Neurology

Sudden focal neurological deficit from cerebral ischaemia (~85% of strokes). The acute task is to exclude haemorrhage on CT and reperfuse within the window; the localisation (territory) and Bamford class are the high-yield exam skills. See the Stroke localisation panel below the cards.

A transient episode of focal neurological dysfunction from ischaemia, classically resolving within 24 hours, WITHOUT acute infarction on imaging. A warning of high early stroke risk — it mandates urgent assessment and immediate antiplatelet.

Spontaneous bleeding into the subarachnoid space, usually from a ruptured berry aneurysm. The classic "thunderclap" headache — sudden, maximal at onset, worst ever — demands urgent CT and, if negative, an LP for xanthochromia.

Venous bleeding from torn bridging veins collecting between the dura and arachnoid. Classically in the ELDERLY or alcoholics (brain atrophy stretches the veins), often after trivial trauma, with a fluctuating or insidious course. CT shows a CRESCENT-shaped collection crossing suture lines.

Arterial bleeding (classically the middle meningeal artery at the pterion) collecting between the skull and dura. Typically a young patient after a temporal head injury, with the classic "lucid interval" then rapid deterioration. CT shows a BICONVEX (lens) collection limited by sutures.

Thrombosis of the cerebral venous sinuses, causing raised ICP and venous infarction (which may be haemorrhagic). Easily missed — it presents with headache ± seizures/focal signs in a prothrombotic context (pregnancy/puerperium, COCP, dehydration, thrombophilia).

A common primary headache disorder of recurrent moderate–severe headaches, classically unilateral, pulsatile, with nausea, photophobia/phonophobia and aggravation by activity, ± aura. The exam tests acute vs preventive treatment and the COCP/aura interaction.

The most severe primary headache — strictly unilateral, excruciating periorbital pain in clusters (attacks daily for weeks, then remission), with ipsilateral cranial autonomic features and a RESTLESS, agitated patient (unlike migraine where they lie still).

The commonest primary headache: bilateral, mild–moderate, pressing/tightening "band around the head", without the nausea, aura or activity-aggravation of migraine. Often related to stress, fatigue and poor posture.

Sudden, severe, brief, electric-shock-like facial pain in the trigeminal distribution, usually from vascular compression of the nerve root. Paroxysms are triggered by light touch (washing, shaving, chewing). Carbamazepine is first-line.

Raised intracranial pressure with no mass lesion, hydrocephalus or venous thrombosis — classically a young obese woman, often on a precipitant drug. The threat is progressive visual loss from papilloedema. A diagnosis of exclusion after venous imaging.

A progressive neurodegenerative disorder from dopaminergic neuron loss in the substantia nigra, defined by the motor triad of bradykinesia, rigidity and a resting tremor, classically ASYMMETRIC. The exam tests distinguishing it from essential tremor, drug-induced parkinsonism and the Parkinson-plus syndromes.

A common, often inherited, postural/action tremor of the hands (and sometimes head/voice) — the chief mimic of early Parkinson disease. The discriminators: it is symmetric, present on action (not at rest), and classically improves with alcohol.

The commonest dementia: insidious, progressive impairment of recent memory first, then language, visuospatial and executive function. Amyloid-β plaques and tau neurofibrillary tangles with cholinergic deficit underlie it. Managed with cholinesterase inhibitors.

The second commonest dementia, from cerebrovascular disease. Classically a STEPWISE decline (each step after a vascular event) in a patient with vascular risk factors and focal neurological signs — distinct from the smooth decline of Alzheimer.

A dementia defined by the triad of FLUCTUATING cognition, recurrent VISUAL HALLUCINATIONS and spontaneous PARKINSONISM, with REM sleep behaviour disorder. Crucially, patients have severe SENSITIVITY to antipsychotics — a key safety point.

An early-onset dementia (often <65) from frontal/temporal lobar degeneration, presenting with EARLY personality/behavioural change or progressive language breakdown, with memory relatively preserved early on — the opposite emphasis to Alzheimer.

Dementia with BOTH Alzheimer and significant vascular pathology — common in older patients. The exam trap (and Raahat’s lost mark): a stem that shows BOTH hippocampal/amnestic features AND vascular changes; the answer integrates both, rather than anchoring on the single cleanest label ("Alzheimer’s").

A progressive neurodegeneration of motor neurons with MIXED upper and lower motor neuron signs and — characteristically — NO sensory involvement and NO sphincter/eye-movement involvement until late. Amyotrophic lateral sclerosis is the commonest form. Riluzole modestly extends survival.

An autosomal-dominant trinucleotide (CAG) repeat disorder causing progressive chorea, cognitive decline and psychiatric disturbance, with onset usually in mid-adulthood. Shows ANTICIPATION (earlier/worse with successive generations). No cure — management is supportive.

