Extrapyramidal Side Effects (EPSE) Examination – OSCE Guide

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Anton Malakhveitchouk November 27, 2023

This guide discusses how to approach performing a focused examination of a patient to identify extrapyramidal side effects (EPSE) from
antipsychotic medications in an OSCE setting.

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Background
The extrapyramidal system plays a critical role in fine-tuning motor control, influencing speech, facial expressions, posture, and spontaneous
motor activity.1

Extrapyramidal side effects are associated with antipsychotic medications and are a type of drug-induced movement disorder.

They are most commonly associated with typical antipsychotics (e.g. haloperidol, risperidone). These medications often cause EPSEs due
to their antagonistic effect on dopamine D2 receptors, disrupting the normal balance of neurotransmission in the basal ganglia, which is
integral to controlling movement and coordination.2

However, it is crucial to recognise that other pharmaceutical agents, including certain antidepressants, lithium, anticonvulsants, and
antiemetics, can also precipitate these effects.2,3

EPSEs may be divided into two broad categories: hypokinetic (may resemble Parkinson’s disease) and hyperkinetic (may resemble
Huntington’s disease).2

There are four common extrapyramidal side effects. These can be remembered through the ADAPT mnemonic:4

Acute Dystonia
Akathisia
Parkinsonism
Tardive dyskinesia

Parkinson’s disease vs Huntington’s disease

Parkinson’s disease and Huntington’s disease are two motor pathologies that both affect the basal ganglia.

Parkinson’s disease results from degenerations of neurons in the substantia nigra, resulting in a dopamine deficiency in the basal ganglia. It
is characterised by the mnemonic TRAP:5

Tremor (rest)
Rigidity (cogwheel)
Akinesia (or bradykinesia)
Postural instability

Huntington’s disease results from neuronal degeneration in the basal ganglia and cerebral cortex. It is characterised by choreiform
movements and cognitive decline.

Hypokinetic EPSEs

Acute dystonia

Acute dystonia is characterised by involuntary muscle contractions leading to abnormal postures or repetitive movements, affecting
various body parts. This can be incredibly painful and is thus important to treat immediately.

It typically presents within 1 – 5 days after drug exposure. It may affect any skeletal muscle, including the back and extremities (opisthotonos),
neck (torticollis), jaw (trismus), eyes (oculogyric crisis), abdominal wall, pelvic muscles (tortipelvic crisis), facial, and tongue muscles
(buccolingual crisis).2,4

Intramuscular administration of antimuscarinic (e.g. benztropine) or diphenhydramine may relieve dystonia in minutes.4

Parkinsonism

Parkinsonism is a clinical syndrome of resting tremor, cogwheel rigidity and general slowing of motor functions. Notable characteristics
include masked facies, a stooped posture, and a slow, shuffling gait.2,4 Patients often experience gait imbalance and difficulty rising from a
seated position.

Although the most common cause of parkinsonism is Parkinson’s disease, antipsychotics (drug-induced parkinsonism) and other conditions
can also cause parkinsonism due to interfering with the dopaminergic pathway.

Management of drug-induced parkinsonism involves discontinuation or dose reduction of the causative medication. Patients can be
switched to an atypical antipsychotic. In some cases, medications used for Parkinson’s disease can be used, including amantadine,
antimuscarinic agents (e.g. benztropine), dopamine agonists and levodopa.4

Hyperkinetic EPSEs

Akathisia

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Akathisia is characterised by a subjective feeling of internal restlessness and a compelling urge to move, leading to the objective
observation of repetitive movements comprising leg crossing, swinging, or shifting from one foot to another.2,4

It typically presents within four weeks of starting or increasing the dosage of the offending medication. Misdiagnosis is common due to its
non-specific symptoms that are often difficult to describe by patients and can often be confused with anxiety or agitation, leading to
inadvertent exacerbation of the condition when antidepressant or antipsychotic medications are increased.

