Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing fasciitis is a soft tissue infection that is characterized by extensive necrosis of the subcutaneous fat, neurovascular structures, and fascia. Cerebral infarction after facial necrotizing fasciitis has been rarely reported. A 61-year-old woman with diabetes was admitted with painful swelling of her right cheek. One day later, she was stuporous and quadriplegic. A computed tomographic scan of her face revealed right facial infection in the periorbital soft tissue, parotid, buccal muscle, and maxillary sinusitis. A computed tomographic scan of the brain revealed cerebral infarction in the right hemisphere, left frontal area, and both cerebellum. Four days later, she died from cerebral edema and septic shock. Involvement of the cerebral vasculature, such as the carotid or vertebral artery by necrotizing fasciitis, can cause cerebral infarction. Facial necrotizing fasciitis should be treated early with surgical treatment and the appropriate antibiotic therapy.
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PMID:Fulminant cerebral infarction of anterior and posterior cerebral circulation after ascending type of facial necrotizing fasciitis. 2293 95

Cerebral vasospasm associated with hyperthyroidism has not been reported to cause cerebral infarction. The case reported here is therefore the first of cerebral infarction co-existing with severe vasospasm and hyperthyroidism. A 30-year-old woman was transferred to our hospital in a stuporous state with right hemiparesis. At first, she complained of headache and dizziness. However, she had no neurological deficits or radiological abnormalities. She was diagnosed with hyperthyroidism 2 months ago, but she had discontinued the antithyroid medication herself three days ago. Magnetic resonance imaging and angiography showed cerebral infarction with severe vasospasm. Thus, chemical angioplasty using verapamil was performed two times, and antithyroid medication was administered. Follow-up angiography performed at 6 weeks demonstrated complete recovery of the vasospasm. At the 2-year clinical follow-up, she was alert with mild weakness and cortical blindness. Hyperthyroidism may influence cerebral vascular hemodynamics. Therefore, a sudden increase in the thyroid hormone levels in the clinical setting should be avoided to prevent cerebrovascular accidents. When neurological deterioration is noticed without primary cerebral parenchyma lesions, evaluation of thyroid function may be required before the symptoms occur.
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PMID:Severe Cerebral Vasospasm in Patients with Hyperthyroidism. 2818 50


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