Rapid review: neurology

• Neurology comes in patterns. Your first job is to place the patient in the right pattern group: vascular, fit, acute weakness, dizziness, cognitive change, movement disorder, coma.
• In every group, the single most dangerous diagnosis is named first, and the one test that changes management is done before anything else.
• Time is treatment: stroke thrombolysis, subarachnoid haemorrhage securement and giant cell arteritis vision protection are all minutes and hours.
• Dizziness is usually benign but posterior circulation stroke hides inside it; use the HINTS test and a low threshold for imaging.
• Weakness is localised by pattern (asymmetric, fatiguable, ascending, UMN/LMN mix) rather than by memorised lists.
• Dementia is a syndrome, not a diagnosis; ask which cortex is failing, and treat reversible causes first.
• Coma care is ABCDE plus a structured search for cause, not a named drug.
• Cord and nerve root emergencies are diagnosed by the combination of symptoms and the urgency of the imaging, not by waiting for paralysis.

By the end of this revision page you should be able to:

1. For each major neurologic presentation, name the most likely dangerous diagnosis, the best first test and the best first treatment.
2. Recognise the commonest wrong answer for stroke, headache, seizure, weakness, dizziness, dementia, movement disorder, coma and cord compression.
3. Choose the right first investigation for an acute neurologic problem and say what it excludes.
4. Outline the first medical and surgical steps for stroke, subarachnoid haemorrhage, status epilepticus, Guillain-Barre syndrome, myasthenia and cord compression.
5. Link each block to the full MedGrasp topic for the detail you need on the ward.

This is a revision sheet, not a textbook. Each block below gives five things for one classic presentation: the presenting picture in clinical words, the single most likely diagnosis, the best first test, the best first treatment, and the commonest wrong answer, followed by the location of the full topic in plain text. Numbers are taken from the same guideline editions cited by those topic pages. A final algorithm comes first because it governs every presentation after it.

Presenting picture. Sudden, focal loss of brain function corresponding to a vascular territory: face and arm weaker than the leg and dysphasia in a middle cerebral artery territory stroke, visual field loss, ataxia, dysarthria or a brainstem syndrome. Symptoms are present at onset and progress or remain; the time of last known well is usually clear to the bystander even if the patient is not.

Single most likely diagnosis. Acute ischaemic stroke, most often from large-vessel atherosclerosis, cardioembolism or small-vessel disease.

Best first test. Non-contrast CT of the head as soon as possible to exclude haemorrhage, followed immediately by CT or MR angiography of the head and neck arteries when thrombectomy is a possibility. Glucose, oxygen saturation, ECG and cardiac monitoring are part of the same first set.

Best first treatment. Intravenous alteplase 0.9 mg/kg, given within 4.5 hours of known onset in eligible patients, plus aspirin after brain imaging, urgent mechanical thrombectomy for proximal large-vessel occlusion, and organised stroke unit care with blood pressure, glucose, fluids and temperature controlled. ^[2] Decompressive hemicraniectomy is considered for large hemispheric infarction. ^[1]

Commonest wrong answer. To delay or withhold reperfusion because the deficit looks mild or fluctuating, and to give antihypertensive treatment aggressively in a patient who is a candidate for thrombolysis; blood pressure is lowered only to the guideline thresholds before reperfusion. ^[1] See the full topic: neurology/ischaemic-stroke-and-tia.

Presenting picture. Sudden focal deficit with headache, vomiting and a fall in conscious level that develops over minutes; hypertension is common and there may be no history of trauma.

Single most likely diagnosis. Spontaneous intracerebral haemorrhage, usually from hypertensive small-vessel disease or cerebral amyloid angiopathy.

Best first test. Urgent non-contrast CT of the head, which shows haematoma, location, size and ventricular extension within minutes.

Best first treatment. Reversal of anticoagulation if present, rapid blood pressure lowering for small to moderate haematomas, neurosurgical review for cerebellar haemorrhage or mass effect, and management of complications. Early prediction of poor outcome from any single score alone is unsafe. See the full topic: neurology/intracerebral-haemorrhage.

