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)

We report the case of a 25-year-old woman undergoing a laparoscopic cholecystectomy, who suffered, one min after the beginning of intraperitoneal insufflation of CO2 (2.5 L at a pressure of 10 mmHg), a sudden decrease to 0.8 L.min-1 of the aortic blood flow (ABF), monitored in the descending aorta by an oesophageal echo-Doppler probe, associated with a decrease of PetCO2 to 15 mmHg and of SpO2 readings to 88%. Despite the lack of simultaneous changes in heart rate and arterial pressure, pulmonary gas embolism (GE) was suspected. The pneumoperitoneum was exsufflated and CPR was started because of circulatory inefficiency. Ten min later, efficient spontaneous cardiac activity restarted, whereas PetCO2 and ABF returned rapidly to normal values. At this time, a typical gas noise was clearly obtained through the oesophageal Doppler transducer. The patient remained in deep coma (GCS:6) with a left sided hemiplegia. However, she fully recovered after four sessions of hyperbaric oxygenation. Simultaneous continuous monitoring of ABF and PetCO2 allows an undelayed recognition of major circulatory disturbances, before significant changes in heart rate and arterial pressure occur.
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PMID:[Diagnosis of heart arrest caused by CO2 embolism during laparoscopic surgery by monitoring of aortic blood flow and capnography]. 857 8

An 81-year-old woman developed left hemiplegia and coma due to a right hemisphere infarct and died 6 days later. When first seen in coma she had the classical signs of descending central herniation in the diencephalic stage. The CT scan of the third day showed a large hypodense area occupying the superficial and deep territories of the middle and anterior cerebral arteries on the left as well as a frontal cortico-subcortical hypodense area indicative of an older infarct on the opposite hemisphere. No mass effects were apparent. She followed a downhill course with signs of brainstem deterioration. A second CT scan a few hours before death revealed the expected pattern of brain shift and herniations. This case adds to the available evidence showing that the clinical signs of encroachment of supratentorial structures upon the basal forebrain can be reproduced by an acute mono-hemispheral lesion without visible mass effects. It indicates, further, that the role of intracranial displacements in the genesis and short-term prognosis of coma remains an unsettled matter. In at least a few number of cases, diaschisis might play a major role.
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PMID:[Coma and transtentorial herniation syndrome due to acute non-expansive hemispheric lesion]. 872 80

Of the 26 cystinotic patients over 19 years of age followed in our institution, 7 developed CNS complications at a mean age of 23 years. Two forms were observed. The first, associating cerebellar and pyramidal signs, mental deterioration and finally pseudo-bulbar palsy, may be called cystinosis encephalopathy. The other form resembled a stroke-like episode with coma and hemiplegia or milder symptoms. Hydrocephalus was rare and not associated with clinical symptoms in this series. Cysteamine was administered for longer than 6 months to 4 of the patients with encephalopathy. Two had an almost complete disappearance of their symptoms including the gross abnormalities of MR imaging in one; one improved partially and remained stable, and one continued to deteriorate but was suspected of non-compliance. These results suggest that cysteamine may be an effective treatment of cystinosis encephalopathy and encourage prescription of this drug in cystinosis in order to prevent this complication.
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PMID:Clinical polymorphism of cystinosis encephalopathy. Results of treatment with cysteamine. 883 Jan 79

