The Netter Collection of Medical Illustrations VOLUME 7 PART l

Plate 13-11 Brain: PART I

Other Cranial Neuralgias Cutaneous head and neck nerves Auricular branch
of vagus nerve (X)
GLOSSOPHARYNGEAL NEURALGIA From ophthalmic division
Glossopharyngeal neuralgia is estimated to be 70 times of trigeminal nerve (V1) Medial branches
less common than trigeminal neuralgia. This is a severe, Supraorbital nerve of dorsal rami
paroxysmal, lancinating pain within the glossopharyn- Supratrochlear nerve of cervical spinal
geal nerve distribution, usually deep in the throat, nerves
behind the tongue, and/or the ear. Characteristic trig- Palpebral branch of
gers include swallowing, coughing, chewing, swallow- lacrimal nerve Greater occipital
ing cold drinks, or touching the preauricular area. Infratrochlear nerve nerve (C2)
During these painful paroxysms, some patients may External nasal branch of 3rd occipital
experience an associated bradycardia and/or asystole, anterior ethmoidal nerve nerve (C3)
which may result in syncope. Eight to 10 percent of From 4th, 5th,
patients will have concurrent trigeminal neuralgia. From maxillary division 6th, and 7th
of trigeminal nerve (V2) nerves in
Magnetic resonance imaging (MRI), with special Infraorbital nerve succession
attention to this nerve, is indicated to rule out second- Zygomaticofacial nerve below
ary causes, including aberrant blood vessels, multiple Zygomaticotemporal nerve
sclerosis, or various mass lesions. Medical therapies are Branches from
similar to those for trigeminal neuralgia. Spontaneous From mandibular division cervical plexus
remissions also occur. Medically refractory individuals of trigeminal nerve (V3) Lesser occipital
may require microvascular decompression or an abla- Mental nerve nerve (C2)
tive procedure, including a rhizotomy. In most cases, a Buccal nerve Great auricular
rhizotomy with surgical division of the glossopharyn- Auriculotemporal nerve nerve (C2, 3)
geal nerve and the upper rootlets of the vagus nerve Transverse cervical
provide relief. Glossopharyngeal neuralgia nerve (C2, 3)
Supraclavicular
OCCIPITAL NEURALGIA nerves (C3, 4)
This is a paroxysmal, lancinating pain within the distri-
bution of the greater, lesser, and/or third occipital nerve, Medial surface of
often starting at the upper neck or base of the skull and tympanic membrane
radiating to the back of the head. The stabbing, electric and eustacian tube
shocklike pain may be provoked by exposure to cold,
light touch (i.e., brushing one’s hair, or head and neck Glossopharyngeal
movement). Neurologic examination may demonstrate nerve (IX)
local nerve tenderness and percussion (Tinel sign) and
may elicit painful paroxysms or paresthesias along the Posterior 1/3 of tongue,
affected nerve’s cutaneous distribution.
Glossopharyngeal posterior pharynx, tonsils,
The occipital nerve is derived from the second cervi- neuralgia can cause severe carotid body and carotid sinus
cal (C2) root, and therefore pain from C2 will manifest
in a similar distribution. Similarly, skull base and upper stabbing pain in the throat, back
cervical joint pathology may refer pain to the upper
neck and posterior head. A cranial and/or cervical of tongue, tonsils, neck, or deep in
spine MRI focusing on the craniocervical junction is
recommended. the ear on one side. Pain lasts seconds

An occipital nerve block with local anesthetic and to minutes, and may occur spontaneously or be triggered by maneuvers such as swallowing, talking, coughing, or
glucocorticoids mixture is often the treatment of choice
because this can be both therapeutically and diagnosti- clearing the throat. Some patients may have severe bradycardia or asystole with episodes of pain.
cally useful. After a block, the pain should ease tempo-
rarily, sometimes for weeks or months. Pain relief may It is important to inquire about neuropathic in con- â•…
be accompanied by temporary diminished sensation or trast to neuralgic symptoms. Persistent pain or sensory
dysesthesias within the occipital nerve distribution. dysfunction, that is, paresthesias, hypoesthesia, or with a smoking history who report new unilateral facial
Relief with an occipital block should be interpreted allodynia, suggest neuropathy with underlying nerve pain or when weight loss or persistent cough is present.
with caution because other primary headache syn- damage. If a magnetic resonance image (MRI) is A chest x-ray or CT scan of the chest may be diagnostic.
dromes, such as migraine and cluster, are also reported normal, evaluation for connective tissue disease and
to respond to greater occipital nerve blockade. other inflammatory etiologies should be undertaken. Isolated mental or inferior alveolar nerve neuropa-
thies occur in patients with various metastatic cancers,
LESS COMMON CRANIAL NEURALGIAS Two other situations deserve special mention. Persis- including hematologic malignancies as well as lung,
Neuralgic-type pain may arise from any nerve or nerve tent unilateral facial pain may rarely be the presenting breast, prostate, and kidney cancers. Patients present
branch within the head or neck. This includes other symptom of lung cancer and is speculated to be due to with numbness of the chin, lower lip or the gingiva of
nerves derived from the cervical plexus, such as the referred pain from compression or invasion of the vagus the lower teeth, with or without associated pain. This
great auricular nerve, as well as terminal branches of nerve. Lung malignancy must be suspected in patients “numb chin syndrome” is usually the consequence of
the trigeminal nerve, for instance, supraorbital or infra- bone metastases or leptomeningeal seeding, but it may
orbital nerves. Neuralgia may develop spontaneously or manifest without obvious cause.
subsequent to nerve trauma. The great auricular nerve,
carrying lower-ear and jaw-line sensation, may be
damaged during parotidectomy, rhytidectomy (face-
lift), or carotid endarterectomy.

328 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 13-12 Headache

Idiopathic Intracranial
Hypertension (IIH),
Pseudotumor Cerebri

Idiopathic intracranial hypertension (IIH), previously Obese young
called pseudotumor cerebri, is a disorder of elevated woman: persistent
intracranial pressure of unknown cause. It most often headache
occurs in obese women of childbearing age. Patients
commonly describe daily headaches, often severe and Normal optic disc on funduscopic exam
progressive, that may worsen with cough or strain,
often accompanied by nausea. The headaches may Important to exclude mimics Papilledema
awaken the patient from sleep. Papilledema is a diag- of idiopathic intracranial Concentrically contracted visual fields, large blind spots
nostic hallmark, and may be associated with blurred hypertension (IIH), such as,
vision, enlarged blind spots, or visual-field defects. sinus thrombosis,
Additional symptoms include transient visual obscura- hypervitaminosis A; use
tions (blurring or loss of vision lasting seconds) or pho- of steroids, tetracycline,
topsia (brief sparkles or flashes of light) in one or both or nalidixic acid; chronic
eyes, often provoked by positional changes and Valsalva otitis media with dural sinus
maneuver. Horizontal diplopia due to unilateral or occlusion; endocrinopathy
bilateral sixth nerve palsies may be present. Pulse- Addison or Cushing disease,
synchronous tinnitus, described as a “whooshing sound” hypoparathyroidism
like pulsating running water or wind, is common and is
thought to represent vascular pulsations transmitted by Cerebrospinal fluid pressure elevated â•…
cerebrospinal fluid under high pressure to the venous fields help guide treatment. The therapeutic goals are
sinuses. symptomatic relief by analgesia and reduction of CSF inhibiting choroid plexus CSF secretion. It also may
pressure. Weight reduction is very important in the decrease appetite leading to weight loss.
Diagnostic criteria include demonstrating elevated management of overweight patients with IIH. If the
intracranial pressure by lumbar puncture, with an patient has no visual loss and mild-to-moderate head- Patients with visual loss require urgent treatment
opening pressure greater than 200╯mm H2O in the non- ache, weight loss and pain management may be all with corticosteroids to rapidly decrease intracranial
obese and greater than 250╯mm H2O in the obese. that is necessary. If the patient is taking medicines that pressure. However, because of their many potential
Lumbar puncture needs to be performed in the lateral exacerbate intracranial hypertension, these should be side effects (weight gain, fluid retention, and rebound
decubitus position with legs extended and with the discontinued. increased intracranial pressure on withdrawal of use),
patient relaxed. Falsely elevated pressures may occur in corticosteroids are not suitable for long-term care.
a sitting or prone position, or with anxiety. Cerebrospi- Acetazolamide is the most commonly used medical
nal fluid (CSF) composition is normal. Neuroimaging therapy for IIH. It is a carbonic anhydrase inhibitor and Medically intractable IIH can be treated with surgical
studies tend to be unremarkable, although magnetic is thought to influence intracranial hypertension by procedures, such as optic nerve sheath fenestration or
resonance imaging (MRI) may show findings of intra- CSF shunting. Surgery is primarily indicated for visual
cranial hypertension, including dilated optic nerve loss or worsening vision due to papilledema.
sheaths and an empty sella turcica. Diagnosis may
require examination by an ophthalmologist because
early or mild papilledema can be difficult to detect.
Dilated funduscopic exam also helps differentiate true
papilledema from pseudopapilledema secondary to
optic disc drusen, tilted optic discs, or other mimickers.
Photographs of the optic disc can serve as a baseline for
serial monitoring. Formal visual perimetry should be
performed. The most common finding is an enlarged
blind spot; arcuate defects, inferonasal visual loss, or
generalized visual field constriction may also be seen.

As IIH is by definition idiopathic, secondary causes
of intracranial hypertension must be excluded: (1) mass
lesions (i.e., intracranial tumor or abscess), (2) decreased
CSF absorption via arachnoid granulations (e.g., adhe-
sions after meningitis or subarachnoid hemorrhage),
(3) increased CSF production (e.g., choroid plexus
papilloma), and (4) venous outflow obstruction (e.g.,
cerebral venous sinus thrombosis). Because venous
sinus thrombosis may mimic IIH, imaging of cerebral
veins with magnetic resonance venography (MRV) is
indicated with the standard MRI. Secondary intracra-
nial hypertension also occurs with various metabolic,
toxic, and hormonal disturbances, including imbalances
in growth hormone, thyroid hormone, or aldosterone,
and medications, including tetracycline, vitamin A,
lithium, amiodarone, and corticosteroids (especially on
withdrawal).

Permanent visual loss is the major morbidity associ-
ated with IIH, and management strategies depend on
the degree and progression of papilledema. Serial pho-
tographs of the optic disc and serial testing of visual

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 329

Plate 13-13 Brain: PART I

Headache is orthostatic, worse in an upright
position; often aggravated by exertion, bending
over, or Valsalva maneuver

Intracranial Hypotension/ Hearing may seem muffled or
Low Cerebrospinal Fluid– exaggerated; may have
pressure Headache associated pulsatile tinnitus

Orthostatic headache, a headache occurring in an Head pain dramatically improves in a recumbent position
upright position and relieved in a recumbent position,
is the hallmark of a low cerebrospinal fluid (CSF)– Sagittal MRI (left) with descent of cerebellar tonsils, crowding of the
pressure headache. Typically bilateral, these headaches
may be throbbing or constant and are often aggravated posterior fossa, and reduction of pre-pontine space. Coronal MRI with
by exertion, bending over, or Valsalva maneuvers. They gadolinium (right) demonstrates diffuse pachymeningeal enhancement.
may be accompanied by a variety of symptoms, includ-
ing neck pain or stiffness, nausea, and photophobia. â•…
Associated hearing changes, such as “muffled hearing,”
tinnitus, or hyperacusis, are often present. Dizziness, normal-to-low (<60╯mm H2O) opening pressure and show fluid collections outside the arachnoid space,
visual blurring, diplopia (from sixth nerve palsy), radic- normal-to-high CSF protein. Mild pleocytosis (WBC engorgement of the epidural venous plexus, or menin-
ular arm symptoms, and, rarely, facial numbness may 10-50) may also occur. geal diverticula. The presence of a meningeal diverticu-
also occur. The headaches may be daily (often late in lum does not, of course, guarantee that it is the site of
the day) or intermittent. They may also present in an Most headaches due to low CSF pressure are self- CSF leak. The most reliable method for detecting the
acute thunderclap presentation, mimicking subarach- limited. Conservative measures, such as bed rest, caf- actual site of the leak is to identify extravasation of CSF
noid hemorrhage. feine, and increased fluid intake, are advocated as into the paraspinal soft tissues, which is best seen on a
first-line treatments. A persistent headache may require computed tomography (CT) myelogram. When more
The low CSF pressure or volume may relate to an epidural blood patch. If the site of the leak is known, conservative measures fail, surgical intervention may be
hypovolemia, overshunting of CSF, or a CSF leak. the blood patch can be relatively targeted toward this considered.
When the patient is upright, there is traction on the site. In spontaneous CSF leaks, MRI of the spine might
anchoring pain-sensitive structures of the brain, with
brain descent or “sagging” in its cranial vault. Symp-
toms localizing to the cranial nerves and brainstem are
thought to be due to traction or compression of these
structures, although the hearing changes may relate to
alteration of pressure in the perilymphatic system of the
inner ear. CSF leaks may occur after any trauma to the
meninges, including a lumbar puncture, an epidural
injection, or spinal surgery. They may also occur spon-
taneously through weak meningeal diverticula or weak
dura, as can be seen in connective tissue disorders.
When the CSF leak is identified, it is most often at the
level of the spinal cord, but rarely, intracranial leaks
may occur through defects in the cribriform plate or
sinuses. These patients may have clear nasal drainage,
indicative of CSF rhinorrhea.

Patients with an orthostatic headache should be eval-
uated with a magnetic resonance image (MRI) of the
brain with contrast, looking for diffuse pachymeningeal
enhancement, descent of the cerebellar tonsils (mimick-
ing a Chiari I malformation), crowding of the posterior
fossa, decreased ventricle size, descent of the optic
chiasm, reduction of the prepontine space, pituitary
enlargement, engorgement of cerebral venous sinuses,
and subdural fluid collections. A normal MRI brain
does not rule out low CSF pressure headache and may
be normal in up to one third of cases. If the clinical
history is suggestive, other testing may be useful to
identify the presence of a CSF leak. A radioisotope
cisternogram involves injecting a radionuclide into the
CSF and monitoring how fast it ascends and diffuses
around the brain. A CSF leak can be demonstrated
directly by radiotracer accumulation in the extra-
arachnoid space or indirectly by a delay in radiotracer
ascent to the cerebral convexities. If CSF rhinorrhea
is suspected, nasal pledgets are placed with the cister-
nogram to determine if there is radioactivity in the
nasal secretions. Beta-2 transferrin, which is present in
CSF, may be detected in CSF rhinorrhea. Lumbar
puncture may not be necessary for the diagnosis of low-
pressure headache. When performed, this may show a

330 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 13-14 Headache

Pain on chewing Temporal cephalalgia,
Loss of weight, scalp tenderness
weakness Visual disturbances
Blindness may
Giant Cell Arteritis develop rapidly
Low-grade fever,
Giant cell arteritis (GCA), also known as temporal arte- malaise
ritis, is a generalized vasculitis affecting large- and
medium-sized vessels. This arteritis involves the aorta Symmetric pain
and its extracranial vessels, including the external and stiffness of
carotid artery with its superior temporal division and, shoulder and hip
less commonly, the occipital scalp artery. Unlike other girdle muscles
forms of vasculitis, GCA rarely involves the skin,
kidneys, and lungs. Anterior ischemic optic neuropathy

Signs and symptoms of GCA may begin quite Elevated
abruptly or sometimes gradually over a number of sedimentation
months before becoming clinically recognizable. Its rate
classic symptoms relate to the inflammation of, and
reduced blood flow through, the involved arteries. Most Rigid, tender, nonpulsating temporal Biopsy specimen of superficial temporal artery: almost
patients present with bilateral headache, often com- arteries may be visible or palpable total obliteration of lumen with some recanalization.
plaining of scalp pain with normally non-noxious High-power insert shows infiltration with lymphocytes,
stimuli, such as brushing their hair. Transient visual plasma cells, and giant cells; fragmentation of internal
loss, or even permanent visual loss, may result from elastic lamina.
involvement of the posterior ciliary, ophthalmic, and
retinal arteries. Painful cramping or claudication often â•…
occurs with the use of the jaw while chewing or on
movement of the tongue. Many patients have associated scalp artery, a magnetic resonance angiogram, duplex system, or even a myocardial infarction. Involvement of
systemic symptoms, such as fever, malaise, sweating, ultrasonography, or a positron emission tomography the aorta very rarely may lead to aortic dissection or
and weight loss. Examination may reveal that the tem- (PET) scan. aneurysm. Prompt treatment with corticosteroids is
poral and occipital vessels are firm, tender, and pulsel- required to prevent permanent sequelae, especially
ess. Sausage-shaped thickenings or nodularity may be When unrecognized and untreated, GCA can lead to visual loss. Headache and systemic symptoms usually
palpable along the vessel wall. a variety of complications. The most devastating is improve within 48 hours of starting treatment, but
sudden permanent unilateral or sequential bilateral visual loss and ischemic complications are often irre-
The incidence of GCA increases with advancing age vision loss from anterior ischemic optic neuropathy versible. Biopsy should be obtained within 24 hours of
and must be considered in all patients older than 50 (AION) or retinal artery occlusion, cerebrovascular starting steroids.
years who develop a new headache, have a change in ischemia—more commonly in the vertebral basilar
their previous headache characteristics, or have acute-
onset transient visual loss. Polymyalgia rheumatica
(PMR) is an overlapping disease, and symptoms of
PMR are found in more than one third of biopsy-
proven cases of GCA. These PMR symptoms include
neck pain, morning stiffness, and myalgias in shoulder
and pelvic muscles.

Erythrocyte sedimentation rate (ESR) and C-reactive
protein (CRP) are nonspecific markers of inflammation
that, when elevated—often to very high levels (60 to
120╯mm/hr for ESR and greater than 40 for CRP)—are
supportive of the diagnosis of GCA. Sedimentation
rate is reported to be normal in about 5% of patients
with GCA. Normochromic anemia, low albumin, and
thrombocytosis are often present.

Diagnosis can only be established with certainty by
biopsy of the temporal artery and demonstration of
focal inflammation, giant cells, and interruption of the
internal elastic lamina. Of importance, none of the
testing options have a sensitivity of 100%. Because
vessel involvement can be segmental, the biopsy may
also be falsely negative. If the biopsy is negative but the
clinical suspicion remains high, such as in an elderly
patient with a new headache and jaw claudication or
systemic symptoms, other tests should be performed,
looking for signs of vessel inflammation. These would
include another site for artery biopsy, such as the
contralateral temporal artery or posterior occipital

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 331

P late 13-15 Brain: PART I

Contiguous Structure Sinusitis
Headaches
Nasal cavities
SINUS HEADACHE Ethmoid air cells
Most patients presenting with “sinus headache” actually Lens of eye
have migraine. This misdiagnosis may arise based on Greater wing
the location of pain and may be even more tricky if the of sphenoid
patient’s migraine is triggered by weather changes or if
it is associated with parasympathetic symptoms, such as Optic Axial CT showing opacification with
nasal congestion, lacrimation, or rhinorrhea. When nerve (II) fluid of the right sphenoid sinus
inflammation of the sinuses is the source of headache, Temporal
it is almost always accompanied by facial tenderness and lobe
pain, nasal congestion, or nasal discharge. Inflamma- of brain
tion of the sinuses is called sinusitis, or rhinosinusitis
when the nasal passages are also affected. Sphenoid sinuses

Patients perceive maxillary sinus pain in the cheek, Temporomandibular disorder
gums, and upper teeth. Frontal sinus pain tends to
involve the forehead, while ethmoid sinusitis causes Jaws closed Articular tubercle
pain behind or between the eyes. Sphenoid sinusitis is Mandibular fossa
characterized by pain in variable locations, including
the frontal, occipital, temporal, or vertex locations. Articular
disk
Symptoms lasting fewer than 7 days tend to be viral Joint capsule
in origin. In contrast, acute bacterial rhinosinusitis
presents with more than 7 days of purulent rhinorrhea, Open position Anterior dislocation
nasal congestion, facial or dental pain/pressure, an
accompanying cough, halitosis, and, if severe, fever Dental disease Glaucoma-Primary closed angle
(50% of adults). Fungal sinusitis may be acute or Fixed, mid-dilated pupil
chronic (lasting more than 12 weeks) and is of par-
ticular concern in patients who are immunocomÂ

P late 13-16 Headache

Headache CAUSES OF THUNDERCLAP HEADACHE Diagnosis/Testing
Typical Presentation

Subarachnoid Sudden and severe HA ϩ/Ϫ N/V; may CT w/o contrast; LP for xanthochromia
hemorrhage have ophthalmoplegia or altered
mentation

Intracranial Sudden and severe HA; focal neurologic CT w/o contrast
hemorrhage signs; seizures; altered; mentation

Cerebral venous May mimic Idiopathic intracranial Examine for papilledema; MRV;
sinus thrombosis hypertension CT w/contrast for empty delta sign

Arterial dissection Sudden unilateral HA ϩ/Ϫ neck pain; Examine for Horner sign; MRI/MRA
may be posttraumatic; may mimic head and neck (CTA or carotid U/S
migraine if MRI not available)

Reversible cerebral Recurrent thunderclap HA; photophobia Cerebral angiogram is the gold standard:
vasoconstriction or nausea possible however, can start with MRA or CTA
syndrome