Withdrawal akathisia can also occur with the discontinuation or dose reduction of antipsychotic medications and is typically self-limited,
often resolving within six weeks.2,4

Administration of antimuscarinic (e.g. benztropine) or diphenhydramine may relieve akathisia. If caused by a first-generation antipsychotic,
patients can be switched to an atypical antipsychotic. Additional therapeutic strategies specific to akathisia include beta-blocker (ex:
propranolol), amantadine, clonidine, benzodiazepines and mirtazapine.4

Differentiating akathisia from anxiety and agitation

Akathisia, anxiety and agitation all cause restlessness. However, it is important to differentiate these as they have different treatments.
Confusing akathisia for agitation could lead to the inappropriate administration of antipsychotics, which would further exacerbate the
symptoms.

Anxiety is a feeling of worry or unease. It may present with physical signs such as nervousness, restlessness, tension, tachycardia, sweating
and gastrointestinal discomfort. However, anxiety primarily affects thoughts and feelings rather than directing a particular movement. The
restlessness associated with anxiety is generally less intense than akathisia and is less driven by an urge to move.

Agitation is a state of increased arousal or restlessness, which can manifest as both psychological and physical symptoms. Individuals may
present with irritability, anger or aggression that may include verbal outbursts. It does not typically arise as a side effect of medications and is
common in conditions such as dementia, manic episodes of bipolar disorder, depression, and psychosis. It is also associated with substance
use.

In akathisia, the restlessness is largely driven by an internal sensation that is predominantly physical rather than emotional.

Tardive dyskinesia

Tardive dyskinesia is characterised by involuntary, choreoathetoid movements that primarily affect the orofacial and tongue muscles,
extending to the trunk and extremities.2,4

Symptoms are typically painless but may impede social interactions and impact daily functions such as chewing, swallowing, and speaking. It
is crucial to detect and treat early as there are cases where symptoms can become irreversible.

Tardive dyskinesia may improve temporarily with an increase in antipsychotic medication and temporarily worsen with a decrease. Tardive
dyskinesia is much less common with modern antipsychotics, and the incidence is less common today. It is also important to note that it may
be seen in other populations, such as patients with dementia.

Treatment options include reducing the dose or discontinuing the causative medication and possibly switching to an atypical antipsychotic.
Other interventions include dopamine-depleting medications such as tetrabenazine.4

Neuroleptic malignant syndrome (NMS)

NMS is a life-threatening reaction to medications with dopamine receptor-antagonist properties characterised by altered mental status,
fever, muscle rigidity and autonomic dysfunction.6

Patients typically develop NMS within hours or days after exposure to causative drugs, with most cases falling between 2 weeks and 30 days.
The clinical course typically begins with muscle rigidity followed by fever within several hours of onset and mental status changes that can
range from mild drowsiness, agitation or confusion to delirium or coma.

NMS is accompanied by autonomic instability, including labile blood pressure, tachypnoea, tachycardia, excessive salivation (sialorrhea),
sweating (diaphoresis), flushing, skin pallor and incontinence.6

Immediate management is critical. The causative medication should be discontinued. General management includes aggressive hydration,
cooling blankets to manage hyperthermia, and correcting metabolic abnormalities.

Bromocriptine (dopamine agonist) and dantrolene (muscle relaxant) can be used in severe cases.6

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Introduction
Wash your hands and don PPE if appropriate.

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Introduce yourself to the patient, including your name and role.

Confirm the patient’s name and date of birth.

Briefly explain what the examination will involve using patient-friendly language.

Gain consent to proceed with the examination.

Ask the patient if they have any pain before proceeding with clinical examination.

Painful muscle spasms may occur in acute dystonia

General inspection
Most EPSEs can be observed through observation alone.

