Patients with acute neurological symp-toms frequently present to the emergencydepartment. The commonest presenta-tions include headache and seizures.Careful clinical evaluation and promptinvestigation are required to excludesinister causes and initiate correct treat-ment.

Headache

Most patients presenting urgently withheadache will not have sinister under-lying pathology but the primary aim ofacute assessment is the rapid identifica-tion of those with such pathology(Table 1). A careful history is critical, inparticular determination of the rate ofonset and location of the headache aswell as any associated features.

Intracranial haemorrhage

Subarachnoid haemorrhage (SAH)(Fig 1) must be excluded in any patientwith abrupt (‘thunderclap’) onsetheadache even in the absence of any neu-rological signs. The headache is instanta-neous and reaches its peak rapidly(seconds to minutes).1 Meningism,nausea and vomiting are common butnot invariable. Seizures and loss of con-sciousness may occur at onset. If anurgent radiologist reported computedtomographic (CT) brain scan of thebrain is normal, a lumbar puncture (LP)must be performed more than eighthours after ictus to assess cerebrospinal

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Susan E Tomlinson BMed FRACP(Australia),

Clinical Research Fellow, Department of

Molecular Neuroscience, Institute of

Neurology, London

Michael G Hanna

MBChB(Hons) BSc(Hons) MD FRCP, Consultant

Neurologist and Professor in Clinical

Neurology, Centre for Neuromuscular

Disease, National Hospital for Neurology;

Department of Molecular Neuroscience,

Institute of Neurology, London

Clin Med 2007;7:272–7

Acute neurologyHeadache type Causes

Primary headache syndrome eg migraine, cluster migraine headache, tension headache

Secondary headache Intracranial haemorrhage: subarachnoid, subdural,

intracerebral

Meningitis or encephalitis

Increased intracranial pressure: idiopathic or secondary

Cerebral venous sinus thrombosis

Arterial dissection, arteritis, arterial occlusion

Intracranial hypotension

Extracranial process: cervicogenic headache, sinusitis,

glaucoma

Malignant hypertension

Temporal arteritis (usually over age 55 years)

Table 1. Causes to consider in emergency presentation of headache.

Fig 1. Non-contrast computed tomograph of the brain showing subarachnoidhaemorrhage with hydrocephalus and blood extending into the lateral and fourthventricles.

fluid (CSF) red cell count and xan-thochromia. Arterial aneurysm is thecommonest cause of SAH. GlasgowComa Score (GCS) should be monitoredsince obstructive hydrocephalus andraised intracranial pressure (ICP) mayoccur. Urgent neurosurgical assessmentis essential for definitive treatment toprevent rebleed which is associated withhigh mortality. Nimodipine may reducecerebral vasospasm and should beadministered when advised by theneurosurgical team.2

Intracerebral haemorrhage (Fig 2)usually causes acute onset focal neuro-logical deficit ‘stroke’ and may be accom-panied by headache, especially ifaccompanied by uncontrolled hyperten-sion. Careful control of blood pressureand neurological monitoring for signs ofraised pressure are important. Neuro-surgical evacuation may be required in asmall proportion of patients.

Subdural haemorrhage (SDH) (Fig 3)may be spontaneous or secondary totrauma (sometimes minor trauma in theelderly). SDH should always be thoughtof in an older patient with gradual onsetheadache, particularly if there is focalneurology. Once diagnosed, urgent neu-rosurgical advice should be soughtregarding the need for evacuation versusmonitoring.

