Ad, TD, Akathisia 120454

ACUTE DYSTONIA
TARDIVE DYSKINESIA
AKATHISIA
DR. SAGAR JHA
INTERN, NMCTH
ACUTE DYSTONIA
 Acute medication-induced dystonia
 Dystonic reactions, in general, are movement disorders characterized by
involuntary contractions of muscles.
 Different muscle groups can be affected and the reaction may be further
categorized based on the specific muscles involved.
 For example:
• Oculogyric crisis involves the ocular muscles
• Laryngeal dystonia involves the larynx
PREVALENCE
 Approximately 10%, but more common: in young males, in the neuroleptic‐
naive, with high‐potency drugs (e.g. haloperidol).
 Dystonic reactions are rare in the elderly.
 Time taken to develop: Hours of starting antipsychotics (minutes if the IM or IV
route is used).
ACUTE DYSTONIA
ETIOLOGY
 Most commonly, it occurs in response to antidopaminergic agents and dopamine

receptor antagonists, such as antiemetics (i.e. metoclopramide)
and antipsychotics (i.e. haloperidol and chlorpromazine).
 These medications can block dopamine’s function at the D2 receptor, thereby
causing involuntary muscle contraction of muscle groups, commonly in the face
and neck.
 Sometimes, serotonergic agents can also induce the reaction.
ACUTE DYSTONIA
CLINICAL FEATURES
 Muscle spasm in any part of the body along with

accompanying pain.
 Eyes rolling upwards (oculogyric crisis).
 Head and neck twisted to the side (torticollis).
 The patient may be unable to swallow or speak clearly.
 In extreme cases, the back may arch or the jaw dislocate.
ACUTE DYSTONIA
TREATMENT
 Stop any medication that is responsible for the reaction.
 An acute dystonic reaction is usually treated with anticholinergic
agents (e.g. benztropine) or benzodiazepines (e.g. diazepam).
 Most often these medications are administered intravenously since individuals
may have difficulty swallowing.
 Response to IV administration will be seen within 5 minutes while response to
IM administration takes around 20 minutes.
 Botulinum toxin may be effective.
 rTMS may be helpful.
TARDIVE DYSKINESIA
 Tardive dyskinesia is a syndrome characterized by abnormal involuntary
movements, typically involving the orofacial region, limbs, and trunk.
PREVALENCE
 5% of patients per year of antipsychotic exposure.

 More common in:
• elderly females
• those with affective illness
• those who have had acute EPS early in treatment
 Time taken to develop: Months to years
TARDIVE DYSKINESIA
ETIOLOGY
 It is likely that the disorder is related to an increased sensitivity of dopamine

receptors in the basal ganglia.
 This is supported by the observation that drugs that block dopamine, such as
antipsychotic medications, suppress TD, whereas dopamine agonists worsen the
disorder.
 Drugs causing:
• Older Antipsychotics(Chlorpromazine, Fluphenazine, Haloperidol,
Prochlorperazine, Thioridazine)
• Anti-emetics (Metoclopramid)
• Anti-depressants(amitriptyline, fluoxetine, phenelzine, sertraline, trazodone)
• Anti-Parkinson medicines (levodopa)
• Antiseizure medicines (phenobarbital and phenytoin)
TARDIVE DYSKINESIA
CLINICAL FEATURES
 The dyskinetic movements occur at rest and can usually be temporarily suppressed
volitionally or by purposeful action, distraction, or sleep.
 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(truncal dyskinesia)
• respiratory dyskinesia is characterized by grunting and irregular breathing patterns.
 Severe oral dyskinesia may result in dental and denture problems that can progress to
ulceration and infection of the mouth as well as muffled or unintelligible speech.
 Severe orofacial tardive dyskinesia can impair eating and swallowing, which in turn can
produce significant health problems.
 Gait disturbances due to limb dyskinesia may leave patients vulnerable to falls and injuries.
TARDIVE DYSKINESIA
TREATMENT
 Stop anticholinergic if prescribed.
 Reduce dose of antipsychotic medication.
 Change to an antipsychotic with lower propensity for TD.
 Clozapine is the antipsychotic most likely to be associated with resolution
of symptoms.
 Quetiapine may also be useful in this regard
 Both valbenazine and deutetrabenazine have a positive risk–benefit
balance as add‐on treatments.
 There is also some evidence for tetrabenazine and Ginkgo biloba as add‐
on treatments.
 TD may respond to ECT
AKATHISIA
 Akathisia comes from the Greek word “akathizein”, which means inability to sit still.
 Akathisia is a syndrome of motor restlessness seen predominantly in the context of
antipsychotic and some antidepressant medication use.
 The core feature of akathisia is mental unease and dysphoria characterised by a sense
of restlessness.
PREVALENCE
 Wide variation but approximately 25% for acute akathisia 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’.
AKATHISIA
ETIOLOGY
 The exact etiology is unknown.
 Believed to be due to the blockage of dopamine type 2 receptors in the
brain leading to imbalance between cholinergic/dopaminergic systems
in the brain.
 Drugs causing:
• First and second generation antipsychotics
• Antidepressants(at high doses)
• Metoclopramide(anti emetic)
• Reserpine, methyldopa(Anti hypertensives)
• Diltiazem(calcium channel blockers)
AKATHISIA
CLINICAL FEATURES
 It has subjective, as well as motor, components.
 Subjectively, patients experience muscle tension, difficulty finding a comfortable
body position, and inability to stop moving; they feel as though they are “jumping
out of their skin.”
 Objectively, akathisia classically manifests by
• rocking from foot to foot while standing
• frequently crossing and uncrossing the legs when seated
• constantly pacing up and down
• foot stamping when seated
 Sleep may be disturbed because of physical discomfort.
AKATHISIA
TREATMENT
 Reduce the antipsychotic dose.
 Change to an antipsychotic drug with lower propensity for akathisia .
 A reduction in symptoms may be seen with: propranolol 30–80 mg/day
(evidence poor); clonazepam (low dose).
 5‐HT 2 antagonists such as cyproheptadine, mirtazapine, trazodone,
mianserin and cyproheptadine may help, as may diphenhydramine.
 Anticholinergics are generally unhelpful.
REFERENCES
 The Maudsley, Prescribing Guidelines in Psychiatry, 13th edition

 Kaplan & Sadock’s Comprehensive Textbook of Psychiatry, 10th edition
U! !
K YO
H A N
T

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ACUTE DYSTONIA

 Most commonly, it occurs in response to antidopaminergic agents and dopamine

 Muscle spasm in any part of the body along with

 5% of patients per year of antipsychotic exposure.

 It is likely that the disorder is related to an increased sensitivity of dopamine

 The Maudsley, Prescribing Guidelines in Psychiatry, 13th edition

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