Intended for healthcare professionals

Clinical Review

Lesson of the week: Carotid dissection causing stroke in a child with migraine

BMJ 1997; 314 doi: https://doi.org/10.1136/bmj.314.7076.291 (Published 25 January 1997) Cite this as: BMJ 1997;314:291
  1. V Ganesan, research fellowa,
  2. F J Kirkham, senior lecturera
  1. a Neurosciences Unit Institute of Child Health Wolfson Centre London WC1N 2AP
  1. Correspondence to: Dr Ganesan

    Introduction

    The aetiology of stroke in childhood and adolescence often remains obscure. Up to 50% of published cases are said to be idiopathic, but often the search for an underlying cause is not exhaustive. Arterial dissection, usually of the internal carotid artery, is an important cause of stroke in this age group, accounting for 6% of cases in our series of 115 patients (unpublished data). Migrainous infarction, on the other hand, is rare in all ages and should be a diagnosis of exclusion. Unfortunately, in a patient with a history of headache it is often tempting to make this diagnosis. This case shows that other, potentially treatable, disease may be missed as a consequence.

    Case report

    A 15 year old left handed boy fell off his skateboard, sustaining a blow to the right occiput without loss of consciousness. The next day he developed right occipital headache, blurred vision, nausea, and left hemiparesis, which extended to his face. The limb weakness and headache resolved over 24 hours but the facial weakness persisted. He had blurred vision and felt nauseated but did not vomit. Despite bedrest and simple analgesics, his symptoms did not resolve and he was admitted to hospital on the third day with a presumptive diagnosis of hemiplegic migraine. That night, he fell out of bed, hitting his head again. It became clear the following morning that his condition had deteriorated, and he became disorientated, with a recurrence of the left hemiparesis. Power in the hand was Medical Research Council grade 0/5 and in the leg grade 2/5. There were no other clinically relevant findings. He had a history of migraine without aura which had been controlled by pizotifen. Two years earlier he had had one previous episode of headache with a focal deficit (left facial weakness) lasting 16 hours. Magnetic resonance imaging of the brain had shown normal results.

    T2 weighted magnetic resonance imaging five days after the onset of symptoms showed extensive high signal and swelling in the region of the right middle cerebral artery, suggestive of infarction. He was unable to tolerate magnetic resonance angiography and was managed conservatively with a working diagnosis of migrainous cerebral infarction. Seventy two hours later, despite complete resolution of his headache, his hemiparesis had not improved. There was evidence of reduced flow in the right middle cerebral artery on transcranial Doppler ultrasonography. Magnetic resonance angiography at this time showed reduced flow in the right internal carotid artery and absent flow in the distal right middle cerebral artery. Magnetic resonance imaging showed that the previously noted area of high signal on T2 weighted imaging had spread. Intra-arterial digital subtraction angiography showed irregular narrowing of the right internal carotid artery with reduced flow, which, in the absence of any proximal internal carotid artery disease, suggested right internal carotid artery dissection (fig 1).

    FIG 1
    FIG 1

    Contrast study (intra-arterial digital subtraction angiogram) showing tapered irregular narrowing of the right internal carotid artery, suggestive of dissection

    He was extensively investigated for other risk factors for juvenile stroke. Detailed cardiac, metabolic, and haematological investigations yielded normal results. He was given anticoagulant treatment and improved slowly, requiring prolonged rehabilitation. At the time of writing, he had a residual dense hemiparesis and had not regained any useful function of his hand, although he was able to walk independently. He has had to forgo an apprenticeship in the building trade. Anticoagulant treatment was discontinued after six months.

    Discussion

    Cervicocephalic arterial dissection is an important cause of stroke in childhood and adolescence.1 It may occur spontaneously (although there is often a history of trauma, which may be minor)2 and affect many vessels. In children the anterior circulation is more usually affected.1 Pain in the ipsilateral head, neck, or eye is typical and there may be Horner's syndrome if the cervical sympathetic chain is affected. There is evidence to suggest that migraine increases the risk of arterial dissection.3

    A focal neurological deficit may form part of the migrainous aura, but a recent study estimated that the risk of stroke was doubled in those with migraine4; this seems to be greatest in young women, especially those taking the contraceptive pill.5 The International Headache Society emphasises that other causes of stroke should be excluded before migrainous cerebral infarction is firmly diagnosed6; a history of migraine in a patient with acute stroke is not sufficient. Unfortunately, this stipulation is often ignored both in published findings and in clinical practice.

    Non-atheromatous cerebrovascular disease, including arterial dissection, is common in childhood stroke; imaging the cerebral circulation is important in establishing aetiology. Magnetic resonance imaging and magnetic resonance angiography permit non-invasive imaging of cervicocephalic vessels and are useful in the diagnosis of carotid dissection.2 An abnormal but non-diagnostic study, as in this case, may prompt the clinician to consider contrast angiography, which remains the gold standard.

    Prompt anticoagulant treatment is of confirmed therapeutic benefit in carotid dissection,2 although its efficacy in the presence of an established infarction is less clear.

    From the available published findings, which emphasise the importance of early diagnosis and treatment of carotid dissection, the outcome in this case might well have been improved by earlier anticoagulant treatment. A history of migraine must not preclude prompt and thorough investigation of juvenile stroke.

    References

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    View Abstract