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Table2.4 Common causes oftransient loss ofconsciousness
History Examination Investigations
Epileptic
seizure
(E p. 362)
Alcohol
withdrawal
(E p. 380)
Functional
seizures
Rigors Feels cold/ hot, no
Eclampsia
(E p. 501)
Transient
arrhythmia/
Stokes– Adams
Narcolepsy Excessive daytime
Vasovagal
syncope
(E p. 274)
Known epilepsy, may
have aura, post- ictal
confusion/ weakness
Usually >50units/ wk
alcohol consumption,
last drink >24h ago
Unusual features, long
duration, memory of
event, eyes shut
LOC, coarse shaking,
infective symptoms
Pregnant, may be
unaware
Palpitations, pale,
sudden LOC ±limb
jerking; rapid recovery
with ushing
sleepiness, collapse,
sleep paralysis
±hallucinations
Feels light- headed ±hot,
then collapse while
standing, ±ne limb
jerking, ±urinary incontinence, rapid recovery,
no post- ictal phase
Often normal, may
have tongue or limb
trauma
Anxious, sweaty,
tachycardic, tremor
±chronic liver failure
Responsive to pain,
normal respiration,
no injuries
Febrile, source of
infection (eg UTI,
pneumonia), no injury
iBP, palpable uterus,
peripheral oedema
Evidence of cardiac
disease, injury
following fall,
irregular/ absent
pulse during attack
Often normal; loss of
postural muscle tone
and tendon reexes
during attacks
Bradycardia and
hypotension during
episode, GCS 5/ 5
within min, no focal
neurology
Often normal, may
have focal lesion
or metabolic cause
iMCV and γGT;
dplatelets, mild
anaemia
Normal
investigations
iWBC, NØ or
LØ, and CRP, +ve
urine dipstick
Proteinuria, foetal
heart on Doppler
Arrhythmia
or heart block
on ECG, 24h
ECG and BP
monitoring, echo
HLA typing, sleep
studies
±postural drop
(systolic drop
of 20mmHg or
more)
363SEIZURES
Box 2.5 Assessing a ‘rstt’
HistoryDetailed account from rst- hand witness, documented carefull y.
InvestigationsFBC, U+E, LFT, glucose, Ca
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.
ManagementAdmit only if GCS <5 or drowsy; discuss with senior doctor regarding
suspicion of seizures and need to give up driving (E p. 633, yr ban) and safety
advice; do
not start antiepileptic medication— this decision should be made by a neur-
ologist in an urgent out- patient clinic (‘rst t’ clinic).
2+
, Mg2+, PO
3−
, clotting, medication levels,
4
I Box 2.6 Causes ofseizures elsewhere inthisbook
Raised ICP E p. 372 Hypertensive emergency E p. 276
Hypoglycaemia E p. 337 Hypoxia E p. 284
Hypocalcaemia E p. 410 Meningitis/ encephalitis E p. 372
Hyper/ hyponatraemia E pp. 408–9 Eclampsia E p. 501
364 CHAPTER2 Neurology
Neurodegenerative disorders
Parkinson’s disease(E OHCM1 p. 490.)
$ Common neurological disorder (aects ~% of >60yr). Cardinal fea-
tures 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; SPECT if indistinguishable from essential
tremor; exclude other causes of ‘Parkinsonism’, eg drug induced (haloperidol). Refer to a specialist early before initiating treatment.
Management MDT (PD doctors, specialist nurses, PT, OT, SALT). Anti-
parkinsonian medications should be started and titrated by specialists.
Levodopa enhances dopamine transmission but eectiveness reduces over
years. st line either levodopa with peripheral dopa- decarboxylase inhibitor
(eg carbidopa) if symptoms interfere with lifestyle, or levodopa, dopamine
agonists (eg ropinirole), or monoamine oxidase inhibitors (eg selegiline) if
they do not. Problematic ‘on–o ’ and ‘end-of-dose’ phenomena with levodopa may require the addition of MAO- B inhibitor, dopamine agonist, or
COMT-inhibitor (eg tolcapone). Administration is at strict times, so drug
chart timings may need changing. In NBM patients deliver usual medicines
via NG tube or convert to topical route (eg rotigotine).
