CASC Knowledge Essentials14 · Physical signs and investigations

14 · Physical signs and investigations

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Written by Resident Doctor Committee · Published

14.1 Four antipsychotic movement disorders

Syndrome

Recognise it

Treatment principle

Acute dystonia

Painful sustained contraction, often soon after starting/increasing a dopamine blocker: torticollis, jaw spasm, tongue involvement, oculogyric crisis

Antimuscarinic treatment; airway involvement is an emergency

Drug-induced parkinsonism

Bradykinesia, rigidity, reduced facial expression, shuffling gait ± rest tremor; often days to weeks

Review dose/drug; sometimes a short course of an antimuscarinic

Akathisia

Inner restlessness, often with pacing, rocking or repeated leg movements, often after a medication change

Review dose/titration; propranolol may help selected patients

Tardive dyskinesia

Repetitive involuntary movements, especially lip-smacking, chewing and tongue movements; usually longer exposure

Specialist medication review; antimuscarinics can worsen it

Timing helps, but is not diagnostic. Metoclopramide and other dopamine-blocking antiemetics can cause the same problems. Procyclidine treats acute dystonia; severe cases may need parenteral treatment. Laryngeal dystonia can obstruct the airway.

Akathisia: the patient feels driven to move

The patient may describe being unable to sit still or feeling as though they must escape their own body. Visible movements can be subtle or absent. Mistaking this for worsening psychosis and increasing the antipsychotic can make it worse. Severe distress, including suicidal thoughts, needs direct assessment.

Restless legs has a different pattern: unpleasant leg sensations at rest, worse in the evening/night, relieved by movement. Propranolol is unsuitable in asthma, significant bradycardia or hypotension.

Describe the movement precisely

Term

Meaning

Rest tremor

Present with the limb supported and inactive

Postural tremor

Appears while holding a position

Intention tremor

Increases as the limb approaches a target

Rigidity

Resistance through passive movement, relatively independent of speed

Cogwheeling

Ratcheting resistance, often from tremor superimposed on rigidity

Spasticity

Velocity-dependent resistance; points to an upper motor neurone lesion

Lithium: fine postural tremor may be an ordinary side effect; coarse tremor with ataxia or confusion suggests toxicity. Drug-induced parkinsonism is often symmetrical, but can be asymmetric. Persistence after withdrawal may reveal underlying Parkinson's disease.

Antimuscarinics can worsen cognition, constipation, urinary retention and tardive dyskinesia. Match the scale to the problem: Barnes → akathisia; Simpson–Angus → parkinsonism; AIMS → abnormal involuntary movements.

14.2 Weakness and neurological localisation

Pattern

Findings

Upper motor neurone

Weakness, increased tone, brisk reflexes, extensor plantar response; an acute lesion can initially be flaccid

Lower motor neurone

Weakness, reduced tone/reflexes; later wasting and fasciculations

Polyneuropathy

Distal, often symmetrical sensory loss and reduced ankle reflexes; consider alcohol, diabetes and nutritional deficiency

Cerebellar

Incoordination, intention tremor, dysdiadochokinesia, dysarthria, broad-based unsteady gait

Functional weakness

Positive inconsistency between voluntary and automatic movement; may coexist with neurological disease

MRC power: 0 = no contraction; 1 = contraction without movement; 2 = movement with gravity removed; 3 = against gravity; 4 = against resistance but weak; 5 = normal. Pain, fatigue and understanding can affect the result.

Hoover's sign: apparently weak voluntary hip extension improves during resisted flexion of the opposite hip. This supports functional weakness in context; it does not show that the person is pretending. Sudden focal weakness still needs an urgent neurological differential.

Romberg is not a cerebellar test in isolation

Standing uses vision, proprioception and vestibular input. Marked deterioration on closing the eyes suggests that vision was compensating for impaired position sense or vestibular input. Cerebellar unsteadiness is usually evident with the eyes open too.