Presenting picture. A sudden, fully resolving focal neurologic deficit (lasts minutes, often under an hour) caused by temporary focal brain ischaemia: transient dysphasia, monocular visual loss, or limb weakness. Resolution does not mean benign.

Single most likely diagnosis. Transient ischaemic attack, most often embolic, from atherosclerosis, atrial fibrillation or a proximal source.

Best first test. Same-day brain imaging (MRI with diffusion-weighted sequences where available, otherwise CT), vascular imaging of the carotids and a full cardiovascular assessment including ECG and rhythm monitoring.

Best first treatment. Immediate single antiplatelet treatment and urgent 48-hour specialist assessment with secondary prevention started within days, not weeks. ^[1] Carotid endarterectomy is offered for symptomatic tight stenosis. See the full topic: neurology/ischaemic-stroke-and-tia.

Presenting picture. Recurrent, often unilateral, pulsating or throbbing headache lasting 4 to 72 hours, with nausea and/or photophobia and phonophobia, and worsening with routine activity; some patients have an aura of fully reversible focal neurologic symptoms before the headache.

Single most likely diagnosis. Migraine with or without aura (International Classification of Headache Disorders, 3rd edition).

Best first test. Clinical diagnosis; brain imaging is not needed when the history is typical and there are no red flags. An ECG and normal examination suffice.

Best first treatment. Acute attacks: simple analgesic (aspirin or paracetamol) plus an antiemetic, escalating to an oral triptan when needed, with advice to limit acute medicines to prevent medication-overuse headache. Prevention: beta-blocker, topiramate or amitriptyline, chosen by comorbidity. ^[5]

Commonest wrong answer. To scan every headache, or to keep changing the acute drug every month instead of setting a sensible limit on acute treatment. See the full topic: neurology/primary-headache-disorders.

Presenting picture. Sudden, severe "thunderclap" headache reaching peak within seconds (classically during exertion or straining), with neck stiffness, vomiting and sometimes loss of consciousness or a focal deficit; meningism on examination.

Single most likely diagnosis. Aneurysmal subarachnoid haemorrhage.

Best first test. Urgent non-contrast CT of the head; if negative but suspicion remains high, lumbar puncture (CSF xanthochromia) or CT angiography of the cerebral arteries.

Best first treatment. Secure the aneurysm (endovascular coiling or neurosurgical clipping) within the first day or two, plus oral nimodipine for all patients, blood pressure and temperature control, and management of hydrocephalus and delayed cerebral ischaemia. ^{[3] [4]}

Commonest wrong answer. To label this as benign "worst headache" or migraine and send the patient home, or to lumbar puncture before checking imaging and contraindications. See the full topic: neurology/subarachnoid-haemorrhage.

Presenting picture. A new persistent headache in a person over 50, often with scalp or temporal artery tenderness, jaw claudication on chewing, visual symptoms (amaurosis fugax, diplopia, sudden visual loss) and constitutional upset; polymyalgia rheumatica symptoms coexist in 40 to 60 percent. ^[6]

Single most likely diagnosis. Giant cell (temporal) arteritis, a large-vessel granulomatous vasculitis.

Best first test. Raised erythrocyte sedimentation rate and C-reactive protein with a temporal artery ultrasound looking for the halo sign; temporal artery biopsy remains the reference, and CT or MR angiography assesses large-vessel involvement.

Best first treatment. High-dose oral glucocorticoid started the same day, without waiting for confirmation: 40 to 60 mg prednisolone-equivalent daily, with intravenous methylprednisolone (0.25 to 1 g daily for up to 3 days) when there is visual loss or threatened vision, plus tocilizumab in selected relapsing or high-risk disease. ^[6]

Commonest wrong answer. To await biopsy before treating, or to use the low doses used for polymyalgia rheumatica in a patient with visual symptoms. See the full topic: musculoskeletal/giant-cell-arteritis-and-polymyalgia-rheumatica.

Presenting picture. An episode of abnormal, excessive neuronal discharge manifesting as a transient, stereotyped disturbance of behaviour, motor function, sensation or consciousness: a generalised tonic-clonic seizure, or a focal seizure with impaired awareness or motor signs; status epilepticus is any seizure lasting 5 minutes or more, or repeated seizures without full recovery between them.