Meningitis and encephalitis

Headache, fever, meningism and alteredconsciousness raise the suspicion ofmeningitis or encephalitis. The mostcommon causes of community-acquiredbacterial meningitis are Streptococcuspneumoniae and Neisseria meningitidis.Patients may become drowsy or haemo-dynamically unstable in a short period oftime. If bacterial meningitis is suspected,blood cultures should be taken andantibiotics commenced immediately.Delayed antibiotic treatment may resultin adverse outcome. Patients shouldundergo CT of the brain (or magneticresonance imaging (MRI) if available)followed by LP. A recent review con-cluded that dexamethasone given fromthe time of administration of the firstdose of antibiotics improves morbidityand mortality in adults with community-

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Patients with acute neurology commonly present in the emergency department;headache and seizures are among the most common presentations

Acute headache requires careful clinical evaluation. Rapid imaging may be requiredto exclude subarachnoid haemorrhage (SAH) or structural pathology. Furtherassessment of infection or haemorrhage with a lumbar puncture may beconsidered in the absence of structural pathology

A patient presenting with sudden onset of severe headache should be consideredto have an SAH until proven otherwise

In acute seizures the immediate priority is to stop seizure activity, followed byrapid evaluation to determine the underlying cause

Key Points

KEY WORDS: headache, meningitis, seizure, subarachnoid haemorrhage

Fig 2. A large left-sided acute intraparenchymal haemorrhage adjacent to the leftlateral ventricle. There is extension of haemorrhage into the lateral, third and fourthventricles. The lateral ventricles appear dilated. There is some mass effect with minormidline shift. The basal cisterns are still visualised.

acquired bacterial meningitis.3 LP shouldbe deferred until after brain imaging ifthere are features of ICP, focal neuro-logical deficits or the occurrence ofseizures: in these situations the patientmay be at risk of brain herniation.

Current international guidelines forempiric antibiotic treatment recommendvancomycin and a third-generationcephalosporin (ceftriaxone or cefo-taxime) until organism identificationand sensitivities are known.4 Cephalo-sporin resistant S. pneumoniae is lessprevalent in the UK than in other coun-tries (eg USA, Australia, Spain). Localcentres may advise initial treatment withcephalosporins alone, but with the rec-

ommendation that clinicians have a lowthreshold for addition of vancomycin ifthere is a delay to LP and/or if the patienthas any risk factors for exposure to resis-tant S. pneumoniae.5 Ampicillin shouldbe added if the presence of Listeria mono-cytogenes is possible.

The risk of immunocompromise andhistory of recent travel should be docu-mented. These features may prompttailoring of initial antimicrobial treat-ment until microbial clarification isobtained.

The clinical presentations of bacterialmeningitis, viral meningitis and viralencephalitis may overlap. Early seizuresand confusion are more likely to occur in

encephalitis. Brain MRI will often showtemporal lobe changes in viral ence-phalitis. In patients with viral meningitisand encephalitis, CSF shows mono-nuclear pleocytosis and Gram stain isnegative. In patients with bacterialmeningitis there are predominantlypolymorphs in the CSF. Viral polymerasechain reaction may assist in diagnosingthe commoner viral causes of meningitisor encephalitis (eg herpes simplex). EEGmay be helpful in viral encephalitis andshow temporal lobe changes (eg slowingor 2–3 Hz spike/wave).6

Symptomatic management with anal-gesia, anti-emetics and adequate hydra-tion is often adequate in uncomplicatedviral meningitis. If there is clinical suspi-cion of encephalitis (seizure, delirium,obtundation), antiviral treatment shouldbe commenced. Herpes simplex virus isthe commonest cause and treatment iswith aciclovir 10 mg/kg three times a day.

Increased intracranial pressure

Headache which is worse in the morning,exacerbated by Valsalva manoeuvres andassociated with nausea and vomitingmay suggest increased ICP, but manyacute headache patients without raisedICP may exhibit these clinical features.The finding of focal neurological signswith papilloedema strongly points toraised ICP. Imaging should be performedto exclude an underlying structurallesion or cerebral venous sinus throm-bosis (CVST). LP should be consideredonly if a structural lesion is excluded onimaging. Intermittent severe headache,sometimes with episodes of loss of con-sciousness, may occasionally be due tointermittent obstruction of CSF flow, forexample by a third ventricle colloid cyst.

