Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The investigations were carried out in 30 control cases, in 20 patients with acute transient cerebral circulatory failure, 20 patients with intracerebral haemorrhage, and 22 patients with thrombotic encephalomalacia. The determinations of uropepsin activity were done on the 1st, 3rd, 7th and 14th days of the disease. Uropepsin activity in 24-hour urine was determined by the method of West, Ellis and Scott. In the group of patients with acute transient cerebral circulatory failure abnormalities in urinary uropepsin activity were not significant. The mean activity of uropepsin in 24-hour urine in patients with intracerebral haemorrhage and brain infarction on the 1st day of the disease was significantly higher than in controls. The rise in the activity of this enzyme in patients with encephalomalacia was lower in relation to patients with intracerebral haemorrhages. During improvement of the condition of patients with brain stroke the uropepsin activity in 24-hour urine decreased.
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PMID:[Urinary uropepsin activity in patients with different forms of stroke]. 25 64

The authors determined peripheral-blood ammonia level in patients with cerebral strokes. The determinations were done by the method of Konitzer et al. on the 1st, 3rd and 7th days of the disease. The results of determinations were subjected to statistical analysis with the t test of Student. It was found that the mean serum ammonia level in patients with cerebral stroke on the 1st day of the disease was higher than in the control group. The difference was statistically significant. The level of ammonia in the blood of patients with cerebral haemorrhage was significantly higher on the 1st day of the disease than in patients with encephalomalacia. The difference was statistically significant with error probability of 0.05.
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PMID:[Levels of ammonia in patients with stroke]. 63 30

An uncommon type of stroke in children is presented. An intracranial arteriovenous malformation in a 13-year-old boy spontaneously occluded about 22 months after surgical intervention. Precipitating factors, such as bacterial infections, could not be demonstrated in this patient, who had been attending school since the time of the craniotomy. The histological features of venous encephalomalacia in the galenic territory are contrasted with hemorrhagic encephalomalacia as seen after arterial occlusions: in the former, hemorrhages are more widespread and edema is more pronounced.
Stroke
PMID:Spontaneous thrombosis of deep cerebral veins: a complication of arteriovenous malformation. 112 16

Catalase-like activity was determined in the cerebrospinal fluid of 16 patients with cerebral haemorrhage, 24 cases od encephalomalacia due to thrombosis, and 10 controls. It was demonstrated that catalase-like activity in the cerebrospinal fluid of patients with cerebral stroke is significantly raised in relation to the activity observed in controls. This rise is patricularly evident in the first 24 hours after the onset. The rise was statistically significant only in the group of encephalomalacia.
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PMID:[Catalase-like activity in cerebrospinal fluid in patients with cerebral stroke]. 120 96

The use of transcranial Doppler sonography (TDS) in combined ultrasound diagnosis was the first to allow a noninvasive assessment of cerebral circulation. Altogether 50 patients in acute stroke period were examined. The results obtained were verified at surgery, cerebral angiography or autopsy. Changes in the velocity of the blood flow, its reversal, different Doppler sonogram pattern appeared controversial for cerebral and subarachnoid haemorrhages caused by the occlusion of the internal carotid artery or other factors of encephalomalacia. TDS employment promotes the improvement in the diagnosis of the cause underlying the acute impairment of cerebral circulation and in the prognosis of cerebral coma. The findings are correlated with routine echo-pulsography and Doppler sonography.
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PMID:[Transcranial Doppler sonography combined with other ultrasonic methods in the diagnosis of stroke]. 278 53

The authors report a comparative analysis of the results of angiographic investigations and computer tomography in patients with clinical manifestations of stroke. Attention is called to the accuracy of the information obtained in computer tomography with regard to the extent of focal encephalomalacia and stage of evolution. Signs are described making possible differentiation between vasogenic lesions and other pathological processes of identical or similar features in computer tomography.
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PMID:[The value of computer tomography in the diagnosis of encephalomalacic foci]. 714 11

Mitochondrial myopathy, encephalopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome is one of the mitochondrial encephalomyopathies that has distinct clinical features including stroke-like episodes with migraine-like headache, nausea, vomiting, encephalopathy and lactic acidosis. We report a 27-year-old woman who presented with partial seizure, stroke-like episodes including hemiparesis, hemianopia and hemihypethesia, sensorineural hearing loss, migraine-like headache, and lactic acidosis. Brain computed tomographic scan showed encephalomalacia in the right parieto-occipital area and recent hypodensity in the left temporoparieto-occipital area with cortical atrophy. Muscle biopsy revealed ragged-red fibers and paracrystaline inclusions in the mitochondria. Genetic study revealed an A to G point mutation at nucleotide position (np) 3243 of mitochondrial DNA. External ophthalmoplegia and ptosis were also found during two exaggerated episodes in this patient. Therefore, the overlapping syndrome of chronic progressive external ophthalmoplegia in the MELAS syndrome is considered in this case. Furthermore, we also found carnitine deficiency in this patient and she was responsive well to steroid therapy. Muscle biopsy also revealed excessive lipid droplets deposits. Therefore, the carnitine deficiency may occur in MELAS syndrome with the A to G point mutation at np 3243. We recommend the steroid or carnitine supplement therapy be applied to the MELAS syndrome with carnitine deficiency.
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PMID:CPEO and carnitine deficiency overlapping in MELAS syndrome. 748 81

