|Year : 2006 | Volume
| Issue : 1 | Page : 32-35
Subarachnoid hemorrhage: An unusual presentation of cerebral venous sinus thrombosis
T Bindu1, S Panda1, HS Chandrashekar2, Ravi S Shankar2, D Nagaraja1
1 Departments of Neurology, Neuroimaging , NIMHANS, Bangalore, India
2 Departments of Interventional Radiology, NIMHANS, Bangalore, India
Department of Neurology, NIMHANS, Hosur Road, Bangalore - 560029
Source of Support: None, Conflict of Interest: None
| Abstract|| |
The diagnosis of cerebral venous thrombosis (CVT) requires high index of suspicion owing to the varied spectrum of its clinical manifestations. Its diagnosis may be more elusive if the patient presents with subarachnoid hemorrhage (SAH). We report four cases of CVT that presented with SAH and will discuss the importance of looking for clues for the early diagnosis of CVT. Three men and one woman presented with severe headache and images initially suggested SAH with no associated parenchymal bleeding. In all patients, SAH involved the sulci of the convexity and spared the basal cisterns. Angiography showed occlusion of intracranial venous sinuses without revealing any other cause of SAH. All the patients showed improvement with anticoagulant therapy.
Keywords: Cerebral venous thrombosis, subarachnoid hemorrhage
|How to cite this article:|
Bindu T, Panda S, Chandrashekar H S, Shankar RS, Nagaraja D. Subarachnoid hemorrhage: An unusual presentation of cerebral venous sinus thrombosis. Ann Indian Acad Neurol 2006;9:32-5
|How to cite this URL:|
Bindu T, Panda S, Chandrashekar H S, Shankar RS, Nagaraja D. Subarachnoid hemorrhage: An unusual presentation of cerebral venous sinus thrombosis. Ann Indian Acad Neurol [serial online] 2006 [cited 2020 Nov 29];9:32-5. Available from: https://www.annalsofian.org/text.asp?2006/9/1/32/22819
Subarachnoid hemorrhage (SAH) usually suggests the presence of a vascular lesion, such as ruptured aneurysm. However, a small number of patients may have SAH due to other etiologies. Therefore, it is an issue of paramount importance to pick clues to suspect nonaneurysmal origin of SAH like cerebral venous thrombosis (CVT). This is important as the management is entirely different and the outcome of a potentially treatable condition like CVT depends on early diagnosis and treatment. CVT presenting as SAH is rarely reported in the literature. To date, eleven patients with CVT and a Computed Tomography (CT)-based diagnosis of SAH have been reported of which seven had SAH without parenchymal involvement. We report four cases of CVT who presented as SAH and discuss the pointers that may lead to the early diagnosis of CVT.
A 32-year-old man presented with headache for two days and three episodes of generalized tonic clonic seizures. He was habituated to excess of alcohol. On examination, he was fully conscious, fundi were normal and there were no cranial nerve palsies or focal neurological deficits. Meningeal signs were present. Nonenhanced CT of brain showed hyperdensity in the left Sylvian fissure, anterior interhemispheric fissure and in bilateral frontoparietal convexities, which were not enhancing on contrast infusion [Figure - 1]A. There were no parenchymal bleeds. CSF was uniformly bloodstained with fresh RBCs, sugar 54 mg/dl and protein 105 mg/dl. Digital subtraction angiography showed superior sagittal sinus and right transverse sinus thrombosis [Figure - 1]B. Therapy with heparin followed by oral anticoagulant was initiated along with anticonvulsant drugs . The patient improved significantly within a week.
A 50-year-old man presented with headache for four days, altered sensorium for two days and recurrent episodes of focal seizures of the left upper limb. He was not an alcoholic or smoker. On examination, he was in deep altered sensorium, flexing the right upper limb to pain without any vocalization or eye opening. Pupils were bilaterally 3 mm in size and not reacting to light. Fundi were normal and extra ocular movements were frozen. Neck stiffness was not present. Nonenhanced CT brain showed hyperdensity in the right Sylvian fissure and posterior interhemispheric fissure suggestive of bleed [Figure - 2]A. MRI brain with MR venogram confirmed thrombosis of superior sagittal sinus, left transverse sinus and straight sinus [Figure - 2]B. Since the patient's condition was unstable, DSA could not be done. No conditions that could result in CVT were found despite an extensive etiologic workup. He was treated with heparin followed by oral anticoagulant and he significantly improved.
A 27-year-old woman presented with acute onset of headache and weakness of the left upper limb and lower limb. She had been on oral contraceptive pills prior to the onset of symptoms. On examination, she was conscious, fundi were normal and she had left hemiparesis. There were no meningeal signs. Non-enhanced CT of brain showed nonenhancing hyperdensities in the right frontal convexity, right cingulate sulcus and in the anterior interhemispheric fissure without parenchymal bleed [Figure - 3]A. Digital subtraction angiography showed thrombosis of all the major sinuses, i.e. superior sagittal sinus, straight sinus and bilateral transverse sinuses [Figure - 3]B. She improved within five days with interruption of oral contraceptives and initiation of anticoagulant therapy without any further worsening.
