01Purpose and principlesWhat the assessment is for and the core concepts behind it.
Weakness assessment separates the patient's experience from measurable impairment. Ask whether performance varies with repetition, time of day, heat, exertion or rest; whether pain blocks movement; and whether symptoms affect one movement, one limb, one side or all four limbs. Medication and exposure review should include corticosteroids, statins, alcohol, recreational nitrous oxide, neurotoxic chemotherapy, sedatives and agents that can worsen neuromuscular transmission. Recent infection, vaccination, travel, tick exposure, systemic inflammation and family history may change the differential.
Examine muscle bulk, involuntary movement and fasciculation before tone and power. Test power with the joint stabilised, first against gravity and then resistance, comparing sides and matching the patient's capacity. Distribution often localises better than absolute grade: shoulder abduction and hip flexion are proximal; finger abduction and ankle dorsiflexion are distal; pyramidal patterns affect extensors more in the upper limb and flexors more in the lower limb. Neck flexion, eye closure, sustained upgaze, speech and cough may reveal risk missed by limb scores.
Sensory symptoms include positive phenomena—pins and needles, burning, electric shocks, allodynia—and negative phenomena—numbness or loss of position. Define surface territory, depth, symmetry and a proximal boundary. A hemisensory deficit may be cerebral, but a sharply split midline pattern has limitations as a localising sign. A spinal level, dissociated modality loss, length-dependent gradient, dermatome or single-nerve field can be decisive when reproducible and supported by reflexes and power.
Weakness and sensory loss may not share one cause. A patient with prior stroke can develop carpal tunnel syndrome; cervical myelopathy can coexist with peripheral neuropathy; immobility can produce compressive nerve injury. Retain more than one localisation when the signs demand it, and use repeat examination, focused imaging, laboratory tests and neurophysiology to test the anatomical model.
Key points
- Clarify what 'weak' means: loss of force, fatigability, heaviness, pain-limited effort, stiffness, incoordination, breathlessness, low endurance and impaired initiation describe different physiology.
- Establish onset, maximum severity and trajectory before detailed examination. Sudden focal weakness is vascular until assessed; progression over hours to days raises inflammatory, compressive, toxic, metabolic and neuromuscular emergencies.
- Map function through tasks—buttons, jars, overhead activity, rising, stairs, foot clearance and falls—then test the individual movements that reproduce the reported limitation.
- Upper motor neurone evidence comes from the whole pattern: distribution, drift, tone, reflexes, clonus and plantar response. Acute central lesions may have normal or reduced tone initially.
- Lower motor neurone localisation combines weakness with wasting, fasciculation, reduced tone and depressed reflexes, then uses myotomes, dermatomes and named-nerve territories to separate root, plexus and nerve.
- Fatigable ocular, bulbar or proximal weakness with preserved sensation suggests neuromuscular-junction dysfunction; symmetric proximal weakness with preserved sensation suggests myopathy, but overlap demands specialist testing.
- Test sensory modalities separately. Pinprick and temperature sample small-fibre/spinothalamic function; vibration and joint position sample large-fibre/dorsal-column function; light touch alone is an incomplete screen.
- Move from normal toward the symptom boundary with the patient's eyes closed, compare sides and repeat inconsistent responses. Avoid drawing a precise dermatome from one uncertain pinprick answer.
- Pain and guarding can create apparent weakness. Optimise position and analgesia, test around the painful joint and describe the limitation instead of converting it automatically into an MRC grade.
- Functional weakness or sensory disturbance is diagnosed through positive internal inconsistency interpreted by an experienced clinician, not through normal imaging or a belief that symptoms are voluntary.
- End with a syndrome statement including tempo, symmetry, proximal versus distal distribution, upper versus lower motor neurone signs, sensory modality and territory, cranial involvement and respiratory or autonomic risk.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Sudden unilateral face, arm or leg weakness with language, neglect, gaze or field disturbance is a cerebral vascular syndrome until proven otherwise. Pure motor stroke remains possible without cortical features and early CT can be normal.
Upper motor neurone signs below a level, impaired hand dexterity, gait stiffness, a truncal sensory boundary and bladder dysfunction support cord disease. Segmental wasting or reduced arm reflexes can coexist at the lesion level.