We reported 6 cases of excellent motor recovery after a large infarction in the middle cerebral artery territory including the cortex. All patients were men (aged 67 to 80); 4 had left hemiplegia and 2 had right hemiplegia. They had abrupt onset of focal neurologic symptoms and signs, suggesting embolic stroke. The consciousness level, according to the Japan coma scale, was grade II in 4 patients and normal in the other 2. Atrial fibrillation was present in 4 patients and premature atrial and ventricular contractions were seen in 1 each. Hypertension was present in 3 patients and diabetes mellitus in 1. The motor plegia gradually improved after 1 to 3 days and almost completely disappeared at 12 days after onset. All patients were eventually able to walk alone without any aids. However, aphasia persisted in 2 patients with left hemispheric damage and left unilateral spatial neglect in 3 patients with right hemispheric damage. A cerebral blood flow analysis by single photon emission computed tomography, using [123I] isopropyliodoamphetamine or technetium 99m hexamethylpropylenamine oxime, demonstrated increased blood flow in the frontal lobe cortex surrounding the infarcted region in 5 patients. These patients showed good recovery from motor deficit, even though, motor symptoms did not begin to improve until 1 to 3 days after onset of stroke. We suggest that there is a subgroup of stroke patients, whose severe motor deficit starts to improve even 3 days after onset of a large infarction in the middle cerebral artery territory including the cerebral cortex.
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PMID:[Analysis of patients with excellent motor recovery after large infarction in the middle cerebral artery territory including the cortex]. 886 42

We report a 36-year-old woman with right hemiplegia, anosognosia, and rapidly deteriorating course. She was well until the end of January, 1995 when she had an onset of fever, sputum, and cough. A 5 x 5 tumor was found in her left lower lobe. She was admitted to the Pulmonary Medicine on May 24, 1995 when she was 36-year-old. General physical examination was unremarkable. Bone scintigraphy revealed increased uptake in the skull, sternum, right scapula, vertebrae, right femur, and in ribs. Cranial CT scan revealed a large mass lesion in the right frontal subcortical region with central low density and peripheral high density areas, and small low density lesions in the right thalamic area and in the right posterior frontal region; ring enhancement was observed in the latter two lesions. On the second day of admission, she noted left-sided weakness which improved by corticosteroid treatment. On June 17, there was a sudden onset of left hemiparesis and a neurologic consultation was asked. Upon neurologic examination, she appeared somnolent but could understand verbal commands. She showed constructional apraxia, neglect of the left hemisphere, and anosognosia. Cranial nerves were unremarkable. Motor-wise, she showed flaccid left hemiplegia. Deep tendon reflexes were exaggerated on the left and the plantar response was extensor bilaterally. Nuchal stiffness was noted. Her cranial CT scan on June 17 revealed enlargement of the right frontal mass lesion. The subsequent course was complicated by DIC and progressive worsening of her consciousness. On June 18, she was comatose and pupillary light reflex was lost. She developed Cheyne-Stokes respiration and expired on that evening. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had a primary adenocarcinoma in the lung with multiple metastases including the brain. The fulminant terminal course was ascribed to hemorrhage within the tumor and subsequent central type of transtentorial herniation. Opinions were divided regarding the cause of hemorrhage; some participants thought hemorrhage was caused by DIC. Post-mortem examination revealed an adenocarcinoma arising at the S6 segment of the left lung with multiple organ metastases. In the brain, a huge hemorrhagic metastasis was found in the right frontal lobe and a non-hemorrhagic metastasis in the right thalamic region. Probably, the size of the metastases influenced the occurrence of hemorrhage. The direct cause of the death was transtentorial herniation.
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PMID:[A 36-year-old woman with acute onset left hemiplegia and anosognosia]. 912 37

This hospital based study was carried out on 185 adult patients of cerebral malaria. Out of 185 patients, 62 (33.5%) died and 123 (66.5%) survived. Neurological sequelae were present in 13 (10.5%) of 123 survivors at the time of discharge (i.e. 10-15 days after recovery from coma) from the hospital. These were in form of psychosis in 5 patients (4%), cerebellar ataxia in 4 patients (3.2%), extrapyramidal rigidity in 2 patients (1.62%) and hemiplegia in 2 patients (1.62%).
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PMID:Incidence and outcome of neurological sequelae in survivors of cerebral malaria. 925 38

The recuperation after a head trauma is divided in three phases. Awakening from coma is the initial phase that normally occurs at the intensive care unit. The period of hospitalization when the threatens of death and neurological instability disappear is the intermediate phase. The post concussional syndrome occurs in the late phase, when the patients have been discharged from the hospital. This syndrome, despite the absence of abnormalities in the clinical examination, causes an assortment of ailments that preclude normal activities. Organic neurological sequelae such as hemiplegia, speech disorders, cranial nerve lesions and mental disorders take also place in this phase. An adequate rehabilitation plan for the patient and his family must take into account all these issues.
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PMID:[Late effects of head trauma]. 933 75

