Cases reported "Atrophy"

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11/21. Brain tumor with ipsilateral cerebral hemiatrophy in children.

    A series of six cases of cerebral tumor with ipsilateral cerebral hemiatrophy, including four cases admitted at our institute, were studied. Various common clinical features were noted in these six cases. The mechanism whereby ipsilateral hemiatrophy of the cerebrum arises from brain tumor has been discussed on the basis of symptomatologic and clinicopathologic findings noted in these 6 cases. 1) The onset of the disease was between 8 and 14 years of age with a mean of 11 years and 8 months; thus all the 6 patients being juvenile. 2) Presenting symptoms developed from 1 year and 2 months to 4 years before admission, with an average of 2 years and 1 month. The clinical course was therefore relatively chronic in every case. 3) Presenting symptoms were: decline of school work, hemiparesis and loss of consciousness. These symptoms were all progressive throughout the course. The principal symptoms were hemiparesis, hemihypoesthesia, character and emotional changes, deterioration of mental faculties and behavioral abnormalities. No sign or symptom of significant increase of intracranial pressure were observed in any case. 4) Ipsilateral cerebral hemiatrophy on the tumor side was evidenced by carotid angiography and by pneumoencephalography. 5) The common site of tumor in this series was the thalamus and its surrounding areas. 6) The tumor was invariably a pinealoma which seemed to be ectopic in every case. 7) The obtained histopathological findings suggest that the ipsilateral cerebral hemiatrophy was due to thinning of the cerebral cortex with degeneration and disappearance of ganglion cells, demyelination in the subcortex and destruction of axons. Our speculated mechanism of ipsilateral cerebral hemiatrophy due to thalamic tumor is that thalamic tumor causes the degeneration and disappearance of thalamic ganglion cells and nerve fibers, consequently occurring secondary Waller's degeneration of afferent and projecting fibers from the thalamus as well as retrograde degeneration of efferent fibers, thus resulting in an extensive atrophy of the cerebral cortex and subcortical tissue.
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12/21. Ocular histopathologic studies of neonatal and childhood adrenoleukodystrophy.

    Histopathologic studies of the eyes of one patient (a boy who died at 14 years of age) with childhood adrenoleukodystrophy and two patients (girls who died at 24 and 31 months of age) with neonatal adrenoleukodystrophy showed the accumulation of the characteristic bileaflet inclusions in optic nerve macrophages, retinal neurons, and macrophages and loss of ganglion cell and nerve fiber layer. Additionally, in the two cases of neonatal adrenoleukodystrophy, changes resembling early retinitis pigmentosa were found, with accumulation of characteristic inclusions in the retinal pigment epithelium and pigment-laden macrophages. One of the patients with neonatal adrenoleukodystrophy also had an anterior subcapsular cataract and cystoid macular edema.
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13/21. GM1 gangliosidosis, type 2: ocular clinicopathologic correlation.

    The clinical and pathological manifestations of a case of juvenile GM1 gangliosidosis are presented and the pathological findings compared with those previously reported for GM1 gangliosidosis in man and in animal models. The most striking finding in the present case was the marked degeneration of the retinal ganglion cell and nerve fiber layers. Although such extensive ganglion cell loss was not observed in any of the other cases reviewed, the presence of multimembranous inclusion bodies in retinal ganglion cells strongly suggests that the pathological process was similar in all cases. Much remains to be learned about the function of gangliosides in the healthy retina and about the pathophysiological consequences of deranged ganglioside metabolism. The many parallels, including those observed in pathological studies, between the human and animal forms of GM1 gangliosidosis allow an optimistic appraisal of the value of further research using the animal models.
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14/21. pathology of olivopontocerebellar atrophy with glutamate dehydrogenase deficiency.

    We report the neuropathologic findings in the first patient with recognized glutamate dehydrogenase (GDH) deficiency to come to postmortem examination. He had progressive cerebellar ataxia beginning at age 21. He died at age 47 of pulmonary emboli. Postmortem examination revealed pancerebellar, olivary, and mild pontine atrophy, demyelination of the posterior columns, degeneration of anterior horn and dorsal root ganglion cells, and reduction of myelinated fibers in the sural nerve. In addition, there was neuronal storage of lipopigment diffusely throughout the CNS and the autonomic neurons, with cell distention, atrophy, and loss in selected areas.
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15/21. Neuropathology of secondary generalized epilepsy--(Lennox-Gastaut syndrome)--a case report.

    Neuropathological considerations were performed on a case, who went into Lennox syndrome after an acute encephalopathy at the infantile period, and moreover who fell into an akinetic-mute state derived from brain damage by herniation caused by a head injury and subsequent status epilepticus. Neuropahtological background in the present case of Lennox syndrome is thought to be based on the widespread unilateral cerebral lesions and the basal ganglional, especially thalamic, degenerations derived secondarily from the diffuse cerebral damage. The patient revealed akinetic mutism with the disappearance of the epileptic seizures and the desynchronization of the EEG's, when the brain lesions formed at the adult period spread over the opposite hemispheric limbic system and the brain stem tectum.
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16/21. Achalasia of the cardiac sphincter and the pylorus?

