Neurology: Neurological Emergencies (Complete)

• Overview: At a Glance | Reduced Consciousness and Coma | Acute Confusion (Delirium) | Raised Intracranial Pressure
• Headache: Acute Headache: Red Flags | Giant Cell Arteritis
• Infection: Bacterial Meningitis | Encephalitis
• Seizures: Status Epilepticus | First Seizure and Mimics
• Spine: Metastatic Spinal Cord Compression | Cauda Equina Syndrome | Spinal Abscess and Other Acute Myelopathies | Autonomic Dysreflexia
• Neuromuscular: Guillain–Barré Syndrome | Myasthenic Crisis
• Other emergencies: Head Injury | NMS and Serotonin Syndrome | Parkinson's Disease Emergencies
• Revision: Drug Reference Table | Spot the Emergency | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🧠 Neurological emergencies are a race against time - "time is brain". In status epilepticus, meningitis and spinal cord compression, delay means permanent disability or death. Stroke has its own chapter (Stroke Emergencies). This chapter is a practical guide to recognising them and acting in the first hours.
Your four questions for every patient: Is the airway safe, and what is the GCS? When was the patient last known to be well? Where is the lesion (brain, spinal cord, nerve, muscle)? Which time-critical treatment is needed - thrombolysis, antibiotics, anti-seizure drugs, steroids, surgery?

At a Glance

For stroke, TIA, intracerebral haemorrhage, subarachnoid haemorrhage and cerebral venous sinus thrombosis, see the Stroke Emergencies chapter.

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Reduced Consciousness and Coma

Assess: Use the Glasgow Coma Scale:

• Eyes: 1–4.
• Verbal: 1–5.
• Motor: 1–6 - the best predictor of outcome.

Report it as its parts (e.g. E2 V2 M5 = 9). GCS 8 or less usually means the airway is at risk.

Immediate actions - treat the reversible causes first:

• ABC; oxygen; recovery position or airway adjuncts.
• Capillary glucose - treat hypoglycaemia at once (IV thiamine first if alcohol or malnutrition is likely).
• Naloxone if opioid toxicity is possible (pinpoint pupils, slow breathing).
• Temperature - hypothermia, hyperthermia.
• Look for head injury, a rash (meningococcal), neck stiffness, needle marks, medical alert bracelets.
• Focal signs and pupils.

Causes:

• Structural: Stroke (especially basilar), intracerebral or subarachnoid haemorrhage, subdural or extradural haematoma, tumour, abscess, hydrocephalus.
• Metabolic and toxic (commonest - usually no focal signs, pupils reactive):
  • Hypoglycaemia; hyponatraemia; hypercalcaemia.
  • Hypercapnia; hypoxia.
  • Uraemia; liver failure.
  • Drugs and alcohol.
  • Sepsis; hypothyroidism; Wernicke's.
• Infection: Meningitis, encephalitis.
• Seizures: Post-ictal state, non-convulsive status epilepticus.

Pupils as clues:

• Pinpoint: Opioids, pontine haemorrhage.
• Unilateral fixed dilated: Third nerve compression from uncal herniation - a neurosurgical emergency.
• Bilateral dilated: Anticholinergic or sympathomimetic drugs, severe hypoxic injury.
• Reactive with no focal signs: Think metabolic or toxic.

Investigations:

• Blood gas (glucose, sodium, CO2, lactate, carboxyhaemoglobin).
• FBC, U&E, LFTs, calcium, ammonia, CRP, blood cultures.
• Paracetamol and salicylate levels; toxicology.
• CT head; ECG.
• LP if infection is possible (once safe); EEG if non-convulsive status is suspected.

💡 Clinical Pearl: Locked-in syndrome (basilar artery stroke) can look like coma - the patient is awake but cannot move. Always ask an apparently unresponsive patient to look up and down and blink: vertical eye movements may be preserved.

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Acute Confusion (Delirium)

What it is: An acute, fluctuating disturbance of attention and awareness caused by an underlying medical problem. It affects up to a third of older medical inpatients and is linked to longer stays, falls, institutional care and death. It is often missed - especially the quiet, hypoactive form.

Screen: The 4AT - a score of 4 or more suggests delirium. Get a collateral history: what is the person usually like?

