Cerebral Venous Sinus Thrombosis Presenting Research Articles

Communicating hydrocephalus due to cerebral venous sinus thrombosis treated with ventriculoperitoneal shunt

Cerebral venous sinus thrombosis (CVT) is a rare cerebrovascular disease with variable presentation. CVT rarely causes hydrocephalus. Communicating hydrocephalus due to CVT is extremely rare. We describe a patient of CVT presenting with chronic headache and communicating hydrocephalus. The patient was successfully treated with ventriculoperitoneal (VP) shunt. A 40 year old man presented with moderate to severe headache since six months and progressive visual loss since two months. Head Computed tomogram showed mild hydrocephalus without obstruction. Lumbar puncture (LP) demonstrated elevated pressure but was otherwise normal. Magnetic resonance venogram showed extensive CVT. Repeated CSF drainage and thecoperitoneal shunt did not relieve the severe headache hence a VP shunt was placed. Post shunt headache subsided with resolution of hydrocephalus. CVT can present as communicating hydrocephalus. Gradual reduction of intra-ventricular pressure by repeated LPs followed by VP shunt can safely treat hydrocephalus due to CVT.

Cerebral venous sinus thrombosis presenting as cerebral metastasis in a patient with choriocarcinoma following a non-molar gestation

► A patient with choriocarcinoma and neurologic symptoms was diagnosed with cerebral venous thrombosis (CVT). ► Her risk factors for CVT included methylene tetrahydrofolate reductase gene mutation and malignancy. ► Chemotherapy was continued despite the CVT to achieve choriocarcinoma remission.

Cerebral Venous Sinus Thrombosis Presenting With Auditory Hallucinations and Illusions

Cerebral venous sinus thrombosis may present with seizures or neuropsychiatric symptoms, but does not typically present with hallucinations. We present a case of venous thrombosis of the right sigmoid and transverse sinuses that presented with auditory hallucinations and illusions. We describe a 45-year-old woman with a history of myasthenia gravis, stable on oral prednisone and monthly intravenous immunoglobulin infusions, who started on a progesterone/estrogen combination contraceptive pill for menorrhagia 3 weeks before admission and presented with symptoms of headache, fever, and auditory hallucinations and illusions. The patient's cerebrospinal fluid showed lymphocytic pleocytosis. Two electroencephalograms showed significant right temporal lobe slowing. Magnetic resonance venogram of the brain showed venous sinus thrombosis of the right sigmoid and transverse sinuses. Magnetic resonance imaging showed a cortical venous infarct in the right middle temporal gyrus. The patient's auditory hallucinations and illusions resolved spontaneously weeks after presentation. This case suggests that auditory hallucinations and illusions should be added to the already broad spectrum of presenting features of cerebral venous sinus thrombosis. The nondominant right middle temporal gyrus may play a role in such auditory hallucinations.

Cerebral Venous Sinus Thrombosis in an Adult Patient Presenting as Headache and Acute Subdural Hematoma

We report a 55-year-old man with cerebral venous sinus thrombosis presenting as acute subdural hematoma. He was treated with an intravenous infusion of heparin sodium and the occluded superior sagittal sinus was recanalized. According to our literature review, acute subdural hematoma caused by cerebral venous sinus thrombosis is relatively rare, and only a single case has reported thus far. We speculate that dehydration was the reason for cerebral venous sinus thrombosis in the present case, and the sudden rise in intracranial pressure in addition to hemodynamic stress caused by cerebral venous sinus thrombosis resulted in the collapse of a bridging vein and caused an acute subdural hematoma.

Cerebral Venous Sinus Thrombosis Presenting as Transient Ischemic Attacks in a Case With Homozygous Mutations of MTHFR A1298C and CG677T

We report a case with recurrent, transient attacks of slurred speech, weakness, and numbness of the right half of the face and the right arm without seizure activity, accompanied by headache and double vision. Neurologic examination revealed bilateral papilledema and right abducens palsy. Brain magnetic resonance imaging revealed thrombosis of the dural venous sinuses and the cortical veins, with no evidence of parenchymal lesion. Homozygous mutations were found for methylenetetrahydrofolate reductase (MTHFR) A1298C and MTHFR CG677T. Anticoagulation with heparin and warfarin resulted in prompt cessation of the transient attacks, as well as the signs and symptoms of increased intracranial pressure. This report documents that, although rare, transient ischemic attacks can result from cerebral venous thrombosis.

Cerebral Venous Sinus Thrombosis: Unusual Imaging Appearance

Cerebral venous sinus thrombosis (CVST) has widely varied clinical and radiological manifestations ranging from asymptomatic minimal brain oedema to severe haemorrhagic infarcts associated with focal deficits, coma and even death. Cerebral venous sinus thrombosis presenting with lobar or subdural hematomas are rare and the cause may easily be overlooked. We present a case of CVST with an atypical radiological picture of intra-arenchymal, subdural and subarachnoid haemorrhage.

