This document discusses drug-induced movement disorders caused by antipsychotic medications. It covers the classification of both acute and chronic movement disorders including dystonia, parkinsonism, akathisia, and tardive dyskinesia. It discusses the pathophysiology, risk factors, signs and symptoms, time of onset, scales used for assessment, management, and prevention of these medication-induced movement disorders. It also lists other medications that can cause movement disorders and the DSM-5 diagnostic categories for medication-induced movement disorders.

1. DR PRERNA KHAR
JR-II
DRUG INDUCED
MOVEMENT DISORDERS

2. TOPICS TO BE COVERED
• Introduction
• Classification
• Pathophysiology
• Types of Movement Disorders
• Management
• DSM diagnostic categories
• References

3. INTRODUCTION
• Medication-induced movement disorder
(Extra-Pyramidal Side Effects, EPSE)
occurs due to treatment with antipsychotic
medications.
• Though they are commonly caused by the
typical antipsychotics, but can also be caused
by the atypical.

4. IMPLICATIONS
• The movement disorders associated with
antipsychotics are disabling and distressing and
result in behavioral disturbances(violence and
aggression), non-adherence,and exacerbation of
psychosis.
• Some of the motor signs may be misinterpreted as
psychotic symptoms.
• The bradykinesia, limb stiffness, and mask-like facies
seen in Parkinsonism are a social and functional
handicap.
• The restlessness and agitation associated with
akathisia have similar effects.

5. CLASSIFICATION
ACUTE
• Acute Dystonia
• Parkinsonism
• Acute Akathesia
CHRONIC
• Tardive dystonia
• Chronic akathisia
• Tardive dyskinesia

6. PATHOPHYSIOLOGY
• Though the pathophysiology of MIMD has not been
clearly elucidated yet, but certain theories and
hypothesis suggest the interplay between:
– genetic predisposition,
– dopaminergic system hypersensitivity in the basal
ganglia,
– decreased functional reserve, and
– over activation of the cholinergic system.

7. RISK FACTORS

8. 1.DYSTONIA
OPISTHOTONUS
OCULOGYRIC CRISIS

9. • Signs And Symptoms
-Occulogyric Crisis
-Torticollis
-Inability to swallow or speak freely
(Glossopharyngeal spasm)
-Opisthotonus/jaw dislocation
• Mechanism: interference with presynaptic dopamine
receptors, or there may be a mismatch between excess
release of dopamine and coincident hypersensitivity of
dopamine receptors.
- Overactivation on unblocked D1 receptors.

10. • Prevelance: Approx 10%
More common in-:Young males
Neuroleptic Naïve
High potency drugs
Rare in elderly.
• Time Taken To Develop:
- Acute: Hours of starting AP (mins if IM)
- Tardive Dsytonia: Months to years.

11. • Treatment:
-Anticholinergic drugs ( Trihexyphenydyl)
- If Unable to swallow/ acute- IM (20 mins) or IV
(5mins)
- Switch to antipsychotic with lower propensity to cause
EPS.
- Tardive dystonia may respond to ECT.
- Botulinum toxin: If above fail.
- rTMS (Repetitive Transcranial Magnetic Stimulation)

12. 2.PSEUDOPARKINSONISM
• Signs & Symptoms:
-Tremor/Rigidity.
-Bradykinesia
- Bradyphrenia(slowed thinking)
- Salivation
The above can be mistaken for depression/ negative
symptoms of Schizophrenia

14. PSEUDOPARKINSONISM PARKINSON’S DISEASE
Apraxic Slowness Bradykinesia
Essential tremor, myoclonus Resting tremor
Paratonic rigidity Lead pipe rigidity
Frontal ataxia Postural instability
Slow, shuffling apraxic gait Slow, shuffling gait with
festination, retropulsion

15. • Rating Scales: Simpson Angus EPS Rating
Scale.
• Prevalence: Aprrox 20%
MC in: -Elderly Females
-Preexisting Neurological Damage
• Time Taken To Develop: days to weeks after
starting AP/ if dose is increased.

16. • Treatment:
- Decrease the dose of AP
- Prescribe anti-cholinergic. Review use every 3
months as most don’t require long term
- Change to AP with lower propensity to cause
EPS.

17. 3.AKATHESIA (Restlessness)
• Signs & Symptoms:
- Foot stomping when seated.
- Crossing/uncrossing legs.
- Pacing up and down.
• Rating Scale: Barnes Akathesia Rating Scale
-Hillside akathesia rating scale
-Prince Henry Hospital akathesia scale
• Prevalence: 25%
-Less with SGAs

18. • Pseudoakathesia:
• In a relatively small number of people, repetitive
restless movements characteristic of akathisia may
not be accompanied by any sense of inner restlessness
or compulsion to move.
• More common in male and older patients.
• May coexist with negative symptoms and tardive
dyskinesia

19. • Mechanism Of Akathesia:
- Due to dopamine receptor blockade in brain
areas other than the striatum.
-When akathisia occurs alone in the absence of
Parkinsonian symptoms, it may be due to
dopaminergic blockade in the mesocortical
tract rather than in the nigrostriatal pathway.

20. • Time Taken To Develop:
- Hours to weeks after starting.
- Increasing the dose.
- Tardive Akathesia-longer to develop, can last even
after withdrawing the AP
• Treatment
- Decrease the dose.
- Change to AP with lower propensity.
- Propranolol:30-80 mg/day
- Low dose clonazepam
- Anticholinergics are generally not helpful

21. Treatment Algorithm for Akathesia

22. 4.TARDIVE DYSKINESIA
• Signs & Symptoms:
-Grimacing
-Tongue protrusion (fly catching)
-Lip smacking/ chewing
- Pressing lip against the cheek (Bonbon sign)
-Choreiform hand movements(pill rolling/ paino playing)
-Rapid eye/leg movements.
-Severe movements-difficulty in speaking /eating
/breathing.
- Irregular breathing, belching, grunting sounds
whistling,sucking.

