Geriatrics - July 2017

Acute myocardial infarction, unstable angina and stable angina 51

cardiovascular disease in the developing 6. White HD, Chew DP. Acute myocardial TREATMENT APPROACHES
world: global implications. Eur Heart J. 2010 infarction. Lancet. 2008 Aug 16; 372 (9638):
Mar; 31(6):642-8. 570-84.
3. Abrams J. Clinical practice. Chronic stable
angina. N Engl J Med. 2005 Jun 16;352 7. Boden WE, Eagle K, Granger CB. Reper-
(24):2524-33. Review. No abstract avail- fusion strategies in acute ST-segment
able. Erratum in: N Engl J Med. 2005 Dec elevation myocardial infarction: a compre-
22;353(25):2728. hensive review of contemporary mana-
4. Snow V, Barry P, Fihn SD, et al. Primary care gement options J Am Coll Cardiol. 2007
management of chronic stable angina Sep 4;50(10):917-29.
and asymptomatic suspected or known
coronary artery disease: a clinical practice 8. Van de Werf, Bax J, Betriu A, et al. Mana-
guideline from the American College of gement of acute myocardial infarction in
Physicians. American College of Physicians; patients presenting with persistent
American College of Cardiology Chronic ST-segment elevation: the Task Force on
Stable Angina Panel. Ann Intern Med. 2004 the Management of ST-Segment Ele-
Oct 5;141(7):562-7. Erratum in: Ann Intern vation Acute Myocardial Infarction of the
Med. 2005 Jan 4;142(1):79. European Society of Cardiology. Eur
5. Fox K, Garcia MA, Ardissino D, et al. The Heart J. 2008 Dec;29(23):2909-45. Epub
Task Force on the Management of Stable 2008 Nov 12.
Angina Pectoris of the European Society of
Cardiology. Guidelines on the manage- 9. Kalra S, Duggal S, Valdez G, et al. Review of
ment of stable angina pectoris: executive acute coronary syndrome diagnosis and
summary: The Task Force on the management. Postgrad Med. 2008
Management of Stable Angina Pectoris of Apr;120(1):18-27.
the European Society of Cardiology. Eur
Heart J. 2006 Jun;27(11):1341-81. 10. Hamm CW, Bassand JP, Agewall S, et al.
The Task Force for the management of

acute coronary syndromes (ACS) in

patients presenting without persistent

ST-segment elevation of the European
Society of Cardiology. Eur Heart J. 2011

Dec;32(23):2999-3054.

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52 ENDOCRINE CONDITIONS

Initiating and titrating basal insulin
treatment in patients with type 2 diabetes

Dr M Koning Step 1 recommends metformin and life-
MBChB MMed (Int Med) style changes. Basal insulin can be added
 Specialist endocrinologist in private in Step 2 or Step 3, where basal insulin is
practice, Pretoria added as a third drug.4