Common causes - "PINCH ME":

• Pain.
• Infection (UTI, pneumonia, cellulitis, but also meningitis and encephalitis).
• Nutrition (and thiamine).
• Constipation; also urinary retention.
• Hydration and electrolytes (sodium, calcium, glucose).
• Medication - anticholinergics, opioids, benzodiazepines, steroids, new drugs; drug or alcohol withdrawal.
• Environment - ward moves, lack of glasses or hearing aids, sleep loss.
• Also: hypoxia, stroke, head injury (subdural), MI, organ failure.

Management (NICE CG103):

• Treat the causes.
• Supportive care: Reorientation, familiar faces, glasses and hearing aids, a calm environment, sleep, mobilisation, hydration and nutrition.
• Avoid restraints, unnecessary catheters and ward moves.
• Drugs only if the person is very distressed or a risk to themselves or others, and other measures have failed: e.g. haloperidol 0.5 mg, at the lowest dose for the shortest time.
• Avoid haloperidol in Parkinson's disease and dementia with Lewy bodies - seek specialist advice.
• Capacity: Assess decisions as they arise (Mental Capacity Act); involve family; consider safeguards if the person is deprived of liberty.

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Raised Intracranial Pressure

Mechanism: The skull is a closed box. A growing mass, swelling or blocked CSF flow raises the pressure inside, reducing brain blood flow. Eventually the brain is pushed through openings in the skull (herniation), which compresses the brainstem.

Causes:

• Haemorrhage.
• Large infarct.
• Tumour; abscess.
• Trauma.
• Hydrocephalus.
• Meningitis, encephalitis.
• Cerebral venous sinus thrombosis.
• Acute liver failure.
• Idiopathic intracranial hypertension (chronic).

Clinical pattern:

• Headache - worse on lying down, coughing or straining, and in the morning.
• Vomiting.
• Papilloedema.
• Falling GCS.
• Sixth nerve palsy (a "false localising" sign).
• Uncal herniation: Ipsilateral fixed dilated pupil (third nerve) and hemiparesis.
• Cushing's triad (late, pre-terminal): hypertension, bradycardia, irregular breathing.

Management:

• Urgent CT and neurosurgical referral.
• Head up 30°; keep the neck straight; avoid tight tube ties (they obstruct venous drainage).
• Airway: Intubate if GCS is 8 or less. Keep CO2 normal; brief hyperventilation only as a bridge to surgery.
• Osmotherapy: Mannitol (e.g. 0.25–1 g/kg IV) or hypertonic saline, per local protocol.
• Dexamethasone for oedema around a tumour or abscess - not for head injury or stroke.
• Treat seizures, fever and hyperglycaemia; maintain BP and oxygen.
• Definitive treatment: Evacuate the haematoma, drain the CSF (external ventricular drain), decompressive craniectomy, or remove the tumour.

⚠️ Safety Pearl: Never do a lumbar puncture when raised ICP or a mass lesion is possible (reduced GCS, focal signs, papilloedema, new seizures) until CT has excluded it - it can cause fatal herniation. Give antibiotics first if meningitis is suspected.

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Acute Headache: Red Flags

Most headaches are benign (migraine, tension-type). These features point to a dangerous cause:

• Thunderclap onset (maximum within about a minute) - SAH until proven otherwise (see the Stroke Emergencies chapter); also reversible cerebral vasoconstriction syndrome, artery dissection, pituitary apoplexy.
• Fever, neck stiffness, rash or confusion - meningitis or encephalitis.
• Features of raised ICP - worse lying down or on straining, vomiting, papilloedema: tumour, haemorrhage, CVST.
• New headache over 50, with jaw claudication or scalp tenderness - GCA.
• Pregnancy or postpartum - pre-eclampsia, CVST, pituitary apoplexy.
• New focal signs, seizures or altered consciousness.
• Immunosuppression or cancer - infection, metastases.
• Head injury, especially on anticoagulants - subdural haematoma.
• Painful red eye with haloes and vomiting - acute angle-closure glaucoma.
• Headache in several household members - carbon monoxide poisoning.
• Headache on standing, eased lying flat - low CSF pressure (after LP or spontaneous).

