8. Neurology Emergencies

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Neurology Emergencies

Edited by Anne-Maree Kelly

8.1 Headache

Anne-Maree Kelly


Headache is a common ailment that is often due to a combination of physical and psychological factors. The vast majority are benign and self-limiting and are managed by patients in the community. Only a very small proportion of patients experiencing headache attend emergency departments (ED) for treatment. The challenges are to distinguish potentially life-threatening causes from the more benign and to manage effectively the pain of headache.

Aetiology, pathophysiology and pathology

The structures in the head capable of producing headache are limited. They include:

The bulk of the intracranial contents, including the parenchyma of the brain, the subarachnoid and pia mater and most of the dura mater, are incapable of producing painful stimuli.

The pathological processes that may cause headache are:

ent Tension. This usually refers to contraction of muscles of the head and/or neck and is thought to be the major factor in the so-called ‘tension headache’.

ent Traction. Traction is caused by stretching of intracranial structures due to a mass effect, such as with a space-occupying lesion. Pain caused by this mechanism is characteristically constant, but may vary in severity.

The pathophysiological causes of headache are summarized in Table 8.1.1.

Table 8.1.1

A pathophysiological classification of headache

  Extracranial Intracranial
Tension/traction Muscular headache
‘Tension headache’
Intracranial tumour
Cerebral abscess
Intracranial haematoma
Vascular Migraine Severe hypertension
Inflammatory Temporal arteritis Meningitis
Sinusitis Subarachnoid haemorrhage
Otitis media  
Tooth abscess  


Clinical features

In the assessment of a patient with headache, history is of prime importance. Specific information should be sought about the timing of the headache (in terms of both overall duration and speed of onset), the site and quality of the pain, relieving factors, the presence of associated features, such as nausea and vomiting, photophobia and alteration in mental state, medical and occupational history and drug use.

Intensity of the pain is important from the viewpoint of management but is not a reliable indicator of the nature of underlying pathology. This said, sudden, severe headache and chronic, unremitting or progressive headache are more likely to have a serious cause.

Physical examination should include temperature, pulse rate and blood pressure measurements, assessment of conscious state and neck stiffness and a neurological examination, including funduscopy (where indicated). Abnormal physical signs are uncommon, but the presence of neurological findings makes a serious cause probable. In addition, a search should be made for sinus, ear, mouth and neck pathology and muscular or superficial temporal artery tenderness.

Headache patterns

Some headaches have ‘classic’ clinical features: these are listed in Table 8.1.2. It must be remembered that, as with all diseases, there is a spectrum of presenting features and the absence of the classic features does not rule out a particular diagnosis. Every patient must be assessed on their merits and, if symptoms persist without reasonable explanation, further investigation should be undertaken.

Table 8.1.2

Classic clinical complexes and cause of headache

Preceded by an aura Migraine
Throbbing unilateral headache, nausea
Family history
Sudden onset Subarachnoid haemorrhage
Severe occipital headache; ‘like a blow’
Worst headache ever
Throbbing/constant frontal headache Sinusitis
Worse with cough, leaning forward
Recent URTI
Pain on percussion of sinuses
Paroxysmal, fleeting pain Neuralgia
Distribution of a nerve
Trigger manoeuvres cause pain
Hyperalgesia of nerve distribution
Unilateral with superimposed stabbing Temporal arteritis
Claudication on chewing
Associated malaise, myalgia
Tender artery with reduced pulsation
Persistent, deep-seated headache Tumour: primary or secondary
Increasing duration and intensity
Worse in morning
Aching in character
Acute, generalized headache Meningitis
Fever, nausea and vomiting
Altered level of consciousness
Neck stiffness±rash
Unilateral, aching, related to eye Glaucoma
Nausea and vomiting
Raised intraocular pressure
Aching, facial region Dental cause
Worse at night
Tooth sensitive to heat, pressure  


URTI: upper respiratory tract infection.

