Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral venous thrombosis (CVT) is a disease with multiple known etiologies that present with a remarkably wide spectrum of clinical signs and symptoms. We present a case of a 34-year-old man with a history of meningeal symptoms for 1 week after receiving a lumbar injection for lower back pain. He subsequently developed dense right hemiplegia and global aphasia. Head magnetic resonance imaging revealed superior sagittal sinus thrombosis. The patient was started on intravenous heparin but deteriorated neurologically. Urokinase infusion directly into the superior sagittal sinus was performed, with striking functional and neurologic improvement. Lupus anticoagulant was positive. We also present the case of a 24-year-old pregnant woman who developed an acute onset of meningeal symptoms and resultant left hemiparesis. Head magnetic resonance angiography revealed thrombosis of right transverse and sigmoid sinuses. Protein S deficiency was found. She was started on intravenous heparin, then enoxaparin, with improvement in symptoms. These cases demonstrate that CVT can be a cause of stroke in young patients with hypercoagability disorders, and a heightened awareness of CVT will promote optimal medical care and functional outcomes. Excellent functional recovery is likely with early recognition and treatment of the underlying etiology, as well as successful lysis of the clot.
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PMID:Cerebral venous thrombosis in young adults: 2 Case reports. 1134 48

Cerebral venous thrombosis (CVT), which typically progresses from either acute or subacute onset, presents with symptoms related to intracranial hypertension (e.g., headache and papilledema) and brain parenchymal lesions (e.g., aphasia and hemiplegia). Anticoagulation therapy is generally accepted as a treatment for CVT and often leads to good clinical outcomes. However, we experienced a case of CVT with an uncommon clinical course. The patient was a 63-year-old man who presented with headache, papilledema, visual loss, and diplopia; his condition gradually deteriorated, and he was diagnosed with CVT via cerebral angiography. The sinus thrombus was extensive and resistant to anticoagulation therapy, and lumbar puncture revealed a progressive increase in cerebrospinal fluid (CSF) pressure. We performed a lumboperitoneal (LP) shunt procedure, which yielded marked improvement in the symptoms. The main mechanism of neurological dysfunction in CVT is venous outflow obstruction caused by venous thrombus, which results in brain edema, and/or venous infarction, which induces focal neurological signs. Another mechanism is impaired CSF absorption in the thrombosed sinuses, resulting in intracranial hypertension. We speculated that the latter mechanism strongly influenced our case, thus explaining the uncommon clinical course and effectiveness of the LP shunt procedure. Although LP shunting is not a common treatment for CVT, this case report could indicate the usefulness of this procedure for CVT with chronic progression and resistance to anticoagulation therapy.
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PMID:Report of Dramatic Improvement after a Lumboperitoneal Shunt Procedure in a Case of Anticoagulation Therapy-Resistant Cerebral Venous Thrombosis. 2665 61