Type 2 diabetes mellitus (T2DM) is a Evidence from clinical trials shows that
chronic disease that causes significant early introduction of basal insulin is effec-
micro- and macrovascular complications tive at keeping glucose levels within the
when suboptimally treated. It affects more target range with doses of <0.4 U/kg/day,
than 350 million people worldwide and resulting in a low risk of hypoglycaemia
the prevalence is increasing rapidly, and only moderate weight gain.3,5
particularly in developing countries. It is However, when insulin is only initiated at a
crucial that patients are managed opti- later stage, the dose required to achieve
mally to decrease the risk of these optimal glucose control is much higher,
complications. resulting in an increased risk for hypogly-
caemia and excessive weight gain.3
INITIATING INSULIN Long-term studies investigating the effect
of intensive glycaemic control cardiovas-
If a patient does not reach the goals for cular (CV) outcomes have produced
glycaemic control on oral agents, adding mixed results. A meta-analysis including
a basal insulin to the regime should be these trials suggests that intensive glucose
considered. The goal for HbA1c varies control reduces the risk of CV complica-
according to different guidelines. The tions without increasing mortality – at least
EASD, IDF and German Diabetes Asso- in some patients.3 The ORIGIN study
ciation recommend a target of <6.5 %, showed that insulin therapy does not
while the ADA recommends a target of increase the risk of complications in
<7 %.1 Locally, the Society for Endo- people with T2DM and CV-risk factors.3
crinology, Metabolism and Diabetes for
South Africa (SEMDSA) recommends a BARRIERS AGAINST INITIATION
target of <7 % for HbA1c for the majority OF (BASAL) INSULIN
of patients, a fasting glucose of
4-7 mmol/L and a postprandial glucose of Failure to start basal insulin may be due to
5-10 mmol/L. The goal is <6.5 mmol/L for several factors, including fear (of the
young patients with newly diagnosed patient and the physician); especially fear
diabetes and no complications and of hypoglycaemia, as well as a fear of
<7.5 mmol/L for the elderly, high-risk weight gain.1 Physicians are often reluc-
patients or those with hypoglycaemia tant to initiate insulin, as they lack
unawareness. 4 The target for elderly and confidence in the patient’s ability to
frail patients has to be less stringent, to manage insulin therapy, or because of
reduce the complications of hypogly- uncertainties regarding initial insulin
caemia.3 It is therefore important to take dosing and titration. Patients may also
into account the individual patient’s age, have several other barriers to insulin initia-
complications, comorbidities and risk of tion, such as a lack of self-confidence to
hypoglycaemia when deciding about the manage insulin therapy, psychological
target that should be aimed for. 2 insulin resistance (PIR), a need for frequent
blood-glucose monitoring and pain asso-
In the SEMDSA Guidelines of 2012, a ciated with insulin use.1 In insulin-naïve
step-wise approach for the management patients, PIR is common, and contributes
of T2DM is recommended. to long delays in initiating insulin and

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Initiating and titrating basal insulin treatment in patients with type 2 diabetes 53

extensive periods of hyperglycaemia.2 e.g., if the patient’s fasting blood TREATMENT APPROACHES
Several studies showed the benefit of glucose is 12 mmol/L, the starting dose
earlier rather than later addition of basal will be 12 U.)
insulin. These benefits should be explained n Target for fasting blood glucose:
to the patient and might help overcome 5.6 mmol/L
the barriers. n Insulin titration: increments of 2 U at a
time
BASAL INSULIN TITRATION n Insulin titration frequency: every third day
ALGORITHMS n Driver of titration: patients are as good
(and even better) than physicians. In
When the decision is made to initiate one study they reached their targets in a
insulin therapy, it makes sense to first shorter time period.
target fasting glycaemia, as it contributes
the most to HbA1c.1 This can be done by If the patient’s HbA1c remains above target,
adding a basal insulin or insulin analogue in spite of target fasting glucose reached,
(such as glargine or Levemir) to metformin, prandial insulin should be added.
with or without the continuation of a
sulphonylurea. In most studies, this combi- REFERENCES
nation improved glycaemic control, 1. Arnolds S, et al. Common standards of
without causing severe hypoglycaemia or
excessive weight gain. In a large, pooled basal insulin titration in T2DM. J Diabetes Sci
analysis of prospective, randomised, Technol. 2013:7(3):771-788.
controlled clinical trials in patients with 2. Ovre D and Fonseca V. Benefits of timely
T2DM, more than half of the patients previ- basal insulin control in patients with type 2
ously uncontrolled on up to two oral diabetes. J of Diabetes and its Com-
agents with baseline HbA1c of between plications. 2015;29:295-301.
8.7 and 9.1 % achieved a target HbA1c of 3. H a n e f e l d M . U s e o f i n s u l i n i n t y p e 2
<7 % 24 weeks after starting basal insulin.5 diabetes: What we learned from recent
clinical trials on the benefits of early insulin
RECOMMENDATIONS initiation. Diabetes and Metabolism.
2014;40:391-399.
Most of the studies made the following 4. Amod A, et al. The 2012 SEMDSA Guideline
recommendations :1 for the management of Type 2 diabetes.
n Starting dose: 10 U per day JEMDSA. 2012:17(2), Supplement 1:S1-S95.
5. Fonseca V, et al. An analysis of early insulin
(Alternatively, the patient’s fasting blood glargine added to metformin with or
glucose can be used as a guide, without sulfonylurea: impact on glycaemic
control and hypoglycaemia. Diabetes,
Obesity and Metab. 2011;13:814-822.