The medical records of 89 children followed at a multidisciplinary Meningomyelocele Clinic at the Children's Clinics for Rehabilitative Services were reviewed. Almost all children in southern Arizona with meningomyelocele are followed at this clinic. Eight children (foreign nationals) were excluded because they were not eligible for neurosurgery/neurology services at the clinic. The remaining 81 children have been followed at the clinic from 0.25 to 21 years. Seventeen children (21%; age: 1.3-17 years, mean: 9.1 +/- 4.4 years; follow-up: 1.3-16 years) manifested seizures at some time during their course. All children with seizures had shunted hydrocephalus. Neonatal seizures occurred in 2 children currently not receiving medication. An additional 3 children had an acute symptomatic seizure associated with an intraventricular hemorrhage during ventriculoperitoneal shunt revision, 2 of whom later developed epilepsy. Fourteen children (17.3%) had epilepsy; 12 were taking antiepileptic drugs. Seizures were controlled on medication in 5 children. EEG abnormalities were present in 12 children (focal slowing 4, focal spikes 8, diffuse slowing 3, generalized or bilaterally synchronous spike-wave 4). Most of these children (12/14) had evidence of additional central nervous system (CNS) pathology (i.e., areas of encephalomalacia or past stroke 7, cerebral malformations 2, CNS calcifications 1, and frequent apneic spells/cardiac arrest 2). We conclude that epilepsy occurs in approximately 17% of children with meningomyelocele, and most have other CNS pathology to account for their seizures.
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PMID:Epilepsy in children with meningomyelocele. 757 45

Conventional MRI (cMRI) has shown that brain abnormalities without clinical stroke can manifest in patients with sickle cell disease (SCD). We used quantitative MRI (qMRI) and psychometric testing to determine whether brain abnormalities can also be present in patients with SCD who appear normal on cMRI. Patients 4 years of age and older with no clinical evidence of stroke were stratified by cMRI as normal (n = 17) or abnormal (n = 13). Spin-lattice relaxation time (T1) of gray and white matter structures was measured by the precise and accurate inversion recovery (PAIR) qMRI method. Patient cognitive ability was assessed with a standard psychometric instrument (WISC-III or WISC-R). In all 30 patients with SCD, qMRI T1 was lower than in 24 age- and race-matched controls, in cortical gray matter (P < .0006) and caudate (P < .0009), as well as in the ratio of gray-to-white matter T1 (P < .008). In the 17 patients who were shown to be normal by cMRI, qMRI T1 was still lower than in controls, in both cortical gray matter (P < .02) and caudate (P < .004). Histograms of voxel T1 show that the proportion of voxels with T1 values intermediate between gray and white matter (ie, consistent with encephalomalacia) was 9% higher than controls in patients shown to be normal by cMRI (P < .05) and 15% higher than controls in patients shown to be abnormal by cMRI (P < .0005). The full scale intelligence quotient (FSIQ) of all patients with SCD was 75, compared to the FSIQ of 88 in a historical control group of patient siblings (P < .001). The FSIQ of patients shown to be normal by cMRI was 79, significantly lower than the FSIQ of patient siblings (P < .04). The FSIQ of 71 in patients shown to be abnormal by cMRI was significantly lower than both the patient siblings (P < .005) and the patients shown to be normal by cMRI (P < .04). Patients shown to be abnormal by cMRI scored lower than patients shown to be normal by cMRI, specifically on the subtests of vocabulary (P = .003) and information (P = .03). Cognitive impairment is thus significant, even in patients with SCD who were shown to be normal by cMRI, suggesting that cMRI may be insensitive to subtle neurologic damage that can be detected by qMRI. Because cognitive impairment can occur in children normal by cMRI, our findings imply that prophylactic therapy may be needed earlier in the course of SCD to mitigate neurologic damage.
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PMID:Quantitative MRI of the brain in children with sickle cell disease reveals abnormalities unseen by conventional MRI. 962 65

The brain organization for movement in a 20-year-old man with a history of intrauterine or perinatal right middle cerebral artery stroke was studied. [(15)O]-water positron emission tomography demonstrated a normal pattern of activation during finger movement in the right hand. Movement of the hemiparetic left hand was associated with activation in the supplementary motor area bilaterally and in the left premotor cortex. Blood flow increase was observed in the right temporal lobe adjacent to an extensive area of encephalomalacia, suggesting atypical motor function in the temporal lobe.
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PMID:Motor organization after early middle cerebral artery stroke: a PET study. 983 Oct 1


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