A thiamine-deficiency neuropsychiatric emergency. Wernicke encephalopathy is the acute, REVERSIBLE triad (confusion, ophthalmoplegia, ataxia); if untreated it progresses to Korsakoff syndrome — irreversible anterograde amnesia with confabulation. Give IV thiamine BEFORE glucose.

A potentially REVERSIBLE cause of dementia: the classic triad of gait apraxia, urinary incontinence and cognitive impairment ("wet, wacky, wobbly") with ventriculomegaly but a normal CSF pressure. CSF shunting can improve it — so it must not be missed among the dementias.

A chronic autoimmune demyelinating disease of the CNS, defined by neurological episodes DISSEMINATED IN TIME AND SPACE. Typically a young woman with relapsing-remitting attacks (optic neuritis, sensory, motor, cerebellar). Diagnosis combines clinical episodes, MRI lesions and CSF oligoclonal bands.

An acute, immune-mediated, ASCENDING demyelinating polyneuropathy, classically a few weeks after an infection (especially Campylobacter jejuni). Progressive symmetrical weakness with areflexia; the danger is respiratory failure and autonomic instability. Treated with IVIG or plasma exchange (NOT steroids).

An autoimmune disorder of the neuromuscular junction (antibodies against the post-synaptic acetylcholine receptor) causing FATIGABLE muscle weakness — worse with use and at the end of the day. Ocular and bulbar muscles are typically affected; the emergency is a myasthenic (respiratory) crisis. Associated with thymoma.

Inflammation of the meninges. The neuro emphasis is the CSF interpretation (bacterial vs viral vs TB vs fungal) and the do-not-delay-antibiotics rule. Community non-blanching rash → immediate benzylpenicillin; hospital → IV ceftriaxone (± amoxicillin for Listeria) + dexamethasone for pneumococcal.

Inflammation of the brain parenchyma, causing altered behaviour/cognition, reduced consciousness and seizures (± fever) — distinct from meningitis by the prominent cerebral dysfunction. HSV-1 (temporal-lobe) is the key treatable cause; start IV ACICLOVIR empirically and early.

A focal collection of pus within the brain parenchyma, from contiguous spread (sinusitis, otitis, dental) or haematogenous seeding (endocarditis, right-to-left shunt). Presents with the combination of raised ICP, focal deficit and infection. Imaging shows a RING-ENHANCING lesion.

Primary or, more commonly, METASTATIC intracranial tumours. They present with progressive focal deficit, raised-ICP headache (worse on waking/lying), seizures, or personality change. The exam tests the subtype clues and the steroid-for-oedema point.

A benign tumour of the vestibulocochlear nerve’s Schwann cells at the cerebellopontine angle. The classic presentation is UNILATERAL sensorineural hearing loss with tinnitus; as it grows it affects adjacent cranial nerves (V, VII). Bilateral tumours suggest neurofibromatosis type 2.

A pathological rise in intracranial pressure that threatens cerebral perfusion and risks herniation ("coning"). Recognised by the headache/vomiting/papilloedema triad and falling GCS with pupil change; managed by treating the cause and temporising measures. The neuro emphasis: do NOT LP if a mass/raised ICP is suspected.

Compression of the spinal cord — an emergency because delay causes permanent paralysis. Metastatic malignant spinal cord compression (MSCC) is the classic cause. Presents with progressive limb weakness, a SENSORY LEVEL and sphincter disturbance; needs urgent MRI of the WHOLE spine and high-dose steroids.

Damage to the spinal cord (trauma, ischaemia) producing characteristic patterns depending on which tracts are involved. The exam tests recognising the syndrome from the dissociation of motor, pain/temperature and dorsal-column (proprioception/vibration) signs.

Demyelination of the DORSAL COLUMNS and CORTICOSPINAL TRACTS (and peripheral nerves) from vitamin B12 deficiency (or nitrous oxide abuse, which inactivates B12). A reversible cause of a mixed sensory/UMN picture — treat B12 promptly. The classic trap: giving folate first can precipitate it.

Compression of the cauda equina (lumbosacral nerve roots below the cord, ~L1/L2 down) — a surgical EMERGENCY. Usually a large central disc prolapse. The red-flag features (saddle anaesthesia, bladder/bowel dysfunction, bilateral sciatica) mandate emergency MRI and decompression to prevent permanent incontinence.

An acute, idiopathic (likely post-viral, HSV-linked) LOWER-motor-neuron facial nerve palsy. The key discriminator is that it involves the WHOLE side of the face including the FOREHEAD (forehead-sparing implies an UMN/central cause such as stroke). Early prednisolone improves recovery.

