Psycotropics, anti psycotics 1st and second generation,anti parkinsons, anti depressants mood stabilizers, sedative hypnotics side effects, management of side effects

1. Management of adverse effects
of psychotropics
Part I
Prepared by: Dr Prabidhi Adhikari
Moderator: Prof. Dr Mohan Belbase

2. Contents:
• Introduction
• Classification
• Adverse effects of anti depressants
• Adverse effect of antipsychotics
• References

3. Introduction
• A psychotropic drug is a chemical substance that changes the function of
the nervous system and results in alterations of perception, mood, cognition, and
behavior.
• Five main classes of psychotropic drugs are distinguished primarily by the effects
that result from their actions on neurotransmitters.
• Psychotropic drugs exert their actions by either mimicking the effects, blocking
the activity, or altering the storage, release, or uptake of neurotransmitters

4. Classification:
• Antidepressants
• Antipsychotics
• Mood stabilizing drugs
• Anxiolytics and hypnosedatives
• Antiepileptic drugs
• Anti parkinsonism drugs
• Miscellaneous

5. Adverse effects
AE is a harmful and undesired effect resulting from a medication or intervention
and procedures
Can be:
Acute or chronic
Mild, moderate and severe
Impact of adverse effects:
Discontinuation of medication
Diminished quality of life related to troublesome side effects
Increase risk of other comorbidities
Life threatening

6. Adverse effects of anti depressants
Antidepressants are drugs used to treat depression, anxiety and other disorders.
Broadly classified into:
1.SSRI
2.SNRI
3.TCA
4.MOAs
5.Atypical antidepressants
6. NAMDA modulators
6.Serotonin Modulators
Most prevalent side effects include sexual dysfunction, drowsiness, weight gain,
insomnia, anxiety, dizziness, headache, dry mouth, blurred vision, nausea, rash, and
tremor.

7. SSRI (Adverse effects)
SSRIs block reuptake of 5HT , increase serotonin level in synapses and enhance
neurotransmission

8. SNRI (Adverse effects)
Block serotonin and norepinephrine reuptake in the synapse, increasing postsynaptic
receptors' stimulation.

9. TCA (Adverse effects)
• Inhibits the reuptake of norepinephrine and serotonin
• Also has antagonizing affinity for muscarinic M1 receptors and histamine H1
receptors.
• TCA thus can cause sedation and anticholinergic side effects.

10. MAOS and RIMA
MAOIs inhibit the monoamine oxidase enzyme responsible for catabolizing serotonin,
norepinephrine, and dopamine.

11. Adverse effects of anti depressants….
Suicidality
• Associated with an increased risk of suicidal thoughts and acts
• More in adolescents and young adults and those having history of suicidal
behavior
• Explain about potential risk
• Monitor closely about suicidal behavior, self harm particularly during start of
treatment and dose change

12. Adverse effects of anti depressants….
Sexual dysfunction
Can occur with all antidepressants
Most common with SSRI and venlafaxine
men: delayed ejaculation, erectile dysfunction
men and women: decreased sexual desire, anorgasmia
History and examination:
Arizona Sexual Experience Scale
Changes in Sexual Functioning Questionnaire
Psychotropic Related Sexual Dysfunction Questionnaire

13. Adverse effects of anti depressants….
Management
• likely to be both dose-dependent and fully reversible
• Wait for spontaneous remission: may occur in a small number of people (5–10%)
but can take up to 4–6months
• Rule out: other causes , comorbidity and substance use
• Dose reduction (if in remission)
• Switching antidepressant
(Lower‐risk: agomelatine, bupropion, mirtazapine, vilazodone, vortioxetine and
moclobemide)

