INDEX

SN TITLE PAGE
1. Chapter 1- Treatment of First Episode Schizophrenia 2

2. Chapter 2- Treatment of Relapse or Acute Exacerbation of Schizophrenia 4

3. Chapter 3- Treatment of Depression (Single or Recurrent episodes) 6

4. Chapter 4- Treatment of acute mania or hypomania 8

5. Chapter 5- Management of Alcohol Use Disorder 11

6. Chapter 6- Management of Anxiety Disorders 14

7. Chapter 7- Management of Obsessive compulsive disorder 16

8. Chapter 8- Management of Treatment Resistant Obsessive Compulsive 19

Disorder

9. Chapter 9- Management of Rapid Cycling Bipolar Affective Disorder 22

10. Chapter 10- Management of Aggressive, Violent Patients 24

11. Chapter 11- Assessment and Management of Suicide/Self-harm 27

12. Chapter 12- Protocol for ECT- Evaluation, Work-Up, Application, Handling 31
Complications

13. Chapter 13- General Principles of Prescribing In Pregnancy 34

14. Chapter 14- Management of Dementia 36

15. Chapter 15- Management of Delirium 39

16. Chapter 16- Management of Developmental Disorder 42

17. Chapter 17- Management of Attention Deficit Hyperactivity Disorder 46

18. Chapter 18- Management of Medically Unexplained Symptoms 48

19. Chapter 19- Treatment of Antipsychotic-induced Akathisia 50

20. Chapter 20- Treatment Protocol for Insomnia 52

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 Chapter - 1

Treatment Protocol for First Episode Schizophrenia

Schizophrenia is a chronic, and frequently devastating neuropsychiatric disorder, affecting

about one percent of the world’s general population [1]. It imposes a disproportionately large
economic burden in terms of hospitalization, chronic treatment and rehabilitation, and lost
productivity [2]. Antipsychotic drugs are effective in both the acute and maintenance phase of
schizophrenia. The individual response to antipsychotics varies in view of inter-individual
differences in pharmacokinetics and tolerability, suggesting that there is no clear cut first line
antipsychotic [1, 2].
General Principles of Prescribing Antipsychotics: [3]
1. The minimum effective dose of antipsychotic in schizophrenia (first episode or relapse) is
advocated.
2. The use of single antipsychotic (with or without additional mood stabilizer or sedative) is
recommended.
3. Antipsychotics should not be used for the purpose of sedation.
4. Combination of antipsychotics should be used only where response to a single antipsychotic
(including clozapine) has been clearly demonstrated to be inadequate.
5. PANSS scoring should be done at baseline and then weekly to see for the response.
6. Patient and guardian have to be explained the need for regular blood monitoring in patients
taking clozapine. In case of suspicion of development of agranulocytosis or signs/ symptoms
of myocarditis/ seizure, Clozapine has to be stopped urgently and consult the physician.
Flowchart:

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 Discuss with patient and/or guardian, then start antipsychotic
as per clinical and economical profile, preferably atypical
antipsychotics

Titrate, if necessary, to minimum effective dose

Adjust dose according to clinical response and side effects

Assess over 4-6 weeks

Continue at Change drug If not tolerated or poor compliance,

the effective either SGA change drug and repeat as above
dose or FGA and
follow as
above

Clozapine

(Take written consent after explaining side

effects and need for regular blood
monitoring)

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Reference:

1. Jablensky, A., Sartorius, N., Ernberg, G., Anker, M., Korten, A., Cooper, J.E., Day, R., and
Bertelsen, A. Schizophrenia: Manifestations, incidence and course in different cultures. A
World Health Organization ten-country study. Psychol. Med. Monogr 1992; Suppl. 20: 1–97.
2. Rice DP. The economic impact of schizophrenia J. Clin. Psychiatry 1999; 60 Suppl 1: 4–
6.
3. Armenteros JL et al. Antipsychotics in early onset schizophrenia: systematic review and
metaanalysis. Eur Child Adolesc Psychiatry 2006; 15: 141-148.
4. Agid O et al. An algorithm based approach to first episode schizophrenia: response rates
over 3 prospective antipsychotic trial with retrospective data analysis. J Clin Psychiatry 2011;
72 (11): 1439-1444.

Chapter - 2
Treatment Protocol for Relapse or Acute Exacerbation of Schizophrenia

Schizophrenia is a chronic, and frequently devastating neuropsychiatric disorder, affecting

about one percent of the world’s general population [1]. It imposes a disproportionately large
economic burden in terms of hospitalization, chronic treatment and rehabilitation, and lost
productivity [2]. Antipsychotic drugs are effective in both the acute and maintenance phase of
schizophrenia. A relapse is the return of symptoms or worsening of residual symptoms
(symptoms that haven't completely disappeared).
There are many reasons why people who have recovered from Schizophrenic symptoms may
have a relapse: [3, 4]
1. When drug adherence is doubtful or known to be poor.
2. Psychosocial stressful circumstances.
3. Inadequate rest and sleep
4. Alcohol or other substance use.

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Treatment of relapse or acute exacerbation of schizophrenia (adherence is doubtful or
known to be poor)

Confused or
Investigate reasons for poor
disorganized -Simplify drug regimen
adherence
-Reduce anticholiergics

-Consider compliance aids

Lack of
insight or Poorly tolerated treatment
support

-Discuss with the patient and guardian -Discuss with patient and guardian

-Consider compliance therapy, depot -Switch to acceptable drugs

antipsychotics or liquid/ dispersible
antipsychotics

Treatment of relapse or acute exacerbation of schizophrenia (when full adherence to

medication is
confirmed)

Investigate psychological and social precipitants

Provide appropriate support and/or therapy
Continue usual drug treatment

Acute drug treatment

required

Add short term sedatives

Or
Switch to a different acceptable antipsychotic if appropriate
(at least 2 antipsychotic trials for 4-6 weeks)
Discuss with patient and guardian
Assess over at least 6 weeks

Treatment ineffective

Switch to Clozapine

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 Reference:

1. Jablensky, A., Sartorius, N., Ernberg, G., Anker, M., Korten, A., Cooper, J.E., Day, R., and
Bertelsen, A. Schizophrenia: Manifestations, incidence and course in different cultures. A
World Health Organization ten-country study. Psychol. Med. Monogr 1992; Suppl. 20: 1–97.
2. Rice DP. The economic impact of schizophrenia J. Clin. Psychiatry 1999; 60 Suppl 1: 4–
6.
3. Armenteros JL et al. Antipsychotics in early onset schizophrenia: systematic review and
metaanalysis. Eur Child Adolesc Psychiatry 2006; 15: 141-148.
4. Haro JM et al. Remission and relapse in the outpatient care of schizophrenia: 3 year
results from the schizophrenia outpatient health outcomes study. J Clin Psychopharmacol
2006; 26: 571-578.

Chapter -3
Treatment of Depression (Single or Recurrent episodes)

Depression is a widely recognized public health problem which essentially warrants judicious
use of antidepressants, although, of late, psychological treatment have found a place as an
alternative treatment option in milder forms of depression [1].
Principles of prescribing in depression
1. Discuss with the patient choice of drug and utility/availability of non-pharmacological

treatments.

2. Discuss with the patient the likely outcome such as the symptom reduction and the possible

time frame.

3. Prescribe a dose of antidepressant (after titration) that is likely to be effective

4. For a single episode, continue treatment for at least 6-9 months after resolution of the

symptoms (Multiple episodes may require longer).

5. Withdraw antidepressants gradually; always inform the patient of the risk of discontinuation

and identification of early signs of relapse [1, 2, 4].

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 Flow chart:

Discuss the choice of drug with the patient

Include:

Therapeutic effect

Adverse effect

Discontinuation effect

Start antidepressant

Titrate gradually to therapeutic dose. Assess efficacy after

2 weeks

Assess weekly for further 1-2 Continue for 6-9 months at full Switch to a different
weeks treatment dose antidepressant

If still no response, consider Consider longer term treatment in Titrate to therapeutic dose
increasing the dose recurrent depression
Assess efficacy over 3-4
weeks. Increase dose as
necessary

Switch to a different antidepressant

Titrate to therapeutic dose. Assess efficacy over 3-4 weeks, increase

dose as necessary

Refer to suggested options for treatment resistant depression

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 Reference:
1. National Institute for Health and Clinical excellence. Depression – the treatment and
management of depression in adults (update) CG90.2009. [Link]
2. American Psychiatric Association. Practice guidelines for the treatment of patients with
major depressive disorder. 3rd edition.2010. Washington DC: American Psychiatric
Association: 2010.
3. Crismon ML et al. The Texas Medication Algorithm project: report of texas consensus
conference panel on medication treatment of Major depressive disorder. J Clin Psychiatry
1999; 60: 142-156.
4. Zajecka J, Kornstein SG, Blier P. Residual symptoms in major depressive disorder:
prevalence, effects, and management. J Clin Psychiatry. 2013 Apr;74(4):407-414.

Chapter – 4
Treatment of acute mania or hypomania

Drug treatment is the mainstay of treatment for mania and hypomania. Both antipsychotics
and mood stabilizers are effective. Sedative and anxiolytics drugs may add to the effect of
antipsychotics and mood stabilizers. The use of antidepressants or other drugs known to
induce hypomania or mania (e.g. steroids, antimalarials etc.) and substances (alcohol and
cannabis) should be identified routinely and if found should be immediately stopped [1, 3].
The choice of drug should be made taking into account of the patient’s clinical profile, past or
family history of response, drug availability and monitoring facilities and socioeconomic
factors.
The following are strategies for treatment of mania and hypomania [1, 2, 4, 5]:
Reference:
1. American Psychiatric Association. Guideline watch: Practice guideline for the treatment of patients
with bipolar disorders, 2nd Edn, Washington, DC, American Psychiatric Association; 2005
2. National institute for Health and clinical excellence. Bipolar disorder. The management of bipolar
disorder in adults, children and adolescents, in primary and secondary care. Clinical guidance 38.
2006. [Link]
3. Smith LA et al. Pharmacological interventions for acute bipolar mania: a systematic review of
randomized placebo-controlled trials. Bipolar Disord 2007;9: 551-560

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4. Goodwin GM. Evidence-based guidelines for treating bipolar disorder: revised second edition-
recommendations from the British Association for Psychopharmacology. J Psychopharmacol 2009;
23: 346-388
5. Geddes JR, Miklowitz DJ. Treatment of bipolar disorder. Lancet. 2013 May 11;381(9878):1672-82.

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 Is the patient taking
Diagnose patient as acute
antidepressants/ other
mania or hypomania
drugs/substance
known to induce mania

Is patient taking Antimanic Stop those

medications? drugs
immediately

No Yes

Consider -an antipsychotic (if If taking an antipsychotic-Check

symptoms are severe or compliance and dose. Increase dose if
behaviour disturbed) necessary. Consider adding lithium or
valproate

Or

If taking lithium
Lithium (if future Check Serum Lithium Levels and adjust
adherence is likely) dose to give levels 0.8-1.2 mmol/l and/or
adding an antipsychotic

Or

Valproate (avoid in women

If taking Valproate
of child bearing potential)
Check plasma level. Increase dose up to
50-125mg/l. Consider adding an
antipsychotic.

