Hyperbaric oxygen therapy of air embolus in the cerebral venous sinuses after intracranial surgery: a case report.

A case with cerebral venous air embolism (CVAE) after neurosurgery and treated with hyperbaric oxygen therapy (HBOT) is presented. This is a rare and potentially fatal complication that neurosurgeons should be aware of. A 52-year-old male was diagnosed with an intracerebral hematoma. An emergency evacuation of the hematoma was performed with a craniotomy and the postoperative CT scan showed a complete evacuation of the hematoma, but it also revealed a CVAE. The patient was immediately referred to HBOT and received three sessions within 48 h. The CT scan after the first HBOT showed no CVAE, venous thrombosis, or new hematoma.

Sturge-Weber syndrome with spontaneous intracerebral hemorrhage in childhood.

A girl aged 2 years 10 months suddenly went into a deep coma and demonstrated left hemiplegia. At birth, she had exhibited a left-sided facial port-wine stain typical of Sturge-Weber syndrome (SWS) and involving the V1 and V2 distributions of the trigeminal nerve. Computed tomography showed a right thalamic hemorrhage with acute hydrocephalus. Magnetic resonance imaging with Gd enhancement 8 months before the hemorrhage had shown a patent superior sagittal sinus (SSS) and deep venous system. Magnetic resonance imaging and MR angiography studies 2 months before the hemorrhage had revealed obstruction of the SSS and right internal cerebral vein (ICV). Given that a digital subtraction angiography study obtained after the hemorrhage did not show the SSS or right ICV, the authors assumed that impaired drainage was present in the deep venous system at that stage. The authors speculated that the patient's venous drainage pattern underwent compensatory changes because of the occluded SSS and deep venous collectors, shifting outflow through other cortical venous channels to nonoccluded dural sinuses. Sudden congestion (nearly total to total obstruction) of the ICV may have caused the thalamic hemorrhage in this case, which is the first reported instance of pediatric SWS with intracerebral hemorrhage and no other vascular lesion. Findings suggested that the appearance of major venous sinus occlusion in a child with SWS could be a warning sign of hemorrhage.

Iatrogenic venous thrombosis secondary to supplemental medicine toxicity.

OBJECTIVE: We described a case of cerebral venous sinus thrombosis in a patient taking multiple supplements as part of a naturopathic anti-aging regimen. METHODS: Case report. RESULTS: The patient presented with a thalamic infarct associated with a thrombus in the vein of Galen. He reported no previous history of endocrinopathy and no known hypercoagulability risk factors. He was treated with therapeutic anticoagulation resulting in improvement. Diagnostic workup revealed hyperthyroidism and gonadotrophic deficiency attributed to significant supplement medicine usage. CONCLUSION: This case highlights a potential risk of dietary supplements. Use of these supplements may be a risk factor for idiopathic cerebral venous thrombosis.

Dural arteriovenous fistulas with aggressive course: clinical and angiographic correlations in two patients.

Cranial dural arteriovenous fistulas (DAVFs) usually present with non-aggressive symptoms. We here report two patients who presented a peculiar clinical picture related to DAVFs, with focal neurological signs and haemorrhagic (case 1) or ischaemic lesions (case 2) respectively. The clinical and angiographic findings and putative pathophysiological mechanisms are discussed.

Scalp arteriovenous malformation draining into the superior sagittal sinus associated with an intracranial arteriovenous malformation: just a coincidence? Case report.

OBJECTIVE AND IMPORTANCE: Recent experimental and clinical evidence suggests that hemodynamic changes in the venous system can induce the formation of new arteriovenous malformations (AVMs). In a rat model, increased venous pressure induces the formation of soft tissue and dural AVMs. We report a clinical observation that may support these data. CLINICAL PRESENTATION: A 4-year-old boy with a midline scalp AVM draining into the superior sagittal sinus had an associated intracranial/parenchymal AVM. The cerebral AVM increased venous pressure in the superior sagittal sinus as revealed by angiography. INTERVENTION: The scalp AVM was resected, and the intracranial AVM was treated by use of the gamma knife. CONCLUSION: On the basis of reported experimental data and the morphological and hemodynamic characteristics in this patient's two lesions, we suggest that the scalp AVM might have been induced by hypertension in the superior sagittal sinus. This clinical observation supports the notion suggested by experimental studies that hemodynamic changes can induce the formation of associated AVMs.

