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Biomedical subjects

M Tsujihata

Publications and source records attributed to M Tsujihata.

At least 145 records · Page 8Linked to original sources
PubMed1981

[The Tolosa-Hunt syndrome: report of a case with recurrent (9 times) painful ophthalmoplegia (author's transl)].

A 48-year-old woman was referred to the First Dept. of Int. Med., Nagasaki Univ. Sch. Med., in August, 1979, with a six-month history of recurrent episodes of right-sided painful ophthalmoplegia and diplopia. An epidode affected the right eye, lasted one to two weeks, and relapsed every month. On examination she had a complete ptosis on the right side and pain on the right eye. All extraocular muscle supplied by the 3rd nerve were paralysed. The pupils were equal in size both sides, reacting to light completely. Visual acuity was normal except myopia. All the other cranial nerves and the remainder of central nervous system was normal. Results of thyroid function tests and of lumbar puncture were normal. The glucose tolerance test showed a mild diabetic pattern. Blood and CSF cultures for bacteria, fungi, and acid-fast bacillus were negative. The skull, brain CT scan, and carotid angiogram were within normal limits. A tentative diagnosis of Tolosa-Hunt syndrome was made after an unproductive search for a cause for this woman's painful ophthalmoplegia and unsuccessful treatment of ophthalmoplegia with antibiotics or diet therapy for mild hyperglycemia. The patient was given prednisolone 30 mg daily orally when she had the 9th attack of painful ophthalmoplegia Pain, ptosis, and diplopia disappeared in 5 days and she did not show any recurrence of symptoms over the next 7 months.

Female↗
PubMed1980

Beriberi neuropathy. Morphometric study of sural nerve.

Seven biopsied sural nerves from patients with beriberi were morphometrically evaluated. In teased fiber analysis the mean frequency of myelinated fibers showing axonal degeneration and segmental demyelination was 37.5 and 5.3%, respectively. In two cases with frequency of segmental demyelination higher than 5%, segmental demyelination was shown by statistical criteria to have occurred on certain fibers in a clustered fashion. Therefore, the segmental demyelination in beriberi may be secondary to axonal degeneration. Electromyographic findings and slow improvement of muscle weakness were compatible with axonal degeneration of motor fibers. Determinations of fiber densities revealed preferential decrease of the density of large myelinated fibers with the preservation of the density of small myelinated and unmyelinated fibers. The preferential nerve fiber involvement in beriberi was not associated with pain in the lower limbs and this fact is contrary to the expectation of the proponents of the gate control theory.

Adolescent↗
PubMed1980

Ultrastructural localization of acetylcholine receptor at the motor endplate: myasthenia gravis and other neuromuscular diseases.

Peroxidase-conjugated alpha-bungarotoxin (P-BGT) was used for the ultrastructural localization of the acetylcholine receptor in motor endplates. Brachial biceps muscle specimens were obtained from six patients with myasthenia gravis (MG) (two ocular and four generalized), five other patients with neuromuscular diseases (limb-girdle dystrophy, polymyositis, and amyotrophic lateral sclerosis) and two controls. In all patients with generalized MG, most of the endplates showed a marked decrease in P-BGT binding. In one of two patients with ocular MG, the amount and distribution of P-BGT binding appeared normal, whereas the other patient showed a slight decrease in P-BGT binding. There was a loose correlation between clinical severity of MG and acetylcholine receptor index or antiacetylcholine receptor antibodies. On the other hand, the amount and distribution of acetylcholine receptor in other neuromuscular diseases was well preserved, even at the endplates denuded of their nerve terminals in amyotrophic lateral sclerosis (ALS) cases.

Humans↗
PubMed1979

Muscular dystrophy in six young girls.

Clinical and genetic studies were made on progressive muscular dystrophy in six young girls. No chromosome abnormality was observed in these patients. The pedigree of one case implied a sex-linked recessive trait, and clinical features were identical with Duchenne dystrophy. The clinical manifestations of two sisters in another family were less severe than in their brother with Duchenne dystrophy. The clinical differences among these three cases are well explained by the Lyon hypothesis. Three other cases were compatible with childhood muscular dystrophy of autosomal recessive inheritance.