Complications Depression, dementia (late stage): Parkinson’s disease may have
pathological overlap with Lewy body dementia (E p. 385) 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
$ Degenerative disease aecting upper and lower motor neurons.
Diagnosis Primarily clinical but EMG can help. Progressive motor weakness
(UMN and LMN E p. 355) and behavioural change; sensation unaected.
Fasciculations progress to spasticity, poor swallow, and dementia.
Management Early referral to neurology- led MDT including MND nurse,
PT, OT, SALT, palliative care, and dietetics.
non-invasive ventilation, and riluzole. Quinine and baclofen for cramps.
Exercise programmes. Prognosis3– 5yr.
ComplicationsAspiration, respiratory failure, frontotemporal dementia.
Huntington’s disease
$ Incurable inherited (autosomal dominant) disorder characterized by
involuntary limb movements (chorea), dementia, and behavioural disturbance (depression, psychoses). Onset at 30– 50yr.
Friedreich’sataxia
$ Inherited (autosomal recessive) disorder characterized by progressive limb
and gait ataxia, dysarthria, loss of proprioception, absent tendon reexes in the
legs, and extensor plantar responses. Inability to walk occurs 75yr after disease
onset. May also develop heart failure and DM. Supportive management.
5
NICE guidelines available at Mguidance.nice.org.uk/ NG7
6
Resources for patients, carers, and doctors at Mwww.mndassociation.org
7
NICE guidelines available at Mguidance.nice.org.uk/ NG42
5
7
Consider gastrostomy,
6
STROKE/CVA/TIA EMERGENCY
2Stroke/CVA/TIA emergency
2 Airway
2 Breathing
2 Circulation
2 Disability
3Call for senior help early. Patient may need urgent aspirin, thromb-
olysis, thrombectomy, or transfer to Hyperacute Stroke Unit (HASU).
If GCS is reduced Epp. 352–3.
•
5L/ min O
•
Check blood glucose; treat if too low (E p. 336) or high (Ep. 338)
•
Check temp; treat if too low (blankets) or high (IV/ PR paracetamol)
•
Monitor O
•
Venous access, FBC, ESR, U+E, LFT, lipids, CBG, trop, coag,G+S
•
NBM and start IV uids for hydration (eg 0.9% saline at 00mL/ h)
•
ECG looking for atrial brillation, utter, 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 ndings
•
Request urgent CT head ±CT angiogram ±CT perfusionscan
•
Consider aspirin/ thrombolysis/ thrombectomy after CT (Boxes 2.7– 2.9)
•
Reassess, starting with A, B, C…
2Box 2.7 Consider thrombolysis witht- PA inCVAif
• ≤4.5h from onset (possibly 4.5– 6h, but benetsless)
• Access to specialist stroke services
• Non- haemorrhagic stroke (excludedbyCT)
• Signicant symptoms and not improving
• Contraindications as for cardiac thrombolysis (Epp. 564–5).
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort—
If no palpable pulse—
If GCS ≤8—
if SOB or sats<94%
2
sats, RR, HR, cardiac trace, temp,andBP
2
CALL ANAESTHETIST
CALL ARREST TEAM
CALL ARREST TEAM
365
2Box 2.8 Consider intra- arterial thrombectomyif
• CT shows no haemorrhage and little sign of early ischaemicchange
• CTA/MRA shows large proximal occlusion of the anterior circulation
• An established and experienced thrombectomy service is available
• It can be initiated as rapidly as possible (ideally within6h)
• Modied Rankin <3
+ National Institute of Health Stroke Scale >5.