14. Adverse effects of anti depressants….
Management
• Drug holidays: intermittently missing one or two doses prior to planned sexual activity
may possibly help but risks discontinuation symptoms.
• Phosphodiesterase inhibitors: sildenafil (25 to 100 mg )and tadalafil (5 to 10 mg) for ED
• Bupropion: may be useful in women at higher doses (300mg/day)
• Mirtazapine: Evidence is mixed
• Transdermal testosterone: efficacy in women with SSRI/SNRI‐emergent loss of libido and
in men who continue to take serotonergic antidepressants with low or low‐normal
testosterone levels

15. Adverse effects of anti depressants….
Bleeding
• SSRIs will deplete platelet serotonin, leading to a reduced ability to form clots
• SSRIs increase the risk of GI, uterine, cerebral and peri‐operative bleeding
• SSRIs may also increase gastric acid secretion and therefore may be indirectly
irritant to the gastric mucosa
• Increase the risk of peptic ulcer
• The risk of is highest during the first 30 days

16. Adverse effects of anti depressants….
Management
• Try to avoid SSRIs in patients receiving NSAIDs, aspirin or oral anticoagulants or in
those with a history bleeding disorder
• If SSRI use cannot be avoided, monitor closely and prescribe gastroprotective
proton pump inhibitors.
• Use of less potent serotonin reuptake inhibitors

17. Sleep disturbances
Educating patients on behavior techniques and sleep hygiene, modification of use
of caffeine and common sympathomimetic agents
If fluoxetine is activating, take in the morning to help reduce insomnia
Trazodone or a hypnotic like benzodiazepines for insomnia
Mirtazapine for insomnia

18. Gastrointestinal side effects:
Nausea, diarrhea, constipation, dry mouth
Management:
Histamine 2 antagonists such as ranitidine, or proton pump inhibitors
Mirtazapine because of its 5-HT3 receptor antagonistic properties
Use of divided dosing or taking medications with a small amount of food
Use of loperamide, lactobacillus, diphenoxylate hydrochloride. Cyproheptadine,
psyllium for diarrhea

19. Constipation
• Prevention and early recognition are critical.
management strategies include:
• Adequate hydration
• Use of osmotic agents such as sorbitol, lactulose, or polyethylene glycol, and
• Stimulant laxatives such as senna or bisacodyl
• Bulk-forming, fiber-based laxatives are generally not recommended for slow-
transit constipation such as that caused by anticholinergic effects.

20. Arrythmia
• Tricyclic antidepressants (TCAs) have arrhythmogenic activity
• Result of potent blockade of cardiac sodium channels and variable activity at
potassium channels.
• TCAs are best avoided completely in patients at risk of serious arrhythmia
• ECG changes include PR, QRS and QT prolongation
• ECG monitoring : baseline, 1 week after each increase in dose and periodically
throughout treatment

21. • Non‐tricyclics generally have a very low risk
• Sertraline is recommended post MI, but other SSRIs and mirtazapine are also
likely to be safe
• Bupropion, citalopram, escitalopram, moclobemide, lofepramine and venlafaxine
should be used with caution or avoided in those at risk of serious arrhythmia
• Advice from cardiology should be sought

22. Hyponatremia
• Onset is usually within 30 days of starting treatment (median 11 days)
• Dose independent

23. Management
• Explain about symptoms: dizziness, nausea, lethargy, confusion, cramps, seizures
• Serum sodium should be determined (at baseline and 2 and 4 weeks, and then
3‐monthly) for those at high risk
• Determine High risk group
• older age , female gender
• major surgery, history of hyponatremia or a low baseline Na
• co‐therapy with other drugs associated with hyponatremia
• reduced renal function, glomerular filtration rate [GFR]

24. Mild hyponatremia
Fluid restriction
Increase sodium intake
if symptoms persist, the antidepressant should be discontinued.
If serum sodium is >125mmol/L, monitor sodium daily until normal
Severe hyponatremia
If serum sodium is < 125 mmol/L, specialist medical care required
Risk of seizures, coma and respiratory arrest
Rapid correction may be harmful

