• 15L/min O2 if SOB/sats <94%; beware if previous COPD/CO2 retainer
• If hypoxic 
p. 276
• Bag and mask ventilation if poor/absent respiratory effort.
| ► Airway | Check airway is patent; consider manoeuvres/adjuncts |
| ► Breathing | If no respiratory effort— CALL ARREST TEAM |
| ► Circulation | If no palpable pulse— CALL ARREST TEAM |
| ► Disability | If GCS ≤8— CALL ANAESTHETIST |
►► Call for senior help early if patient unwell or deteriorating.
• 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 p. 276
• Bag and mask ventilation if poor/absent respiratory effort.
• VBG, FBC, U+E, LFT, glucose, Ca2+, troponin, clotting, G+S, bld cultures, paracetamol, salicylate and alcohol levels
• Control seizures ( p. 348)
• 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.
• 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
• 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.
⇄ Box 11.1↓GCS covered elsewhere
• 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.
Table 11.1 Common causes of reduced GCS
| Cause | Signs |
| Intoxication | 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 |
| Meningism | Neck stiffness, photophobia, Kernig’s sign, Brudzinski’s sign, straight leg raise ( p. 134) |
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.
Meningism Meningitis, encephalitis, subarachnoid haemorrhage.
Ask about (notes, relatives, contacts, nurses) Baseline, speed of onset, headache, chest pain, palpitations, vomiting, seizures, weight loss; PMH Cardiac, respiratory, DM, kidney, liver, psychiatric, stroke/TIA, seizures, dementia; DH Elicit PMH from DH, consider the possibility of overdose; SH Alcohol, recreational drugs (overdose or withdrawal).
Obs GCS (Table 11.2), temp, BP, HR, O2 sats, O2 requirements, RR, pupil size.
Neuro obs GCS, limb movements, pupil size and reactivity, HR, BP, RR, temp.
Look for Respiration Rate, depth, distress, added sounds, air entry on both sides; Pulse Rate/rhythm; Abdomen Rigidity, pulsatile mass, organomegaly; distension; Neuro Pupil responses, papilloedema (late sign), limb tone, plantars; Skin Rashes, injection marks, trauma; DRE constipation.
Investigations blds FBC, U+E, LFT, Ca2+, glucose, troponin, CRP, clotting, bld cultures, toxicology screen (paracetamol, salicylate, alcohol); ABG pH, ↓O2 or ↓↑CO2; ECG Arrhythmias; CXR 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; AXR Faecal impaction; LP After a CT scan if CT normal.
Table 11.2 GCS scoring (3/15 minimum)
| Eyes | Open spontaneously | 4 | Motor | Obeys commands | 6 |
| Open to command | 3 | Localizes pain | 5 | ||
| Open to pain | 2 | Flexes/withdraws to pain | 4 | ||
| No response | 1 | Abnormal flexion to pain | 3 | ||
| Voice | Talking and orientated | 5 | Extension to pain | 2 | |
| Confused/disorientated | 4 | No movement | 1 | ||
| Inappropriate words | 3 | ||||
| Incomprehensible sounds | 2 | ||||
| No vocalizations | 1 |
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.
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.
| ► Airway | Check airway is patent; consider manoeuvres/adjuncts |
| ► Breathing | If no respiratory effort—CALL ARREST TEAM |
| ► Circulation | If no palpable pulse—CALL ARREST TEAM |
| ► Disability | If GCS ≤8—CALL ANAESTHETIST |
►► 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
• 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:
• 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)
• Thiopental or propofol on ICU/HDU
• Transfer to ICU for general anaesthetic, intubation, EEG monitoring.
► Box 11.2 Life-threatening causes
| ► Airway | Check airway is patent; consider manoeuvres/adjuncts |
| ► Breathing | If no respiratory effort—CALL ARREST TEAM |
| ► Circulation | If no palpable pulse—CALL ARREST TEAM |
| ► Disability | If GCS ≤8—CALL ANAESTHETIST |
►► 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.
• 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
• 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 ( pp. 534–535) 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
• 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 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).
• Call for anaesthetist and senior help
• Paraldehyde 0.4mL/kg PR as above unless already given
► Box 11.3 Life-threatening causes
► Worrying features Preceding headache or head injury, duration >5min, prolonged post-ictal phase, adult onset, recent depression (overdose).
