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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cortical blindness is defined as a loss of vision due to bilateral retrogeniculate lesions (geniculocalcarine blindness). Gerstmann's syndrome is a combination of disorientation for left and right, finger agnosia, and profound agraphia, alexia, and acalculia. It is due to a lesion in the left angular gyrus, situated at the confluence of the temporal, parietal, and occipital lobes. We report on a patient who suffered from severe underdiagnosed eclampsia and who developed bilateral extensive medial temporal, parietal, and calcarine ischemic infarctions during an eclamptic fit. In addition, ischemia destroyed the left angular gyrus. The combination of these lesions led to Gerstmann's syndrome with additional cortical agnosia and cortical diplopia. For the first few months following the ischemic insult, the patient had been cortically blind. Thereafter, the patient slowly regained a visual acuity of 0.1 in both eyes. She then experienced monocular and binocular diplopia. Her ocular motility was normal; there was no phoria or tropia. Monocular and binocular diplopia slowly became less severe over the following year. Now, 2 years after the incident, the patient has a visual acuity of 0.2 in both eyes and no double vision. However, the handicapping symptoms of Gerstmann's syndrome, which make leading a normal life impossible, have persisted--the patient still cannot cope alone, mainly due to the severe disorientation for left and right. The picture of cortical agnosia, cortical diplopia, and Gerstmann's syndrome is a very rare combination. Visual recovery and rehabilitation in cortical blindness are severely affected and made difficult by the symptoms of Gerstmann's syndrome. In our case the reason for such a dramatic clinical picture was eclampsia, whose prodomes had not been diagnosed in time.
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PMID:Eclamptogenic Gerstmann's syndrome in combination with cortical agnosia and cortical diplopia. 749 36

It is not unusual to observe hemichorea in patients with diabetes mellitus, with origins attributable to recent ischemia. Our patient was a 66-year-old female with diabetes mellitus who suddenly developed right hemichorea, mild muscle weakness of the right upper extremity, ideational apraxia, and acalculia. Her blood glucose was 600 mg/dL, and HbA1c was 13.3%. After the patient underwent head magnetic resonance imaging (MRI), a new cerebral infarction was observed in the left frontal lobe, and treatment was started with edaravone and cilostazol. At the same time, insulin treatment was also started for hyperglycemia. The acalculia and ideational apraxia improved approximately 1 week after treatment initiated, and the hemichorea also decreased. ECD-SPECT was performed on admission, and it was observed that blood flow was decreased in the left frontal lobe and striatum, but increased in the thalamus; two weeks later on follow-up ECD-SPECT, blood flow had increased slightly in the left forebrain and striatum, while it had decreased slightly in the thalamus. This suggests that the cause of hemichorea was related to ischemia. When the activity of the pallidum is impaired, it is presumed that the inhibitory activity towards the thalamus weakens and the thalamic cells become over-excited, causing chorea.
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PMID:Hemichorea in a diabetes mellitus patient following acute ischemic stroke with changes in regional cerebral blood flow. 2574 12