Cerebral venous sinus thrombosis as a rare cause of thunderclap headache and nonaneurysmal subarachnoid haemorrhage

Sirs: In a clinical setting, isolated thunderclap headache is commonly assumed to be benign in origin once subarachnoid haemorrhage (SAH) has been excluded [1]. However, cerebral venous sinus thrombosis (CVST) is an infrequent, alternative cause of sudden-onset headache and is not conclusively excluded by normal conventional CT and LP. CVST is also a recognised rare cause of SAH. Here, we report a case of CVST presenting with thunderclap headache and complicated by delayed SAH. A previously well 53-year-old woman presented with spontaneous, sudden-onset occipital headache as her sole symptom. Neurological examination including fundoscopy was normal, with no evidence of meningism. Acute head CT and subsequent LP performed 16 hours after onset were unremarkable (opening pressure 19 cm, CSF acellular with no bilirubin detectable on spectrophotometry). The headache resolved completely within 24 hours and the patient was discharged with a diagnosis of primary thunderclap headache. The following day, she represented with sudden-onset headache at rest accompanied by mild neck stiffness. Her symptoms resolved before a further suddenonset headache occurred two days later. Examination remained normal throughout. Repeat, unenhanced head CT demonstrated a small, high left frontal SAH along the cranial convexity without involvement of the basal cisterns (Fig. 1a). CT angiography detected no arterial aneurysm, but its venous phase showed changes suggestive of superior sagittal sinus thrombosis, which was confirmed on MR venography (Fig. 1b). Screening for secondary causes of thrombosis was negative. She was initially treated with intravenous unfractionated heparin to allow rapid reversal in case of rebleeding, before being warfarinised under cover from low molecular weight heparin. She remained well at follow-up six months later. Repeat MR angiography showed resolution of the superior sagittal sinus thrombosis, with no other vascular or brain parenchymal abnormalities. Thunderclap headache is an unusual presentation of CVST, perhaps seen in fewer than 20 % of cases [2]. Rarely, there may be no concomitant findings to suggest the presence of a CVST, such as focal neurological signs, seizures or features of raised intracranial pressure. Most patients with CVST have a raised opening pressure and abnormal CSF constituents, but absence of these features does not conclusively rule out the diagnosis. In a previous series of 38 cases, nine patients had both opening pressure and CSF constituents measured, and in one of them all parameters were normal [3]. SAH is a very rare complication of cerebral venous thrombosis, with only 30 cases reported to date. It has been suggested that venous intraparenchymal haemorrhages may rupture into the subarachnoid space, thus causing sudden-onset headache in CVST [2, 4]. However, we hypothesise that our patient’s first headache was caused by the CVST, as there was no evidence of SAH on initial brain CT and bilirubin was not detectable in the CSF. The second or third episode of headache may have been caused by SAH. LETTER TO THE EDITORS

Cerebral venous sinus thrombosis presenting with excessive subarachnoid hemorrhage in a 14-year-old boy

Cerebral venous thrombosis presenting with subarachnoid hemorrhage (SAH) is very rare. We report a case of cerebral venous sinus thrombosis as an initial manifestation of SAH. A 14-year-old boy was admitted with progressive headache, nausea, vomiting, diplopia, and gait disturbance. Cerebral computed tomography scan showed a widely SAH in the basal cisterns, bilateral sylvian fissures, and anterior interhemispheric fissure. Cerebral angiography was performed to detect any aneurysm in intracranial vasculature as a cause of SAH; however, the totally thrombosed superior sagittal sinus, galenic vein, and straight sinus were the sole abnormal findings.

Cerebral venous sinus thrombosis presenting as subdural haematoma

The authors report a 39-year-old woman who presented with intermittent, excruciating nuchal and occipital headache. Magnetic resonance imaging and magnetic resonance angiography scans showed bilateral subdural haematomas with veno-occlusive disease of the superficial and deep venous systems. There were bridging collaterals with scalp veins, bleeds from which could explain the subdural haematoma. There was acute on chronic veno-occlusive disease with an acute rise in intracranial pressure and a bleed from the vein of Galen.

Cerebral venous sinus thrombosis and thrombophilia presenting as pseudo-tumour syndrome following mild head injury

Cerebral venous sinus thrombosis (CVT) after mild head injury is infrequent. A 38-year-old patient presented with a Glasgow Coma score (GCS) of 15 after a road traffic accident. CT scan revealed a temporal contusion. He was treated with measures to prevent cerebral oedema and anticonvulsants. Three weeks later he presented with features of pseudo-tumour syndrome. Investigations revealed the presence of cerebral venous sinus thrombosis, protein C deficiency and elevated titres of antiphospholipid antibodies. He was treated with anticoagulants and showed improvement. This case report highlights that multiple "hits" may lead to CVT and hence laboratory screening of patients with CVT is necessary even if the clinical situation seemingly provides sufficient explanation for a thrombotic event. The presence of acquired and inherited causes of thrombophilia need not always lead to symptomatic thrombosis. As illustrated by this case, a second hit, such as trauma, may be the precipitating factor that unmasks the prothrombotic state.