24. • Pathogenesis:
• -Dopamine Receptor Supersensitivity
Chronic DA blockade leads to super sensitivity of
postsynaptic DA receptors. (upregulation)
• GABA insufficiency Hypothesis
Decreased activity of striatal GABA neurons, and
reduced GABA turnover and increase GABA
receptors.
• Neurodegenerative Hypothesis
Caused due to generation of free radicals and
excititoxicity, particularly in the striatum
 Cholinergic Degeneration
Due to overactivation of cholinergic neurons in the
striatum when released from Dopaminergic inhibition
after antipsychotics are administered.

25. • Increased proliferation of D2 receptors in certain
parts of the striatum
• Neuroleptic accumulation in neuromelanin cells with
nigral damage
• Oxidative stress – free radical production with chronic
neuroleptic use
• Altered corticostriatal input, cortical damage
• Related to neurobiology of schizophrenia itself
• Endocrine factors (oestrogen in women)

28. • Rating Scales: AIMS (Abnormal Involuntary
Movement Scale)
• Prevalence: 5% of pts/ yr of AP exposure.
MC in : Elderly women
-Those with affective illness.
-EPS in early phase of T/T.
-Total Neuroleptic load, typical,
injectables, intermittent treatment
-Negative schizophrenia
-Diabetes mellitus, Smoking, Alcohol
• Anticholinergic medications worsen the TD or
make the latent TD manifest.

31. Can be a/w neurocognitive defecits.
• Time Taken To Develop: Months to years.
• TD is a/w greater mortality, severe psychopathology.
• Can occur after smaller doses of convential drugs/
drug naïve pts

32. Differential Diagnosis
• Wilson’s disease
• Huntington’s chorea
• Syndenham’s chorea
• Neuroacanthocytosis
• Hallervorden-Spatz disease
• SLE
• Encephalitis
• Toxins (Hg, CO)
• Early onset chorea
• Basal ganglia calcification
• Other drugs
• Hepatic encephalopathy
• Senile chorea
• Multiple sclerosis
• Acute intermittent porphyria
• Ataxia telangiectasia

33. • Treatment:
-Stop anticholinergic if prescribed.(controversial)
- Reduce dose of AP(can initially worsen TD)
- Change to AP with lower propensity.
- Clozapine-Resolution of symptoms/ Quetiapine.
- Tetrabenazine(licensed only in UK) (DA depletor) 25-
200mg/day
- Ginkgo Biloba
- Vitamin E (400-600 IU/ day)
- BZD (reduce the anxiety associated with it)

34. • Preventive Measures:
• -Frequently assess the need for continuation of antipsychotic,
especially if affective illness or dementia is diagnosed
• Continuous versus intermittent treatment
• Lowest effective dose
• Avoiding older high-potency agents
• Administration of AIMS at 6-monthly intervals if on typicals
and 12-monthly intervals on atypicals (3 and 6-monthly,
respectively, if at high risk.)
• Preferable use of atypicals, especially olanzapine or
risperidone at <6 mg/d (Glazer, 2000)

35. APA TASK FORCE RECOMMENDATIONS
(1997, 2004)
• Establish objective evidence that antipsychotics are
effective for an individual
• Using the lowest effective dose
• Cautious use in children, the elderly and in mood
disorders
• Regular examination of patients for TD
• Consider alternatives, obtain informed consent, and
consider dosage reduction if TD present
• If worsening, consider (a) stopping the drug, (b)
change to another drug, (c) clozapine

36. 5.WITHDRAWAL EMERGENT DYSKINESIA
• Withdrawal dyskinesias may take the form of
generalized chorea, athetosis, tongue protrusion,
chewing movements, facial grimacing, finger, toe,
ankle movements, ballistic movements, vocalizations,
and spasmodic torticollis.
• The movements worsen with increasing level of
arousal or anxiety.
• The most widely accepted theory is that of
dopaminergic hypersensitivity.
• Usually time-limiting-lasting 4-8 wks. (if persists-TD)
• Treatment: Re-assurance that withdrawal dyskinesia
usually disappears within a few weeks. If symptoms
are distressing then restart therapy and slow down
titration.

37. OTHER MEDICATIONS CAUSING
MOVEMENT DISORDERS
• Antiemetics like Domperidone, Metoclopramide.
• Antidepressant- amoxapine.
• Valproate and Lithium- hand tremors. (medication
induced postural tremor.)

38. DSM 5 Diagnostic Categories Of
Medication Induced Movement
Disorders
• Neuroleptic Induced Parkinsonism.
• Other Medication induced Parkinsonism.
• Medication induced acute Dystonia
• Medication induced Acute Akathesia.
• Tardive Dyskinesia.
• Tardive Dystonia
• Tardive Akathisia
• Medication induced Postural tremor.

39. REFERENCES
• Maudsley Prescriber’s guide 4th
edition.
• Antipsychotic-Induced Movement
Disorders: Evaluation and Treatment: Dr Maju
Matheww, Psychiatry 2005.
• Pseudoparkinsonism: A review of a common
nonparkinsonian hypokinetic movement disorder
:Kurlan et al. Advances in Parkinson’s Disease. Vol.2,
No.4, 108-112 (2013)
• DSM 5