|Year : 2010 | Volume
| Issue : 2 | Page : 85-89
Subarachnoid hemorrhage with transient ischemic attack: Another masquerader in cerebral venous thrombosis
Bhawna Sharma, Vipin Satija, Parul Dubey, Ashok Panagariya
Department of Neurology, SMS Medical College, Jaipur, India
|Date of Web Publication||28-Mar-2012|
7, Raj Niketan, Moti Doongri Road, Jaipur
Cerebral venous thrombosis has a wide spectrum of clinical manifestations that may mimic many other neurological disorders and lead to frequent misdiagnoses or delay in diagnosis. The most frequent symptoms and signs are headache, seizures, focal deficits, and papilledema. A number of rare atypical manifestations have been described. Cerebral venous thrombosis may present with an isolated intracranial hypertension type picture, thunderclap headache, attacks of migraine with aura, isolated psychiatric disturbances, pulsatile tinnitus, isolated or multiple cranial nerve involvement, and occasionally as subarachnoid hemorrhage (SAH) or transient ischemic attack. Our patient presented with thunderclap headache and transient ischemic attack like episode with obvious SAH on CT scan. Acute SAH suggests the presence of a vascular lesion, such as ruptured aneurysm, and CVT is not generally considered in the diagnostic workup of SAH. The case emphasizes the importance of cerebral venous study in nonaneurysmal cases of SAH. It is important to have a high index of suspicion in such atypical cases to avoid delay in diagnosis.
Keywords: Cerebral venous thrombosis, masquerader, subarachnoid hemorrhage, transient ischemic attack
|How to cite this article:|
Sharma B, Satija V, Dubey P, Panagariya A. Subarachnoid hemorrhage with transient ischemic attack: Another masquerader in cerebral venous thrombosis. Indian J Med Sci 2010;64:85-9
|How to cite this URL:|
Sharma B, Satija V, Dubey P, Panagariya A. Subarachnoid hemorrhage with transient ischemic attack: Another masquerader in cerebral venous thrombosis. Indian J Med Sci [serial online] 2010 [cited 2013 May 22];64:85-9. Available from: http://www.indianjmedsci.org/text.asp?2010/64/2/85/94405
| ¤ Introduction|| |
Cerebral dural venous sinus and cortical venous thrombosis present with a myriad of neurological manifestations. Most common clinical features include headache, focal or generalized seizures, focal neurological deficits, and intracranial hypertension. Acute subarachnoid hemorrhage (SAH) or transient ischemic attacks are rare presentations of cerebral venous thrombosis (CVT). , A high index of clinical suspicion is required in these situations when such presentations occur in isolation, so that appropriate treatment can be initiated as promptly as possible. The report also emphasizes the routine inclusion of venous angiogram in patients with SAH, especially in those in which aneurysm has not been detected on arterial study.
| ¤ Case Report|| |
A 40-year-old nonhypertensive male presented with sudden onset severe left-sided headache followed by an episode of right-sided weakness which lasted for 15 min and recovered spontaneously. There was no history of loss of consciousness, seizure, vomiting, any preceding fever, or any similar history of headache or transient ischemic attack (TIA) in past. He had history of chronic alcohol intake but had no other addictions. On examination blood pressure was 150/90 mmHg and neck stiffness was present. Rest of the systemic and neurological examination was normal. There was no papilledema or any focal deficit.
Noncontrast computed tomogram revealed SAH in left-sided frontoparietal and right frontal cortical sulci [Figure 1], [Figure 2] and [Figure 3]. MR angiogram did not show aneurysm or any other vascular abnormality [Figure 4]. Patient was managed on conservative lines for nonaneurysmal SAH. But severe headache was persistent in the absence of any hydrocephalus on a subsequent CT scan.
|Figure 1: NCCT head shows SAH in bilateral cerebral convexites in left frontoparietal cortical sulci and right frontal cortical sulci|
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|Figure 2: NCCT head shows SAH in bilateral cerebral convexites in left frontoparietal cortical sulci and right frontal cortical sulci|
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DSA cerebral vessels were then carried out on the third day of illness which was suggestive of a normal arterial study but showed occlusion of superior sagittal sinus, right transverse sinus, and right sigmoid sinus. Subsequently done MR venogram brain also confirmed these findings [Figure 5] and [Figure 6]. On further enquiry there was no preceding dehydration, ear discharge, or symptoms suggestive of any other infective focus. Routine blood hematology and biochemistry were normal. Coagulation profile (PT, PTT), homocysteine, and antiphospholipid antibody levels were within normal limits. Workup for the thrombophilic profile was negative. HIV ELISA was negative. The patient was anticoagulated with low-molecular-weight heparin and was later shifted to oral anticoagulants maintaining the international normalized ratio between 2 and 2.5. His headache gradually subsided and he was discharged on oral anticoagulants.
|Figure 5: MR venogram brain showing superior sagittal sinus, right transverse, and right sigmoid sinus thrombosis|
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|Figure 6: MR venogram brain showing superior sagittal sinus, right transverse, and right sigmoid sinus thrombosis|
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| ¤ Discussion|| |
CVT has a wide spectrum of clinical manifestations and modes of onset that may mimic many other neurological disorders and lead to frequent misdiagnoses or delay in diagnosis. A typical clinical profile is determined by the underlying sinus/venous system involved, mode of onset (acute, subacute or chronic), and nature of primary disease giving rise to CVT. The most frequent symptoms and signs are headache (95%), focal seizures with or without secondary generalization (47%), focal deficits including unilateral or bilateral paresis (43%), and papilledema (41%).  Twenty percent presented with a isolated intracranial hypertension (IIH) type picture (headache, visual disturbance, and papilledema).
A number of rare atypical manifestations have been described with CVT. CVT may present with thunderclap headache, attacks of migraine with aura, isolated psychiatric disturbances, pulsatile tinnitus, isolated or multiple cranial nerve involvement, and occasionally as SAH or TIA. , Our patient presented with a thunderclap headache and TIA like episode with obvious SAH on a CT scan. SAH was evident bilaterally on cerebral convexities. The exact cause of SAH associated with CVT is unknown. Venous hemorrhagic infarct can be responsible for secondary rupture into subarachnoid spaces and cause SAH.  Our patient did not have any parenchymal abnormality. Dural sinus thrombosis with secondary venous hypertension may lead to SAH into the subarachnoid space due to the rupture of fragile, thin-walled cortical veins.  Possibly either of these two mechanisms might be responsible for SAH in our case.
Isolated TIA like presentation in CVT has been only rarely reported. Cortical vein involvement alone without extension to the dural sinuses may present with a "stroke-like" episode without intracranial hypertension.  The postulated mechanism of the transitory focal deficit include sudden venous engorgement of the drained brain parenchyma.  In our case, transient hemiparesis might have been because of irritative effects of SAH.
Another interesting point is the site of SAH occurring in CVT. These include the presence of SAH at cerebral convexities but with basal cistern sparing. Recognition of these subtleties may give a clue to an underlying unusual nonaneurysmal cause and will encourage further investigations.  Acute SAH suggests the presence of a vascular lesion, such as ruptured aneurysm, and CVT is not generally considered in the diagnostic workup of SAH. The case also emphasizes the importance of cerebral venous study in nonaneurysmal cases of SAH.
Cerebral venous sinus thrombosis is a potentially life-threatening condition if it is undiagnosed, but is a treatable disorder. It is important to have a high index of suspicion in such atypical cases, especially when such presentations occur in isolation, to avoid delay in diagnosis.
| ¤ References|| |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]