Dysfunction of peripheral nerves, most commonly a length-dependent, symmetrical "glove-and-stocking" sensorimotor neuropathy. The exam tests identifying the CAUSE (diabetes the commonest) and the predominantly-motor vs predominantly-sensory pattern.

Dysfunction of a spinal nerve ROOT, usually from a disc prolapse or degenerative spondylosis, producing pain, sensory change and weakness in that root’s DERMATOME and MYOTOME — distinct from the diffuse pattern of peripheral neuropathy. Most settle conservatively.

Injury or entrapment of a single peripheral nerve (mononeuropathy), producing a focal motor/sensory deficit in that nerve’s territory. The exam tests recognising the classic deficits: carpal tunnel (median), wrist drop (radial), claw hand/Froment (ulnar), and foot drop (common peroneal).

Dysfunction of the autonomic nervous system, most commonly from long-standing diabetes. Produces postural hypotension, gastrointestinal dysmotility, bladder dysfunction and other autonomic features — often alongside a peripheral sensory neuropathy. Management is largely symptomatic.

X-linked recessive disorders of the dystrophin gene. Duchenne (dystrophin ABSENT) is severe and presents in early childhood; Becker (dystrophin REDUCED) is milder and later. Boys present with proximal weakness, calf PSEUDOHYPERTROPHY and Gowers sign, with a markedly raised creatine kinase.

A common sensorimotor disorder: an irresistible URGE to move the legs, worse at rest and in the evening/night, relieved by movement. Often associated with iron deficiency (check ferritin) and certain drugs; can disturb sleep significantly.

A tendency to recurrent UNPROVOKED seizures. Classification (focal vs generalised) drives drug choice. The high-yield exam points: sodium valproate is highly teratogenic (avoid in women of childbearing potential), and the first-line drugs differ by seizure type.

A seizure lasting ≥5 minutes, or repeated seizures without recovery between them — a neurological emergency. A timed, stepwise protocol: benzodiazepine first, then a second-line antiepileptic, then anaesthesia, while checking glucose and (in pregnancy) treating eclampsia.

An ACUTE, FLUCTUATING disturbance of attention and cognition with an altered level of consciousness, caused by an underlying organic insult (infection, drugs, metabolic, retention, pain). The exam point is distinguishing it from dementia (acute + fluctuating + inattention + clouded consciousness) and finding/treating the cause.

A permanent, NON-PROGRESSIVE disorder of movement and posture from an injury to the developing brain (antenatal, perinatal — including hypoxic-ischaemic encephalopathy — or early postnatal). The motor disorder is static but its clinical expression changes with growth; comorbidities (epilepsy, learning disability) are common.

A granulomatous vasculitis of medium/large arteries (especially the branches of the external carotid) in the OVER-50s. A sight-threatening emergency: new headache, scalp tenderness and jaw claudication with a very high ESR. Treat with high-dose steroids IMMEDIATELY — before the biopsy — to prevent irreversible blindness.

An autoimmune disorder of the neuromuscular junction in which antibodies against presynaptic voltage-gated CALCIUM channels reduce acetylcholine release. The mirror image of myasthenia gravis: PROXIMAL weakness that IMPROVES with repeated use, with autonomic features, and a strong association with SMALL-CELL LUNG CANCER (paraneoplastic).

The commonest inherited peripheral neuropathy (hereditary motor and sensory neuropathy), usually autosomal dominant (PMP22 duplication in CMT1A). A slowly progressive, length-dependent motor-predominant neuropathy producing the classic distal wasting, pes cavus and an "inverted champagne bottle"/stork-leg appearance.

A group of neurodegenerative "atypical parkinsonism" syndromes that mimic Parkinson disease but have additional features and respond POORLY to levodopa: progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and corticobasal degeneration (CBD). The exam skill is spotting the red-flag feature that makes it "Parkinson-plus" rather than idiopathic PD.

A fluid-filled cavity (syrinx) expanding within the central spinal cord, often cervical and frequently associated with a Chiari I malformation. As it expands it first interrupts the decussating spinothalamic fibres, producing a classic DISSOCIATED sensory loss in a "cape" distribution — loss of pain/temperature with preserved light touch/proprioception.

Compression of the cervical spinal cord by degenerative changes (osteophytes, disc, ligamentum flavum) — the commonest cause of spinal cord dysfunction in older adults. An insidious, often painless, mix of upper-limb clumsiness/numbness and a spastic gait with UPPER motor neuron signs in the legs. Easily missed, and a delayed diagnosis costs recovery.

A chronic, disabling multi-system condition whose cardinal feature is post-exertional malaise — a disproportionate worsening of symptoms after activity, typically delayed by hours to days and taking a disproportionately long time to recover from. NICE NG206 (2021) reframed both the diagnosis and the management substantially.