Dysmetria means overshooting/undershooting a target; dysdiadochokinesia means impaired rapid alternating movements. Cerebellar limb signs are usually ipsilateral. Alcohol-related cerebellar damage, neuropathy and Wernicke encephalopathy can coexist; do not wait for the full Wernicke triad before treating.

14.3 Cranial nerves and visual pathways

Finding

Localisation

Monocular visual loss

Retina or optic nerve, before the chiasm

Bitemporal hemianopia

Optic chiasm; think of a pituitary-region lesion

Homonymous hemianopia

Contralateral pathway behind the chiasm

Superior homonymous quadrantanopia

Often contralateral temporal optic radiations

Inferior homonymous quadrantanopia

Often contralateral parietal optic radiations

Relative afferent pupillary defect

Asymmetric optic-nerve or substantial retinal dysfunction

Before the chiasm: one eye. At the chiasm: both temporal fields. Behind it: the opposite visual field. Drawn for MRCPsychiatrist

Facial sensation: trigeminal, except the angle of the jaw, which is supplied by upper cervical nerves. A peripheral facial-nerve lesion weakens the ipsilateral forehead and lower face; a supranuclear lesion often relatively spares the forehead.

Hearing: Rinne normally gives air conduction greater than bone conduction. Bone greater than air suggests conductive loss. Weber goes towards conductive loss, away from sensorineural loss; profound unilateral deafness can complicate interpretation.

A normal-looking disc does not exclude optic neuritis

Optic neuritis can cause reduced acuity, poor colour vision and pain on eye movement despite normal fundoscopy. Acute visual loss needs ophthalmic assessment, even after emotional stress.

Papilloedema is optic-disc swelling due to raised intracranial pressure. Headache, vomiting and transient visual obscurations may accompany it. A normal fundus does not exclude neurological disease.

14.4 Cognitive domains and lobar syndromes

Attention comes first. Someone with delirium may fail a memory task because they never registered the information.

Domain

Deficit

Example task

Attention

Distractibility; difficulty holding/manipulating information

Months backwards, digit span

Episodic memory

Poor new learning and delayed recall

Learn and later recall information

Executive function

Poor planning, inhibition, switching or abstraction

Fluency, go/no-go, alternating sequences

Language

Naming, comprehension, fluency or repetition impaired

Name objects, follow commands

Visuospatial function

Poor spatial organisation or neglect

Clock drawing, figure copying

Praxis

Cannot perform a learned act despite adequate basic movement

Demonstrate a familiar action

Recognition

Cannot recognise familiar objects, faces or stimuli

Object/face recognition

The useful localisation patterns are:

  • Frontal: disinhibition, apathy, perseveration, poor planning.

  • Dominant parietal: Gerstmann syndrome: agraphia, acalculia, finger agnosia and left–right disorientation.

  • Non-dominant parietal: neglect and poor awareness of a deficit.

  • Medial temporal: impaired new learning.

These are network clues, not rigid one-lobe rules. A low MMSE, MoCA or ACE score can reflect delirium, depression, sensory or language difficulties, education, medicines or dementia. A normal score does not exclude disease. Loss of independent function helps separate dementia from MCI, allowing for previous ability and physical disability.

14.5 Thyroid and other physical findings

State

Clinical picture

Typical blood pattern

Overt primary hypothyroidism

Cold intolerance, constipation, weight gain, dry skin, fatigue, slowing, low mood; cognition may suffer

TSH ↑, free T4 ↓

Subclinical hypothyroidism

Often few symptoms

TSH ↑, free T4 normal

Thyrotoxicosis

Heat intolerance, weight loss, tremor, tachycardia, anxiety, irritability

TSH ↓, free T4 and/or T3 ↑

Goitre means enlargement, not overactivity. Lithium-associated hypothyroidism can often be treated while lithium continues. Low free T4 with an inappropriately normal/low TSH suggests a different problem, such as central hypothyroidism or non-thyroidal illness. Acute illness can distort results.