Clinical investigations

For the majority of patients with headache no investigation is required. The investigation of suspected subarachnoid haemorrhage and meningitis is discussed elsewhere in this book. If tumour is suspected, the investigations of choice are magnetic resonance imaging (MRI) or a contrast-enhanced computed tomography (CT) scan. An elevated erythrocyte sedimentation rate (ESR) may be supporting evidence for a diagnosis of temporal arteritis. With respect to sinusitis, facial X-rays are of very limited value.

Tension headache

The pathological basis of tension headaches remains unclear, but increased tension of the neck or cranial muscles is a prominent feature. A family history of headaches is common and there is an association with an injury in childhood or adolescence. The most common precipitants are stress and alteration in sleep patterns.

Aspirin, non-steroidal anti-inflammatory agents (NSAIDs) and paracetamol (acetaminophen) have all been shown to be effective in the treatment of tension headaches, with success rates between 50 and 70%. Ibruprofen 400 mg or ketoprofen 25–50 mg appear to be the most effective, followed by aspirin 600–1000 mg and paracetamol 1000 mg.


Migraine can be a disabling condition for the sufferer. Most migraine headaches are successfully managed by the patient and their general practitioner, but a small number fail to respond or become ‘fixed’ and sufferers may present for treatment at EDs. As most patients (up to 80% in some studies) have tried oral medications prior to presenting, parenterally administered agents are usually indicated for ED treatment.

Migraine is a clinical diagnosis and, in the ED setting, a diagnosis of exclusion. Other causes of severe headache, such as subarachnoid haemorrhage and meningitis, must be ruled out before this diagnosis is made. Of particular note, the response of a headache to antimigraine therapy should not be used to assume that the cause was migraine. There have been reports that the headaches associated with subarachnoid haemorrhage and meningitis have, on occasion, responded to these agents.


The pathophysiology of migraine is complex and not completely understood. It is a chronic neurovascular disorder characterized by dysfunction of the central and peripheral nervous system and intracranial vasculature.

The headache pain of migraine seems to result from the activation of the trigeminovascular system. The triggers for the development of migraine headache are probably chemical and are thought to originate in the brain, the blood vessel walls and the blood itself. These triggers stimulate trigeminovascular axons, causing pain and the release of vasoactive neuropeptides. These neuropeptides act on mast cells, endothelial cells and platelets, resulting in increased extracellular levels of arachidonate metabolites, amines, peptides and ions. These mediators and the resultant tissue injury lead to a prolongation of pain and hyperalgesia.

Serotonin has also been specifically implicated in migraine. By activation of afferents, it causes a retrograde release of substance P. This in turn increases capillary permeability and oedema.

Classification and clinical features

Migraine is defined as an idiopathic recurring headache disorder with attacks that last 4–72 hours. Typical characteristics are unilateral location, pulsating quality, moderate or severe intensity and aggravation by routine physical activity. There is also usually nausea, photophobia and phonophobia.

In some patients, migraine is preceded by an ‘aura’ of neurological symptoms localizable to the cerebral cortex or brainstem, such as visual disturbance, paraesthesia, diplopia or limb weakness. These develop gradually over 5–20 minutes and last less than 60 minutes. Headache, nausea and/or photophobia usually follow after an interval of less than an hour.

Several variant forms of migraine have been defined, including ophthalmoplegic, abdominal, hemiplegic and retinal migraine, but all are uncommon. In ophthalmoplegic migraine, the headache is associated with paralysis of one or more of the nerves supplying the ocular muscles. Horner’s syndrome may also occur. Abdominal migraine manifests as recurrent episodes of abdominal pain for which no other cause is found. Retinal migraine, which is fortunately very rare, involves recurrent attacks of retinal ischaemia which may lead to bilateral optic atrophy. Hemiplegic migraine is a stroke mimic.


The complexity of the mechanisms involved in the genesis of migraine suggests that there are a number of ways to interrupt the processes to provide effective relief from symptoms.