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Giant Cell Arteritis

Mechanism: Inflammation of medium and large arteries, especially branches of the carotid artery. The feared complication is sudden permanent blindness from ischaemic optic neuropathy, which often affects the second eye within days.

Who and what: Age over 50, with:

• New headache (often temporal).
• Scalp tenderness (pain combing hair).
• Jaw claudication (pain chewing).
• Visual symptoms - blurring, double vision, transient visual loss.
• Polymyalgia symptoms; fever, weight loss.
• A tender, thickened, pulseless temporal artery.

Investigations:

• ESR and CRP (usually raised).
• Fast-track temporal artery ultrasound (halo sign) or biopsy - within 1–2 weeks of starting steroids.

Treatment (BSR) - do not wait for test results:

• Without visual symptoms: Prednisolone 40–60 mg daily immediately.
• With visual loss or ischaemic visual symptoms: IV methylprednisolone (e.g. 500 mg–1 g daily for 3 days), or prednisolone 60 mg, and same-day ophthalmology review.
• Bone protection and a gastroprotection review.
• Taper steroids slowly over 12–18 months.
• Tocilizumab for relapsing or refractory disease (NICE TA518).

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Bacterial Meningitis

Mechanism: Bacterial infection of the meninges. In adults the commonest organisms are Streptococcus pneumoniae and Neisseria meningitidis; Listeria affects older, immunocompromised and pregnant people. Untreated, it kills within hours.

Clinical pattern:

• Headache, fever, neck stiffness, photophobia, vomiting.
• Altered consciousness; seizures; focal signs.
• Non-blanching rash - meningococcal disease; septic shock can occur with or without meningitis.
• Older and immunosuppressed people may only be confused or drowsy.

Immediate management (NICE NG240):

• Before hospital: If meningococcal disease is suspected (non-blanching rash), give benzylpenicillin IM or IV - but do not delay transfer.
• ABC; sepsis care (fluids for shock); senior review.
• Blood cultures and blood for meningococcal and pneumococcal PCR.
• Antibiotics within 1 hour of arrival - if the LP will be delayed more than about an hour, give antibiotics first:
  • Ceftriaxone 2 g IV every 12 hours (high dose).
  • Add amoxicillin 2 g IV every 4 hours for Listeria risk: aged 60 or over, immunocompromised, pregnancy, diabetes or alcohol dependence.
  • Penicillin allergy or recent travel to areas with resistant pneumococci: follow local microbiology advice.
• Dexamethasone (e.g. 10 mg dexamethasone phosphate, 8.3 mg dexamethasone base, IV every 6 hours) - start with or shortly after the first antibiotic dose. Continue for 4 days if pneumococcal (or H. influenzae) meningitis is confirmed; stop if another cause is found.
• Lumbar puncture when safe. CT first if there are:
  • Focal neurological signs.
  • Reduced GCS (e.g. 12 or below) or a falling GCS.
  • Papilloedema.
  • New seizures.
  • Immunocompromise.
  Do not do an LP in septic shock, coagulopathy or rapidly spreading purpura.
• Notify UKHSA (public health) urgently. Close contacts of meningococcal cases receive antibiotic prophylaxis (e.g. single-dose ciprofloxacin).

CSF interpretation:

⚠️ Safety Pearl: Never delay antibiotics for a CT scan or LP in suspected bacterial meningitis. Take blood cultures, give ceftriaxone (and dexamethasone), then investigate.

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Encephalitis

Mechanism: Inflammation of the brain tissue itself, usually from a virus (herpes simplex is the commonest treatable cause) or an autoimmune process.

Clinical pattern:

• Altered behaviour, personality change or confusion.
• Fever, headache.
• Seizures.
• Focal signs - dysphasia, hemiparesis.
• Reduced consciousness.
• Can be mistaken for psychiatric illness or delirium.

Management (ABN/BIA encephalitis guidance):

• IV aciclovir 10 mg/kg every 8 hours, started within 6 hours of arrival if encephalitis is suspected and results are not available. Use ideal body weight in obesity. Keep the patient well hydrated (it can cause kidney injury).
• LP (once safe): CSF lymphocytes, protein, glucose, and HSV PCR (plus VZV and enterovirus). HSV PCR can be negative in the first days - repeat it if suspicion remains.
• MRI - temporal lobe changes in HSV encephalitis.
• EEG - seizures, non-convulsive status.
• HIV test in everyone.
• Duration: At least 14 days for proven HSV encephalitis (21 days if immunocompromised), with repeat LP to confirm the PCR is negative.

Autoimmune encephalitis:

• Anti-NMDA receptor: Young women - psychiatric symptoms, seizures, abnormal movements, autonomic instability, reduced consciousness. Look for an ovarian teratoma.
• Anti-LGI1: Older adults - memory loss, faciobrachial dystonic seizures, hyponatraemia.
• Treatment: IV methylprednisolone, IV immunoglobulin or plasma exchange; remove any tumour.

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Status Epilepticus

Definition: A convulsive seizure lasting 5 minutes or more, or repeated seizures without recovery in between. Seizures become harder to stop and cause brain injury the longer they continue.

Immediate care:

• ABC - high-flow oxygen; protect from injury; recovery position after the seizure; do not put anything in the mouth.
• Check glucose - treat hypoglycaemia (IV thiamine first if alcohol or malnutrition is likely).
• Time the seizure.
• IV access; bloods including anti-seizure drug levels, U&E, calcium, magnesium, CK; blood gas.
• Look for causes:
  • Missed anti-seizure medication.
  • Alcohol withdrawal.
  • Infection.
  • Stroke; tumour; head injury.
  • Drug toxicity.
  • Hyponatraemia.
  • Eclampsia (pregnancy or postpartum - give magnesium sulfate).

Drug treatment (NICE NG217):

• First line - benzodiazepine (at 5 minutes):
  • IV lorazepam 4 mg (0.1 mg/kg, maximum 4 mg) if IV access and resuscitation facilities are available, or
  • Buccal midazolam 10 mg (or rectal diazepam 10–20 mg) in the community or without IV access.
  • Repeat once after 5–10 minutes if the seizure continues. Follow the patient's own emergency plan if one exists.
• Second line (if seizures continue after 2 doses of benzodiazepine) - one of:
  • Levetiracetam IV (e.g. 60 mg/kg, maximum 4.5 g, over about 10–15 minutes) - quick to give, with fewer side effects.
  • Phenytoin IV (20 mg/kg, no faster than 50 mg/minute, with ECG and BP monitoring).
  • Sodium valproate IV (40 mg/kg, maximum 3 g). Avoid in women and girls of childbearing potential unless there is no alternative (MHRA).
  If one fails, try another second-line drug with expert advice.
• Third line (refractory status, usually at about 30–60 minutes): General anaesthesia in ICU (e.g. propofol or midazolam infusion) with EEG monitoring, or phenobarbital.

Other points:

• Functional (dissociative) seizures can mimic status. Clues:
  • Eyes forcibly closed.
  • Side-to-side head movements, pelvic thrusting.
  • Fluctuating or very long episodes with preserved awareness.
  • No hypoxia or rise in lactate.
  If in doubt, treat - but avoid repeated escalating doses without senior review.
• Non-convulsive status epilepticus: Ongoing reduced consciousness or confusion after a seizure, with subtle twitching - needs an EEG.

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First Seizure and Mimics

Is it a seizure? The most important tool is an eyewitness account.

• Suggests an epileptic seizure:
  • Prolonged jerking.
  • Tongue bitten on the side.
  • Head turning.
  • Blue face.
  • Prolonged confusion afterwards (post-ictal).
  • Muscle aches.
• Suggests syncope:
  • A trigger (standing, pain, heat).
  • Warning (lightheaded, sweaty, tunnel vision).
  • Pallor.
  • Brief jerks lasting a few seconds ("convulsive syncope").
  • Rapid recovery.
• Exertional collapse, palpitations or an abnormal ECG: Think cardiac syncope - arrhythmia, long QT. See the Cardiac Emergencies chapter.

Assessment:

• Look for provoking causes: Hypoglycaemia, hyponatraemia, hypocalcaemia, alcohol or benzodiazepine withdrawal, drugs (tramadol, bupropion, recreational drugs), head injury, infection.
• 12-lead ECG in everyone.
• Bloods; CT head if there is head injury, focal signs, persistent confusion, anticoagulation or immunosuppression.

After a first unprovoked seizure (NICE NG217):

• Refer to a specialist (first seizure clinic), to be seen within 2 weeks.
• MRI and EEG as directed by the specialist.
• Do not usually start anti-seizure medication after a single seizure without specialist advice.
• Safety advice: No bathing alone (shower instead), no swimming alone, care with heights, cooking and machinery.
• Driving (DVLA group 1): Must stop driving and inform the DVLA - usually 6 months off driving after a first unprovoked seizure (longer if a high recurrence risk, and 12 months for epilepsy).

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Metastatic Spinal Cord Compression

Mechanism: Cancer spreads to a vertebra (or epidural space) and compresses the spinal cord or cauda equina. It is the first presentation of cancer in about a quarter of cases. Outcome depends on function at diagnosis - patients who can walk at diagnosis usually keep walking.

Common primaries: Breast, prostate, lung, kidney, myeloma.

Red flags for spinal metastases (in someone with cancer, or at risk of cancer):

• Thoracic back pain.
• Progressive, severe or unremitting pain.
• Pain worse on lying flat, coughing or straining, or at night.
• Band-like pain around the chest or abdomen.
• Localised spinal tenderness.

Neurological signs of compression:

• Leg weakness, difficulty walking.
• A sensory level.
• Bladder or bowel dysfunction (often late).

Management (NICE NG234):

• Contact the acute oncology / MSCC coordinator immediately.
• Whole-spine MRI - urgently, and immediately if there are neurological symptoms or signs.
• Dexamethasone 16 mg daily (orally or IV, in the morning) with a PPI, unless lymphoma is suspected (steroids can prevent diagnosis). Monitor glucose.
• Flat bed rest with spinal alignment if there is pain suggesting spinal instability, until assessed.
• Definitive treatment: Surgical decompression and stabilisation (for suitable patients - instability, single-level disease, good prognosis) or radiotherapy.
• Analgesia; VTE prevention; bladder and bowel care; rehabilitation.

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Cauda Equina Syndrome

Mechanism: Compression of the nerve roots below the end of the spinal cord (L1–L2), most often by a large central disc prolapse. Other causes include tumour, epidural abscess, haematoma and trauma. Delay can leave permanent bladder, bowel and sexual dysfunction.

Red flags - any of these with back pain or sciatica:

• Bilateral sciatica or bilateral leg symptoms.
• Saddle (perineal) numbness - "numb when wiping".
• Bladder dysfunction - difficulty starting, reduced sensation, painless retention, overflow incontinence.
• Bowel dysfunction - loss of control or sensation.
• Sexual dysfunction - new erectile problems, reduced genital sensation.
• Reduced anal tone or sensation on examination (a late sign).

Management:

• Bladder scan - a large post-void residual (e.g. above about 200 mL) supports the diagnosis.
• Emergency MRI of the lumbosacral spine - the national pathway (GIRFT) aims for MRI within about 4 hours of request, 24/7.
• Urgent spinal surgical review and decompression.
• Safety-netting: Patients with back pain and sciatica who are sent home must be told the red flags in plain language, and to return immediately if they occur.

💡 Clinical Pearl: By the time painless urinary retention or a lax anal sphincter appears, the damage is often permanent. Act on early symptoms - bilateral sciatica, altered saddle sensation, or subtle bladder change.

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Spinal Abscess and Other Acute Myelopathies

• Spinal epidural abscess:
  • Who: People who inject drugs; diabetes; immunosuppression; S. aureus bacteraemia; recent spinal procedures or epidural.
  • Features: Back pain, fever and progressive neurological deficit. The full triad is often absent early.
  • Tests: Raised CRP and ESR; blood cultures; contrast MRI of the whole spine.
  • Treatment: IV antibiotics covering S. aureus (per local guidance, until cultures are known); urgent surgical decompression if there is a deficit.
• Acute transverse myelitis:
  • Inflammation of the cord - MS, neuromyelitis optica spectrum disorder (AQP4 antibodies), MOG antibody disease, infection, or idiopathic.
  • Weakness, a sensory level and bladder problems developing over hours to days.
  • MRI; LP; antibodies.
  • High-dose IV methylprednisolone; plasma exchange if severe.
• Spinal cord infarction: Sudden back pain and paraplegia - after aortic surgery or aortic dissection. Look for the aorta!
• Traumatic cord injury: Immobilise the spine; maintain BP (neurogenic shock - hypotension with bradycardia); spinal injuries unit.
• Spinal haematoma: On anticoagulants, or after an epidural or LP - emergency MRI and decompression.

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Autonomic Dysreflexia

Mechanism: In people with a spinal cord injury at or above T6, a stimulus below the injury (most often a full bladder or blocked catheter) triggers a massive, uncontrolled sympathetic surge. Signals from the brain that would normally calm it cannot get past the injury.

Clinical pattern:

• Sudden severe hypertension - even a modest rise can be dangerous, as resting BP is often low.
• Pounding headache.
• Flushing and sweating above the injury; pale, cold skin below.
• Bradycardia; nasal congestion; anxiety.
• Risk of stroke, seizures and death.

Management:

• Sit the patient up and lower the legs; loosen tight clothing and leg bags.
• Find and remove the trigger:
  • Bladder - check or change the catheter, or catheterise.
  • Bowel - constipation (use lidocaine gel before rectal examination).
  • Pressure sores, ingrown toenails, tight clothes.
  • Fractures; labour.
• If BP stays high: A fast-acting antihypertensive - e.g. sublingual GTN or immediate-release nifedipine, per spinal injuries unit guidance.
• Monitor BP closely; seek spinal injuries unit advice. Many patients carry an autonomic dysreflexia card.

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Guillain–Barré Syndrome

Mechanism: An acute immune attack on peripheral nerves, often 1–4 weeks after an infection (Campylobacter diarrhoea, respiratory viruses, CMV, Zika).

Clinical pattern:

• Progressive, symmetrical weakness - usually starting in the legs and ascending - over days to 4 weeks.
• Reduced or absent reflexes.
• Tingling and often back or limb pain.
• Facial and bulbar weakness.
• Respiratory muscle weakness - about 1 in 4 need ventilation.
• Autonomic instability: Arrhythmias, BP swings, ileus, urinary retention.
• Miller Fisher variant: Ophthalmoplegia, ataxia and areflexia; anti-GQ1b antibodies.

Investigations:

• Nerve conduction studies.
• LP: Raised protein with a normal cell count ("albuminocytological dissociation") - can be normal in the first week.
• Exclude mimics: spinal cord compression (MRI), hypokalaemia, hypophosphataemia, myasthenia, botulism, porphyria.

Management:

• Monitor FVC regularly (e.g. every 4–6 hours, or more often if declining). Saturations fall late.
• ICU referral if FVC is below 20 mL/kg or falling quickly, there is bulbar weakness or aspiration, or the patient has autonomic instability.
• IV immunoglobulin 0.4 g/kg daily for 5 days (or plasma exchange) - for people who cannot walk unaided, ideally within 2 weeks of onset.
• Steroids do not help.
• Supportive:
  • Cardiac monitoring.
  • VTE prophylaxis.
  • Neuropathic pain relief.
  • Pressure care; bowel and bladder care.
  • Swallow assessment.
  • Psychological support.
  • Rehabilitation.

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Myasthenic Crisis

Mechanism: Myasthenia gravis is an autoimmune attack on acetylcholine receptors (or MuSK) at the neuromuscular junction. In a crisis, weakness of breathing and swallowing muscles needs ventilatory support.

Triggers:

• Infection; surgery; pregnancy.
• Starting high-dose steroids.
• Stopping or reducing treatment.
• Drugs:
  • Aminoglycosides, macrolides, fluoroquinolones.
  • Magnesium.
  • Beta-blockers.
  • Some anaesthetic agents, immune checkpoint inhibitors.

Clinical pattern:

• Fatigable weakness - worse with repetition and through the day.
• Ptosis, diplopia.
• Bulbar weakness - nasal speech, choking, weak cough.
• Neck flexion weakness.
• Breathlessness, especially lying flat.

Management:

• Serial FVC and swallow assessment; ICU if FVC is below 20 mL/kg, there is bulbar weakness, or hypercapnia.
• IV immunoglobulin or plasma exchange - plasma exchange may work faster.
• Stop or avoid trigger drugs; treat infection with "safe" antibiotics.
• Pyridostigmine is often paused if the patient is ventilated (it increases secretions), then restarted.
• Steroids are started or increased cautiously - they can worsen weakness for the first 1–2 weeks.
• Cholinergic crisis (rare - excess pyridostigmine) causes weakness with sweating, salivation, small pupils, diarrhoea and fasciculations.
• Look for a thymoma (CT chest).

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Head Injury

Assessment:

• ABCDE with cervical spine protection.
• GCS and pupils.
• Mechanism of injury.
• Loss of consciousness and amnesia.
• Vomiting; seizures.
• Anticoagulant or antiplatelet use.
• Look for signs of basal skull fracture: "panda eyes", Battle's sign (bruising behind the ear), CSF leak from the nose or ear, blood behind the eardrum.

CT head within 1 hour (NICE NG232) for adults with any of:

• GCS below 13 on initial assessment, or below 15 at 2 hours after the injury.
• Suspected open or depressed skull fracture.
• Any sign of basal skull fracture.
• Post-traumatic seizure.
• Focal neurological deficit.
• More than one episode of vomiting.

CT head within 8 hours if there has been loss of consciousness or amnesia, plus any of:

• Age 65 or over.
• Bleeding or clotting disorder.
• Dangerous mechanism (e.g. fall from height, pedestrian hit by vehicle).
• More than 30 minutes of retrograde amnesia.

People taking anticoagulants: Consider CT within 8 hours even without other indications (NICE NG232).

Types of bleed:

• Extradural haematoma:
  • Usually a temporal bone fracture tearing the middle meningeal artery.
  • Classically a lucid interval followed by rapid deterioration.
  • Biconvex (lens-shaped) on CT.
  • Emergency surgery.
• Acute subdural haematoma: Torn bridging veins; crescent-shaped on CT; often with brain injury - high mortality.
• Chronic subdural haematoma:
  • Older people, alcohol, anticoagulants - often after a trivial or forgotten fall.
  • Weeks of fluctuating confusion, headache, drowsiness or falls.
  • Neurosurgical drainage (burr holes) if symptomatic.
• Traumatic subarachnoid haemorrhage and contusions.

Management:

• Neurosurgical referral for significant bleeds, a falling GCS or skull fractures.
• Reverse anticoagulation for intracranial bleeding.
• Avoid hypoxia and hypotension (both worsen brain injury).
• Discharge with written head injury advice and a responsible adult - return if drowsiness, vomiting, worsening headache, confusion, weakness or seizures develop.

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NMS and Serotonin Syndrome

Both are drug-induced emergencies with fever, rigidity and autonomic instability. They are told apart by the drug, the speed of onset and the neuromuscular signs:

Severe hyperthermia (above 41°C) in either needs ICU - sedation, paralysis and ventilation may be needed. Avoid physical restraint.

Other causes of drug-induced hyperthermia:

• Malignant hyperthermia - volatile anaesthetics or suxamethonium; treat with dantrolene.
• Anticholinergic toxicity - dry, flushed skin, urinary retention, delirium.
• Sympathomimetics - cocaine, amphetamines.

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Parkinson's Disease Emergencies

• Missed or delayed doses: People with Parkinson's can deteriorate within hours if doses are late. They become rigid, unable to swallow, and at risk of aspiration, falls and delirium. Give medication on time - within 30 minutes of the usual time ("Get It On Time").
• Nil by mouth (surgery, stroke, vomiting):
  • Give levodopa via an NG tube (dispersible preparations).
  • Or use a rotigotine transdermal patch, using a dose conversion calculator and specialist advice.
  • Never just stop treatment.
• Parkinsonism–hyperpyrexia syndrome: An NMS-like state (rigidity, fever, high CK, confusion) after sudden withdrawal of dopaminergic drugs. Restart the drugs urgently; supportive care in HDU.
• Avoid dopamine-blocking drugs:
  • Haloperidol and most other antipsychotics.
  • Metoclopramide, prochlorperazine.
  For nausea, use domperidone (check QT) or ondansetron (avoid with apomorphine). For agitation or hallucinations, seek specialist advice (low-dose quetiapine or clozapine are sometimes used).
• Acute confusion or hallucinations: Look for infection, constipation, retention and drug changes before reducing Parkinson's medication.
• Deep brain stimulation: Contact the DBS team before MRI or diathermy. Sudden device failure can cause severe symptoms.