Rapid, usually symmetric ascending weakness with areflexia, sensory symptoms, facial or bulbar involvement and autonomic instability suggests Guillain–Barré syndrome. Reflexes can be preserved in variants, and respiratory decline may occur without dyspnoea.
Distal symmetric burning, numbness or loss of vibration beginning in the feet, with absent ankle reflexes and later distal weakness, is typical. Early hands-before-feet, asymmetry or marked motor loss is atypical and needs reconsideration.
Variable ptosis, diplopia, nasal speech, chewing fatigue, dysphagia, head drop or proximal weakness that worsens with sustained activity, without sensory loss, supports neuromuscular-junction disease and demands bulbar-respiratory assessment.
Symmetric proximal and neck weakness with preserved sensation may accompany rash, myalgia, dark urine, systemic inflammation, endocrine disease or medication exposure. CK can be normal in some myopathies and extremely raised in rhabdomyolysis.
A reproducible discrepancy between voluntary and automatic movement, such as validated hip-abductor or Hoover-type findings, may support functional weakness when the overall syndrome fits. It is a rule-in diagnosis communicated non-judgementally.
03Method and interpretationA systematic approach to the test and its findings.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Capillary glucose, ECG and urgent blood chemistryFirst step - Why
- Identify immediate metabolic mimics or causes and complications of profound weakness.
- Interpretation and limitations
- Check glucose promptly in every acute focal syndrome. Potassium, calcium, magnesium, renal function and acid-base status can change muscle and nerve excitability; ECG abnormalities may make electrolyte correction an emergency.
- 02
FBC, ESR or CRP, thyroid tests, B12, folate, HbA1c and CK - Why
- Screen selectively for common haematological, endocrine, nutritional, inflammatory, metabolic and muscle causes.
- Interpretation and limitations
- Choose tests from phenotype and exposure. A raised CK supports muscle injury but is not specific, while normal CK does not exclude endocrine, steroid-related, inclusion-body or some inflammatory muscle disorders.
- 03
CT or MRI of the brain - Why
- Evaluate acute central deficits, structural lesions, demyelination and selected inflammatory patterns.
- Interpretation and limitations
- Use emergency stroke imaging for sudden focal weakness. MRI protocol and timing depend on the question; a negative scan does not by itself diagnose functional symptoms or peripheral disease.
- 04
MRI of the relevant spinal region - Why
- Detect cord compression, inflammation, infarction, neoplasm and root or cauda equina pathology.
- Interpretation and limitations
- A coherent sensory level, upper motor neurone pattern or sphincter syndrome determines urgency and coverage. Discuss emergency imaging rather than relying on plain radiographs or delaying for outpatient tests.
- 05
Nerve conduction and electromyographic studies - Why
- Characterise peripheral distribution, axonal loss, demyelination, denervation, myopathy and transmission failure.
- Interpretation and limitations
- Early studies can be non-diagnostic, especially in acute neuropathy or recent radiculopathy. The referral should state timing, suspected level, anticoagulation and the specific question so appropriate nerves and muscles are sampled.
- 06
Respiratory function and swallow assessment - Why
- Identify ventilatory and aspiration risk in neuromuscular, bulbar and high-cervical disease.
- Interpretation and limitations
- Use serial locally specified vital-capacity and inspiratory measures with clinical signs; single-breath count is only an adjunct. Normal oxygen saturation may persist despite rising carbon dioxide and falling ventilatory reserve.
04Clinical next stepsHow the result changes management or prompts escalation.
01New unilateral weaknessTreat onset as time-criticalFirst stepAbrupt face or limb power loss, drift or loss of function, whether persistent, improving or discovered on waking.+
- 1Perform ABCDE, glucose and a concise stroke examination; establish last known well, functional impact, seizure activity, headache, trauma, anticoagulants and pre-event disability.
- 2Activate urgent stroke imaging and specialist assessment rather than waiting for routine blood results or symptom resolution; include posterior-circulation and dissection clues.
- 3Follow the stroke team's reperfusion and antithrombotic plan, document swallowing and serial deficit, and investigate mimics only without delaying treatment eligibility decisions.