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Erectile dysfunction in men over 65 55

Erectile dysfunction in men over 65 TREATMENT APPROACHES

Dr E Rudolph the prevalence of erectile dysfunction
MHSSH; PGDip CBT globally by 2025, with the biggest
 Psychosexologist, London increase in developing countries that
have expanding populations, such as
CN Boffard South Africa.
MHSSH; PGDip CBT
 Psychosexologist, London IMPACT ON SOCIETY

“A man is only as old as his arteries” Erectile dysfunction has been found to
– Sir William Osler have a great impact on a man’s overall
quality of life and wellbeing, affecting his
Erectile dysfunction is the persistent self-esteem, sexual desire and personal
inability to attain or maintain an erection relationships.8 A man experiencing this
sufficient for sexual performance1 and is may feel shock, despair, embarrassment,
the result of a problem within the complex loss of vitality, fear of failure, frustration
interaction between the hormonal, and a sense of hopelessness.9 These
vascular and neurological process in the emotions could lead to risk-taking behav-
male body.2 This experience can cause iours, such as smoking, drinking and
the individual marked distress. It is a condi- substance abuse, as well as the develop-
tion that affects men both physically and ment of challenging psychological
psychologically; having a great impact on symptoms. It is widely known that mental
one’s wellbeing, quality of life and health concerns have a great impact on
personal relationships.3 Although it is not society, and erectile dysfunction has also
life-threatening, it is considered a marker been found to be both a cause and
for other physical conditions, such as effect of depression, with symptoms of
cardiovascular disease.1 Even as early as depression such as anhedonia, change
the1940s, Alfred Kinsey indicated that in sleeping patterns and selective focus
ageing was a significant risk factor for of negative experiences confounding
developing erectile dysfunction.2 the issue.2

PREVALENCE In studies that have assessed the quality
of life pre- and post-treatment for erectile
It is a widely known fact that as a man dysfunction, the results continuously show
ages, his likelihood of developing erectile that patients report an improvement in
dysfunction increases.2 Various studies overall sexual response, including desire,
have shown that in a general adult popu- arousal and orgasm. Sexual satisfaction
lation in the United States, 18-31 % of men and quality of life have also been shown
are affected by erectile dysfunction, and to improve. This has been found to posi-
this increases to 78 % in men over 75,4,5 tively affect partners as well2 since
Unfortunately, in South Africa there is a erectile dysfunction can have a
paucity of data on this particular popula- profoundly negative effect on both the
tion. Studies, such as that of De Klerk, have patient and his partner.3
found prevalence rates of 77 % in a black
and mixed-race urban population in the Studies conducted in the United States
Western Cape.6 The largest study ever and the United Kingdom have explored
conducted on ageing in men was the the financial burden that the problem
Massachusetts Male Ageing Study,7 places on society, with results showing
which although conducted nearly 20 that the cost of erectile dysfunction
years ago, projected a 111 % increase in increases with male ageing.2,10 It was
found that outpatient visits and treatment-
seeking behaviour accounted for the