Idiopathic intracranial hypertension ischaracterised by headache, often severeand pulsatile, with papilloedema. Theremay be transient visual obscurations orwhooshing in the ears. This condition typ-ically affects women of childbearing ageand is associated with elevated body massindex. There may be a history of recentweight gain or use of certain medications(eg tetracyclines, vitamin A). LP confirmselevated opening pressure (>25 cm H20).Other causes of increased ICP must be

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Fig 3. A large right acute-on-chronic right-sided subdural collection with significantmass effect and early subfalcine herniation.

excluded and CSF constituents and cere-bral imaging be normal.7 Untreated papil-loedema may result in permanent visualloss. Treatment aims to lower ICP withacetazolamide, serial LP, shunting of CSFfluid or optic nerve sheath fenestration.Weight loss may help.8

Cerebral venous sinusthrombosis

Although uncommon, CVST is animportant diagnosis to consider inpatients presenting with severe headache.Predisposing factors include pregnancy,the postpartum period, prothrombotic

states, dehydration and sepsis (especiallyintracranial infection). The headache isusually generalised and acute or subacutein onset. There may be features of raisedICP, meningism, drowsiness, seizures(often focal), papilloedema and focalneurological deficit due to stroke(venous infarct).9 A non-contrast brainCT in the acute phase may show an‘empty delta’ sign and hyperintensity inthe sagittal, straight and transversesinuses (Fig 4). Initial treatment is withtherapeutic doses of heparin followed byoral warfarin. Secondary intracranialvenous haemorrhage does not neces-sarily contraindicate anticoagulation but

neurological advice should be sought.10

Duration of warfarin therapy depends onpersistence of underlying cause.

Migraine

Sudden onset of a severe headache, oftenunilateral, associated with nausea, vom-iting and photophobia is typical of anacute migraine. However, this diagnosisshould not be made in patients presentingwith these symptoms for the first timeunless all the above causes (intracranialhaemorrhage, meningitis, encephalitis,ICP, CVST) have been considered andexcluded by appropriate investigations.Patients known to have migraine maydescribe an antecedent prodrome or auraand may have a family history ofmigraine. Simple analgesia such as aspirinand non-steroidal anti-inflammatorydrugs (NSAIDs) in combination withanti-emetics may be adequate to controlthe acute event. 5-hydroxytryptamine-1agonists (triptans) administered at theonset of a migraine may avert a full attackbut should not be used in patients withcardiovascular disease.11 After discharge,migraine patients may require ongoingmanagement of their symptoms by theirgeneral practitioner or a neurologist.Opiate seeking patients sometimes pre-sent with apparent acute migraine toobtain pethidine or other opioids. Theuse of NSAIDs and triptans by acutephysicians will help to reduce thisbehaviour.

Extracranial causes

Extracranial causes such as temporalarteritis, cervicogenic headache, sinusitisand glaucoma should be considered.History may point to the underlyingdiagnosis. Spontaneous or traumatic ver-tebrobasilar or carotid dissection canpresent with neck pain or headache andmay be associated with stroke. MRI brainwith MR angiogram may be required.

Seizure

A detailed history from the patient and,if possible, an eyewitness is importantwhen assessing a patient with a blackout

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Fig 4. Hyperintensity within the straight sinus extends into the torcular, with furtherextension into the superior sagittal sinus. This is likely to represent acute thrombus.The suprasellar, ambient and quadrigeminal cisterns are effaced.

suspected to be a generalised seizure.Syncope is the main differential; some-times an initial syncopal event may befollowed by a seizure if brain hypoxia isprolonged (eg if the patient is main-tained in a vertical position). Featuresprior to the collapse should be askedabout specifically (eg pallor, diaphoresis,palpitations, chest pain) which maypoint to syncope. In contrast, a specificaura (eg epigastric rising, olfactorysymptoms, focal motor or sensory symp-toms) is more suggestive of a seizure.Incontinence and tongue biting are morecommon in seizures but can sometimesaccompany cardiac syncope. Recoveryfrom syncope is usually more rapid thanafter a generalised seizure when a patientis often confused and may complain ofheadache and limb stiffness.

