Cases reported "Brain Diseases"

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11/125. The auditory pathology of anoxia.

    A case of anoxic encephalopathy is reported, with study on a whole-auditory-pathways basis, and the method of processing tissues is outlined. Pathologic changes are found throughout the central part of the auditory pathway. The importance of including the superior ventral cochlear nucleus (SVCN) with cochlear structures in correlating findings with audiometric data is supported. The previously advanced tonotopic frequency pattern, with zonal vulnerability, of the spheroid cells of SVCN is supported.
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12/125. Successful surgical relief of seizures associated with hamartoma of the floor of the fourth ventricle in children: report of two cases.

    OBJECTIVE AND IMPORTANCE: To discuss the physiopathology and surgical handling of seizures due to hamartoma of the floor of the fourth ventricle in two children. CLINICAL PRESENTATION: Two girls aged 3 years at the time of their operations presented with seizures due to a lesion of the floor of the fourth ventricle. The seizures began within the first days of life and consisted of hemifacial contraction, then head deviation, blinking of the eyelids, and intermittent dysautonomic manifestations. The interictal neurological condition seemed normal in one patient and showed a slight development delay in the other. An ictal electroencephalogram showed slow waves in the posterior areas. A magnetic resonance imaging scan revealed a mass that remained unchanged on serial examinations bordering the fourth ventricle, with an isointense signal on T1-weighted sequences and high-intensity signals on T2-weighted sequences without gadolinium enhancement. An ictal single-photon emission computed tomographic scan showed hyperperfusion in the lesion in both girls. INTERVENTION: The operation consisted of resection and disconnection of the lesion. An electrical recording was obtained in one patient during the operation while she was anesthetized; the recording, made by means of a depth electrode with five contacts inside the lesion, indicated that repetitive theta rhythmic discharges were present. Neuropathology was consistent with a hamartoma. In both girls, the seizures disappeared after their operations, and antiepileptic drugs were withdrawn (follow-up periods, 8 and 3 yr, respectively). CONCLUSION: Considering the results of single-photon emission computed tomography, the intralesional electrical record, and the relief of seizures after the operation, we postulate that the seizures arose from inside the lesion. This particular kind of noncortical seizure is similar to gelastic seizure due to hypothalamic hamartoma.
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13/125. Calcified cysticerci provoke perilesional edema and seizures.

    In cases of cysticercosis, seizures and other symptoms occur in persons with only calcified brain lesions. The presence of perilesional edema has been documented in association with calcified lesions in symptomatic patients, but the frequency of this complication and characteristics of the patients who develop it are not known. patients in peru and the united states with neurocysticercosis, documented by positive results of serological testing and with only calcified lesions as shown using computerized tomography, were studied using magnetic resonance imaging. Perilesional edema was observed in slightly more than one-third of the patients, and some patients had frequent, severely disabling episodes. Those with an increased proportion of enhancing calcified lesions were more likely to show perilesional edema. edema around calcified lesions is common in this population and is associated with seizures and neurological morbidity.
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14/125. Psychiatric illness associated with systemic lupus erythematosus.

    Estimates of the frequency of mental changes associated with systemic lupus erythematosus (SLE) range from 3% to 65%. Variations in classifying and reporting symptoms account for much of the difficulty in determining the true incidence. Other problems in study design also make it difficult to compare results of various studies, although it appears that psychiatric illness associated with SLE falls into two categories: organic and functional disorders. The former occur in 22% to 29% of patients having SLE and rheumatoid arthritis and are associated with a poorer prognosis and higher mortality. The latter occur in 18% to 35% of SLE patients and slightly less in patients with rheumatoid arthritis. Several possible causes for mental changes of SLE have been proposed. The case of a patient with SLE having an acute psychotic episode illustrates the possible roles of premorbid personality, mental and environmental stress, and steroid therapy in precipitating psychiatric illness in SLE.
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15/125. Valproate-induced encephalopathy.

    A 50-year-old woman taking carbamazepine (CBZ) 1200 mg daily for her partial epilepsy developed acute confusion after valproate (VPA) add-on treatment for 10 days. The administration of VPA started from 1000 mg daily and, 3 days later, increased to 1500 mg daily. Beside a mildly elevated serum ammonia level (81 microg/dL), her electroencephalogram showed diffuse background slowing intermixed with 2-2.5 Hz of high-amplitude slow waves, which indicated a diffuse encephalopathy. The serum levels of VPA and CBZ were 49.1 mg/L and 8.6 mg/L, both being non-toxic. The liver functions appeared normal. She recovered rapidly after discontinuation of VPA. In this patient, a safe previous administration of VPA did not preclude the occurrence of encephalopathy. A relatively large initial VPA dosage could possibly be the culprit.
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16/125. Clinical studies on cerebral schistosomiasis japonica in the philippines.

    The author examined the cerebral schistosomiasis japonica (CSJ) in the philippines which is one of the areas heavily infected with S. japonicum. Seventy-five subjects were selected randomly from 307 patients with CSJ, who showed neurological symptoms such as convulsions, paroxysmal disturbance of consciousness and hemiparesis. The mean age of the subjects was 33. Of the 71 patients who had paroxysmal disease, 54 had convulsions, in 33 of which it was of the Jacksonian type, and 24 had psychomotor seizures and 1 autonomic seizures. Thus, 58 patients or 82% of the paroxysmal disease group showed a sign of the localized lesion of the brain. Fifty-one patients (72%) of this group had attacks more than once a month, and the onset of the paroxysmal disease was later than 20 years old in 49 (69%). EEGs were judged as abnormal in 24 (32% of total subjects), borderline in 13 (17%) and normal in 38 (51%). The characteristic abnormal or borderline findings of EEG were random and paroxysmal slow waves with asymmetry. Discussion was made in reference to the strong suspicion that the cerebral symptoms of the subjects, the paroxysmal diseases in particular, were a syndrome associated with schistosoma japonicum and to the difference between CSJ in japan and that in the philippines.
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17/125. osteopetrosis, renal tubular acidosis without urinary concentration abnormality, cerebral calcification and severe mental retardation in three Turkish brothers.