A wide variety of pharmacological agents and combinations of agents have been tried for the treatment of migraine, with varying results. Interpreting the evidence is challenging, as the majority of the studies have small sample sizes, compare different agents or combinations of agents, are conducted in settings other than EDs and the outcome measure(s) tested varies widely. For mild to moderate migraine headache in patients who have not taken other medication, aspirin 900 mg combined with metoclopramide 10 mg is effective. Most ED patients, however, have either tried their usual medication or have significant nausea or vomiting making oral therapy inappropriate.

The effectiveness of commonly used agents is summarized in Table 8.1.3. Dosing and administration are summarized in Table 8.1.4. At present, the most effective agents appear to be the phenothiazines (chlorpromazine and prochlorperazine) and the triptans, each of which has achieved>70% efficacy in a number of studies. Note that triptans are contraindicated in patients with a history of ischaemic heart disease, uncontrolled hypertension or with the concomitant use of ergot preparations.

Table 8.1.3

Pooled effectiveness data from ED studies of the treatment of migraine

Agent No. of studies Total patients Clinical success rate (%) NNT: clinical success
Chlorpromazine (IV) 6 171 85 1.67
Prochlorperazine (IM or IV) 6 171 71 2.17
Sumatriptan (6 mg SC) 21 3139 71 2.17
Ketorolac (IM or IV) 6 155 66 2.44
Tramadol (IM or IV) 3 191 60 2.86
Metoclopramide (IV) 7 300 58 3.03
Magnesium sulphate (IV) 3 117 41 6.25


Clinical studies in adults, defined ‘success’ endpoint, minimum of 50 patients studied in aggregate, NNT calculated assuming placebo effectiveness rate of 25%.

Table 8.1.4

Drug dosing and administration

Agent Drug dosing/administration
Chlorpromazine (IV) 12.5 mg intravenously, repeated every 20 minutes as needed to a maximum dose of 37.5 mg, accompanied by 1 L normal saline over 1 hour to avoid hypotension
25 mg in 1 L normal saline over 1 hour, repeated if necessary
Prochlorperazine (IM or IV) 10 mg/12.5 mg (depending on packaging)
Sumatriptan (SC, IN) 6 mg SC, 20 mg IN
Metoclopramide (IV) 10–20 mg
Ketorolac (IM or IV) 30 mg IV, 60 mg IM
Tramadol (IM) 100 mg

Pethidine (meperidine) is not indicated for the treatment of migraine. Its reported effectiveness is only 56%, it has a high rate of rebound headache and it carries a risk of dependence. The data on dihydroergotamine are difficult to interpret because it is often used in combination with other agents (e.g. metoclopramide); however, it has also been shown to be less effective than chlorpromazine and sumatriptan in acute treatment and to have a high rate of unpleasant side effects. Sodium valproate and haloperidol have also shown moderate effectiveness in small studies, but there are insufficient data to draw a valid conclusion or recommend them as treatment options. Lignocaine (lidocaine) has been shown to be no more effective than placebo. The efficacy of intravenous magnesium sulphate (1 or 2 mg) remains unclear. It was shown in a small placebo-controlled trial to be effective but, in another study, the combination of magnesium with metoclopramide was less effective than metoclopramide and placebo.

Rebound or recurrent headache is common in ED patients treated for migraine (approximately 30%). There is evidence that oral or IV dexamethasone, in addition to standard migraine therapy for selected patients, reduces the proportion of patients who experience early recurrence (so-called rebound headache). A meta-analysis of published papers reports a 26% reduction in the relative risk of headache recurrence within 72 hours. Doses used were 10 mg IV or 8 mg orally.

Trigeminal neuralgia

Trigeminal neuralgia is a debilitating condition in which patients describe ‘lightning-’or a ‘hot poker-’like pain that is severe and follows the distribution of the trigeminal nerve. Individual episodes of pain last only seconds, but may recur repeatedly within a short period and can be triggered by minor stimuli, such as light touch, eating or drinking, shaving or passing gusts of wind. It is most common in middle or older age.

