Neurology

Reversible Cerebral Vasoconstriction Syndrome classically causes recurrent thunderclap headaches over days to weeks. Imaging can be normal early — the absence of an infarct doesn't exclude it — but it can progress to ischaemic stroke (often watershed territory), convexity SAH, or PRES-like vasogenic oedema, sometimes presenting with a new focal neurological deficit.

• Triggers: vasoactive/serotonergic substances (SSRIs, triptans, nasal decongestants, cannabis, other sympathomimetics), the postpartum period, and stress.
• Differential for the same clinical picture: aneurysmal SAH (always exclude first), primary angiitis of the CNS, migraine, idiopathic intracranial hypertension, mass lesion, and MS.
• Imaging: CT angiogram may show multifocal segmental vasoconstriction ("string of beads"); a localised convexal SAH (confined to a few sulci, not the basal cisterns) is a recognised RCVS finding. Catheter (digital subtraction) angiography remains the gold standard when the diagnosis is unclear.

• A well-demarcated extra-axial lesion — think meningioma. Intra-axial possibilities include abscess, cyst, and stroke; also consider hydrocephalus.
• Any patient with a VP shunt and a new headache: consider both shunt malfunction and an abdominal CSF pseudocyst — a recognised complication (roughly 1–5% of shunts) where CSF collects around the peritoneal catheter tip within a fibrous capsule.
• Cerebral venous sinus thrombosis in a patient with inflammatory bowel disease — IBD is a prothrombotic state, especially with active disease, and CVST needs to be actively excluded in this group.

Brief, severe, electric-shock-like facial pain in a trigeminal distribution, often triggered by light touch. Atypical features — younger age, bilateral pain, or sensory loss — should prompt MRI to exclude a secondary cause: stroke, mass effect from a tumour, or a vascular malformation/compressive vessel.

First-line medical therapy is carbamazepine (or oxcarbazepine); gabapentin, pregabalin and lamotrigine are alternatives or adjuncts. Refractory or secondary cases may need surgical options such as microvascular decompression.

Neurogenic (type 2) myocardial injury from a catecholamine surge and autonomic dysfunction can raise troponin after an acute stroke, sometimes with a stress-cardiomyopathy (Takotsubo) picture. The ECG and echo are often unremarkable — no significant wall motion abnormality — but don't assume this every time; a genuine concurrent ACS is still possible and should be considered on its own merits.

• Check an anti-factor Xa level if the patient is on a factor Xa inhibitor (apixaban, rivaroxaban) — this tells you whether they were actually therapeutically anticoagulated, which matters for both the likely mechanism and thrombolysis eligibility decisions.
• TTE (± TOE for higher sensitivity) to look for a cardioembolic source — LV or atrial thrombus, valvular disease, PFO.
• Review adherence and dosing, and consider whether a different agent or dose is warranted — don't assume the drug "failed" without checking these first.

Posterior circulation stroke, central vertigo and CVST can all present similarly — vertigo, headache, cerebellar signs. Look specifically for CVST features: a severe, worsening headache, new seizures, or focal neurological signs.

Primitive reflexes that re-emerge with frontal lobe dysfunction — a frontal lobe lesion (stroke, trauma, tumour), or diffuse processes like dementia, Parkinson's disease, or encephalopathy.

• Grasp, rooting and sucking reflexes.
• Palmomental reflex — stroking the thenar eminence causes contraction of the ipsilateral chin/mentalis muscle.
• Glabellar tap (Myerson's sign) — repetitive tapping on the glabella normally causes blinking that quickly habituates; persistent blinking that fails to habituate is classically associated with Parkinson's disease.

An upgoing (extensor) plantar response can be the earliest sign of an evolving UMN lesion, sometimes preceding other findings — don't dismiss it while other signs are still developing.

On finger tapping/finger fractionation testing, a progressive decrement in amplitude and speed with repetition is characteristic of Parkinsonian bradykinesia. A new stroke instead tends to cause a fixed reduction in speed and dexterity from the outset, without that progressive decrementing pattern.

• Symptoms and signs that don't localise to a single anatomical lesion, and are often inconsistent between examinations.
• Hoover's sign: weakness of hip extension on direct testing that resolves when the contralateral leg is actively flexed against resistance (involuntary hip extension) — a well-validated positive sign of functional leg weakness.
• A brisk crossed adductor reflex or palmomental reflex points toward organic UMN (pyramidal) pathology, which helps weigh against a purely functional presentation when the picture is ambiguous.