25. Restarting treatment
• Prescribe a drug from a different class.
• Consider noradrenergic drugs such as nortriptyline and lofepramine, mirtazapine
or an MAOI such as moclobemide.
• Begin with a low dose, increasing slowly, and monitor closely.
• If hyponatremia recurs and continued antidepressant use is essential, consider
water restriction and/or careful use of demeclocycline.
• Consider ECT

26. Orthostatic hypotension
• Risk factors assessment : include systemic diseases causing autonomic instability
(e.g., diabetes, alcohol dependence, Parkinson’s disease), dehydration, drug-drug
interactions, and age.
• Gradual titration, and dosing distributed throughout the day (in order to minimize
peak levels).
• Ample consumption of water and increased salt intake (supplementing 1-2
g/day), if not contraindicated, can reduce symptomatic hypotension.
• Abdominal binders and leg compression stockings can reduce venous pooling and
improve symptoms.

27. Elevated blood pressure
• Venlafaxine, desvenlafaxine and levomilnacipran may raise your blood pressure
• Avoid in hypertensive patients if possible
• Restriction of salt
• Use of anti hypertensive
• Use of beta blockers like propranolol

28. Others
• Bupropion for emotional flattening, cognitive slowing, or apathy
• Benzodiazepines for jitteriness and anxiety, especially at initiation of treatment
and especially for anxious patients
• For urinary hesitancy, give an alpha 1 blocker such as tamsulosin
• Lowered seizure threshold and rare seizures : Avoid in patient with history of
seizure disorder

29. Serotonin syndrome
• Life-threatening condition precipitated by the use of serotonergic drugs.
• Overactivation of both the peripheral and central postsynaptic 5HT-1A and,
most notably, 5HT-2A receptors
• May be a consequence of therapeutic medication use, accidental interactions
between medications or recreational drugs, or intentional overdose.
•
• Often precipitated by the addition of one or more of these medications in
patients who were previously stable on a serotonergic agent.
• It is important for providers to take a careful medication history when adding
new medications.

30. Drugs causing serotonin syndrome
• SSRIs
• Serotonin modulators, such as trazodone,
• Dopamine-norepinephrine reuptake inhibitors such as bupropion,
• Tri-cyclic antidepressants and Monoamine oxidase inhibitors
• St. John’s wort, a popular supplement
• linezolid, methylene blue
• Tryptophan
• Amphetamines, cocaine, MDMA (Ecstasy) and levodopa
• Meperidine, tramadol, pentazocine, metoclopramide, valproate, carbamazepine,
dextromethorphan, and cyclobenzaprine

32. Evaluation
• No laboratory test confirms the diagnosis
• Patients may have leukocytosis, elevated creatine phosphokinase, and decreased
serum bicarbonate concentration.
• Patients may develop labile blood pressure, heart rate and cardiac dysrhythmias
• Disseminated intravascular coagulation
• Rhabdomyolysis, renal failure, metabolic acidosis, myoglobinuria,
• Respiratory failure.

33. Diagnosis
• Serotonin syndrome is diagnosed clinically
• Requires a thorough review of medications and a careful physical exam.
• Symptoms tend to develop rapidly after exposure to the precipitating drug
• 30% within one hour, 60% within 6 hours, and nearly all patients with toxicity
developing symptoms within 24 hours of exposure.

34. Diagnosis
• The Hunter Serotonin Toxicity Criteria (HSTC) include the use of a serotonergic
agent plus 1 or more of the 5 following criteria:
• Spontaneous clonus
• Inducible clonus plus agitation or diaphoresis
• Ocular clonus plus agitation or diaphoresis
• Tremor and hyperreflexia
• Hypertonia
• Temperature above 38°C plus ocular or inducible clonus
• Clonus and hyperreflexia are most important for the diagnosis; however, severe
muscle rigidity may mask these symptoms

36. Dosing
• Cyproheptadine is a histamine-1 receptor antagonist with nonspecific 5-HT1A and
5-Ht2A antagonistic properties.
• Starting dose is 12 mg, followed by an additional 2 mg every two hours as long as
symptoms persist.
• As the patient improves, continued at a dose of 8 mg every 6 hours until
symptoms resolve.