Think about ► Life-threatening See Box 11.2; Most likely Idiopathic (>50%), epilepsy, alcohol withdrawal, hypoglycaemia, hypoxia, trauma; Other Kidney or liver failure, pseudoseizures, overdose (tricyclics, phenothiazines, amphetamines); Non-seizure Brief limb jerking during a faint, rigors, syncope, arrhythmias. See Table 11.3.
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; PMH previous seizures, cerebrovascular/cardiac/respiratory/hepatic/renal/psychiatric disease, DM, alcohol, pregnancy, surgeries; DH Anticonvulsants, hypoglycaemics, benzodiazepines; SH Occupation, driving, hobbies, social support, alcohol intake, last drink, illicit drugs, recent travel; FH Epilepsy.
Obs 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).
Investigations blds VBG, FBC, U+E, LFT, glucose, Ca2+, Mg2+, blood cultures, anticonvulsant levels; ABG If hypoxia or metabolic upset suspected; Urine Consider drug screen, β-hCG if pre-menopausal ♀; ECG To exclude dysrhythmia; CT 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; MRI Is the neuroimaging of choice in suspected epilepsy; LP If meningitis or encephalitis suspected; EEG May help to exclude encephalitis or as out-patient investigation for epilepsy.
Treatment Stop seizure using treatment outlined on p. 348. 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.
Box 11.4 Describing a seizure
If witnessing or describing seizures, document exactly what happened:
Onset Position, activity, any warning, starting in one limb or all over, presence of tonic phase (arched back, muscle spasm).
During Loss of awareness, limb movements, eye movements, jaw and lip movements, breathing, peripheral or central cyanosis, incontinence (urinary and faecal), duration, HR, and rhythm.
Afterwards Tongue trauma, sleepy, limb weakness (Todd’s paresis p. 352).
Table 11.3 Common causes of transient loss of consciousness
| History | Examination | Investigations | |
| Epileptic seizure ( p. 352) |
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 ( p. 352) |
Usually >50units/wk alcohol consumption, last drink >24h ago | Anxious, sweaty, tachycardic, tremor ±chronic liver failure | ↑MCV and γGT; ↓platelets, mild anaemia |
| Pseudo-seizures/psychogenic | Unusual features, short duration, memory of event | Responsive to pain, normal respiration, no injuries | Normal investigations |
| Rigors | 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 ( p. 518) |
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 |
| Narcolepsy | 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 ( p. 266) |
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) |
Box 11.5 Assessing a ‘first fit’
History Detailed account from first-hand witness, documented carefully.
Investigations FBC, U+E, LFT, glucose, Ca2+, Mg2+, PO43−, clotting, medication levels, urine and serum toxicology screen (including paracetamol and salicylate); CT to exclude structural causes (non-urgent, unless recent trauma or altered neurology); consider LP after CT only if infection suspected; MRI is the neurologists’ imaging of choice in suspected epilepsy, but can be arranged from their clinic.
Management Admit only if gcs <15 or drowsy; discuss with senior doctor regarding suspicion of seizures and need to advise to stop driving ( p. 619, 1yr ban); do not start antiepileptic medication—this decision should be made by a neurologist in an urgent out-patient clinic (‘first fit’ clinic).
⇄ Box 11.6 Causes of seizures elsewhere in this book
Epilepsy ( OHCM10 p. 490.)1
Abnormal and unprovoked discharge of a group of neurons causes a seizure. Epilepsy is the recurrence of ≥2 such seizures.
Symptoms 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.
Awareness 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.
Signs ↓GCS, tongue trauma, limb weakness, incontinence, Todd’s paresis (transient weakness following a seizure; mimics a TIA), post-ictal state.
Investigations Often normal; MRI and EEG (±provocation) may aid diagnosis and seizure classification. Consider EEG/video telemetry.
Treatment 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 ( p. 372).
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 ( p. 452), contact a neurosurgeon, otherwise hourly neuro obs and reassess if ↓GCS.
Parkinson’s disease ( OHCM10 p. 494.)2
Common neurological disorder (affects 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.
Investigations 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.
Management 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.
Complications Depression, dementia (late stage): Parkinson’s disease may have pathological overlap with Lewy body dementia ( p. 377) 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.