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56 ENDOCRINE CONDITIONS

greatest proportion of costs, and genito- n Previous sexual history, including issues
urinary consultations and treatment of gender identity or sexual orientation
measures, such as prostheses, accounted
for a lower proportion. The impact of the n Daily and nocturnal tumescence
problem is further compounded by the n Partner issues, i.e., history of trauma,
high correlation to other serious condi-
tions, such as diabetes mellitus, sexual dysfunction or psychosocial issues
cardiovascular disease, hypertension, n Lifestyle, i.e., substance use, smoking,
depression or problems with the prostate,
such as benign prostatic hyperplasia or alcohol intake, exercise
prostate cancer.2 This places a further
economical strain on the health-care A genital examination should be
system. In order to better evaluate the performed by an appropriate clinician,
cost of such a dysfunction, Wessells et al10 especially in the case of penile curvature
suggest that a better understanding of during tumescence, Peyronie’s disease,
treatment-seeking behaviour, patient- painful erections, symptoms of hypog-
treatment preference, satisfaction and onadism or any urological symptoms.1
overall outcome, and a better under-
standing of pathogenesis is necessary. For The International Index of Erectile
the South African population, the afford- Function (IIEF) can be used as a diagnostic
ability of PDE-5 inhibitors has only recently tool, and has become a standard meas-
improved, making treatment of erectile urement in clinical trials.13 Ideally, men in
dysfunction more accessible to many relationships should be assessed with their
population groups, but certainly not all. partners present, as Hackett et al1 suggest
that co-existing sexual concerns, sexual
DIAGNOSTIC ISSUES satisfaction and sexual health can thus be
identified and managed. They further
For all clinicians, erectile dysfunction suggest that it is highly likely that all couples
should be taken seriously, as it has repeat- will have some psychological element
edly been shown to be an independent contributing to their problem, and there-
marker for serious cardiovascular risk or fore almost all couples could benefit from
diabetes mellitus.1 Investigations should basic psychosexual education.1 This should
thoroughly assess a man’s personal, take place following the initial assessment,
medical and lifestyle history and should if not during. By helping a couple under-
commence with identifying reversible risk stand the pathophysiology, aetiology,
factors, such as smoking, hyperlipidaemia, physiological and psychological effects of
hypogonadism and hypertension. the problem on their relationship, it could
Correcting these, could greatly reduce ultimately improve the compliance and
one’s risk.1 outcome of treatment.

When assessing a male patient for Levinson14 suggested, “each cultural
possible erectile dysfunction, a clinician group in South Africa has different diag-
should conduct a thorough sexual nostic acceptability”. In many cultures, a
history.11 This should include questions psychogenic aetiology is considered
regarding: unacceptable, and according to
n O riginal precipitating factors and date Levinson, traditional Western medicine
tends to focus on how the condition
of onset develops and how to treat it; rarely why it
n P redisposing factors has developed. Furthermore, psycho-
n Maintaining factors therapy is considered more acceptable
n Medical history, including medical, among the white population than African
cultures. Therefore, in treating older South
psychiatric and surgical history African males, cultural considerations and
n P revious erectile capacity expectations should be taken into
n Current relationship status account and managed when suggesting
treatment options. This should be discuss-
HANDBOOK OF GERIATRIC MEDICINE ed in detail with the patient.

















































Diagnosis and management of generalised anxiety disorder and panic disorder in adults 81

Table 1. Diagnostic criteria for generalised anxiety disorder TREATMENT APPROACHES

A. Excessive anxiety and worry (apprehensive expectation), occurring more days
than not for at least 6 months, about a number of events or activities (such as work
or school performance).

B. T he individual finds it difficult to control the worry.

C. T he anxiety and worry are associated with three (or more) of the following six
symptoms (with at least some symptoms having been present for more days than
not for the past 6 months):

Note: Only one item is required in children.

1. R estlessness or feeling keyed up or on edge.

2. Being easily fatigued.

3. Difficulty concentrating or mind going blank.

4. Irritability.

5. Muscle tension.

6. S leep disturbance (difficulty falling or staying asleep, or restless, unsatisfying
sleep).

D. T he anxiety, worry, or physical symptoms cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.

E. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition
(e.g., hyperthyroidism).

F. T he disturbance is not better explained by another mental disorder (e.g., anxiety or
worry about having panic attacks in panic disorder, negative evaluation in social
anxiety disorder [social phobia], contamination or other obsessions in obsessive-
compulsive disorder, separation from attachment figures in separation anxiety
disorder, reminders of traumatic events in posttraumatic stress disorder, gaining
weight in anorexia nervosa, physical complaints in somatic symptom disorder,
perceived appearance flaws in body dysmorphic disorder, having a serious illness
in illness anxiety disorder, or the content of delusional beliefs in schizophrenia or
delusional disorder).