Keep the physical differential open: chest pain can be cardiac despite anxiety. Fever and breathlessness on clozapine may be pneumonia, aspiration or myocarditis. Sedation and impaired swallowing increase aspiration risk; constipation with distension/vomiting is urgent.

14.6 ECG essentials

Standard settings: speed 25 mm/s, voltage 10 mm/mV. One small square = 40 ms; one large square = 200 ms. For a regular rhythm, rate ≈ 300 ÷ large squares between R waves. For an irregular rhythm, count QRS complexes over ten seconds and multiply by six.

Interval

Meaning

Number to know

PR

Atrioventricular conduction

About 120–200 ms

QRS

Ventricular depolarisation

≥120 ms is broad

QT

QRS onset to T-wave end

Varies with heart rate; use QTc

Measure QRS onset to T-wave end. QTc then adjusts for heart rate. PeaBrainC, CC BY-SA 4.0. PeaBrainC, CC BY-SA 4.0, via Wikimedia Commons

Bazett: QT/√RR. Fridericia: QT/∛RR. Use seconds in both. Bazett can overestimate QTc during tachycardia, including clozapine-related tachycardia.

QTc: thresholds and what changes the risk

BHRS antipsychotic guidance uses 440 ms in men, 470 ms in women as action thresholds; 500 ms is a major concern requiring urgent review. Check the tracing, potassium, magnesium, calcium, other medicines, bradycardia and cardiac disease. Syncope/presyncope with significant prolongation needs urgent rhythm assessment.

Stopping/changing the culprit is often required, with specialist input. Clozapine is an exception to an automatic switch because abrupt substitution can cause severe relapse; obtain specialist assessment.

Pattern

Think of

Independent P waves and QRS complexes

AV dissociation: possible complete heart block, but interpret rates and their relationship

Irregularly irregular, no consistent P waves

Atrial fibrillation; assess rate and thromboembolic risk

Regional ST elevation in related leads

Possible acute coronary occlusion: assess as an emergency

Widespread ST elevation + PR depression

Pericarditis in the right clinical setting

Broad QRS after tricyclic overdose

Sodium-channel blockade and serious cardiotoxicity

Peaked T waves/progressive conduction disturbance

Hyperkalaemia; check urgently

A normal ECG does not exclude acute coronary syndrome or myocarditis. Lead positions: V1/V2 in the fourth intercostal spaces beside the sternum; V4 in the fifth at the midclavicular line; V3 between V2/V4; V5/V6 level with V4. Misplacement can mimic pathology.

14.7 Starvation, purging and substance-related signs

Starvation: bradycardia, hypotension, hypothermia, weakness, lanugo and oedema. Purging: dental erosion, parotid swelling, knuckle calluses and potassium depletion. Normal electrolytes do not prove stability. During refeeding, phosphate, potassium and magnesium can fall from normal baseline values. Weight trajectory, observations and function matter.

With alcohol, distinguish withdrawal (tremor, sweating, tachycardia), liver disease (jaundice, ascites, other stigmata), and neurological/nutritional damage. Asterixis is negative myoclonus seen in metabolic encephalopathy, not a specific sign of alcohol use. Confusion, ataxia or ocular signs with nutritional vulnerability suggest Wernicke encephalopathy.

Opioid withdrawal: dilated pupils, yawning, tears, rhinorrhoea, piloerection, aches, diarrhoea. Intoxication: sedation, respiratory depression, often small pupils. Fever, an infected injection site or a new murmur suggests infection, including endocarditis.

14.8 Know what an investigation can and cannot establish

Apparently reassuring result

What it does not exclude

Normal FBC/inflammatory markers

Every medical cause of psychiatric symptoms

Negative urine drug screen

Exposure outside the assay or detection window

Normal routine EEG

Epilepsy

Normal structural brain scan

Dementia or functional neurological disorder

Choose tests to answer a clinical question. Electrolytes, renal function, calcium, glucose, thyroid tests and targeted nutritional/infection tests answer different questions. New focal signs, rapid cognitive decline, delirium, suspected toxicity and an atypical first presentation should keep the physical differential active.