37. Adverse effects of antipsychotics
• Side effects range from :
• minor tolerability issues [mild sedation , dry mouth]
• unpleasant [constipation, akathisia, sexual dysfunction]
• painful [acute dystonia ]
• disfiguring [weight gain , tardive dyskinesia]
• life threatening [myocarditis, agranulocytosis].
• 1st generation: EPS
• 2nd generation: Metabolic syndrome

40. EPS(Extra pyramidal symptoms)
• Acute dystonia
• Parkinsonism
• Akathisia
• Tardive dyskinesia

41. Acute dystonia
• Sudden sustained involuntary muscle
contraction
• Can be both painful and very
frightening
• Can occur any part of the body.
• The patient may be unable to
swallow or speak clearly.
• In extreme cases the back may arch,
or the jaw dislocate

43. Prevalence
• Conventional antipsychotics range between 5% and 30% (Sachdev, 1995)
• Recent studies suggest that they are not uncommon and affect 30-40% of
patients exposed to classical antipsychotic drugs.
• Haloperidol and the long-acting depot fluphenazines have the highest incidence.
• More common in young males, neuroleptic‐naïve
• Rare in the elderly
Time taken to develop
• Can occur within hours of starting antipsychotics (minutes if the IM or IV route is
used)

44. Treatment :
• Anticholinergic drugs: given orally, IM or IV depending on the severity of
symptoms
• Response to IV administration will be seen within 5 minutes
• Response to IM administration takes around 20 minutes
1st line
Anticholinergics:
• Benztropine 2mg im/iv q 15-30 min max 8mg
• Trihexyphenidyl 5 mg im q 15-30 min max 20 mg
Antihistamines:
Diphenhydramine 50 mg im/iv 15-30 min up to 200mg

45. 2nd line
Patients that fail to respond completely to anticholinergic therapy
IV or IM lorazepam at 0.05 to 0.10 mg/kg or
IV diazepam at 0.1 mg/kg
Maintenance
Benztropine 1-2 mg po 6 hourly upto 8mg/day
Trihexyphenidyl 2-5 mg po 6 hourly upto 20 mg/day
Diphenhydramine 25-50 mg po q 6 hourly 15-30 up to 200mg/day ; 1mg/kg in child
Amantadine 100mg po 6-8hrs 300mg/day
Other consideration
Reduction of dose
Slow down titration
Change antipsychotics

46. Akathisia
• A subjectively unpleasant state of inner restlessness where there is a strong
desire or compulsion to move
• E.g. foot stamping when seated
• Constantly crossing/uncrossing legs
• Rocking from foot to foot
• Constantly pacing up and down
• Akathisia can be mistaken for psychotic agitation and has been linked with
suicidal ideation and aggression towards others

47. Prevalence:
• approximately 25% with FGAs
• lower with SGAs In decreasing order: aripiprazole, risperidone, olanzapine,
quetiapine and clozapine
Time taken to develop:
• Acute akathisia occurs within hours to weeks of starting antipsychotics or
increasing the dose
• Akathisia that has persisted for several months or so is called ‘chronic akathisia’.
• Tardive akathisia tends to occur later in treatment and may be exacerbated or
provoked by antipsychotic dose reduction or withdrawal

48. Management
• Reduce the antipsychotic dose
• Change to an antipsychotic drug with lower propensity for akathisia
• propranolol 30–80 mg/day
• clonazepam (low dose)
• 5‐HT 2 antagonists such as cyproheptadine,
• mirtazapine, trazodone, mianserin 21 and cyproheptadine, diphenhydramine