Ischemic stroke New neurologic deficits, in specific MRI w/DWI: Large or subacute/chronic;
vascular distribution may show on CT
Secondary
Thunderclap Headache and Pituitary apoplexy HA; visual changes ϩ/Ϫ altered mentation CT or MRI (MRI more sensitive)
Other Headache Presenting
in the Emergency Department Third ventricular Recurrent severe headaches, sometimes CT w/ contrast or MRI
colloid cyst with relieved with recumbency
Most patients who seek care in an emergency depart- hydrocephalus
ment have a primary headache disorder. Nevertheless,
an emergency medicine physician must evaluate for the Spontaneous intra- Postural HA, worse upright ϩ/Ϫ MRI with gadolinium; in some cases
possibility of an underlying, secondary cause for the cranial hypotension symptoms of low CSF pressure cisternogram, CT myelogram
pain. New headaches beginning during vigorous exer- occasionally
tion or after head/neck trauma require consideration of
an intracranial hemorrhage or cervicocephalic arterial Posterior reversible HA with vision changes, seizures or CT or MRI (MRI more sensitive)
dissection. Most concerning are those patients present- leukoencephalopathy altered mentation; marked hypertension
ing with an explosive, debilitating, or “thunderclap” head- (PRES) on occasion
ache often referred to as the “worst headache of my life”
or “I felt like I was hit with a sledge hammer.” Because of Intracranial infection Fever, chills, meningismus, leukocytosis Lumbar puncture for CSF, glucose,
the urgency of diagnosis, every individual experiencing (e.g., bacterial protein, and cells; MRI may show
these symptoms must initially be investigated for a sub- meningitis) meningeal enhancement. CT before
arachnoid or intracranial hemorrhage. If either type lumbar puncture if concern for mass
hemorrhage is ruled out, other pathologic mechanisms effect
for an acute severe headache require consideration (see
table at right). Glaucoma Ipsilateral HA with slowly responsive Ophthalmology consult
mid-dilated pupil
Equally important is the patient presenting with an
acute headache and new-associated neurologic symp- Primary sexual or Sudden onset before, during, or right after Diagnosis of exclusion especially if this
toms, particularly focal motor or sensory loss, language exertional HA orgasm or peak of exertion. is the first episode. Consider MRI/MRA
dysfunction, or encephalopathic symptomatology, such to rule out aneurysm with SAH
as confusion or seizures. Other historical details in the
acute headache patient also cause significant concern Primary Primary cough HA Sudden onset with cough or strain, Diagnosis of exclusion
warranting further and immediate evaluation. These 1 second to 30 minute duration
include older age, immunocompromise, recent infec-
tion or fever, history of cancer, clotting or bleeding Primary thunderclap Max intensity in Ͻ 1 minute; lasts 1 hour Diagnosis of exclusion
disorders (particularly including therapeutic anticoagu- HA to 10 days
lation), progressively worsening headache severity, or
symptoms of systemic illness, that is, weight loss, DWI, Diffusion-weighted imaging, HA, headache, N/V, nausea/vomiting.
fatigue, myalgia, or unexplained anemia.
â•…
Any patient whose clinical presentation with head-
ache includes fever, alteration in consciousness or men- SUBARACHNOID AND INTRAPARENCHYMAL patient, especially if there is associated neck pain or
tation, or an overall toxic appearance requires an urgent HEMORRHAGE stiffness, needs to lead the clinician to question the
evaluation for a possible underlying infection. Nuchal possibility of SAH. Intraparenchymal hemorrhage is
rigidity usually indicates meningeal irritation, which Although the classic thunderclap presentation typically more likely to cause relatively rapid evolution of focal
can be seen with either subarachnoid hemorrhage or heralding the rupture of an intracerebral aneurysm with neurologic symptoms as well as seizures and altered
meningitis. Papilledema reflects increased intracranial subarachnoid hemorrhage (SAH) is not easily over- mentation, depending on the size and location of the
pressure and warrants further investigation for disor- looked, occasional SAH patients present with more hematoma. If the blood tracks into the cerebrospinal
ders causing mass effect, such as tumor, infection, hem- subtle symptoms. Any headache that is unusual for the fluid (CSF), intraparenchymal hemorrhage may also
orrhage, or idiopathic intracranial hypertension.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 333

Plate 13-17 Brain: PART I

Subarachnoid hemorrhage signs and symptoms

Sudden, severe, Transient or persistent alteration in consciousness
explosive headache ranging from disorientation to deep coma.
Fever, sweating, vomiting
and tachycardia are
frequently present.

Diplopia and/or photo-
phobia also common

Signs of meningeal irritation
Kernig sign: resistance to
full extension of leg at
knee when hip is flexed

Less than 135°

Thunderclap Headache and Intracerebral hemorrhage (hypertensive) Brudzinski sign: flexion of both hips and knees
Other Headache Presenting CT scan showing when neck is passively flexed
in the Emergency Department large putaminal
hemorrhage Moderate-sized
(Continued) intracerebral
hemorrhage involving
cause meningeal irritation and neck stiffness. A history left putamen, with
of anticoagulation, especially in an older patient pre- rupture into lateral
senting with headache is particularly concerning for ventricle; brain
hemorrhage. A computed tomography (CT) scan is distorted to opposite
diagnostic. Information on evaluation and management side; scar of healed
of intracranial hemorrhage is detailed in Section 9. hemorrhage on right
side
REVERSIBLE CEREBRAL VASOCONSTRICTION
SYNDROME Acute hypertensive crisis/posterior Reversible cerebral vasoconstriction syndrome
Reversible cerebral vasoconstriction syndrome is char- reversible encephalopathy syndrome (PRES)
acterized by recurrent thunderclap headaches. Pain
peaks within minutes, last minutes to hours, sometimes MRA shows
more than 1 day, and tends to recur over a few days to irregularity of
2 weeks. Patients may have associated focal neurologic both anterior
deficits, and one third of patients experience seizures. cerebral arter-
Risk factors include hypertension, preeclampsia/ ies that was
eclampsia (i.e., postpartum angiopathy), sympathomi- not present on
metic drugs or serotonergic agents (drug-induced repeat imaging
cerebral vasculopathy), catecholamine-secreting tumors 3 weeks later.
(i.e., pheochromocytoma), and binge alcohol drinking.
â•…
Cerebrospinal fluid is normal or near normal (mild
elevations in protein or white blood cells). MRI and CT ACUTE HYPERTENSIVE CRISIS/POSTERIOR be associated with hypertensive encephalopathy or
may be normal, may show features similar to posterior REVERSIBLE ENCEPHALOPATHY malignant hypertension with retinal hemorrhages/
reversible encephalopathy syndrome (PRES), or may SYNDROME (PRES) exudates, papilledema, intracranial hemorrhage, or
show evidence of intracranial hemorrhage, especially other organ damage, including pulmonary edema or
cortical subarachnoid hemorrhage. The diagnostic gold Patients with hypertensive crisis may present with acute malignant nephrosclerosis. The cause for the hyperten-
standard is conventional angiography demonstrating or subacute posterior headaches sometimes accompa- sion needs to be identified. Immediate commencement
multifocal segmental vasoconstriction subsequently nied by dyspnea, chest pain, lightheadedness, focal neu- of rapidly acting antihypertensive therapies is the
reversible within 12 weeks after onset. However, mag- rologic deficits, and epistaxis. Markedly elevated blood primary treatment; general symptom management is
netic resonance angiography (MRA) and computed pressure (generally greater than 180/120╯mm╯Hg) may also needed for the dyspnea, chest pain, and so forth.
tomography angiography (CTA) are less invasive and
may provide supporting diagnostic evidence. Although
there is no evidence-based study to support a specific
therapy, nimodipine is the treatment most often recom-
mended for the vasospasm.

334 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

P late 13-18 Headache

Cerebral venous sinus thrombosis

Normal MRV Venous
thrombosis

Superior sagittal sinus Sagittal section

Tentorium cerebelli
Great cerebral vein (Galen)

Falx cerebri

Inferior sagittal sinus

Thunderclap Headache and Sphenoparietal sinus Superior sagittal sinus
Other Headache Presenting Anterior and posterior Straight sinus
in the Emergency Department intercavernous sinuses Transverse sinus
Superior petrosal sinus Confluence of sinuses
(Continued) Basilar venous plexus Falx cerebelli
Inferior petrosal sinus Occipital sinus
Posterior reversible leukoencephalopathy, also termed To jugular foramen Sigmoid sinus
posterior reversible encephalopathy syndrome (PRES),
is a syndrome involving vasogenic edema preferentially Pituitary apoplexy MRI showing pituitary tumor apoplexy. Sagittal
affecting the white matter of the posterior brain, includ- Compressed image shows fluid-fluid level within the area of
ing the occipital lobes and cerebellum. On MRI, the optic chiasm recent hemorrhage.
vasogenic edema appears as a relatively symmetric Compressed
increased T2 signal, not conforming to a particular cranial nerve III â•…
vascular distribution. Patients present with headache Hemorrhagic
that may be accompanied by seizures, visual changes, pituitary tumor COLLOID CYST
and altered mentation. This syndrome may be associ- Pituitary gland A colloid cyst is a benign cyst that arises in the anterior
ated with hypertensive encephalopathy, preeclampsia/ third ventricle just posterior to the foramen of Monro.
eclampsia, and certain cytotoxic and immunosuppres- in the setting of a pituitary macroadenoma. Patients Because of its location, it can act as a ball-valve tran-
sant drugs. may present with a sudden and severe headache, siently obstructing the ventricular outflow and causing
ophthalmoplegia, visual disturbance, nausea/vomiting, obstructive hydrocephalus. Patients may present with
CEREBRAL VENOUS THROMBOSIS altered mentation, meningismus, and sometimes fever. intermittent symptoms of increased intracranial pres-
Cerebral venous thrombosis (CVT) most often has a In the emergency room, this may mimic a severe sure, including sudden and severe headaches with
subacute presentation; however, a minority of patients migraine or aseptic meningitis, and in severe cases may
present with thunderclap headache. Headaches are per- cause adrenal crisis, coma, or death. Although pituitary
sistent and tend to be worse in the morning, in a recum- pathology is usually noted on a noncontrast CT scan of
bent position, and with Valsalva maneuvers, such as the head, an MRI is more sensitive.
coughing or straining. Headaches may be accompanied
by other signs of increased intracranial pressure, such
as papilledema, seizures, and altered mentation. If
venous infarction occurs, focal neurologic deficits may
be present. If the venous thrombosis is in the superior
sagittal sinus, a CT scan with contrast may show a
filling defect around the thrombus, called the “empty
delta” sign. However, CT and MRI may be unremark-
able, requiring MR venography for diagnosis. When
diagnosis is established, causative or predisposing con-
ditions need to be identified, including thrombophilic
states or occult malignancy. Patients are generally
treated with anticoagulation.

PITUITARY APOPLEXY
Acute pituitary apoplexy is an uncommon syndrome
due to hemorrhage or infarction of the pituitary gland

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 335

Plate 13-19 Brain: PART I

Colloid cyst

AB

Colloid cyst. (A) Axial, FLAIR and (B) coronal, T1-weighted gadolinium Colloid cyst of 3rd ventricle and surgical
enhanced images demonstrate a round cystic mass in the region of the approach via right prefrontal (silent) cerebral
foramina of Monro, with dilatation of the lateral ventricles. The signal cortex.
characteristics are variable. This cyst is hypointense on T2-weighted
images and bright on T1-weighted imaging, with minimal peripheral
enhancement.

Bacterial meningitis

Thunderclap Headache and Thrombophlebitis of superior sagittal sinus and Inflammation and suppurative process on surface of
Other Headache Presenting suppurative ependymitis, with beginning hydrocephalus leptomeninges of brain and spinal cord
in the Emergency Department
Arterial dissection
(Continued)
Area of Internal carotid Common
nausea/vomiting; these often improve in a recumbent scan Thrombus artery carotid
position. If obstructive hydrocephalus is prolonged, artery Intimal tear allows blood flow to dissect beneath intimal layer,
deterioration with altered mentation, seizures, coma, detaching it from arterial wall. Large dissection may occlude
and death may occur. Diagnosis is made by CT or MRI, vessel lumen
and early surgical intervention is necessary for symp-
tomatic colloid cysts. Detached intima

POST-TRAUMATIC HEADACHE Carotid dissection: Ultrasound of the carotid artery with clot
Most headaches after trauma are of the benign tension- formed between layers of the artery (near the upper right internal
type. However, a history of trauma should alert the carotid artery [RICA] label)
physician to the possibility of hemorrhage, especially in
the setting of anticoagulation. This includes subarach- â•…
noid and intraparenchymal hemorrhage as mentioned
above, as well as subdural or epidural hematoma (see INTRACRANIAL INFECTION papilledema, or altered mentation must have a CT or
Section 14). Subdural hematomas may manifest insidi- Meningitis or meningoencephalitis must be suspected MRI before lumbar puncture, to exclude a brain abscess
ously with headache, decreased level of consciousness, in any patient with new headache accompanied by with associated mass effect. In a patient with a new
balance or gait difficulty, cognitive impairment or neck stiffness or fever, nausea/vomiting, and photoÂ

SECTION 14â•…

HEAD TRAUMA

P late 14-1 Brain: PART I

SKULL: ANTERIOR VIEW

Frontal bone Coronal suture
Glabella
Supraorbital Parietal bone
notch (foramen) Nasion
Sphenoidal bone
Orbital surface
Lesser wing

Nasal bone Greater wing

Skull: Anterior and Lacrimal bone Temporal bone
Lateral Aspects
Zygomatic bone Ethmoidal bone
The anterior, or facial, aspect of the skull is composed Frontal process Orbital plate
of the frontal part of the calvaria (skullcap) above and Orbital surface Perpendicular plate
the facial bones below. The facial contours and propor­ Temporal process Middle nasal concha
tions are largely determined by the underlying bones, Zygomaticofacial
and it is a commonplace observation that they show foramen Inferior nasal concha
considerable variations associated with age, sex, and Vomer
race. The outer surface of the frontal bone underlies Maxilla Mandible
the brow. The facial skeleton is irregular, a feature Zygomatic process
accentuated by the presence of the orbital openings, the Orbital surface Ramus
piriform aperture, and the superior and inferior dental Infraorbital foramen Body
arches of the oral cavity. Frontal process Mental foramen
Alveolar process Mental tubercle
The convex anterior surface of the frontal bone is Anterior nasal spine Mental protuberance
relatively smooth, but there are frontal tuberosities, or
elevations, on each side. In early life, a median suture Orbital surface Right orbit: frontal and slightly lateral view Supraorbital notch
separates the two halves of the developing bone. This of frontal bone â•… Posterior and
suture normally fuses between ages 6 and 10 years but Orbital surface of lesser Anterior
occasionally persists as the metopic suture. The two wing of sphenoid bone ethmoidal foramina
orbital openings are roughly quadrangular and have Superior orbital fissure Orbital plate of
supraorbital, infraorbital, medial, and lateral borders. Optic canal (foramen) ethmoidal bone
The supraorbital notch, or fissure, carries the corre­ Orbital surface of greater Lacrimal bone
sponding nerve and vessels. The infraorbital foramen, wing of sphenoid bone Fossa for lacrimal sac
located about 1╯cm below the infraorbital margin, Orbital surface of Orbital process of
transmits the nerve and vessels of the same name. The zygomatic bone palatine bone
orbits are somewhat pyramidal in shape, with the quad­ Zygomaticofacial foramen Orbital surface
rangular openings, or bases, directed forward and Inferior orbital fissure of maxilla
slightly outward, whereas the apexes correspond to the Infraorbital groove Infraorbital foramen
medial ends of the superior orbital fissures.
The lateral wall and roof are continuous anteriorly The lateral wall and floor of the orbit are also con­
The superior wall (roof) separates the orbital contents but diverge posteriorly to bound the superior orbital tinuous anteriorly but are separated posteriorly by the
from the brain and meninges in the anterior cranial fissure, which lies between the greater and lesser wings inferior orbital fissure, most of which is located between
fossa. Anteromedially, it is hollowed out by a variably of the sphenoid bone and opens into the middle cranial the greater wing of the sphenoid bone and the orbital
sized frontal sinus, and anterolaterally, there is a shallow fossa. The fissure transmits the oculomotor (III) and surface of the maxilla. The inferior orbital fissure con­
lacrimal fossa for the orbital part of the lacrimal gland. trochlear (IV) nerves, the lacrimal, frontal and nasocili­ nects the orbit with the pterygopalatine and infra­
Posteriorly, the optic canal (foramen) lies between the ary branches of the ophthalmic nerve, the abducens temporal fossae. The maxillary nerve passes from the
two roots of the lesser wing of the sphenoid bone, just (VI) nerve, the ophthalmic veins, and small meningeal pterygopalatine fossa into the orbit through the inferior
above the medial end of the superior orbital fissure; it vessels. orbital fissure and continues forward as the infraorbital
transmits the optic (II) nerve and ophthalmic artery.

The inferior wall (floor) is formed mainly by the
orbital surface of the maxilla, which separates the orbit
from the maxillary sinus (antrum). A groove for the
infraorbital nerve and vessels ends in the infraorbital
foramen.

The thin medial wall separates the orbit from the
ethmoidal air cells, the anterior part of the sphenoidal
sinus, and the nasal cavity. At its anterior end, the lac­
rimal fossa is continuous below with the short nasolac­
rimal canal that opens into the inferior nasal meatus.
The thicker lateral wall separates the orbit from the
temporal fossa anteriorly and from the middle cranial
fossa posteriorly. The orbital surface of the zygomatic
bone shows a foramen for the zygomatic nerve, which
bifurcates within the bone to emerge on the cheek and
temporal fossa as the zygomaticofacial and zygomatico­
temporal nerves, respectively.

338 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 14-2 Head Trauma

SKULL: LATERAL VIEW

Sphenoidal bone Parietal bone Temporal fossa Temporal bone
Greater wing Superior temporal line
Coronal suture Inferior Squamous part
Frontal bone Pterion temporal line Zygomatic process
Supraorbital Articular tubercle
notch (foramen) Groove for pos-
terior deep tem-
Glabella poral artery
Supramastoid crest
Ethmoidal bone
Skull: Anterior and Lateral Orbital plate External acoustic
Aspects (Continued) meatus
Lacrimal bone Mastoid process
nerve. Anastomotic channels between the orbital and Fossa for Lambdoid suture
pterygoid venous plexuses, and orbital fascicles from lacrimal sac
the pterygopalatine ganglion, also traverse this fissure. Occipital bone
Nasal bone
The anterior nasal (piriform) aperture is bounded by Sutural
the nasal and maxillary bones. The nasal bones articu­ Maxilla (wormian)
late with each other in the midline, with the frontal Frontal process bone
bone above and with the frontal processes of the maxil­
lae behind. The irregular lower borders of the nasal Infraorbital External
bones give attachment to the lateral nasal cartilages. foramen occipital
Anterior protuberance
The lower face is supported by both the maxillary nasal spine (inion)
alveolar processes and the mandible. The inferior Alveolar process
margin of each maxilla projects downward as the curved Mandible Asterion
alveolar process, which unites in front with its fellow to Zygomatic bone
form the U-shaped alveolar arch containing the sockets Zygomaticofacial Head of condylar process
for the upper teeth. The roots of the teeth produce foramen Mandibular notch
slight surface elevations, the most obvious of which are Coronoid process
produced by the canine teeth. The upper border of the Temporal process Ramus
body of the mandible is called the alveolar part and Zygomatic arch Oblique line
contains sockets for the lower teeth, whose roots also Body
produce slight surface elevations. Mental foramen

Viewed from the side, the skull is divided into the Infratemporal fossa exposed Sphenoidal bone
larger ovoid braincase and the smaller facial skeleton. by removal of zygomatic Greater wing
The two are connected by the zygomatic bone, which arch and mandible* Infratemporal crest
acts as a yoke (zygon) between the temporal, sphenoid Pterygomaxillary fissure Lateral plate of
(greater wing) and frontal bones, and the maxilla. Other Inferior orbital fissure pterygoid process
features on the lateral aspect of the skull include parts Infratemporal surface of maxilla
of the sutures between the frontal, parietal, sphenoid, Alveolar foramina Pterygoid hamulus
and temporal bones (which form most of the braincase), Tuberosity of maxilla (of medial plate of
and the sutures between such facial bones as the nasal, pterygoid process)
lacrimal, ethmoid, and maxilla. Clearly seen are the *Superficially, mastoid process forms posterior boundary.
parts of the mandible and the temporomandibular joint, â•… Foramen Temporal bone
the external acoustic meatus and the various foramina ovale
that transmit nerves and vessels of the same name. Not External acoustic
readily visible are the foramen ovale and the foramen meatus
spinosum. Mandibular fossa

Certain features deserve particular mention. The Pterygopalatine fossa Articular tubercle
curved superior and inferior temporal lines arch upward Styloid process
and backward over the frontal bone from the vicinity of
the frontozygomatic suture, pass over the coronal Sphenopalatine foramen
suture and the parietal bone, and then turn downward
and forward across the temporal squama to end above bone may extend forward to articulate directly with the The infratemporal fossa is an irregular space lying
the mastoid process. The superior and inferior tempo­ frontal bone, thus excluding the sphenoid. This area is below the infratemporal crest. It is continuous above
ral lines provide attachments, respectively, for the the pterion, and its internal surface is deeply grooved by with the temporal fossa through the gap between the
temporal fascia and the upper margin of the temporal the anterior branches of the middle meningeal vessels. crest and the zygomatic arch. It is bounded medially
muscle, which occupies most of the temporal fossa. This It is situated about 3.5╯cm behind the frontozygomatic by the lateral plate of the pterygoid process and the
fossa is bounded above by the superior temporal line, suture (usually palpable as a slight ridge) and 4╯cm infratemporal surface of the maxilla, and laterally, by
and below it is bounded by the infratemporal crest, above the zygomatic arch. As the most common site of the ramus of the mandible. It communicates through
separating the greater wing of the sphenoid bone from damage to these vessels from a skull fracture, it is a the pterygomaxillary fissure with the pterygopalatine
the pterygoid processes. The anteroinferior corner of surgical landmark. fossa.
the parietal bone usually fills the angle between the
greater wing of the sphenoid and the frontal bone,
although sometimes the squamous part of the temporal