    Deficiency of carbonic anhydrase ii (CA II) isoenzyme produces metabolic disorders of bone, kidney and brain. In this report we describe the clinical, radiological, pathological and genetic findings in three brothers who were affected with the autosomal recessive syndrome of osteopetrosis, renal tubular acidosis (RTA) and cerebral calcification. The RTA was hybrid type, but urinary concentration ability was intact. Additional features were severe mental retardation, stunted growth, microcephaly, dental malocclusion, high-arched palate, and broad thumbs. Previous reported patients with this syndrome were predominantly from the middle east and mediterranean region. This is the first report with CA II deficiency from the Turkish population. The presence of mental retardation and relative infrequency of skeletal fractures in our patients resembles the clinical course of patients with the Arabic mutation of the CA II gene, but this mutation was not found in our patients.
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18/125. Ophthalmological abnormalities in children with cerebral white matter disorders.

    The use of magnetic resonance imaging (MRI) in children with severe neurological impairment has defined a subgroup with increased T2-signals from cerebral white matter. The causes of white matter abnormalities are for the most part unknown, despite extensive investigation. Their clinical correlates and characteristics have still to be systematically analysed and described. We have compared clinical, ophthalmological and electro-ophthalmological findings in such children to delineate neurological and MRI patterns and have sought to correlate with the progression of disease. Clinical and electro-ophthalmological investigations were performed in 26 children with cerebral white matter abnormalities of unknown aetiology; 25 of the 26 children showed abnormalities, 23 clinical and 18 electro-ophthalmological. optic nerve abnormalities, severe visual impairment and strabismus were the most common. Electro-ophthalmological abnormalities were increased latencies and abnormal waveform of the visual evoked potentials (VEP). Children with progressive disease all had abnormal VEP, whereas none of the ten children with a normal VEP deteriorated. We conclude that children with cerebral white matter abnormalities almost invariably had ophthalmological and often VEP abnormalities. Normal VEP was correlated with non-progressive disorder, as was hypoplasia or malformation of the papilla, whereas abnormal VEP were associated with progressive disease.
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19/125. Immunohistochemical study of six cases of Taylor's type focal cortical dysplasia: correlation with electroclinical data.

    PURPOSE: Cortical specimens from six patients operated on for drug-resistant epilepsy diagnosed as Taylor's type focal cortical dysplasia were submitted to neuropathological and immunohistochemical studies. methods: All patients were submitted to presurgical investigations including clinical and neuropsychological evaluations, EEG/video telemetry of ictal and interictal events, magnetic resonance imaging, and ictal and interictal single-photon emission computed tomography (SPECT). Recordings from electrocorticography (ECoG) were obtained in four cases and from subdural electrode implantation in two. Postsurgical follow-up was assessed according to Engel's score. immunohistochemistry (IHC) was processed for parvalbumin (PV), calbindin D28-K (CB), nonphosphorylated neurofilaments (SMI-311), glial fibrillary acidic protein (GFAP) in all cases. RESULTS: We found continuous/quasi-continuous spikes and sharp-wave patterns in three cases and frequent repetitive bursting of polyspikes and ECoG seizures in two cases. Every patient showed cortical dyslamination, abnormal and giant neurons, and balloon cells. GFAP immunoreactivity was found in astrocytes and some balloon cells that were less intensely stained. Nonphosphorylated neurofilaments SMI-311 immunoreactivity was found in normal and giant neurons and in some balloon cells, making visible thin neuropils. PV immunoreactivity was present in normal interneurons and in fibers in layers IV-V. PV-negative balloon cells were surrounded by abundant PV-positive fibers. CB immunoreactivity was found mostly in interneurons in layers II-III. CONCLUSIONS: Our research is inconclusive. More cases should be investigated, and we must draw more accurate anatomic correlations between the ECoG recordings and surgical specimens studied with IHC.
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20/125. Molecular tracking of antigen-specific T cell clones in neurological immune-mediated disorders.

    T cells recognizing self or microbial antigens may trigger or reactivate immune-mediated diseases. Monitoring the frequency of specific T cell clonotypes to assess a possible link with the course of disease has been a difficult task with currently available technology. Our goal was to track individual candidate pathogenic T cell clones, selected on the basis of previous extensive studies from patients with immune-mediated disorders of the CNS, including multiple sclerosis, HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) and chronic lyme neuroborreliosis. We developed and applied a highly specific and sensitive technique to track single CD4( ) and CD8( ) T cell clones through the detection and quantification of T cell receptor (TCR) alpha or beta chain complementarity-determining region 3 transcripts by real-time reverse transcriptase (RT)-PCR. We examined the frequency of the candidate pathogenic T cell clones in the peripheral blood and CSF during the course of neurological disease. Using this approach, we detected variations of clonal frequencies that appeared to be related to clinical course, significant enrichment in the CSF, or both. By integrating clonotype tracking with direct visualization of antigen-specific staining, we showed that a single T cell clone contributed substantially to the overall recognition of the viral peptide/MHC complex in a patient with HAM/TSP. T cell clonotype tracking is a powerful new technology enabling further elucidation of the dynamics of expansion of autoreactive or pathogen-specific T cells that mediate pathological or protective immune responses in neurological disorders.
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