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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the course of investigating a 10-year-old boy because of progressive deterioration of intellectual functioning, ataxia, and hemiplegia, an absence of serum hexosaminidase activity was noted. A skin biopsy examined by electron microscopy showed axonal accumulations of dense osmiophilic deposits. Because of the patient's age at onset and the slowly progressive nature of his ilness, we are reporting an atypical juvenile case of Sandhoff disease.
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PMID:Progressive cerebellar ataxia, spasticity, psychomotor retardation, and hexosaminidase deficiency in a 10-year-old child: juvenile Sandhoff disease. 55 67

The tibialis anterior (TA) is a muscle activated mainly during walking. Its use during the step cycle was studied in 10 patients (55.8 +/- 8.8 years) with chronic hemiplegia (duration 3-18 years) and related to the muscle fibre composition, size and expression of isoforms of myosin heavy chains (MHCs). In the average step cycle the integrated surface EMG of the paralysed TA did in the majority of the hemiplegic patients not exceed 10% of that recorded during maximal contraction of the normal leg. The type I fibre percentage in the paralysed TA subject was 57.4% as compared with 79.4% in normal muscles (P less than 0.05). The range of axonal conduction velocities in the peroneal nerve did not differ in paralysed and non-paralysed leg, suggesting that there was no selective loss of one class of motoneurons. The type II fibres consisted of IIA (66%) and IIB (31%), in contrast to the normal TA muscle where less than 1% of the muscle fibres are of type IIB. The incidence of fibres in the biopsies with both slow and fast MHCs had a mean value of 3.5% (range 0.7-9%). The type I and type II muscle fibres had normal sizes with cross-sectional area 4511 +/- 962 microns 2 and 6181 +/- 1062 microns 2. No selective type II atrophy was seen. Occasional hypertrophic type I and II fibres were seen in 4 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disuse of anterior tibial muscle during locomotion and increased proportion of type II fibres in hemiplegia. 179 69

Severe head injury or diffuse axonal injury is frequently associated with spastic hemiplegia/paraplegia. However, the causative lesion has not been well elucidated. Especially, the relationship between the gliding contusion and spastic hemiplegia has not been inferred yet. We have analyzed 6 brain concussion cases and 19 cases of diffuse axonal injury. None of the concussion cases experienced hemiplegia in their courses. Among the 19 cases, 10 were left with persistent and disabling hemiplegia/quadriplegia, whereas 5 showed persistent but mild hemiplegia. Among the 10 cases, one was incapacitated by a brainstem hemorrhage. The remaining 9 cases exhibited, in the parasagittal white matter, small hemorrhagic spots in the acute phase CT, low-density areas in the chronic phase CT, and/or T2 high and T1 low signal lesions in the MRI. In 8 cases, the lesion was in accord with the hemiplegic side, but in one case the low density area was on the ipsilateral side. Two of the 3 cases showing quadriplegia exhibited bilateral parasagittal lesions. None of the 5 mild hemiplegia cases and 10 nonhemiplegia cases showed such abnormality. Superficial brain contusions were found in 17 cases altogether, but they were not at all correlated with the occurrence of hemiplegia. Thus, it was concluded that parasagittal white matter shearing injury or so called gliding contusion could be the manifestation of injury to the corticospinal tract in the corona radiata.
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PMID:[Parasagittal white matter shearing injury (so-called gliding contusion): possible radiological evidence of spastic hemiplegia in diffuse axonal injury]. 809 Feb 65