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 339

P late 14-3 Brain: PART I

Skull: Midsagittal Section Sphenoidal bone Parietal bone Temporal bone
Greater wing Coronal suture Squamous part
The rigid braincase is formed by the bones of the cal­ Lesser wing Petrous part
varia (see Plate 14-4) and the base of the skull (see Plate Anterior clinoid Grooves for Internal acoustic meatus
14-5), which is divided into anterior, middle, and pos­ process branches of middle Groove for superior
terior cranial fossae (see Plates 14-6 and 14-7). These Optic canal meningeal vessels petrosal sinus
divisions are less visible on a sagittal section of the skull. Sella turcica Opening of
Body Palatine bone vestibular aqueduct
The occipital bone bounds most of the posterior cranial Sphenoidal sinus Vomer (bony nasal septum) Groove for
fossa. It is pierced by the foramen magnum, through Medial and lateral sigmoid sinus
which the medulla oblongata and spinal cord, sur­ plates of
rounded by their meninges, become continuous; it also pterygoid Lambdoid suture
transmits the vertebral arteries, a few small veins, the process
spinal roots of the accessory (XI) nerves, and the recur­ Occipital bone
rent meningeal branches from the upper spinal nerves. Frontal bone
The occipital condyle articulates with the homolateral Frontal sinus Groove for
superior atlantoarticular process. The hypoglossal (XII) transverse sinus
nerve passes through the corresponding canal. The Ethmoidal bone External occipital
jugular foramen lodges the superior bulb of the internal Crista galli protuberance
jugular vein (in which the sigmoid and inferior petrosal Cribriform plate (inion)
sinuses end); the glossopharyngeal (IX), vagus (X), and Perpendicular Jugular foramen
accessory nerves pass through it anteromedial to the plate (bony Groove for inferior
bulb, and it provides an entry for the recurrent menin­ nasal petrosal sinus
geal branches of the vagus and small meningeal branches septum) Hypoglossal canal
of the ascending pharyngeal and occipital arteries. The
basilar part of the occipital bone unites with the body Nasal bone Foramen magnum
of the sphenoid to form a sloping platform anterior to Inferior nasal Occipital condyle
the pons and medulla oblongata. concha Basilar part

The squamous part of the temporal bone is grooved by Maxilla
the posterior branches of the middle meningeal vessels Anterior
and the sulcus along the superior border of its petrous nasal spine
part is for the superior petrosal sinus. The inferior Nasal surface
petrosal sinus lies in the sulcus between the petrous Incisive canal
temporal and occipital bones. The internal acoustic
meatus is a canal about 1╯cm long, ending in a cribri­ Palatine process
form septum that separates it from the internal ear. It
transmits the facial (VII) nerve and its nervus interme­ Alveolar process
dius, the vestibulocochlear (VIII) nerve, and the inter­
nal auditory (labyrinthine) artery. Frontal bone Opening of sphenoidal sinus

The sphenoid bone has a central body from which two Nasal bone
greater and two lesser wings and two pterygoid pro­
cesses arise. The body contains two air sinuses sepa­ Ethmoidal bone Sphenopalatine foramen
rated by a septum that is often incomplete. Its concave Cribriform plate
upper surface, the sella turcica, houses the pituitary Superior nasal concha Sphenoidal bone
gland. The optic canal transmits the optic (II) nerve and Middle nasal concha
the ophthalmic artery. Lacrimal bone Body

The nasal cavity is roofed over mainly by the cribri­ Inferior nasal concha Medial Plates of pterygoid process
form plate of the ethmoid bone, augmented anteriorly Lateral
by small parts of the frontal and nasal bones, and pos­ Maxilla
teriorly, by the anteroinferior surface of the sphenoidal Nasal surface Pterygoid hamulus
body. Its floor is formed by the palatine processes of the Palatine process
maxillae and by the horizontal plates of the palatine Alveolar process Perpendicular plate Palatine bone
bones. The incisive canal transmits the nasopalatine Horizontal plate
nerves and branches of the greater palatine arteries.
Each lateral wall is formed above by the nasal surface View of lateral nasal wall with nasal septum removed
of the ethmoid bone that covers the ethmoidal labyrinth â•…
and supports thin, shell-like projections, the superior
and middle nasal conchae. These overhang the corre­ pterygoid plate. The maxillary and palatine bones artic­ meatuses. The lower opening of the nasolacrimal duct is
sponding nasal meatuses. Below, each lateral wall is ulate with a separate bone, the inferior nasal concha, near the anterior end of the inferior meatus. The sphe-
formed by the nasal surface of the maxilla, the perpen­ overhanging the inferior nasal meatus. The sphenoidal nopalatine foramen behind the middle concha transmits
dicular plate of the palatine bone and the medial air sinuses open into the nose through the sphenoidal the nasopalatine nerve.
aperture in the sphenoethmoidal recess posterosuperior
to the superior concha. The frontal and maxillary air The nasal cavity is subdivided by a more-or-less ver­
sinuses open into the middle meatus through a semilu- tical septum formed by the perpendicular ethmoidal
nar hiatus, and the multiple air cells forming the eth­ plate and the vomer. The triangular gap between them
moidal labyrinth open into the superior and middle anteriorly is filled in by the nasal septal cartilage (not
shown in the illustration).

340 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 14-4 Head Trauma

Superior view

Frontal bone
Coronal suture
Bregma
Parietal bone
Sagittal suture
Parietal foramen (for emissary vein)
Lambda
Lambdoid suture
Sutural (wormian) bone
Occipital bone

Inferior view

Calvaria Frontal bone
Frontal crest

The calvaria, or skullcap, is the roof of the cranium and of the anterior ends of the lips of the groove for the Groove for superior sagittal sinus
is formed by the frontal, parietal, and occipital bones. superior sagittal sinus. There are other, narrower
It is ovoid in shape and widest toward the posterior grooves for meningeal vessels. The largest of these, the Coronal suture
parts of the parietal bones, but there are individual middle meningeal arteries and veins, leave their imprints Parietal bone
variations in size and shape associated with age, race, in particular on the parietal bones, and the channels Granular foveolae
and sex; thus minor degrees of asymmetry are common. containing them may become tunnels where the antero­ (for arachnoid granulations)
inferior angles of the parietal bones meet the greater Diploë
The anterior part, or brow, is formed by the frontal wings of the sphenoid bone. The skull varies in thick­ Grooves for branches of
bone, which extends backward to the coronal suture ness, and the area around the pterion is thin. It is middle meningeal vessels
between the frontal bone and the parietal bones. The Groove for superior sagittal sinus
latter bones curve upward and inward to meet at the Sagittal suture
midline sagittal suture. Posteriorly, the parietal bones Lambdoid suture
articulate with the triangular upper part of the occipital Occipital bone
squama along the lambdoid suture. The meeting points
of the sagittal suture with the coronal and lambdoid â•…
sutures are termed, respectively, bregma and lambda. In
the fetal skull, they are the sites of the anterior and relatively easily fractured by a blow to the side of the
posterior fontanelles. The vertex, or highest point, of head, with possible tearing of the middle meningeal
the skull lies near the middle of the sagittal suture. vessels. The resulting hemorrhage can be serious if it is
Parietal foramina are usually present; they transmit not recognized and treated promptly.
emissary veins passing between the superior sagittal
sinus and the veins of the scalp. The cut edge of the skullcap reveals that the constitu­
ent bones possess outer and inner laminae of compact
The deeply concave internal, or endocranial, surface bone separated by the diploë, a layer of cancellous bone.
of the calvaria is made up of the inner aspects of the The outer lamina is thicker and tougher than the more
bones, sutures, and foramina mentioned above. The brittle inner lamina.
bones show indistinct impressions produced by related
cerebral gyri, more evident grooves for dural venous
sinuses and meningeal vessels, and small pits, or foveolae,
for arachnoid granulations. Thus there is a median
groove in the frontal, parietal, and occipital bones
extending backward from the frontal crest to the inter­
nal occipital protuberance; it increases in width poste­
riorly and lodges the superior sagittal sinus. The frontal
crest seen in the midline is produced by the coalescence

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 341

P late 14-5 Brain: PART I

External Aspect Maxilla
of Skull Base Incisive fossa
Palatine process
The inferior surface of the base of the skull, the norma Intermaxillary suture
basilaris, is formed anteriorly by the arched hard palate, Zygomatic process
fringed by the maxillary alveolar processes and teeth;
posteriorly by the wider occipital squama, pierced by Zygomatic bone
the foramen magnum; and, in between, by an irregular
area comprising several bony processes for muscular Frontal bone Palatomaxillary suture
and tendinous attachments, articular and other fossae,
and many foramina. The bones and fissures shown in Sphenoid bone Palatine bone
the illustration need no added description, but the Pterygoid process Horizontal plate
nerves and vessels traversing the foramina will be listed. Hamulus Greater palatine
Medial plate foramen
The incisive foramen transmits the terminal branches Pterygoid fossa Pyramidal process
of the nasopalatine nerves and greater palatine vessels. Lateral plate Lesser palatine
The major and minor palatine foramina are traversed Scaphoid fossa foramina
by the corresponding arteries and nerves. The choanae Greater wing Posterior nasal spine
are the posterior nasal apertures. Foramen ovale
Foramen spinosum Choanae
The foramen ovale pierces the greater sphenoidal Spine Vomer
wing near the lateral pterygoid plate and the sulcus for Ala
the auditory tube; the mandibular nerve, the accessory Temporal bone Groove for auditory
meningeal artery, and communications between the Zygomatic process (pharyngotympanic,
cavernous sinuses and pterygoid venous plexus pass Articular tubercle eustachian) tube
through it. The foramen spinosum, anteromedial to the Mandibular fossa
sphenoidal spine, transmits the middle meningeal Styloid process Foramen lacerum
artery and the meningeal branch of the mandibular Petrotympanic fissure
nerve. Carotid canal
(external opening)
The foramen lacerum is an irregular canal between the Tympanic canaliculus
sphenoidal body, the apex of the petrous part of the External acoustic meatus
temporal bone and the basilar part of the occipital bone. Mastoid process
The upper end of the carotid canal opens into it, and Mastoid canaliculus
the internal carotid artery with its nerves and veins, on Stylomastoid foramen
emerging from the canal, turn upward to enter the Petrous part
cavernous sinus. Meningeal branches of the ascending Mastoid notch (for
pharyngeal artery and emissary veins from the cavern­ digastric muscle)
ous sinus pass through the foramen lacerum, and the Occipital groove
deep and greater petrosal nerves unite within it to form (for occipital artery)
the nerve of the pterygoid canal. Jugular fossa (jugular
foramen in its depth)
The anterior part of the mandibular fossa articulates Mastoid foramen
with the mandibular head and belongs to the temporal
squama, but the posterior nonarticular part is derived Parietal bone
from the tympanic plate. The tympanosquamous fissure
between them is continued medially as the petrotympanic Occipital bone
fissure, through which the chorda tympani nerve Hypoglossal canal
emerges. The stylomastoid foramen behind the root of Occipital condyle
the styloid process transmits the facial (VII) nerve and Condylar canal and fossa
the stylomastoid branch of the posterior auricular Basilar part
artery. Pharyngeal tubercle
Foramen magnum
The lower opening of the carotid canal is anterior to Inferior nuchal line
the jugular fossa, which lodges the superior bulb of the External occipital crest
internal jugular vein. The canal bends at right angles Superior nuchal line
within the petrous part of the temporal bone, and its External occipital protuberance
upper end opens into the foramen lacerum. The tym-
panic canaliculus pierces the ridge between the carotid â•…
canal and the jugular fossa and conveys the tympanic
branch of the glossopharyngeal (IX) nerve to the tym­ occipital artery. The anterior end of the hypoglossal canal which serve mainly for muscular and ligamentous
panic plexus. The mastoid canaliculus opens on the (for the hypoglossal [XII] nerve and some small men­ attachments. However, the most notable feature is the
lateral wall of the fossa and transmits the auricular ingeal vessels) is above the anterior end of the occipital foramen magnum, through which the medulla oblongata
branch of the vagus (X) nerve. The jugular foramen in condyle. Behind the condyle is a shallow condylar fossa, and spinal cord become continuous. The vertebral
the depth of the fossa may be partly or completely usually pierced by a condylar foramen conveying an emis­ arteries, spinal roots of the accessory nerves, and recur­
divided into three parts by bony spicules. The antero­ sary vein between the sigmoid sinus and cervical veins. rent meningeal branches from the upper cervical nerves
medial compartment transmits the inferior petrosal ascend through the foramen magnum, while down
sinus and a meningeal branch of the ascending pharyn­ The posterior part of the base of the skull is formed through it pass the anterior and posterior spinal
geal artery; the intermediate part transmits the glos­ predominantly by the occipital squama; these are arteries.
sopharyngeal, vagus, and accessory (XI) nerves; and the marked by nuchal lines, occipital crest, and so forth,
posterolateral part conveys the sigmoid sinus to the
superior bulb of the internal jugular vein. Often seen
near the posterior border of the mastoid process is a
mastoid foramen, which is traversed by an emissary vein
from the sigmoid sinus and a meningeal twig from the

342 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

P late 14-6 Head Trauma

INTERNAL ASPECTS OF BASE OF SKULL: BONES

Bones, Markings, and Frontal bone Middle cranial fossa Anterior cranial fossa
Orifices of Skull Base Groove for superior sagittal sinus
Frontal crest Posterior cranial fossa
The internal surface of the base of the skull has adapted Groove for anterior meningeal vessels
its shape to the configuration of the adjacent parts of Foramen cecum â•…
the brain. It consists of three cranial fossae, the anterior, Superior surface of orbital part
middle, and posterior, which are separated by conspicu­ Lateral to the sellae is a shallow, sinuous groove for
ous ridges and increase in size and depth from front Ethmoidal bone the internal carotid artery; at its anterior end on the
to back. Crista galli medial side may be a small tubercle, the middle clinoid
Cribriform plate process.
The anterior cranial fossa is the shallowest of the three
fossae and lodges the lower parts of the frontal lobes of Sphenoidal bone The lateral parts of the middle fossa are related in
the brain. The sulci and gyri of the lobes are mirrored Lesser wing front to the orbits, on each side to the temporal fossae,
in the irregularities of the bony surfaces. It is limited Anterior clinoid process and below to the infratemporal fossae. The middle fossa
anteriorly and laterally by the frontal bone. On each Greater wing communicates with the orbits through the superior
side, the floor is formed by the slightly domed and Groove for middle meningeal orbital fissures.
ridged orbital plate of the frontal bone, which supports vessels (frontal branches)
the orbital surface of the homolateral frontal lobe of the Body
brain and its meninges and separates them from the Jugum
orbit. Posterior extensions from the frontal air sinuses Prechiasmatic groove
may expand the orbital plates for varying distances, and Tuberculum sellae
the medial parts of these plates overlie the ethmoidal Sella Hypophyseal fossa
labyrinths. turcica Dorsum sellae
Posterior clinoid process
On each side of the midline crista galli are the grooved Carotid groove (for int. carotid artery)
ethmoidal cribriform plates that help to form the roof of Clivus
the nasal cavity, lodge the olfactory bulbs, and provide
numerous orifices for the delicate olfactory nerves. A Temporal bone
small pit exists between the frontal crest and the crista Squamous part
galli, the foramen cecum, which occasionally transmits a Petrous part
tiny vein from the nose to the superior sagittal sinus. Groove for lesser petrosal nerve
The crista galli and frontal crest give attachment to the Groove for greater petrosal nerve
anterior end of the falx cerebri. Arcuate eminence
Trigeminal impression
Posterior to the ethmoid and frontal bones, the floor Groove for superior petrosal sinus
of the anterior cranial fossa is formed by the anterior Groove for sigmoid sinus
part of the body of the sphenoid bone, the jugum sphe-
noidale, and on each side, by the lesser wings of this bone. Parietal bone
These lesser wings slightly overlap the anterior part of Groove for middle meningeal
the middle cranial fossa and project into the stems vessels (parietal branches)
of the lateral cerebral sulci, thus forming the upper Mastoid angle
boundaries of the superior orbital fissures.
Occipital bone
The medial ends of the posterior borders of the lesser Clivus
wings end in small, rounded projections, the anterior Groove for inferior petrosal sinus
clinoid processes, which provide attachments for the ante­ Basilar part
rior ends of the free border of the tentorium cerebelli. Groove for posterior meningeal vessels
Each anterior process is grooved on its medial side by Condyle
the internal carotid artery, and each may be joined to Groove for transverse sinus
the inconstant middle clinoid process by a thin osseous Groove for occipital sinus
bar, thus forming a narrow bony ring around the artery Internal occipital crest
as it emerges from the cavernous sinus. Internal occipital protuberance
Groove for superior sagittal sinus
The middle cranial fossa is intermediate in depth
between the anterior and posterior fossae. It is narrow The lesser wings of the sphenoid are attached to its
and elevated medially but expands and becomes deeper body by two roots, separated from each other by the
at each side to lodge and protect the temporal lobes of optic canals that transmit the optic (II) nerves and oph­
the brain. It is bounded anteriorly by the posterior thalmic arteries. Behind the prechiasmatic sulcus is
borders of the lesser wings of the sphenoid bone and a median elevation, the tuberculum sellae, and the
the anterior margin of the prechiasmatic sulcus; poste­ hypophyseal fossa housing the pituitary gland. The fossa
riorly by the superior borders of the petrous parts of is limited behind by the dorsum sellae, an upward-
the temporal bones, which are grooved by the superior projecting bony plate with a concave upper border
petrosal sinuses and by the dorsum sellae of the sphe­ expanding laterally into the posterior clinoid processes.
noid; and laterally by the greater wings of the sphenoid,
the frontal angles of the parietal bones, and the tempo­
ral squamae.

The floor in the median area is formed by the body of
the sphenoid bone, containing the sphenoidal air sinuses.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 343

P late 14-7 Brain: PART I

INTERNAL ASPECTS OF BASE OF SKULL: ORIFICES

Foramen cecum Emissary vein to
superior sagittal sinus

Nasal slit Anterior ethmoidal
Anterior ethmoidal artery, vein, and nerve
foramen

Foramina of Olfactory nerves
cribriform plate

Bones, Markings, and Posterior ethmoidal Posterior ethmoidal
Orifices of Skull Base foramen artery, vein, and nerve

(Continued) Optic canal Optic nerve (II)
Superior orbital fissure Ophthalmic artery
Various other, more-or-less symmetric openings exist
on each side. The foramen rotundum pierces the greater Oculomotor nerve (III)
wing of the sphenoid bone just below and behind the Trochlear nerve (IV)
inner end of the superior orbital fissure, and then it Lacrimal, frontal, and
opens anteriorly into the pterygopalatine fossa. The nasociliary branches
foramen ovale also penetrates the greater sphenoidal of ophthalmic nerve (V1)
wing posterolateral to the foramen rotundum and leads Abducent nerve (VI)
downward into the infratemporal fossa. The smaller Superior ophthalmic vein
foramen spinosum lies posterolateral to the foramen
ovale and opens below into the infratemporal fossa Foramen rotundum Maxillary nerve (V2)
close to the sphenoidal spine; the sulcus for the middle Foramen ovale Mandibular nerve (V3)
meningeal vessels starts at this foramen. The foramen Accessory meningeal
lacerum is an irregular aperture between the body and
greater wing of the sphenoid bone and the apex of the artery
petrous part of the temporal bone; it marks the point Lesser petrosal nerve
of entry of the internal carotid artery into the cavernous
sinus. Behind the foramen lacerum is the shallow depres- Foramen spinosum Middle meningeal artery and vein
sion for the trigeminal (semilunar) ganglion on the anterior Meningeal branch of mandibular
surface of the petrous temporal bone, and lateral to this
are two narrow grooves leading to the hiatuses for the nerve
lesser (minor) and greater (major) petrosal nerves.
Sphenoidal emissary foramen (of Vesalius) (inconstant)
The arcuate eminence is produced by the superior
semicircular canal of the internal ear. Anterolateral to Foramen lacerum Greater petrosal nerve
this eminence is a thin plate of bone, the tegmen tympani,
forming the roof of the tympanic cavity and mastoid Carotid canal for Internal carotid artery
antrum and extending forward and medially to cover Hiatus for Internal carotid nerve plexus
the bony part of the auditory (pharyngotympanic) tube. Lesser petrosal nerve

The posterior cranial fossa is the largest and deepest of Hiatus for Greater petrosal nerve
the cranial fossae and lodges the cerebellum, pons, and
medulla oblongata. It is bounded anteriorly by the Internal acoustic meatus Facial nerve (VII)
dorsum sellae, the back of the body of the sphenoid Opening of Vestibulocochlear nerve (VIII)
bone, and the basilar part of the occipital bones; poste­ vestibular aqueduct Labyrinthine artery
riorly by the squama of the occipital bone below the Endolymphatic duct
sulci for the transverse sinuses and the internal occipital
protuberance; and laterally by the petrous and mastoid Mastoid foramen Emissary vein (and
parts of the temporal bones, the mastoid angles of (inconstant) occasional branch
the parietal bones, and the lateral parts of the Jugular foramen of occipital artery)
occipital bone.
Inferior petrosal sinus
The posterior fossa is pierced by a number of foram­ Glossopharyngeal nerve (IX)
ina and is grooved by various dural venous sinuses. A Vagus nerve (X)
large median opening in the floor of the fossa, the Accessory nerve (XI)
foramen magnum, penetrates the occipital bone. The Sigmoid sinus
medulla oblongata and spinal cord and their surround­ Posterior meningeal artery
ing meninges become directly continuous immediately
below the foramen. The petrous part of the temporal Condylar canal Emissary vein and meningeal
bone and the occipital bone are separated by the petro- (inconstant) branch of ascending
occipital fissure and the sulcus for the inferior petrosal sinus; pharyngeal artery
the fissure ends behind, in the jugular foramen. The
inferior petrosal and sigmoid sinuses pass through the Hypoglossal Hypoglossal nerve (XII)
anterior and posterior parts of this foramen, respec­ canal Medulla oblongata
tively, while the glossopharyngeal (IX), vagus (X), and Foramen Meninges
accessory (XI) nerves occupy an intermediate position magnum Vertebral arteries
as they leave the skull. Meningeal branches
â•…
Two canals are associated with the occipital condyles: of vertebral arteries
the hypoglossal canal, for the twelfth cranial nerve, and Spinal roots of accessory
the condylar canal.
nerves

Above the jugular foramen, the internal acoustic The internal opening of the inconstant mastoid
meatus tunnels into the petrous part of the temporal foramen is close to the sulcus for the sigmoid sinus, which
bone. It is about 1╯cm long and is separated laterally winds downward from the transverse sinus to the
from the internal ear by a thin bony plate pierced jugular foramen, where it ends in the superior bulb of
by many apertures for fascicles of the facial (VII) and the internal jugular vein. The internal occipital protuber-
vestibulocochlear (VIII) nerves. Behind the orifice ance is related to the confluence of the superior sagittal,
of this meatus is the slitlike opening of the vestibular straight, occipital, and transverse sinuses. The margins
aqueduct, which lodges the blind end of the endolym­ of the sulci for the transverse sinuses give attachment
phatic duct. to the tentorium cerebelli.