A 33-year-old man presented with headache for three days and two episodes of generalized tonic clonic seizures. He was habituated to excess of alcohol. On examination, he was conscious and oriented. Fundi were normal and there were no cranial nerve palsies or focal neurological deficits. Meningeal signs were present. Nonenhanced CT of brain showed hyperdensities in the interhemispheric fissure, bilateral frontoparietal convexities and left Sylvian fissure which were not enhancing on contrast [Figure - 4]A. There were no parenchymal bleeds. CT venogram showed thrombosis of the superior sagittal sinus [Figure - 4]B. After instituting anticoagulants with antiepileptic drugs, he improved.
| Discussion|| |
The most common cause of nontraumatic SAH is rupture of an intracranial aneurysm (85%). Less common causes are blood dyscrasias, cerebral amyloid angiopathy, primary, metastatic or meningeal neoplasms, vasculitis, drug abuse, cerebral venous occlusive disease, bacterial meningitis, spinal cord vascular malformations and spinal cord tumors, arterial dissection, dural arteriovenous fistula and pituitary apoplexy. In this report, CVT has been highlighted as a cause of nonaneurysmal SAH. All the four patients presented initially with severe headache with or without seizures. Radiological imaging done at presentation initially showed blood in the cerebral convexities with no parenchymal bleed or direct signs of CVT. Digital subtraction angiography done in two patients, MRI with MR venogram in one patient and CT venogram done in one patient confirmed thrombosis and occlusion of intracranial venous sinuses. However, they did not reveal any other cause of SAH. Risk factors for CVT were identified, namely, chronic alcoholism in two patients and oral contraceptive drug intake in one patient.
Patients with CVT commonly present with severe headache and focal neurological symptoms and signs. Imaging usually reveals single or multifocal parenchymal venous infarcts with haemorrhagic transformation and direct signs of CVT like dense delta and cord sign on plain CT and empty delta sign on contrast enhanced CT. The cases presented demonstrate the rare possibility of imaging evidence of blood in the subarachnoid space without any parenchymal bleed or direct signs of CVT, thus radiologically suggesting SAH. Subsequent angiographic evaluation confirmed the diagnosis of CVT. The presentation of CVT in the form of SAH has been rarely reported in the literature. Lumbar puncture in patients with CVT commonly show red blood cells. In a series of 32 patients with CVT, 50% had more than 100 erythrocytes/mm 3sub of CSF. However, no SAH was demonstrable in 23 patients with available CT scans., To date, eleven patients with CVT and a CT-based diagnosis of SAH have been reported. Further, only seven patients with isolated cortical vein thrombosis with CT evidence of SAH in the absence of parenchymal involvement has been reported till date.
The exact pathophysiology of SAH associated with CVT is not known. Venous hemorrhagic infarction can be responsible for secondary rupture into subarachnoid spaces causing SAH. However, none of the patients reported here had intraparenchymal signs of bleeding on CT or MR imaging. Dural venous thrombosis with secondary venous hypertension may lead to SAH due to rupture of thin walled fragile cortical veins. Some of these veins may be dilated secondary to sinus thrombosis. On CT scan, it may be difficult to know initially whether SAH is of aneurysmal or nonaneurysmal in origin. Noncontrast CT images of all the four patients demonstrated hyperdensities suggestive of bleed in the sulcal subarachnoid space with sparing of basal cisterns. Since, the SAH is due to the increased venous pressure following CVT, the site of rupture is perhaps in the cortical veins over the cerebral surface. This would explain the tendency for the subarachnoid blood to be seen in the brain convexities and the interhemispheric fissure as seen in three of the patients. Hence, an important radiological clue could be the sparing of the basal cisterns in SAH associated with CVT, even in the absence of parenchymal involvement. This should prompt the clinician to ask for vascular imaging of not only intracranial arteries, but also venous sinuses at the earliest. Digital subtraction angiography, which is the gold standard for detecting aneurysm, will show abnormalities such as filling defects within the sinuses, nonvisualization of a segment of the sinuses, with or without reversal of flow in the venous phase in CVT.
Concurrently, clinical clues should be sought to strengthen the possibility of CVT. The presence of severe headache is not discriminating between CVT and aneurysmal bleed except if it is acute and thunderclap in nature as in aneurysmal SAH. However, patients with CVT often present with associated focal or generalized seizures and may have focal motor or language deficits shortly after onset. It is important that such patients should also be enquired and investigated for risk factors for CVT like puerperal state, infections of ear or sinuses, connective tissue disorders and prothrombotic states. CVT is a potentially serious, but fully treatable condition and its outcome depends upon early diagnosis and timely treatment., Recognition of these clinical and radiological signs can prevent delayed diagnosis of CVT even in the presence of apparent confounding presentations.
Interestingly, all the patients improved with anticoagulant therapy despite subarachnoid bleed being present radiologically. In the previous reports as well, antithrombotic agents were instituted in all the cases., Once the diagnosis of CVT is confirmed, the treatment of these patients needs to be done as per the accepted protocol of therapy with anticoagulants., As noted in all the four cases, there was no worsening of the clinical condition. Hence, SAH in this specific clinical setting is not a contradiction for anticoagulation.
| Conclusion|| |
SAH is a rare initial presentation of CVT. The presence of subarachnoid blood in the cerebral convexities sparing the basal cisterns even in the absence of parenchymal lesions and direct signs of CVT could be a radiological clue to nonaneurysmal origin of SAH like CVT. The above signs should prompt further studies to demonstrate the presence of CVT. In the exceptional circumstance of SAH in CVT, anticoagulation is the mainstay of treatment.
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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]
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