The relationship between spastic hemiplegia in diffuse axonal injury (DAI) and neuroradiological findings was studied in 100 cases. These cases were prospectively collected from the files of Automobile Insurance Rating Organization in Japan between 1993 from to 1996. Requirements for entry to this study were as follows: presence of initial unconsciousness after head injury without any lucid interval. Existence of CT scan or MRI film obtained within 12 hours of injury showing no significant mass effects, as well as follow-up CT scan or MRI film obtained more than 3 months after the injury. Psychosocial outcome was described both by the medical professional and the caregiver. The hemiplegia was rated severe, mild, or none. The outcome and diffuse ventriculomegaly were classified as reported by the authors previously. Spastic hemiplegia or quadriplegia was documented in the chronic stage in 63 cases, including 53 severe cases with difficulty in walking and 10 mild cases with only pyramidal signs detected. Chi-square analysis showed significant correlation between hemiplegia and the DAI outcome level or ventriculomegaly rating. Focal brain contusion was noticed in 33 cases, but did not correlate with the hemiplegia at all. Radiological findings included 25 cases of parasagittal white matter injury (gliding contusion), 20 cases of callosal injury, 19 cases of basal ganglionic region injury, 5 cases of brain-stem injury, and 3 cases of cerebellar injury. Chi-square analyses of hemiplegia and contralateral presence of these injuries were significant in the former three types of injury. Presence of at least one of these 3 lesions was defined as GCB injury. There were altogether 46 GCB injury cases which were significantly correlated with contralateral hemiplegia by chi-square analysis and by Spearman rank analysis. Partial correlation analysis with hemiplegia as the target variable indicated highly significant correlation only with GCB injury and outcome level. In conclusion, spastic hemiplegia in DAI is a manifestation of primary shear injury. Neuroradiological findings of GCB injury were statistically able to be significantly correlated with the presence of hemiplegia, and suggested pyramidal tract injury either at the corona radiata or the internal capsule level.
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PMID:[Shearing injuries of parasagittal white matter, corpus callosum and basal ganglia: possible radiological evidences of hemiplegia in diffuse axonal injury]. 926 60

A 51-year-old woman with no significant family history exhibited progressive presenile dementia followed by right-sided spastic hemiplegia and died 27 months after the onset of her illness. Brain MRI demonstrated a widespread abnormality in the cerebral deep white matter and corpus callosum. Neuropathologically, extensive destruction of axons and myelin and abundant axonal spheroids were found in the deep white matter, preferentially of the frontoparietal areas. The corpus callosum was also severely damaged. The cerebral cortex and subcortical U fibers remained intact. The pathological features were different among the lesions, reflecting the sequential degenerative processes of the white matter. This case is, to our knowledge, the third sporadic case of neuroaxonal leukoencephalopathy with axonal spheroids.
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PMID:Neuroaxonal leukoencephalopathy with axonal spheroids. 1213 5

We describe extended and repeat magnetic resonance (MR) examinations in the case of a 16-year-old male who developed acute left-sided sensorimotor hemiplegia after a single dose of inhaled heroin. MRI revealed symmetrical hyperintense signals in T 2 -weighted images and massive diffusion disorders in the diffusion weighted images predominantly in parieto-occipital subcortical white matter and both ventral globi pallidi with preservation of U fibers and no brain oedema. MR spectroscopy data were compatible with combined hypoxic and mitochondrial damage resulting in axonal injury without demyelination. Normal values and variations had been obtained from spectra of five age-matched subjects. This is the first reported MR follow-up study of leukoencephalopathy occurring acutely after a first inhaled dose of heroin. We postulate that toxic spongiform leukoencephalopathy in heroin addicts may be the outcome of a complex mechanism directly triggered by heroin and causing mitochondrial as well as hypoxic injury in specific and limited areas of white matter.
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PMID:Acute leukoencephalopathy after inhalation of a single dose of heroin. 1277 33