344 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 14-8 Head Trauma

Skull Injuries Open fracture Depressed fracture

The mechanical forces resulting in traumatic brain “Ping-pong ball”
injuries may produce a variety of different structural depression of
injuries, each of which requires different surgical or skull in an
medical treatment. infant

Before the introduction of computed tomography Indriven fragments of bone
(CT) scans, plain skull radiographs were of vital impor­ Basilar skull fractures
tance in evaluating patients with head injuries. The C
presence of a skull fracture strongly suggested the pos­
sibility of a significant, underlying intracranial injury. B
Fracture is present in 66% to 100% of patients with A
epidural hematoma; 18% to 60% with acute subdural
hematoma; and 40% to 80% with contusions or intra­ Longitudinal (A) and transverse (B) “Panda bear” or “raccoon” sign due to leakage of blood from
cerebral hematoma. Such intracranial injuries are now fractures of petrous pyramid of temporal anterior fossa into periorbital tissues. Absence of conjunctival
immediately identified by CT, and an associated skull bone, and anterior basal skull fracture (C) injection differentiates fracture from direct eye trauma.
fracture is often noticed only in passing.
Rhinorrhea
There are, however, several types of skull fracture
that are of clinical significance. The most classic is the Otorrhea or Battle sign: postauricular hematoma
basilar skull fracture, which may be associated with ear hemorrhage â•…
cerebrospinal fluid (CSF) leak and cranial nerve inju­ post-traumatic epilepsy. They definitely are associated
ries. Basilar skull fracture has been reported in up to with potentially significant underlying brain injury. The primary concern over frontal sinus fractures is
25% of patients sustaining a head injury. Even with CT, Common practice until recently was to operate on all the status of the posterior wall of the sinus, with the
basilar skull fractures may not be identified because of such fractures. Contemporary literature, however, has possibility of dural violation and the risk of CSF leak,
their orientation to the plane of the scan. Special thin shown that the risk of post-traumatic epilepsy is not pneumocephalus, and infection. As a general rule,
cuts or coronal views may be required. The majority of significantly increased, and the risk of infection may be unless there is overt evidence of CSF leak or pneumo­
basilar skull fractures occur through the petrous bone greater in those patients treated operatively than non­ cephalus with posterior wall fragments in-driven more
or the anterior cranial fossa. Clival fractures are less operatively. It thus appears possible to manage conser­ than 3 to 4╯mm, nonoperative management is usually
common. Petrous bone fractures occur either trans­ vatively all but the most contaminated and comminuted successful. Some, however, advocate surgery on the
versely or longitudinally, and their orientation predis­ fractures with reasonable safety. majority of frontal sinus fractures to prevent the devel­
poses to various complications. opment of a mucocele.

The classic clinical presentation of a petrous bone
fracture is with the Battle sign—a retromastoid hema­
toma. Raccoon eyes—periorbital hematomas—may be
seen with anterior skull base fractures. CSF leaks, otor­
rhea or rhinorrhea, have been reported in approxi­
mately 10% of patients with basal skull fractures.
Otorrhea is typically associated with petrous fractures,
whereas rhinorrhea may emanate from either frontal
fossa fractures through the cribriform plate or the
petrous bone through the eustachian canal. In either
case, with bed rest and head elevation, the CSF leak
ceases spontaneously in more than 85% of patients.
The administration of antibiotics is not advised because
this may predispose to antibiotic-resistant infection.
Persisting leaks may be treated with a lumbar drain;
only a small number require direct or endoscopic surgi­
cal repair.

If there is any question as to whether drainage from
the nose or ear represents CSF, the fluid can be checked
for glucose, which typically is greater than 30╯mg/mL
in CSF, or β-2-transferrin, which is found only in
the CSF.

Cranial nerve injuries may complicate up to 5% of
basal skull fractures, the most common of which is
facial nerve injury in association with petrous fractures.
Such an injury may occur in up to 50% of patients with
transverse and 20% with longitudinal fractures. The
facial nerve is especially prone to injury in the narrow
fallopian canal as swelling occurs or by compression
from fracture fragments. If facial paralysis is immediate
and complete, the chances of recovery are small. More
minor injuries tend to recover well, and steroids are
often used for treatment. Some advocate early surgical
exploration and decompression of the nerve.

Two other types of skull fractures require specific
clinical management: open depressed and frontal sinus
fractures.

Open, or compound, depressed skull fractures
have been said to be associated with infection and

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 345

P late 14-9 Brain: PART I
Normal brain
Concussion

A concussion is a type of traumatic brain injury that Traumatic forces to the
changes the way the brain normally works and is caused head can change the way
by traumatic forces to the head or body. Most concus­ the brain works
sions occur without loss of consciousness. The Centers
for Disease Control and Prevention estimates that Injured brain
between 1.6 and 3.8 million concussions occur in sports Repetitive concussions can
and recreational activities each year. Concussions or cause chronic traumatic
mild traumatic brain injuries can result in short- and encephalopathy and result
long-term health risks. In athletes, there is a correlation in loss of white matter
between repetitive concussions and a neurodegen­
erative disease called chronic traumatic encephalopathy. Healthy neuron
There is also an entity called “second impact syn­
drome.” The potential public health problem of con­ Tau-microtubule Microtubule
cussion is such that more than 40 states in the United complexes in axon
States have either laws or pending bills addressing the
problem of concussions in youth sports. Tau bound to Disintegrating
microtubule microtubule
At the level of the neuron, linear and rotational forces Microtubule Dissociated
can lead to structural and metabolic changes that subunits fall apart tau subunit
transiently impair function and contribute to physical,
cognitive, and emotional symptoms. The molecular Diseased neuron Aggregated tau protein Tau subunits assemble
substrate for these acute clinical changes is the subject within neurofibrillary tangle and form neurofibrils
of much current research on cellular ionic transients in
sodium and calcium, axonal integrity, bioenergetics, â•…
neurovascular coupling, and genetics. What is apparent
in sufferers of a concussion is that symptoms may neurodegenerative disease termed chronic traumatic in deceased players from other sports, for example,
persist for days, weeks, or months after a concussive encephalopathy. This disease was first described in 1928 football, hockey, and wrestling. Although the cases vary
event. as dementia pugilistica in deceased boxers. The clinical in severity of neuropathology, they share the common
syndrome associated with this pathology, so-called feature of increased deposition of aggregated tau
Clinical Symptomatology. The signs and symptoms “punch drunk” condition, was believed to be limited protein within neurofibrillary tangles, which is similar
of concussions are diverse. Typically, individuals have to boxers who displayed progressive cognitive, emo­ to neurodegenerative diseases such as Alzheimer
difficulty with thinking and memory skills, and their tional, and behavioral symptoms, such as depression, disease. In addition, earlier stages of chronic traumatic
emotions may be affected. The physical problems agitation, and dementia, years after repeated traumatic encephalopathy are being reported in athletes as young
include headache, nausea, and visual disturbances. The brain injuries. Recently, however, many other cases of as 18 years old, where there is evidence of white matter
Centers for Disease Control and Prevention advocates chronic traumatic encephalopathy have been described loss in brain imaging.
that any athlete suspected of having a concussion should
be immediately removed from play, evaluated by a
health-care professional, and only allowed to return
when cleared by a health-care professional. At present,
there are no “neuroprotective” drugs that can be used
for this condition, and it is recommended that for
safety, physical and mental activities that excessively
stimulate the injured brain should be discontinued.
Furthermore, a graded return-to-play system is recom­
mended as the safest way to bring an athlete back to full
contact activities.

Second Impact Syndrome. Second impact syndrome
is the most devastating, yet rare, consequence of repeat
concussion in the postinjury phase. This condition
occurs when an individual experiences a second trau­
matic episode to the brain before the brain has fully
recovered from the initial traumatic injury. These sub­
jects rapidly develop global cerebral edema, coma,
severe neurologic impairment, and the potential for
death. This rare condition has been observed mainly in
youths younger than 21 years. At present, there are no
methods for determining the recovery period after a
concussion or even the duration of a “window of vul­
nerability” after a concussion. Hence much of the
current emphasis in the management of concussion and
return-to-playing of sports in young athletes is on
reducing any potential for second impact syndrome.

Repeat Concussions and Chronic Traumatic Enceph-
alopathy. Individuals who suffer an isolated concus­
sive event should recover completely if they allow an
appropriate time for recovery, with rest and cessation
of sports. In contrast, brain autopsy studies of former
professional athletes in contact sports, such as box­
ing, football, and hockey, have revealed a chronic,

346 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

P late 14-10 Head Trauma

Temporal fossa hematoma Shift of normal
Skull fracture midline structures
crossing middle Compression of
meningeal artery posterior cerebral
artery
Herniation of temporal Shift of brainstem
lobe under to opposite side
tentorium cerebelli may reverse
lateralization of
signs by tentorial
pressure on
contralateral
pathways

Acute Epidural Hematoma

The overall incidence of acute epidural hematoma Compression of oculomotor (III) Herniation of Compression of corticospinal
(EDH) after head injury is approximately 5%, but it nerve leading to ipsilateral cerebellar tonsil and associated pathways,
approaches 10% in patients presenting in coma. EDHs pupil dilation and third resulting in contralateral
are almost always traumatic in nature. There are rare cranial nerve palsy hemiparesis, deep tendon
reports of spontaneous occurrence in association with hyperreflexia, and Babinski sign
anticoagulation or thrombocytopenia. The classic clini­
cal presentation is with a loss of consciousness that is Subfrontal hematoma Posterior fossa hematoma
followed by a lucid interval and then by progressively Frontal trauma: Occipital trauma and/or
severe headache and decreasing level of consciousness. headache, poor fracture: headache,
However, most EDHs result from motor vehicle colli­ cerebration, meningismus, cerebellar
sions, and greater than 60% of patients are unconscious intermittent and cranial nerve signs,
at the scene or on hospital arrival. disorientation, Cushing triad
anisocoria
Computed tomography scan shows a variably sized
oval or “lens-shaped” hyperdensity between the bone Bone flap turned down from cracking uncut
and the dura. segment of margin, exposing epidural hematoma,
which is removed by suction, spoon, or Penfield
The most common clinical location for an EDH is dissector
the temporal fossa, typically associated with a temporal
bone fracture that lacerates the middle meningeal â•…
artery and leads to arterial bleeding. This can result in
the well-known transtentorial herniation syndrome. As 8 without focal neurologic deficit can be managed sufficient blood to be lifesaving. Definitive treatment is
the ipsilateral temporal lobe is forced medially, the third conservatively with serial CT scanning and close evacuation through a large “trauma” bone flap. An
nerve is trapped against the brainstem, resulting in ipsi­ neurologic observation in a neurosurgical center. active bleeding point is virtually always found on the
lateral pupillary dilation. As more pressure develops, • It is strongly recommended that patients with an dura. Occasionally, bleeding may be seen to be coming
the ipsilateral posterior cerebral artery may be so acute EDH in coma (GCS < 9) with anisocoria from underneath the temporal lobe, and the middle
severely compressed as to result in an occipital lobe undergo surgical evacuation as soon as possible. meningeal artery will be found lacerated at or within
stroke that is typically seen on CT scan a day or two In a truly urgent situation when, for example, weather the foramen spinosus. With rapid, aggressive treat­
after the event. With increasing shift of the brain to the or distance precludes getting the patient to a center ment, mortality across all age groups and all GCS
opposite side, the brainstem is compressed, and the with neurosurgical capabilities, a burr hole may release scores is less than 10%.
cerebral peduncle is forced into the edge of the tento­
rium, creating a so-called Kernohan notch and result­
ing in hemiparesis ipsilateral to the dilated pupil. If the
compression remains severe for too long, Duret hemor­
rhages occur in the brainstem from compression or
tearing of the small perforating arteries coming off the
basilar artery. Such hemorrhages can be seen on mag­
netic resonance imaging (MRI) and portend a poor
prognosis.

Venous epidural hematomas may also occur and are
most common in the posterior fossa in children.

The following are recently published guidelines by
the Brain Trauma Foundation (New York) for the treat­
ment of EDH:

• An EDH greater than 30 cm3 should be surgically
evacuated regardless of the patient’s score on the
Glasgow Coma Scale (GCS).

• An EDH less than 30 cm3 and with less than
15-mm thickness and with less than a 5-mm
midline shift in patients with a GCS greater than

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 347

P late 14-11 Brain: PART I

Acute Subdural Hematoma

Acute subdural hematoma (ASDH) is the primary “Question mark” skin incision
structural abnormality in up to 30% of patients after (black); outline of free bone
severe traumatic brain injury (TBI) and, in most flap and burr holes (red)
instances, is associated with other significant structural Catheter to monitor intracranial
injuries such as contusions. pressure, emerging through burr
hole and stab wound
The injury occurs typically after a high-speed motor
vehicle collision. ASDH, however, is being increasingly Skin flap reflected (Raney clips control
seen in elderly patients after same-height falls, and bleeding); free bone flap removed and
especially in patients on anticoagulant or antiplatelet dura opened; clot evacuated by
medication. Bleeding is typically venous in nature, irrigation, suction, and forceps
resulting from shearing of cortical veins, bridging veins, Bone and skin flaps
or veins from one of the cerebral venous sinuses. replaced and sutured

A computed tomography (CT) scan typically shows Jackson-Pratt drain,
a hyperdense crescent of blood between the dura and emerging from
the brain. Despite a relatively small amount of blood, subdural space via
there is typically significant underlying hemispheric burr hole and
cerebral edema with associated midline shift. An entity stab wound
known as a hyperacute ASDH has been described on
CT: the presence of mixed hyperdensity indicates Section showing acute subdural hematoma on right side
ongoing active bleeding. Contusions are also frequent and subdural hematoma associated with temporal lobe
and typically will worsen after surgical evacuation of intracerebral hematoma (“burst” temporal lobe) on left
the ASDH.
â•…
The decision to operate is based on a number of
factors, but increasing, age is an extremely strong inde­ CONTUSIONS DIFFUSE AXONAL INJURY
pendent factor indicating a poor prognosis.
Contusions are parenchymal mass lesions that occur in Diffuse axonal injury (DAI) or shear injury, as the name
The following recommendations by the Brain up to 35% of patients with severe TBI. Approximately implies, results from stretching and tearing of axons
Trauma Foundation (New York) have been proposed 30% will enlarge progressively or become associated throughout the brain. Although the injury is diffuse,
for surgical management: with significant surrounding edema. Although most can two of the most common areas of involvement are the
be managed medically, it has been recommended that corpus callosum and the posterolateral quadrants of the
• An ASDH with a thickness greater than 10╯mm or surgery be considered in the following setting: patients upper brainstem. CT scans may show discrete punctu­
a midline shift greater than 5╯mm should be surgi­ with GCS scores of 6 to 8 with frontal or temporal ate hemorrhages in these and other white matter tracts.
cally evacuated regardless of the patient’s GCS. contusions greater than 20 cm3 in volume, with midline Magnetic resonance imaging (MRI) is very sensitive to
shift of at least 5╯mm and/or cisternal compression on DAI lesions, which appear hyperintense on T2-weighted
• All patients with ASDH with GCS less than 9 CT scan, and any patients with any lesion greater than images. Severe DAI is unfortunately associated with a
should undergo intracranial pressure monitoring. 50 cm3 in volume should be treated operatively. poor outcome.

• A patient with a GCS less than 9 and with an
ASDH less than 10╯mm thick and a midline shift
less than 5╯mm should undergo surgical evacuation
of the lesion if the GCS decreases by 2 or more
points between injury and hospital admission and/
or the patient presents with asymmetric or fixed
and dilated pupils and/or the intracranial pressure
(ICP) exceeds 20╯mm╯Hg.

• Patients with ASDH and indications for surgery
should have evacuation performed as soon as
possible.

The issue of “as soon as possible” for surgical inter­
vention has been widely studied. In a landmark paper
in 1981, it was found that patients undergoing surgery
within 4 hours of injury had a lower (30%) mortality
rate than those undergoing surgery at later than 4 hours
(90%). A subsequent paper in 1991 did not find any
significant difference in mortality for patients undergo­
ing surgery within or after 4 hours. It has been sug­
gested that the degree and extent of underlying brain
injury is probably the more important determinant of
recovery than is the absolute timing of surgery.

The goal of surgery is the most complete evacuation
of the ASDH as is possible through a large “trauma
craniotomy” flap. Attention should be directed to coag­
ulating any bleeding cortical veins or bridging veins.
If there appears to have been avulsion of a vein from
one of the venous sinuses, unless there has been ade­
quate exposure of the area, such is best controlled by
packing with hemostatic agents. If there is significant
brain swelling, it is often best not to replace the crani­
otomy flap.

Unfortunately, despite the most aggressive neuro­
critical care, the mortality rate from ASDH remains
high, ranging from 40% to 60% across all GCS catego­
ries and greater than 70% in patients presenting in coma.

348 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 14-12 Head Trauma
CT scan
CT Scans and MR Images of Intracranial Hematomas showing a
large right
CT SCANS AND MRIS OF INTRACRANIAL HEMATOMAS parietal epi-
dural hema-
Normal brain toma. Note
CT scan at level the biconvex
of the frontal shape of the
horns of the hyperintense
lateral ventricles blood and
the signif-
icant midline
shift of the
ventricles.

CT scan showing CT scan of a
a large acute chronic sub-
subdural hema- dural hema-
toma. The hyper- toma showing
intense blood a large hypo-
covers the sur- intense mass
face of the along the
right hemi- surface of the
sphere and left fronto-
causes a temporal
large midline region, with
shift. an associated
midline shift

Normal T-1 T-2 weighted
weighted MRI MRI showing
of the brain multiple small
at the level hyperintense
of the lateral bright signals
ventricles in the white
matter, typical
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS of diffuse
axonal injury

â•…
349

Plate 14-13 Brain: PART I

Vascular Injury Rupture of internal carotid Superior and inferior Supraorbital vein
artery into cavernous sinus ophthalmic veins Supratrochlear
CAROTID-CAVERNOUS FISTULA Superior petrosal sinus (greatly dilated) vein
Carotid-cavernous fistula (CCF), occurring in less Angular vein
than 3% of head-injured patients, is the most well- Bruit
characterized sequela of intracranial vascular injury, Pulsating Pulsating
having first been described in 1757. Although CCF may exophthalmos exoph-
arise from other causes such as ruptured intracavernous thalmos
aneurysm or infection, trauma is the most common Chemosis
cause. CCF occurs when there has been an injury to the
cavernous sinus segment of the carotid artery, resulting Bruit obliterated by
in redirection, overfilling, and pressurization of the Dilation carotid compression
venous inflow and outflow of the cavernous sinus. The of retinal
resulting clinical syndrome is characterized by pulsating Retromandibular veins, papill-
exophthalmos and a bruit. (posterior edema, and
facial) vein progressive
The carotid artery enters the cavernous sinus as it Internal car- loss of vision
exits the foramen lacerum at the base of the skull. It otid artery
then rises toward the posterior clinoid process before Internal Facial (anterior Tachycardia, cardiac
acutely turning anteriorly for approximately 2╯cm (the jugular vein facial) vein hypertrophy, dyspnea,
horizontal segment), leaving the cavernous sinus just
below the anterior clinoid. There are several small Pterygoid plexus and increased blood
branches of the carotid inside the cavernous sinus, volume may occur
including the meningohypophyseal trunk and the artery
of the inferior cavernous sinus. The cavernous sinus Endovascular balloon occlusion of fistula
itself is an intricate plexus of venous channels surround­
ing the carotid artery. It lies lateral to the pituitary Balloon inflated with Outer catheter advanced
gland and sphenoid sinus, extending from the superior radiopaque fluid over inner catheter to
orbital fissure to the apex of the petrous bone. Among occluding fistula engage balloon cuff
many other venous and sinus connections, the superior
and inferior ophthalmic veins and the central retinal Carotid arteriography, early phase, reveals prom- Balloon liberated by slight
artery drain into the cavernous sinus, the former inent opacificaton of cavernous sinus (arrows) pull on inner catheter. Balloon
accounting for the exophthalmos and the latter for the via carotid-cavernous fistula neck spontaneously constricted
possibility of intracranial hemorrhage. The third, by tense latex tie. All catheters
fourth, and all three branches of the fifth cranial nerve including the superior ophthalmic vein, the carotid then withdrawn.
run within the lateral wall of the cavernous sinus; the artery, and the superior petrosal sinus.
sixth nerve passes directly through the sinus alongside â•…
the carotid, whereas ocular sympathetic fibers form a Large series of patients with CCFs treated endovas­
plexus on the wall of the carotid. cularly have demonstrated a 99% occlusion rate with Another serious secondary insult is intracranial hyper­
less than 5% complications. tension. It is reasonably well established that maintain­
The classic signs and symptoms of the complete syn­ ing intracranial pressure (ICP) below 20╯mm╯Hg
drome resulting from CCF include pulsating exoph­ SECONDARY COMPLICATIONS OF at all times is associated with greater than 90% sur­
thalmos, a bruit that patients often appreciate, chemosis TRAUMATIC BRAIN INJURY vival; controlling ICP below this level for greater than
(conjunctival injection), diplopia, visual loss, and head­ A significant number of patients die or are left severely 50% of the time is associated with greater than 50%
ache. These may evolve over the course of several weeks disabled after TBI, not by the primary injury itself but survival; and an inability to ever bring ICP below
or months. Their pathophysiologic basis can be deduced by the secondary insults that follow. The most common 20╯mm╯Hg, is accompanied by a greater than 90%
readily from the previously described anatomy. of these are hypotension and hypoxia. mortality.