Single most likely diagnosis. A provoked or symptomatic seizure (metabolic disturbance, infection, structural lesion, alcohol, drug) in a first episode; epilepsy when there have been recurrent unprovoked seizures.

Best first test. Clinical diagnosis of epilepsy is usually from the history and a witness account; EEG and brain imaging (MRI) are confirmatory once stability allows, and metabolic causes (glucose, sodium, calcium, renal and liver function, infection screen) are excluded.

Best first treatment. In a discrete seizure, protect the airway, place the patient in the recovery position and do not force anything into the mouth. In status epilepticus, give a benzodiazepine (intravenous lorazepam or intramuscular midazolam) as first-line treatment, then a loading dose of an intravenous antiseizure medicine such as levetiracetam, fosphenytoin or valproate if the seizure continues. ^[7] In epilepsy, choose the first antiseizure drug by seizure type and patient factors, taking valproate precautions seriously. ^[7]

Commonest wrong answer. To label a first fit as epilepsy and start long-term treatment after a single event, or to use the wrong first antiseizure drug for the seizure type. See the full topics: neurology/seizures-and-epilepsy and neurology/status-epilepticus.

Presenting picture. An acute or subacute, ascending, symmetric flaccid weakness with areflexia, often after a respiratory or gastrointestinal infection, with mild sensory symptoms; autonomic dysfunction and respiratory failure may develop over days.

Single most likely diagnosis. Guillain-Barre syndrome (acute inflammatory demyelinating polyradiculoneuropathy), with variants including Miller Fisher syndrome.

Best first test. Nerve conduction studies and electromyography, with lumbar puncture showing albuminocytologic dissociation; pulmonary function (vital capacity) is the bedside test that decides airway and ventilation.

Best first treatment. Supportive care on a monitored ward with attention to respiratory function and autonomic stability, plus specific disease treatment with intravenous immunoglobulin or plasma exchange; deep vein thrombosis prophylaxis and physiotherapy. ^[9]

Commonest wrong answer. To send a patient home because the weakness is still mild, or to mistake the neuropathic picture for a spinal cord lesion. See the full topic: neurology/peripheral-neuropathy-and-guillain-barre-syndrome.

Presenting picture. Fatiguable weakness that worsens on repeated effort and recovers with rest, often starting with ptosis, diplopia, dysarthria or dysphagia, with proximal limb weakness later; a crisis is worsening weakness with respiratory or bulbar failure.

Single most likely diagnosis. Myasthenia gravis, usually from acetylcholine receptor antibodies, with Lambert-Eaton myasthenic syndrome as the important differential in older smokers with proximal weakness and autonomic features.

Best first test. Serological testing for acetylcholine receptor, MuSK and LRP4 antibodies; bedside response to an anticholinesterase and repetitive nerve stimulation or single-fibre electromyography confirm. CT of the thymus is part of the work-up.

Best first treatment. Symptomatic treatment with an anticholinesterase (pyridostigmine), and disease-modifying treatment with immunosuppression (corticosteroids and steroid-sparing agents); thymectomy in selected patients, and rescue with intravenous immunoglobulin or plasma exchange for crises. ^[8]

Commonest wrong answer. To miss myasthenic or cholinergic crisis by waiting for laboratory confirmation, or to give magnesium, aminoglycosides or neuromuscular blocking drugs that worsen weakness. See the full topic: neurology/myasthenia-gravis-and-lambert-eaton-syndrome.

Presenting picture. A young adult with two or more episodes of focal neurologic symptoms (optic neuritis, internuclear ophthalmoplegia, brainstem or spinal cord syndrome) that evolve over days, resolve partially, and are disseminated in space and time.

Single most likely diagnosis. Relapsing-remitting multiple sclerosis, defined by the McDonald 2017 criteria applied to clinical and MRI findings. ^[10]

Best first test. MRI of the brain and spinal cord (dissemination in space) with gadolinium, plus lumbar puncture for oligoclonal bands when the clinical picture is atypical.