After a stroke, recovery that continues beyond 3 or 4 weeks has been attributed to plasticity, a reorganization of the brain in which functions previously performed by the ischemic area are assumed by other ipsilateral or contralateral brain areas. Neuronal plasticity has been variously attributed to redundancy (parallel distributed pathways), changes in synaptic strength, axonal sprouting with formation of new synapses, assumption of function by contralateral homologous cortex, and substitution of uncrossed pathways. Transcranial magnetic stimulation, positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and 128-electrode high-resolution electroencephalography have been successfully applied to demonstrate cortical reorganization after hemiplegia. Recording the motor potential is a promising noninvasive method for the localization of motor control after hemispheric lesions. Most patients with hemiparetic stroke show some improvement, usually during the first 3 to 6 months after the ictus. Improvement and prognosis depend on a number of variables including volume and location of the infarction, age of the patient, and the elimination of risk factors to avoid future episodes (i.e., dietary control of lipids, the elimination of tobacco, and the control of diabetes and hypertension). Currently, emphasis has been placed on fibrinolytic treatment in the first 3 hours to prevent or minimize neurological deficit. Aside from the above listed factors, improvement after stroke may be due to reorganization of the brain, particularly the cerebral cortex, and repair of damaged tissue and recanalization. It is also important to relate such changes to functional improvement and successful rehabilitation.
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PMID:Brain reorganization after stroke. 1468 16

The recurrent laryngeal nerves were examined by electron microscopy in five control, four subclinical and four clinical laryngeal hemiplegic horses. In addition, the peroneal nerve was examined in two horses in the latter group. The distally distributed loss of large myelinated fibres in the left recurrent laryngeal nerve seen by light microscopy was confirmed. In addition, active axonal pathology was found to be more evident than indicated by light microscopic investigations. The onion bulb formations observed indicated the repetitive nature of the damaging influence to nerve fibres. Although the pathological changes were most obvious in the distal left recurrent laryngeal nerve, alterations similar in type and distribution were present in other areas of the left and right nerves, and in the distal hindlimb nerves. The observation of fibres with inappropriately thick myelin sheaths relative to their axonal calibre, was confirmed statistically by determining the regressions of axis cylinder perimeter against the number of myelin lamellae. In conclusion, the peripheral nerve pathology of equine laryngeal hemiplegia was demonstrated to be a distally distributed loss of myelinated fibres, with considerable active axonal damage, in conjunction with axonal atrophy. These features suggest that this disease may be classified as a distal axonopathy.
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PMID:Equine laryngeal hemiplegia. Part II. An electron microscopic study of peripheral nerves. 1603 Dec 25

Individual nerve fibres were isolated from the recurrent laryngeal and some distal hindlimb nerves, in an investigation of equine laryngeal hemiplegia. One hundred teased fibres were obtained from each of three sampling sites on both left and right recurrent laryngeal nerves, from 15 Thoroughbred horses. These fibres were graded descriptively and internode lengths measured. A distal distribution of pathology was demonstrated in all groups studied, but was most severe in the clinical group of horses. The predominant change was one of short thinly myelinated internodes interspersed amongst normally myelinated internodes, indicating remyelination of previously demyelinated areas of nerve fibre. Such pathological change was also reflected by the decreased mean internode length, and its increased variability associated with disease. However, it was determined statistically that these abnormal internodes were grouped along particular nerve fibres, rather than being randomly distributed between all nerve fibres. This is thought to indicate myelin sheath changes secondary to underlying axonal pathology. Thus it was concluded that the primary pathology was likely to be axonal in nature, while the high incidence of demyelination changes was a reflection of the chronic nature of the disease process. Thus, the distal distribution of pathology, the primary axonal involvement, the presence of changes in left and right recurrent laryngeal and distal limb nerves, all support the classification of equine laryngeal hemiplegia as a distal axonopathy.
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PMID:Equine laryngeal hemiplegia. Part III. A teased fibre study of peripheral nerves. 1603 Dec 32

Evidence of long central nerve fibre degeneration (axonal spheroids) in the lateral cuneate nuclei was found in all eight Thoroughbreds affected clinically and subclinically with equine laryngeal hemiplegia, but in only one of six control animals. It was considered that these spheroids may signify a central nervous component of the disease process of laryngeal hemiplegia although until further investigations are performed no firm conclusions regarding the relationship of these findings with laryngeal hemiplegia could be made. Examination of the left and right nucleus ambiguus of clinical and subclinical laryngeal hemiplegic horses revealed no pathological alterations.
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PMID:Equine laryngeal hemiplegia. Part V. Central nervous system pathology. 1603 Dec 34


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