Degenerative disease affecting upper and lower motor neurons.3
Diagnosis Primarily clinical but EMG can help. Progressive motor weakness (UMN and LMN p. 353) and behavioural change; sensation unaffected. Fasciculations progress to spasticity, poor swallow, and dementia.
Management 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.
Complications Aspiration, respiratory failure, frontotemporal dementia.
Incurable inherited (autosomal dominant) disorder characterized by involuntary limb movements (chorea), dementia, and behavioural disturbance (depression, psychoses). Onset at 30–50yr.
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.
| ► Airway | Check airway is patent; consider manoeuvres/adjuncts |
| ► Breathing | If no respiratory effort—CALL ARREST TEAM |
| ► Circulation | If no palpable pulse—CALL ARREST TEAM |
| ► Disability | If GCS ≤8—CALL ANAESTHETIST |
►► Call for senior help early. Patient may need urgent aspirin, thrombolysis, thrombectomy, or transfer to Hyperacute Stroke Unit (HASU).
If GCS is reduced pp. 344–345.
• 15L/min O2 if SOB or sats <94%
• Check blood glucose; treat if too low ( p. 328) or high ( p. 330)
• 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)
► Box 11.9 Key differentials
Neurological disability due to sudden loss of perfusion of an area of brain.5
Causes Ischaemia (85%, eg af, carotid stenosis) or haemorrhage (15%).
Symptoms Sudden-onset focal neurology though onset can be stuttering.
Signs 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
| TACS | All of: | |
| PACS | ||
| LACS | ||
| POCS | Any of: |
Source: data from Bamford J, et al. Lancet 1991;337:1521 (subscription required).
*Loss of vision on the same side in both eyes ( Fig. 3.1 p. 135).
†Includes dysphasia, visuospatial problems, ↓GCS.
Prognosis lacs/pacs/pocs have similar prognoses (15% 1yr mortality vs 60% live independently) but tacs is worse (60% vs 5%).
Investigations blds 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.
Treatment See emergency treatment p. 354; 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; p. 356); if concerns, keep NBM+IV fluids and request salt assessment. Monitor bp, but do not try to lower bp without discussing with a senior ( p. 271). 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).
Complications Aspiration, dependence, further event, bleed, ↑ICP.
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.
Symptoms/signs 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.
Management If <3h since symptoms began p. 354; 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*
| Age | ≥60yr | 1 point | |
| BP | Systolic >140mmHg and/or diastolic ≥90mmHg | 1 point | |
| Clinical features | Unilateral weakness | 2 points | |
| Speech disturbance without weakness | 1 point | ||
| Other signs | 0 points | ||
| Duration | ≥60min | 2 points | |
| 10–59min | 1 point | ||
| <10min | 0 points | ||
| Diabetes | Yes | 1 point | |
| Total score | 7d risk | Management | |
| 0–3 | 1.2% | Urgent out-patient ‘TIA clinic’ follow-up (1wk) | |
| 4–5 | 5.9% | Discuss with stroke physician—likely to need admission for urgent investigation | |
| 6–7 | 11.7% | ||
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%.
Box 11.10 Not safe to swallow? Do a ‘ward swallow’
For any patient with ↓GCS or suspected neurological disability, perform a ‘ward swallow’ assessment. Give them a spoonful of water, then a sip or water, and then a cup of water, each time observing for the following and not proceeding if they occur at any time:
If any of these features are present, keep NBM+IV fluids and request a SALT assessment.
► Worrying features ↓HR, ↑/↓BP, ↓GCS, severe headache, pyrexia, neck stiffness, photophobia, vomiting, papilloedema.
Think about Try to establish an anatomical pattern to abnormalities that will narrow the differential diagnosis (see Table 11.6).
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); PMH Previous neurology, migraines, epilepsy, eye problems, recent infections, ↑bp, irregular heartbeat, dm, psychiatric disorder DH Focus to symptom pattern (eg if peripheral neuropathy, ask about isoniazid, metronidazole) SH Alcohol, recreational drugs; FH Nerve or muscle problems.
Obs BP, HR, GCS ( pp. 344–345 if ↓), glucose, neuro obs.
Look for Perform a complete neurological exam ( pp. 134–138) including cerebellar signs and gait; cvs exam for af and carotid bruit.