If response is inadequate
If taking lithium or Valproate and mania
Combine antipsychotic and
is severe
Valproate or lithium
Check plasma level/add an antipsychotic

If taking Carbamazepine
Consider adding an antipsychotic
Adding short term
benzodiazepines may be
considered (Lorazepam or
Clonazepam) Adding short term benzodiazepines may
be considered

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 Chapter - 5
Management of Alcohol Use Disorder

Various conditions resulting from different patterns of alcohol consumption include acute
alcohol intoxication, harmful alcohol use, the alcohol dependence syndrome, and the alcohol
withdrawal state.
Alcohol dependence is a cluster of physiological, behavioural and cognitive phenomena in
which the use of alcohol takes on a much higher priority for a given individual than other
behaviours that once had greater value.
Alcohol intoxication:
»Assess airway and
breathing.
»Put the person on
Look for: If there is disturbance
in the level of their side to prevent
» Smell of alcohol on the aspiration in case they
consciousness,
breath cognition, perception, vomit.
» Slurred speech affect or behaviour »Refer to emergency
» Uninhibited behaviour following recent
consumption of alcohol ward if necessary or
observe until effects of
Assess: Alcohol Intoxication alcohol have worn off.
» Level of consciousness is likely »If methanol poisoning
» Cognition and is suspected, refer to
emergency ward for
further management

Alcohol withdrawal:

Alcohol withdrawal occurs following cessation of heavy alcohol consumption, typically

between 6 hours and 6 days after the last drink. It can also be seen if person took lesser
quantity than his usual daily intake.
Management is as follows:

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 » Treat in hospital or
detoxification centre if available.
Look for chances of » If withdrawal is
Look for: severe withdrawal: complicated by delirium:
» Tremor in hands » Past episodes of severe – Treat the withdrawal with
» Sweating diazepam.
alcohol withdrawal including
» Vomiting – Manage in a safe
» Increased Pulse and BP delirium and seizures
» Other medical or environment.
» Agitation
psychiatric problems or – Keep well hydrated.
Ask about: benzodiazepine dependence – Refer to medical emergency
» Headache » If withdrawal is
» Severe withdrawal
» Nausea complicated by a seizure,
» Anxiety symptoms already present
treat with diazepam in the first
only a few hours after
instance and do not use
stopping drinking
anticonvulsants to prevent
further seizures

Detoxification:

Mild
- Sweating, anxious, tremor; lasts hours to 1 – 2 days
- Rx as Out-patient; ensure support, caregiver
- Lorazepam regime; start 4 – 12 mg. tds po and taper over 10 days
- Thiamine 100 mg. daily po; MVT tablet daily; Vit B Complex 2 daily tablets
Severe
- Treat as in-patient
- Thiamine 100 mg. daily, IV initially then po
- Ensure adequate hydration – IV 5% Dextrose water (After giving Inj Thiamine 100mg)
- Inj. Lorazepam 2-4 mg. every 2 – 4 hours until stable in first 24 hours;
- Then stabilization dose in 3 divided doses the following day;
- Then taper over 3-5 days
- MVT one tablet daily; Vit. B tablets daily
- Reduce external stimuli
- Monitor clinical status, and intervene as indicated
- If history of withdrawal seizures, Diazepam is effective
- Psychosis → Haloperidol 0.5-5mg tds, po or IMI

3. Alcohol dependence
Assess for:
» A strong desire or sense of compulsion to take alcohol
» Difficulties in controlling alcohol use in terms of its onset, termination or levels of use
» A physiological withdrawal state when alcohol use has ceased or been reduced, as shown
by the characteristic withdrawal syndrome for alcohol; or use of the same (or a closely
related) substance with the intention of relieving or avoiding withdrawal symptoms

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» Evidence of tolerance, such that increased doses of alcohol are required in order to achieve
effects originally produced by lower doses
» Progressive neglect of alternative pleasures or interests because of alcohol use, increased
amount of time necessary to obtain or take alcohol or to recover from its effects
» Alcohol use persisting despite clear evidence of overtly harmful consequences, such as
harm to the liver, depressive mood states, or impairment of cognitive functioning

If 3 or more features are present then, following should be done:

Intervention:
Explain both the short-term and long-term risks of continuing use.
» Arrange detoxification if necessary. During detoxification, treat withdrawal symptoms.
» Assess motivation. Apply Brief Interventions.
» Advise complete cessation of alcohol.
» Advise daily consumption of thiamine 100 mg.
» After detoxification, prevent relapse with medication (naltrexone, acamprosate or
disulfiram).
» Assess and treat any medical or psychiatric co-morbidity.
» Address housing and employment needs.
» Provide information and support to person, carers and family members.
» Provide psychosocial interventions such as family counselling or therapy, problem-solving
counselling or therapy, cognitive behavioural therapy, motivational enhancement therapy, or
contingency management therapy.
» Follow up frequently initially.
Pharmacological treatment for alcohol dependence (Relapse Prevention):

Acamprosate:
For adults of 18–65 years weighing 60 kg and over, the starting dose is 1998 mg daily (666
mg three times daily). For adults weighing less than 60 kg, the dose should be reduced to
1332 mg daily: 666 mg (morning), 333 mg (midday) and 333 mg (night).

Naltrexone:
50 mg p.o. OD. Side-effects include nausea (especially in the early stages of treatment),
headache, abdominal pain, reduced appetite and tiredness. Prior to commencing naltrexone
renal and liver function tests must be done. Patients on naltrexone should not be given opioid
analgesics. Hepatotoxicity has been described with high doses, so use should be avoided in
acute liver failure.

Disulfiram:
Disulfiram can cause extremely unpleasant physical effects in presence of alcohol due to
accumulation of acetaldehyde. Continued drinking can lead to arrhythmias, hypotension and
collapse. Clinician must ensure that no alcohol has been consumed for at least 24 h
beforehand. Dosage range from 250-750mg OD p.o.

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 References:
1. Mental Health Gap Action Programme. mhGAP intervention guide for mental, neurological
and substance use disorders in non-specialized health settings: version 1.0. Geneva: World
Health Organization 2010.
2. Albanese AP. Management of alcohol abuse. Clin Liver Dis 2012. 16(4):737-62.
3. Gist RS, Sullivan M, Serianni RP. Management of substance abuse in the hospital setting. Int
Anesthesiol Clin 2011. 49(1):15-30.

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Chapter -6
Management of Anxiety Disorders

Anxiety is a normal emotion experienced by everyone. Differentiation between normal and

pathological anxiety must be done first. Normal anxiety allows individuals to function
optimally but pathological anxiety results in both social and occupational dysfunction.
Anxiety symptoms may be psychological, physical or both. Symptoms may be part of an
anxiety disorder or may be the effects of a general medical condition or substance.
Approach to diagnosing and treating anxiety disorder:
Within the spectrum of anxiety disorders, each disorder has a characteristic set of symptoms.
Three symptom groups have been identified viz. panic, phobic and general anxiety.
Step 1:
• Exclude - underlying medical condition and substance abuse
• Common medical conditions include:
- asthma
- cardiac disease such as angina
- hyperthyroidism
• Common substances include: caffeine-containing beverages and over-the-counter
medications or illicit drugs.
1. ASSESSMENT OF PATIENT
This includes:
- detailed history of panic, phobic, general anxiety symptoms
- mental state examination
- physical examination
Panic Symptoms Phobic Symptoms General Anxiety
- Acute onset of - Fear in relation to - Excessive anxiety
intense fear a specific object or and worry
- palpitations and situation - Poor concentration
chest pain - Avoidance of the - Irritability
- sweating offending situation - Restlessness
- tremulous - Anxious - Constant anxiety
- shortness of breath participation in - Difficult to control
- choking sensation such a situation worry
- dizziness
- fear of dying

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 2. INVESTIGATIONS
Initial laboratory tests include:
- Full blood count
- Chemistry profile
- Thyroid function test
- Drug screen
- ECG

3. MANAGEMENT
‘Stepped care’ approach is recommended to help in choosing the most effective intervention.
Treat the primary disorder first.
Psychological therapy is more effective than pharmacological therapy and should be used as
first line where possible.
Consider combination therapy for complex anxiety disorders that are refractory to treatment.
High-intensity psychological intervention and self-help (based on CBT principles) should be
encouraged
PATIENT EDUCATION
- Lifestyle modification
- Avoiding excessive caffeine
- Coping with daily stresses
- Sleep hygiene
- Provide verbal and written information on the likely benefits and disadvantages of each
mode of treatment.

PRESCRIBING ANXIOLYTICS
Benzodiazepines - for acute situational anxiety.
- Use should be limited to 4 weeks.
- Clonazepam 0.5mg bd/tds
Antidepressant agents are the drugs of choice in the treatment of anxiety disorders.
- Tricyclic antidepressants – imipramine 25mg to 150mg for panic disorder
- SSRIs- as per patient profile

References:
1. Taylor, D., Kapur, S., & Taylor, D. The Maudsley prescribing guidelines in psychiatry 2012.
2. Bandelow, B., Sher, L., Bunevicius, R., Hollander, E., Kasper, S., Zohar, J. WFSBP Task
Force on Anxiety Disorders, OCD and PTSD. Guidelines for the pharmacological treatment
of anxiety disorders, obsessive–compulsive disorder and posttraumatic stress disorder in
primary care. International Journal of Psychiatry in Clinical Practice 2012, 16(2), 77–84.

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 Chapter – 7
Management of Obsessive compulsive disorder

Obsessive compulsive disorder (OCD) is a chronic psychiatric disorder characterized by

recurrent intrusive thoughts (obsessions) and/ or repetitive compulsory behaviours
(compulsions) that are ego-dystonic, time consuming and cause significant psychosocial
dysfunction [1]. The illness runs a chronic course with episodic exacerbation of symptoms
due to various bio psychosocial factors [2]. The patient suffering from OCD needs to
evaluated and treated as per the consensus of few standard protocols which are as follows:
1. The patient should undergo a detailed evaluation to identify the bio psychosocial factors
contributing to the causality or maintenance of the OC symptoms. The patient has to undergo
a baseline Y-BOCS rating and subsequently at intervals of 1 week to see the change in
symptom severity with pharmacological and non-pharmacological interventions.
2. Investigations should include ESR, ASO titre and others as per the clinician’s decision.
3. Associated co-morbidities such as tic disorder, impulse dyscontrol disorder, Body
dysmorphic disorder (BDD) and hypochondriasis etc. should be evaluated.
4. The following disorders have to be differentiated from OCD such as Major depression
(depressive ruminations), Bipolar disorder (racing of thoughts), psychotic disorder (intrusive
thoughts and delusions), organic mental disorder (intrusive thoughts and stereotypes), and
other anxiety disorders. The patient’s level of insight into his psychopathology needs to be
assessed [2, 3].
5. First line pharmacotherapy should include adequate trials for at least 12 weeks at the
maximum recommended dosages of one of the following: Clomipramine 100-250mg/day,
Fluoxetine 20-80mg/day, Fluvoxamine 100-300mg/day, Sertaline 100-200mg/day,
Escitalopram 20-40mg/day, Paroxetine 25-50mg/day and Venlafaxine 75-225mg/day. The
dose escalation should be gradual watching for the side effects and the trial should be given
for 8-12 weeks before switching the drug [3, 4,5].
6. Intensive psychological intervention techniques should be carried out including ERP and
CBT, with a minimum of at least 20 hours of actual ERP [4].