Best first treatment. A relapse is treated with a short course of high-dose intravenous corticosteroid; long-term, a disease-modifying therapy is chosen by disease severity, escalation and monitoring strategy. ^[10]

Commonest wrong answer. To treat every change in symptoms as a new relapse, or to start a disease-modifying therapy without matching its intensity to the disease and monitoring for progressive multifocal leukoencephalopathy where relevant. See the full topic: neurology/multiple-sclerosis.

Presenting picture. A relentless, usually asymmetric, mixed upper and lower motor neurone weakness over months, with fasciculations, cramps, dysarthria and dysphagia; sensations and cognition may be partly affected in some variants.

Single most likely diagnosis. Amyotrophic lateral sclerosis, the commonest motor neurone disease phenotype, diagnosed by progressive UMN and LMN signs in more than one body region with supportive electrophysiology.

Best first test. Electromyography and nerve conduction studies to confirm lower motor neurone dysfunction, with brain and spinal cord MRI to exclude structural mimics; respiratory tests and swallowing assessment guide early support.

Best first treatment. Multidisciplinary care from diagnosis: riluzole where offered, non-invasive ventilation as respiratory function falls, gastrostomy for dysphagia and careful nutritional support, with attention to communication and caregiver needs. ^[11]

Commonest wrong answer. To attribute progressive weakness in a older patient to spinal stenosis or "just ageing" without considering motor neurone disease, or to delay respiratory and nutritional support. See the full topic: neurology/amyotrophic-lateral-sclerosis.

Presenting picture. The sensation of movement: true vertigo (spinning) suggests a vestibular disorder; presyncope suggests a cardiovascular cause; dysequilibrium in older adults suggests sensory or visual-vestibular impairment; non-specific dizziness is common and non-localising.

Single most likely diagnosis. Benign paroxysmal positional vertigo (BPPV) when vertigo is brief, provoked by head position and accompanied by a characteristic (and often fatigable) positional nystagmus.

Best first test. A positional test (Dix-Hallpike for posterior canal BPPV, supine roll for horizontal canal) performed by a trained clinician; the HINTS examination (head impulse, nystagmus, test of skew) is used for acute vestibular syndrome. ^[15]

Best first treatment. For BPPV, a canalith repositioning manoeuvre (for example the Epley manoeuvre); for acute vestibular neuritis, supportive antiemetics, early vestibular rehabilitation and, where appropriate, antiviral therapy only on evidence; for any patient, treat the cause rather than the symptom. Transient vertigo triggered by standing should lead to orthostatic blood pressure checking. ^[15]

Commonest wrong answer. To give long courses of vestibular suppressants (betahistine, prochlorperazine) for peripheral vertigo, or to miss posterior circulation stroke in new acute vestibular syndrome. Acute vestibular syndrome not explained by BPPV or postural hypotension in an adult should be referred immediately for stroke assessment. ^[15]

Red flags for central vertigo. Vertical nystagmus, diplopia, dysarthria, dysphagia, ataxia, limb weakness, a skew deviation, or continuous vertigo in an older patient with vascular risk factors. See the full topic: neurology/vertigo-dizziness-and-syncope-approach.

Presenting picture. A progressive decline in cognitive function, usually with memory impairment plus one or more of aphasia, apraxia, agnosia or executive dysfunction, severe enough to interfere with daily function; delirium is excluded by time course and fluctuation.

Single most likely diagnosis. Alzheimer disease is the commonest cause, presenting with prominent episodic memory failure and posterior cortical features; other common types are vascular dementia, dementia with Lewy bodies and frontotemporal dementia.

Best first test. A cognitive screen (for example an ACE-III or MoCA) and a basic reversible-cause screen (full blood count, urea and electrolytes, glucose, calcium, thyroid-stimulating hormone, vitamin B12 and folate, plus syphilis serology where appropriate), followed by structural brain imaging (CT or MRI) for all patients.

