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[A case report of subacute panencephalitis associated with specific T cells sensitized to proteolipid protein (PLP) synthetic peptides identified with rubella virus].

A 37-year-old woman was admitted to the hospital on October 4, 1991 because of fever, headache, and abnormal behavior. Although she was treated with aciclovir, she developed encephalitis, which slowly manifested itself over the next month as meningeal irritation, loss of consciousness, partial seizure, and quadriparesis. Her cerebrospinal fluid showed mild lymphocytic pleocytosis without protein elevation. Serum IgG antibody titer to rubella virus was elevated, but the rubella virus could not be detected in the cerebrospinal fluid by PCR amplification. Her consciousness level improved slowly, and by the end of November she suffered only dystonic posture of her right arm and hand. By the middle of December, there were no abnormal neurological findings except some extrapyramidal tract signs and symptoms, such as tremor and rigidity. The serum rubella virus IgG titer had fallen back into the normal range. Her illness was diagnosed as subacute panencephalitis, and she recovered completely about 5 months after the onset of the disease. The lack of rubella virus in the cerebrospinal fluid suggests that panencephalitis may not be dependent on virus replication within the central nervous system. Specific T cells sensitized to proteolipid protein synthetic peptides (PLP158-166) identified with rubella virus were detected in this case during the active stage. These observations imply that subacute panencephalitis may be dependent on an immune-mediated mechanism and that PLP-specific T cells may play an important role in pathogenesis of the disease.

Adult↗

[Changes in blink reflex (OM) after lesions of the nervous system in various locations].

Electrically evoked blink reflex (BR) as a one of the non-invasive methods is used to diagnose function of central nervous system, specially of brainstem. It seems that this method is not fully appreciated in neurological practice. On the basis of literature and own experience the authors present typical pictures of BR on EMG analysis related to the lesions of respective parts of reflex arc and suprasegmental structures involving pyramidal and extrapyramidal tracts.

Blinking↗

[Myopathology of the intrinsic laryngeal muscles in neurodegenerative diseases, with reference to the mechanism of vocal cord paralysis].

To investigate the mechanism of the vocal cord abductor paralysis (VCAP) in the neurodegenerative diseases, the intrinsic laryngeal muscles (the crycothyroid, the interarytenoid, and the posterior crycoarytenoid muscles) from 41 autopsied cases were histologically examined: 10 cases of amyotrophic lateral sclerosis (ALS), 10 of Parkinson's disease (PD), 9 of multiple system atrophy (MSA), 4 of Machado-Joseph disease (MJD), 4 of progressive supranuclear palsy (PSP), 1 of familial amyloidotic polyneuropathy (FAP), and 3 of cerebrovascular diseases as a control. According to the distribution of the neurogenic changes among above-described three intrinsic laryngeal muscles, three forms were raised: 1. The totally paralytic form showing that all the three muscles developed neurogenic atrophy. This form includes ALS, MJD, and FAP. 2. The posterior muscle-paralytic form showing that only the posterior crycoarytenoid muscle was selectively involved. This form includes MSA. 3. The nonparalytic form showing no morphological abnormalities in any of the intrinsic laryngeal muscles. This type includes PD and PSP. In this nonparalytic form, supranuclear mechanism such as pyramidal or extrapyramidal tract involvement may cause VCAP through the increased laryngeal muscles tone. Considering that VCAP can be seen in any of the above-described forms, our results indicate that the mechanism of VCAP is different among the neurological disorders.

Atrophy↗

[A case of acquired stuttering resulting from striatocapsular infarction].

Acquired stuttering resulting from a striatocapsular infarction is reported. A 54-year-old man was admitted to our hospital because of acute onset of stuttering and right facial palsy. The patient spoke very slowly. Speech was characterized by repetitions and prolongations. We considered that there was no aphasia, because comprehensive faculty was normal and neither paraphasia nor word-finding difficulty was recognized. Brain CTs and MRI revealed a striatocapsular infarction extending from the putamen to the caudate nucleus in the left hemisphere. Previously, there were reports of stuttering derived from parkinsonism and lesions in the supplementary motor area and thalamus. Therefore, we proposed that the stuttering arose from a collapse of basal ganglia circuits that connect the cerebral cortex and basal ganglia, including the extrapyramidal tract system.

Cerebral Infarction↗