References:
1. International classification of diseases 10 Classification of Mental and Behavioural Disorders
Diagnostic Criteria for Research, World Health Organization: Geneva; 1993.

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2. Zohar J, Insel TR. Obsessive Compulsive Disorder. Psychobiological approaches to
diagnosis, treatment and pathophysiology. Biol Psychiatry. 1987; 22: 667-87.
3. Rapport JL. The waking nightmare: An overview of obsessive compulsive disorder. J Clin
Psychiatry 1990; 51: 25-8.
4. Pallanti S, Quercioli L. Treatment refractory Obsessive Compulsive Disorder:
Methodological issues, operational definitions and therapeutic lines. Prog
Neuropsychopharmacol Biol Psychiatry. 2006; 30; 400-12.
5. Farris SG, McLean CP, Van Meter PE, Simpson HB, Foa EB. Treatment response, symptom
remission, and wellness in obsessive-compulsive disorder. J Clin Psychiatry 2013
Jul;74(7):685-90.

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Differentiate OCD from: Look for co-morbidities such as:
• Major depression (depressive ruminations)
• Tic disorder
• Bipolar disorder (racing of thoughts)
• psychotic disorder (intrusive thoughts and • Impulse dyscontrol disorder,
delusions), • BDD
• organic mental disorder (intrusive thoughts and • Hypochondriasis etc.
stereotypes)
• Other anxiety disorders. Evaluate bio psychosocial factors

Establish diagnosis of OCD as per diagnostic

classificatory system (ICD/DSM recent version)

Y-BOCS rating- Baseline, subsequently at interval of 1 week

First line pharmacotherapy should include adequate Intensive psychological intervention

trials for 8- 12 weeks at the maximum techniques
recommended dosages of one of the following:
ERP
Clomipramine 100-250mg/day,
CBT
Fluoxetine 20-80mg/day,
(minimum of at least 20 hours of
Fluvoxamine 100-300mg/day,
actual ERP)
Sertaline 100-200mg/day,

Escitalopram 20-40mg/day,

Paroxetine 25-50mg/day and

Venlafaxine 75-225mg/day.

The dose escalation should be gradual watching for

the response & side effects

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 Chapter - 8
Management of Treatment Resistant Obsessive Compulsive Disorder

Obsessive compulsive disorder (OCD) is a chronic psychiatric disorder characterized by

recurrent intrusive thoughts (obsessions) and/ or repetitive compulsory behaviors
(compulsions) that are ego-dystonic, time consuming and cause significant psychosocial
dysfunction [1]. The illness runs a chronic course with episodic exacerbation of symptoms
due to various bio psychosocial factors and variable response to treatment [2]. The patient
should receive a trial of at least 3 SRIs , one of should be Clomipramine at the maximum
recommended dosage for a trial of at least 12 weeks and actual ERP for a minimum of 20
hours to mark it as treatment resistant OCD [4, 5]. The patient suffering from treatment
resistant OCD needs to evaluated and treated as per the consensus of few standard protocols
which are as follows:
1. The following disorders have to be differentiated from OCD such as Major depression
(depressive ruminations), Bipolar disorder (racing of thoughts), psychotic disorder (intrusive
thoughts and delusions), organic mental disorder (intrusive thoughts and stereotypes), and
other anxiety disorders. The patient’s level of insight into his psychopathology needs to be
assessed [2, 3].
2. Associated co-morbidities such as tic disorder, impulse dyscontrol disorder, body dysmorphic
disorder (BDD) and hypochondriasis etc. should be evaluated.
3. The patient should undergo a detailed evaluation to identify the bio psychosocial factors
contributing to the causality or maintenance of the OC symptoms as well as improper
compliance.
4. The patient has to undergo a baseline Y-BOCS rating and subsequently at intervals of 1 week
to see the change in symptom severity to mark as partial response (< 35% improvement in Y-
BOCS baseline score) or non-response or treatment resistant (< 25% improvement in Y-
BOCS baseline score) .
5. The question of inadequate first line anti-obsessional treatment should be evaluated (a trial of
at least 3 SRIs, one of should be Clomipramine at the maximum recommended dosage for a
trial of at least 12 weeks and actual ERP for a minimum of 20 hours).
6. In case of partial response to SSRIs, the following strategies can be sought: augmentation
strategies, combination strategies, using SSRIs in tandem with behavior therapy or novel
treatment options.

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7. Augmentation can be tried judging the patients comorbidities and clinical profiles with agents
like clonazepam (0.5- 3 mg/day), buspirone (10-40mg/day), lithium (Serum Lithium level of
0.4-1.0 meq/l), typical and atypical antipsychotics (lower doses) [5,6].
8. Combination treatment lower doses of Clomipramine (75-150mg/day) (than when used
alone) with SSRI or MAOI can be tried. Specific precautions to be taken for early
identification of side effects, adverse events like 5-HT syndrome [4, 5].
9. In case of refractory cases, experimental treatment approaches such as IV Clomipramine,
TMS, ECT and Psychosurgery etc. have been suggested.

References:
1. International classification of diseases 10 Classification of Mental and Behavioural Disorders
Diagnostic Criteria for Research, World Health Organization: Geneva; 1993.
2. Zohar J, Insel TR. Obsessive Compulsive Disorder. Psychobiological approaches to
diagnosis, treatment and pathophysiology. Biol Psychiatry. 1987; 22: 667-87.
3. Rapport JL. The waking nightmare: An overview of obsessive compulsive disorder. J Clin
Psychiatry 1990; 51: 25-8.
4. Pallanti S, Quercioli L. Treatment refractory Obsessive Compulsive Disorder:
Methodological issues, operational definitions and therapeutic lines. Prog
Neuropsychopharmacol Biol Psychiatry. 2006; 30; 400-12.
5. Walsh KH, Mc Dougle CJ. Pharmacological augmentation strategies for treatment resistant
Obsessive Compulsive Disorder. Expert Opin Pharmacother 2004; 5:2059-67.
6. Dold M, Aigner M, Lanzenberger R, Kasper S. Antipsychotic augmentation of serotonin
reuptake inhibitors in treatment-resistant obsessive-compulsive disorder: a meta-analysis of
double-blind, randomized, placebo-controlled trials. Int J Neuropsychopharmacol. 2013
Apr;16(3):557-74.

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 Failure of trial of at least 3 SRIs , one of should be Clomipramine at the maximum recommended dosage
for a trial of at least 12 weeks + actual ERP for a minimum of 20 hours

Partial response (< 35% improvement in Y-BOCS baseline score) or

Non-response or treatment resistant (< 25% improvement in Y-BOCS baseline score) .

Differentiate OCD from: Look for co-morbidities such as:

• Major depression (depressive ruminations) • Tic disorder

• Bipolar disorder (racing of thoughts) • Impulse dyscontrol disorder,
• psychotic disorder (intrusive thoughts and
• BDD
delusions),
• organic mental disorder (intrusive thoughts • Hypochondriasis etc.
and stereotypes)
Evaluate bio psychosocial factors
• Other anxiety disorders.

Partial response/No-response

Combination treatment Augmentation

lower doses of Clomipramine (75- Clonazepam (0.5- 3 mg/day),

150mg/day)
Buspirone (10-40mg/day),
+
Lithium (Ser Li level of 0.4-1.0 meq/l),
SSRI or MAO-Inhibitor
Typical and atypical antipsychotics

If, no response

Experimental Interventions
IV Clomipramine,
TMS,
ECT

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 Chapter - 9
Protocol for Management of Rapid Cycling Bipolar Affective Disorder

Rapid cycling in bipolar disorder (as defined in DSM-IV-TR) refers to occurrence of four or
more mood disturbances within a single year that meet criteria for a major depressive, mixed,
manic, or hypomanic episode. These episodes are demarcated by either partial or full
remission for at least 2 months or a switch to an episode of opposite polarity (e.g. from a
major depressive to a manic or mixed episode). It is less responsive to drug treatment than
non-rapid cycling bipolar disorder and associated with greater suicidal risk [1, 2]. The factors
reported to be contributing to cycling include use of antidepressants, drug or alcohol use,
hypothyroidism and psychosocial stressors. The response to treatment is variable, some
requiring more than 2 mood stabilisers and spontaneous or treatment related remissions
occurring in others [3].
These are the standard strategies to treat rapid cycling bipolar disorder which is accepted
across various settings [1, 3]:
1. Withdraw antidepressants immediately (irrespective of complaints of depressive symptoms or
dysphoria)
2. Evaluate the possible factor contributing to rapid cycling (i.e. drug or alcohol use,
hypothyroidism and psychosocial stressors) by blood investigation and detailed evaluation of
psychosocial milieu of the patient.
3. Optimise mood stabiliser treatment (using plasma level), preferably Sodium
Valproate/Divalproex /Carbamazepine/Oxcarbazepine
Consider combining mood stabilisers e.g Valproate+ Lithium
Lithium may be relatively less effective but this is not certain
4. Consider other (usually adjunct) treatment options:
• Quetiapine (200-600mg/day)
• Lamotrigine (upto 200 mg/day, lower dose with valproate, precaution for drug rash)
• Olanzapine (10-20mg/day)
• Risperidone (2-6mg/day)
• Aripiprazole (15-30mg/day)
• Topiramate (upto 300mg/day)
• Thyroxine supplementation (50-200µg/day)
• Clozapine (usual dose if inadequate response or intolerance to other drugs)

- 22 -
5. Adjunct benzodiazepines if there is agitation, insomnia or to reduce the antipsychotic use;
Benzodiazepines to be tapered gradually after reduction of severity of clinical symptoms.
6. Thyroxine supplementation (50-200µg/day)(in case of thyroid dysfunction); Nimodipine
(upto 180mg/day) if required.
The choice of drug is determined by patient factors, with few comparative efficacy data to
guide choice. Quetiapine has best supporting data and may be considered an effective adjunct
treatment option [4, 5].