2Box 2.9 Key dierentials
Hypo/ hyperglycaemia E pp. 337, 340–1 Other intracranial pathology E pp. 355–7
Encephalitis/ meningitis E p. 372 Seizure/ Todd’s paresis E pp. 361–3
Overdose E pp. 497–9 Severe liver/ renal failure E pp. 327–31, 395
Bell’s palsy E p. 357 Hypertensi ve encephalopathy E pp. 280–1
366 CHAPTER2 Neurology
Stroke
$ Neurological disability due to sudden loss of perfusion of an area of brain.
CausesIschaemia (85%, eg AF, carotid stenosis) or haemorrhage (5%).
SymptomsSudden- onset focal neurology though onset can be stuttering.
Signs
Check for irregular heartbeat, carotid bruit, and LVF. The Bamford
stroke classication (Table 2.5) allows easy recognition of the area
of brain aected, as well as prognostication; Posterior circulation strokes
(POCS) aect the territory of the vertebrobasilar artery (occipital lobes,
brainstem, and cerebellum); Anterior circulation strokes involve the internal
carotid artery territory, which supplies the rest of the brain. These are
further subcategorized as
terior circulation stroke
Investigations bldsFBC, U+E, LFT, glucose, lipids, clotting;ECG; CXR;
±CT angiogram ±CT perfusion scan urgently if within thromb-
CT head
olysis/ thrombectomy window, GCS persistently low, on oral anticoagulants/ known bleeding disorder, severe headache at onset of stroke or
evidence of iICP; otherwise CT head within 24h. TACS/ PACS also
need
echo, carotid Doppler, and 24hECG. Common practice in cases of
high clinical suspicion of stroke and negative CT is to proceed to MRI.
Treatment
See emergency treatment E p. 365; if candidate for thromb-
olysis9 ±interventional thrombectomy, move fast to ensure timely treatment.
Otherwise, aspirin 300mg/ 24h PO/ PR for 4d (provided no haemorrhage on
CT). Assess swallow (Box 2.0); if concerns, keep NBM+IV uids and request
SALT assessment. Do not lower BP acutely unless haemorrhage (aim SBP 30–
40mmHg). Do not use LMWH acutely (risk of haemorrhagic transformation).
Do not prescribe TEDS (risk of pressure ulcers); consider intermittent pneumatic compression to prevent DVT. Stroke ward care for early mobilization and
rehabilitation with MDT (stroke doctor, stroke nurse, PT, OT, dietician).
Complications Aspiration, dependence, further event, bleed, iICP,
malignant MCA syndrome.
Table2.5 Bamford stroke classication
TAC S All of: Motor/ sensory decit in ≥2 of face, arm,leg
PAC S Either:
LACS Motor and/ or sensory decit aecting ≥2 of face, arm,leg
POCS Any of: Ipsilateral cranial nerve palsy + contralateral motor/ sensory decit
Source:data from Bamford J, etal. Lancet 99;337:52 (subscription required).
*
Loss of vision on the same side in both eyes (Fig.3. p. 31).
†
Includes dysphasia, visuospatial problems,dGCS.
8
NICE guidelines available at Mguidance.nice.org.uk/ CG28
9
See Box 2.7 and resources from the International Stroke Trial collaborators, available at
Mhttps://www.ed.ac.uk/clinical-brain-sciences/research/completed-studies-trials/ist-3-trial
Homonymous hemianopia
Higher cortical dysfunction
2 out of 3 of TACS criteriamet
or:
Higher cortical dysfunctionalone
or:
Isolated motor decit not meeting LACS criteria
No higher cortical dysfunction or hemianopia
Bilateral motor/ sensory decit
Disordered conjugate eye movement
Cerebellar dysfunction
Isolated hemianopia or cortical blindness
total anterior circulation stroke
(PACS), and
lacunar stroke
*
†
(TACS),
(LACS).
8
partial an-
Transient ischaemic attack(TIA)
$ A transient episode of neurological dysfunction caused by focal brain
ischaemia without infarction. Symptoms typically last less than an hour,
but prolonged episodes canoccur.