Aetiology and pathophysiology

Evidence suggests that the pathological basis of trigeminal neuralgia is demyelination of sensory fibres of the trigeminal nerve in the proximal (CNS) portion of the nerve root or, rarely, in the brainstem, most commonly due to compression of the nerve root by an overlying artery or vein.

Trigeminal neuralgia is classified as classic trigeminal neuralgia (no cause identified) and symptomatic trigeminal neuralgia (secondary to another condition). Characteristics associated with symptomatic trigeminal neuralgia are trigeminal sensory deficits and bilateral involvement.

Clinical investigations

In approximately 15% of cases, there is a structural cause for trigeminal neuralgia. For this reason, there is some support for routine neuroimaging (CT, MRI) in these patients. Electrophysiological assessment of trigeminal reflexes can also be helpful in distinguishing classic from symptomatic trigeminal neuralgia. The choice between the two approaches will depend on availability, expertise, cost and patient and treating clinician preference.


The mainstay of therapy for trigeminal neuralgia is carbamazepine. The usual starting dose is 200–400 mg/day in divided doses, increased by 200 mg/day until relief up to a maximum of 1200 mg/day. The average dose required is 800 mg/day. Where available, oxcarbazepine 600–1800 mg/day is an effective alternative. For patients who fail first-line therapy, there is some evidence to support the addition of lamotrigine or a change to baclofen. Referral for consideration of surgery is appropriate in patients who are refractory to medical therapy.

Temporal (giant cell) arteritis

Giant cell arteritis is the most common form of vasculitis in patients aged over 50 years. It affects large and middle-sided blood vessels with a predisposition for the cranial arteries arising from the carotid arteries. Loss of vision is the most common severe complication. Involvement of extracranial arteries including the aorta is more frequent than previously assumed. Inflammation markers in blood are usually elevated, but specific laboratory tests for the diagnosis of giant cell arteritis are not available. Imaging using ultrasonography, magnetic resonance imaging and positron emission tomography can be useful to confirm, localize and assess the extent of vascular involvement. Temporal artery biopsy is the gold standard for diagnosis. Glucocorticoids are still the standard therapy (50–100 mg/day). Patients with acute visual changes secondary to giant cell arteritis should receive parenteral corticosteroid therapy and be admitted until their condition stabilizes.

Further reading

1. American Academy for Neurology. AAN summary of evidence-based guideline for clinicians: trigeminal neuralgia.<www.aan.com/practice/guideline/uploads/303.pdf>[Accessed Jan. 2013].

2. Colman I, Friedman BW, Brown MD, et al. Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomized controlled trials for preventing recurrence. Br Med J. 2008;336:1359–1361.

3. Derry CJ, Derry S, Moore RA. Sumatriptan (subcutaneous route of administration) for acute migraine attacks in adults. Cochrane Database Syst Rev. 2012;2:CD009665.

4. Friedman BW, Kapoor A, Friedman MS, et al. The relative efficacy of meperidine for the treatment of acute migraine: a meta-analysis of randomized controlled trials. Ann Emerg Med. 2008;52:705–713.

5. Kelly AM, Holdgate A. Emergency care evidence in practice series, emergency care community of practice: migraine in the emergency department Melbourne: National Institute of Clinical Studies; 2006; <www.nhmrc.gov.au/_files_nhmrc/file/nics/material_resources/Management%20of%20acute%20migraine%20colour.pdf>[Accessed Jan. 2013].

6. Kelly AM. Specific pain syndromes: headache. In: Mace S, Ducharme J, Murphy M, eds. Pain Management and procedural sedation in the emergency department. New York: McGraw-Hill; 2006.

7. Kelly AM, Walcynski T, Gunn B. The relative efficacy of phenothiazines for the treatment of acute migraine: a meta-analysis. Headache. 2009;49:1324–1332.

8. Sumamo Schellenberg E, Dryden DM, et al. Acute migraine treatment in emergency settings Comparative effectiveness review No 84 (Prepared by the University of Alberta Evidence-based Practice Center under Contract No 290-2007-10021-I.) AHRQ Publication No 12(13)-EHC142-EF Rockville, MD: Agency for Healthcare Research and Quality; 2012; <www.effectivehealthcare.gov/reports/final.cfm>[Accessed Jan. 2013].