50. Pseudo parkinsonism
Signs and symptoms:
• Tremor and/or rigidity
• Bradykinesia
decreased facial expression,
flat monotone voice,
 slow body movements,
inability to initiate movement
• Bradyphrenia (slowed thinking)
• Salivation

51. Prevalence:
Approximately 20%
more common in:
elderly females
those with pre‐existing neurological damage (head injury, stroke, etc.)
Time taken to develop:
Days to weeks after antipsychotic drugs are started, or the dose is increased

52. Treatment:
Reduce the antipsychotic dose
Change to an antipsychotic with lower propensity for pseudo parkinsonism
Prescribe an anticholinergic
Many patients do not require long‐term anticholinergic agents.
Use should be reviewed at least every 3 months.
Do not prescribe at night (symptoms usually absent during sleep)
Amantadine at 100‐400 mg daily(who need to avoid anticholinergics)

53. Tardive dyskinesia
Signs and symptoms
• A wide variety of movements can occur such as:
• lip smacking or chewing
• tongue protrusion (fly catching)
• choreiform hand movements (pill rolling or piano playing)
• pelvic thrusting Severe orofacial movements can lead to difficulty speaking,
eating or breathing.
• Movements are worse when under stress

54. Prevalence
• 5% of patients per year of antipsychotic exposure.
common in:
• elderly females
• those with affective illness
• those who have had acute EPS early in treatment
• may be associated with neurocognitive deficits
Time taken to develop:
• Months to years
• Approximately 50% of cases are reversible

55. Pathophysiology

56. Management:
• Stop anticholinergic if prescribed
• Reduce dose of antipsychotic medication
• Change to an antipsychotic with lower propensity for TD
• Use of Clozapine is best supported .
• Quetiapine , olanzapine,risperidone, aripiprazole may also be useful
• Both valbenazine and deutetrabenazine have a positive risk–benefit balance as
add‐on treatments
• There is also some evidence for tetrabenazine 25-200 mg/day and Ginkgo biloba
as add‐on treatments.

57. • Benzodiazepines: clonazepam 1-4 mg/day; diazepam 6-20 mg/day
• VITAMIN E 400-600 IU/Day
• Pyridoxine
• Amino acids
• Botulinum toxins
• Donepezil : 10 mg/day
• Levetiracetam : up to 3000mg/day
• Melatonin: 10 mg/day
• Sodium oxybate : 8 gm/day
• rTMS

58. Neuroleptic malignant syndrome(NMS)
• NMS is an acute disorder of thermoregulation and neuromotor control.
• Secondary to decrease dopaminergic activity in CNS
• Blockade of dopamine D2 receptor
• Decrease availability of dopamine
• Occurs 4-14 days after start of treatment
• Symptoms evolve over 24 to 48 hours and untreated symptoms last up to 10 to
14 days

59. Pathophysiology of NMS

60. Characterized by muscular rigidity, hyperthermia, altered consciousness, and
autonomic dysfunction, following exposure to antipsychotic medication
Elevated creatine kinase ,leukocytosis , altered LFT’s

61. Mortality:
20-30 %, higher if depot medication involved
Risk factors :
Concurrent medical and neuropsychiatric issues
Dehydration
Psychomotor agitation
Comorbid neurological disorder
Low serum iron
Preexisting catatonia
Mood disorder
History of NMS
High-potency FGAs seem to have the highest incidence, while SGAs and low potency
FGAs have lower incidences.

62. TREATMENT RESTARTING ANTISYCHOTICS
Psychiatric unit :
withdraw antipsychotics
monitor vitals
Hydration and temperature control
ICU admission may be required
I.M LORAZEPAM [BZD’S ]
Medical unit :
bromocriptine+ dantrolene sedation with
BZD’S
Artificial ventilation if required
L-dopa, apomorphine, carbamazepine
ECT
• Stop antipsychotics for 5 days [allow NMS
to resolve completely ]
• Begin very small dose and increase
slowly
• Close Monitoring of vitals
• Aripiprazole , quetiapine ,clozapine .
• Avoid depot/ LAI and high potency FGA’S.