Although a CCF can typically be seen on computed Hypoxia (oxygen saturation less than 90%) and/ An important, but still uncontrolled problem is the
tomography (CT) or magnetic resonance imaging or hypotension (systolic blood pressure less than damaging biochemical cascade that is initiated shortly
(MRI), angiography is necessary to define the anatomy 90╯mm╯Hg) was found to occur in greater than one after injury. The final common pathway to energy
of the fistula and to identify the associated abnormal third of patients with severe TBI in the National Coma failure, and ultimately to cell death, relates to loss of
venous drainage so as to allow for planning of optimal Data Bank. A single episode of hypotension at any point calcium homeostasis and to mitochondrial damage.
treatment. Because traumatic CCFs rarely resolve is associated with a doubling of mortality; of hypoxia Opening the cellular membranes to calcium influx
spontaneously, surgical intervention is usually indi­ with a 33% increase; and the combination with a 75% is triggered by a variety of mechanisms, including
cated. The timing of intervention depends on the increase. Thus every effort should be made to prevent oxygen free-radical production, excitatory neuro­
degree and extent of visual loss. Visual deterioration is or minimize the occurrence of these events. toxicity, caspases, and cytokines. The resulting damage
due to ischemia secondary to increased intraocular may exceed that created by the primary injury. Ran­
pressure and subsequent hypoxia as a result of reduced domized controlled clinical trials of pharmacologic
arterial flow and venous hypertension. agents to block this biochemical cascade have not
yielded benefit.
Before the development of endovascular surgical
techniques, the most common treatment approach
involved occluding the internal carotid artery in the
neck as well as intracranially just distal to its exit from
the cavernous sinus. Unfortunately, this usually meant
sacrificing the ophthalmic artery as well, given its origin
just below the anterior clinoid process, with the associ­
ated risk of further visual loss.

The current treatment of choice is selective endovas­
cular balloon occlusion of the fistulous connection
itself, preserving the carotid artery and its branches.
The fistula may be accessed by a variety of routes,

350 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

P late 14-14 Head Trauma

Initial Assessment and “ABC” assessment
Management of Head Injury A—airway: Suction to
free oropharynx from
As with any potentially life-threatening injury, the blood and other material;
airway, breathing, and circulation (ABC) protocol takes intubate after cervical
precedence. In a comatose patient in whom the airway spine evaluation
has not been secured in the prehospital phase, intuba­
tion takes priority. Even brief episodes of hypoxia are B—breathing: Evaluate rate,
associated with significantly worse outcomes. Rapid- rhythm, and breath sounds;
sequence intubation utilizing agents such as thiopental vmreeodnnutiicltaeotrePAatocBoGr2ail(seteovePlolaswo2er and
or propofol with a muscle relaxant is optimal in mini­ ICP);
mizing the risk of aspiration, but it also renders unin­
terpretable the findings on neurologic examination. C—circulatory status: Start intravenous infusion of
Thus it is preferable that a reliable Glasgow Coma lactated Ringer or normal saline solution, followed
Score is established before intubation. Initial ventila­ by blood if indicated; obtain immediate laboratory
tion should aim to normalize Pao2 and Pco2, at greater work and x-rays; administer anticonvulsants if indicated,
than 90% and 35 to 40╯mm╯Hg, respectively. Hyper­ plus pressor agent if required (shock rarely due to
ventilation is not advised unless attempting to treat head injury alone; search for cause)
suspected increased intracranial pressure (ICP), and
then for only short periods. Monitor central venous
pressure in shock.
Hypotension (systolic blood pressure < 90╯mm╯Hg)
may increase mortality markedly after head injury. Lac­ Intravenous line Maxillary or
tated Ringer solution or normal saline are the resuscita­
tion fluids of choice. Glucose solutions should be mandibular
avoided because hyperglycemia may worsen the out­ fractures Pupillary
come. Hypertonic saline (HS) is being used increas­ dilation;
ingly. Effective resuscitation can be accomplished with Measure Ruptured aorta ocular
as little as 1 to 2╯mL/kg, and HS may have a variety of urine
neuroprotective effects. If an adequate systolic blood Insert flow Hemopericardium palsies
pressure cannot be restored with 2 to 3 liters of crystal­ indwelling hourly
loid, packed RBCs should be given. Foley
catheter
It is important to rigorously follow the Advanced
Trauma Life Support guidelines. Up to 70% of severely Rhinorrhea,
head-injured patients will have thoracic, abdominal, or otorrhea
major orthopaedic injuries, which may require more
immediate attention than the head injury. On occasion, Babinski sign Fractures, Ruptured Ruptured Sucking chest wounds,
a patient may be so hemodynamically unstable as to (neurologic paralysis bladder spleen, fractured ribs,
require urgent thoracotomy, laparotomy, or endovascu­ examination) liver, flail chest,
lar intervention before the head injury can be fully Back injuries intestine, hemothorax,
evaluated. Simultaneous ICP monitoring during the kidney pneumothorax
ongoing intervention should be considered.
Conduct complete physical examination and repeat periodically
It is important to obtain a computed tomography â•…
(CT) scan of the head as soon as possible during initial
management so as to determine the degree and extent 7 days unless the patient seizes. Dilantin and Keppra to decubiti, can begin after 30 minutes on a backboard,
of structural damage to the brain and prepare for imme­ are the most frequently used drugs for this purpose. especially in hypotensive patients.
diate operative intervention, if appropriate. When a
large mass lesion or early evidence of significantly At some early point, the spine must be evaluated A plain radiograph of the spine, supplemented with
increased ICP (such as obliteration of the basal cisterns) because spinal injury occurs in more than 5% of CT scan, will rule out the majority of bony injuries, but
is present, mannitol 0.5 to 1.0╯mg/kg may be given to severely head-injured patients. Cervical immobilization the possibility remains of a significant ligamentous
reduce ICP. However, mannitol may initiate a diuresis must be maintained with a collar until structural injury injury. Magnetic resonance imaging (MRI) within the
that causes or exacerbates hypotension. to the cervical spine is definitively excluded. It is impor­ first 24 to 48 hours of injury has been advocated as a
tant to remove a hard backboard as soon as possible, reliable method of assessing for ligamentous damage,
Additional problems are posed by patients on anti­ while maintaining the patient flat, to immobilize the but many physicians prefer to leave a cervical collar in
coagulants or antiplatelet medications. If such a history thoracolumbar spine. Skin ischemia, potentially leading place until clinical assessment is complete.
cannot be elicited, an important component to the
initial laboratory studies is determination of the inter­
national normalized ratio (INR) and clotting time. In
patients with any evidence of traumatic intracranial
bleeding, the INR must be corrected with vitamin K
and fresh frozen plasma. Many are using recombinant
factor VIIa for this purpose. Dealing with current
antiplatelet agents is particularly problematic because
platelet function may be impaired for up to 7 days.
Platelet transfusions may be helpful. Desamino-d-
arginine vasopressin (DDAVP) can be administered
as well.

Unless a patient is on chronic steroid therapy, ste­
roids are contraindicated as a treatment for head injury.
Anticonvulsant prophylaxis should be initiated as soon
as possible after severe head injury and maintained for

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 351

Plate 14-15 Brain: PART I

Eye opening (E) E
Spontaneous . . . . 4
Glasgow Coma Score Open
your
Teasdale and Jeanette introduced the Glasgow Coma eyes
Score (GCS) in 1974 as an objective measure of level
of consciousness after traumatic brain injury (TBI). To speech . . . . . . . 3
The GCS quickly became universally accepted as the
best clinical measure of the severity of TBI, allowing Spontaneous = 4 To pain = 2 To pain . . . . . . . . . 2
for a reliable, standardized method of assessing and Nil (no response) = 1 Nil . . . . . . . . . . . . 1
reporting sequential evaluation across all health-care Response to speech = 3
providers. The GCS measures level of consciousness, Motor response (M) M
not neurologic deficits. An appropriate neurologic Obeys . . . . . . . . . 6
examination should accompany the GCS. Show
me 2
The GCS evaluates three independent neurologic fingers
responses: eye opening, motor response, and verbal
response All parameters may be significantly affected by Localized . . . . . . . 5
systemic factors such as severe hypotension or signifi­
cant drug/alcohol intoxication or by local factors, Obeys = 6 Withdraws = 4 Withdraws . . . . . . 4
including ocular trauma, intubation, extremity frac­
tures, and spinal cord injury. Iatrogenic paralysis/ Localizes = 5
sedation affects the score and may render the GCS
inapplicable. Abnormal
flexion . . . . . . . . . 3
The eye opening and verbal responses are simple to
record. The motor response has traditionally been Abnormal Extensor
recorded as the best reaction in response to deep pres­ flexor response . . . . . . . 2
sure or pain. Thus a patient who is hemiplegic may still response = 3
receive a motor score of 6. In their original paper,
Teasdale and Jennett specifically proscribed the manner Extensor Nil . . . . . . . . . . . . 1
in which the evaluation of all three parameters was to response = 2 Nil (no response) = 1
be undertaken. Noxious stimuli to the nailbed were to Verbal response (V)
be applied to elicit decorticate or decerebrate responses, What Yesterday Scream, V
while painful stimuli to the head neck or trunk were year Mother groan, Oriented . . . . . . . 5
used to test for localization. Eye opening in response is this? moan
to pain was to be tested distant to the face to prevent a Inappropriate Incomprehensible Confused
grimacing reflex from keeping the eye shut. 2012 words = 3 sounds = 2 conversation . . . . . 4

It is generally accepted that a GCS of 13 to 15 is Oriented = 5 1997 No response Inappropriate
associated with minor TBI, a GCS of 9 to 12 reflects words . . . . . . . . . . 3
moderately severe TBI, and a GCS of 3 to 8 indicates Confused Nil = 1
severe TBI. It is common practice to attach a modifier conversation = 4 Incomprehensible
(“t”) after the score if a verbal response cannot be sounds . . . . . . . . . 2
recorded due to intubation.
Nil . . . . . . . . . . . . 1
The GCS cannot be used in preverbal children, and
a children’s coma scale has been developed. The eye and Coma score (E + M + V) = 3 to 15)
motor responses mirror those of the GCS. For the
verbal response, a score of 5 is given if the child smiles, â•…
orients to sounds, follows objects, and interacts. Scores
of 4 to 1 include both a component related to crying during ongoing evaluation, a decline of two or more A good recovery is defined as a resumption of a
and one to interaction. Thus a score of 4 indicates that points is generally considered clinically significant. normal life despite minor ongoing disability. With
the child cries consolably and interacts inappropriately; moderate disability, a patient is disabled but indepen­
3, that crying is inconsistently consolable and there is Efforts in developing the GCS have been extended dent, able to perform all activities of daily living, and
moaning; 2, that the child cries inconsolably and is to outcome assessment. The Glasgow Outcome Scale work in a sheltered setting. Severely disabled patients
restless; and 1, that there is an absence of crying or (GOS) was introduced in 1975 and is the cornerstone are conscious but totally dependent on others for care.
interaction. in outcome assessment, with high intrarater reliability. In the persistent vegetative state, the patient is unre­
There are five potential outcomes, that is, death, per­ sponsive and speechless but may open the eyes and
Several studies have shown an association between sistent vegetative state, severe disability, moderate dis­ appear to be able to track.
both a prehospital and in-hospital GCS and outcome. ability, and a good outcome.
As an example, patients having a GCS of 6 to 15 in the
field were 30 times more likely to have a good outcome
than with a GCS less than 6. A prospective study of
emergency medical service (EMS) and in-hospital GCS
determination found a positive predictive value of 77%
for a poor outcome (dead, vegetative, or severely dis­
abled) in patients with a GCS of 3 to 5 and 26% with
a GCS of 6 to 8.

From a clinical perspective, the GCS is routinely
recorded at regular intervals during the neurocritical
care phase of TBI management. Various clinical deci­
sions have come to be based on GCS thresholds, such
as the need for intubation and consideration of ICP
monitoring when the GCS is less than 8. Similarly,

352 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

P late 14-16 Head Trauma

DEVICES FOR MONITORING INTRACRANIAL PRESSURE

Neurocritical Care and Intraparenchymal ICP
Management after montior Intraventricular
Traumatic Brain Injury cannula
Subarachnoid
Care of the severely injured patient is challenging and pressure screw
often requires a team approach. Systemic and intracra­
nial physiology may vary at different times. In 1996, Epidural
the Brain Trauma Foundation in conjunction with transducer
the American Association of Neurologic Surgeons
published the first evidence-based guidelines for the Means to establish
medical management of severe TBI. external ventricular
drainage
The first priority in severe TBI is to establish com­
plete and rapid physiologic resuscitation, which includes â•…
a secure airway and maintenance of O2 saturation of
greater than 90% and arterial systolic pressure greater Mannitol is the most commonly used pharmacologic cerebral oxygen delivery. Effective doses of mannitol
than 90╯mm╯Hg. If not already performed, endotrachial agent to lower ICP. The primary action of mannitol is range from 0.25╯g/kg to 1╯g/kg and lead to ICP reduc­
intubation should be undertaken in any patient with a in inducing an osmotic gradient between plasma and tion within 15 to 30 minutes.
GCS less than 9 or one who remains hypoxic despite cells, thus drawing edema fluid from the brain into the
supplemental oxygen. It is routine to place an arterial circulation. This causes an expansion of blood volume Because mannitol is an osmotic diuretic, it is excreted
line for continuous blood pressure (BP) recording. and a potential elevation in blood pressure but ulti­ entirely by the kidneys and thus should be used with
Central or Swan Ganz lines may be helpful in guiding mately results in a diuresis that may lower blood pres­ caution in patients with renal failure. It is important to
fluid resuscitation. sure. Secondary effects of mannitol include a reduction follow serum sodium and osmolality and limit use if
in blood viscosity, which increases cerebral blood and serum sodium is elevated to greater than 155╯mEq/L
The optimal resuscitation and maintenance intrave­ or osmolality is greater than 320╯mOsm/L.
nous fluids have been discussed earlier.

Once the patient is medically and surgically stabi­
lized, the next priority is to establish intracranial pres­
sure (ICP) monitoring in patients with a GCS less than
9 who have abnormal computed tomography (CT)
scans. ICP monitoring is also important in comatose
patients with normal CT scans if two of the following
are present: age greater than 40 years, systolic BP less
than 90╯mm╯Hg, or there is unilateral or bilateral
motor posturing.

There are various devices for ICP monitoring. The
intraventricular catheter is considered the gold stan­
dard and also allows for the drainage of cerebrospinal
fluid (CSF) when ICP is elevated. However, placement
of a ventricular catheter may be difficult in the swollen
and/or shifted brain, and a variety of parenchymal
monitors may serve as reasonable substitutes.

Brain oxygen saturations (PBo2) are being increas­
ingly monitored in severe TBI; however, their true
usefulness is unclear. Early information suggests that
PBo2 less than 20╯mm╯Hg may be associated with worse
outcomes, but it is unclear whether this represents the
severity of the underlying brain injury or a potentially
treatable “secondary injury.”

Less commonly used is cerebral microdialysis, which
can measure a variety of neurotransmitters and metabo­
lites, such as glutamate, aspartate, and lactate. It is like­
wise unclear how information obtained in this way will
play a role in the institution of a specific therapy.

The central tenant of severe TBI management is
control of ICP and, by extension, cerebral perfusion
pressure (CPP). CPP is the mean arterial pressure
minus the ICP and is the driver of cerebral blood
flow. As has been noted, persistently elevated ICP
(>20╯mm╯Hg) is associated with significant mortality.
An optimal CPP is generally in the range of 60 to
70╯mm╯Hg.

First-line therapies for ICP control include sedation,
paralysis, head-of-bed elevation to 20 to 30 degrees,
and avoidance of hyperthermia (>38.5°â•C› ).

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 353

P late 14-17 Brain: PART I

DECOMPRESSIVE CRANIECTOMY

Increased intracranial pressure refactory to medical management

Neurocritical Care and Obliteration of sulci
Management after Traumatic Obliteration of subarachnoid space
Brain Injury (Continued)
Decompressive craniectomy
Hypertonic saline (3%) is being increasingly used to Coronal suture
treat intracranial hypertension. Its mechanism of action Cranial flap
is clearance of edema fluid through bulk flow. Addi­
tional potential benefits include immunomodulation— Slit ventricles
prevention of leukocyte adherence and release of Effacement of cisterns
prostaglandins—and inhibition of excitotoxity. Typi­
cally, administered doses are intermittent boluses of After bifrontal craniectomy
250╯mL or a continuous infusion of 1╯mL/kg/hr. As
with mannitol, use should be limited if serum sodium Strip of bone
exceeds 155╯mEq/L or osmolality 320╯mOsm/L. remaining over
superior sagittal
Hyperventilation can rapidly decrease ICP by caus­ sinus
ing vasoconstriction and reducing intracranial blood
volume. Prolonged prophylactic hyperventilation was CT appearance after extensive bifrontal Subtemporal
previously a mainstay of ICP management but has been craniectomy for ICP control. Note that all decompression
found to worsen outcome, probably by inducing is­ of the cranial bone from the coronal suture
chemia. Currently, it is recommended that hyperventi­ forward has been removed.
lation should only be used for short periods and that
Pco2 be kept above 30╯mm╯Hg. ╅

If the ICP is uncontrollable despite these measures, before hospital discharge to minimize the risk of infec­ the quality of survival. A Cochrane meta-analysis of
high-dose barbiturate therapy may be necessary. This tion, especially if the bone has been implanted, and what little prospective, randomized data currently exist
suppresses metabolism and lessens cerebral blood-flow other complications associated with DC. Greater than yielded 50% odds of unfavorable outcome after DC.
requirements. The patient must, however, be hemody­ 20% of patients will develop symptomatic hydrocepha­ The Decompressive Craniotomy (DECRA) Trial of
namically stable because barbiturates can have a direct lus or subdural hygromas after DC. This is related in DC was recently published, and in adults with diffuse
cardiac depressant effect. Pentobarbital is the barbitu­ part to the brain being exposed to atmospheric pressure TBI and uncontrollable intracranial hypertension, it
rate most commonly used. A typical loading dose is once the ICP has normalized. found early bifrontal DC decreased intracranial pres­
10╯mg/kg over 30 minutes, followed by 5╯mg/kg hourly sure and intensive care unit (ICU) length of stay but
for three doses, with a maintenance dose of 1╯mg/kg/hr. Although DC can be highly effective in controlling was associated with more unfavorable outcomes.
Continuous electroencephalographic monitoring is elevated ICP, it remains unclear whether it improves
necessary as the goal of therapy is to induce burst
suppression.

Decompressive craniectomy (DC) has come to sup­
plant barbiturates as the “final” treatment for intracta­
ble ICP elevations. Originally introduced in the 1960s,
the procedure fell out of favor because, although mor­
tality was lowered after severe TBI, the quality of sur­
vival was unchanged. The procedure involves removal
of large portions of the skull in an attempt to control
ICP. Over the past decade, numerous published articles
on DC have used different ICP-based criteria for
undergoing the procedure, such as ICP greater than
20╯mm╯Hg for more than 30 minutes or ICP greater
than 30╯mm╯Hg for more than 20 minutes. Regardless
of the criteria used, there is a direct correlation between
the amount of bone removed and the ability to control
ICP. There is a less than 40% reduction in ICP if bone
removal is less than 8000 mm3 and greater than 80%
reduction with removal of more than 12,000 mm3.

The DC may be unilateral or bilateral. When unilat­
eral, bone is removed from the supraorbital ridge ante­
riorly to the inion posteriorly, superiorly to within 1╯cm
of the superior sagittal sinus and inferiorly to the floor
of the temporal fossa. Bilateral DC is typically bifrontal
from the supraorbital ridge to behind the coronal
suture (including a generous subtemporal decompres­
sion), leaving a 1-cm strip of bone over the superior
sagittal sinus. The bone is saved for later replacement
either by implantation into an abdominal subcutaneous
pocket or by freezing. It is typically replaced within 1
to 3 months. Some advocate replacement of the bone

354 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

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Laws ER, Jane Jr JA. Pituitary tumors: long-term outcomes and 987–96. DW, et al; Surgical Management of Traumatic Brain Injury
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Leksell L. Stereotactic radiosurgery. J Neurol Neurosurg Psychia- van den Bent MJ, Carpentier AF, Brandes AA, Sanson M, Taphoorn mas. Neurosurgery 2006;58(Suppl):S16–24.
try 1983;46:797–803. MJ, Bernsen HH, et al. Adjuvant procarbazine, lomustine, and Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell
Louis DN, Ohgaki H, Wiestler OD, Cavenne WK, editors. WHO vincristine improves progression-free survival but not overall DW, et al; Surgical Management of Traumatic Brain Injury
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Section 13—Headache
Brenner M, Oakley C, Lewis DW. Unusual headache syndromes

in children. Curr Pain Headache Rep 2007;11:383–9.
Dodick DW, Turkel CC, DeGryse RE, Aurora SK, Silberstein SD,

Lipton RB, et al. OnabotulinumtoxinA for treatment of chronic
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placebo-controlled phases of the PREEMPT clinical program.
Headache 2010;50:921–36.