Best first treatment. Confirm the subtype and start a cholinesterase inhibitor (donepezil, rivastigmine or galantamine) for mild to moderate Alzheimer disease, adding memantine for moderate to severe disease, with non-pharmacological support and caregiver support throughout; manage vascular risk and review drugs that impair cognition. ^{[12] [13]}

Commonest wrong answer. To assume memory loss is normal ageing, or to chase a single drug without first excluding depression, medication effect, infection, metabolic disturbance and normal pressure hydrocephalus. See the full topics: neurology/alzheimer-disease-and-dementia and psychiatry/dementia-neurocognitive-disorders.

Presenting picture. An acute or subacute disturbance of attention and awareness with a fluctuating course, disorganised thinking and perceptual disturbance, over hours to days, usually in an older or hospitalised patient; it is a medical emergency masquerading as confusion.

Single most likely diagnosis. Delirium secondary to infection, medication (especially anticholinergics, opioids, benzodiazepines), metabolic disturbance, hypoxia, pain, urinary retention or constipation; alcohol or benzodiazepine withdrawal is an important and reversible cause.

Best first test. The 4AT or CAM bedside screen, then an urgent search for cause: infection, drug side effects (especially new ones), hypoxia, dehydration, electrolytes, glucose, renal and liver function, pain and bladder/bowel status; no lumbar puncture without a clear indication.

Best first treatment. Treat the cause first; supportive measures include reorientation, adequate fluids and nutrition, sleep hygiene, glasses and hearing aids, mobilisation and avoidance of restraints and sedatives. Antipsychotics are used only for severe agitation that threatens safety, in the lowest effective dose and shortest duration. See the full topic: psychiatry/delirium.

Presenting picture. Parkinson disease: asymmetric resting tremor, bradykinesia and muscular rigidity with postural instability later, plus non-motor features (REM sleep behaviour disorder, constipation, anosmia, orthostatic hypotension); a tremor disorder without these signs is usually not Parkinson disease.

Single most likely diagnosis. Idiopathic Parkinson disease, diagnosed clinically by bradykinesia plus rest tremor or rigidity, once drug-induced parkinsonism, vascular parkinsonism and atypical parkinsonian disorders (multiple system atrophy, progressive supranuclear palsy, corticobasal syndrome) have been considered.

Best first test. Clinical diagnosis; a dopaminergic imaging scan (DaTscan) helps when the clinical picture is unclear, and MRI excludes secondary causes and structural mimics.

Best first treatment. Levodopa (with a decarboxylase inhibitor) is the most effective symptomatic treatment; a dopamine agonist or monoamine oxidase-B inhibitor may be preferred in younger patients or to delay dyskinesia, with device-aided therapies (deep brain stimulation, infusion therapies) later. Anticholinergics should be avoided in older adults. ^[14]

Commonest wrong answer. To call any tremor Parkinson disease, or to start high-dose levodopa in a young patient without counselling about long-term motor complications, or to fail to review dopamine-blocking drugs as a reversible cause. Other movement disorders worth localising: essential tremor (action and postural tremor, alcohol-responsive), dystonia (sustained abnormal postures, task-specific), Huntington disease (chorea with cognitive and psychiatric change) and restless legs syndrome. See the full topics: neurology/parkinson-disease and neurology/tremor-dystonia-and-movement-disorders.

Presenting picture. A patient who is unarousable and unresponsive, with the brain no longer supporting wakefulness or awareness; the depth of coma, the pattern of breathing, pupil responses and motor posturing give the first clues to level and cause.

Single most likely diagnosis. The cause is found by structure: structural (haemorrhage, infarct, tumour, hydrocephalus, herniation), metabolic or toxic (hypoxia, hypoglycaemia, uraemia, liver failure, sepsis, drug overdose, Wernicke encephalopathy), or infectious (meningitis, encephalitis).

Best first test. Airway, breathing and circulation first; then immediate glucose, oxygen saturation, core temperature and, where needed, blood gases; urgent CT of the head if trauma or a focal or structural cause is suspected; toxicology and infection screens by context.