9. Yoon YJ, Kim JH, Kim SY, et al. A comparison of efficacy and safety of non-steroidal anti-inflammatory drugs versus acetaminophen in the treatment of episodic tension-type headache: a meta-analysis of randomized placebo-controlled trial studies. Korean J Fam Med. 2012;33:262–271.

8.2 Stroke and transient ischaemic attacks

Philip Aplin and Mark Morphett


Ischaemic strokes and transient ischaemic attacks (TIAs) are most commonly due to atherosclerotic thromboembolism of the cerebral vasculature or emboli from the heart. Other causes should be considered in younger patients, those presenting with atypical features or when evaluation is negative for the more common aetiologies.

Haemorrhagic and ischaemic strokes cannot be reliably differentiated on clinical grounds alone, therefore further imaging, most commonly CT scanning, is required prior to the commencement of antiplatelet, thrombolytic or interventional therapies.

The risk of a completed stroke following a TIA is high – up to 15% in the first week. Clinical scoring systems, such as the ABCD2 score, have been proposed as an assessment tool for a stroke risk following TIA. Patients with TIA identified as low risk for progression to stroke (e.g. ABCD2<4) are increasingly managed through integrated rapid TIA assessment clinics in an outpatient setting, with admission reserved for those at higher risk.

Differentiating strokes from other acute neurological presentations may be difficult in the emergency department. This issue has implications for the use of high-risk therapies, such as thrombolysis.

The early phase of stroke management concentrates on airway and breathing, rapid neurological assessment of conscious level, pupil size and lateralizing signs and blood sugar measurements. Hyperglycaemia may worsen neurological outcome in stroke and so glucose should not be given in likely stroke patients unless a low blood sugar level is objectively demonstrated.

Outcomes in stroke patients are improved when they are admitted to a dedicated stroke unit. This involves a multidisciplinary approach to all aspects of stroke management.

Treating doctors should be fully aware of the risks/benefits and indications/contraindications of thrombolytic therapy in treating acute strokes. Currently, tPA should be considered for use in selected acute ischaemic strokes when administered within 4.5 hours of symptom onset, but controversies remain.

More complex imaging modalities, such as CT perfusion and diffusion/perfusion MRI, continue to be evaluated in acute stroke work-up in an attempt to define better the patient group that will benefit from aggressive vessel opening strategies.

In the setting of acute large cerebral vessel occlusion, intra-arterial therapies, such as clot retrieval devices, continue to be evaluated and improved. The place of these interventions in acute stroke therapy is the subject of ongoing research.


Cerebrovascular disease is the third highest cause of death in developed countries, after heart disease and cancer. A stroke is an acute neurological injury secondary to cerebrovascular disease, either by infarction (80%) or by haemorrhage (20%). The incidence of stroke is steady and, although mortality is decreasing, it is still a leading cause of long-term disability. Transient ischaemic attacks (TIAs) are defined as transient episodes of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia, without acute infarction. Causes are similar to those of ischaemic stroke, particularly atherosclerotic thromboembolism related to the cerebral circulation and cardioembolism. Diagnosis of the cause of TIAs with appropriate management is important in order to prevent a potentially devastating stroke.


Brain tissue is very sensitive to the effects of oxygen deprivation. Following cerebral vascular occlusion, a series of metabolic consequences may ensue, depending on the extent, duration and vessels involved, which can lead to cell death. Reperfusion of occluded vessels may also occur, either spontaneously or via therapeutic intervention, with the potential for reperfusion injury. An area of threatened but possibly salvageable brain may surround an area of infarction. The identification of this so-called ischaemic penumbra and therapeutic efforts to ameliorate the extent of irreversible neuronal damage, have been the subject of ongoing research efforts.