358 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

INDEX

A Anencephaly, 6 Astrocytoma, pilocytic, 299, 302
ABC assessment, for head trauma, 351 Aneurysm Ataxias
Abducens nerve (VI), 5, 112
Abnormal involuntary movements, 158 intracerebral, 208 cerebellar, 248, 270
Abscess intracranial, subarachnoid hemorrhage and, 238–242 episodic, 194
Angioma, pontine cavernous, 237 Friedreich ataxia, 197
brain, 276, 314 Angioplasty, endovascular ICA, 216 Ataxic cerebral palsy, 18, 176
spinal epidural, 277 Angular gyrus, 55 Atherosclerosis, 209
Absence seizures, 69 Anomalous origins of cerebral arteries, 201 carotid artery, 213–216
Abuse Anorexia nervosa, 108 intracranial, 216
alcohol Anosognosia, 56 vertebral artery in neck, 217
Anterior aspects of skull, 338–339 Athetoid cerebral palsy, 18, 176
criteria, 92 Anterior cerebral arteries, 202–203, 209–212 Athetosis, 170
treatable dementia caused by, 63 Anterior choroidal artery, 202 Atonic cerebral palsy, 18, 176
child, 109–110 Anterior circulation Atonic seizures, 69
elder, 100 dissection, 216 Atrial fibrillation, 207, 223
intimate partner, 99 ischemia, 209–216 Atrial myxomatous tumor emboli, 224
prescription drug, 95 Anterior hypothalamic area, 115–116 Atrophy
Acamprosate, 93 Anterior pituitary hormone deficiencies, 140–141 in frontal and temporal lobes, 60
Accessory nerve (XI), 5 Anti-B-cell agents, in multiple sclerosis treatment, 263 of olfactory bulbs and tracts, 57
N-Acetylhomotaurine, 93 Anti-Borrelia burgdorferi antibodies, 282 Attention-deficit/hyperactivity disorders (ADHD), 107
Acoustic pathway, 46 Anti-N-methyl-D-aspartate receptor encephalitis, 102 Auditory radiations, 145
Acrocephalosyndactyly, 11 Antidiuretic hormone (ADH), 125, 137, 141 Aura, migraine, 319, 321
Acrocephaly, 11 Antiepileptic drugs Auscultation, in evaluation of stroke, 206
Action potentials, 74 molecular targets of, 76 Autism spectrum disorders, 31
Action tremor, 171 for status epilepticus, 72 Autoantibodies, of paraneoplastic disorder, 268–269
Acute disseminated encephalomyelitis, 250–251, 264–265 Antiphospholipid antibody syndrome, 231 Autoimmune disorders
Acute epidural hematoma, 347 Antipsychotic medications, 91, 102 acute disseminated encephalomyelitis, 264–265
Acute hemorrhagic leukoencephalopathy, 265 Antisocial personality disorder, 98 acute hemorrhagic leukoencephalopathy, 265–266
Acute hypertensive crisis, 334–335 Antithrombin III, 230 multiple sclerosis, 248–263
Acute necrotizing myopathy, 272 Anxiety disorders neuromyelitis optica, 264
Acute personality changes, 101–102 generalized (GAD), 84 paraneoplastic immune-mediated disorders, 268–269
Acute subdural hematoma, 348 panic disorder, 86 sensory neuropathies, 272
Adenohypophysis, 136 pediatric, 105 stiff-man syndrome, 267
Adiposity signals, 129 social (SAD), 85 Autonomic nervous system
Adrenal crisis, 143 Aphasia, 55 hypothalamic control of, 118
Adrenocorticotropic hormone (ACTH), 117, 125, 128, rehabilitation, 245 neuropathy, 272
130 Apnea, 134 nuclei and tracts, 218
Adult-onset primary dystonia, 168 Apnea test, 156 Autosomal recessive disorders, 194
Afferent connections, in cerebellum, 184, 190 Apoplexy, pituitary, 143, 335 Avulsion fracture, of metaphysis, 109
Afferent neurons, 50 Arachnoid, 15 Axial rudiment, 2
Afferent pathways, cerebellar, 185–186 Arachnoid cyst, 314 Axodendritic synapses, 47
African trypanosomiasis, 291 Arachnoid granulations, 15 Axons
Agenesis, of corpus callosum, 7, 29 Arcuate cerebellar tract, 186 acutely demyelinated, 258–259
Aggression to others, 106 Arcuate fibers, 38 descending hypothalamic, 131
Agyria, 6, 29 Arnold-Chiari malformation, 8 diffuse axonal injury, 348
AIDS dementia complex, 286 Arrhinencephalia, 7 ensheathment, 25
Akinetic mutism, 149 Arterial dissection, 334 inhibitory and excitatory fibers, 49
Akinetic-rigid syndrome, 161–167 Arterial supply to brain and meninges movement through, 47
Alar plate, 4–5, 20 anomalous origins, 201 myelinated, 257
Alcohol abuse anterior cerebral arteries, 202–203 preganglionic sympathetic, 128
criteria, 92 basilar artery, 201–202 B
treatable dementia caused by, 63 cervical segments, 200 B cells
Alcohol use disorders circle of Willis, 201 antigen-presenting, 255
risk factors, 92 external carotid artery, 201 ectopic follicle, 260
treatment, 93 internal carotid artery, 200 naive, 268
Alcohol withdrawal syndrome, 94 meningeal arteries, 203–204 Babinski sign, 62, 298
Alexia without agraphia, 55 middle cerebral arteries, 203 Baby blues, 82
Allantois, 2 ophthalmic artery, 202 Bacterial meningitis, 274–275, 336
Alzheimer disease, 80 posterior cerebral arteries, 202 Ballism, 170
clinical manifestations, 59 supratentorial arteries, 201 Basal ganglia, 27
disconnection of subcorticocortical circuits in, 39 vertebral artery extracranial, 200–201 anatomy, 158–160
memory circuits and, 53 Arterial thrombosis, platelet role, 229 and gait disorders, 196
pathology, 57–58 Arteriovenous malformations, 237 paraneoplastic disorders, 270
γ-Aminobutyric acid (GABA), 28 Arthropod-borne virus infections, 285 Basal ganglia and movement disorders
role in epilepsy neurobiology, 74–76 Ascending arousal pathways, 132 cerebral palsy, 176
Amnesia, 54 Ascending pharyngeal artery, 200 chorea/ballism, 170
Amnion, 2 Ascending reticular activating system, 101, 149 hyperkinetic, 168–169
Amphiphysin antibody, 271–272 Aseptic meningitis, 285 myoclonus, 173
Amygdala, 41–42, 44, 58, 80, 85, 131 Asperger disorder, 31 Parkinsonian syndrome, 161–167
Amygdaloid body, 158–160 Association neurons, 50 psychogenic, 175
Amyloid plaques, 58 Association pathways, cortical, 37 tics and Tourette syndrome, 172
Anatomic relationships Astrocytes, 21, 51
of hypothalamus, 112 Astrocytic tuft, in pallidum, 164 359
of pituitary gland, 138

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Index

Basal ganglia and movement disorders (Continued) C Cerebral cortex (Continued)
tremor, 171 Calcarine fissure, 42, 80 neuron types in, 50
Wilson disease, 174 Calcarine sulcus, 35 NMDA receptor encephalitis, 270
Calcitonin gene-related protein (CGRP), 318
Basal plate, 4–5, 20 Caloric testing with ice water, 151, 155 Cerebral edema, diffuse, 275
Basilar artery, 201–202, 209 Calvaria, 232, 341 Cerebral emboli
Caput succedaneum, 12
occlusion, 219–220 Cardiac arrest, 153 donor sources and embolic materials, 223–224
Basilar bifurcation, aneurysm, 239 Cardiac emboli, 208 recipient arteries, 223
Basilar plexus, 233 Cardiovascular function, hypothalamic regulation of, 131 treatment, 224
Basilar-type migraine, 321 Carotid artery disease, 210 Cerebral hemispheres
Basket cell, 181, 183–184 Carotid artery stenosis, 207 at 3 months, 27
Battle sign, 345 Carotid-cavernous fistula, 350 dominant, language dysfunction, 55
Bed nucleus of stria terminalis, 85 Carotid endarterectomy, 214–215 nondominant, higher cortical dysfunction, 56
Bed positioning, after stroke, 244 Carotid sinuses, 131 unilateral lesion, with compression of brainstem, 152
Benign hereditary chorea, 170 Cataplexy, 133 Cerebral malaria, 291
Benign paroxysmal vertigo of childhood, 326 Catechol-O-methyltransferase, 165–166 Cerebral palsy, 18, 176
Benign rolandic epilepsy, 70 Catecholamines, 131 Cerebral peduncle, sclerotic areas, 261
Benzodiazepine receptor agonists, 103 Caudal neuropore, 3 Cerebral venous sinus thrombosis, 335
Benzodiazepines, in alcohol withdrawal, 94 Caudate nucleus, 44, 158–160 Cerebral venous system, 233
Berry aneurysms, 242 Cerebrocerebellar connections, 191
Bifrontal craniectomy, 354 hemorrhage, 236 Cerebrocerebellar projections, 189
Bilateral cerebral hemisphere disease, 152 tail of, 43 Cerebrospinal fluid (CSF)
Biopsy Cavernous sinus, 112, 138, 200, 232–233 analysis, for multiple sclerosis, 252
efferent vein to, 114 diversion, in treatment of hydrocephalus, 17
brain, 266 meningioma, 304 low CSF-pressure headache, 330
temporal artery, 331 CD4+ T cells, 253–255 in neurosarcoidosis, 295
Bipolar disorder, 83 Cell adhesion molecules, in multiple sclerosis relapse, Cerebrovascular disease, pediatric, 243
Blastopore, 2 Cerebrovascular occlusive disease, 209
Blindness 256–258 Cerebrum
sudden unilateral, 248 Cell groups, hypothalamic, 115–116 inferior surface of cerebral hemisphere, 36
transient monocular, 210–211 Cell migration, in developing neocortex, 28 internal capsule, 158
Blood supply, of hypothalamus and pituitary gland, 114 Cell types, pituitary, 136 medial surface of cerebral hemispheres, 35–36
Body stalk, 2 Cellular diversity, in embryonic brain and spinal cord, 20 superolateral surface, 34–35
Body weight, hypothalamic regulation of, 129 Central diabetes insipidus, 137 Cervical dystonia, 169
Bone morphogenetic proteins (BMPs), 20, 27 Central nervous system (CNS) Cervical flexure, 4
Bones of skull, 338–344 Cervical nerve, first, 5
Border zone ischemia, 153 at 49 days, 10 Cervical nerve root, injuries at birth, 26
Border zone strokes, 211 inflammatory events during multiple sclerosis relapse, Chemical synaptic transmission, 48
Borderline personality disorder, 97 Chemotherapy, for brain tumors, 315
Brachial plexus, injuries at birth, 26 256–258 Chiari II malformation, 9
Brachiocephalic trunk, 200 tumors, differential diagnosis, 314 Chiasmatic cistern, 15
Brachycephalia, 11 Central (rolandic) sulcus, 34, 46, 144 Child abuse, 109–110
Brain Central tract, 24–25 Choanae, 342
arterial supply to, 200–204 Cephalic flexure, 4, 10 Cholinergic neuronal degeneration, 58
biopsy, 266 Cephalohematoma, 12 Chondroid chordomas, 313
embryonic, cellular diversity in, 20 Cerebellar ataxia, 248, 270 Chordomas, 313
external development, in second and third trimesters, 14 Friedreich, 197 Chorea, 170
fetal, growth in first trimester, 10 Cerebellar cognitive affective syndrome, 193 paraneoplastic, 270
inferior surface, 36 Cerebellar cortex Choroid plexus, 43
initial formation of, 3 and corticonuclear circuitry, 183–184 at 212 months, 27
medial surface, 35–36 and nuclei, 181–182 of fourth ventricle, 156
morphogenesis of, 4–5 Cerebellar corticonuclear projection, 190 of lateral ventricle, 15, 158–160
superolateral surface, 34 Cerebellar disorders papilloma, 312
tuberculosis of, 283 differential diagnosis, 194 of third ventricle, 138
Brain abscess, 276 of gait, 195 Chronic active plaques, 261
Brain damage, hypoxic-ischemic, 153 Cerebellar peduncles, 178, 180 Chronic paroxysmal hemicrania, 323
Brain death, 155 Cerebellitis Chronic silent plaques, 259
Brain tumor acute, 194 Chronic subcortical vascular disease, 226
as cause of seizures, 73 complicating varicella, 289 Chronic traumatic encephalopathy, 346
clinical presentations of, 298 Cerebellomedullary cistern, 15 Ciliary ganglion, 118
intraventricular, 312 Cerebellovestibular pathways, 189 Cingulate gyrus, 35–36, 80
pediatric, 301–302 Cerebellum, 5, 10 Cingulum, 38
right temporal, 66 efferent pathways, 187–188 Circle of Willis, 201, 217
treatable dementia caused by, 63 and fourth ventricle, 178 Circuit formation, in spinal cord, 23
treatment modalities, 315 gross anatomy, 179 Circuitry
Brain wave activity, 66 hemorrhage, 236–237 of basal ganglia, 160
Brainstem infarction, 219 cerebellar neuronal, 183–184
compression of, 152 modular organization, 190 cerebrocerebellar, 191
encephalitis, 271 motor examination, 192 Circumlocution, 59
and gait disorders, 196 subdivisions and afferent pathways, 185–186 Cirrhosis, postnecrotic type, 174
gliomas, 301–302 Cerebral abscess, 314 Cistern of corpus callosum, 15
lesions, in multiple sclerosis, 248 Cerebral aqueduct (of Sylvius), 10, 15 Claw toes, 197
nuclei and areas in, 149 Cerebral arteries Climbing fiber, 183–184
reflexes, 150, 155 anterior, 202–203 Climbing fiber pathways, 186
Broca aphasia, 55, 245 middle, 203 Cluster headache, 323–324
Brown adipose tissue, 126 posterior, 202 Coagulopathies
Brudzinski sign, 238, 275, 334 territories of, 201 antiphospholipid antibody syndrome, 231
Bruises, from child abuse, 110 Cerebral cortex, 85 inherited thrombophilias, 230
Bulbar paralysis, 219–220 development of, 28 platelet role in arterial thrombosis, 229
Bulimia nervosa, 108 function and association pathways, 37 Coccygeal nerve, 5
Bull’s eye rash, 282 and gait disorders, 196 Cochlear nerve, 310
Bullying, 106 inputs to hypothalamus, 123
major association bundles, 38

360 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Index

Cognitive-behavioral therapy, for insomnia, 103 Cryptococcal meningitis, 293 Dura mater, 15, 58
Cognitive processing therapy, for PTSD, 87 Cyanosis, in tonic-clonic seizure, 68 venous sinuses of, 232–233
Cold-stimulus headache, 325 Cyclic pattern of abusive relationships, 99
Colloid cyst, 335–336 Cyclic vomiting syndrome, 326 Dyslexia, developmental, 30
Cysticercus, of pork tapeworm, 280 Dysphagia, after stroke, 246
ventricular, 312 Cytogenetic disease, Prader-Willi syndrome, 113 Dyspraxia, constructional, 56
Color imaging, of corpus callosum, 40 Cytokines, inflammatory, 127–128 Dysthymic disorder, 104
Columns of fornix, 43–44 Cytomegalovirus coinfection, 287 Dystonia, 168–169
Coma D
Decerebrate rigidity, 148, 151 E
basilar artery occlusion and, 220 Decompression, microvascular, 327 Eastern equine encephalitis, 285
decorticate rigidity, 148 Decompressive craniectomy, 354 Eating disorders, pediatric, 108
differential diagnosis, 152 Decorticate rigidity, 148 Ectoderm, of embryonic disc, 2
irreversible, 155 Deep brain stimulation, 167 Ectopic B cell follicle, 260
Commissural fibers, 40 Deep cerebral nuclei, 182 Edema
Compression, chiasmatic, 139 Deep cervical lymph node
Computed tomography (CT) angiogram, 213 diffuse cerebral, 275
Computed tomography (CT) scan immunostimulatory events leading to relapse, 254 in trichinosis, 292
for coma, 151 multiple sclerosis in remission, 253 Effector T cells, 254–255
evaluation of stroke, 207 Defects of higher cortical function, testing for, 52 Efferent neurons, 50
in intracerebral hemorrhage, 236 Dehydration, endocrine response to, 125 Efferent pathways, cerebellar, 187–188
of intracranial hematomas, 349 Delayed sleep phase syndrome, 135 Efferent vein, to cavernous sinus, 114
Concentration, testing for, 52 Delirium, 101–102 Elder abuse, 100
Concussion, 346 Dementia Electrocardiogram, 207, 228
Conduct disorder, 106 frontotemporal, 60 Electrodes, subdural, 77
Conduction block, in multiple sclerosis relapse, 257–258 with Lewy bodies, 61 Electroencephalography (EEG), 66
Congenital brain malformations, as cause of seizures, 73 treatable, 63 absence pattern, 69
Congenital cerebral aneurysm, 238 vascular, 62 benign rolandic epilepsy, 70
Consciousness Dementia paralytica, 281 focal (partial) seizures, 67
altered, focal seizures with, 67–68 Demyelination hypsarrhythmia, 70
brain death, 155 in multiple sclerosis relapse, 258–259 neonatal seizures, 71
coma, 148 of white matter, 261 periodic wave pattern, 294
Dendritic cells, 253–255 status epilepticus, 72
differential diagnosis of, 152 Dendritic crest synapses, 47 tonic-clonic seizures, 68
disorders of, 149 Dendrodendritic synapses, 47 Electrophoresis, CSF, 252
emergency management and assessment, 150–151 Dental caries, 113 Emboli, cerebral, 223–224
hypoxic-ischemic brain damage, 153 Dentate gyrus, 35–36, 42 Emboliform nucleus, 180, 188–189
minimally conscious state, 154 Dentate nucleus, 178, 180, 188 Embolism, 204–205
neurologic examination, 151 Dentoalveolar abscess, 332 cardiac, 208
vegetative state, 154 Depressed fractures of skull, 12, 345 top-of-the-basilar artery, 220–221
ventilatory patterns and apnea test, 156 Depression Embryo
Constructional dyspraxia, 56 associated symptoms and comorbidities, 81 at 20-21 days, 3
Continuous positive airway pressure (CPAP), 134 in multiple sclerosis, 249 at 18 days, 2
Contusions, 348 postpartum, 82 from 28 through 36 days, 4–5
Conversion disorder, 89–90 Depressive disorders, pediatric, 104 Emergency management and assessment, for coma,
Convulsive status epilepticus, 72 Depressive pseudodementia, 63
Copaxone. See Glatiramer acetate Dermatomyositis, 271–272 150–151
Coronary heart disease, 226 Descending hypothalamic tract, 116 Emotional responses, blunted, 56
Corpus callosum, 35, 123 Detoxification Encephalitis
agenesis of, 7, 29 alcohol, 93
cistern of, 15 opioid, 96 anti-N-methyl-D-aspartate receptor, 102
color imaging of, 40 Developmental dyslexia, 30 brainstem, 271
glioma, 300 Diabetes insipidus, central, 137 Eastern equine, 285
splenium of, 43, 145 Diagnostic imaging, MRI, for multiple sclerosis, herpes simplex, 54, 290
Corpus striatum, 27 NMDA receptor, 270
Cortical necrosis, diffuse, 153 250–251 varicella-zoster, 289
Cortical organization of neurons, 50 Dialectical behavior therapy, 97 Encephalocele, 6
Cortical ridge, 253–254 Diaphragma sellae, 112, 138 Encephalopathy
Cortical spreading depression, 319 Diastematomyelia, 9 AIDS, 286
Corticobasal degeneration, 164–165 Diencephalon, 5 chronic traumatic, 346
Corticocortical circuits, 39 hypertensive, 227
Corticonuclear circuitry, 183–184 at 5 12 weeks, 19 hypoxic-ischemic, 153, 228
Corticonuclear microcomplexes, 190 in NMDA encephalitis, 270 metabolic disease with, 63
Corticospinal tract, 180 nuclei and areas in, 149 posterior reversible encephalopathy syndrome,
dysfunction, in multiple sclerosis, 249 Diffuse axonal injury, 348
Corticotrophs, 136 Diffusion tensor imaging, 40 334–335
Corticotropin deficiency, 140 Dimethyl fumarate (BG-12), 263 Endarterectomy, carotid, 214–215
Corticotropin-releasing hormone (CRH), 130 Diplegia, in cerebral palsy, 18, 176 Endoscopic transnasal trans-sphenoidal approach, 315
Cough headache, 325 Diploë, 341 Endovascular balloon occlusion, selective, 350
Cranial fossa, 343 Disconnection syndrome, 55 Energy balance, 129
Cranial nerves Disruptive behavior disorders, 106 Entorhinal cortex, 42, 53
at 36 days, 5 Dissection Ependymal lining, of brain cavities, 10, 14
ganglions, neurons of, 24 anterior circulation, 216 Ependymoma, ventricular, 312
injury, complicating skull fracture, 345 arterial, 334 Epidural hematoma, acute, 347
paraneoplastic disorders, 271 vertebral artery, 217–218 Epidural hemorrhage, 205
Cranial neuralgias, 327–328 Disulfiram, 93 Epilepsy
Cranial neuropathies, 240 Dopamine, role in parkinsonism, 166
Craniectomy, decompressive, 354 Dorsal median sulcus, 178 epileptic syndromes, 70
Craniopharyngiomas, pituitary tumors and, 306–308 Dorsal root ganglia, in midlumbar spine, 266 neurobiology of, 74–76
Craniosynostosis, 11 Drug-induced mechanisms, in etiology of stroke, 208 status epilepticus, 72
Creutzfeldt-Jakob disease, 294 Drug-induced parkinsonism, 165 treatment of, 77–78
Cribriform plate, foramina of, 344 Epileptic seizures
Crista galli, 343 absence (petit mal), 69
atonic, 69
causes of, 73