    A patient with a recurrent achalasia of the cardia was found, after a Heller cardiomyotomy, also to have pyloric insufficiency necessitating gastric resection. The pylorus appeared to contain virtually no ganglia at all. On the basis of an experiment with rabbits, in which vagotomy was shown to have no appreciable effect on the ganglion cells in the pylorus, it was concluded that the abnormality demonstrated in this patient could not be attributed to a possible injury of the vagus nerves but was probably due instead to achalasia of the pylorus.
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17/21. PET study of cerebral glucose metabolism and fluorodopa uptake in patients with corticobasal degeneration.

    We measured cerebral glucose utilization and fluorodopa metabolism in the brain of patients with corticobasal degeneration using position emission tomography. The clinical pictures are distinctive, comprising features referable to both cerebral cortical and basal ganglionic dysfunctions. Brain images of glucose metabolism can demonstrate specific abnormalities with a marked asymmetry in the parietal cortex (the primary motor and sensory cortex and the lateral parietal cortex), the thalamus, the caudate nucleus and the putamen of the dominantly affected hemisphere related to clinical symptoms in six patients. [18F]dopa uptake also reduced in an asymmetric pattern, both the caudate nucleus and the putamen in four patients. This unique combination study measuring both cerebral glucose utilization and fluorodopa metabolism in the nigrostriatal system can provide efficient information about the dysfunctions which are correlated with individual clinical symptoms.
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18/21. Electron microscopic observations in a case of long-standing profound sensorineural deafness.

    The ultrastructural pathology in an ear with long-standing profound deafness is presented. endolymphatic hydrops was present, although there had been no vestibular symptoms. Although hair cells were absent, the intercellular junctional complex at the endolymphatic surface of the organ of corti was maintained, suggesting "healing" by migration or proliferation of supporting cells to fill the empty spaces. Severe atrophy of the stria vascularis was present, and crystalline deposits were found within the strial remnant. An encapsulated tectorial membrane was interpreted in light of ultrastructural findings as either herniation of the fibrillar connective tissue of the spiral limbus into the scala media or alternatively demonstrating abnormal continuity between the connective tissue of the spiral limbus and the remnant of tectorial membrane. Neural degeneration was severe in all cochlear turns. However, more nerve fibers were seen in the proximal portion of Rosenthal's canal than at the habenula perforata or in the organ of corti, and central processes from the ganglion area were more numerous than peripheral processes. The ganglion cell population was reduced to approximately 10% of normal, and only unmyelinated cell bodies were found. Few recognizable neural fibers were seen within the organ of corti, although bizarre collections of apparent cellular debris and cell processes containing many mitochondria or vesicles were seen in regions normally containing neural fibers.
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keywords = ganglion
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19/21. Isolated infraspinatus atrophy in a collegiate volleyball player.

    PURPOSE: To describe a case of isolated infraspinatus atrophy due to suprascapular nerve entrapment by a labral ganglion cyst in a volleyball player and to propose a mechanism for its formation. CASE SUMMARY: A female volleyball player was evaluated for shoulder pain and found to have atrophy of the infraspinatus muscle. magnetic resonance imaging (MRI) showed a loculated ganglion cyst impinging on the suprascapular nerve. DISCUSSION: Several etiologies for isolated infraspinatus atrophy in volleyball players are cited in the literature. It is suggested here that the rapid deceleration in the volleyball spike can result in a superior labral lesion (SLAP), which can lead to ganglion cyst formation. These ganglion cysts can then cause isolated infraspinatus atrophy by impinging on the suprascapular nerve at the spinoglenoid notch. RELEVANCE: In one study, isolated infraspinatus atrophy was found in 12% of elite volleyball players. Since infraspinatus atrophy may result from impingement of the suprascapular nerve by ganglion cysts and not just traction injuries, imaging studies, such as an MRI, should be considered in the evaluation of these patients.
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ranking = 2.5
keywords = ganglion
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20/21. atrophy of the infraspinatus muscle caused by a suprascapular ganglion.

    CASE SUMMARY: Herein is reported a case of a 21-year-old ice hockey player with a suprascapular ganglion causing atrophy of the infraspinatus muscle. DISCUSSION: Lesions of the suprascapular nerve can be caused by trauma of compression. While the suprascapular nerve entrapment syndrome results in atrophy of both the supraspinatus and the infraspinatus muscles, compression of the nerve distal to the spinoglenoid notch leads to isolated weakness of the infraspinatus muscle.
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