Symptoms/ signsAs for stroke but resolve completely (classically within 24h,
though no precise cut- o time distinguishes ischaemia from infarction);
note that transient loss of consciousness, ‘dizzy turns’, or +ve symptoms
(seeing lights, sounds, tingling, movements) are unlikely to beaTIA.
ManagementIf <3h since symptoms began E p. 365. Start aspirin 300mg/
24h. Any suspected TIA should be considered high risk for stroke so refer
immediately for specialist assessment (ideally <24 hours from onset).
8
CVA preventionThe risk of further events after TIA or stroke can be re-
duced 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/ 2h PO. Clopidogrel is usually rst choice if tolerated.
Encourage smoking cessation, healthy diet, and moderate exercise.
Carotid endarterectomy should be considered within 2wk if symptomatic carotid stenosis>70%.
T Box 2.0 Not safe toswallow? Do a ‘ward swallow’
For any patient with dGCS or suspected neurological disability, perform a ‘ward swallow’ assessment. Give them a spoonful of water,
then a sip of water, and then a cup of water, each time observing for
the following and not proceeding if they occur at anytime:
• Delayed swallowing (>2s to initiate swallow)
• Drooling
• Cough during or within min of swallowing
• Dysphonia/‘wet voice’ after swallowing.
If any of these features are present, keep NBM+IV uids and request
a SALT assessment.
367STROKE
0
0
NICE clinical knowledge summary available at Mcks.nice.org.uk/topics/stroke-tia
368 CHAPTER2 Neurology
Backpain
2Worrying features Bladder/ bowel changes, fever, weight loss, age
<20yr or >55yr, steroids, thoracic pain, previous cancer, progressive neurological decit, swelling, wakes them up at night, not relieved by rest, perianal
anaesthesia, pulsatile abdominalmass, trauma, immunosuppression.
Think about 2 Serious Cord compression, cauda equina syndrome,
malignant metastases, myeloma, infection, fracture, aortic aneurysm;
CommonMechanical back pain (Table2.6), renalcolic.
Ask aboutTrauma/ lifting (mechanism), location of pain, duration, aggra-
vating/ 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;
neurological problems, osteoporosis, anaemia, cancer;
gesia;
FHJoint or back problems;SHOccupation (lifting, prolonged sitting).
Look for Scoliosis, kyphosis, bony or paraspinal tenderness; re-
duced range of movement (especially exion), pain on straight leg raise
(E p. 47); lower limb neurological decit (motor, sensory, reexes); expansile abdominal mass;
PR dtone or sensation (sacral/ saddle anaesthesia).
InvestigationsIf you suspect mechanical back pain and worrying fea-
tures are not present, no further investigation required; otherwise consider:
blds FBC, ESR, CRP, Ca
2+
, ALP, PSA; CXR ±spinal X- ray if post
trauma or risk of pathological fracture;
compression or cauda equina suspected; urgent if suspected malignancy,
infection, or fracture; routine if suspect inammatory disorder;
Table2.6 Common causes ofbackpain
History Examination Investigations
3
compression
3Cauda
equina
syndrome
Mechanical
back pain
Spondylitis ‘Inammatory type’ pain,*
Vertebral
collapse
fracture
*Pointers to an inammatory aetiology include:morning stiness, pain that improves with exercise but not rest, alternating buttock pain, nocturnal pain during second 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).
See Mwww.sheeld.ac.uk/ FRAX/ — a WHO validated tool to assess fracture risk (and need for
DEXA or osteoporosis treatment) in those without worrying features (E Box 7.4p. 459).
(±pain) below lesion,
incontinence
Leg weakness and pain
(often bilateral), urinary
and/ or faecal incontinence
Pain, worse on
movement, brought on
by lifting/ trauma
joint pain, no trauma,
family history
Sudden- onset pain in an
elderly patient
Weakness, numbness
Cord
Dermatomal
distribution; UMN below
lesion, LMNat lesion
dperianal sensation,
danal tone, dleg power,
sensation, and reexes
Pain reproduced by
straight leg raise,
unilateral neurology
dlumbar exion, pain on
squeezing pelvis; ±painful
red eye (E pp. 448–50)
Central pain over a
discrete vertebra;
reduced ROM
PMHPrevious back/ joint pain,
DH Steroids, anal-
MRISpine:as emergency if cord
Emergency/ urgent
MRI to look for
lesion
Emergency/ urgent
MRI to look for
lesion
Imaging rarely
needed and only in
specialist settings
RhF– ve, iESR,
sacroiliitis on X- ray,
MRI inammation
Fracture on X- ray
(wedge- shaped
vertebral body)
DEXA.