Adolescent↗
PubMed1979

Limb muscle endplates in ocular myasthenia gravis: quantitative ultrastructural study.

Motor endplate ultrastructure in the biceps brachii was quantitatively analyzed in five patients with ocular myasthenia gravis (56 endplates), six patients with generalized myasthenia gravis (83 endplates), and five controls (64 endplates). Ultrastructural changes of the motor endplates were observed in nonweak limb muscles of patients with ocular myasthenia gravis as well as in generalized myasthenia; these changes were mostly restricted to the postsynaptic region. Decrease of the mean presynaptic and postsynaptic membrane length, and postsynaptic membrane density, were more remarkable in generalized myasthenia than in ocular myasthenia. Widening of the primary and secondary synaptic clefts was also observed more frequently in generalized myasthenia. There was no correlation between ultrastructural alterations and the duration of symptoms or treatment, severity of disease, or titers of antiacetylcholine receptor antibody.

Adolescent↗
PubMed1978

Active state properties of denervated and immobilized muscle: comparison with dystrophic muscle.

Possible roles of neurotrophic mechanisms and muscle activity in the contractile abnormalities of muscular dystrophy were studied by comparing human dystrophic muscle to denervated and immobilized muscle. As evident in denervated muscle from the decreased acceleration of twitch development (decreased active state intensity of shortening), and isoproterenol-induced decrease of twitch with shortened decay of the active state, part of the abnormality in the subcellular calcium transport system in dystrophic muscle seems to be influenced by disordered neural regulation. Other active state abnormalities relating to activation processes and contractile proteins in dystrophic muscle were also demonstrated in both denervated and immobilized muscle, with some being more marked in immobilized muscle. The findings indicate that a neurogenic hypothesis cannot entirely explain the pathogenesis of progressive muscular dystrophy.

Adult↗
PubMed1976

The motor end plate in myasthenia gravis and in experimental autoimmune myasthenia gravis. A quantitative ultrastructural study.

Neuromuscular junction ultrastructure in rat forelimb digit extensor muscle was sequentially and quantitatively investigated in experimental autoimmune myasthenia gravis (EAMG). Experimental animals received a single dose of highly purified eel-electroplax acetylcholine receptor protein plus complete Freund's adjuvant and B. pertussis organisms. During the first 7 days (latent period) after immunization the experimental end plates remained normal. Between day 7 and 11 (acute phase) mononuclear cells infiltrated those regions of muscle where the end plates were located and the was sudden degeneration of the postsynaptic regions with splitting away of the abnormal junctional folds from the underlying muscle fibers. Macrophages entered the gaps arising between the muscle fibers and the separating postsynaptic folds and removed the degenerating folds by phagocytosis. The nerve terminals were displaced from their usual location but maintained their structural integrity. After day 11 (chronic phase) the inflammatory reaction subsided and the nerve terminals returned to the highly simplified postsynaptic regions. Subsequently the postsynaptic folds were reconstituted and again they degenerated. The degeneration involved especially the tips of the folds where acetylcholine receptor sites are concentrated. Immature junctions with poorly differentiated postsynaptic regions and nerve sprouts near end plates were also observed. In two animals that relapsed on day 27 and 33, respectively, degeneration of the postsynaptic folds was more intense than in the remaining animals that had not relapsed during the chronic phase. Morphometric analysis of the end plates demonstrated significant decreases in the postsynaptic membrane length, in the postsynaptic membrane density and in the postsynaptic to presynaptic membrane length ratio in chronic EAMG. In addition, the concentration of synaptic vesicles in the nerve terminals was increased in acute and chronic EAMG while the nerve terminal area was decreased in acute EAMG. The alterations in the nerve terminal may be secondary to the postsynaptic changes. The postsynaptic region is the primary target of the autoimmune reaction in EAMG and the ultrastructural and morphometric abnormalities of the end plate in the chronic phase of the syndrome closely resemble those which have been observed in human myasthenia gravis.

Animals↗