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 361

Index

Epileptic seizures (Continued) Frontal forceps, 40 Head injury, prognosis of coma related to, 151
focal (partial), 67–68 Frontal lobe, 14, 34 Head measurement, for hydrocephalus, 17
myoclonic, 69 Head process, 2
neonatal, 71 gyral atrophy of regions of, 57 Head trauma. See also Traumatic brain injury
tonic, 69 Frontotemporal dementia, 60
tonic-clonic, 68–69 Full outline of unresponsiveness score (FOUR), 150 as cause of seizures, 73
Functional MRI, cerebellum, 191 Glasgow coma score, 352
Episodic ataxias, 194 Funduscopic examination, 206 initial assessment and management, 351
Episodic memory, 53 G treatable dementia caused by, 63
Epstein-Barr virus, trigger for multiple sclerosis, 248 Gait disorders vascular injury, 350
Equilibrium disorders, with brain tumor, 298 Headache. See also Migraine
Erb palsy, 26 after stroke, 246 contiguous structure headaches, 332
Erythema migrans, 282 differential diagnosis, 195–196 cranial neuralgias, 327–328
Essential myoclonus, 173 Gamma-aminobutyric acid (GABA), 132, 184 giant cell arteritis, 331
Essential tremor, 171 Gene mutations, prothrombin, 230 idiopathic intracranial hypertension, 329
Ethmoidal bone, 338–340, 343 Generalized anxiety disorder (GAD), 84 intracranial hypotension, 330
Evoked potentials, in diagnosis of multiple sclerosis, 252 pediatric, 105 pain sensitive structures and pain referral, 318
Excitatory postsynaptic potential (EPSP), 49, 75 Generalized seizures pediatric, 326
Excitatory synapses, 48 absence (petit mal), 69 presenting in emergency department, 333–336
Executive function atonic, 69 tension-type, 325
myoclonic, 69 thunderclap, 333
in Alzheimer disease, 59 neurobiology of, 76 trigeminal autonomic cephalalgias, 323–324
deficits, 193 tonic, 69 Heart, sources of cerebral emboli, 223–224
testing, 52 tonic-clonic, 68–69 Heat conservation, 126
Exercises, passive range of motion, after stroke, 244 Generalized stiff person syndrome, 267 Hematomas
Exertional headache, 325 Genetics acute epidural, 347
Exophthalmos, pulsating, 350 of bipolar disorder, 83 intracranial, 349
Explicit memory, 53 in causation of seizures, 73 subdural
External carotid artery, 201 of major depressive disorder, 81
Extracranial hemorrhage, in newborn, 12 Genu recurvatum, 288 acute, 348
Extrapyramidal system, paraneoplastic disorders, 270 Germ cell tumors, intracranial, 309 from child abuse, 110
Eye movements Ghrelin, 129 treatable dementia caused by, 63
abnormal, 219–221 Giant cell arteritis, 208, 210, 331 Hemianopsia, 321
cerebellar lesion effects, 192 Giant congenital aneurysms, 239 Hemichorea, 170
in intracerebral hemorrhage, 236 Giant vertebrobasilar aneurysm, 242 Hemicrania continua, 324
Eye opening, in Glasgow Coma Scale, 352 Gilenya. See Fingolimod Hemiparesis, 211
Eye response, 150 Glasgow Coma Scale, 150, 352 Hemiplegia, in cerebral palsy, 18, 176
F Glatiramer acetate, in multiple sclerosis treatment, Hemispherectomy, 78
Facial nerve (VII), 5, 310 Hemorrhage
Factor V Leiden, 230 262–263 extracranial, 12
Falx cerebri, 27, 232 Glaucoma, 332 intracerebral, 204–205, 235–237
Fastigial nucleus, 187–188 Glia limitans disruption, 256 intracranial, 13
Fat in epidural space, 277 Glial cells, 51, 182 postpartum, 142
Feedback, to cerebral cortex, 191 Glioblastoma, 300 subarachnoid, 154, 204–205, 333–334
Fever, 127–128 Gliomas, 299 Hensen’s node, 2
Fibromuscular dysplasia, 210 Global aphasia, 55, 245 Herpes simplex encephalitis, 54, 290
Fimbria Globose nuclei, 188 Herpes zoster, 289
of fornix, 160 Globus pallidus, 145, 158–160 High endothelial venule, 253
of hippocampus, 42–43 Glossopharyngeal nerve (IX), 5 Higher cortical function
Fingolimod, in multiple sclerosis treatment, 262–263 Glossopharyngeal neuralgia, 328 defects of, 52
Fistula, carotid-cavernous, 350 Glucose tolerance test, abnormal, 113 dysfunction, nondominant hemisphere, 56
Flat affect, 91 Glutamate Hindbrain, 4–5
Flexor responses, appropriate localizing and, 148 generation of neuronal diversity in, 22
Floor plate, 20 in cerebellum, 184 Hippocampus, 42, 58, 80, 85
Fluid and electrolyte balance, 125 role in epilepsy neurobiology, 74–75 depth electrode to, 77
Focal dysplasia, 30 Glutamic acid decarboxylase, 267 Histopathology
Focal ischemic lesions, in cerebral palsy, 18 Golgi body, 47 of meningioma, 304
Focal (partial) seizures, 67–68 Golgi cells, 181–182 of multiple sclerosis, 259, 261
neurobiology of, 75–76 Gonadotrophs, 136 Hollenhorst plaque, 206
Follicular dendritic cells, 255 Gonadotropin deficiency, 140–141 Holoprosencephaly, 7
Food intake, hypothalamic regulation of, 129 Gracile fasciculus, 156 Hook bundle of Russell, 187, 189
Foot, dystonic, in Rett syndrome, 32 Gracile nucleus, 185 Hoover test, 90
Foot deformity, in spinal dysraphism, 9 Granular foveola, 232 Hormone fluctuation, as migraine trigger, 320
Foramen magnum, 344 Granular layer, cerebellar cortex, 181 Human immunodeficiency virus (HIV), 286–287
Foramen of Luschka, 15 Granule cells, 183, 189 Human leukocyte antigen-G (HLA-G), 260
Foramen of Magendie, 15 Gray matter, heterotopic, 7 Hunger signal, 129
Forebrain, 4–5 Gray ramus communicans, 118 Huntington disease, 170
axial sections through, 145, 160 Great cerebral vein (of Galen), 35 Hydranencephaly, 6
embryonic, 2 Growth hormone deficiency, 140–141 Hydrocephalus
limbic, 41 Gummatous neurosyphilis, 281 normal-pressure, 16, 63–64, 196
morphogenesis, and regional differentiation, 27 Gyri, 34–35 surgical treatment of, 17
neural plate of, 3 atrophy of, 57 Hyperhomocysteinemia, 230
regions associated with hypothalamus, 45 parahippocampal, 123 Hyperkinetic movement disorder, 168–169
Fornix, 35, 43, 123, 138 Gyrus cinguli, 45 Hypertension, idiopathic intracranial, 329
Fractures H Hypertensive encephalopathy, 227
open, of skull, 345 Habenula, 80, 123 Hypnic headache, 325
in young children, 109 Habenular commissure, 178 Hypochondriasis, 89
Friedreich ataxia, 197 Hallucinations, focal seizures with, 67 Hypoglossal canal, 344
Frontal bone, 338–343 Hamartomas, hypothalamic, 124 Hypoglossal nerve (XII), 5
Frontal encephalocele, 6 Head and neck, cutaneous nerves, 328 Hypophyseal portal system, 114
Hypophysis, 2, 10, 136, 143
362 Hypotension, intracranial, 330
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Index

Hypothalamic dysfunction, 270 Inferior nasal concha, 338 Lancet-Adams syndrome, 173
Hypothalamic sulcus, 4–5, 35 Inferior olivary nucleus, 190 Language dysfunction
Hypothalamus, 85 Inferior olive, 187
Inferior sagittal sinus, 232–233 dominant hemisphere, 55
anatomic relationships of, 112 Inferior surface of brain, 36 in frontotemporal dementia, 60
blood supply of, 114 Inflammation, systemic, hypothalamic response to, in migraine, 319, 321
cell groups, 115–116 in stroke, 211
control of 127–128 Language function test, 52
Information, storage and retrieval, 54 Lateral aspects of skull, 338–339
autonomic nervous system, 118 Inherited thrombophilias, 230 Lateral (sylvian) fissure, 34
pituitary gland, 117 Inhibitory postsynaptic potential (IPSP), 75 Lateral geniculate body, 46, 144, 156
developmental disorders of, 113 Inhibitory synapses, 48 Lateral geniculate nucleus, 145
forebrain regions associated with, 45 Injury patterns of child abuse, 110 Lateral hypothalamic area, 132
function and dysfunction, 124 Innominate artery, occlusive lesions, 217 Lateral longitudinal stria, 40–41
limbic and cortical inputs to, 123 Insomnia, 103 Lateral medullary syndrome, 218–219
nuclei of reticular formation, 149 Insula, 35 Lateral nuclei, hypothalamic, 116
olfactory inputs to, 119 Intention tremor, 171, 192, 249 Lateral vestibular nucleus, 180
regulation of Intercavernous sinuses, 232–233 Lead identification, in EEG, 66
cardiovascular function, 131 Intercellular adhesion molecule-1 (ICAM-1), 256–258 Lens placode, 2
food intake, body weight, and metabolism, 129 Interferon-β, in treatment of multiple sclerosis, 262 Lenticular nuclei, degenerative changes in, 174
sleep, 132–135 Interfollicular channel, 253 Lentiform nucleus, 44, 158–159
temperature, 126 Internal carotid artery, 112, 200 Leptin, 129
water balance, 125 Leptomeninges, infection of, 274
relationships to pituitary, 136 aneurysms, 241 Lesioning procedures, 167
response to systemic inflammation, 127–128 branches, 204 Lesions
somatosensory inputs to, 121 Internal carotid artery disease, 209–216 brainstem, 152
and stress response, 130 International Carotid Stenting Study, 215
taste information to, 122 Interneurons, 50 in multiple sclerosis, 248
visual inputs to, 120 Interpeduncular cistern, 15 into cavernous sinus, 138
Hypothermia Intervention programs, for antisocial personality disorder, in cerebral cortex, 37
paroxysmal, 126 demyelinating, in multiple sclerosis, 261
treatment for hypoxic-ischemic brain damage, 153 98 hypothalamic, 124
Hypoxia, 204, 228 Interventional radiology, repair of berry aneurysms, 242 mass, pituitary, 139
Hypoxic-ischemic brain damage, 153 Interventricular foramen, 10, 15 tumefactive, 251–252
I Intimate partner abuse, 99 Leukoencephalopathy
Idiopathic intracranial hypertension, 329 Intoxication, opioid, 95 acute hemorrhagic, 265
Idiopathic Parkinson disease, 161–164 Intracerebral hemorrhage, 204–205, 235–237 perinatal telencephalic, 7, 18
Idiopathic torsion dystonia, 168 Intracranial aneurysm, subarachnoid hemorrhage and, posterior reversible, 335
Immune-mediated injury, organ-specific, 268 progressive multifocal, 278
Immune response, hypothalamic control of lymphoid 238–242 Lewy bodies
tissue in, 128 Intracranial germ cell tumors, 309 dementia with, 61
Immunocompromised host, infections of, 278–279 Intracranial hemorrhage, in newborn, 13 in Parkinson disease, 163
Immunostaining, of Lewy bodies, 61 Intracranial hypotension, 330 Lewy body disease, 164–165
Impersistence, motor, 56 Intracranial pressure Lhermitte sign, 248–249
Inclusion bodies, Negri, 290 Limb paralysis, 219
Incontinence, in tonic-clonic seizure, 68 devices for monitoring, 353–354 Limbic encephalitis, 270
Indusium griseum, 40–41, 80 increased, 351 Limbic system, 41, 58, 80
Infantile spasms, 70 Intracranial pressure triad, 298 inputs to hypothalamus, 123
Infarction Intracranial vertebral artery disease Lissencephalia, 6
cerebellar, 219 cerebellar infarction, 219 Lissencephaly, 29, 73
completed, 205 lateral medullary syndrome, 218–219 Listeriosis, 278–279
lacunar, 225–226 medial medullary infarction, 219 Livedo reticularis, 231
myocardial, 207 Intraparenchymal hemorrhage, 333–334 Lobes
postpartum pituitary, 142 Intraparenchymal venules, 262 of brain, 14, 34
thalamic, 145 Intrasellar cystic craniopharyngioma, 308 of cerebellum, 179
Infarcts Intraventricular cannula, 353 frontal, gyral atrophy of regions of, 57
thalamic, 221–222 Ischemia frontal and temporal, atrophy in, 60
watershed, 18 anterior circulation, 209–216 occipital, hemorrhage, 236
Infections of nervous system vertebrobasilar territory, 219 parietal, in corticobasal degeneration, 165
brain abscess, 276 Ischemic stroke, 194, 204–206 of pituitary, 136–137
Creutzfeldt-Jakob disease, 294 Island of Reil, 14 Locked-in syndrome, 246
herpes simplex virus encephalitis, 290 Isocortical region, 45 Locus ceruleus, 58, 85
herpes zoster, 289 Isolated downbeat nystagmus, 194 Longitudinally extensive transverse myelitis (LETM), 264
HIV, 286–287 J Low CSF-pressure headache, 330
in immunocompromised host, 278–279 Jugular foramen, 344 Low-grade gliomas, 299
intracranial, 336 Juvenile myoclonic epilepsy, 70 Lower brachial plexus injury, 26
meningitis Juxtarestiform body, 180 Lower extremity, weakness in, 90
aseptic, 285 K Lugaro cell, 182
bacterial, 274–275 Kayser-Fleischer ring, 174 Lumbar puncture, 274
neurocysticercosis, 280 Kernig sign, 275, 334 Lumbosacral enlargement of spinal cord, 10
neurosarcoidosis, 295 Klumpke palsy, 26 Lyme disease, 282
parameningeal, 277 Knee jerk, repetitive, 248 Lymph nodes
parasitic, 291–293 Korsakoff syndrome, 54 deep cervical, 253–254
poliomyelitis, 288 L entrapment, 262
rabies, 290 Lacrimal bone, 338–340 Lymphoid tissue, hypothalamic control, in immune
spirochetal, 281–282 Lactotrophs, 136
tetanus, 284 Lacunar stroke, 225–226 response, 128
tuberculosis of brain and spine, 283 Lambert-Eaton syndrome, 266, 271–272 Lymphoma, primary CNS, 314
Infectious disease, in etiology of stroke, 208 Lamina terminalis, 5, 27, 80 M
Inferior cerebellar peduncle, 180, 218 Macroadenomas, pituitary, 141, 306–307
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS Magnetic resonance angiography, 210, 213–214

363

Index

Magnetic resonance imaging (MRI) Middle cerebral arteries, 203, 209–212 Narcolepsy, 133
of brain abscess, 276 aneurysm clipping, 241 Nasal bone, 338–340
diagnostic, for multiple sclerosis, 250–251 Nasal cavity, 340
of intracranial hematomas, 349 Midsagittal section of skull, 340 Natalizumab, in multiple sclerosis treatment,
Migraine, 208
Magnetic resonance venography, 234 263
Magnocellular neurons, 117 aura, 321 Neglect, as elder abuse, 100
Major depressive disorder, 81 management, 322 Negri inclusion bodies, 290
pathophysiology, 319 Neocortex, developing, 28
pediatric, 104 presentation, 320 Neonatal seizures, 71
Malaria, cerebral, 291 Migration of neurons, defective, 29 Neopallium, 10
Mammillary bodies, 42, 112 Milk let-down reflex, 121 Neoplasm, predicted by seropositivity, 269
Mammillothalamic tract, 116 Minimally conscious state, 154 Nerve biopsy, 266
Mandible, 338–339 Mitochondrial encephalomyopathies, 194 Neural crest, 2
Mandibular nerve, 122 Mitoxantrone, in multiple sclerosis treatment, 263
Marantic emboli, 224 Mitral valve prolapse with clots, 224 derivatives of, 3–5, 21
Mass lesions, pituitary, 139 Modular organization of cerebellum, 190 Neural crest progenitor, 22
Mastoid foramen, 344 Molecular layer of cerebellar cortex, 181, 183 Neural groove, 3
Maxilla, 338–340, 342 Monoaminergic fibers, 186 Neural plate of forebrain, 3
Maxillary nerve, 122 Mood disorders Neural stem cells, 20, 22
Maxillary sinus pain, 332 bipolar disorder, 83 Neural tube, 20
McArdle disease, 196 major depressive disorder, 81
Meckel-Gruber syndrome, 6 postpartum depression, 82 cells derived from, 21
MECP2 gene mutation, in Rett syndrome, 32 Mossy fiber pathways, 185–186 defective formation of, 6–7
Medial dorsal nucleus, 144 Mossy fibers, 184, 189 Neuralgia
Medial eminence, 178 Motor and sensory cortices, 37 cranial, 327–328
Medial geniculate body, 46, 156 Motor and sensory deficits, in intracerebral hemorrhage, postherpetic, 289
Medial longitudinal stria, 40–41 Neurenteric canal, 2
Medial medullary infarction, 219 236 Neurinomas, acoustic, 310
Medial nuclei, hypothalamic, 115–116 Motor aura, 321 Neurobiology of epilepsy, 74–76
Medial surface of cerebral hemispheres, Motor examination, cerebellar, 192 Neuroblast, 21
Motor neuron syndromes, 272 Neurocritical care management, after traumatic brain
35–36 Motor neurons, destruction by poliovirus, 288
Median aperture, 15 Motor response, 150–151 injury, 353–354
Median preoptic neurons, 132 Neurocysticercosis, 280
Medulla, nuclei of reticular formation, 149 in Glasgow Coma Scale, 352 Neurodegenerative disorders, 194
Medulla oblongata, 10, 14, 35, 178, 187 Movement disorders Neurofibrillary tangles, 57–58

mature and at 5 12 weeks, 19 abnormal involuntary movements, 158 in parkinsonism, 163–164
Medulloblastoma, 301–302 cerebral palsy, 176 Neurogenesis, in developing neocortex, 28
Melanin-concentrating hormone, 116 chorea/ballism, 170 Neurohypophysis, 136–137
Melatonin, 120 hyperkinetic, 168–169 Neuroimmunologic syndromes, primary and
Memory myoclonus, 173
Parkinsonism, 161–167 paraneoplastic processes, 266
circuits, 53 psychogenic, 175 Neurologic examination for coma, 151
short-term, multiple sclerosis effects, 249 tics and Tourette syndrome, 172 Neurometabolic cause of seizures, 73
testing, 52 tremor, 171 Neuromuscular junction disorders, 195, 272
Memory loss Wilson disease, 174 Neuromyelitis optica, 251, 264
in Alzheimer disease, 59 Moyamoya, 243 Neurons
in basilar artery embolism, 221 Mucosa, olfactory, 119
Meningeal arteries, 203–204 Multifocal dystonia, 168 cerebellar, orientation of, 184
Meninges, and superficial veins, 232 Multiinfarct dementia, 62 differentiation and growth, 23
Meningiomas, 304–305 Multiple sclerosis diversity, in spinal cord and hindbrain, 22
Meningitis clinical manifestations, 249 loss, in entorhinal hippocampal circuit, 53
aseptic, 285 diagnosis median preoptic, 132
bacterial, 274–275, 336 migration along radial glial cells, 28
cryptococcal, 293 CSF analysis, 252 parvicellular, 117
tuberculous, 283 evoked potentials, 252 proliferation and migration disorders, 29
Meningocele, 8 MRI, 250–251 structure and synapses, 47
Meningoencephalitis, syphilitic, 281 tumefactive lesions, 251–252 types, in cerebral cortex, 50
Meningomyelocele, 8 differential diagnosis, 314 Neuropathology of Parkinson disease, 163–164
Meningovascular syphilis, 281 gross CNS pathology, 261 Neurosarcoidosis, 295
Mental foramen, 339 histopathology, 261 Neurosyphilis, 281–282
Mesencephalic tectum, tumor compressing, 309 pathophysiology, 253–255 Neurotransmitters
Mesencephalon, 4–5 progressive, enigma of, 260 in cerebellum, 184
mature and at 5 12 weeks, 19 relapses, 256–259 role in epilepsy neurobiology, 74
Metabolic disease, with encephalopathy, 63 treatment, 262–263 Night terrors, 135
Metabolism, hypothalamic regulation of, 129 visual manifestations, 248 Nocardiosis, 278
Metastatic tumors to brain, 303 Myasthenia gravis thymoma, 271–272 Node of Ranvier, 257, 259
Metencephalon, 5, 10 Myelencephalon, 10 Non-germ cell tumors, 309
N-Methyl-D-aspartate (NMDA) receptor Myelin, stripping by macrophages, 258 Nonconvulsive status epilepticus, 72
encephalitis, 270 Myelination, 24–25 Nonlanguage cues, abnormal recognition of, 56
role in epilepsy neurobiology, 75 Myelomeningocele, 6, 9 Nonsyndromic craniosynostosis, 11
Microadenoma, pituitary, 307 Myocardial infarction, 207 Normal-pressure hydrocephalus, 16, 63–64, 196
Microaneurysm, cerebral, 235 Myocardiopathy with thrombi, 224 North American Symptomatic Carotid Endarterectomy
Microcephaly, 11 Myoclonic seizures, 69
Microglial cells, 21, 51 Myoclonus, 173 Trial, 215
T cell-mediated activation, 256 Myopathy Notochordal plate, 2
Microgyria, 6 acute necrotizing, 272 Novantrone. See Mitoxantrone
Microvascular decompression, 327 inflammatory, 195 Nuclei
Midbrain, 4–5 N
embryonic, 2 Naive CD4+ T cells, 253–255 cerebellar, 181–182
nuclei and areas in, 149 Naltrexone, 93 hypothalamic, 115–116
Middle cerebellar peduncle, 180 thalamic, 46, 144
Nucleus ambiguus, 218–219
364 Nucleus interpositus anterior, 188
Nucleus interpositus posterior, 188
Nucleus reticularis tegmenti pontis, 186

