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Atypical presentations of subarachnoid haemorrhage
  1. J KELLY
  1. Queen Mary's Hospital, Sidcup, Kent, UK
    1. Department of Medicine, Institute of Clinical Science
    2. Royal Victoria Hospital, Belfast BT12 6TJ, N Ireland

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      Sir,I was interested to read the report on atypical presentations of subarachnoid haemorrhage (SAH) by Johnston and Robinson.1 The following case serves as a reminder that prominent focal neurological signs may occur in SAH, occasionally dominating the clinical picture and causing diagnostic confusion, particularly in the context of a false-negative computed tomography (CT) scan.

      A previously well 51-year-old man presented with sudden onset of headache and right-sided weakness. On examination, he was aphasic with a right homonymous hemianopia and dense right-sided weakness. CT head was performed 6 hours after the onset of symptoms and was normal. The possibility of SAH was considered but was felt to be unlikely given the prominent focal signs, absence of nuchal rigidity and vomiting, and normal CT (which has a 95% sensitivity for the diagnosis of SAH within the first 24 hours2). Early middle cerebral artery infarction was felt to be more likely, particularly as routine tests confirmed the presence of diabetes and hypertension. A decision was taken to treat supportively and repeat the CT in 2–3 days to confirm the presence of ischaemic stroke.

      The following day, the headache and focal signs had resolved. The patient was alert but mildly confused. Shortly after, he became comatose. Repeat CT remained normal. Lumbar puncture revealed uniformly blood-stained cerebrospinal fluid with xanthochromia, confirming the diagnosis of SAH.

      Although the majority of patients with SAH present in a classical manner with sudden onset of severe headache,2 atypical presentations occur and may cause diagnostic confusion, particularly if the CT scan is unremarkable. Indeed, misdiagnosis is common even when presentation is typical: in one recent series of 136 cases of SAH with a classical presentation referred to a neurosurgical centre, the diagnosis was initially missed by general practitioners and hospital physicians in around half of cases, leading to a significantly worse outcome in these patients.2

      Clinical differentiation of SAH from ischaemic stroke may occasionally be difficult: headache may be a prominent feature in ischaemic stroke or transient ischaemic attack, occurring in 17% of patients with middle cerebral artery territory infarction.3 Similarly, focal neurological signs occur in around 20% of patients with SAH.4

      The possibility of SAH should always be considered in patients presenting with focal neurological signs and headache, with a low threshold for lumbar puncture where CT scanning is non-diagnostic.


       This letter was shown to the authors of reference 1 who responded as follows:

      Sir,In reply to the letter by Dr Kelly, it is apparent that SAH can occur in the presence of prominent focal neurological signs. Indeed the diagnosis may be delayed due to the perceived low probability of SAH or due to a reluctance to perform lumbar puncture in the presence of a focal neurological deficit. While the presence of focal neurological signs is more suggestive of ischaemic/haemorrhagic stroke than SAH,1-1 the presence of a focal neurological deficit is not an adverse prognostic factor in SAH.1-2 Recurrent transient focal neurologic deficits have been described in a patient 13 days after a SAH. At that time, multiple cerebral infarcts were demonstrated by CT brain scan and the patient was anticoagulated with heparin without any adverse consequences.1-3

      I agree with Dr Kelly that SAH should be considered as a diagnosis in any patient presenting with a focal neurological deficit and a normal CT brain scan.


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