01Purpose and principlesWhat the assessment is for and the core concepts behind it.
Neurological diagnosis begins with a map rather than a disease list. First identify the main functional systems affected—motor, sensory, visual, language, coordination, cognition, autonomic or consciousness—and determine whether the pattern is focal, multifocal, diffuse or length-dependent. Next place the abnormality along the neuroaxis. Only then combine localisation with tempo, age, exposures and systemic context to generate causes. This sequence reduces anchoring on a familiar diagnosis and makes investigation purposeful.
Motor localisation uses power distribution, tone, reflexes, plantar responses, muscle bulk and fasciculation together. An upper motor neurone lesion commonly produces pyramidal-pattern weakness, increased tone, brisk reflexes and an extensor plantar response, but acute cerebral or spinal lesions can initially be flaccid. Lower motor neurone dysfunction produces weakness, wasting, fasciculation and reduced reflexes in a segmental, root or nerve pattern. A normal examination between episodes does not exclude fatigability, seizure, transient ischaemia or functional neurological disorder.
Sensory localisation depends on modality as well as territory. Spinothalamic pathways convey pain and temperature, whereas dorsal columns carry vibration and joint position. A dissociated deficit, sensory level, crossed face-body pattern, dermatomal band or stocking distribution is more useful than the statement 'reduced sensation'. Cortical sensory tests such as extinction and graphesthesia are interpretable only when primary sensation, attention and comprehension are adequate.
Localisation guides urgency but does not confer certainty. Stroke may present without classic lateralising signs; metabolic disease can mimic a focal syndrome; a structural lesion can coexist with delirium; and functional signs can coexist with organic pathology. Reassess after resuscitation, glucose correction, analgesia or seizure recovery, document change and use specialist advice when the pattern remains internally inconsistent or clinically dangerous.
Key points
- Localise before naming a disease: decide whether the dominant lesion lies in cerebral cortex, subcortical white matter, brainstem, cerebellum, spinal cord, anterior horn cell, root, plexus, peripheral nerve, neuromuscular junction or muscle.
- Time course narrows mechanism. Maximal-at-onset deficit favours vascular or seizure-related disease; minutes to hours can be vascular, toxic or migrainous; days suggests inflammatory, infectious or metabolic disease; months to years suggests degenerative, compressive or hereditary disease.
- A unilateral upper motor neurone pattern below a facial lesion may arise in the contralateral hemisphere or ipsilateral cord; facial involvement, cortical signs and the exact pattern of sensory change separate these levels.
- Cortical clues include aphasia, neglect, apraxia, visual-field loss, seizures and cortical sensory dysfunction. Pure motor or pure sensory syndromes without cortical features can reflect compact subcortical pathways.
- Crossed findings—ipsilateral cranial-nerve dysfunction with contralateral limb weakness or sensory loss—strongly suggest a brainstem lesion, although the complete syndrome may be incomplete early.
- A spinal-cord syndrome produces long-tract signs below a level, sometimes with segmental lower motor neurone findings at the level; bladder, bowel, sexual dysfunction and a truncal sensory level are high-value clues.
- Root disease follows a myotome and dermatome with a reduced corresponding reflex; mononeuropathy follows a named nerve; polyneuropathy is usually length-dependent and symmetric, but important inflammatory neuropathies need not be.
- Neuromuscular-junction disease causes fatigable weakness with preserved sensation; myopathy favours proximal weakness with preserved sensation and usually preserved reflexes until weakness is advanced.
- Positive symptoms such as tingling, flashing lights or jerking often reflect irritative activity; negative symptoms such as loss of vision, power or sensation reflect impaired function, but this distinction never replaces urgent assessment of onset and evolution.
- Multiple lesions are possible. Diabetes, cancer, vascular disease and systemic inflammation can generate coexisting central and peripheral abnormalities, so do not force every sign into one anatomical site.
- A localisation statement should contain side, level and tract or structure—for example, 'left hemispheric cortical syndrome affecting language and right face-arm motor pathways'—and should explicitly list discordant findings.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Contralateral face and limb deficit accompanied by aphasia, neglect, gaze deviation, homonymous field loss, apraxia, seizure or cortical sensory impairment points above the brainstem. Dominant-hemisphere language dysfunction and non-dominant visuospatial neglect are especially localising.
Diplopia, dysarthria, dysphagia, vertigo or abnormal eye movements with long-tract limb signs, particularly crossed cranial-nerve and body findings, suggests brainstem disease. Sudden onset may represent posterior-circulation stroke even when FAST is negative.