[Fatal sinus vein thrombosis in a patient with mixed connective tissue disease and secondary antiphospholipid antibody syndrome]. / Letale Sinusvenenthrombose bei einer Patientin mit Mischkollagenose und sekundärem Antiphospholipid-Antikörper-Syndrom.

BACKGROUND: The antiphospholipid (Huges) syndrome is a complication of connective tissue diseases characterized by thromboembolic occlusions of arterial and venous blood vessels. CASE REPORT: At the age of 13, the patient developed connective tissue disease with arthritis and myositis. The course of her disease was characterized by frequent relapses despite immunosuppressive treatment. She developed deep venous thrombosis of her right leg as a manifestation of secondary antiphospholipid antibody syndrome at the age of 15 and was subsequently started on oral anticoagulation therapy. Approximately 10 months later, however, she decided to try alternative medicine and stopped both anticoagulation and immunosuppressive therapy. Only after 4 weeks she developed seizures followed by respiratory arrest with the need for cardiopulmonary resuscitation. Despite intensive care she died 2 days later with the signs of severe cerebral edema causing herniation of the brainstem. Autopsy confirmed the diagnosis of severe edema of the brain as a result of extensive thrombosis of all sinus veins. CONCLUSION: A complete sinus vein thrombosis is a rare manifestation of antiphospholipid antibody syndrome. The lethal thrombosis in this case occurred during a period of reactive hypercoagulability after termination of immunosuppressive and/or anticoagulation therapy. This case report underlines the need for long-term anticoagulation in patients with the antiphospholipid syndrome.

Reversible dural arteriovenous malformation-induced venous ischemia as a cause of dementia: treatment by surgical occlusion of draining dural sinus: case report.

We report a unique case of thalamic dementia caused by tentorial dural arteriovenous malformation (AVM), which was successfully treated by surgical occlusion of the straight sinus after attempts to occlude the dural AVM by endovascular procedures had failed. The tentorial dural AVM was fed by bilateral posterior meningeal arteries and occipital arteries, with early retrograde venous drainage into the straight sinus, inferior sagittal sinus, basal vein of Rosenthal, and dural veins in the falx cerebri. The venous ischemia in bilateral thalamus was revealed as low-density areas in computed tomographic scans, as high-intensity areas in T2-weighted magnetic resonance images, and as decreased cerebral blood flow and increased cerebral blood volume in single-photon positron emission computed tomography. Because this patient was not amenable to cure by endovascular embolization, an open surgical approach, surgical occlusion of the draining venous channel (the straight sinus), was performed. Postoperatively, dural AVM in angiography and venous ischemia in bilateral thalamus were resolved, as revealed by magnetic resonance imaging and single-photon positron emission computed tomography. Dementia caused by bilateral thalamic ischemia was also resolved. This case clearly illustrates the pathophysiological mechanism of venous ischemia in the bilateral thalamus to cause reversible dementia.

Recovery from primary deep cerebral venous sinus thrombosis with recanalisation.

A 50-year-old woman with idiopathic deep cerebral sinus and vein thrombosis (DCVT) had cerebellar disturbance prior to impaired consciousness. CT and MRI revealed haemorrhagic infarction in the cerebellum and signal changes suggesting infarction in the thalamus and basal ganglia bilaterally. The straight sinus and internal cerebral vein (ICV) were dense on CT. On angiography, the vein of Galen (VG) and straight sinus were not seen. Following clinical recovery, CT and MRI became normal, and angiography showed recanalization of the VG and ICV. The relationship between cerebellar infarction and DCVT, and signal changes on CT and MRI are discussed.