Perform a brief general inspection of the patient, looking for signs of EPSEs:

Pain: acute dystonia can be incredibly painful

Difficulty breathing, swallowing, or speaking could indicate signs of acute dystonia.
Posture: abnormal posture, such as abnormal muscular contractions, twisted neck (torticollis), back (opisthotonus) or jaw (trismus) that
may be seen in acute dystonia
Facial expression: look for blunted affect or grimacing. Blunted affect may present as reduced emotional expression, while grimacing
could manifest as involuntary contractions of facial muscles
Blink rate: observe the patient’s blink rate, noting that less than ten blinks per minute could indicate a hypokinetic state, while more than
30 could suggest a hyperkinetic condition. Vigorous blinking could be a sign of a Tic.
Motor restlessness (akathisia): akathisia presents as a subjective urge to move, coupled with observable excessive movement.
Patients may engage in excessive pacing or vocalise the need to move.
Abnormal involuntary movements: these can be seen in tardive dyskinesia. Look for chorea (sudden, quick involuntary movements in
any skeletal muscle), athetosis (slow, writhing movements), and tics (sudden, quick, patterned movements). While chorea could affect
any skeletal muscle, athetosis is noticeable mainly in the shoulders, fingers, and lower face. Common tics include throat clearing,
vigorous blinking, sniffing, and shaking head.

Differentiating a blunted affect from mask-like facies

Mask-like facies and affective blunting both cause changes in facial expressions that may be picked up in a physical examination.

Affective blunting is a reduction in the expression and experience of emotions. This may also be associated with reduced vocal inflection
(prosody), decreased expressive gestures, and may appear emotionally indifferent. Their reactions to both positive and negative events may
be severely limited or absent. Affective blunting is generally more common in psychiatric disorders such as schizophrenia and depression.

Mask-like facies (hypomimia) is a reduction in facial expressivity and is a motor symptom. Mask-like facies is more common in patients with
parkinsonism and is generally associated with other signs such as rigidity and bradykinesia. Unlike affective blunting, a patient with mask-like
facies may experience emotions and display appropriate emotional responses in conversation.

Tremor
Observe for a resting tremor associated with parkinsonism, characterised by involuntary movements in a limb at rest, typically slowing down
at around 4 – 6 cycles per second. A prominent tremor in the second digit that causes it to rub against the palmar surface of the thumb may
be observed (“pill-rolling tremor”).

A resting tremor can be confused with a postural tremor and intention tremor:

Postural tremors appear promptly with unsupported postures (such as in extended hands) and are more rapid than resting tremors. It is
the most common tremor seen in psychiatry and can be attributed to a range of causes, such as essential tremor, anxiety, caffeine,
theophylline, lithium, valproate, beta-adrenergic agonists, and/or withdrawal from alcohol, benzodiazepines, or barbiturates.
Intention tremor is a broad, coarse, low-frequency tremor seen when a body part approaches a target. It consists of rhythmic shifting
from one side to the other of the target (dysmetria).

Gait

Sitting to standing

Ask the patient to stand from their seated position with their arms across their chest to screen for postural instability. Make sure
to stand close to the patient so that you can intervene if they lose their balance.

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Imbalance and difficulty rising from a seated position may also be present in parkinsonism.

Observe gait

Ask the patient to walk to the end of the examination room and then turn and walk back whilst you observe their gait:

Parkinsonism gait will have short steps, diminished arm swinging, and rushed (festinating). When turning, several steps are required.
Patients may appear unable to rotate at the waist (en bloc turning”). The patient may get stuck (freeze).

Tone
Assess tone in the muscle groups of the neck, upper limbs, and lower limbs, comparing each side. Looking for rigidity (parkinsonism) and
dystonia. Before beginning, it is important to explain to the patient what you will be doing and why.

Rigidity is a velocity-independent increase in muscle tone associated with parkinsonism. During the assessment, it is crucial to move the
limbs both quickly and slowly to observe any differences in resistance.

Cogwheel rigidity: characterised by a ratcheting sensation, often due to an underlying tremor superimposed on hypertonia
Lead pipe rigidity: a uniform increase in muscle tone throughout the movement, often associated with neuroleptic malignant syndrome

Dystonia may manifest as sustained muscle contractions or intermittent spasms. Pay attention to any unintended contractions or abnormal
postures. Dystonia more often affects the axial muscles, causing torticollis or rotation of the lower spine.