369BACK PAIN
Mechanical back pain including disc prolapse
SymptomsLow back pain, worse on coughing/ moving, may radiate toleg.
SignsPainful leg raise, tender around vertebra, radicular pain, normalPR.
Risk assessNICE use the STarT Back Screening Tool.
3
Uses pain distribu-
2
tion, 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 Table2.7.
Treatment Reassurance, education, and resumption of normal activities for
all (including early mobilization, avoid lifting, maintain posture). Exercise
and CBT programmes if recovery predicted to be slow and painful.
Short- term NSAIDs but recognize risks and limited benet. Reassess urgently if bilateral symptoms or urinary/ faecal incontinence.
Table2.7 Types ofmechanical backpain
‘Sprain’ Muscular pain and spasm without neurology
Disc prolapse ‘Slipped disc’, may compress the nerve root causing a
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
Lumbar spinal
stenosis
3
Cord compression
unilateral radiculopathy (eg sciatica)
patients; conservative management; spinal fusion if severe
Narrowing of the spinal canal eg due to OA, causes leg
aching and heaviness on walking (spinal claudication)
CausesTumour, 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 (Ep. 483).
InvestigationsUrgent MRI spine, look forcause.
TreatmentCatheterize; refer immediately to orthopaedics/ neurosurgeons.
ComplicationsWeakness, reduced sensation, incontinence, impotence.
3
Cauda equina syndrome
CausesCentral disc prolapse, tumour, abscess/ TB, haematoma, trauma.
SymptomsUrinary incontinence or retention (may be painless), faecal in-
continence, bilateral leg weakness andpain.
Signs Bilateral reduced power (LMN) and sensation, reduced perianal
(saddle) sensation, reduced anal tone, bilateral absent ankle reexes.
InvestigationsUrgent MRIspine.
TreatmentCatheterize; refer immediately to orthopaedics/ neurosurgeons.
ComplicationsWeakness, reduced sensation, incontinence, impotence.
Vertebral collapse fracture
CausesTrauma, osteoporosis, tumour.
SymptomsSudden- onset back pain; may be mild trauma if pathological.
SignsCentral vertebral tenderness, reduced mobility.
InvestigationsSpinalX- ray.
TreatmentAnalgesia, assess ability to cope, treat osteoporosis (Ep. 459).
2
NICE guidelines for low back pain available at Mguidance.nice.org.uk/ NG59
3
STarT Back Screening Tool available at Mhttps://startback.hfac.keele.ac.uk/
370 CHAPTER2 Neurology
Headache
2Worrying features dGCS, sudden onset, severe, recurrent
vomiting, photophobia, rash, neck stiness, focal neurology, seizures,
papilloedema, diHR,diB P.
Think about 2Emergencies Intracranial haemorrhage (subarachnoid,
subdural, extradural), meningitis, encephalitis, iICP, temporal arteritis,
acute glaucoma, hypertensive crisis;
tion, migraine, extracranial (sinuses, eyes, ears, teeth), trauma, post- LP,
post- nitrates;
Other Cluster, postcoital, hypoglycaemia, hyponatraemia.
See Table2.8 and Box2..
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, eye pain/watering, rhinorrhoea;
PMHPrevious headaches, migraines (and usual symptoms);DHNitrates,
analgesics, antihypertensives;
druguse.
ObsTemp, GCS, glucose, HR, BP, uid balance. Cushing’s reexIs a late
sign of iICP:dHR andiB P.