Source: Reprinted with permission from the American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013:222.

specificity.8 Greater GAD-7 scores corre- PANIC DISORDER
late with more functional impairment.8 The
scale was developed and validated PD is characterised by episodic, unex-
based on DSM-IV criteria, but it remains pected panic attacks that occur without
clinically useful after publication of the a clear trigger.5  Panic attacks are defined
DSM-5 because the differences in GAD by the rapid onset of intense fear (typi-
diagnostic criteria are minimal. The cally peaking within about 10 minutes)
PRO-MIS Emotional Distress – Anxiety avail- with at least four of the physical and
able from the American Psychiatric psychological symptoms in the DSM-5
Association at http://www.psychiatry.org/ diagnostic criteria (see Table 3).5 
practice/dsm/dsm5/online-assessment-
measures, are intended to aid clinical Another requirement for the diagnosis of
evaluation of GAD and monitor treatment PD is that the patient worries about further
effectiveness. attacks or modifies his or her behaviour in
maladaptive ways to avoid them. The
most common physical symptom

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82 NEUROPSYCHIATRIC CONDITIONS

Table 2. GAD-7 screening tool Not at Several More Nearly
all days than every
Over the last 2 weeks, how often have you half the day
been bothered by the following problems? days

(Use “✓” to indicate your answer) 0 1 2 3
0 1 2 3
1. F eeling nervous, anxious, or on edge 0 1 2 3
2. Not being able to stop or control worrying 0 1 2 3
3. Worrying too much about different things 0 1 2 3
4. Trouble relaxing 0 1 2 3
5. Being so restless that it is hard to sit still 0 1 2 3
6. Becoming easily annoyed or irritable
7. Feeling afraid as if something awful might =___ +___ +___ +___

happen
Total score_____

Note: Total score for the 7 items ranges from 0 to 21. Scores of 5, 10, and 15 represent cut-offs for
mild, moderate, and severe anxiety, respectively. Although designed primarily as a screening and
severity measure for GAD, the GAD-7 also has moderately good operating characteristics for panic
disorder, social anxiety disorder, and posttraumatic stress disorder. When screening for anxiety
disorders, a recommended cut-off for further evaluation is a score of 10 or greater.

GAD: generalised anxiety disorder

Source: Reprinted from Spitzer RL, Williams JB, Kroenke K, et al. Patient health questionnaire (PHQ) screeners. http://www.
phqscreeners.com/overview.aspx?Screener=03_GAD-7. Accessed July 22, 2014.

accompanying panic attacks is palpita- epilepsy or transient ischaemic attacks).
tions.9 Although unexpected panic Other psychiatric disorders (e.g., other
attacks are required for the diagnosis, anxiety disorders, major depressive disorder,
many patients with PD also have bipolar disorder); use of substances such as
expected panic attacks, occurring in caffeine, albuterol, levothyroxine, or decon-
response to a known trigger.9 The severity gestants; or substance withdrawal may also
measure for panic disorder–adult (http:// present with similar symptoms and should
www.psychiatry.org/File %20Library/ be ruled out.5
Practice/DSM/DSM-5/SeverityMeasure
ForPanicDisorderAdult.pdf) is an assess- Complicating the diagnosis of GAD and
ment scale that can complement the PD is that many conditions in the differen-
clinical assessment of patients with PD. tial diagnosis are also common co-
morbidities. Additionally, many patients
DIFFERENTIAL DIAGNOSIS with GAD or PD meet criteria for other
AND COMORBIDITY psychiatric disorders, including major
depressive disorder and social phobia.
When evaluating a patient for a sus- Evidence suggests that GAD and PD
pected anxiety disorder, it is important to usually occur with at least one other
exclude medical conditions with similar psychiatric disorder, such as mood,
presentations (e.g., endocrine conditions anxiety, or substance-use disorders.10 
such as hyperthyroidism, pheochromocy-
toma, or hyperparathyroidism; cardio- When anxiety disorders occur with other
pulmonary conditions such as arrhythmia conditions, historic, physical, and labora-
or obstructive pulmonary diseases; neuro- tory findings may be helpful in distin-
logic diseases such as temporal lobe guishing each diagnosis and developing
appropriate treatment plans.