Flowchart:
DIAGNOSIS OF RAPID CYCLING

STEP Withdraw antidepressants

1
STEP Evaluate the possible factor contributing to rapid cycling (drug or alcohol use,
2 hypothyroidism and psychosocial stressors)
STEP Optimise mood stabiliser Preferably Sodium Valproate/Divalproex
3 treatment(using plasma /Carbamazepine/Oxcarbazepine
levels) Consider combining mood stabilisers
STEP Consider other (usually Quetiapine
4 adjunct) treatment options Lamotrigine
Olanzapine
Risperidone
Aripiprazole
Topiramate
Thyroxine
Clozapine

References:
1. Calabrese JR et al. Current research on rapid cycling bipolar disorder and its treatment. J
Affect Disord 2001; 67; 241-55.
2. Kupka RW et al. Rapid and non-rapid cycling bipolar disorder: a meta-analysis of clinical
studies. J Clin Psychiatry 2003; 64: 1483-94.

- 23 -
3. Coryell W et al. The long term course of rapid-cycling bipolar disorder. Arch Gen Psychiatry
2003; 60: 914-20.
4. Vieta E et al. Quetiapine in the treatment of rapid cycling bipolar disorder. Bipolar Disorder
2002; 4: 335-40.
5. Zupancic ML. Role of atypical antipsychotics in rapid cycling bipolar disorder: a review of
the literature. Ann Clin Psychiatry. 2011 May; 23(2):141-149.
----------------------------------------------------------------------------------------------------------------
Chapter - 10
Management of Aggressive, Violent Patients

DEFINITIONS
Aggression is any form of behaviour directed towards the goal of harming or injuring another
living being who is motivated to avoid such treatment.
Violence is harmful behaviour inflicted upon another person or property involving the use of
force. Violence is defined as the act that leads to physical harm or destruction.
Aggression may or may not result in violence but all violence is aggression.
Phases of dealing with aggression or violence:
Phase 1: De-escalation
Phase 2: Physical restraint
Phase 3: Sedation
Phase 4: Mechanical restraint
Phase 5: Post sedation / Seclusion / Transfer
Phase 1: De-escalation
De-escalation is a process to defuse a potentially violent or aggressive situation without
having to resort to physical restraint.
During physical restraint there is a risk of injury to both the patient and the staff, therefore
there is a need for verbal intervention, which could help to reduce the threat of violence and
return the patient to a calm state of mind.
- Show concern or empathy
- Speak quietly but clearly and calmly; don’t argue
- Assist patient to stay in control
- Set limits firmly but do not threaten
- Allow extra personal space
- Deal with the issue at hand
- Ensure safe environment and remove all potential weapons
- 24 -
- Ensure safe exit point for staff
- Encourage patient to talk and make use of appropriate listening skills
- Offer medication to patient; initially oral therapy
- Allow patient to find a solution to the problem
Phase 2: Physical Restraint
- Team leader to co-ordinate
- Evacuation of staff and patients not involved
- Obtain assistance of at least 4 other staff members
- Inform the patient that the intention is to restrain and sedate
- Each person should hold a limb and the team leader should hold the patient’s head while
talking to the patient
Phase 3: Sedation (See flow chart)
- Initially offer patient oral therapy
- If patient refuses and de-escalation techniques have failed, use intramuscular or
intravascular therapy
- Lorazepam 2mg – 4mg IMI/IVI stat – give slowly over 3 minutes
- Do not risk needle-stick injury if IV is difficult
- If patient not sedated after 20 minutes, administer Haloperidol 5mg IMI stat which may be
repeated using 5mg every hour to a maximum of 20mg
- Obtain collateral information from family members or those accompanying the patient
Phase 4: Mechanical Restraint
- Prior informed written consent from guardian and/or patient
-Not to be used as a punitive measure, but for the safety of the patient and others, until
sedation takes effect
- Not to be used for longer than 30 minutes at a time.
- Restrain in a semi-prone position ensuring that the limbs are not contorted, to prevent
aspiration and compression injury
Phase 5: Post Sedation/Seclusion/Transfer
- Assign a staff member to be with patient until he/she becomes ambulant or until transfer
effected
- Once sedated or calm, to attempt history taking, physical mental state examination and
special investigations (esp. blood glucose) to evaluate cause of behavioural disturbance
- Blood pressure, pulse rate and respiration to be monitored every 5 – 10 minutes in first hour
and then every 15 minutes until ambulant
- 25 -
 - If BP drops below 100/60, elevate lower limbs of patient
- If BP does not respond, IV fluids need to be commenced
- Document all nursing care and medication accurately
- Transfer of patient to a psychiatric ward after consultation with family members
-Admission procedure as per admission guidelines of concerned hospital (1, 2, 3).
Guidelines For The Rapid Tranquillisation Of Aggressive, Violent Patients

INITIAL CONSIDERATIONS
1. DE-ESCALATION – Talking down, time out, distraction, privacy and quiet.
2. MEDICATIONS – Note any Psychotropic medication received in last few hours.
3. ADVANCE DIRECTIVES – Patient preferred treatment choices.

OFFER ORAL THERAPY

HALOPERIDOL 5 –10mg (Max 30mg/24hrs) – not for the neuroleptic naïve

Review temperature, pulse, blood pressure and respiratory rate every 5 – 10 minutes for
one hour and then hourly until patient is ambulatory.

INTRAMUSCULAR THERAPY
LORAZEPAM 2 – 4 mg IMI (Max 6mg/24hrs) Sedation in 30 – 45 minutes;
peaks in 1 – 3 hours, lasts 4 – 6 hours
+/-
HALOPERIDOL 5mg IMI (Max 18mg / 24hrs) Sedation in 10 minutes;
peaks in 20 minutes
+
PROMETHAZINE 25-50 mg IMI
OR
OLANZAPINE 5 – 10mg IMI (Max 20mg/24 hrs) 2 hour interval between
injections; peaks 15 – 45 minutes

IF NO IMPROVEMENT, REVIEW AND CONSULT SENIOR COLLEAGUE

Consider Consider
DIAZEPAM 10mg IV slowly Zuclopenthixol acetate CLOPIXOL
over 5-10 minutes ACUPHASE IM 50 – 150mg
(Sedation in 1 – 2 hrs, peaks in 36 hours,
lasts 72 hours)

NB: For elderly patients, halve doses and titrate according to response
References:
1. Gillies D, Sampson S, Beck A, Rathbone J. Benzodiazepines for psychosis-induced
aggression or agitation. Cochrane Database Syst Rev. 2013 Apr 30;4.
2. Miller L, Riddle MA, Pruitt D, Zachik A, dosReis S. Antipsychotic treatment patterns and
aggressive behavior among adolescents in residential facilities. J Behav Health Serv Res.
2013 Jan;40(1):97-110.

- 26 -
3. Powney MJ, Adams CE, Jones H. Haloperidol for psychosis-induced aggression or agitation
(rapid tranquillisation). Cochrane Database Syst Rev. 2012 Nov 14;11.
----------------------------------------------------------------------------------------------------------------

Chapter - 11
Assessment and Management of Suicide/Self-harm

Suicide is the act of deliberately killing oneself. Self-harm is a broader term referring to
intentional self-inflicted poisoning or injury, which may or may not have a fatal intent or
outcome. Any person over 10 years of age experiencing any of the following conditions
should be asked about thoughts or plans of self-harm in the last month and about acts of self-
harm in the last year (1, 2, 3):

Risk Factors for Suicide

o Male
o Elderly
o Single, divorced, widowed
o Living alone, poor social support
o Unemployed
o low socioeconomic status
o Previous suicide attempt or self-harm
o Any mental disorder
o Alcohol/ drug abuse/dependence
o Concurrent physical disorder
o Recent bereavement

Following algorithm should be followed:

- 27 -
 » Medically treat injury or
poisoning.
1. Has the person attempted
a medically serious act of » If medical hospitalization
self-harm? is needed, continue to
If person requires monitor the person closely
urgent medical to prevent suicide.
treatment for act of
self-harm

Observe for evidence of self-

injury
Look for: In all cases:
Keep the person in a
» Signs of poisoning or secure and supportive
intoxication
environment at the health
» Signs / symptoms requiring facility while being
urgent medical treatment such assessed (do not leave
as: them alone).
– bleeding from self-inflicted » Care for the person with
wound
self-harm.
– loss of consciousness
– extreme lethargy » Offer and activate
psychosocial support.
Ask about: If NO, assess for » Consult mental health
» Recent poisoning or other imminent risk of specialist.
self-harm / suicide » Maintain regular contact
self-harm
and follow-up.

- 28 -
2. Is there an imminent risk of
self-harm / suicide? If there are: » Take the following precautions:
» current thoughts or
plan to commit suicide / – Remove means of self-harm.
self-harm – Create secure and supportive
OR environment; if possible, offer
» history of thoughts or separate, quiet room while waiting.
Yes plan of self-harm in the – Do not leave the person alone.
past month or act of – Supervise and assign a named
self-harm in the past staff member or a family member to
Ask person and carer about: ensure safety.
year in a person who is
» Current thoughts or plan to commit now extremely – Attend to mental state and
suicide or self-harm agitated, violent, emotional distress.
» History of thoughts or plan of self- distressed or » Consult mental health specialist
harm in the past month or act of self- uncommunicative » Maintain regular contact and
harm in the past year
follow-up.
» Access to means of self-harm
Look for: There is imminent risk
of self-harm / suicide.
» Severe emotional distress
» Hopelessness
» Extreme agitation
» Violence
» Uncommunicative behaviour If there is no imminent » Offer and activate psychosocial
» Social isolation risk of self-harm / support.
suicide, but history of
thoughts or plan of » Consult mental health specialist
self-harm in the past » Maintain regular contact and
No month or act of self- follow-up.
harm in the past year

Manage the
3. Does the person have concurrent
concurrent priority mental, If concurrent priority conditions conditions in
conjunction with the
neurological or drug use above actions.
disorders?

» Depression
» Alcohol or drug use disorders
» Bipolar disorder
» Psychosis
» Epilepsy
» Behavioural disorders

- 29 -
 Manage pain
4. Does the person have chronic pain? If chronic pain is present
and treat any
relevant medical
disease.

5. Does the person have emotional

symptoms severe enough to warrant
clinical management?
If YES, additional
clinical management of
symptoms is warranted

» Difficulty carrying out usual work, school,

domestic or social activities
» Marked distress or repeated help-seeking
» Repeated self-medication for emotional
distress or unexplained somatic symptoms

References:

1. Mental Health Gap Action Programme. mhGAP intervention guide for mental, neurological
and substance use disorders in non-specialized health settings: version 1.0. Geneva: World
Health Organization 2010.

2. Kalmár [Link] possibilities of suicide prevention in adolescents. A holistic approach to

protective and risk factors. Neuropsychopharmacol Hung 2013. 15(1):27-39.