Look forVolume status (E p. 402); evidence of meningism:neck sti-
ness, photophobia, Kernig’s sign (fully ex hip and passively extend knee,
+ve if painful in head or neck); non- blanching rash (check whole body);
red eye (E pp. 448–50), 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;
and send
tures;
blds FBC, ESR, U+E, LFT, glucose, CRP, clotting, and bld cul-
ABG Especially if dGCS.CT head ±LPDiscuss with a senior whether
these are required (E p. 580);
Treatment Exclude emergencies and treat other causes with simple
analgesia (E pp. 92–4) and uids if dehydrated (E pp. 402–5); ask to
be contacted if symptoms fail to improve or worsen:
New onsetGCS <5 (Epp. 352–3).
New- onset focal neurology Re- evaluate for meningitis, encephalitis, or iICP
(E p. 372):5L/ min O
Sudden (onset <2min), severe, and constant Consider a subarachnoid
, consider ABx— call a senior urgently.
2
haemorrhage (E p. 372): 5L/ min O
Unwell, deranged obs Always consider meningitis/ sepsis (E p. 372), classic
symptoms in <30%:5L/ min O
Red, painful eye, dacuity Acute glaucoma (E p. 449), urgent ophthal-
mology referral.
Temporal tendernessConsider temporal arteritis (Ep. 373).
Hypertensive(BP >200/ 20mmHg) (Epp. 278–81).
4
NICE guidelines available at Mguidance.nice.org.uk/ CG50
CommonDehydration, tension, infec-
SH Recent stressors, alcohol intake, illicit
4
otherwise secure IV access
EEGMay help diagnose encephalitis.
, lie at— call a senior urgently.
2
, IV uids, discuss ABx with senior.
2
Table2.8 Common causes ofheadache
Subarachnoid
or warning
bleed
Subdural or
extradural
haematoma
Meningitis
septicaemia
±
Raised ICP Vomiting, blurred vision,
Encephalitis Drowsy, confused, vomiting,
Temporal
arteritis
Migraine Previous mig raines, visual
Cluster Severe recurrent daily
Tension Bilateral, band- like pressure,
Sinusitis Frontal pain, blocked/
Trigeminal
neuralgia
Exertional Sudden, explosive bilateral
Acute
glaucoma
Drug
induced
History Examination Investigations
Rapid onset, severe pain,
vomiting, dGCS if severe
Trauma, confusion,
vomiting
Unwell, irritable, drowsy,
photophobia, feels ill ±rash
dizzy, drowsy, worse on
coughing/ bending, seizures
seizures, preceding ulike illness, non- specic
symptoms
Age >55yr, visual
disturbances, weight loss,
polymyalgia, jaw pain/
claudication
aura; unilateral, throbbing,
nausea, ±vomiting
headaches, unilateral
worse when stressed
runny nose
Frequent, brief ‘stabbing’
pains; unilateral in
distribution of CN V;
previous facial herpes zoster
pain typically on exercise
or orgasm
Age >50yr, blurred vision,
pain in one eye, often
occurs at night
Many medications can induce headaches, particularly nitrates, Ca2+
channel antagonists, and metronidazole with alcohol
May be normal, neck
stiness, photophobia,
focal neurology
d/ uctuating GCS;
may be signs of iICP
Febrile ±septic, neck
stiness, photophobia
±non- blanching rash
Pupillary abnormalities,
focal neurology; late
signs:papilloedema,
Cushing’s reex
Pyrexia, dGCS,
confusion, focal
neurology, neck
stiness, photophobia
Tender, palpable,
non- pulsatile temporal
artery, tender scalp
Photophobia, visual
eld defects, may have
focal neurology
Agitated, rhinorrhoea,
lacrimation, sweating
Normal; occasional
scalp tenderness
Tender above or
below eyes
Normal; may identify
‘trigger point’
May mimic migraine or
SAH, but meningism
absent
dvisual acuity, dilated,
±oval pupil, red
around cornea, tender
Bleed on CT;
xanthochromia in
CSF after 2h
Blood seen on CT
iWCC, iCRP;
CSF:neutrophilia
±dglucose
Abnormal CT:
enlarged ventricles
±focal lesion
CT/ MRI:oedema,
temporal lobe
changes; CSF:iLØ
±protein
iCRP, iii ESR with
anaemia, iplts and
iALP, biopsy
Usually none.