02Rapid generalised progressionPrioritise airway and ventilationWeakness spreading over hours or days, especially with facial, neck, bulbar, cough or autonomic involvement.+
- 1Seek urgent neurology and critical-care review, assess speech, secretion handling, cough, respiratory pattern and autonomic observations, and measure serial respiratory function through the local protocol.
- 2ConfirmatoryCheck electrolytes, glucose, ECG, infection and drug or toxin exposure while arranging neurophysiology, antibody or CSF testing as specialist-led; do not wait for confirmatory tests if ventilation is threatened.
- 3Institute monitored swallow, thrombosis, pressure-area and mobility care and use disease-specific immunotherapy only under the responsible specialist pathway.
03Chronic sensory complaintPhenotype before broad testingPersistent distal, dermatomal, focal or multifocal numbness, paraesthesia or neuropathic pain without current emergency signs.+
- 1Map modality and territory, test strength and reflexes, examine feet and gait, and review diabetes, alcohol, nutritional risk, renal disease, medicines, cancer treatment, infection and family history.
- 2Use focused blood tests for the common and plausible causes; choose imaging for a central or root pattern and neurophysiology for atypical, progressive, asymmetric or motor-predominant peripheral disease.
- 3EscalationAddress foot protection, falls and pain while arranging follow-up; escalate new motor loss, rapid ascent, autonomic disturbance, sphincter symptoms or a reproducible sensory level.
05Risks, monitoring and follow-upComplications, safety checks and further assessment.
- Chart power by named movement rather than a global limb score, including the testing position and whether pain, fatigue or attention limited effort.
- Repeat reflexes, sensory boundary, plantar responses and gait when central or spinal disease is evolving, and record any newly concordant level or asymmetry.
- In rapidly progressive weakness, serially measure respiratory and bulbar function using the receiving service's protocol and escalate trend before oxygen saturation falls.
- For peripheral sensory loss, monitor skin integrity, footwear, falls, driving and functional decline as well as symptom intensity.
- Review potentially contributory medicines and exposures after laboratory or neurophysiological results; do not stop essential therapy without balancing indication and specialist advice.
- Safety-net inability to rise or walk, spreading weakness, dysphagia, breathlessness, new bladder dysfunction and stroke-like symptoms with a clear emergency route.
06Special situationsVariants, exceptions and circumstances that change the usual approach.
MRC grades are ordinal
The distance between grades is not equal, and grade 4 covers a wide range. Named movements, function and serial technique give more meaning than summing scores mechanically.
Fatigue has several meanings
General exhaustion after effort is not the same as reproducible decrement in a specific muscle. Clarify recovery with rest and seek ocular, bulbar or respiratory involvement before inferring junctional disease.
Small fibres can be missed
Burning pain and temperature loss may occur with preserved vibration, reflexes and routine nerve-conduction studies because standard studies principally assess larger myelinated fibres.
Areflexia is not universally peripheral
Acute spinal shock can transiently reduce reflexes, and severe neuropathy can mask briskness from a coexisting cord lesion. Interpret reflexes with plantar responses, tone and level.
Hoover signs need context
Complementary hip movement can demonstrate preserved automatic strength, but poor comprehension, pain or bilateral disease can invalidate the test. Use it as one positive sign, not a trick.
Oxygenation can mislead
Neuromuscular hypoventilation may retain carbon dioxide before hypoxaemia develops. Weak cough, bulbar change and declining respiratory measurements should prompt escalation despite a reassuring pulse oximeter.
07Common pitfallsFrequent interpretation and management errors.
- 01
Equating pain-limited movement with neurological paresis and assigning an unjustified power grade.
- 02
Using grip strength alone to declare the entire upper limb normal.
- 03
Testing only light touch and concluding that all sensory modalities are intact.
- 04
Forcing a variable sensory boundary into a dermatome without repetition or corroborating reflex and motor signs.
- 05
Waiting for hypoxaemia before escalating progressive bulbar or neuromuscular weakness.
- 06
Diagnosing functional neurological disorder because MRI and nerve studies are normal.
- 07
Assuming symmetric distal numbness is diabetic without reviewing tempo, severity, medicines and atypical motor or autonomic features.