3. Wilkinson P. Non-suicidal self-injury. Eur Child Adolesc Psychiatry 2013. 2013 Feb;22
Suppl 1:S75-9.
----------------------------------------------------------------------------------------------------------------

- 30 -
 Chapter - 12
Protocol for ECT- Evaluation, Work-Up, Application, Handling Complications

Electroconvulsive therapy (ECT) is an important, effective and relatively safe treatment

procedure for a variety of neuropsychiatric disorders. The present days ECT devices usually
deliver constant current by varying the time of exposure and stimulus waveforms being brief
pulse square wave or ultra-brief pulse square wave [1, 2] .
Pre-ECT evaluation/ work up should include the following: [1, 3, 7]
1. Informed consent has to be taken in written from both the patient and guardian (Only
guardian in case the patient is a minor), after explaining the method, benefit and risks
involved in the ECT procedure (preferably in written format). Consent can cover anaesthetic
procedures and the electrical stimulation.
2. Complete medical history, detailed physical, neurological, and preanesthesia examination
should be done.
3. Complete dental examination including the state of dentition, any artificial dentures etc.
should be done.
4. Laboratory evaluation should include routine blood and urine examination, X-ray chest and
ECG. Pre-ECT Mini Mental Status Examination (MMSE) should be performed and post
ECT assessment should be done once in a week to look for any cognitive impairment.
5. X-ray spine is needed if there is evidence of a spinal disorder. CT brain/ MRI should be
performed in case of suspected seizures or any intra cranial space occupying lesions.
6. Detailed history of concomitant medications being used should be assessed which have
possible effect on the seizure threshold or seizure duration and the drugs which have potential
interactions with the medications used during ECT. Concomitant use of drugs like
Benzodiazepines, antiepileptic mood stabilisers, Lithium, Bupropion and Clozapine have to
be avoided.
7. Patient should be nil orally for 5-6 hours before the ECT procedure, with empty bladder and
bowel. The mouth should be checked for dentures or other foreign objects.
8. An IV (intravenous line) should be established.
9. A bite block, 100% oxygen and emergency equipment for establishment of airway and
defibrillator should be immediately available in case of requirement.
10. Muscarinic anticholinergic agent like Inj. Atropine 0.3 to 0.6 mg IM has to be administered
30-45 minutes before the treatment procedure. Another option is the use of Glycopyrrolate
(0.2-0.4 mg IM/ slow IV), which produces less cognitive dysfunction, nausea, but has
- 31 -
 comparatively less cardio protective effect than atropine. The choice of ECT anaesthesia and
muscle relaxant has to be decided by the anaesthesia team [2, 4]

ECT Application:
1. ECT can be used in clinical diagnosis like Major depression (Unipolar or bipolar, particularly
psychotic depression), mania (or mixed episodes), schizophrenia with acute exacerbation
(catatonic subtype), schizoaffective disorder and other conditions like Parkinson’s disease,
Neuroleptic malignant syndrome (NMS), intractable seizure disorder.
2. ECT can be used in psychiatric patients presenting with suicidal/ homicidal risk, food refusal,
catatonia, severe psychomotor agitation or retardation / past history of response to ECT/ poor
response or intolerance to the side effects of psychotropics in the past/ patient preference.
Failure to respond to or intolerance of pharmacotherapy or for rapid definitive response in the
current episode can also warrant the use of ECT.
3. ECT sessions should be given at a frequency of 2-3 sessions/ week on an average of 8-10
session [6-12 sessions properly spaced depending on the clinical condition]. In catatonia or
NMS less number of ECT sessions are required (4-6 sessions). An adequate ECT trial should
be 8-10 sessions, after which term like ECT resistance can be considered; Maximum up to 14
ECT sessions can be tried [3, 4]

Complications and their management:

1. CNS:
a. In case of subshock, a gap of > 30 seconds (wait and watch) should be allowed. The
stimulation then has to be increased by 1.5 times and the second treatment should be
administered. The principle should be that the patient should have an adequate motor/ EEG
seizure before leaving the treatment room.
b. In case of inadequate duration of seizure, O2 (100%) inhalation for short duration/
theophylline/ caffeine can be tried, the stimulation has to be increased 1.5 times and second
treatment should be administered.
c. In case of prolonged seizures (> 180 sec. by Motor/EEG measurement), the seizure has to be
terminated by infusion of IV Diazepam/ Lorazepam or Thiopentone. Non-convulsive status
should be suspected if there is lack of recovery after anaesthesia [6, 7].

- 32 -
 2. Neurocognitive:
a. Post- ECT confusion/ delirium/ agitation: The patient be temporarily restrained to reduce the
risk of injury to self or others. Slow IV or IM Diazepam /Lorazepam can be useful.
b. Memory deficits: They can be reduced by avoiding sine-waveform, suprathreshold stimulus,
greater frequency and the number of treatments.
c. Post-ECT headache is common and can be treated with Paracetamol or other NSAIDS [5, 7,
8].
3. Dental and Musculoskeletal injuries or TM joint dislocation: can be prevented by
precaution during the treatment procedure. Myalgia can be treated with NSAIDS [5].
4. Cardiovascular and Respiratory complications can be prevented by good initial medical
evaluation, use of muscarinic anticholinergics or glycopyyrolate before the treatment session.
In case of rare ventricular tachycardia or fibrillation, defibrillation should be done with the
help of cardiologist or respiratory physician [5, 6, 7].
References:
1. American Psychiatric Association Task Force on Electroconvulsive Therapy. The Practice
of Electroconvulsive Therapy. 2nd edition. Washington, DC, American Psychiatric Press,
2001. Chapter 1, 2.
2. Rey JM, Walter G. Half a century of ECT use in young people. American Journal of
Psychiatry1997; 154:595–602.
3. American Psychiatric Association Task Force on Electroconvulsive Therapy. The Practice
of Electroconvulsive Therapy. 2nd edition. Washington, DC, American Psychiatric Press,
2001, Chapters 3,4,6.
4. Krystal AD, Coffey CE. Neuropsychiatric considerations in the use of electroconvulsive
therapy. Journal of Neuropsychiatry and Clinical Neuroscience 1997; 9:283–292.
5. Kelly KG, Zisselman M. Update on electroconvulsive therapy (ECT) in older adults.
Journal of the American Geriatrics Society 2000; 48:560–566.
6. American Psychiatric Association Task Force on Electroconvulsive Therapy. The Practice
of Electroconvulsive Therapy. 2nd edition. Washington, DC, American Psychiatric Press,
2001, Chapter 5.
7. Enns MW, Reiss JP. Electroconvulsive therapy. Canadian Journal of Psychiatry 1992;
37:671–686.
8. Euba R. Electroconvulsive therapy and ethnicity. J ECT. 2012 Mar;28(1):24-6.
----------------------------------------------------------------------------------------------------------------------------

- 33 -
 Chapter - 13
General Principles of Prescribing In Pregnancy

The risk of spontaneous major malformation of the fetus during pregnancy is approximately
2-3%. The potential risks of drugs include major malformation (first trimester exposure),
neonatal toxicity (third trimester exposure) and long term neurobehavioral effects [1, 2]. The
safety of psychotropic in pregnancy cannot be clearly established in view of the lack of
ethical prospective trials. The following are few general principles of prescribing in
pregnancy.
In all women of child-bearing potential
1. Always discuss the possibility of pregnancy-many pregnancies are unplanned.
2. Try to avoid using drugs that are contraindicated during pregnancy in women of reproductive
age (especially Valproate and Carbamazepine). If these drugs are prescribed, women should
be made fully aware of their teratogenic properties even if not planning pregnancy. Prescribe
Folate preferably 2 weeks prior to conception [2, 3].
If mental illness is newly diagnosed in a pregnant woman
1. Try to avoid all drugs in the first trimester (when major organs are being formed) unless
benefit outweighs risk.
2. If non drug treatment is not effective/appropriate, use an established drug at the lowest
effective dose [2, 3].
If a woman taking psychotropic drugs is planning a pregnancy
1. Consider discontinuing treatment if the woman is well and at low risk of relapse.
2. Discontinuation of treatment for woman with serious mental illness and at a high risk of
relapse is unwise, but consideration should be given to switching to a low risk drug. Be aware
that switching drugs may increase the risk of relapse [3, 4].
If a woman taking psychotropic medications discovers that she is pregnant
1. Abrupt discontinuation of treatment post conception for women with serious mental illness
and at a high risk of relapse is unwise; relapse may ultimately be more harmful to the mother
and the child than continued, effective drug therapy.
2. Consider remaining with current medication rather than switching, to minimize the number of
drugs to which the fetus is exposed [5].
In all pregnant women
1. Ensure that the parents are as involved as possible in all decisions.
2. Use as few drugs as possible and at their lowest effective dose.

- 34 -
3. Use the drug with the lowest known risk to the mother and fetus.
4. Dose adjustment is required with the progression of the pregnancy. Dose increases are
required in the third trimester of pregnancy when blood volume expands by around 30%.
Plasma level monitoring of the drugs should be regularly done.
5. Consider referral to specialist perinatal services.
6. Ensure adequate fetal screening.
7. Inform the obstetric team of psychotropic use and possible complications.
8. Monitor the neonate for withdrawal effects after birth.
9. Document all the decisions [1, 2, 5].
Recommendations for the use of psychotropic drugs in pregnancy
Psychotropics Recommendations
1. Anti-depressants Nortryptiline, Fluoxetine
First generation antipsychotics have (Haloperidol, Trifluoperazine, Chlorpromazine)
been widely used, although safety is not fully established. No clear evidence that any
antipsychotic is a major teratogen, although there is limited data for Olanzapine and
Clozapine. Screen for adverse metabolic effects [8].
Consider using an antipsychotic as a mood stabilizer rather than an anticonvulsant drug.
Avoid Lithium and anticonvulsants unless risks and consequences of relapse outweigh the
known risk of teratogenesis. In women of child bearing potential taking Carbamazepine
(safer) or Valproate, should receive prophylactic Folic acid administration [7].
Non-drug measures are preferred. Benzodiazepines are probably not teratogenic but are best
avoided in late pregnancy [2, 5, 6].