Bilateral weakness, a definable truncal sensory level, upper motor neurone signs below the lesion and sphincter or autonomic disturbance support cord involvement. Neck or back pain, malignancy, infection, trauma and anticoagulation change the emergency differential.
Radicular pain plus myotomal weakness, dermatomal sensory loss and a depressed reflex suggests a root. Plexopathy crosses several roots and nerves, while a named-nerve lesion respects that nerve's motor and cutaneous territory and often has a focal compression history.
Symmetric distal sensory loss, reduced ankle reflexes and later distal weakness suggests a dying-back peripheral neuropathy. Marked asymmetry, proximal weakness, rapid progression, motor predominance or autonomic failure should prompt a different and often urgent pathway.
Fluctuating ocular, bulbar, neck or proximal limb weakness that worsens with use, with preserved sensation and generally normal reflexes, suggests impaired neuromuscular transmission. Dysphagia, weak cough or breathlessness may signal impending ventilatory failure.
Symmetric proximal weakness affecting rising, stairs, lifting the arms or neck flexion with intact sensation points toward muscle. Rash, myalgia, dark urine, endocrine features, medication exposure or very rapid evolution refine cause and urgency.
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
Bedside glucose, observations and repeat neurological examinationFirst step - Why
- Identify reversible mimics, physiological instability and evolution while preserving a timed baseline.
- Interpretation and limitations
- Hypoglycaemia can produce focal or diffuse dysfunction and must be corrected promptly. Record consciousness, pupils, speech, fields, limb findings and time last known well; deterioration or a changing level can be more important than a single normal sign.
- 02
Emergency CT head with vascular imaging when indicated - Why
- Detect haemorrhage, mass effect, large infarction and arterial occlusion in an acute central syndrome.
- Interpretation and limitations
- A normal early non-contrast CT does not exclude ischaemic stroke. CT angiography or perfusion is selected by the stroke pathway and potential reperfusion decision, not ordered as an untargeted localisation test.
- 03
MRI brain or spine using a question-specific protocol - Why
- Resolve posterior-fossa, inflammatory, demyelinating, neoplastic, cord and small ischaemic lesions with greater tissue contrast.
- Interpretation and limitations
- Choose anatomical coverage and sequences with radiology or neurology. MRI can remain normal in some clinical disorders and should not delay time-critical treatment or transfer when CT-based pathways are appropriate.
- 04
Targeted laboratory screen - Why
- Find metabolic, toxic, infectious, inflammatory, haematological or endocrine contributors suggested by phenotype.
- Interpretation and limitations
- Typical initial tests may include FBC, U&E, calcium, glucose, liver tests, CRP and selected thyroid, B12, CK, infection or autoimmune studies. Indiscriminate panels create incidental results and do not substitute for localisation.
- 05
Nerve conduction studies and electromyography - Why
- Distinguish axonal from demyelinating neuropathy and assess root, anterior horn, neuromuscular-junction or muscle dysfunction.
- Interpretation and limitations
- Timing matters because denervation and conduction abnormalities may lag symptoms. Results sample selected nerves and muscles and must be reconciled with the examination rather than interpreted as whole-body imaging.
- 06
Lumbar puncture with planned cerebrospinal-fluid studies - Why
- Assess infection, inflammation, malignancy or selected haemorrhage presentations after safety review.
- Interpretation and limitations
- Do not perform reflexively in a patient with mass-effect risk, haemodynamic instability or an immediately treatable emergency. Opening pressure, paired serum tests and correct tubes must be planned before puncture.
04Clinical next stepsHow the result changes management or prompts escalation.
01Sudden focal deficitActivate an acute stroke assessmentFirst stepA new lateralised motor, sensory, visual, language, balance or brainstem deficit with abrupt or uncertain onset.+
- 1Establish last known well, perform ABCDE, check capillary glucose, record an NIHSS-informed examination where trained and identify anticoagulants, bleeding risk, seizure and head trauma without delaying transfer.
- 2EscalationContact the local stroke pathway immediately for urgent brain and vascular imaging; posterior-circulation symptoms and disabling deficits deserve escalation even when a simple screening tool is negative.
- 3Let stroke specialists decide thrombolysis, thrombectomy, antithrombotic and blood-pressure management from imaging, timing and individual contraindications; document neurological change and swallow status.