Large anterior circulation ischaemic strokes can be associated with increasing mass effect and intracranial pressure in the hours to days following onset. Secondary haemorrhage into an infarct may also occur, either spontaneously or related to therapy. Clinical deterioration often follows.

Ischaemic strokes

These are the results of several pathological processes (Table 8.2.1):

ent Ischaemic strokes are most commonly due to thromboembolism originating from the cerebral vasculature, the heart or, occasionally, the aorta. Thrombosis usually occurs at the site of an atherosclerotic plaque secondary to a combination of shear-induced injury of the vessel wall, turbulence and flow obstruction. Vessel wall lesions may also be the site of emboli that dislodge and subsequently occlude more distal parts of the cerebral circulation. Atherosclerotic plaque develops at the sites of vessel bifurcation. Lesions affecting the origin of the internal carotid artery (ICA) are the most important source of thromboembolic events. The more distal intracerebral branches of the ICA, the aorta and the vertebrobasilar system are also significant sites. Acute plaque change is likely to be the precipitant of symptomatic cerebrovascular disease, particularly in patients with carotid stenosis. Hence, the most effective therapies will probably not only target the consequences of acute plaque change, such as thrombosis and embolism, but also aim for plaque stabilization using such agents as antiplatelet drugs, statins and antihypertensive drugs along the lines used in the management of acute coronary syndromes.

ent Approximately 20% of cerebrovascular events are due to emboli originating from the heart. Rarely, emboli may arise from the peripheral venous circulation, the embolus being carried to the cerebral circulation via a patent foramen ovale.

ent Lipohyalinosis of small arteries is a degenerative process associated with diabetes and hypertension that mainly affects the penetrating vessels that supply areas, such as the subcortical white matter, and is the postulated cause of lacunar infarcts.

ent Dissection of the carotid or vertebral arteries may cause TIAs and stroke. This may occur spontaneously or following trauma to the head and neck region, particularly in young people not thought to be at risk of stroke. Distal embolization from the area of vascular injury is the main pathological process involved.

ent Haemodynamic reduction in cerebral flow may occur as a result of systemic hypotension or severe carotid stenosis. In these cases, cerebral infarction typically occurs in a vascular watershed area.

ent The cerebral vasoconstriction that may occur in association with subarachnoid haemorrhage (SAH), migraine and pre-eclampsia and with drugs, such as sympathomimetics and cocaine, may precipitate stroke.

ent Less common vascular disorders, such as arteritis, venous sinus thrombosis, sickle cell disease and moyamoya disease, may be causes of stroke.

ent Venous sinus thrombosis may occur spontaneously or in relation to an underlying risk factor, such as an acquired or congenital prothrombotic disorder, dehydration or meningitis. The consequences depend on the extent and localization of the thrombosis. Stroke secondary to venous thrombosis is due to venous stasis, increased hydrostatic pressures and associated haemorrhage.

Table 8.2.1

Causes of stroke

Ischaemic stroke

Arterial thromboembolism

 Carotid and vertebral artery atheroma

 Intracranial vessel atheroma

 Small vessel disease – lacunar infarction

 Haematological disorders – hypercoagulable states


 Aortic and mitral valve disease

 Atrial fibrillation

 Mural thrombus

 Atrial myxoma

 Paradoxical emboli


Severe vascular stenosis or a combination of these factors


 Vasoconstriction – drug induced, post-SAH, pre-eclampsia

Other vascular disorders

 Arterial dissection

 Gas embolism syndromes

 Moyamoya disease


Intracerebral haemorrhage

Hypertensive vascular disease

Lipohyalinosis and microaneurysms




Arteriovenous malformations

Amyloid angiopathy

Bleeding diathesis



 Thrombocytopenia/disseminated intravascular coagulation


Secondary haemorrhage into a lesion – tumour or infarction

Haemorrhagic stroke

Haemorrhagic stroke is the result of vessel rupture into the surrounding intracerebral tissue or subarachnoid space. Subarachnoid haemorrhage is the subject of a separate chapter in this book (see Chapter 8.3).