References:
1. McElbatton PR. Pregnancy: General principles of drug use in pregnancy. Pharm J 2003;
270:232-234
2. National Institute for Health and Clinical Excellence. Antenatal and postnatal mental health.
Clinical managaement and service guidance. [Link]/.
3. Gentile S. Antipsychotic therapy during early and late pregnancy. A systematic review.
Schizophr Bull 2010; 36518-544

- 35 -
4. Ernst CL et al. The reproductive safety profile of mood stabilizers, atypical antipsychotics
and broad spectrum psychotropics. J Clin Psychiatry 2002; 63 Suppl 4:42-55.
5. Schneid-Kofman N et al. Psychiatric illness and adverse pregnancy outcome. Int J Gynaecol
Obstet 2008; 101:53-56.
6. Reis M et al. Maternal use of antipsychotics in early pregnancy and delivery outcome. J Clin
Psychopharmacol 2008; 28:279-288.
7. Félegyházy Z, Adler M. Affective disorders and their treatment during pregnancy and after
birth -- a review. Neuropsychopharmacol Hung. 2013 Mar;15(1):40-8.
8. Robinson GE. Treatment of schizophrenia in pregnancy and postpartum. J Popul Ther Clin
Pharmacol. 2012;19(3):e380-6.
----------------------------------------------------------------------------------------------------------------
Chapter - 14
Management of Dementia

Dementia is a syndrome due to disease of the brain, usually of a chronic or progressive

nature, in which there is disturbance of multiple higher functions, including memory,
thinking, orientation, comprehension, calculation, learning capacity, language and judgement
[4, 6]. Consciousness is not clouded. Impairments of cognitive function are accompanied and
occasionally preceded by deterioration in emotional control, social behaviour or motivation
[1, 4]. Some of the most common forms of dementia are: Cortical dementias like Alzheimer's
disease, fronto-temporal dementia, Pick’s dementia and dementia with Lewy bodies and Sub-
cortical dementias like vascular dementia [1, 2]. The particular assembly of symptoms that
each patient manifests as a result of dementing changes along the course of the disease varies
between patients. Considering that many drugs (and other non drug treatments) have
significant side effects and costs, producing guidelines for the treatment of this disease is not
always clear-cut [3, 5, 7]. Patient with dementia can present behavioural and psychological
symptoms. The main features of behavioural problems are agitation, aggression and apathy,
whereas psychological problems can present wit psychosis, depression, insomnia, anxiety etc
[5, 6].
The recommendations for management of dementia is given in the form of a flow chart as
follows:

- 36 -
 Forgetfulness

History
Physical examination
Mental status examination
Neuropsychological assessment
Caregiver assessment

Meets diagnostic criteria of No Non-dementia memory disturbance including age

dementia related cognitive changes, delirium, amnesia,
depression

Yes

Cause of dementia apparent Yes Pt. With h/o anoxia, trauma, other definitive
cause (huntington’s dis, Parkinson dis), if stable,
required no other diagnostic assessment

No

Labrotary tests abnormal, Yes Specific diagnosis of hypothyroidism, B12

medical illness deficiency, systemic illness, HIV encephalopathy
etc.

No

Yes
Neuroimaging indicated & Tumor, abscess, hydrocephalous, subdural
abnormal? hematoma, multiple sclerosis, stroke or
vascular dementia

No

Yes
Motor system disorders Extrapyramidal syndrome of PSP, DLB, other
present? movement disorder

No - 37 -
 Yes Depression
Evidence of depression?

Alzheimer’s Lewy Body Other type

Dementia Dementia of dementia

TREATMENT OPTIONS

Consider treatment with If behavioural Non-pharmacological

Acetylcholine esterase symptom appears management
inhibitor

Donepezil 5-10mg/day Start low, go slow Educational

programme for
Rivastigmine 6-12mg/day Haloperidol .25-.5mg/day caregiver
Galantmine 16- Quetiapine 12.5-50mg/day
24mg/day
Olanzapine 2.5-5mg/day

- 38 -
 Reference:

1. Savva GM, Zaccai J, Matthews FE, Davidson JE, McKeith I, Brayne C. Prevalence,
correlates and course of behavioural and psychological symptoms of dementia in the
population. Br J Psychiatry. 2009;194:212–219.
2. National Institute for Health and Clinical Excellence. Dementia - Supporting people with
Dementia and their Carers in Health and Social Care. 2006.
3. Black W, Almeida OP. A systematic review of the association between the Behavioral and
Psychological Symptoms of Dementia and burden of care. Int Psychogeriatr. 2004;16:295–
315.
4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders,
4th Edn Washington, DC: American Psychiatric Association 2000.
5. Ballard C., Day S., Sharp S., Wing G., Sorensen S. Neuropsychiatric symptoms in dementia:
importance and treatment considerations. Int. Rev. Psychiatry 2008. 20, 396–404.
6. Ballard C., Gauthier S., Corbett A., Brayne C., Aarsland D., Jones E. Alzheimer’s disease.
Lancet 2011. 377, 1019–1031.
7. van de Glind EM, van Enst WA, van Munster BC, Olde Rikkert MG, Scheltens P, Scholten
RJ, Hooft L. Pharmacological Treatment of Dementia: A Scoping Review of Systematic
Reviews. Dement Geriatr Cogn Disord 2013. 36(3-4):211-228.

----------------------------------------------------------------------------------------------------------------
Chapter - 15
Management of Delirium

It is acute or sub acute onset of impaired cognitive functioning as a result of diffuse brain
dysfunction. The central feature is a fluctuating level of consciousness.
CLINICAL FEATURES
• Change in the level of consciousness
• Changes in behaviour i.e. increased or decreased activity
• Thought processes are fragmented and incoherent. Sleep disturbance
• Hallucinations tend to be visual or tactile, and delusions are transitory and fragmented
• Mood may be anxious, irritable or fearful. Labile mood
• Perplexity is characteristic.
• Memory is markedly affected; registration and new learning are impaired
• Disorientation is more marked for time than place or person
• Neurological signs e.g. unsteady gait, tremor, asterixis, myoclonus, paratonia
CAUSES
• CNS disorders e.g. trauma, seizures, vascular disease and degenerative disease
- 39 -
• Metabolic disorder e.g. hypoxia, hypoglycaemia, thiamine deficiency, anaemia, renal or
hepatic failure, electrolyte imbalance
• Cardiopulmonary disorder e.g. CCF, MI, arrhythmia, shock, respiratory failure
• Systemic illness e.g. substance intoxication or withdrawal, infection, neoplasm, postoperative
state, temperature dysregulation
MANAGEMENT OF DELIRIUM
Basic principle – Treatment of underlying cause is the most important step
General Principle – Alleviate distress, control anxiety, reassure patient. Prevent self harm,
monitor vital signs, maintain adequate fluid balance, nurse in a well-lit room and prevent
further complications. Regularly monitor symptoms and behaviours as they can fluctuate
rapidly.
Specific management – Appropriate investigations to identify underlying cause e.g. blood
screen including full blood count, urinalysis, chest x-ray, arterial blood gases. Additional tests
if indicated include blood cultures, LP, CT, EEG, drug screen
Pharmacological management –
• Withdraw all non-essential drugs.
• Haloperidol is frequently used because it has few anticholinergic side effects, few active
metabolites, and a relatively small likelihood of causing sedation and hypotension.
Haloperidol 1-5mg two to three times a day orally or intramuscularly. Risperidone,
Olanzapine and Quetiapine are increasingly being used, due to their more tolerable side effect
profile.
• Benzodiazepines as monotherapy are generally reserved for patients with delirium caused by
seizures or withdrawal from alcohol/ sedative hypnotics
• Regular monitoring is mandatory. Once patient stabilizes, gradually taper and discontinue
medication.
By treating the underlying cause, the features of delirium should resolve in a matter of days.
The symptomatic treatment should then be withdrawn. A delirium persisting for more than
ten days requires repeat investigation into cause and its management.
Environmental Interventions –
• Provide support and orientation: communicate clearly, repeated verbal reminders, clear
signposts with a clock, calendar and day’s schedule.
• Ensure staff consistency and family support.
• Provide an unambiguous environment: allow adequate space, avoid extremes of sensory
experience, avoid medical jargon and ensure adequate lighting.
• Maintain competency: identify and correct sensory impairments, encourage self-care and
participation in treatment, allow maximum periods of uninterrupted sleep and maintain
activity level.

Flowchart

- 40 -
 Flowchart for management of delirium**
E.g. change in level of
Clinical features of delirium consciousness, disorientation and
memory impairment

Investigate underlying E.g. blood + urine serum, CXR ±

cause ECG, LP, CT

Underlying cause diagnosed

Treat underlying cause

General principles of E.g. reassure, prevent self-

management harm, monitor vital signs

Pharmacological Environmental intervention

management

Withdraw non-essential • Support + intervention

drugs • Unambiguous
Haloperidol/ atypical environment
antipsychotic • Maintain competency
Benzodiazepines

If delirium persists > 10 days

REPEAT

References:

1. Tabet, N., Howard, R. Pharmacological treatment for the prevention of delirium: review of
current evidence. International Journal of Geriatric Psychiatry 2009, 24(10), 1037–1044.
2. Fong, T. G., Tulebaev, S. R., Inouye, S. K. Delirium in elderly adults: diagnosis, prevention
and treatment. Nature reviews. Neurology 2009, 5(4), 210–220.
3. Alakkassery S, Flaherty JH. Delirium in the elderly. J Med Liban 2012. 60(4):214-219.
----------------------------------------------------------------------------------------------------------------

- 41 -
 Chapter - 16
Management of Developmental Disorder

Developmental disorder is an umbrella term covering disorders such as intellectual disability

/ mental retardation as well as pervasive developmental disorders including autism. These
disorders usually have a childhood onset, impairment or delay in functions related to central
nervous system maturation, and a steady course rather than the remissions and relapses that
tend to characterize many other mental disorders. Despite a childhood onset, the
developmental disorders tend to persist into adulthood.
Pervasive developmental disorders
The features are impaired social behaviour, communication and language, and a narrow range
of interests and activities that are both unique to the individual and carried out repetitively.
They originate in infancy or early childhood. Usually, but not always, there is some degree of
intellectual disability. Behaviours mentioned above are often seen in individuals with
intellectual disabilities as well (1, 3).
Intellectual disability
Intellectual disability is characterized by impairment of skills across multiple developmental
areas (i.e., cognitive, language, motor and social) during the developmental period. Lower
intelligence diminishes the ability to adapt to the daily demands of life. Intelligence Quotient
(IQ) tests can provide guidance to the person’s abilities, but should be used only if the tests
have been validated for use in the population in which they are being applied (2, 3).
Family psychoeducation
Psychoeducation involves the person with developmental disorder and the family, depending
on the severity of the condition and availability and significance of the family member role in
daily life (3).
Parent or significant family member needs to be trained to:
» Accept and care for the child with developmental disorder.
» Learn what is stressful to the child and what makes them happy; what causes their problem
behaviours and what prevents them; what are the child’s strengths and weaknesses and how
best they learn.
» Understand that people with developmental disorders may have difficulties when they face
new situations.
» Schedule the day in terms of regular times for eating, playing, learning and sleeping.
» Involve them in everyday life, starting with simple tasks one at a time.
» Keep them in schools as far as possible; attending mainstream schools even if it is part time
is preferable.
» Be careful about their general hygiene and train them in self-care.
» Reward their good behaviour after the act and give no reward when the behaviour is
problematic.
» Protect them from abuse.
» Respect their right to have a safety zone within a visible boundary where they can feel safe,
comfortable and move around and play freely the way they like.
» Communicate and share information with other parents who have children with similar
conditions.

- 42 -
2.2 Advice to teachers
» Make a plan on how to address the child’s special educational needs. Simple tips include:
– Ask the child to sit at the front of the class.
– Give the child extra time to understand assignments.
– Break long assignments into smaller pieces.
– Look for bullying and take appropriate action to stop it.

- 43 -
 1. Does the child have a delay in
development?