Assessment

Neck

1. Support the patient’s head gently.

2. Ask the patient to relax and allow you to control the movement.

3. Passively rotate the head towards the shoulder, observing for rigidity or dystonia.

Upper limb

1. Support the patient’s arm.

2. Guide through circumduction of the shoulder, flexion/extension of the elbow, and wrist circumduction.

3. Compare the tone on both sides, noting any asymmetry or unilateral abnormalities.

Lower limb

1. Roll each leg on the examination bed, observing for any resistance or abnormal postures.

2. Lift each knee briskly off the bed while ensuring the heel remains in contact with the bed. A rise in the knee with the heel lifting off could
indicate increased tone.

3. Compare the tone on both sides, noting any asymmetry or unilateral abnormalities.

To complete the examination

Explain to the patient that the examination is now finished.

Thank the patient for their time.

Dispose of PPE appropriately and wash your hands.

Summarise your findings.

Example summary
“Today I performed a physical examination on a 29-year-old man who is taking antipsychotic medication for schizophrenia to assess
clinical features of EPSE. On general inspection, the patient demonstrated a blunted affect and marked restlessness, getting up and pacing
before and after the examination. A tremor was noted in his right hand that was present at rest and resolved with movement. Observation of
gait was notable for bradykinesia, reduced arm swinging and hesitation when turning. Assessment of Tone revealed rigidity in the neck.
The vitals were stable. These findings are consistent with the clinical features of EPSE.

For completeness, I would like to perform the following further assessments and investigations.”

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Further assessments and investigations
Consider completing a movement disorder assessment scale. Several scales can be used to evaluate different types of movement
disorders:2,8

For assessing hypokinetic or parkinsonian signs, commonly used scales include the Unified Parkinson’s Disease Rating Scale motor
exam section and the Simpson-Angus scale
The Unified Huntington’s Disease Rating Scale and Abnormal Involuntary Movement Scale (AIMS) evaluate hyperkinetic or tardive-like
signs
The Barnes Akathisia Rating Scale (BARS) may be used to assess the presence and severity of akathisia
The Extrapyramidal Symptoms Rating Scale addresses both hyperkinetic and hypokinetic signs, providing a comprehensive
assessment tool for various movement disorders

Perform a neurological and cerebellar examination if concerned about neurological pathology.

Assess the drug chart for neuroleptics, dopamine-blocking antiemetics and sodium valproate.

Reviewer

Dr Aisling Campbell

Consultant Psychiatrist

University College Cork

References
1. Lee, J., & Muzio, M. R. (2022). Neuroanatomy, Extrapyramidal System. In StatPearls. StatPearls Publishing. Available from: [LINK]
2. Sanders, R. D., & Gillig, P. M. (2012). Extrapyramidal examinations in psychiatry. Innovations in clinical neuroscience, 9(7-8), 10–16.
Available from
3. Blair, D. T., & Dauner, A. (1992). Extrapyramidal symptoms are serious side-effects of antipsychotic and other drugs. The Nurse
practitioner, 17(11), 56–67.
4. D’Souza, R. S., & Hooten, W. M. (2023). Extrapyramidal Symptoms. In StatPearls. StatPearls Publishing. Available from: [LINK]
5. Jankovic J. (2008). Parkinson’s disease: clinical features and diagnosis. Journal of neurology, neurosurgery, and psychiatry, 79(4), 368–
376.
6. Berman B. D. (2011). Neuroleptic malignant syndrome: a review for neurohospitalists. The Neurohospitalist, 1(1), 41–47.
7. Oregon Health & Science University. Abnormal Involuntary Movement Scale (AIMS). Available from: [LINK]
8. Barnes T. R. (2003). The Barnes Akathisia Rating Scale–revisited. Journal of psychopharmacology (Oxford, England), 17(4), 365–370.

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