HANDBOOK OF GERIATRIC MEDICINE

Diagnosis and management of generalised anxiety disorder and panic disorder in adults 83

Table 3. Diagnostic criteria for panic disorder TREATMENT APPROACHES

A. R ecurrent unexpected panic attacks. A panic attack is an abrupt surge of intense
fear or intense discomfort that reaches a peak within minutes, and during which
time four (or more) of the following symptoms occur:

Note: The abrupt surge can occur from a calm state or an anxious state.

1. Palpitations, pounding heart, or accelerated heart rate.

2. Sweating.

3. Trembling or shaking.

4. S ensations of shortness of breath or smothering.

5. F eelings of choking.

6. C hest pain or discomfort.

7. Nausea or abdominal distress.

8. Feeling dizzy, unsteady, lightheaded, or faint.

9. Chills or heat sensations.

10. Paraesthesias (numbness or tingling sensations).

11. Derealisation (feelings of unreality) or depersonalisation (being detached from
oneself).

12. F ear of losing control or “going crazy”.

13. Fear of dying.

Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache,
uncontrollable screaming or crying) may be seen. Such symptoms should not count
as one of the four required symptoms.

B. At least one of the attacks has been followed by one month (or more) of one or
both of the following:

1. P ersistent concern or worry about additional panic attacks or their
consequences (e.g., losing control, having a heart attack, “going crazy”).

2. A significant maladaptive change in behaviour related to the attacks
(e.g., behaviours designed to avoid having panic attacks, such as avoidance
of exercise or unfamiliar situations).

C. The disturbance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication) or another medical condition
(e.g., hyperthyroidism, cardiopulmonary disorders).

D. The disturbance is not better explained by another mental disorder (e.g., the panic
attacks do not occur only in response to feared social situations, as in social anxiety
disorder; in response to circumscribed phobic objects or situations, as in specific
phobia; in response to obsessions, as in obsessive-compulsive disorder; in response
to reminders of traumatic events, as in posttraumatic stress disorder; or in response
to separation from attachment figures, as in separation anxiety disorder).

Source: Reprinted with permission from the American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th
ed. Washington, DC: American Psychiatric Association; 2013:208–209.

TREATMENT section will differentiate between GAD
and PD; otherwise, treatments refer to
Some studies evaluating anxiety treat- anxiety-related symptoms in general.
ments assess non-specific anxiety-related
symptoms rather than the set of symptoms Medication or psychotherapy is a
that characterise GAD or PD. When reasonable initial treatment option for
possible, the treatments described in this GAD and PD.11 Some studies suggest that

