Acute ischemic stroke involving the entire vascular distribution of a carotid or middle cerebral artery can cause massive cerebral edema. This study evaluated external decompression for the treatment of massive stroke and analyzed possible prognostic factors. Twenty-four patients with acute massive cerebral infarction, which had progressed to tentorial herniation and impending death, underwent ex ternal decompression after medical therapy failed to achieve an effective response. The neurological outcome 2 months after surgery using the Glasgow Outcome Scale was severe disability in 14 patients, vegetative state in two, and death in eight. The overall mortality was 33%. Various characteristics (age, sex, etiology, side of hemispheric infarction, pupillary asymmetry, Japan Coma Scale, distribution of in farction, hemorrhagic infarction, midline shift, tentorial herniation) were evaluated to determine the factors associated with high mortality after surgical intervention. There was no statistically significant relationship between any variable and mortality. Mortality was especially high in the patients with preoperative consciousness level of 200, anterior, middle, and posterior cerebral artery territory infarc tion, and stage III of tentorial herniation. Postoperatively, all patients with severe disability returned to a clear level of consciousness.Six patients with dominant hemisphere stroke had some measure of communicative skills in spite of aphasia. External decompression is a life-saving treatment for pa tients with massive cerebral infarction and can provide a reasonable quality of life even for those with dominant hemisphere strokes. Decompressive surgery should be considered and performed as soon as possible if computed tomography demonstrates signs of descending tentorial herniation.
To clarify the genotype-phenotype correlation of 5p-syndrome, FISH analyses were performed for six patients by using a series of probes spanning 5p13.1-p15.33. Genotypically, break points of deletion were quite different. Three of the six patients were diagnosed as interstitial deletion on chromosome 5p by G-banding method and FISH analysis; however, all of them proved to be entire distal deletions of 5p caused by unbalanced chromosomal translocations. Furthermore, one 5p-syndrome patient was diagnosed only by the FISH analysis using a single probe but not by ordinary chromosomal analyses. Therefore, when ordinary chromosomal analysis cannot detect any deletion in a patient who is phenotypically suspected of 5p-syndrome, multiple FISH analysis or parental chromosomal analysis would be needed for correct diagnosis. Interestingly, one patient with terminal deletion between 5p15.31-pter lacks mental retardation and cat-like crying, indicating that this region might not be responsible for those cardinal features of 5p-syndrome. Further studies on genotype-phenotype correlation will help us better understand 5p-syndrome and also determine functional mapping of the 5p region.
A 56-year-old man presented with a very rare true neurenteric cyst in the conus medullaris without evidence of vertebral or visceral anomaly manifesting as a 6-month history of mild low back and bilateral inguinal pain. No motor weakness was found in the bilateral lower extremities. He had also suffered dysesthesia in the bilateral feet for several weeks before admission. Lumbar spine magnetic resonance (MR) imaging demonstrated a cystic intradural extramedullary mass at the L1-2 levels without enhancement after gadolinium injection. MR imaging, computed tomography, and radiography detected no vertebral anomaly. Lumbar laminectomy at the L1-2 levels was performed and the lesion was incompletely removed. Histological examination showed the cystic wall lined with ciliated columnar epithelium. Neurenteric cyst should be considered in the diagnosis of isolated cystic mass lesion at the lumbosacral region even in the absence of vertebral or visceral abnormality.
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