02Cord or cauda equina signalProtect threatened neural structuresA sensory level, bilateral long-tract signs, new bladder or bowel dysfunction, saddle change or progressive weakness with spinal pain.+
- 1Stabilise trauma when relevant, document power, reflexes, perianal sensation and bladder function sensitively, check for sepsis and malignancy features, and obtain senior review at once.
- 2Arrange emergency MRI of the appropriate spinal region through the local spinal, neurosurgical or metastatic-cord-compression route; avoid delaying imaging for a complete outpatient-style work-up.
- 3DefinitiveUse cause-specific treatment only with the responsible pathway—for example antibiotics, decompression or corticosteroid decisions—and repeat the examination while awaiting definitive care.
03Peripheral or neuromuscular syndromeDefine distribution and respiratory riskProgressive lower motor neurone, length-dependent, fatigable or proximal weakness without a clear acute cerebral pattern.+
- 1Map power by movement, reflexes, sensory modalities, cranial and bulbar function, gait and autonomic symptoms; review tempo, infection, toxins, medicines, diabetes, systemic disease and family history.
- 2EscalationMeasure respiratory function urgently when weakness is rapid, ascending, bulbar or neck-predominant, and escalate autonomic instability, weak cough, dysphagia or falling vital capacity to neurology and critical care.
- 3Select blood tests and neurophysiology from the localisation, recognising that early studies may be non-diagnostic; arrange timely reassessment rather than using a normal initial test as closure.
05Risks, monitoring and follow-upComplications, safety checks and further assessment.
- Repeat the same core neurological examination after any clinical change so that apparent progression is not an artefact of different techniques or undocumented baselines.
- Track respiratory rate, oxygenation, cough, voice, swallowing and locally specified vital-capacity measures in rapidly progressive peripheral, bulbar or neuromuscular weakness.
- Record bladder function, post-void residual where appropriate and evolving saddle or truncal sensation when spinal localisation remains possible.
- Revisit localisation when imaging is negative, because early ischaemia, small posterior-fossa lesions, inflammatory disease and functional neurological disorder can all require clinical follow-up.
- Document medication exposure, renal and hepatic function and any correction of glucose or electrolytes so subsequent examinations can be interpreted in physiological context.
- Provide explicit safety-netting for new weakness, speech or vision change, severe headache, seizure, sphincter disturbance, breathlessness or rapid spread of sensory symptoms.
06Special situationsVariants, exceptions and circumstances that change the usual approach.
Face involvement separates levels
A hemispheric lesion can affect face and limbs together, whereas a cervical cord lesion spares the face. A brainstem lesion may produce an ipsilateral cranial-nerve deficit with contralateral limb findings.
Acute lesions may be flaccid
Spasticity and brisk reflexes take time to develop. Early stroke or spinal shock can produce low tone and reduced reflexes, so chronology prevents mislabelling an acute central lesion as peripheral.
Reflex arcs have two sides
A brisk reflex suggests loss of descending inhibition only when the local sensory nerve, motor nerve, root, neuromuscular junction and muscle can still complete the arc.
Sensory levels need confirmation
Patients may describe a boundary that does not correspond exactly to a cord segment. Test several modalities from normal toward abnormal, compare both sides and look for corroborating motor, reflex and autonomic signs.
Aetiology can be multifocal
Mononeuritis multiplex, metastases and demyelination can create several anatomically separate lesions. A single-lesion rule should never erase genuinely discordant, reproducible findings.
Functional signs are positive findings
Internal inconsistency such as a validated Hoover sign can support functional weakness, but diagnosis requires appropriate expertise and does not imply fabrication or exclude simultaneous structural disease.
07Common pitfallsFrequent interpretation and management errors.
- 01
Naming multiple sclerosis, stroke or neuropathy before stating where the lesion is likely to be.
- 02
Calling any brisk reflex an upper motor neurone sign without considering anxiety, symmetry and the integrity of the reflex arc.
- 03
Excluding posterior-circulation stroke because facial droop or arm weakness is absent on a simple screening test.
- 04
Assuming a normal early scan disproves a clinically coherent neurological syndrome.
- 05
Describing sensory loss without modality, boundary, side, reproducibility or comparison with a named nerve or dermatome.
- 06
Using a functional diagnosis solely because tests are negative rather than eliciting positive diagnostic features.
- 07
Forgetting that a patient can have two lesions, such as cervical myelopathy plus diabetic polyneuropathy.