If there is a Manage nutrition

delay in problems,
development or including iodine
the mentioned deficiency and
oddities in medical
communication/ conditions,
Assess child’s development using
behaviour
developmental milestones or comparing
the child with other children of the same
age.
Are there any
nutritional
deficiencies
including iodine
deficiency and /
or medical
conditions?
Look for:
» Oddities in communication Start family psychoeducation.
» Restricted, repetitive (stereotyped) » Consider parent skills
patterns of behaviour, interests, and training.
activities » Inform about available
» The time, sequence and course of educational and social
these features services and collaborate with
» Loss of previously acquired skills them.
» Family history of developmental » Assess current level of
adaptive functioning in
disorder
consultation with specialist,
» Presence of visual and hearing » Manage associated
impairment
conditions such as visual and
» Associated epilepsy hearing impairment
» Associated signs of motor impairment » Provide support for
or cerebral palsy anticipated difficult situations
in life.
» Facilitate and collaborate
with community-based
rehabilitation services.
» Provide support for carers
» Follow up regularly.

2. Is the delay in development due

to non-stimulating environment or
maternal depression?

» Provide family
psychoeducation and train
If non-stimulating parents on how to provide a
environment or mother stimulating environment for
with depression the child.

» Treat maternal
depression.

- 44 -
3. Look for another priority
mental, neurological, or
substance use disorder

Treat according to relevant

intervention
– Epilepsy
– Depression
– Behavioural disorders

Consider especially:
» Epilepsy
» Depression
» Behavioural disorders

» Manage any underlying

treatable acute physical
problem exacerbating
behavioural problems.

» Consider additional family

psycho-education and parent
4. Does the child have skills training for the specific
problem behaviours? problem behaviour.

» Consider cognitive
behavioural therapy (CBT).

» Provide further support for

care-givers.

Pharmacological
treatment for irritability,
aggression, self-injurious
behaviour:

Tab. Risperidone- 0.5-

1.5mg/day

- 45 -
 References:

1. Danial JT, Wood JJ. Cognitive Behavioral Therapy for Children with Autism: Review and
Considerations for Future Research. J Dev Behav Pediatr. 2013 Aug 2. [Epub ahead of print]
2. Rana F, Gormez A, Varghese S. Pharmacological interventions for self-injurious behaviour in
adults with intellectual disabilities. Cochrane Database Syst Rev. 2013 Apr 30;4.
3. Mental Health Gap Action Programme. mhGAP intervention guide for mental, neurological
and substance use disorders in non-specialized health settings: version 1.0. Geneva: World
Health Organization 2010.

----------------------------------------------------------------------------------------------------------------
Chapter - 17
Management of Attention Deficit Hyperactivity Disorder

Attention deficit hyperactivity disorder (ADHD) is characterized by pervasive and impairing

symptoms of inattention, hyperactivity, and impulsivity according to DSM-IV [1]. The WHO
uses a different name—hyperkinetic disorder (HD)—but lists similar operational criteria for
the disorder [2]. It has been associated with a broad range of negative outcomes for affected
subjects and with a serious financial burden to families and society, which characterizes it as
a major public health problem [3]. Appropriate pharmacological, psychological and
behavioral interventions should be put in a place.
The following is a summary of treatment for Attention Deficit Hyperactivity Disorder:

1. Drug treatment should be initiated only after comprehensive assessment of the mental,
physical health and socio-economic factors.
2. For cases of moderate (or lesser) degrees of severity, psychological interventions are
recommended as initial therapy, with medications subsequently if required.
3. For severe cases (those with pervasive impairment from their ADHD), medications will be
the first line of treatment.
4. Methylphenidate is usually the drug of choice with its licensed indication. Adverse effects
include insomnia, anorexia, raised blood pressure and growth retardation, which can be
managed symptomatically or by dose reduction or giving drug holidays. Decision making
should include consideration of co-morbid conditions (tics, epilepsy), tolerability and adverse
effects, convenience of dosing and patient/parent preference. If using methylphenidate,
modified release preparations is preferable (convenience of single day dosing, improving
adherence, acceptability to schools) or multiple doses of immediate release preparations
(greater flexibility in controlling time/course of action). [3, 4]

- 46 -
5. Atomoxetine is a suitable first line alternative. It may be useful for children who do not
respond to stimulant or when dopaminergic adverse effects (such as tics, stereotypies)
become problematic on stimulants. Parents should be told about adverse effects such as
anorexia and potential emergence of suicidal thinking/ liver dysfunction [4, 5]
6. Third line drugs include Clonidine and TCAs. There is some evidence supporting the use of
Bupropion and antiepileptic like Carbamazepine, Valproate. Low dose of Risperidone is
useful in reducing co-existent aggression. Modafinil has been reported to be effective without
any comparative evidences with standard treatments and its safety is not established [6, 7]
7. Where more than one agent is considered suitable, the product with the lowest cost should be
prescribed.
8. Monitoring should include periodic measurement of height and weight, along with recording
of heart rate and blood pressure. [3, 4, 5]

Reference:
1. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Diseases
(DSM-IV), 4th ed. Washington, DC, American Psychiatric Publishing, 1994
2. World Health Organization: The ICD-10 Classification of Mental and Behavioral Disorders:
Diagnostic Criteria for Research. Geneva, Switzerland, World Health Organization, 1993
3. Goldman LS, Genel M, Bezman RJ, Slanetz PJ: Diagnosis and treatment of attention-
deficit/hyperactivity disorder in children and adolescents: Council on Scientific Affairs,
American Medical Association. JAMA 1998; 279:1100–1107
4. National Institutes of Health: National Institutes of Health Consensus Development
Conference Statement: diagnosis and treatment of attention-deficit/hyperactivity disorder
(ADHD). J Am Acad Child Adolesc Psychiatry 2000; 39:182–193
5. Rappley MD: Attention deficit-hyperactivity disorder. N Engl J Med 2005; 352:165–173
6. Biederman J, Faraone SV: Attention-deficit hyperactivity disorder. Lancet 2005; 366:237–
248.
7. Pringsheim T, Gorman D. Second-generation antipsychotics for the treatment of disruptive
behaviour disorders in children: a systematic review. Can J Psychiatry. 2012 Dec;57(12):722-
727
----------------------------------------------------------------------------------------------------------------

- 47 -
 Chapter - 18
Management of Medically Unexplained Symptoms

People in this category have anxiety, depressive or medically unexplained somatic symptoms.
They do not have any of the conditions covered elsewhere in this document (except possibly
for the condition self-harm).The subjects in this category may experience either “normal”
distress or a mental disorder not covered in other categories.
Flowchart for evaluation and treatment of medically unexplained symptoms.

Does the person have any Yes Treat for the diagnosed
psychiatric or medical condition medical and psychiatric
(ascertained after detailed medical condition.
and psychiatric examination)?
• Do not prescribe antidepressants or benzodiazepines.
• Do not manage complaints with injections or other
ineffective treatments (e.g. vitamins).
• Address current psychosocial stressors
No
• Consider structured physical activity programme, relaxation
training, or problem-solving treatment
Are there prominent • Avoid unnecessary medical tests / referrals and do not offer
medically unexplained Yes placebo or other ineffective treatments
somatic symptoms?

• Acknowledge that the symptoms are not “imaginary”.

• Communicate results of tests / examination, saying that no
dangerous disease has been identified, but that it is
nevertheless important to deal with the distressing
symptoms.
• Ask for the person’s explanations of somatic symptoms.
• Explain how bodily sensations (stomach ache, muscle
tension) can be related to experiencing emotions, and ask
for potential links between the person’s bodily sensations
and emotions.
• Encourage continuation of (or gradual return to) normal
activities.
• Advise the person to re-consult if symptoms worsen.

Follow above instructions, plus:

• In case of bereavement: support culturally appropriate
mourning / adjustment and reactivate social networks
• In case of acute distress after recent traumatic events: offer
Has the person been recently basic psychological support i.e., listen without pressing the
exposed to extreme person to talk; assess needs and concerns; ensure basic
Yes
psychosocial stressors? physical needs are met; provide or mobilize social support
and protect from further harm.
• Do- not offer psychological debriefing
- 48
Differential diagnosis of medically unexplained symptoms:

Psychophysiological symptoms:
Psychological factors affecting physical illness
Nonpathological, transient psychogenic somatic symptoms (all are acute but may become
chronic)
Grief and bereavement, with physical symptoms
Fear, with physical symptoms
Exaggeration or elaboration of physical symptoms (e.g., postaccident, when litigation or
compensation is involved)
Sleep deprivation, with physical symptoms
Sensory overload or deprivation, with physical symptoms
Psychiatric syndromes (other than somatoform disorders):
Mood disorders (e.g., major depression and dysthymia)
Anxiety disorders (e.g., panic disorders)
Substance use, abuse, and withdrawal Psychotic disorders (e.g., schizophrenia, psychotic
depression, and monosymptomatic hypochondriasis)
Adjustment disorders with anxiety or depression, or both
Personality disorders
Dementias
Somatoform disorders:
Somatisation disorder
Hypochondriasis
Body dysmorphic disorder
Somatoform pain disorder
Conversion disorder
Somatoform disorder, not otherwise specified
Voluntary psychogenic symptoms or syndromes:
Factitious, with physical symptoms (e.g., Munchausen syndrome)
Malingering, with physical symptoms

- 49 -
 References:
1. Mental Health Gap Action Programme. mhGAP intervention guide for mental, neurological
and substance use disorders in non-specialized health settings: version 1.0. Geneva: World
Health Organization, 2010.
2. Rubin RH, Voss C, Derksen DJ. eds. Medicine: A Primary Care Approach. Philadelphia: WB
Saunders:390, 1996.
3. Sadock BJ, Sadock VA. Kaplan & Sadock's Synopsis of Psychiatry: e10. New York:
Lippincott Williams & Wilkins, 2007.

----------------------------------------------------------------------------------------------------------------
Chapter - 19
Treatment of Antipsychotic-induced Akathisia

Akathisia is a common antipsychotic-induced adverse effect which consists of subjective

(feeling of inner restlessness and the urge to move) as well as objective components (rocking
while standing or sitting, lifting feet as if marching on the spot and crossing and uncrossing
the legs while sitting) [1, 2]. Numerous risk factors for acute akathisia have been described
and the exact pathophysiology of akathisia is still unknown. Since akathisia is a drug-induced
adverse effect, optimal management involves its prevention by advocating the use of atypical
antipsychotics [1, 3]. The patient having Akathisia needs to evaluated and treated as per the
following recommendations [1, 4]:

Reference:
1. Miller CH, Fleischhacker WW. Managing antipsychotic-induced acute and chronic
akathisia. Drug Saf. 2000 Jan;22(1):73-81
2. Sachdev P. The identification and management of drug-induced akathisia. CNS Drugs. 1995;
4:28-46.
3. Fleischhacker WW et al. The pharmacological treatment of neuroleptic-induced akathisia. J
Clin Psychopharmacol 1990; 10: 12-21.
4. Taylor D, Paton C, Kapur S. Treatment of antipsychotic-induced Akathisia. In The Maudsley
Prescribing guidelines 2010. 11th Edition. 103-104.