A case of large fronto-temporo-parietal epidural hematoma associated with ipsilateral retrobulbar hematoma is reported. A 24-year-old man soon after a head injury due to a traffic accident became comatose with anisocoria and hemiplegia and developed exophthalmos, conjuctival chemosis, downward and lateral displacement of the eyeball. CT scan of the brain and the orbit showed the large epidural clot communicating with an ipsilateral retrobulbar hematoma through a sphenoid bone fracture. The patient underwent emergency surgery. Postoperatively, he improved and was discharged in good conditions. On follow-up one month later he was symptoms free. The available literature is reviewed: our case seems to be the fifth reported.
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PMID:Large epidural hematoma associated with ipsilateral retrobulbar hematoma. Case report. 938 74

We describe a 3-year-old boy with subacute sclerosing panencephalitis (SSPE) who died 4 months after its onset. His initial symptoms were drowsiness and left hemiplegia. He became comatose in 10 days, and developed a decortical posture after 45 days. He suffered from multiple cerebral hemorrhage and infarction 3 months later. Oligodendrocytes were positively stained by immunocytochemical stain with a complement-fixing measles antibody. Light microscopy revealed glial nodules, perivascular cuffing and reactive gliosis. Small arteries showed intimal thickening with resultant occlusion and occasional recanalization. These findings suggested vascular involvement in SSPE. This case illustrates the difference between the fulminant and chronic forms of SSPE.
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PMID:[Fulminant subacute sclerosing panencephalitis: clinical and neuropathological observations]. 939 6

Large supratentorial infarctions play an important role in early mortality and severe disability from stroke. However, data concerning these types of infarction are scarce. Using data from the Lausanne Stroke Registry, we studied patients with a CT-proven infarction of the middle cerebral artery (MCA) territory that covered at least two of three MCA subterritories (deep, superficial anterior [superior] and posterior [inferior] territory). We compared these patients with patients presenting more limited infarction in the MCA territory. Our study group of large MCA (laMCA) infarction contained 208 patients, corresponding to 7.6% of all ischemic infarctions in the Lausanne Stroke Registry. Seventy-two patients had complete infarction in the whole MCA territory (coMCA). Internal carotid artery (ICA) occlusion (41%) and ICA dissection (12%) were more common than in limited superficial MCA (lsMCA) infarct and anterior circulation infarct (p < 0.001). Among the patients without ICA occlusion, atrial fibrillation (33%; p < 0.002) and cardiogenic embolism in general (54%; p < 0.001) were more frequent in laMCA than in lsMCA infarct. Severe neurologic deficit (hemiplegia and hemisensory loss in the face, arm and leg, hemianopia, global aphasia, reduced consciousness) was more common than in other types of infarct. A combination of these symptoms had a positive predictive value for laMCA infarction of 0.73 (sensitivity for left side laMCA infarcts, 0.56). Mortality (17%) and severe disability (50%) were higher with laMCA than for other infarcts (p < 0.001). Sixteen of the 35 deaths could be attributed to brain edema. Reduced consciousness, hemianopia, and coMCA infarction were independent predictors of death or severe disability; for death only, coma was an independent predictor. Patients who died because of brain edema were younger than patients whose death was due to other causes (mean age, 57 versus 73 years; p < 0.001); they also died sooner (mean time of death after stroke, 5 versus 37 days; p < 0.001). Furthermore, patients who developed coma on the day of admission were more likely to die because of brain death (p < 0.001). Large middle cerebral artery infarction is associated with cardiogenic embolism, ICA occlusion, and ICA dissection. It is a major predictor of death and severe disability, although a lower frequency of malignant brain infarction was found than previously reported.
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PMID:Large infarcts in the middle cerebral artery territory. Etiology and outcome patterns. 981 7


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