HANDBOOK OF GERIATRIC MEDICINE

84 NEUROPSYCHIATRIC CONDITIONS

combining medication and psycho- serotonin re-uptake inhibitors (SSRIs) are
therapy may be more effective for patients generally considered first-line therapy for
with moderate to severe symptoms.12 The GAD and PD.19–22 Tricyclic antidepressants
National Institute for Health and Care (TCAs) are better studied for PD, but are
Excellence (NICE) guidelines on GAD and thought to be effective for both GAD and
PD in adults are a useful review of available PD.19,20 In the treatment of PD, TCAs are as
evidence; however, information about effective as SSRIs, but adverse effects may
self-help and group therapies may have limit the use of TCAs in some patients.23 
less utility in the United States because of
their relative lack of availability.11 Venlafaxine, extended-release, is effec-
tive and well tolerated for GAD and PD,
EDUCATION whereas duloxetine has been adequately
Compassionate listening and education are evaluated only for GAD.24 Azapirones,
an important foundation in the treatment of such as buspirone, are better than
anxiety disorders.11 Patient education itself placebo for GAD,25 but do not appear to
can help reduce anxiety, particularly in be effective for PD.26 Mixed evidence
PD.13 The establishment of a therapeutic alli- suggests bupropion may have anxiogenic
ance between the patient and physician is effects for some patients, thus warranting
important to allay fears of interventions and close monitoring if used for treatment of
to progress toward treatment. comorbid depression, seasonal affective
disorder, or smoking cessation.27
Common lifestyle recommendations Bupropion is not approved for the treat-
that may reduce anxiety-related symp- ment of GAD or PD.
toms include identifying and removing
possible triggers (e.g., caffeine, stimulants, Medications should be titrated slowly to
nicotine, dietary triggers, stress), and decrease the initial activation. Because of
improving sleep quality/quantity and the typical delay in onset of action, medica-
physical activity. tions should not be considered ineffective
until they are titrated to the high end of the
Caffeine can trigger PD and other types dose range and continued for at least four
of anxiety. Those with PD may be more weeks. Once symptoms have improved,
sensitive to caffeine than the general medications should be used for 12 months
population because of genetic polymor- before tapering to limit relapse.11 Some
phisms in adenosine receptors.14 Smoking patients will require longer treatment.
cessation leads to improved anxiety
scores, with relapse leading to increased Benzodiazepines are effective in
anxiety. Many studies show an association reducing anxiety, but there is a dose-
between disordered sleep and anxiety, response relationship associated with
but causality is unclear.15 In addition to tolerance, sedation, confusion, and
decreased depression and anxiety, phys- increased mortality.28 When used in
ical activity is associated with improved combination with antidepressants, benzo-
physical health, life satisfaction, cognitive diazepines may speed recovery from
functioning, and psychological wellbeing. anxiety-related symptoms, but do not
Physical activity is a cost-effective improve longer-term outcomes. The
approach in the treatment of GAD and higher risk of dependence and adverse
PD.16,17  Exercising at 60 % to 90 % of outcomes complicates the use of benzo-
maximal heart rate for 20 minutes three diazepines.29 NICE guidelines recommend
times weekly has been shown to decrease only short-term use during crises.11 
anxiety16; yoga is also effective.18
Benzodiazepines with an intermediate-
MEDICATION to-long onset of action (such as
First-line therapies clonazepam) may have less potential for
A number of medications are available for abuse and less risk of rebound.30
treating anxiety (see Table 4). Selective
Second-line therapies
HANDBOOK OF GERIATRIC MEDICINE
Second-line therapies for GAD include
pregabalin and quetiapine, although

Diagnosis and management of generalised anxiety disorder and panic disorder in adults 85 TREATMENT APPROACHES

Table 4. Medications for the treatment of generalised anxiety disorder and panic disorder

First line
Selective serotonin re-uptake inhibitors

Escitalopram
Fluoxetine
Fluvoxamine for PD
Paroxetine
Sertraline
Serotonin-norepinephrine re-uptake inhibitors
Duloxetine for GAD
Venlafaxine, extended-release
Azapirone
Buspirone for GAD
Second line
Tricyclic antidepressants
Amitriptyline†
Imipramine (Tofranil)‡
Nortriptyline (Pamelor)†
Anti-epileptics
Pregabalin† for GAD
Antipsychotics
Quetiapine† for GAD
Hydroxyzine
Third line
Mono-amine oxidase inhibitors§
Isocarboxazid†
Phenelzine†
Tranylcypromine†
Augmentation
Benzodiazepines||
Alprazolam¶
Clonazepam**
Diazepam for GAD
Lorazepam‡

Note: Medications are used for GAD and PD unless otherwise noted. They are listed from most to
least commonly used.
FDA: US Food and Drug Administration; GAD: generalised anxiety disorder; NA: not available; PD:
panic disorder.
† Not FDA-approved for this use, although there is some evidence to support its use.
‡ Not FDA-approved for PD, although there is some evidence to support its use; approved for GAD.
§ Consideration of mono-amine oxidase inhibitors should prompt referral to psychiatry.
|| Benzodiazepines may be used for augmentation during acute treatment. Dependence,
tolerance, and escalating doses to get the same effect over the long term can be problematic with
use of benzodiazepines. Short-term prescribing with emphasis on acute management of uncon-
trolled anxiety is preferred. Slowly tapered dosing can prevent rebound symptoms.
¶ Short-acting benzodiazepines, such as alprazolam, are not preferred because they have a higher
risk of addiction and adverse effects.
** Not FDA-approved for GAD, although there is some evidence to support its use; approved for PD.