- 50 -
Reduce dose of antipsychotic or slow rate of Continue at reduced dose
increase
Effective
Ineffective

Switch to Quetiapine/ Olanzapine (lower doses) Continue

(Clozapine also possible if treatment resistant
Effective
Ineffective

Try an antimuscarinic drug (Trihexyphenidyl 2-8 Continue, but attempt

mg/day; Procyclidine 2.5-10 mg/day; Benzatropine gradual withdrawal
6mg/day), usually effective when other
Effective
parkinsonian features are present

Ineffective

Try benzodiazepines (e.g. Clonazepam 0.5-3 Continue, but attempt

mg/day, Lorazepam 2-6 mg/day, Diazepam 10- gradual withdrawal after
15mg/day) 1-2 weeks
Effective

Ineffective

Continue, if no
Try Propranolol 20-80 mg/day
contraindications, but
Effective attempt gradual withdrawal
after several months
Ineffective

Try Cyproheptadine 16mg/day, or, Other serotonin Continue, if no

antagonists (e.g. Mirtazepine 7.5-15mg/day) contraindications
Effective

Ineffective

Continue, if tolerated;
Try Clonidine 0.2-0.8 mg/day
withdraw very slowly

Effective

- 51 -
 Chapter - 20
Treatment Protocol for Insomnia

Insomnia is a general clinical term used for the difficulty in initiating or maintaining sleep. It
may present as:
1. Primary insomnia
2. Secondary insomnia
Essential features of non-organic insomnia according to ICD-10 are:
(a) Difficulty in falling asleep or maintaining sleep, or of poor quality of sleep;
(b) Sleep disturbance at least three times per week for at least 1month;
(c) Preoccupation with the sleeplessness and excessive concern over its consequences;
(d) Unsatisfactory quantity and/or quality of sleep causing marked distress or interfere with
ordinary activities in daily living.

Duration of insomnia:
• Acute insomnia ( up to 4 weeks)
• Chronic insomnia (more than 4 weeks)
Principles of management:
• Must be multidimensional in nature and include psychosocial, cognitive, behavioral and
pharmacological approaches
• Perpetuating factors like life style, inappropriate use of alcohol or other substances
maladaptive sleep wake schedules, and excessive worry about poor sleep must be evaluated.
• Non-pharmacological interventions must be preferred especially in transient and chronic
insomnia patients.
A. Non-pharmacological Interventions
Non-pharmacological treatment should usually target both dysfunctional attitudes and beliefs
about sleep and maladaptive behaviors that maintain the abnormal sleep pattern.(4,5)
a) Sleep Hygiene
1. Avoid oversleeping and daytime naps
2. Develop a regular routine of rising and retiring the same time each day
3. Do not work at falling asleep, rather read a book until you become drowsy
4. Practice relaxation techniques e.g. deep breathing exercises
5. Reduce noise and light in the bedroom, or try low background music
6. Only use the bed for sleeping, do not watch TV in bed
7. Do not go to bed hungry, but do not overeat either
8. Do not drink beverages that contain caffeine, e.g. coffee, Red Bull in the evening
9. Do not consume alcohol at night.
10. Do not smoke in the evening
11. Exercise every day, but not too strenuously before bedtime
12. Try to lead an active life e.g. go for a brisk walk daily
13. Avoid chronic use of sleeping pills

- 52 -
b) Sleep Restriction Therapy
The goal of this therapy is to regulate the sleep wake cycle by tailoring the time spent in bed
to the patient’s true sleep need. It begins by calculating average total sleep time, which is
accomplished by completing sleep logs to determine baseline mean total sleep time. Sleep
time in bed is reduced to estimated total sleep time that should not be less than 5hours. This
time is increased by a 15 minute increment per week when estimated sleep efficiency [ratio
of time asleep to time spent in bed] is at least 85%.
c) Stimulus Control Therapy
This therapy aims to remove negative conditioning related to sleep and to strengthen sleep-
compatible associations with the bed and bed room environment. There are certain
precautions advised to patients as part of this therapy e.g.
1. Go to bed only when sleepy
2. Use bed for sleep only, do not watch TV, read, eat, and talk on telephone while in bed
3. Get up from bed when not able to sleep (does not watch the clock constantly, not use bright
lights), go to another room and involve in non arousal activities until sleepiness returns
4. Awakening at same time every morning, avoiding naps
d) Cognitive Behavioral Therapy
It identifies faulty beliefs and behaviors about sleep and replaces them with more adaptive
ones. It reduces sleep interfering beliefs and behaviors through stimulus control and
encourages behavior which helps in sleep through sleep hygiene education.
e) Relaxation
This therapy is based on the observation that insomnia patients tend to have high levels of
cognitive, physiologic, and/or emotional arousal. Progressive muscle relaxation, autogenic
training and bio-feedback are used to reduce somatic arousal and to achieve a calm & relaxed
mental state for sleep. Guided imagery, yoga and meditation are also useful to lower presleep
cognitive arousal and increase relaxation.
Relaxation technique should be opted on the patient’s choice which is easy to learn and can
be consistently practiced.
f) Paradoxical Intention
This therapy is used in patients who have intense preoccupation with sleep loss and its
consequences. The patient is asked to try, not to sleep rather than to sleep which reduces their
performance anxiety related to sleep.
g) Thought suppression
Thought stopping and articulatory suppression attempt to interrupt the flow of thought. No
attempt is made to deal with thought material as such but rather to alternate thinking.

PHARMACOLOGICAL INTERVENTIONS
The major classes are benzodiazepine receptors agonists (BzRA), antidepressant drugs (AD),
antihistamines, melatonin, and various herbal remedies including valerian root extracts.

Medications should be started with lowest effective dose, for shorter period, discontinued
gradually and polypharmacy should be avoided. Initially, non-benzodiazepine receptor
agonists should be prescribed which does not produce tolerance and withdrawal
symptoms(1,2,3).

- 53 -
[Link]. Drug Dosage Half life
1. Alprazolam .25-.5 mg PO at bedtime 12-15 hr
2. Clonazepam .5mg PO at bedtime 19-60 hr
3. Lorazepam 1-4 mg PO at bedtime 8-24 hr
4. Midazolam 7.5-15 mg PO at bedtime 2-7 hr
5. Nitrazepam 5-10 mg PO at bedtime 24-30 hr
6. Oxazepam 15-30 mg PO at bedtime 2.8-5.7 hr
7. Triazolam 0.125-0.25 mg PO at bedtime 1.5-5 hr
8. Zolpidem 5-10mgPO at bedtime 1.5-4.5hr
11. Eszopiclone 1-3 mg PO at bedtime 6-9 hr
Antidepressants
Evidence to support their efficacy of antidepressant drugs (ADs) for insomnia is relatively
sparse.
Antidepressants Dosage Half Life (hrs)
i)Trazodone 50-150 mg 7-15
ii)Mirtazapine 7.5-45mg 20-40
iii)Doxepin 50mg 10-50
Ramelteon (M1/M2 receptor agonist)
It is available as an 8 mg tablet, which should be taken approximately 30 minutes prior to
bedtime. The FDA approval contains no limitation on how long the medication may be
prescribed.
Anti-histamines
They are the most widely available over-the-counter preparations for insomnia. Adverse
effects of antihistamines include a range of cognitive and performance impairments. The
relative safety and efficacy of antihistamine with more sustained use has not been examined.
Combination- Non pharmacological and Pharmacological treatment
To achieve treatment goals for patients with insomnia, educational, behavioral and
pharmacologic interventions should be combined (1).

- 54 -
 Presenting symptoms: difficulty falling asleep, frequent
awakening, early morning awakening,
restless or unrefreshing sleep

Acute Insomnia Chronic Insomnia

(> 4 weeks)

Identify triggers Is there daytime impairment?

▪ Psychological (e.g. death, ▪ Difficulties at work, in social
divorce) and family life
▪ Environmental (e.g. noise) ▪ Difficulty in carrying out daily
▪ Lifestyle (e.g. shift work) tasks No
▪ Medical (see table 1)
▪ Medication (see table 1)
Implement sleep
Yes hygiene
Reassure & Monitor

Primary Sleep Disorders Secondary Sleep

▪ Circadian rhythm: Disorders
Address trigger night owl, shift work ▪ Medical Disorders
▪ Sleep Apnoea, snoring, ▪ Psychiatric Disorders
gasping ▪ Substances
▪ Restless legs, abnormal
/medication
movement or behaviour in
sleep

Implement
Sleep hygiene

Address underlying cause

Prefer Non-
pharmacologi
cal
If above fails, then consider interventions For psychiatric disorders,
a short course of hypnotic opt for nocturnal sedating
agent agents

- 55 -
 Causes of Insomnia
• Cardiovascular disease
o Cardiac failure
o Arrhythmias
• Gastrointestinal disease
o Gastro-oesophageal reflux
o Peptic ulcer disease
• Respiratory diseases
o Dyspnoea from any cause
o Asthma
o Chronic obstructive airway disease
• Endocrine disorders
o Menopause
o Hyperthyroidism
o Hypothyroidism
• Neurological diseases
o Parkinson’s
o Alzheimer’s
• Other medical conditions
o Obesity
• Pain from any source or cause
• Substances
o Alcohol
o Caffeine
o Nicotine
o Amphetamines
o Hallucinogens
o Cocaine
• Medications
o Corticosteroids
o Decongestants
o Stimulants e.g. Ritalin
o Beta blockers
o Theophylline
o Amphotericin B
o Ciprofloxacin
• Psychiatric conditions:
o Depression
o Psychosis
o Anxiety disorders
o Delirium
o Dementia

- 56 -
 References:

1. Curry, D. T., Eisenstein, R. D., & Walsh, J. K. Pharmacologic management of insomnia: past,
present, and future. The Psychiatric clinics of North America 2006, 29(4), 871–893.
2. Roehrs, T., & Roth, T. Insomnia pharmacotherapy. Neurotherapeutics: the journal of the
American Society for Experimental NeuroTherapeutics 2012, 9(4), 728–738.
3. Ramar, K., & Olson, E. J. Management of common sleep disorders. American family
physician 2013, 88(4), 231–238.
4. Lande, R. G., & Gragnani, C. Nonpharmacologic approaches to the management of insomnia.
The Journal of the American Osteopathic Association 2010, 110(12), 695–701.
5. Matthews, E. E., Arnedt, J. T., McCarthy, M. S., Cuddihy, L. J., & Aloia, M. S. Adherence to
cognitive behavioral therapy for insomnia: A systematic review. Sleep medicine reviews Apr
16 2013. pii: S1087-0792(13)00004-X. doi: 10.1016/[Link].2013.01.001. [Epub ahead of
print]

___________________________________________________________________________