Risk factors for TIA/stroke and prevention

This particularly applies to cerebral ischaemic events, both TIAs and strokes. Non-modifiable risk factors for ischaemic stroke include:

In terms of primary prevention, hypertension is the most important modifiable risk factor. The benefit of antihypertensive treatment in stroke prevention has been well shown. The other major risk factors for atherosclerosis and its complications – diabetes, smoking and hypercholesterolaemia – often contribute to increased stroke risk. These should be managed according to standard guidelines.

The most important cardiac risk factor for TIA and stroke is atrial fibrillation (AF), both chronic and paroxysmal. Warfarin is recommended to prevent cardioembolism where the risk:benefit ratio of anticoagulation (target INR 2.0–3.0) favours this. Prediction tools, such as the CHADS2 and CHA2DS2-VASc scores, have been developed to standardize the approach to primary stroke prevention in patients with non-valvular AF. Recently, an oral direct thrombin inhibitor (dabigatran) has been shown to be non-inferior to warfarin for stroke prevention in a large industry sponsored trial (the RE-LY trial). On the basis of this trial, dabigatran has been approved for use as an alternative to warfarin with rapid uptake of this medication in the community. Those with contraindications to warfarin or very low stroke risk should initially receive aspirin.

A carotid bruit or carotid stenosis found in an otherwise asymptomatic patient is associated with an increased stroke risk. However, the role of carotid endarterectomy in these patients is controversial. While early trials suggested some minor benefit, more recent studies have refuted this and it is increasingly clear that intensive medical therapy in patients with asymptomatic carotid stenosis reduces stroke risk well below that achieved with either endarterectomy or carotid stenting.

Other major cardiac conditions associated with increased TIA/stroke risk include endocarditis, mitral stenosis, prosthetic heart valves, recent myocardial infarction and left ventricular aneurysm. Less common ones include atrial myxoma, a patent foramen ovale and cardiomyopathies.

Secondary prevention involves detection and modification, if possible, of conditions that may have caused a TIA or stroke in order to prevent further events that may result in worse clinical outcomes. As well as the risk factors already mentioned, many other uncommon conditions, such as arterial dissection and prothrombotic states, may cause TIA and stroke. These will be discussed later in the chapter.

Ischaemic stroke syndromes

The symptoms and signs of stroke or TIA correspond to the area of the brain affected by ischaemia or haemorrhage (Table 8.2.2).

Table 8.2.2

Location of TIA

  Arterial territory
Symptom Carotid Either Vertebrobasilar
Dysphasia +    
Monocular visual loss +    
Unilateral weakness*   +  
Unilateral sensory disturbance*   +  
Dysarthria**   +  
Homonymous hemianopia   +  
Dysphagia**   +  
Diplopia**     +
Vertigo**     +
Bilateral simultaneous visual loss     +
Bilateral simultaneous weakness     +
Bilateral simultaneous sensory disturbance     +
Crossed sensory/motor loss     +


*Usually regarded as carotid distribution.

**Not necessarily a transient ischaemic attack if an isolated symptom. Reproduced with permission from Hankey GJ. Management of first time transient ischaemic attack. Emerg Med 2001;13:70–81.

In ischaemic brain injury, the history and pattern of physical signs may correspond to a characteristic clinical syndrome according to the underlying cause and the vessel occluded. This has a bearing on the direction of further investigation and treatment decisions. Differentiating between anterior and posterior circulation ischaemia/infarction is important in this respect, but is not always possible on clinical grounds alone.

Determining the cause of the event is the next step. Once again, clues, such as a carotid bruit or atrial fibrillation, may be present on clinical evaluation. For accurate delineation of the site of the brain lesion, exclusion of haemorrhage and assessment of the underlying cause, it is usually necessary to undertake imaging studies.