Investigations These should be determined by the location of the lesion determined by clinical examination. blds FBC, u+e, Ca2+, glucose, ESR, CRP, autoantibodies; EMG and nerve conduction studies Can help peripheral neuropathy or myopathy; CT/MRI Imaging and LP.
► Urgent CT brainstem or cerebral (lateralizing) signs, persistent ↓GCS, suspected subarachnoid haemorrhage ( p. 364), head injury ( p. 364).
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.
Table 11.6 Guide to localizing neurological lesions
| Motor power | Sensory | Reflexes and tone | Features | Common causes | |
| Cerebrum | Hemiparesis | Hemisensory loss, neglect | ↑* | Unilateral ±higher cortical dysfunction (eg dysphasia, neglect, dyspraxia) ±hemianopia | Stroke ( p. 355–356), SOL ( p. 359), migraine |
| Cerebellum | Normal | Normal | Normal | Ataxia, nystagmus, slurred speech, intention tremor, past-pointing | POCS ( p. 355), SOL ( p. 359), MS ( p. 359), alcohol, phenytoin |
| Brainstem | Hemiparesis | Hemisensory loss | ↑ | Cranial nerve deficit on opposite side to limb motor/sensory signs | POCS ( p. 355), SOL ( p. 359), MS ( p. 359) |
| 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 ( p. 361), spinal stenosis ( p. 462), MS ( p. 359) |
| Radiculopathy (nerve root damage) | Unilateral weakness (fitting nerve root) | Unilateral paraesthesia or pain (fits nerve root) | Normal/↓ | Shooting, stabbing pain, often worse on postural change or cough | Spinal stenosis ( p. 462); Disc prolapse, ► cauda equina syndrome (both p. 361) |
| Neuropathy | Weakness | Paraesthesia | Normal/↓ | May be mononeuropathy (specific nerve) or polyneuropathy (multiple nerves—distal deficit >proximal) | Mono: trauma, compression, inflammation (eg Bell’s palsy p. 359); Poly: several ( p. 359) |
| Neuromuscular junction | Fatigable weakness | Normal | Normal/↓ | Bilateral; fatigue with repetitive effort | Myasthenia gravis ( p. 359) Lambert–Eaton (paraneoplastic) |
| Myopathy | Bilateral weakness (proximal >distal) | Normal | Normal/↓ | 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.
Space-occupying lesion ( OHCM10 p. 498.)
Causes Tumour, aneurysm, abscess, subdural or extradural haematoma.
Symptoms Focal neurology, seizures, behavioural change, early morning headache, vomiting, visual disturbance.
Signs Focal neurology, papilloedema.
Investigations CT, MRI (brainstem/cerebellum); LP Only if no ↑icp.
Treatment For ↑icp p. 364, surgical removal of lesion.
Spinal stenosis Spinal canal narrowing 2° eg osteoarthritis (spondylosis) causes radiculopathy or myelopathy; consider decompressive laminectomy.
Myasthenia gravis ( OHCM10 p. 512.)
Symptoms Weakness, tired, diplopia, dysarthria; worse in evening than morning.
Signs Muscle fatigability, especially on upward gaze, normal reflexes.
Investigations blds Antibodies to ACh receptor; EMG;
edrophonium test (improvement with edrophonium); CT Chest (15% will have thymoma).
Treatment 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).
Polyneuropathies ( OHCM10 p. 504.)
Causes Acute Guillain–Barré (post-infectious; can rapidly progress to respiratory failure; regular spirometry (fvc) to assess; treat with IV immunoglobulins ±ventilation if worsening); Subacute Drugs (eg isoniazid, metronidazole), toxins (eg lead), nutritional deficiency (eg vitamin B); Chronic Malignancy, paraproteinaemia ( p. 410), connective tissue disease, metabolic disorders (eg uraemia, DM pp. 334–336), hypothyroidism ( pp. 340–341); Hereditary eg Charcot–Marie–Tooth.
Symptoms/signs These may be motor (distal weakness) and/or sensory (paraesthesia).
Investigations blds FBC, vitamin B12, folate, U+E, LFT, glucose, TFT, ESR, serum electrophoresis, anca, ana; Urine Dipstick; CXR; nerve conduction studies.
Treatment Treat or remove the cause if possible.
Complications Wounds, ulcers, joint abnormalities, eg Charcot joint.
Multiple sclerosis ( OHCM10 p. 496.)8
Inflammatory, demyelinating disease of the CNS, leading to multiple neurological deficits separated in time and location.
Symptoms Patients will present variably with motor (weakness, clumsiness), sensory (visual disturbance, numbness), or autonomic deficits (incontinence).
Signs Any focal neurology, including LMN and UMN signs; typically bilateral spastic limbs, visual disturbance, internuclear ophthalmoplegia.
Investigations Areas of inflammation and demyelination on MRI; slowed nerve conduction; LP csf electrophoresis may show oligoclonal bands.
Treatment 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).
Complications Contractures, pressure ulcers, recurrent UTIs, unsafe swallow.
► Worrying features Bladder/bowel changes, incontinence/retention, fever, weight loss, age <20yr or >55yr, steroids, thoracic pain, previous cancer, progressive neurological deficit, swelling, wakes them up at night, not relieved by rest, perianal anaesthesia, pulsatile abdominal mass.
Think about ► Serious Cord compression, cauda equina syndrome, malignant metastases, myeloma, infection, fracture, aortic aneurysm;
Common Mechanical back pain (see Table 11.7), renal colic.
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 PMH Previous back/joint pain, neurological problems, osteoporosis, anaemia; DH Steroids, analgesia; FH Joint or back problems; SH Occupation (lifting, prolonged sitting).
Look for Scoliosis, kyphosis, bony or paraspinal tenderness; reduced range of movement (especially flexion), pain on straight leg raise ( p. 151); lower limb neurological deficit (motor, sensory, reflexes); expansile abdominal mass; PR ↓tone or sensation (sacral/saddle anaesthesia).
Investigations If you suspect mechanical back pain and worrying features are not present, no further investigation required; otherwise consider: blds fbc, esr, crp, ca2+, Alp, PSA; CXR ±spinal x-ray if post trauma or risk of pathological fracture; MRI Spine: as emergency if cord compression or cauda equina suspected; urgent if suspected malignancy, infection, or fracture; routine if suspect inflammatory disorder; DEXA.9
Table 11.7 Common causes of back pain
| History | Examination | Investigations | |
| ►► 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. |
| Spondylitis | ‘Inflammatory type’ pain,* joint pain, no trauma, family history | ↓lumbar flexion, pain on squeezing pelvis; ±painful red eye ( pp. 440–442) |
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).
Symptoms Low back pain, worse on coughing/moving, may radiate to leg.10
Signs 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.
Investigations Imaging in specialist settings. MRI if progressive neurology/features of cord compression/cauda equina syndrome. See Table 11.8.
Treatment 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.
Table 11.8 Types of mechanical back pain
| ‘Sprain’ | Muscular pain and spasm without neurology |
| Disc prolapse | ‘Slipped disc’, may compress the nerve root causing a unilateral radiculopathy (eg sciatica) |
| Spondylosis | Degenerative changes of the spine eg osteoarthritis |
| Spondylolysis | Recurrent stress fracture leading to a defect (typically in L5) |
| Spondylolisthesis | 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) |
Causes Tumour, abscess/TB, trauma, haematoma, central disc prolapse.
Symptoms Weakness and/or numbness of legs, continuous/shooting pains, urinary retention or incontinence, faecal incontinence.
Signs LMN signs at the level of the lesion, UMN signs below, normal above, sharp boundary of reduced sensation, spinal shock ( p. 493).
Investigations Urgent mri spine, look for cause.
Treatment Catheterize; refer immediately to orthopaedics/neurosurgeons.
Complications Weakness, reduced sensation, incontinence, impotence.
Causes Central disc prolapse, tumour, abscess/TB, haematoma, trauma.
Symptoms Urinary incontinence or retention (may be painless), faecal incontinence, bilateral leg weakness and pain.
Signs Bilateral reduced power (LMN) and sensation, reduced perianal (saddle) sensation, reduced anal tone, bilateral absent ankle reflexes.
Investigations Urgent mri spine.
Treatment Catheterize; refer immediately to orthopaedics/neurosurgeons.
Complications Weakness, reduced sensation, incontinence, impotence.
Causes Trauma, osteoporosis, tumour.
Symptoms Sudden-onset back pain; may be mild trauma if pathological.
Signs Central vertebral tenderness, reduced mobility.
Investigations Spinal X-ray.
Treatment Analgesia, assess ability to cope, treat osteoporosis ( p. 451).
► Worrying features ↓GCS, sudden onset, severe, recurrent vomiting, photophobia, rash, neck stiffness, focal neurology, seizures, papilloedema, ↓↑HR, ↓↑BP.
Think about ► Emergencies Intracranial haemorrhage (subarachnoid, subdural, extradural), meningitis, encephalitis, ↑intracranial pressure (ICP), temporal arteritis, acute glaucoma, hypertensive crisis;
Common Dehydration, tension, infection, migraine, extracranial (sinuses, eyes, ears, teeth), trauma, post-LP, post-nitrates; Other Cluster, postcoital, hypoglycaemia, hyponatraemia. See Table 11.9 and Box 11.11.
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; PMH Previous headaches, migraines (and usual symptoms); DH Nitrates, analgesics, antihypertensives; SH Recent stressors, alcohol intake, illicit drug use.
Obs Temp, GCS, glucose, HR, BP, fluid balance. Cushing’s reflex Is a late sign of ↑ICP: ↓HR and ↑BP.
Look for Volume status ( p. 394); 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 ( pp. 440–442), visual disturbance or papilloedema; focal neurology; temporal artery tenderness and pulsatility; tenderness over sinuses; evidence of recent head trauma; dental hygiene, ear discharge.
Investigations In the absence of worrying features it is appropriate to give pain relief without investigations;12 otherwise secure IV access and send blds FBC, ESR, U+E, LFT, glucose, CRP, clotting and bld cultures; ABG Especially if ↓GCS. CT head ±LP Discuss with a senior whether these are required ( p. 566); EEG May help diagnose encephalitis.
Treatment Exclude emergencies and treat other causes with simple analgesia ( pp. 88–91) and fluids if dehydrated ( pp. 394–397); ask to be contacted if symptoms fail to improve or worsen:
New onset GCS <15 ( pp. 344–345).
New-onset focal neurology Re-evaluate for meningitis, encephalitis or ↑ICP ( p. 364): 15L/min O2, consider ABx—call a senior urgently.
Sudden (onset <2min), severe, and constant Consider a subarachnoid ( p. 364): 15L/min O2, lie flat—call a senior urgently.
Unwell, deranged obs Always consider meningitis/sepsis ( p. 364), classic symptoms in <30%: 15L/min O2, IV fluids, discuss ABx with senior.
Red, painful eye, ↓acuity Acute glaucoma ( p. 441), urgent ophthalmology referral.
Temporal tenderness Consider temporal arteritis ( p. 365).
Hypertensive (BP >200/120mmHg) ( pp. 270–273).
Table 11.9 Common causes of headache
| History | Examination | Investigations | |
| 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 |
| Encephalitis | 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 |
| Migraine | 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 |
| Cluster | Recurrent daily headaches, unilateral, ‘stabbing’ | Agitated, rhinorrhoea, lacrimation, sweating | None |
| Tension | Bilateral, band-like pressure, worse when stressed | Normal; occasional scalp tenderness | None |
| Sinusitis | 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’ | None |
| Exertional | 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 | ||
⇄ Box 11.11 Headache covered elsewhere
►► Subarachnoid haemorrhage ( OHAM4 p. 384.)
Potentially devastating bleed (typically aneurysmal) into subarachnoid space.
Symptoms Rapid-onset (<2min), severe, continuous (>2h) headache; often occipital (‘hit around back of head’), vomiting, dizziness; may have seizures.
Signs Neck stiffness, drowsy, photophobia, focal neurology, ↓GCS.
Investigations Urgent CT head; since this may miss small bleeds (20%), if CT normal, then LP (>12h after onset) for xanthochromia.
Treatment 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.
Complications Cerebral ischaemia, rebleeding, hydrocephalus, death.
►► Meningitis ( OHAM4 p. 355, ohCm10 p. 822.)
Symptoms Headache, neck pain, photophobia, seizures, unwell.
Signs ↑hr, ±↓bp, ↑temp, ↓GCS or abnormal mood, neck stiffness, ±rash, focal neurology.
Investigations Treat first; blds ↑wcc, ↑crp; ct then lp ( pp. 566–567).
Treatment Contact a senior; ceftriaxone 4g IV STAT if you have a clinical suspicion of bacterial meningitis. Resuscitate as needed ( pp. 488–489). Contact public health regarding contact tracing (see also sepsis p. 494).
Complications ↑icp, hydrocephalus, focal neurology, seizures, death.
►► Encephalitis ( OHAM4 p. 384.)
Brain inflammation, usually viral. Rare and easily missed in early stages.
Symptoms Abnormal behaviour, seizures, drowsy, headache, neck pain.
Signs Altered personality, ↓GCS, focal neurology, neck stiffness, ↑temp.
Investigations CT followed by LP ( pp. 566–567), send csf for viral pcr; CT/MRI/EEG may all show temporal lobe changes.
Treatment Be guided by microbiology; eg aciclovir 10mg/kg/8h IV (10–14d).
Complications ↑icp, seizures, death.
►► Raised intracranial pressure (ICP) ( oham4 p. 372.)
Causes cva, tumours, trauma, infection (including abscess), cerebral oedema (eg post-hypoxia), electrolyte imbalance, idiopathic.
Symptoms Headache and vomiting (worse in morning and coughing/ bending over), tiredness, visual problems, seizures.
Signs ↓GCS, focal neurology; late signs include Cushing’s reflex (↓hr, ↑bp) ±papilloedema.
Investigations Urgent CT head to assess cause and severity. Consider HIV.
Treatment 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.
Complications Herniation of the brain (‘coning’).
( p. 441), needs urgent ophthalmology review.
Temporal arteritis ( OHAM4 p. 644.)
Symptoms Headache, jaw pain on eating, visual problems, aching muscles.
Signs Temporal artery, tender scalp, pulseless/nodular temporal artery.
Investigations blds ↑↑esr (>50mm/h), ↑crp, ↑plts, ↓Hb all suggestive; definitive diagnosis requires biopsies (multiple sites) in ≤1wk of starting therapy.
Treatment 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.
Complications Blindness (10–50%), TIA/stroke.
Recurrent, pulsatile headaches with strong familial tendency. Suspect an alternative pathology if sudden onset, or >55yr with no previous migraines.
Symptoms Throbbing headache, initially unilateral often with nausea ±vomiting, photophobia; 20% may experience a preceding aura (flashing lights, zigzags, visual loss).
Signs May mimic TIA (visual defects, focal neurology) but slower onset.
Investigations Normal; perform blds, CT, LP as required to rule out alternative/coexistent pathology.
Treatment Abortive Simple analgesia ( pp. 88–91), ±anti-emetic, ±5HT1 agonists (eg sumatriptan); Preventative β-blocker (eg propranolol), or antiepileptics (eg topiramate).
Inflammation of the mucosa of the paranasal sinuses due to bacteria, viruses, or fungi; may become chronic.
Symptoms Blocked nose, nasal discharge, facial pain, unable to smell.
Signs Tender over sinuses (above medial eyebrows, bridge of nose, below eyes), purulent nasal discharge, temp usually normal.
Treatment 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.
Complications Local spread of infection, chronic sinusitis.
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.
Treatment Abortive 5HT1 agonists (eg sumatriptan nasal spray), 15L/min O2; Preventative 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 ( pp. 272–273).
► Worrying features Hypoxia, ↑HR, irregular HR, ↓BP, ↓glucose, chest pain, sudden onset, unable to stand, loss of consciousness.
Think about Vertigo Labyrinthitis, vestibular neuronitis, benign positional vertigo, trauma, ototoxic drugs, Ménière’s, CVA, multiple sclerosis, acoustic neuroma; Imbalance Hypoglycaemia, alcohol intoxication, Wernicke’s encephalopathy, CVA, cerebellar space-occupying lesion, intracranial infection, vitamin B12 deficiency, normal pressure hydrocephalus, Syncope/presyncope ( pp. 456–457).
Ask about See Box 11.12; PMH Previous dizziness, ↑bp, dm, MS, IHD; DH Antihypertensives, diuretics, aminoglycosides, insulin, oral hypoglycaemics; SH Alcohol.
Obs 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.
Investigations The type of dizziness (vertigo, ataxia, postural, syncope) should be determined from history alone; if syncope is suspected, investigate for cardiogenic causes ( p. 266); 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.
Box 11.12 Key questions in ‘dizziness’
The sensation of dizziness is difficult to describe (‘giddy’, ‘funny do’, ‘muzzy headed’) and reflects some critically different underlying pathologies; try to map your patient’s symptoms onto a medical equivalent by asking about:
• Loss of consciousness Suggests seizures ( pp. 350–352) or syncope ( p. 266). The impending sense of loss of consciousness, often with a ‘greying out’ of vision, is described as presyncope; causes and management are similar to syncope
• Postural symptoms Worse on standing after a sedentary period; this suggests postural hypotension and should prompt a review of medications
• Vertigo Is the sensation of the world moving or spinning about the patient and is worse on sudden head movements; this suggests a problem with the labyrinth, vestibular nerve, or brainstem ( p. 367)
• Ataxia Is shown by the inability to stand or walk straight; patients may have problems with fine limb movements; this suggests problems with proprioception or cerebellar function ( pp. 367–368).
Always ask about onset, deterioration, hearing loss, tinnitus, nausea, vomiting.
Box 11.13 Romberg’s test
The cerebellum normally receives information needed to keep us upright from two sensory systems: vision and proprioception (via the spinal dorsal columns). Normally, one system can compensate for loss of the other. With the eyes closed and the feet placed together, a patient who sways excessively or falls is ‘Romberg +ve’, having lost proprioception. With a cerebellar lesion, the patient will struggle to maintain posture even with the eyes open.14
► Worrying features Focal neurology, multidirectional or non-fatiguing nystagmus.
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; 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.
Labyrinthitis As for vestibular neuronitis with hearing loss or tinnitus.
Ménière’s 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.
Nystagmus This is found with many peripheral and central causes of vertigo. Causes include: stroke, MS, space-occupying lesions, labyrinthitis, vestibular neuronitis, benign positional vertigo, trauma, drugs of abuse (alcohol, LSD, PCP, ketamine), medications (lithium, SSRIs, phenytoin), Ménière’s, Wernicke’s encephalopathy; congenital (rare).
Ataxia can be differentiated from vertigo on history; there are two types:
Cerebellar ‘DANISH’ signs (see earlier in this topic); unstable even with eyes open.
Sensory Romberg’s +ve (see Box 11.13), loss of proprioception, preservation of fine coordination; ‘stamping’ gait, spinal/neuropathy signs.
Causes CVA, multiple sclerosis, alcohol toxicity, Wernicke’s encephalopathy, phenytoin, vitamin B12 deficiency, normal pressure hydrocephalus, infection, space-occupying lesions, trauma, paraneoplastic.
Management 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, p. 220), as for Korsakoff’s syndrome, to which it may progress if left untreated.
Causes Cervical spondylosis, MS, peripheral neuropathy, syringomyelia, spinal tumour, spinal infection, vitamin B12 deficiency, Friedreich’s ataxia, syphilis.
Management Urgent MRI if acute onset, otherwise consider tests for peripheral neuropathy ( p. 359), spinal X-rays, routine MRI, nerve conduction studies, neurology referral; often treated with vitamin B12.
1 Guidelines available at 
guidance.nice.org.uk/CG137 and http://www.ilae.org/
2 NICE guidelines available at guidance.nice.org.uk/NG71
3 Resources for patients, carers, and doctors at www.mndassociation.org
4 NICE guidelines available at guidance.nice.org.uk/NG42
5 NICE guidelines available at guidance.nice.org.uk/CG68
6 See Box 11.7 (p. 354) and resources from the international stroke trial collaborators, available free at www.dcn.ed.ac.uk/ist3
7 NICE interpretation of study data; see guidance.nice.org.uk/TA210
8 NICE guidelines available at guidance.nice.org.uk/CG186
9 See www.sheffield.ac.uk/FRAX/—a WHO validated tool to assess fracture risk (and need for DEXA or osteoporosis treatment) in those without worrying features ( Box 16.4 p. 451).
10 NICE guidelines for low back pain available at guidance.nice.org.uk/NG59
11 STarT Back Screening Tool available at https://www.keele.ac.uk/sbst/startbacktool/
12 NICE guidelines available at guidance.nice.org.uk/CG150
13 Pickard JD, et al.BMJ 1989;298:636 available free at www.ncbi.nlm.nih.gov/pmc/articles/PMC1835889/
14 Described by the pioneering C19th German neurologist Moritz Romberg, working among the destitute of Berlin with tabes dorsalis (tertiary neurosyphilis).