Consider MRI
head if new and
>55yr
None
None
May have iLØ,
NØ, or EØ
MRI can
demonstrate
neurovascular
compression
Consider CT/ LP
to rule out SAH
iintraocular
pressure,
ophthalmology
review
371HEADACHE
I Box 2. Headache covered elsewhere
Subdural haematoma E p. 460 Extradural haematoma E p. 460
Acute glaucoma E p. 449 Sepsis E p. 484
372 CHAPTER2 Neurology
3Subarachnoid haemorrhage (E OHAM4p. 402.)
$ 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.
SignsNeck stiness, drowsy, photophobia, focal neurology,dGCS.
InvestigationsUrgentCThead; since this may miss small bleeds (20%), if
CT normal, then
Treatment5L/ min O
and antiemetic, eg metoclopramide 0mg IV/ IM. Refer urgently to neuro-
LP(>2h after onset) for xanthochromia.
, analgesia (codeine 30mg PO or 5mg morphine IV)
2
surgeon for endovascular coiling or neurosurgical clipping and consider
transfer to ICU if dGCS. Lie the patient at and advise not to get up or eat.
Reassess often and request neuro obs. Nimodipine (60mg/ 4h PO) prevents vasospasm and improves outcome.
5
Keep systolic 30–40mmHg,
using IV β- blockers, unless lethargic (suggests vasospasm; may require permissive hypertension). Focal neurology or dGCS carry a worse prognosis.
ComplicationsCerebral ischaemia, rebleeding, hydrocephalus,death.
3
Meningitis (E OHAM4 p. 371, E OHCM1p. 806.)
SymptomsHeadache, neck pain, photophobia, seizures, unwell.
Signs iHR, ±dBP, itemp, dGCS or abnormal mood, neck stiness, ±rash.
InvestigationsTreat rst;blds iWCC, iCRP; CT then LP (Epp. 580–1).
TreatmentContact a senior; ceftriaxone 4g IV STAT if you have clinical suspi-
cion of bacterial meningitis. Resuscitate as needed (E pp. 478–9). Contact
public health regarding contact tracing (see also sepsis Ep. 484).
Complications iICP, hydrocephalus, focal neurology, seizures,death
3
Encephalitis (E OHAM4p. 378.)
$ Brain inammation, usually viral. Rare and easily missed in early stages.
SymptomsAbnormal behaviour, seizures, drowsy, headache, neckpain.
SignsAltered personality, dGCS, focal neurology, neck stiness,itemp.
Investigations CTthenLP(E pp. 580–1), send CSF for viral PCR (can be
normal early in disease);
CT/ MRI/ EEGmay show temporal lobe changes.
TreatmentBe guided by microbiology; eg aciclovir 0mg/ kg/ 8h IV (0– 4d).
Complications iICP, seizures,death.
3
Raised intracranial pressure (ICP) (E OHAM4p. 388.)
CausesCVA, tumours, trauma, infection (including abscess), cerebral oe-
dema (eg post- hypoxia), electrolyte imbalance, idiopathic.
Symptoms Headache and vomiting (worse in morning and coughing/
bending over), tiredness, visual problems, seizures.
Signs dGCS, focal neurology; late signs include Cushing’s reex (dHR,
iBP) ±papilloedema.
InvestigationsUrgentCThead to assess cause and severity. ConsiderHIV.
TreatmentElevate 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/ neurologistearly.
ComplicationsHerniation of the brain (‘coning’).
3Acute glaucoma
(E p. 449), needs urgent ophthalmology review.
5
Pickard JD, etal. BMJ 989;298:636. Mwww.ncbi.nlm.nih.gov/ pmc/ articles/ PMC835889/