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86 NEUROPSYCHIATRIC CONDITIONS

Table 5. Possible behaviour interventions for the treatment of generalised anxiety disorder,
panic disorder, and anxiety-related symptoms33,34

Intervention Comments

Cognitive This intervention is useful in treating anxiety disorders. The cognitive
behaviour portion assists change in thinking patterns that support fears, whereas
therapy* the behaviour portion often involves training patients to relax deeply
and helps desensitise patients to anxiety-provoking triggers.

To be effective, therapy must be directed at the patient’s specific
anxieties and tailored to his or her needs. There are minimal adverse
effects, except that behaviour desensitisation is typically associated
with temporary, mild increases in anxiety.33

Mindfulness- This intervention promotes focused attention on the present,
based stress acknowledgment of one’s emotional state, and meditation for further
reduction† stress reduction and relaxation.

Key features include moment-to-moment awareness cultivated with a
non-judgmental attitude, formal meditation techniques, and daily
practice.34

Note: Formal use of these interventions requires specialised training. In patients whose anxiety and
impairment are severe, referral to a trained behaviour health specialist should be considered.
* For more information, see DiTomasso RA, Golden BA, Morris HJ, eds. Handbook of Cognitive-
Behavioral Approaches in Primary Care. New York, NY: Springer; 2010, and Craske MG.
Cognitive-Behavioral Therapy. Washington, DC: American Psychological Association; 2010.
† For more information, see Brantley J. Mindfulness-based stress reduction. In: Orsillo SM, Roemer L,
eds. Acceptance and mindfulness-based approaches to anxiety: conceptualization and treat-
ment. New York, NY: Springer; 2005:131-145.

neither has been evaluated for PD. PSYCHOTHERAPY AND RELAXATION
Pregabalin is more effective than THERAPIES
placebo, but not as effective as loraz-
epam for GAD. Weight gain is a common Psychotherapy includes many different
adverse effect of pregabalin. There is approaches, such as cognitive behaviour
limited evidence for the use of antipsy- therapy (CBT) and applied relaxation (see
chotics to treat anxiety disorders. Although Table 5).33,34 CBT may use applied relaxation,
quetiapine seems to be effective for GAD, exposure therapy, breathing, cognitive
the adverse effect profile is significant, restructuring, or education. Psychotherapy
including weight gain, diabetes mellitus, is as effective as medication for GAD and
and hyperlipidaemia.31 Hydroxyzine is PD.11 Although existing evidence is insuffi-
considered a second-line treatment for cient to draw conclusions about many
GAD,32 but there are minimal data for its psychotherapeutic interventions, structured
use in PD. Its rapid onset can be appealing CBT interventions have consistently proven
for patients needing immediate relief, and effective for the treatment of anxiety in the
it may be a more appropriate alternative primary care setting.34–36 Psychotherapy
if benzodiazepines are contra-indicated may be used alone or combined with
(e.g., in patients with a history of substance medication as first-line treatment for
abuse). Based on clinical experience, PD37 and GAD,11 based on patient prefer-
gabapentin is sometimes prescribed by ence. Psychotherapy should be performed
psychiatrists to treat anxiety on an weekly for at least eight weeks to assess
as-needed basis when benzodiazepines its effect.
are contra-indicated. Of note, the
placebo response for medications used to Mindfulness has similar effectiveness to
treat GAD and PD is high.13 traditional CBT or other behaviour thera-
pies,38 particularly mindfulness-based
stress reduction.39 A meta-analysis of 36

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