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Index

Nucleus reticularis thalami, 76 Panhypopituitarism, 141 Piriform area, 41
Null cell adenoma, 307 Panic disorder, 86 Piriform cortex, 80
O Papillae, of tongue, 122 Pituitary apoplexy, 143, 335–336
Obesity Papilledema, in pseudotumor cerebri, 329 Pituitary gland
Papilloma, choroid plexus, 312
in lesions of hypothalamus, 124 Parabrachial nucleus, 122 anatomic relationships of, 138
in Prader-Willi syndrome, 113 Parahippocampal gyrus, 123 anterior, hormone deficiencies, 140
pseudotumor cerebri in, 329 Parallel fibers, 181, 184 blood supply, 114
Obsessive-compulsive disorder, 88 Paralysis hypothalamic control of, 117
Obstructive hydrocephalus, 16 mass lesions, effects on visual apparatus, 139
Obstructive sleep apnea, 134 limb, 219 posterior, 137
Occipital artery, 200 sleep, 133 postpartum pituitary infarction, 142
Occipital bone, 339–343 upper extremity, 90 relationship to hypothalamus, 112, 136
Occipital encephalocele, 6 Parameningeal infections, 277 severe hormone deficiencies, 141
Occipital forceps, 40 Paraneoplastic immune-mediated disorders, 268–269 tumors, and craniopharyngiomas, 306–308
Occipital horn, 15 Parasitic infections Pituitary stalk lesions, 124
Occipital lobe, 14, 35, 37 African trypanosomiasis, 291 Plaques
hemorrhage, 236 cerebral malaria, 291 Hollenhorst, 206
Occipital neuralgia, 328 cryptococcal meningitis, 293 of multiple sclerosis, 259, 261
Occipital osteodiastasis, 12 trichinosis, 292 neuritic, 58
Occipital sinus, 232–233 Parasomnias, 135 Plasma proteins, in multiple sclerosis relapse, 257
Occlusion Paraventricular nuclei Platelets, role in arterial thrombosis, 229
basilar artery and branches, 221 hypothalamic, 115–116, 126 Poliomyelitis, 288
cerebral arteries, 212 pituitary, 137 Polycythemia, 208
proximal and midbasilar artery, 219–220 Parietal bone, 338–343 Pons, 5, 10, 14, 112, 116
top-of-basilar artery, 222 Parietal lobe, 14, 34–35, 37 compressed by chordoma of clivus, 313
Ocular manifestations in corticobasal degeneration, 165 hemorrhage, 236
of carotid artery disease, 211 Parietooccipital sulcus, 14, 34 nuclei and areas in, 149
of cerebral aneurysms, 240 Parinaud syndrome, 309 Pontine cavernous angioma, 237
of multiple sclerosis, 248 Parkinsonism Pontine cistern, 138
Oculomotor nerve (III), 5, 112, 148 drug-induced, 165 Pontine nuclei, 185
Olfactory bulb, 10, 14, 28, 41, 53 early manifestations, 161 Pontocerebellum, 185–186
atrophy of, 57 neuropathology, 163–164 Porencephaly, 7
structure of, 119 role of dopamine, 166 Porus acusticus, 310–311
Olfactory ensheathing cells, 25 successive clinical stages, 162 Post-infectious cerebellitis, 193
Olfactory inputs to hypothalamus, 119 Paroxysmal depolarization shift, 75–76 Postanoxic myoclonus, 173
Olfactory placode, 2 Paroxysmal hemicrania, 323–324 Postcommissural fornix, 123
Olfactory tract, 35, 241 Paroxysmal torticollis of infancy, 326 Postdromal phase of migraine, 320
Oligodendrocytes, 24–25, 51 Parvicellular neurons, 117 Posterior carotid artery, 211
Oligodendroglial cells, 22 Passive range of motion exercises, after stroke, 244 Posterior cerebral arteries, 202
Oligodendroglioma, 299 Pathophysiology atheromatous disease of, 222
Olivary afferents and projections to cerebellum, 190 of migraine, 319 Posterior communicating artery, 202
Ophthalmic artery, 202 of multiple sclerosis, 253–255 Posterior cranial fossa, arteries, 218
Ophthalmic herpes zoster, 289 of Rett syndrome, 32 Posterior fossa hematoma, 347
Ophthalmoplegic migraine, 321 Pediatric brain tumors, 301–302 Posterior inferior cerebellar artery, aneurysm, 239
Opioid use disorders, 95 Pediatric cerebrovascular disease, 243 Posterior medial surface of brain, 36
Opioid withdrawal syndrome, 96 Pediatric psychiatry Posterior pituitary gland, 137
Opportunistic infection, in HIV, 287 anxiety disorders, 105 Posterior reversible encephalopathy syndrome, 334–335
Oppositional defiant disorder, 106 attention-deficit/hyperactivity disorders, 107 Postganglionic motor neurons, 23
Optic area, 2 depressive disorders, 104 Postherpetic neuralgia, 289
Optic canal, 344 disruptive behavior disorders, 106 Postictal period after seizure, 68
Optic chiasm, 112, 120, 136, 241 eating disorders, 108 Postpartum depression, 82
compressed, 143, 307–308 Periaqueductal grey, 319 Postpartum pituitary infarction, 142
Optic nerves, 10, 27, 112 Perihypoglossal nuclei, 186 Posttraumatic headache, 336
Optic neuritis, in multiple sclerosis, 248 Perinatal telencephalic leukoencephalopathy, 7, 18 Posttraumatic stress disorder (PTSD), 87
Optic tract, 139 Periodic limb movements, 135 Postural tremor, 171, 192
Optic vesicle, 4 Peripheral motor sensory unit paraneoplastic, 271 Posture
Orbital surface Peripheral nervous system, morphogenesis of, 4–5 in lumbar disc herniation, 195
of cerebral hemisphere, 36 Peripheral neuropathies, 195 modified hyperextension, 164
of zygomatic bone, 338 Perivascular cells, 51 Potassium ion conductance, 74
Orexin neurons, 132–133 Perivascular cuff T cells, 257–258 Pott disease, 283
Organ damage, from daily alcohol use, 92 Periventricular-intraventricular hemorrhage (IVH), 13 Prader-Willi syndrome, 113
Orthostatic headache, 330 Periventricular nuclei, hypothalamic, 115–116 Prechiasmatic optic nerves, 139
Osmolality, regulation of, 125 Persistent vegetative state, 153–154 Precommissural fornix, 80
Otic ganglion, 118, 122 Personality changes, acute, 101–102 Prefrontal cortex, 37, 91
Otorrhea, 345 Petit mal seizures, 69 Preganglionic sympathetic axon, 121
Oxytocin, 117, 137 Petrosal sinuses, 233 Preoccipital notch, 34
P Petrous bone fractures, 345 Preoperative evaluation, for epilepsy treatment, 77
Pain PHACE syndrome, 243 Preoptic nucleus, medial, 115–116
of headache, pain sensitive structures and pain referral, Pharmacologic treatment Prepontine cistern, 15
for alcohol dependence, 93 Prescription drug abuse, 95
318 for GAD, 84 Presynaptic neuron, 51
inputs to hypothalamus, 121 for major depressive disorder, 81 Preventative treatments for migraine, 322
persistent unilateral facial, 328 for panic disorder, 86 Primary brainstem lesion, 152
somatization, 89 Physical abuse, 99–100 Primary fissure, cerebellar, 179, 185
Palatine bone, 340, 342 of child, 109 Primary headache, 318
Pallidotomy, 167 Pilocytic astrocytoma, 299, 302 Primary progressive multiple sclerosis, 248
Pineal gland, 112, 138 Primitive knot, 2
tumors, 309 Primitive streak, 2–3
Pineal recess, 14 Prion disease, 294

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 365

Rhombencephalon, 4–5 Index
Rhomboid fossa of 4th ventricle, 156
Progestins, 21 Right temporal tumor, 66 Somatosensory cortex, 37
Progressive multifocal leukoencephalopathy, 278 Risk factors Somatosensory inputs to hypothalamus, 121
Progressive phases Somatosensory system, spinocerebellar pathways,
for alcohol use disorders, 92
of Alzheimer disease, 59 for cardiovascular disease, 226 186
of vascular dementia, 62 for intracerebral hemorrhage, 235 Somnolence, 124
Progressive supranuclear palsy, 164 Rituximab, in multiple sclerosis treatment, 263 Spasms
Prolactinomas, 308 Rolandic sulcus, 14
Proliferation of neurons, defective, 29 Roof of fourth ventricle, 178 infantile, 70
Prosencephalon, 4–5 Roof plate, 20 in tetanus, 284
Prosocele, 4 S Spastic quadriplegia, 18
Prostaglandins, 127–128 Sacral nerve, first, 5 Spatial disorientation, 59
Protein C deficiency, 230 Sacral spinal cord, 10 Spatial excitatory summation, 49
Protein S, 230 Sarcomatous transformation of chordoma, 313 Spatial neglect, unilateral, 56
Prothrombin gene mutation, 230 Satellite cell formation, 24–25 Sphenoid sinusitis, 332
Pseudotumor cerebri, 329 Scaphocephaly, 11 Sphenoid wing meningioma, 305
Psychogenic movement disorders, 175 Schizencephaly, 29 Sphenoidal bone, 338–340, 342–343
Psychosis, postpartum, 82 Schizophrenia, 91 Sphenoidal electrodes, 77
Pterygopalatine fossa, 339 Schwann cells, 21–22 Sphenoidal emissary foramen, 344
Pterygopalatine ganglion, 118, 122 Schwann sheath, 24 Sphenoidal sinus, 138
Pulvinar, 44, 144, 160 Schwannomas, vestibular, 310–311 Sphenoparietal sinuses, 232–233
Pupillary abnormalities, 220–221 Scoliosis Spina bifida aperta, 8–9
Pupillary light reflex, 151 in Friedreich ataxia, 197 Spina bifida occulta, 8
Purkinje cell cytoplasmic autoantibody-type 1 (PCA-1), in poliomyelitis, 288 Spinal cord
in Rett syndrome, 32 central canal of, 15
269–271 Second impact syndrome, 346 circuit formation in, 23
Purkinje cell layer, 181 Secondary headache, 318 differentiation of regions of, 10
Purkinje cells, 182–184, 187 Secondary progressive multiple sclerosis, 248, 260 embryonic, cellular diversity in, 20
Putamen, 44 Seizures generation of neuronal diversity in, 22
with brain tumor, 298 initial formation of, 3
hemorrhage, 236 causes of, 73 mature and at 5 12 weeks, 19
Pyramid, 14 epileptic, 67–69 morphogenesis of, 4–5
Pyramidal cell, 47 neonatal, 71 myopathies, 195
Pyramidal cerebral palsy, 18 Semantic memory, 53 paraneoplastic disorders, 271–272
Q Sensitization, pain, 318 Spinal cord-medullary junction, 149
Quadrigeminal cistern, 15 Sensory aura, 321 Spinal dysraphism, 7–9
Quadriplegia, in cerebral palsy, 18 Sensory neuropathies, 271–272 Spinal epidural abscess, 277
R Separation anxiety disorder, 105 Spinal medulla, 2
Rabies, 290 Septal nuclei, 80 Spinal nerves, at 36 days, 5
Raccoon sign, 345 Severe anterior pituitary hormone deficiency, 141 Spine
Radiation therapy, for brain tumors, 315 Sex hormones, 118 midlumbar, dorsal root ganglia in, 266
Radiologic repair, of berry aneurysms, 242 Sheehan syndrome, 142 tuberculosis of, 283
Ramsay Hunt syndrome, 289 Shivering, 126 Spinocerebellum, 185–186
Range of motion, passive, after stroke, 244 Shunt procedure, for hydrocephalus, 17, 63 Spinothalamic tract, 218
Raphe nuclei, 39, 149 Sickle cell anemia, 208 Spiral fractures, 109
Rapid eye movement (REM), 132–133 Sickness response, 127–128 Spirochetal infections, 281–282
Sigmoid sinuses, 232–233 Splanchnic nerve, 23
behavior disorder, 135 Signs and symptoms of opioid withdrawal, 96 Splenium of corpus callosum, 43, 145, 158–160, 222
Recent memory, processing circuit for, 53 Sinusitis, 332 Sporadic ataxias, 194
Red nucleus, hypothalamic, 116 Skin innervation, trigeminal nerve divisions, 327 Sporadic Creutzfeldt-Jakob disease, 294
Referral of pain, 318, 328 Skull Stabbing headache, 325
Reflexes anterior and lateral aspects, 338–339 Stages of acute personality changes, 101
base Stages of alcohol withdrawal, 94
brainstem, 150 Stages of parkinsonism, 162–163
corneal, 155 bones, markings, and orifices of, 343–344 Status epilepticus, 72
Registration of memory traces, 54 external aspect of, 342 Status marmoratus, 18
Regulatory T cells, 255 calvaria, 341 Stellate cells, 181, 184
Rehabilitation erosion Stem cells, neural, 20, 22
aphasia, 245 in convexity meningioma, 305 Stenosis, carotid artery, 207
issues related to, 246 in neurosyphilis, 281 Stenting, endovascular, 216
stroke, 244 fractures, in newborn, 12 Steps in multiple sclerosis relapse, 256–259
Relapse in multiple sclerosis injuries, 345 Stiff-man syndrome, 267, 271
peripheral events preceding, 253–255 midsagittal section, 340 Stimulatory immunologic synapse, 254
steps in initiation of, 256–259 osteomyelitis of, 277 Straight sinus, 15, 232–233
Relapsing-remitting multiple sclerosis, 248 Sleep, hypothalamic regulation of, 132 Stress response, 130
Remyelination, 259 Sleep disorders Stria medullaris thalami, 45
Replacement therapies, for pituitary hormone apnea, 134 Stria terminalis, 123
narcolepsy, 133 Stroke
deficiencies, 141 parasomnias, 135 amnesic, 54
Resective surgery, for epilepsy, 78 periodic limb movements, 135 anterior circulation ischemia, 209–216
Respiration, in FOUR score, 150 Sleep spindles, 66 aphasia rehabilitation, 245
Rest tremor, 171 Sleeping sickness, 291 cerebral emboli, 223–224
Restiform body, 180 Small cell lung cancer, 270, 272 clinical evaluation and treatment, 206–208
Restless leg syndrome, 135 Social anxiety disorder (SAD), 85 coagulopathies, 229–231
Reticular formation, 149 pediatric, 105 hemorrhagic, 204–205
Reticulocerebellar projections, 186 Sodium amobarbital test, 77
Retinal changes, in cerebral aneurysm, 240 Sodium ion conductance, 74 intracerebral, 235–237
Retinohypothalamic tract, 120 Somatization, 89 subarachnoid, 238–242
Rett syndrome, 32 hypertensive encephalopathy, 227
Reversible cerebral vasoconstriction syndrome, 334 hypoxia, 228
Rhinencephalic region, 45 initial rehabilitation, 244
Rhinencephalon, 10, 41 ischemic, 194, 205–206
lacunar, 225–226
366 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Temperature, hypothalamic regulation of, 126 Index
Temporal bone, 338–340, 342–343
Stroke (Continued) Temporal excitatory summation, 49 Triggers
pediatric cerebrovascular disease, 243 Temporal fossa hematoma, 347 of migraine, 320
rehabilitative issues, 246 Temporal lobe, 14, 35, 37 of multiple sclerosis, Epstein-Barr virus as, 248
timing and evolution, 206 Temporal lobectomy, 78
uncommon etiologic mechanisms in, 208 Temporalis muscle, 232 Triptan mechanism, in treatment of migraine, 322
and vascular dementia, 62 Temporomandibular disorder, 332 Trochlear nerve (IV), 5, 112
venous sinus thrombosis, 232–234 Tension-type headache, 325 Tuber cinereum, 112, 138
vertebral basilar system disorders, 217–222 Tentorial surface of cerebral hemisphere, 36 Tubercle bacilli, 283
Terminal phase of Alzheimer disease, 59 Tuberculosis, of brain and spine, 283
Subacute onset myelopathy, 271 Testing for defects of higher cortical function, 52 Tuberomammillary nucleus, 132
Subacute sensory neuronopathy, 272 Tetanus, 284 Tuberosity of maxilla, 339
Subarachnoid hemorrhage, 154, 204–205, 333–334 Tethered spinal cord syndrome, 9 Tuberous sclerosis complex, 73
Thalamic infarcts, 221–222 Tumefactive multiple sclerosis, 251–252, 314
and intracranial aneurysms, 238–242 Thalamocortical radiations, 46, 144 Tumors
Subarachnoid pressure screw, 353 Thalamogeniculate arteries, 218, 221–222
Subarachnoid space, 15, 256 Thalamostriate artery, 241 atrial myxomatous tumor emboli, 224
Subclavian artery, occlusive lesions, 217 Thalamotomy, 167 brain. See Brain tumor
Subcorticocortical circuits, 39 Thalamus, 44, 85 CNS, differential diagnosis, 314
Subdivisions of cerebellum, 185–186 metastatic to brain, 303
Subdural electrodes, 77 anatomy, 144–145 of pineal region, 309
Subdural empyema, 277 hemorrhage, 236 pituitary, and craniopharyngiomas, 306–308
Subdural hematoma pathology, 145 Tysabri. See Natalizumab
reticular nucleus, 149 U
acute, 348 Thiamine deficiency, 194 Uncinate fasciculus, 38
from child abuse, 110 Thigh adduction test, 90 Uncommon etiologic mechanism of stroke, 208
treatable dementia caused by, 63 Thoracic nerve, first, 5 Uncus, 35–36, 123
Subdural hemorrhage, 205 Thoracic spinal cord, 10 Unilateral cerebral hemisphere lesion, with compression
in newborn, 13 Thrombophilias, inherited, 230
Subependymoma, ventricular, 312 Thrombosis, 204–205 of brainstem, 152
Subfrontal hematoma, 347 arterial, platelet role, 229 Unilateral spatial neglect, 56
Subgaleal hemorrhage, 12 cerebral venous, 335 Unipolar brush cell, 182
Sublabial trans-septal trans-sphenoid approach, 315 venous sinus, 232–234 Upper brachial plexus injury, 26
Submandibular ganglion, 118 Thunderclap headache, 333 Upper extremity paralysis, 90
Substantia innominata, 80 Thymoma, myasthenia gravis, 271–272 Urinary bladder, neurogenic, 248
Substantia nigra, 36, 91, 160 Thyroid-stimulating hormone, 117 V
Subthalamic nucleus, 167 Thyrotrophs, 136 Vagus nerve (X), 5, 121
Subtypes of alcohol dependence, 92 Thyrotropin deficiency, 140–141
Sulcus limitans, 3–5 Tics, 172 stimulation, for epilepsy, 78
Summation of excitation and inhibition, 49 Timing of stroke, 206 Varicella-zoster virus, 289
SUNCT/SUN trigeminal autonomic cephalalgias, Tolerizing signals, 253 Vascular cell adhesion molecule-1 (VCAM-1), 256–258
augmented, 262 Vascular dementia, 62
323–324 Tonic-clonic seizures, 68–69 Vascular disease, as cause of seizures, 73
Sundowning, 102 Tonic seizures, 69 Vascular malformations, 237
Superior cerebellar peduncle, 180 Top-of-the-basilar artery embolism, 220–221 Vasopressin, 137
Superior hypophyseal artery, 114 Topiramate, 93 Vegetative state, persistent, 153–154
Superior longitudinal fasciculus (SLF), 38 Torticollis Vein of Galen malformation, 243
Superior orbital fissure, 344 muscular, 169 Venous sinus thrombosis
Superior sagittal sinus, 15, 27, 232–233 paroxysmal, of infancy, 326
Superior salivatory nucleus, 319 Tourette syndrome, 172 cerebral venous system, 233
Superolateral surface of cerebrum, 34 Toxoplasmosis, 279 diagnosis and treatment, 234
Suprachiasmatic nucleus, 120 Trabecula, 114 dura mater venous sinuses, 232–233
Supraoptic nuclei Transcranial Doppler, 213 Ventilatory patterns, and apnea test, 156
Transient global amnesia, 54 Ventral lateral nucleus, 144
hypothalamic, 115–116 Transient hydrocephalus, 17 Ventral tegmental area, 149
pituitary, 137 Transient ischemic attack (TIA), 205, 210–212 Ventricles
Suprasellar extension, 306 Transient monocular blindness, 210–211 connections of basal ganglia, 159
Supratentorial arteries to brain, 201 Translabyrinthine approach, removal of vestibular in first trimester, 10
Surveillance fourth, cerebellum and, 178
CSF, reduced, 262 schwannoma, 311 mature brain, 15
step in multiple sclerosis relapse, 256 Transverse sinuses, 232–233 Ventricular system, embryonic, 5
Sutures, skull, 338–339, 341 Traumatic brain injury Ventriculomegaly, 57
Sweating, 126 Ventrolateral preoptic nucleus, 103, 132
Sylvian sulcus, 14 acute epidural hematoma, 347 Ventromedial nucleus, hypothalamic, 116
Sympathetic trunk ganglia, 130 acute subdural hematoma, 348 Verbal response, in Glasgow Coma Scale, 352
Symptomatic hydrocephalus, 16 concussion, 346 Vermis, 189
Synapses intracranial hematomas, 349 Verrucose dysplasia, 30
chemical synaptic transmission, 48 neurocritical care management after, 353–354 Vertebral artery
immunologic, 254, 262 secondary complications of, 350 extracranial, 200–201
neuronal, 47 Treatable dementia, 63 meningeal branches, 204
Syndromic craniosynostosis, 11 Tremor in neck, dissection, 217–218
Systemic causes of seizures, 73 dystonic, 168 Vertebral basilar system disorders
Systemic hyperperfusion, 205 intention tremor, 249 intracranial vertebral artery disease, 218–219
T in parkinsonism, 162 posterior cerebral arteries, 222
T cells, naive CD4+, 253–255 psychogenic, 175 proximal and midbasilar artery occlusion, 219–220
Tapeworm, 280 types of, 171 subclavian and innominate arteries, 217
Taste inputs to hypothalamus, 122 Trichinosis, 292 thalamic infarcts, 221–222
Tau protein, 346 Trigeminal autonomic cephalalgias, 323–324 top-of-the-basilar artery embolism, 220–221
Tectospinal tract, 180 Trigeminal nerve (V), 5, 112 vertebral arteries in neck, 217–218
Telencephalic leukoencephalopathy, perinatal, 7, 18 Trigeminal neuralgia, 327 Vertigo, benign paroxysmal, of childhood, 326
Telencephalic vesicle, 5, 10 Trigeminal sensory nucleus, 190 Vestibular nuclei, 218
Telencephalon Trigeminocerebellar projections, 186 Vestibular schwannomas, 310–311
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367
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Index

Vestibulo-ocular reflex, 192 Visual hallucinations, 61 White ramus communicans, 26, 118
Vestibulocerebellar projections, 189 Visual-spatial function, testing, 52 Wilson disease, 174
Vestibulocerebellum, 185–186 Vomer, 338, 342 Wing beating tremor, 171, 174
Vestibulocochlear nerve (VIII), 5 W Wingless/integration (WNT) signals,
Viral infections, arthropod-borne, 285 Wada test, 77
Visceral sensory inputs to hypothalamus, 122 Warfarin-related intracerebral hemorrhage, 235 20, 27
Visual apparatus, pituitary mass lesion effects, 139 Water balance, regulation of, 125 Y
Visual association areas, 37 Watershed infarcts, 18 Yasargil clip, 241
Visual auras, 321 Wernicke aphasia, 55, 245 Yolk sac, 2
Visual evoked responses, 252 West syndrome, 70 Z
Visual field disturbances White matter, 183 Zoster sine herpete, 289
Zygomatic bone, 338–340, 342
in brain tumor, 298 demyelination, 261
in cerebral aneurysm, 240 and gait disorders, 196
in multiple sclerosis, 248 hemorrhage, 236
in pituitary tumors, 306
in pseudotumor cerebri, 329

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THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS