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Tim Raine

, George Collins

, Catriona Hall

, Nina Hjelde

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, Stephan Sanders

, and Simon Eccles

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► Coma and reduced GCS emergency

►► Call for senior help early if patient unwell or deteriorating.

Airway and C-spine

  • Stabilize cervical spine if there is any risk of injury (eg fall)

  • Look inside the mouth, remove obvious objects/dentures

  • Listen for upper airway compromise (gurgling, stridor, snoring)

  • Wide-bore suction under direct vision if secretions present

  • Jaw thrust/chin lift; oro/nasopharyngeal airway if tolerated.


  • 15L/min O2 if SOB/sats <94%; beware if previous COPD/CO2 retainer

  • If hypoxic Neurology p. [link]

  • Monitor O2 sats and RR

  • Bag and mask ventilation if poor/absent respiratory effort.


  • Venous access, take bloods:

    • VBG, FBC, U+E, LFT, glucose, Ca2+, troponin, clotting, G+S, bld cultures, paracetamol, salicylate and alcohol levels

  • ecg and treat arrhythmias (tachy Neurology p. [link]; brady Neurology p. [link])

  • Start IV fluids if shocked

  • Monitor HR, cardiac trace and BP.


  • Check blood glucose

  • Check for sedatives:

    • Opioids, benzodiazepines, antihistamines, TCAs, baclofen, alcohol

  • Control seizures (Neurology p. [link])

  • Check GCS (Box 11.1), pupil reflexes, limb tone, plantar responses, neuro obs:

    • look for brainstem, lateralizing or meningeal signs (see Table 11.1)

  • Call anaesthetist for airway support if GCS ≤8 or airway concerns.

Table 11.1 Common causes of reduced GCS




May have shallow, slow breathing, pinpoint pupils suggests opioids, ↑↑RR suggests salicylates

Brainstem dysfunction

  • Eyes dilated or slow reacting pupil (unilateral or bilateral), absent corneal reflex, eyes looking in different directions (III, IV, VI lesion), eyes fixed: doll’s head movements (not drifting back to forwards gaze when neck rotated)

  • Swallow water not swallowed spontaneously/no gag reflex

  • Respiration apnoeas, gasping, irregular, or Cheyne–Stokes breathing (alternating rapid breathing and apnoeas)

  • Body increased tone and upgoing plantars unilaterally/ bilaterally/crossed

Lateralizing (cerebral dysfunction)

Facial asymmetry, asymmetrical tone, and plantar responses


Neck stiffness, photophobia, Kernig’s sign, Brudzinski’s sign, straight leg raise (Neurology p. [link])


  • Check temperature

  • Look over whole body for evidence of injury or rashes

  • Ask ward staff for a brief history and check medical notes

  • Examine patient brief RS, CVS, abdo, and neuro exam

  • ABG, but don’t leave the patient alone

  • Request urgent portable CXR

  • Stabilize and treat, see following sections

  • Call for senior help

  • Reassess, starting with A, B, C …


  • Get senior help

  • Treat hypoxia with O2, airway aids, ±ventilation

  • Treat arrhythmias and hypotension urgently

  • Start broad-spectrum antibiotics if sepsis suspected (?meningitis)

  • Treat simple metabolic/intoxication abnormalities:

    • glucose <3.5mmol/L, give 100mL of 20% glucose STAT

    • glucose >20mmol/L, 0.9% saline 1L IV STAT (consider DKA/HHS)

    • opioids (pinpoint pupils and ↓RR), naloxone 0.4mg IV/IM STAT

    • history of chronic alcohol excess, Pabrinex® 2 pairs IV over 10min

    • benzodiazepine overdose alone, flumazenil 200micrograms IV.

Further management

  • Check brainstem function (see Table 11.1):

    • normal stabilize the patient and get an urgent CT head

    • gradual-onset dysfunction consider mannitol and urgent CT head

    • rapid-onset dysfunction give mannitol, normalize PaCO2 with ventilator and contact a neurosurgeon urgently; the patient’s brain is probably herniating due to ↑intracranial pressure

  • If ctnormal consider LP to test for meningitis or encephalitis

  • If CT and LP normal the cause is probably metabolic or intoxication.

Coma and reduced GCS

Think about

No focal neurology

↓O2, ↑CO2, low BP, metabolic (↑/↓glucose, Na+, Ca2+, K+; acidosis/alkalosis, renal/liver failure/decompensation, constipation), overdose (alcohol, opioids, TCAs, benzodiazepines), epilepsy/post-ictal, hypothermia, ↑temp, hypothyroid, malignant HTN.

Brainstem dysfunction or lateralizing signs

CVA, tumour, abscess, haematoma, hypoglycaemia or rarely other metabolic abnormalities.


Meningitis, encephalitis, subarachnoid haemorrhage.

Ask about

(notes, relatives, contacts, nurses) Baseline, speed of onset, headache, chest pain, palpitations, vomiting, seizures, weight loss;


Cardiac, respiratory, DM, kidney, liver, psychiatric, stroke/TIA, seizures, dementia;


Elicit PMH from DH, consider the possibility of overdose;


Alcohol, recreational drugs (overdose or withdrawal).


GCS (Table 11.2), temp, BP, HR, O2 sats, O2 requirements, RR, pupil size.

Table 11.2 GCS scoring (3/15 minimum)


Open spontaneously



Obeys commands


Open to command


Localizes pain


Open to pain


Flexes/withdraws to pain


No response


Abnormal flexion to pain



Talking and orientated


Extension to pain




No movement


Inappropriate words


Incomprehensible sounds


No vocalizations


Source: data from Teasdale G, Jennett B. Lancet 1974 304:81–4.

Originally described in 1974 as a 14-point scale (omitting ‘abnormal flexion’) by neurosurgeons at the University of Glasgow for use in patients with head injuries, this revised scale is now widely used in acute medicine and trauma.

Look for


Rate, depth, distress, added sounds, air entry on both sides;




Rigidity, pulsatile mass, organomegaly; distension;


Pupil responses, papilloedema (late sign), limb tone, plantars;


Rashes, injection marks, trauma;





FBC, U+E, LFT, Ca2+, glucose, troponin, CRP, clotting, bld cultures, toxicology screen (paracetamol, salicylate, alcohol);


pH, ↓O2 or ↓↑CO2;




Evidence of aspiration; CT if the patient has focal neurology or there is no clear diagnosis then an urgent CT head is required, the patient may need to be intubated first;


Faecal impaction;


After a CT scan if CT normal.

► Adult seizures emergency

Neurology While seizures and their consequences are dangerous for patients and anxiety provoking for doctors, they are often self-limiting and over-treatment has risks. To begin with stay calm, keep the patient safe, start timing, observe, gather information, check CBG, and plan ahead. Afterwards, document exactly what you saw.

►► Call for senior help if seizure >5min. All timings are from the start of the first fit; the clock only restarts once the patient has been fit-free for >30min.


  • Start timing; this is very important and easy to forget

  • 15L/minO2 in all patients

  • Keep patient safe and put into recovery position if possible

  • Monitor HR, O2 sats, BP, cardiac trace, temp

  • Venous access (after 3–4min). Take bloods:

    • FBC, U+E, LFT, CK, Ca2+, glucose, bld cultures, AED levels

  • Checkglucose: if <3.5mmol/L give 100mL of 20% glucose STAT (Box 11.2).


  • Call for senior help and attach a cardiac monitor

  • Consider an airway adjunct but do not force teeth apart

  • If IV access: lorazepam 4mg IV/2min, repeat at 10min if no effect

  • If no IV access: diazepam 10mg PR or 5–10mg buccal midazolam, repeat every 10min if no effect up to 3 doses

  • Ask ward staff about history/check notes

  • If alcoholism/malnourished, Pabrinex® 2 pairs IV if not already.


  • Call for anaesthetist and senior help

  • If not taking phenytoin: phenytoin 20mg/kg IV at <50mg/min

  • If taking phenytoin: phenobarbital 10mg/kg IV over 10min (max 1g)

  • Monitor ECG, BP, and temp.


  • Thiopental or propofol on ICU/HDU

  • Transfer to ICU for general anaesthetic, intubation, EEG monitoring.

► Paediatric seizures emergency

►► Call for senior help in all children having a seizure. All timings are from the start of the first fit; the clock only restarts with a fit-free period of >30min.

Step 1

  • Start timing; this is very important and easy to forget

  • Maintain airway, assess ABC, check pupil size, posture, neck stiffness, fontanelle, temp, and for rashes

  • 15L/min O2 in all patients

  • Check glucose: if <3.5mmol/L give 2mL/kg of 10% glucose STAT (Box 11.3):

    • take 10mL of clotted blood and one fluoride bottle (Neurology pp. [link][link]) prior to giving glucose, but don’t let this delay treatment

  • Keep patient safe, be alert for vomit occluding the airway

  • Monitor HR, O2 sats, BP, cardiac trace, temp

  • Venous access, take bloods:

    • FBC, U+E, LFT, CRP, Ca2+, Mg2+, glucose, bld cultures, anticonvulsant levels (if on anticonvulsants), venous blood gas

  • If IV access: further lorazepam 0.1mg/kg IV (max 4mg)

  • If no IV access: diazepam 0.5mg/kg PR (max 10mg)

  • Ask parents or ward staff about history/check notes.

Step 2 (10min after either lorazepam/diazepam)

  • If IV access: further lorazepam 0.1mg/kg IV (max 4mg)

  • If no IV access: paraldehyde 0.4mL/kg PR with 0.4mL/kg olive oil or 0.8mL/kg of a pre-prepared 50:50 solution (max 20mL of mixture).

Step 3 (10min after either lorazepam/paraldehyde)

  • Call for anaesthetist and senior help

  • Paraldehyde 0.4mL/kg PR as above unless already given

  • If not on phenytoin: phenytoin 20mg/kg IV/IO at <50mg/min

  • If on phenytoin: phenobarbital 20mg/kg IV/IO over 20min.

Step 4 (20min after either phenytoin/phenobarbital)

  • Rapid sequence intubation

  • Consider mannitol, pyridoxine, paracetamol, diclofenac.


Think about

► Life-threatening

See Box 11.2;

Most likely

Idiopathic (>50%), epilepsy, alcohol withdrawal, hypoglycaemia, hypoxia, trauma;


Kidney or liver failure, pseudoseizures, overdose (tricyclics, phenothiazines, amphetamines);


Brief limb jerking during a faint, rigors, syncope, arrhythmias. See Table 11.3.

Table 11.3 Common causes of transient loss of consciousness




Epileptic seizure (Neurology p. [link])

Known epilepsy, may have aura, post-ictal confusion/weakness

Often normal, may have tongue or limb trauma

Often normal, may have focal lesion or metabolic cause

Alcohol withdrawal (Neurology p. [link])

Usually >50units/wk alcohol consumption, last drink >24h ago

Anxious, sweaty, tachycardic, tremor ±chronic liver failure

↑MCV and γ‎GT; ↓platelets, mild anaemia


Unusual features, short duration, memory of event

Responsive to pain, normal respiration, no injuries

Normal investigations


Feels cold/hot, no LOC, coarse shaking, infective symptoms

Febrile, source of infection (eg UTI, pneumonia), no injury

↑WBC, NØ or LØ and CRP, +ve urine dipstick

Eclampsia (Neurology p. [link])

Pregnant, may be unaware

↑BP, palpable uterus, peripheral oedema

Proteinuria, foetal heart on Doppler

Transient arrhythmia/Stokes–Adams

Palpitations, pale, sudden LOC ±limb jerking; rapid recovery with flushing

Evidence of cardiac disease, injury following fall, irregular/absent pulse during attack

Arrhythmia or heart block on ECG, 24h ECG and BP monitoring, echo


Excessive daytime sleepiness, collapse, sleep paralysis ±hallucinations

Often normal; loss of postural muscle tone and tendon reflexes during attacks

HLA typing, sleep studies

Vasovagal syncope (Neurology p. [link])

Feels light-headed ±hot, then collapse while standing, ±fine limb jerking, ±urinary incontinence, rapid recovery, no post-ictal phase

Bradycardia and hypotension during episode, GCS 15/15 within min, no focal neurology

±postural drop (systolic drop of 20mmHg or more)

Ask about

Get a detailed description of the fit from anyone who witnessed the episode (see Boxes 11.4 and 11.5); headache, antecedent head trauma, chest pain, palpitations, SOB, alcohol withdrawal;


previous seizures, cerebrovascular/cardiac/respiratory/hepatic/renal/psychiatric disease, DM, alcohol, pregnancy, surgeries;


Anticonvulsants, hypoglycaemics, benzodiazepines;


Occupation, driving, hobbies, social support, alcohol intake, last drink, illicit drugs, recent travel;




GCS, temp, CBG (recheck), BP, O2 sats, alcohol withdrawal score.

Look for

Sweating, tremor, head injury, tongue biting, neck stiffness, papilloedema, focal neurology, urinary or faecal incontinence, pregnancy, infection, limb trauma (eg posterior dislocation of shoulder).



VBG, FBC, U+E, LFT, glucose, Ca2+, Mg2+, blood cultures, anticonvulsant levels;


If hypoxia or metabolic upset suspected;


Consider drug screen, β‎-hCG if pre-menopausal ♀;


To exclude dysrhythmia;


May show a focal lesion, ↑ICP, haemorrhage or infarction, perform as urgent if the patient has a persistent GCS <15 post-fit, focal neurology or if the seizure was <4d post-trauma;


Is the neuroimaging of choice in suspected epilepsy;


If meningitis or encephalitis suspected;


May help to exclude encephalitis or as out-patient investigation for epilepsy.


Stop seizure using treatment outlined on Neurology p. [link]. Correct metabolic upset (glucose, Mg2+, Ca2+, Na+) and exclude life-threatening causes while trying to establish the cause (Box 11.6). Secure airway if still fitting or GCS ≤8. Consider specialist opinion, moving ward, and ITU.


(Neurology OHCM10 p. 490.)1

Neurology Abnormal and unprovoked discharge of a group of neurons causes a seizure. Epilepsy is the recurrence of ≥2 such seizures.


Depends on which neurons are misfiring and when. Classify seizures based on a careful history and close observation. The 2017 system uses simpler language but you should still know the old terms:

Onset and evolution

  • Focal Start unilaterally in a focal area of brain giving stereotyped motor, sensory, or autonomic symptoms (previously ‘partial’)

  • Generalized Start bilaterally in both cerebral hemispheres. Always result in reduced awareness (previously ‘primary generalized’)

  • Focal into generalized Previously ‘secondary generalized’ seizures.


This is important as conscious level impacts on their safety.

  • Focal aware Focal symptoms but awareness remains completely intact. Previously referred to as a ‘simple partial’ seizures

  • Focal impaired awareness Awareness not always present (including a vague lack of awareness). Previously ‘complex partial’ seizures.

Motor involvement

  • Focal motor Focal seizure with movement (eg twitching, jerking)

  • Focal non-motor Affects sensation, emotion, thinking, or experience

  • Generalized motor Either ‘other motor’ or a tonic–clonic seizure (ie initial tonic whole body spasm followed by a clonic jerking phase)

  • Generalized non-motor Absence seizures; the stopping of activity with staring/eye-rolling and sometimes lipsmacking; usually <45s.


↓GCS, tongue trauma, limb weakness, incontinence, Todd’s paresis (transient weakness following a seizure; mimics a TIA), post-ictal state.


Often normal; MRI and EEG (±provocation) may aid diagnosis and seizure classification. Consider EEG/video telemetry.


Changing AEDs should be by specialists. Beware some drugs lower seizure thresholds (fluoroquinolones, cephalosporins, penicillins, pethidine, tricyclics, clozapine). Consider NG/IV AEDs if they are NBM.

Alcohol withdrawal

Always consider the possibility of alcohol withdrawal as a cause or provoking factor for seizures (Neurology p. [link]).

Post-traumatic seizures

Seen in more severe traumatic brain injury, where AEDs are often used prophylactically. Arrange an urgent ct scan if not already done; if haematoma seen (Neurology p. [link]), contact a neurosurgeon, otherwise hourly neuro obs and reassess if ↓gcs.

Neurodegenerative disorders

Parkinson’s disease

(Neurology OHCM10 p. 494.)2

Neurology Common neurological disorder (affectsNeurology 1% of >60yr). Cardinal features include resting tremor, rigidity, and bradykinesia.

Symptoms and signs

Coarse resting tremor (‘pill rolling’, unilateral at onset); rigidity (‘cog-wheeling’); falls, festinant gait; small handwriting, depression, impulsivity, speech/swallow problems; sensation normal.


Clinical diagnosis; single-photon emission CT if indistinguishable from benign essential tremor; exclude other causes of ‘Parkinsonism’, eg drug induced (haloperidol). Refer to specialist early if suspected.


MDT (PD doctors, specialist nurses, PT, OT, SALT). Anti-parkinsonian medications should be started, titrated, and amended by specialists. Levodopa enhances dopamine transmission but effectiveness reduces after some years. First line is either levodopa with a peripheral dopa-decarboxylase inhibitor (eg carbidopa) if symptoms interfere with lifestyle, or a choice of levodopa, dopamine agonists (eg ropinirole), or monoamine-oxidase inhibitors (eg selegiline) if they do not. Problematic ‘on-off’ and ‘end-of-dose’ phenomena with levodopa may require the addition of a MAO-B inhibitor, dopamine agonist, or COMT-inhibitor (eg tolcapone). Administration is at strict times, so drug chart timings may need changing.


Depression, dementia (late stage): Parkinson’s disease may have pathological overlap with Lewy body dementia (Neurology p. [link]) with movement and cognitive dysfunction coming at contrasting stages in each disease.

Parkinson’s-plus syndromes

These share some features of Parkinson’s (eg multisystem atrophy: Parkinson’s plus autonomic and cerebellar dysfunction; progressive supranuclear palsy: Parkinson’s plus impaired upwards gaze). These tend to be refractory to standard therapy.

Motor neuron disease

Neurology Degenerative disease affecting upper and lower motor neurons.3


Primarily clinical but EMG can help. Progressive motor weakness (UMN and LMN Neurology p. [link]) and behavioural change; sensation unaffected. Fasciculations progress to spasticity, poor swallow, and dementia.


Supportive. Early referral to neurology-led MDT care including MND nurse, PT, OT, SALT, palliative care, and dietetics is vital.4 Quinine and baclofen for cramps. Exercise programmes. Prognosis 3–5yr.


Aspiration, respiratory failure, frontotemporal dementia.

Huntington’s disease

Neurology Incurable inherited (autosomal dominant) disorder characterized by involuntary limb movements (chorea), dementia, and behavioural disturbance (depression, psychoses). Onset at 30–50yr.

Friedreich’s ataxia

Neurology Inherited (autosomal recessive) disorder characterized by progressive limb and gait ataxia, dysarthria, loss of proprioception, absent tendon reflexes in the legs, and extensor plantar responses. Inability to walk occurs ~15yr after disease onset. May also develop heart failure and DM. Supportive management.

► Stroke/CVA/TIA emergency

►► Call for senior help early. Patient may need urgent aspirin, thrombolysis, thrombectomy, or transfer to Hyperacute Stroke Unit (HASU).

If gcs is reduced Neurology pp. [link][link].

  • 15L/min O2 if SOB or sats <94%

  • Check blood glucose; treat if too low (Neurology p. [link]) or high (Neurology p. [link])

  • Check temp; treat if too low (blankets) or high (IV/PR paracetamol)

  • Monitor O2 sats, RR, HR, cardiac trace, temp and BP

  • Venous access, FBC, ESR, U+E, LFT, lipids, CBG, trop, coag, G+S:

  • NBM and start IV fluids for hydration (eg 0.9% saline at 100mL/h)

  • ECG looking for atrial fibrillation, flutter or arrhythmia.

  • Take a focused history particularly:

    • exact start time and progression (worsening, static, or improving)

    • intracranial pathology, clotting problems, bleeding (eg GI/PV), pregnancy, trauma/invasive procedures/surgery/thrombolysis

  • Examination: RS, CVS, abdo. Document exact neuro findings

  • Request urgent CT head ±CT angiogram ±CT perfusion scan

  • Consider aspirin/thrombolysis/thrombectomy after CT (Boxes 11.7–11.9)

  • Reassess, starting with A, B, C …


Neurology Neurological disability due to sudden loss of perfusion of an area of brain.5


Ischaemia (85%, eg af, carotid stenosis) or haemorrhage (15%).


Sudden-onset focal neurology though onset can be stuttering.


Check for irregular heartbeat, carotid bruit, and LVF. The Bamford stroke classification (see Table 11.4) allows easy recognition of the area of brain affected, as well as prognostication. Posterior circulation strokes (POCS) affect the territory of the vertebrobasilar artery (occipital lobes, brainstem, and cerebellum). Anterior circulation strokes involve the internal carotid artery territory, which supplies all the rest of brain. These are further subcategorized as Total anterior circulation stroke (tacs), Partial anterior circulation stroke (pacs), and Lacunar stroke (lacs).

Table 11.4 Bamford stroke classification


All of:

  • Motor/sensory deficit in ≥2 of face, arm, leg

  • Homonymous hemianopia*

  • Higher cortical dysfunction


  • Either:

  • or:

  • or:

  • 2 out of 3 of TACS criteria met

  • Higher cortical dysfunction alone

  • Isolated motor deficit not meeting LACS criteria


  • Motor and/or sensory deficit affecting ≥2 of face, arm, leg

  • No higher cortical dysfunction or hemianopia


Any of:

  • Ipsilateral cranial nerve palsy + contralateral motor/sensory deficit

  • Bilateral motor/sensory deficit

  • Disordered conjugate eye movement

  • Cerebellar dysfunction

  • Isolated hemianopia or cortical blindness

Source: data from Bamford J, et al. Lancet 1991;337:1521 (subscription required).

*Loss of vision on the same side in both eyes (Neurology Fig. 3.1 p. [link]).

Includes dysphasia, visuospatial problems, ↓GCS.


lacs/pacs/pocs have similar prognoses (15% 1yr mortality vs 60% live independently) but tacs is worse (60% vs 5%).



FBC, U+E, LFT, glucose, lipids, clotting;

ECG; CXR; CT head

±CT angiogram ±CT perfusion scan urgent if within thrombolysis/thrombectomy window, GCS persistently low, on oral anticoagulants/known bleeding disorder, severe headache at onset of stroke or evidence of ↑ICP; otherwise CT head within 24h. TACS/PACS also need echo, carotid Doppler, and 24h ECG.


See emergency treatment Neurology p. [link]; if candidate for thrombolysis6 ±interventional thrombectomy, move fast to ensure timely treatment. Otherwise, aspirin 300mg/24h po/pr for 14d (provided no haemorrhage on CT). Assess safety of swallow (Box 11.10; Neurology p. [link]); if concerns, keep NBM+IV fluids and request salt assessment. Monitor bp, but do not try to lower bp without discussing with a senior (Neurology p. [link]). Do not use LMWH in acute setting with haemorrhagic or ischaemic strokes (risk of haemorrhagic transformation). Do not prescribe TEDS (high risk of pressure ulcers). Admit to stroke ward for early mobilization and rehabilitation with MDT (stroke doctor, stroke nurse, PT, OT, dietician).


Aspiration, dependence, further event, bleed, ↑ICP.

Transient ischaemic attack (tia)

Neurology A transient episode of neurological dysfunction caused by focal brain ischaemia without infarction. Symptoms typically last less than an hour, but prolonged episodes can occur.


As for stroke but resolve completely (classically within 24h, though no precise cut-off time distinguishes ischaemia from infarction); note that transient loss of consciousness, ‘dizzy turns’, or +ve symptoms (seeing lights, sounds, tingling, movements) are unlikely to be a TIA.


If <3h since symptoms began Neurology p. [link]; otherwise use the ABCD2 score to estimate the 7d risk of stroke and therefore decide on admission, not to diagnose a TIA (see Table 11.5). Start aspirin 300mg/24h.

Table 11.5 ABCD2 score to calculate 7d stroke risk*



1 point


Systolic >140mmHg and/or diastolic ≥90mmHg

1 point

Clinical features

Unilateral weakness

2 points

Speech disturbance without weakness

1 point

Other signs

0 points



2 points


1 point


0 points



1 point

Total score

7d risk




Urgent out-patient ‘TIA clinic’ follow-up (1wk)



Discuss with stroke physician—likely to need admission for urgent investigation



Source: date from Johnston SC, et al. Lancet 2007;369:283 (subscription required).

CVA prevention

The risk of further events after TIA or stroke can be reduced with close attention to risk factors. Medical management includes control of BP, cholesterol, and glycaemia. Antiplatelet therapy options include clopidogrel 75mg/24h PO, aspirin 75mg/24h, and dipyridamole MR 200mg/12h PO. Current health-economic modelling favours the use of clopidogrel for those who have had a stroke, and aspirin/dipyridamole combination therapy after a TIA.7 Encourage smoking cessation, healthy diet, and moderate exercise. Carotid endarterectomy should be considered within 2wk if symptomatic carotid stenosis >70%.

Focal neurology

Think about

Try to establish an anatomical pattern to abnormalities that will narrow the differential diagnosis (see Table 11.6).

Table 11.6 Guide to localizing neurological lesions

Motor power


Reflexes and tone


Common causes



Hemisensory loss, neglect


Unilateral ±higher cortical dysfunction (eg dysphasia, neglect, dyspraxia) ±hemianopia

Stroke (Neurology p. [link][link]), SOL (Neurology p. [link]), migraine





Ataxia, nystagmus, slurred speech, intention tremor, past-pointing

POCS (Neurology p. [link]), SOL (Neurology p. [link]), MS (Neurology p. [link]), alcohol, phenytoin



Hemisensory loss

Cranial nerve deficit on opposite side to limb motor/sensory signs

POCS (Neurology p. [link]), SOL (Neurology p. [link]), MS (Neurology p. [link])

Myelopathy (spinal cord damage)

Bilateral weakness (fitting spinal level)

Bilateral paraesthesia (sensory level)

↑ below level may be ↓ at level

UMN signs below level of cord damage; may see LMN signs at level

Cord compression/central disc herniation (Neurology p. [link]), spinal stenosis (Neurology p. [link]), MS (Neurology p. [link])

Radiculopathy (nerve root damage)

Unilateral weakness (fitting nerve root)

Unilateral paraesthesia or pain (fits nerve root)


Shooting, stabbing pain, often worse on postural change or cough

Spinal stenosis (Neurology p. [link]); Disc prolapse, ► cauda equina syndrome (both Neurology p. [link])





May be mononeuropathy (specific nerve) or polyneuropathy (multiple nerves—distal deficit >proximal)

Mono: trauma, compression, inflammation (eg Bell’s palsy Neurology p. [link]); Poly: several (Neurology p. [link])

Neuromuscular junction

Fatigable weakness



Bilateral; fatigue with repetitive effort

Myasthenia gravis (Neurology p. [link]) Lambert–Eaton (paraneoplastic)


Bilateral weakness (proximal >distal)



Acquired form may be painful with ↑CK

Hereditary (eg muscular dystrophy); alcohol, inflammatory (eg polymyositis), statins, ↓T4

*Acute intracranial pathology may present with ↓tone and reflexes before the characteristic UMN signs develop.

Ask about

Motor problems (weakness, gait disturbance); sensory disturbance (tingling, pain, numbness); features of cerebellar disease (clumsiness, dysphasia, gait disturbance); symptoms of cranial nerve and cerebrum involvement (double vision, blurred vision, vertigo, hearing loss, dysphasia, facial droop); establish speed of onset and signs of underlying disease (weight loss, fever, cough, photophobia, neck stiffness, rashes, behavioural change) or ↑ICP (headache, nausea, morning vomiting);


Previous neurology, migraines, epilepsy, eye problems, recent infections, ↑bp, irregular heartbeat, dm, psychiatric disorder


Focus to symptom pattern (eg if peripheral neuropathy, ask about isoniazid, metronidazole)


Alcohol, recreational drugs;


Nerve or muscle problems.


BP, HR, GCS (Neurology pp. [link][link] if ↓), glucose, neuro obs.

Look for

Perform a complete neurological exam (Neurology pp. [link][link]) including cerebellar signs and gait; cvs exam for af and carotid bruit.


These should be determined by the location of the lesion determined by clinical examination.


FBC, u+e, Ca2+, glucose, ESR, CRP, autoantibodies;

EMG and nerve conduction studies

Can help peripheral neuropathy or myopathy;


Imaging and


Lesion location

Your aim is to determine which region of the nervous system is affected to help target further investigation and aid diagnosis. With motor symptoms there are three main areas:

  • Lower motor neuron (LMN) Peripheral nervous system; wasting, fasciculations, reduced reflexes and tone, forehead involved if CN VII

  • Upper motor neuron (UMN) Central nervous system; increased tone and reflexes with upgoing plantars, if facial weakness forehead spared

  • Mixed Consider motor neuron disease, multiple sclerosis, spinal cord compression (LMN signs at level of compression, UMN signs below), Friedreich’s ataxia (UMN weakness with absent ankle and knee jerks), syphilis (taboparesis), subacute combined degeneration of the cord.

Sensory loss

May map to a particular nerve, a nerve root (dermatome), or affect one side of the body up to the level of a significant lesion within the brain or spinal cord (sensory level). Alternatively, loss may be bilateral and distal (‘glove and stocking’) suggesting peripheral neuropathy (eg DM).

The combination of the anatomical pattern, time course, and associated features should enable you to make a clinical diagnosis for most lesions.

Space-occupying lesion

(Neurology OHCM10 p. 498.)


Tumour, aneurysm, abscess, subdural or extradural haematoma.


Focal neurology, seizures, behavioural change, early morning headache, vomiting, visual disturbance.


Focal neurology, papilloedema.

Investigations CT, MRI



Only if no ↑icp.


For ↑icp Neurology p. [link], surgical removal of lesion.

Spinal stenosis

Spinal canal narrowing 2° eg osteoarthritis (spondylosis) causes radiculopathy or myelopathy; consider decompressive laminectomy.

Myasthenia gravis

(Neurology OHCM10 p. 512.)


Weakness, tired, diplopia, dysarthria; worse in evening than morning.


Muscle fatigability, especially on upward gaze, normal reflexes.



Antibodies to ACh receptor;


edrophonium test (improvement with edrophonium);


Chest (15% will have thymoma).


Anticholinesterase (eg pyridostigmine), immunosuppression; thymectomy (even if no thymoma); plasmapheresis/immunoglobulin in refractory cases.

Myasthenic crisis

Triggered by illness, surgery or drugs; severe fatigue may involve the diaphragm causing respiratory failure requiring ventilation; assess with spirometry (fvc). Requires immunosuppression ±plasmapheresis.

Bell’s palsy

Rapid-onset mononeuropathy of facial nerve (VII); prednisolone (60mg/24h PO) started within 72h reduces symptoms; aciclovir may also help; protect affected eye (tape closed at night, artificial tears, sunglasses, discuss with ophthalmology if eye red, weeping, or cannot close).


(Neurology OHCM10 p. 504.)



Guillain–Barré (post-infectious; can rapidly progress to respiratory failure; regular spirometry (fvc) to assess; treat with IV immunoglobulins ±ventilation if worsening);


Drugs (eg isoniazid, metronidazole), toxins (eg lead), nutritional deficiency (eg vitamin B);


Malignancy, paraproteinaemia (Neurology p. [link]), connective tissue disease, metabolic disorders (eg uraemia, DM Neurology pp. [link][link]), hypothyroidism (Neurology pp. [link][link]);


eg Charcot–Marie–Tooth.


These may be motor (distal weakness) and/or sensory (paraesthesia).



FBC, vitamin B12, folate, U+E, LFT, glucose, TFT, ESR, serum electrophoresis, anca, ana;


Dipstick; CXR; nerve conduction studies.


Treat or remove the cause if possible.


Wounds, ulcers, joint abnormalities, eg Charcot joint.

Multiple sclerosis

(Neurology OHCM10 p. 496.)8

Neurology Inflammatory, demyelinating disease of the CNS, leading to multiple neurological deficits separated in time and location.


Patients will present variably with motor (weakness, clumsiness), sensory (visual disturbance, numbness), or autonomic deficits (incontinence).


Any focal neurology, including LMN and UMN signs; typically bilateral spastic limbs, visual disturbance, internuclear ophthalmoplegia.


Areas of inflammation and demyelination on


slowed nerve conduction;


csf electrophoresis may show oligoclonal bands.


MDT approach

Lifestyle advice (smoking cessation, exercise), disease modification (dimethyl fumarate, alemtuzumab or natalizumab), relapse treatment (methylprednisolone in acute flares), and symptom control (baclofen for spasticity, botulinum toxin for tremor, self-catheterization for retention).


Contractures, pressure ulcers, recurrent UTIs, unsafe swallow.

Back pain

(Neurology OHGP4 p. 476.)

Think about

► Serious

Cord compression, cauda equina syndrome, malignant metastases, myeloma, infection, fracture, aortic aneurysm;


Mechanical back pain (see Table 11.7), renal colic.

Table 11.7 Common causes of back pain




►► Cord compression

Weakness, numbness (±pain) below lesion, incontinence

Dermatomal distribution; UMN below lesion, LMN at lesion

Emergency/urgent MRI to look for lesion

►► Cauda equina syndrome

Leg weakness and pain (often bilateral), urinary and/or faecal incontinence

↓perianal sensation, ↓anal tone, ↓leg power, sensation and reflexes

Emergency/urgent MRI to look for lesion

Mechanical back pain

Pain, worse on movement, brought on by lifting/trauma

Pain reproduced by straight leg raise, unilateral neurology

Imaging rarely needed and only in specialist settings.


‘Inflammatory type’ pain,* joint pain, no trauma, family history

↓lumbar flexion, pain on squeezing pelvis; ±painful red eye (Neurology pp. [link][link])

RhF –ve, ↑ESR, sacroiliitis on X-ray, MRI inflammation

Vertebral collapse fracture

Sudden-onset pain in an elderly patient

Central pain over a discrete vertebrae; reduced ROM

Fracture on X-ray (wedge-shaped vertebral body)

*Pointers to an inflammatory aetiology include: morning stiffness, pain that improves with exercise but not rest, alternating buttock pain, nocturnal pain during 2nd half of night only. Finding ≥2/4 of these should prompt a search for a spondyloarthropathy (eg ankylosing spondylitis, reactive arthritis, psoriatic or IBD-associated arthritis).

Ask about

Trauma/lifting (mechanism), location of pain, duration, aggravating/relieving factors, radiation, pain in joints, pain or tingling in legs, leg weakness, bladder (retention or incontinence), faecal incontinence, altered sensation on passing stool, weight loss; fever


Previous back/joint pain, neurological problems, osteoporosis, anaemia;


Steroids, analgesia;


Joint or back problems;


Occupation (lifting, prolonged sitting).

Look for

Scoliosis, kyphosis, bony or paraspinal tenderness; reduced range of movement (especially flexion), pain on straight leg raise (Neurology p. [link]); lower limb neurological deficit (motor, sensory, reflexes); expansile abdominal mass;


↓tone or sensation (sacral/saddle anaesthesia).


If you suspect mechanical back pain and worrying features are not present, no further investigation required; otherwise consider:


fbc, esr, crp, ca2+, Alp, PSA;


±spinal x-ray if post trauma or risk of pathological fracture;


Spine: as emergency if cord compression or cauda equina suspected; urgent if suspected malignancy, infection, or fracture; routine if suspect inflammatory disorder; DEXA.9

Mechanical back pain including disc prolapse


Low back pain, worse on coughing/moving, may radiate to leg.10


Painful leg raise, tender around vertebra, radicular pain, normal PR.

Risk assess

NICE use the STarT Back Screening Tool.11 Uses pain distribution, impact on ADLs, and patient anxieties to predict rate of recovery.


Imaging in specialist settings.


if progressive neurology/features of cord compression/cauda equina syndrome. See Table 11.8.

Table 11.8 Types of mechanical back pain


Muscular pain and spasm without neurology

Disc prolapse

‘Slipped disc’, may compress the nerve root causing a unilateral radiculopathy (eg sciatica)


Degenerative changes of the spine eg osteoarthritis


Recurrent stress fracture leading to a defect (typically in L5)


Anterior displacement of a vertebra; may present in younger patients; conservative management; spinal fusion if severe

Lumbar spinal stenosis

Narrowing of the spinal canal eg due to OA, causes leg aching and heaviness on walking (spinal claudication)


Reassurance, education, and resumption of normal activities for all (including early mobilization, avoid lifting, maintain posture). Combined exercise and CBT programmes if recovery predicted to be slow and painful.11 Short-term NSAIDs then weak opioids if required. Reassess urgently if bilateral symptoms or urinary/faecal incontinence.

►► Cord compression


Tumour, abscess/TB, trauma, haematoma, central disc prolapse.


Weakness and/or numbness of legs, continuous/shooting pains, urinary retention or incontinence, faecal incontinence.


LMN signs at the level of the lesion, UMN signs below, normal above, sharp boundary of reduced sensation, spinal shock (Neurology p. [link]).


Urgent mri spine, look for cause.


Catheterize; refer immediately to orthopaedics/neurosurgeons.


Weakness, reduced sensation, incontinence, impotence.

►► Cauda equina syndrome


Central disc prolapse, tumour, abscess/TB, haematoma, trauma.


Urinary incontinence or retention (may be painless), faecal incontinence, bilateral leg weakness and pain.


Bilateral reduced power (LMN) and sensation, reduced perianal (saddle) sensation, reduced anal tone, bilateral absent ankle reflexes.


Urgent mri spine.


Catheterize; refer immediately to orthopaedics/neurosurgeons.


Weakness, reduced sensation, incontinence, impotence.

Vertebral collapse fracture


Trauma, osteoporosis, tumour.


Sudden-onset back pain; may be mild trauma if pathological.


Central vertebral tenderness, reduced mobility.


Spinal X-ray.


Analgesia, assess ability to cope, treat osteoporosis (Neurology p. [link]).


Think about

► Emergencies

Intracranial haemorrhage (subarachnoid, subdural, extradural), meningitis, encephalitis, ↑intracranial pressure (ICP), temporal arteritis, acute glaucoma, hypertensive crisis;


Dehydration, tension, infection, migraine, extracranial (sinuses, eyes, ears, teeth), trauma, post-LP, post-nitrates;


Cluster, postcoital, hypoglycaemia, hyponatraemia. See Table 11.9 and Box 11.11.

Table 11.9 Common causes of headache




Subarachnoid or warning bleed

Rapid onset, severe pain, vomiting, ↓gcs if severe

May be normal, neck stiffness, photophobia, focal neurology

Bleed seen on ct; xanthochromia in csf

Subdural or extradural haematoma

Trauma, confusion, vomiting

↓/fluctuating GCS; may be signs of ↑icp

Blood seen on ct

Meningitis ±septicaemia

Unwell, irritable, drowsy, photophobia, feels ill ±rash

Febrile ±septic, neck stiffness, photophobia ±non-blanching rash

↑wcc, ↑crp; CSF: neutrophilia ±↓glucose

Raised ICP

Vomiting, blurred vision, dizzy, drowsy, worse on coughing/bending, seizures

Pupillary abnormalities, focal neurology; late signs: papilloedema, Cushing’s reflex

Abnormal ct: enlarged ventricles ±focal lesion


Drowsy, confused, vomiting, seizures, preceding flu-like illness, non-specific symptoms

Pyrexia, ↓gcS, confusion, focal neurology, neck stiffness, photophobia

ct/mri: oedema, temporal lobe changes; CSF: ↑lØ ±protein

Temporal arteritis

Age >55yr, visual disturbances, weight loss, polymyalgia, jaw pain/claudication

Tender, palpable, non-pulsatile temporal artery, tender scalp

↑crp, ↑↑↑esr with anaemia, ↑plts and ↑alp


Previous migraines, visual aura; unilateral, throbbing, nausea, ±vomiting

Photophobia, visual field defects, may have focal neurology

Usually none. Consider MRI head if new and >55yr


Recurrent daily headaches, unilateral, ‘stabbing’

Agitated, rhinorrhoea, lacrimation, sweating



Bilateral, band-like pressure, worse when stressed

Normal; occasional scalp tenderness



Frontal pain, blocked/runny nose

Tender above or below eyes

May have ↑lØ, nØ or eØ

Trigeminal neuralgia

Frequent, brief ‘stabbing’ pains; unilateral in distribution of CN V; previous facial herpes zoster

Normal; may identify ‘trigger point’



Sudden, explosive bilateral pain typically on exercise or orgasm

May mimic migraine or SAH, but meningism absent

Consider CT/LP to rule out SAH

Acute glaucoma

Age >50yr, blurred vision, pain in one eye, often occurs at night

↓visual acuity, dilated, ±oval pupil, red around cornea, tender

↑intraocular pressure, ophthalmology review

Drug induced

Many medications can induce headaches, particularly nitrates, Ca2+ channel antagonists and metronidazole with alcohol

Ask about

Severity, location, bilateral vs unilateral, speed of onset, character, change with coughing, nausea and vomiting, visual changes (before or currently), trauma, seizures, rashes, neck pain, sweating, neurological symptoms, jaw claudication;


Previous headaches, migraines (and usual symptoms);


Nitrates, analgesics, antihypertensives;


Recent stressors, alcohol intake, illicit drug use.


Temp, GCS, glucose, HR, BP, fluid balance.

Cushing’s reflex

Is a late sign of ↑ICP: ↓HR and ↑BP.

Look for

Volume status (Neurology p. [link]); evidence of meningism: neck stiffness, photophobia, Kernig’s sign (fully flex hip and passively extend knee, +ve if painful in head or neck); non-blanching rash (check whole body); red eye (Neurology pp. [link][link]), visual disturbance or papilloedema; focal neurology; temporal artery tenderness and pulsatility; tenderness over sinuses; evidence of recent head trauma; dental hygiene, ear discharge.


In the absence of worrying features it is appropriate to give pain relief without investigations;12 otherwise secure IV access and send


FBC, ESR, U+E, LFT, glucose, CRP, clotting and bld cultures;


Especially if ↓GCS.

CT head ±LP

Discuss with a senior whether these are required (Neurology p. [link]);


May help diagnose encephalitis.


Exclude emergencies and treat other causes with simple analgesia (Neurology pp. [link][link]) and fluids if dehydrated (Neurology pp. [link][link]); ask to be contacted if symptoms fail to improve or worsen:

New onset

GCS <15 (Neurology pp. [link][link]).

New-onset focal neurology

Re-evaluate for meningitis, encephalitis or ↑ICP (Neurology p. [link]): 15L/min O2, consider ABx—call a senior urgently.

Sudden (onset <2min), severe, and constant

Consider a subarachnoid (Neurology p. [link]): 15L/min O2, lie flat—call a senior urgently.

Unwell, deranged obs

Always consider meningitis/sepsis (Neurology p. [link]), classic symptoms in <30%: 15L/min O2, IV fluids, discuss ABx with senior.

Red, painful eye, ↓acuity

Acute glaucoma (Neurology p. [link]), urgent ophthalmology referral.

Temporal tenderness

Consider temporal arteritis (Neurology p. [link]).


(BP >200/120mmHg) (Neurology pp. [link][link]).

►► Subarachnoid haemorrhage

(Neurology OHAM4 p. 384.)

Neurology Potentially devastating bleed (typically aneurysmal) into subarachnoid space.


Rapid-onset (<2min), severe, continuous (>2h) headache; often occipital (‘hit around back of head’), vomiting, dizziness; may have seizures.


Neck stiffness, drowsy, photophobia, focal neurology, ↓gcs.




head; since this may miss small bleeds (20%), if CT normal, then


(>12h after onset) for xanthochromia.


15L/min O2, analgesia (codeine 30mg PO or 5mg morphine iv) and anti-emetic, eg metoclopramide 10mg iv/im. Refer urgently to neurosurgeon for endovascular coiling or neurosurgical clipping and consider transfer to ICU if ↓gcs. Lie the patient flat and advise not to get up or eat. Reassess often and request neuro obs. Nimodipine (60mg/4h PO) prevents vasospasm and improves outcome.13 Keep systolic <130mmHg, using IV β‎-blockers, unless lethargic (suggests vasospasm; may require permissive hypertension). Focal neurology or ↓gcs carry a worse prognosis.


Cerebral ischaemia, rebleeding, hydrocephalus, death.

►► Meningitis

(Neurology OHAM4 p. 355, Neurology ohCm10 p. 822.)


Headache, neck pain, photophobia, seizures, unwell.


↑hr, ±↓bp, ↑temp, ↓gcs or abnormal mood, neck stiffness, ±rash, focal neurology.


Treat first;


↑wcc, ↑crp; ct then lp (Neurology pp. [link][link]).


Contact a senior; ceftriaxone 4g IV STAT if you have a clinical suspicion of bacterial meningitis. Resuscitate as needed (Neurology pp. [link][link]). Contact public health regarding contact tracing (see also sepsis Neurology p. [link]).


↑icp, hydrocephalus, focal neurology, seizures, death.

►► Encephalitis

(Neurology OHAM4 p. 384.)

Neurology Brain inflammation, usually viral. Rare and easily missed in early stages.


Abnormal behaviour, seizures, drowsy, headache, neck pain.


Altered personality, ↓gcs, focal neurology, neck stiffness, ↑temp.



followed by


(Neurology pp. [link][link]), send csf for viral pcr;


may all show temporal lobe changes.


Be guided by microbiology; eg aciclovir 10mg/kg/8h IV (10–14d).


↑icp, seizures, death.

►► Raised intracranial pressure (ICP)

(Neurology oham4 p. 372.)


cva, tumours, trauma, infection (including abscess), cerebral oedema (eg post-hypoxia), electrolyte imbalance, idiopathic.


Headache and vomiting (worse in morning and coughing/ bending over), tiredness, visual problems, seizures.


↓gcs, focal neurology; late signs include Cushing’s reflex (↓hr, ↑bp) ±papilloedema.




head to assess cause and severity. Consider HIV.


Elevate the head end of the bed to 30° and correct hypotension with 0.9% saline. Discuss with a senior before giving mannitol or dexamethasone (tumours only) to reduce the icp. Involve a neurosurgeon/neurologist early.


Herniation of the brain (‘coning’).

►► Acute glaucoma

(Neurology p. [link]), needs urgent ophthalmology review.

Temporal arteritis

(Neurology OHAM4 p. 644.)


Headache, jaw pain on eating, visual problems, aching muscles.


Temporal artery, tender scalp, pulseless/nodular temporal artery.



↑↑esr (>50mm/h), ↑crp, ↑plts, ↓Hb all suggestive; definitive diagnosis requires biopsies (multiple sites) in ≤1wk of starting therapy.


Start 60mg/24h prednisolone PO and strong analgesia. Discuss with on-call surgeon/ENT to arrange urgent out-patient biopsy and liaise with ophthalmology to exclude visual complications; Doppler USS of the artery can be helpful. Out-patient rheumatology follow-up.


Blindness (10–50%), TIA/stroke.


(Neurology OHCM10 p. 458.)

Neurology Recurrent, pulsatile headaches with strong familial tendency. Suspect an alternative pathology if sudden onset, or >55yr with no previous migraines.


Throbbing headache, initially unilateral often with nausea ±vomiting, photophobia; 20% may experience a preceding aura (flashing lights, zigzags, visual loss).


May mimic TIA (visual defects, focal neurology) but slower onset.


Normal; perform blds, CT, LP as required to rule out alternative/coexistent pathology.



Simple analgesia (Neurology pp. [link][link]), ±anti-emetic, ±5HT1 agonists (eg sumatriptan);


β‎-blocker (eg propranolol), or antiepileptics (eg topiramate).


Neurology Inflammation of the mucosa of the paranasal sinuses due to bacteria, viruses, or fungi; may become chronic.


Blocked nose, nasal discharge, facial pain, unable to smell.


Tender over sinuses (above medial eyebrows, bridge of nose, below eyes), purulent nasal discharge, temp usually normal.


Try a mixture of beclometasone nasal spray 2 sprays to each nostril/12h ±ephedrine nasal drops 1–2 drops in each nostril/6h (7d max) ±saline neb 5mL/2–4h. If severe (eg purulent mucus, systemically unwell) prescribe amoxicillin 500mg/8h PO.


Local spread of infection, chronic sinusitis.

Cluster headaches

Neurology Recurrent, short-lived, severe, unilateral ‘stabbing’ headaches occurring up to several times/day (often in early morning). Patients be come agitated during attacks, and may experience rhinorrhoea, lacrimation or facial sweating.



5HT1 agonists (eg sumatriptan nasal spray), 15L/min O2;


Ca2+ channel blockers (eg verapamil), lithium.

Post-dural puncture

Usually presents within 4–5d of LP, epidural, or spinal anaesthetic, (rarely up to 7d); lie patient flat, treat with analgesia and ↑fluid intake (especially caffeinated drinks). Contact anaesthetist if severe/persistent to consider epidural blood patch.

►► Hypertensive crises

Hypertension usually represents a response to the pain of headache and responds to treatment of the headache. However, BP >200/120mmHg may represent the cause of a headache (Neurology pp. [link][link]).


Think about


Labyrinthitis, vestibular neuronitis, benign positional vertigo, trauma, ototoxic drugs, Ménière’s, CVA, multiple sclerosis, acoustic neuroma;


Hypoglycaemia, alcohol intoxication, Wernicke’s encephalopathy, CVA, cerebellar space-occupying lesion, intracranial infection, vitamin B12 deficiency, normal pressure hydrocephalus,


(Neurology pp. [link][link]).

Ask about

See Box 11.12;


Previous dizziness, ↑bp, dm, MS, IHD;


Antihypertensives, diuretics, aminoglycosides, insulin, oral hypoglycaemics;




Temp, HR, lying and standing BP, glucose, GCS.

Look for

Ability to stand, gait; Romberg’s test (Box 11.13), change with position, cerebellar signs (DANIsh—dysdiadochokinesia, ataxia, nystagmus, intention tremor and past pointing, slurred speech, hypotonia), focal neurology, examine ear using otoscope (effusion, perforation); irregular pulse.


The type of dizziness (vertigo, ataxia, postural, syncope) should be determined from history alone; if syncope is suspected, investigate for cardiogenic causes (Neurology p. [link]); for vertigo and ataxia, acute investigation is rarely required; consider a CT head if a stroke or tumour is suspected or there are cerebellar signs; audiometry if vestibular features.


(Neurology OHCS10 p. 554.)

Treat the sensation of vertigo while determining the underlying cause. Centrally acting antihistamines (eg cyclizine 50mg/8h PO) and phenothiazines (eg prochlorperazine 5mg/8h PO) are particularly effective; betahistine 16mg/8h PO may also be used.

Benign positional vertigo

Sudden-onset vertigo lasting seconds following specific head movements. Treated with Epley manoeuvre (a series of movements to dislodge the vestibular debris causing the symptoms; Neurology ohcs10 p. 554) and referral to physiotherapy for vestibular exercises.

Inner ear inflammation

This causes sudden-onset vertigo, nystagmus, and severe nausea without focal neurology. Reassure and treat as above.

Vestibular neuronitis

Viral infection of the vestibular nerve; improves within 1–2wk but can take 2–3mth to fully resolve.


As for vestibular neuronitis with hearing loss or tinnitus.


Attacks of severe vertigo lasting several hours, with tinnitus and progressive low frequency hearing loss. Treat as above, and refer to ent.

Motion sickness

Rarely encountered in hospital, however cinnarizine 30mg PO 2h before journey is effective.


Ataxia can be differentiated from vertigo on history; there are two types:


‘DANISH’ signs (see earlier in this topic); unstable even with eyes open.


Romberg’s +ve (see Box 11.13), loss of proprioception, preservation of fine coordination; ‘stamping’ gait, spinal/neuropathy signs.

Cerebellar ataxia


CVA, multiple sclerosis, alcohol toxicity, Wernicke’s encephalopathy, phenytoin, vitamin B12 deficiency, normal pressure hydrocephalus, infection, space-occupying lesions, trauma, paraneoplastic.


MRI is the most useful diagnostic test (consider CT if acute onset), neurology referral, some underlying causes are treatable:

  • Wernicke’s encephalopathy Thiamine (vitamin B1) deficiency often as a result of chronic alcohol excess results in confusion, ataxia, ophthalmoplegia, and nystagmus; treated with thiamine (PO/IV, Neurology p. [link]), as for Korsakoff’s syndrome, to which it may progress if left untreated.

Sensory ataxia


Cervical spondylosis, MS, peripheral neuropathy, syringomyelia, spinal tumour, spinal infection, vitamin B12 deficiency, Friedreich’s ataxia, syphilis.


Urgent MRI if acute onset, otherwise consider tests for peripheral neuropathy (Neurology p. [link]), spinal X-rays, routine MRI, nerve conduction studies, neurology referral; often treated with vitamin B12.


2 NICE guidelines available at

3 Resources for patients, carers, and doctors at

4 NICE guidelines available at

5 NICE guidelines available at

6 See Neurology Box 11.7 (p. [link]) and resources from the international stroke trial collaborators, available free at

7 NICE interpretation of study data; see

8 NICE guidelines available at

9 See—a WHO validated tool to assess fracture risk (and need for DEXA or osteoporosis treatment) in those without worrying features (Neurology Box 16.4 p. [link]).

10 NICE guidelines for low back pain available at

11 STarT Back Screening Tool available at Neurology

12 NICE guidelines available at

13 Pickard JD, et al.BMJ 1989;298:636 available free at

14 Described by the pioneering C19th German neurologist Moritz Romberg, working among the destitute of Berlin with tabes dorsalis (tertiary neurosyphilis).