Patterns of clinical features

Anterior circulation ischaemia

The anterior circulation supplies blood to 80% of the brain and consists of the ICA and its branches, principally the ophthalmic, middle cerebral and anterior cerebral arteries. This system supplies the optic nerve, retina, frontoparietal and most of the temporal lobes. Ischaemic injury involving the anterior cerebral circulation commonly has its origins in atherothrombotic disease of the ICA. Atherosclerosis of this artery usually affects the proximal 2 cm, just distal to the division of the common carotid artery. Advanced lesions may be the source of embolism to other parts of the anterior circulation or cause severe stenosis with resultant hypoperfusion distally if there is inadequate collateral supply via the circle of Willis. This is usually manifest by signs and symptoms in the middle cerebral artery (MCA) territory (Table 8.2.3). Less commonly, lesions of the intracranial ICA and MCA may cause similar clinical features.

Table 8.2.3

Signs of middle cerebral artery (MCA) occlusion

Homonymous hemianopia

Contralateral hemiplegia affecting face and arm more than leg

Contralateral hemisensory loss

Dysphasias with dominant hemispheric involvement (usually left)

Spatial neglect and dressing apraxia with non-dominant hemispheric involvement

Embolism to the ophthalmic artery or its branches causes monocular visual symptoms of blurring, loss of vision and field defects. When transient, this is referred to as amaurosis fugax or transient monocular blindness.

The anterior cerebral artery territory is the least commonly affected by ischaemia because of the collateral supply via the anterior communicating artery. If occlusion occurs distally or the collateral supply is inadequate, then ischaemia may occur. This manifests as sensory/motor changes in the leg – more so than in the arm. More subtle changes of personality may occur with frontal lobe lesions, as may disturbances of micturition and conjugate gaze.

Major alterations of consciousness, with Glasgow coma scores<8, imply bilateral hemispheric or brainstem dysfunction. The brainstem may be primarily involved by a brainstem stroke or secondarily affected by an ischaemic or haemorrhagic lesion elsewhere in the brain, owing to a mass effect and/or increased intracranial pressure.

Posterior circulation ischaemia

Ischaemic injury in the posterior circulation involves the vertebrobasilar arteries and their major branches which supply the cerebellum, brainstem, thalamus, medial temporal and occipital lobes. Posterior cerebral artery occlusion is manifested by visual changes of homonymous hemianopia (typically with macular sparing if the MCA supplies this part of the occipital cortex). Cortical blindness, of which the patient may be unaware, occurs with bilateral posterior cerebral artery infarction.

Depending on the area and extent of involvement, brainstem and cerebellar stroke manifest as a combination of: motor and sensory abnormalities, which may be uni- or bilateral; cerebellar features of vertigo, nystagmus and ataxia; and cranial nerve signs, such as diplopia/ophthalmoplegia, facial weakness and dysarthria. Consciousness may also be affected.

Examples of brainstem stroke patterns include (this list is by no means exhaustive):

ent ipsilateral cranial nerve with crossed corticospinal motor signs

ent lateral medullary syndrome: clinical features include sudden onset of vertigo, nystagmus, ataxia, ipsilateral loss of facial pain and temperature sensation (V) with contralateral loss of pain and temperature sensation of the limbs (anterior spinothalamic), ipsilateral Horner’s syndrome and dysarthria and dysphagia (IX and X)

ent internuclear ophthalmoplegia manifesting as diplopia and a horizontal gaze palsy due to involvement of the median longitudinal fasciculus (MLF)

ent ‘locked-in’ syndrome: this is caused by bilateral infarction of a ventral pons, with or without medullary involvement. The patient is conscious due to an intact brainstem reticular formation, but cannot speak and is paralysed. Patients can move their eyes due to sparing of the third and fourth cranial nerves in the midbrain.

ent Acute deterioration of conscious state may be the presentation of acute basilar artery occlusion and should be in the differential diagnosis of coma for investigation.

Lacunar infarcts

Lacunar infarcts are associated primarily with hypertension and diabetes. They occur in the small penetrating arteries supplying the internal capsule, thalamus and upper brainstem. Isolated motor or sensory deficits are most commonly seen.

Clinical features

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