64. ECG Changes—QT Prolongation
• Antipsychotics block cardiac potassium channels and are linked to prolongation of the
cardiac QT interval, a risk factor for the ventricular arrhythmia, torsade de pointes, which is
fatal.
• Other ECG Changes: Atrial fibrillation, giant P waves ,T waves , Heart block.
• Perform ECG at the time of admission and if prior abnormality or additional risk factors
present –yearly check up is done .

66. Metabolic syndrome
Major side effect of the atypical antipsychotics mostly with clozapine ,
olanzapine

67. Weight Gain – Histamine receptor
• Mechanisms : 5HT2C antagonism, H1 antagonism, D2 antagonism, and
increased serum leptin (leading to leptin de sensitization ).
• Weight gain is more in antipsychotic-naïve patients and during early stages of
treatment of psychotic illness , women are at greater risk than men.
HIGH MODERATE LOW
Clozapine
Olanzapine
Chlorpromazine
Iloperidone
Sertindole
Quetiapine
Risperidone
Paliperidone
Amisulpride , Asenapine
Brexpiprazole , Aripiprazole
Cariprazine , Haloperidol
Lumateperone
Lurasidone , Sulpiride
Trifluoperazine
Ziprasidone

69. Management
• Weight gain has consequences on self-image, morbidity and mortality.
• Increase risk of other diseases
• Prevention and RX are matters of clinical urgency.
• Body mass index (BMI) and waist circumference should be recorded.
• With continuing antipsychotic treatment, annual measurement of body weight is
recommended as a minimum.

70. Pharmacological management
• lifestyle interventions
• Switching [aripiprazole, ziprasidone lurasidone]and augmentation strategies
may minimise further weight gain .
• Aripiprazole is studied as an intervention for weight gain with clozapine and
olanzapine.
• Pharmacological methods[ Amantadine, liraglutide ,metformin, topiramate,
zonisamide] should be considered only if nonpharmacological RX is not useful.
• Metformin is a DOC
• Bariatric surgery have role in few .

71. Dyslipidemia
• Statins are used to treat dyslipidemias
• Are effective for increasing high-density lipoprotein and reducing total
cholesterol, low-density lipoprotein, and triglycerides.
Hypertension
• Use of antihypertensive medications
• In the context of metabolic syndrome, preference should be given to ACE
inhibitors, ARBs, and CCBs because thiazide diuretics have the potential to
increase blood glucose.

72. Hyperprolactinaemia
Drugs:
• Risperidone
• Paliperidone
• Amisulpride and sulpride
• FGA’S
Avoid in :
• patients under 25 years of age (i.e. before peak bone mass)
• patients with osteoporosis
• patients with a history of hormone‐dependent breast cancer
• young women.

73. Symptoms
• sexual dysfunction
• menstrual disturbances
• breast growth, Galactorrhea , Include delusions of pregnancy.
• Risk of osteoporosis ,breast cancer
Management approach
Baseline prolactin level should be obtained
At 3 months, ask for symptoms of hyperprolactinemia, look for serum prolactin
level

75. 1st choice
• Addition of Aripiprazole 5mg a day
Second choice
• DA agonists – cabergoline, bromocriptine, amantadine
• Metformin 2.5–3g a day
Others:
• strategies to reduce long‐term risk to bone mineral density (e.g. stopping
smoking, increasing weight‐bearing exercise, and ensuring adequate calcium and
vitamin D3 intake16,26).