Seizures may be caused by idiopathicepilepsy, structural brain pathology oraltered cerebral physiology (eg metabolicdisturbance such as hypoglycaemia oralcohol withdrawal) (Table 2). Manypatients presenting with seizure areknown cases of epilepsy. Possible causesinclude general poor control of the con-dition (eg drug-resistant epilepsy), lackof drug compliance or other triggers suchas lack of sleep. Patients presenting witha first seizure may represent a new case ofidiopathic epilepsy or have underlyingstructural brain pathology, infection orother causes of altered cerebral physi-ology. Acute care includes assessing GCS,monitoring the airway in the postictalperiod and observing for recurrentevents (Table 3).

Admission to hospital for observationand investigation is indicated for anunwitnessed or prolonged event, if thereis serious injury, incomplete recovery ofconsciousness or mentation, or the pres-ence of focal symptoms or signs. Fullneurological examination including fun-doscopy is essential. Ideally, EEG shouldbe performed within the first 24 hoursafter the ictus to increase the chance ofcapturing a diagnostic abnormality.12

Those presenting with a first idiopathicgeneralised seizure must be fast trackedfor outpatient neurological assessmentif they recover fully and have no focalneurological deficits.

Treatment should be directed at the

underlying cause. Anticonvulsant therapyafter a first seizure or in patients withinfrequent seizures may reduce the seizurerecurrence within the first 1–2 years.However, this does not affect long-termremission13 so not all patients should begiven anticonvulsant medication. Patientswith known epilepsy already taking anti-convulsant medication at presentationshould have serum anticonvulsant levelschecked and a search for a precipitant fortheir seizure.

Status epilepticus

Status epilepticus is a medical emer-gency. Lorazepam 0.1 mg/kg can beadministered for seizure termination,repeated in two minutes if ineffective.The patient should be given a loadingdose of phenytoin 1.5 mg/kg to preventfurther events. An underlying causeshould be sought if the patient is notknown to have epilepsy and a triggersought in known epileptics. Occasion-ally, general anaesthesia is required tocontrol status epilepticus.14

Safety concerns

It is important to discuss and documentthe regulations for driving and generalsafety behaviour in patients presentingwith seizures.

Conclusions

Acute neurological problems frequentlypresent to the emergency department.Accurate history taking and detailed clin-ical examination are paramount when

assessing the patient presenting withneurological problems such as headacheor seizure. This clinical assessment willdirect further investigations to identifyand treat serious underlying pathology.

References

1 Linn FH, Rinkel GJ, Algra A, van Gijn J.Headache characteristics in subarachnoidhaemorrhage and benign thunderclapheadache. J Neurol Neurosurg Psychiatry1998;65:791–3.

2 van Gijn J, Rinkel GJ. Subarachnoidhaemorrhage: diagnosis, causes andmanagement. Review. Brain 2001;124(Pt 2):249–78.

3 van de Beek D, de Gans J, McIntyre P,Prasad K. Steroids in adults with acutebacterial meningitis: a systematic review.Lancet Infect Dis 2004;4:139–43.

4 van de Beek D, de Gans J, Tunkel AR,Wijdicks EF. Community-acquiredbacterial meningitis in adults. Review.N Engl J Med 2006;354:44–53.

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Seizure type Causes

Primary seizures Idiopathic epilepsy syndrome

Secondary seizures Medication, illicit drug or alcohol excess or withdrawal

CNS process (eg tumour, infection, stroke, trauma)

Metabolic disorder: glucose, calcium, sodium,

mitochondrial disorder

Cerebral venous sinus thrombosis

Eclampsia

Intracranial haemorrhage

Convulsive syncope of cardiac or neurocardiogenic origin

CNS = central nervous system.

Table 2. Causes to consider in acute presentation with seizure.

• Serum glucose

• Electrolytes (especially sodium and

calcium)

• Arterial blood gas

• Blood alcohol

• Urinary drug screen

• Anticonvulsant levels

• ECG (cardiac rate and rhythm)

• MRI brain

• EEG

• Lumbar puncture and screen for

infection

MRI = magnetic resonance imaging.

Table 3. Investigations to consider inacute presentation with seizure.