Acute neurology: a suggested approach

Kuven K Moodley; Arani Nitkunan; Anthony C Pereira

doi:10.7861/clinmedicine.18-5-418

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Box 1.

The principles of acute neurology

1 Use the history (direct and collateral) to establish a differential or working diagnosis. Be an active listener. Let the patient talk; they will often ‘tell’ you the diagnosis

2 Develop a routine to rapidly screen for neurological deficits.⁹ Where is the problem: brain, spinal cord, peripheral nerve etc? This should only take 4 to 5 minutes

3 Target investigations to define aetiology. Decide on the general underlying pathological process rather than a diagnostic label (eg inflammatory problem affecting the cervical cord to guide investigation¹⁰

4 Ensure the management plan is helpful to the patient (eg pain relief)

5 Involve the multidisciplinary team

6 Decide whether patient needs admission

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Table 1.

Diagnostic modelling in neurology based on the temporal course of symptom onset

Time course	Onset time	Probable aetiology
Hyperacute	Seconds	• Vascular eg stroke • Epileptic seizure
Acute	Minutes	• Vascular • Toxic-metabolic • Compressive lesions • Vasovagal syncope
Subacute	Over 72 hours	• Toxic-metabolic eg B12 deficiency • Inflammation (Infective or immune-mediated) • Closed space pathology eg subdural haemorrhage • Infiltrative or neoplastic process • Myasthenia gravis • Medical decompensation of previous neurological insult (can occur with or without delirium)
Remitting –Relapsing	Back to baseline within a day	• transient ischemic attack (usually recovered in <1 hour) • Periodic disorders (migraine with aura, epilepsy, ocular myasthenia)
Remitting –Relapsing	Returning to baseline but taking days–weeks	• Multiple sclerosis • Toxic-metabolic eg drug toxicity
Stuttering	Usually acute or subacute in onset but patient developing new deficits rather than progression of existing ones	• Stroke-like syndromes due to vasculitis/endocarditis • Autoimmune encephalitis • Myasthenia and atypical forms of Guillain-Barré syndrome
Chronic, progressive	Weeks	• Guillain-Barré syndrome • Malignancy
Chronic, progressive	Months	• Degenerative diseases eg Alzheimer's disease, motor neurone disease • Malignancy

Common diseases may present in an atypical manner

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Box 2.

A suggested approach for a screening neurological examination

• General features: make a note of dress, foetor, level of arousal (Glasgow Coma Scale), insight into presenting problem, ease of communication, recall of personal information, speech (slurred speech or dysarthria / expressive or receptive dysphasia / hypophonia) – if affected, perform a bedside swallow test to assess aspiration risk

• Cranial nerves: gross acuity (able to read your ID badge), fundi, fields, eye movements, pupil size and light responses, facial strength

• Tone: normal, flaccid, spastic or rigid

• Power:

Pronator drift
Characterise the pattern of weakness: pyramidal (brain/spinal cord), proximal>distal (muscle/radiculopathy), distal>proximal (neuropathy, rarer myopathies). Is it lateralising (ie hemiplegia) or localising (paraplegia as seen in cord lesions)

• Neck flexion: this is of particular importance in cases of suspected acute neuromuscular weakness (in extreme cases, patients may present with ‘head-drop’) and should be regarded as a harbinger of diaphragmatic failure

• Reflexes: absent, normal or brisk. Remember reflexes are frequently reduced in diabetic patients

• Sensory: distal light touch sensation, double simultaneous stimulation (the presence of sensory hemi-neglect indicating higher cortical sensory impairment, as may commonly occur with right parietal strokes). Characterise the pattern of light touch sensory loss where possible but bear in mind that the sinister causes of sensory impairment are usually associated with other signs. Organic patterns of isolated light touch sensory impairment include: unilateral (either mononeuropathy or monoradiculopathy), ‘glove and stocking’ (toxic-metabolic axonal polyneuropathies) and dense hemisensory (rare instances of lacunar stroke, more likely to indicate a functional neurological disorder). The initial stages of GBS and inflammatory transverse myelopathy may be predominantly sensory; the presence of a truncal level usually indicates cord pathology)

• Coordination: finger–nose, heel–shin

• Gait including walking on toes and tandem gait

• Blood pressure and pulse (including postural responses) Postural blood pressure measurements should be obtained after lying down for at least 5 minutes of rest and repeated after standing for 3 minutes. Postural hypotension is defined as a reduction of greater than 20 mmHg systolic or 10 mmHg diastolic. Any symptoms that develop during the standing phase of the assessment should be clearly documented