76. Neutropenia/Agranulocytosis
• Mostly associated with clozapine
• About 3% of clozapine-treated patients will develop neutropenia; about 1% will
develop agranulocytosis.
• Increased susceptibility to infection
• Most important management strategy for neutropenia or agranulocytosis is early
detection, which will prevent opportunistic infections.
• Highest risk is during the first months of treatment

77. • Use of lithium to raise granulocyte counts
• Granulocyte colony-stimulating factor-Filgastram
• Dose reduction is not an effective approach to clozapine-associated neutropenia.
• Discontinuation of clozapine is the definitive solution to clozapine-induced neutropenia.
• This approach generally requires switching to another antipsychotic.
• For those patients who only responded to clozapine, clozapine re-challenge after
agranulocytosis has not been successful, but case reports describe successful re-
introduction of clozapine after neutropenia using either lithium or filgastram to increase
neutrophil count

78. Normal level : at least 1500 ul
First 6 months – weekly
Second 6 months every 2 weeks
After 1 yr – every month
If ANC <1500ul – confirm report
Repeat within 24 hours
Monitor 3 times/week until >= 1500ul
Once ANC >= 1500 ul – Normal range ANC monitoring for mild , 4
weekly monitoring initially then normal monitoring for moderate
neutropenia

79. • Mild 1000-1499 ul- continue treatment
• Moderate 500-999 ul – interrupt treatment for suspected clozapine
induced neutropenia, hematological consultation
• Severe < 5oo ul – interrupt treatment ,hematological consultation, do
not rechallenge unless benefit outweighs risks

80. Myocarditis
• Risk of clozapine treatment
• Almost always occurs within the first two months of treatment.
• Recognized quickly
• Slow titration may help
• An ECG and cardiac enzymes assessment
• Laboratory tests :elevated eosinophil count, C-reactive protein, sedimentation
rate, and troponins.

81. • Patients initiating clozapine should be monitored weekly for signs and symptoms
of myocarditis
• If a diagnosis is highly suspected or confirmed, then clozapine should be
discontinued promptly, and general or specialty cardiac follow-up care is needed.
• In many cases cardiac function returns to normal after clozapine is stopped.
• Recurrence rates are high
• If Needed re-initiate in hospital with close monitoring.

82. Sedation
• All antipsychotic medications can cause sedation,
• severity and frequency vary
• Shifting dosing to nighttime, and reducing total daily dose
• Transitioning to a less sedating antipsychotic
• Use of stimulants and modafinil

83. Sialorrhea
• common with clozapine (possibly more than 90% of patients)
• It is often uncomfortable, embarrassing and stigmatizing,
• can result in aspiration pneumonia.
• In some cases, painful swelling of the parotid can co-occur.
Management:
• Start with Lower dose and gradually titrate
• Topical therapy with anticholinergics, typically by administering an ophthalmic or
inhaler preparation sublingually, has been shown to improve symptoms.
• Atropine, Ipratropium, benztropine, trihexyphenidyl, glycopyrrolate, and
pirenzepine can be used

84. Management……….
• Adrenergic agents also appear useful - mechanism is not clear.
• Clonidine has shown encouraging results in individual cases.
• Another alpha-2 agonist, guanfacine, was effective in a single case.
• The alpha-1 antagonist terazosin showed significant promise in a small trial, but
has not subsequently been studied.
• sulpiride, amisulpride and monoamine oxidase inhibitor moclobemide have
shown promising results in several small trials
• botulinum toxin injection has been shown to substantially improve antipsychotic-
induced sialorrhea for 8-16 weeks.
• Amitriptyline has also been tried in a small case series with promising results.

85. References
• Sadock, B. J., & Sadock, V. A. (2022). Kaplan & Sadock's synopsis of
psychiatry: Behavioral sciences/clinical psychiatry (12th ed.)
• Taylor, D. M., Barnes, T. R. E., & Young, A. H. (2018). The Maudsley
prescribing guidelines in psychiatry (13th ed.)
• Stahl, S. M. (2013). Stahl's essential psychopharmacology:
Neuroscientific basis and practical applications (4th ed.)
• American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.)

86. Thank you