Best first treatment. Stabilise the ABCs (secure the airway when protective reflexes are lost), give IV glucose (after thiamine) when hypoglycaemic, naloxone for suspected opioid poisoning, and targeted treatment for the cause: antibiotics for infection, reversal for warfarin or DOAC where appropriate, neurosurgical review for mass effect or herniation. ^[17] Unresponsiveness with loss of protective reflexes puts the patient at risk of aspiration and airway obstruction. ^{[17] [17]}

Commonest wrong answer. To start sedating drugs before the cause is found, or to assess coma as "GCS 3/15" without describing the components and the brainstem reflexes that actually localise the lesion. See the full topic: emergency-medicine/unconscious-patient-and-coma.

Presenting picture. Progressive back pain (often worse when supine, or band-like and radicular), gait difficulty, sensory level, sphincter disturbance and weakness; metastatic compression often starts with pain weeks before neurologic deficit.

Single most likely diagnosis. Metastatic spinal cord compression, most often from breast, lung or prostate cancer, or from myeloma.

Best first test. Whole-spine MRI as soon as possible (within hours, not days) in any patient with suspected compression; a plain X-ray is not sufficient and delays diagnosis.

Best first treatment. Dexamethasone early, plus definitive management matched to the tumour (radiotherapy in most cases, surgery for spinal instability, unknown primary or rapid progression), with careful attention to pain control and bladder/bowel management. ^[16]

Commonest wrong answer. To wait for weakness or incontinence before imaging the spine, or to order a single-region MRI when the level is uncertain. See the full topic: neurology/spinal-cord-compression-and-myelopathy.

Presenting picture. Cauda equina syndrome: low back pain with saddle anaesthesia, bladder or bowel dysfunction (retention or incontinence) and bilateral sciatica, often from a large central disc prolapse. Lumbar radiculopathy alone produces dermatomal pain and reflex change without these features.

Single most likely diagnosis. Cauda equina syndrome is a surgical emergency; lumbar radiculopathy is managed conservatively in most cases.

Best first test. Urgent MRI of the lumbar spine for suspected cauda equina; clinical examination with straight leg raise and a full lower-limb neurologic examination for radiculopathy.

Best first treatment. Urgent neurosurgical or spinal surgical decompression for cauda equina syndrome within hours of diagnosis; for radiculopathy, analgesia, physiotherapy and time, with surgery when intractable pain or progressive deficit. See the full topics: surgery/acute-limb-ischaemia is not related; neurology/clinical-neuroanatomy-and-spinal-cord-syndromes and musculoskeletal/low-back-pain-disc-herniation-and-spinal-stenosis.

• Stroke: time windows matter; non-contrast CT first, reperfusion where eligible, and full neurovascular work-up during the same admission.
• Haemorrhagic stroke is diagnosed on CT; reversal, blood pressure control and neurosurgical review are the early priorities.
• Transient ischaemic attacks are treated as urgently as strokes because the early risk of recurrence is high.
• Migraine is a clinical diagnosis; subarachnoid haemorrhage and giant cell arteritis are clinical emergencies that should not be missed.
• Thunderclap headache demands CT first, with further testing guided by result and suspicion.
• Giant cell arteritis is treated with high-dose glucocorticoid the same day; do not wait for biopsy.
• Seizure management separates the event from the diagnosis: stop the seizure, exclude provoked causes, then plan long-term treatment.
• Weakness is localised by pattern: ascending areflexic (Guillain-Barre), fatiguable (myasthenia), relapsing and MRI-defined (multiple sclerosis), and progressive mixed upper and lower motor neurone (motor neurone disease).
• Dizziness is often benign but posterior stroke hides in the acute vestibular syndrome; use red flags and HINTS.
• Delirium is an emergency of attention, usually with a reversible medical cause; dementia is a progressive syndrome with subtypes and reversible mimics.
• Movement diagnosis is clinical, and drug-induced or structural causes must be excluded before labelling a progressive parkinsonian syndrome.
• Coma care begins with ABCDE; airway, glucose and the search for cause precede any single named treatment.
• Cord compression is a clinical and imaging diagnosis of hours, not days; cauda equina is a surgical emergency.
• Plain text references to full topics are given in each block; follow these (neurology/ischaemic-stroke-and-tia, neurology/subarachnoid-haemorrhage, psychiatry/delirium, etc.) rather than memorising this sheet.