Blepharospasm — involuntary, often chronic contraction/blinking of the eyelids — is usually a primary focal dystonia (benign essential blepharospasm) rather than a functional disorder in its own right, though fatigue, stress and dry eyes can aggravate it.

Post-thrombolysis/thrombectomy monitoring: CT angiogram from the arch to the circle of Willis plus CT perfusion acutely, then a routine 24-hour non-contrast CT brain to check for haemorrhagic transformation.

Neuromyelitis optica spectrum disorder is a separate antibody-mediated astrocytopathy, not a subtype of MS — the distinction matters because some MS disease-modifying therapies can worsen NMOSD. Classic pattern: optic neuritis (often severe, sometimes bilateral or simultaneous) plus longitudinally extensive transverse myelitis (≥3 vertebral segments on MRI), associated with anti-aquaporin-4 antibodies. A related but distinct entity, anti-MOG antibody disease (MOGAD), is now classified separately.

Motor and sensory deficits below the lesion level plus autonomic (bladder/bowel) dysfunction. Get an urgent MRI spine to exclude a compressive cause (surgical emergency) before treating as inflammatory — causes include NMOSD, MOGAD, MS, para-/post-infectious myelitis, and idiopathic disease.

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy — a NOTCH3 mutation causing migraine with aura, recurrent subcortical strokes, cognitive decline and mood disturbance. Management is mainly supportive: vascular risk factor control and genetic counselling, as there's no disease-modifying therapy.

A large (>2 cm) demyelinating lesion that mimics a tumour on imaging, sometimes with mass effect and ring enhancement. Distinguishing it from neoplasm can be genuinely difficult radiologically, and biopsy is sometimes needed.

Cortical ribboning (linear cortical hyperintensity following the gyral ribbon on DWI/FLAIR) is classically taught for Creutzfeldt-Jakob disease (prion disease), and also occurs with other causes of cortical laminar necrosis such as severe hypoxic-ischaemic injury or status epilepticus.

A rare autoimmune endotheliopathy affecting the microvasculature of the brain, retina and inner ear — the triad of encephalopathy, branch retinal artery occlusion (visual disturbance, scotomas) and sensorineural hearing loss. Differential includes MS and CNS vasculitis.

• Metabolic/nutritional screen: B12, folate, iron studies, thiamine (B1), B6, vitamin D, vitamin E. Add serum caeruloplasmin/24-hour urinary copper and zinc where there's a relevant risk factor for copper deficiency (e.g. prior bariatric surgery, malabsorption, high-dose zinc supplementation) rather than as a routine screen for everyone.
• Infective causes: HIV and syphilis (tabes dorsalis) directly cause neuropathy; also consider recent infection as a Guillain–Barré trigger (Campylobacter, EBV, CMV, Zika) where the pattern is acute and ascending.
• MRI brain and spine if a central cause or myelopathy/radiculopathy mimic needs excluding.
• Nerve conduction studies/EMG to characterise demyelinating vs axonal pathology and localise the lesion.

• Autosomal dominant (CAG repeat expansion, with anticipation) — always check family history and involve genetic counselling.
• Psychiatric and cognitive change often precedes or accompanies the onset of chorea — this is not purely a movement disorder.
• Classic exam finding: the "jack-in-the-box" tongue — inability to sustain tongue protrusion, darting in and out involuntarily (motor impersistence).

• A positive Dix-Hallpike shows positional nystagmus with a latency and fatigability, and no other neurological findings — non-fatigable nystagmus or additional neuro signs point to a central cause instead.
• Start the Dix-Hallpike with the side the patient is less symptomatic on to establish a baseline before testing the suspected side.
• Posterior canal BPPV (the most common form) produces upbeating, torsional nystagmus on Dix-Hallpike, with the affected ear being the one facing down.

Diagnosed with the supine roll (Pagnini-McClure) test — geotropic nystagmus (beating toward the ground) is the more common canalithiasis variant, and the affected ear is the side that produces more intense nystagmus when turned.

• First-line treatment: the Lempert ("BBQ") roll — a sequence of 90° rolls totalling 360°, finishing sitting up.
• If that fails: the Gufoni manoeuvre — the patient lies quickly onto the unaffected side, the head is then turned 45° toward the floor and held, before sitting up.

"Sunsetting" eyes — downward eye deviation with visible sclera above the iris, from pressure on the dorsal midbrain — is a classic sign of raised intracranial pressure in infants, alongside a bulging fontanelle, rapidly increasing head circumference, developmental delay or regression, vomiting and irritability. Think hydrocephalus, intracranial haemorrhage, or a mass lesion.