Showing papers by "Kenji Kosaka published in 1991"

Parvalbumin-immunoreactive neurons in the cortex in Pick's disease.

Abstract: Parvalbumin (a calcium-binding protein)-immunoreactive (PV-Ir) neurons in the cerebral cortex were examined in 20 postmortem brains obtained from elderly controls and patients with Pick's disease (PD). The type of PV-Ir neurons and their distribution in control and PD brains were similar. The number of PV-Ir neurons in PD brains did not differ significantly from that in the control brains either. These findings suggested that PV-Ir neurons in the cortex are not affected in PD brains. A significant loss of PV-Ir neurons has already been reported in brains obtained from patients with Alzheimer-type dementia (ATD), and the present results suggest the possibility that the damage of PV-Ir neurons might be comparatively selective for ATD brains.

[A new type of complicated form of hereditary spastic paraplegia showing mental deterioration, quadriplegia with muscular atrophy, sensory disturbance, extrapyramidal disorders, and epilepsy].

Abstract: UNLABELLED This study proposes a new type of complicated form of hereditary spastic paraplegia (HSP) and some problems on a clinico-pathological classification of HSP. The present study includes three male and two female patients from two families (A and B). In the family A, four siblings (two males and two females) were affected. Spastic paraplegia developed as an initial symptom. In the family B, a man was affected with spastic paraplegia which had started at the age of eleven. His two half-sisters are normal. All parents in two pedigrees are healthy. The parents in the family B are first cousins. CLINICAL FEATURES Their physical development was normal, but all of them showed mild mental retardation. Gait disturbance due to spastic paraplegia and mental deterioration developed at the age of high teens. At the age of high 20's, they became unable to walk, because of progressive spastic paraplegia and other complicated neurological impairments including pyramidal disorders in the upper limbs, generalized neurogenic muscular atrophy, sensory disturbance and bradykinesia. Some cases showed rigidity and/or spasticity. At the age of high 30's, they became bed-ridden, because of quadriplegia with generalized muscular atrophy. Three cases in the family A suffered from convulsions which started at the high 30's. Mild athetoid movement in the face and neck was observed in three cases in the family A. All patients became apathetic and indifferent at least by the age of 40. Laboratory findings and data: CT scan yielded brain atrophy and dilatation of the lateral ventricles, atrophy of the corpus callosum and hyperostosis of the cranium.(ABSTRACT TRUNCATED AT 250 WORDS)

Study on argyrophilic inclusions of multisystem atrophy (Oppenheimer)

Abstract: UNLABELLED Non-hereditary olivo-ponto-cerebellar atrophy (OPCA) and striato-nigral degeneration (SND) have been looked upon as a single disease entity called multisystem atrophy (MSA) by Oppenheimer. This study revealed that both intracytoplasmic argyrophilic inclusions (AI) in pontine neurons and glial (argyrophilic) cytoplasmic inclusions (GCIs) widely distributed in the CNS are characteristics of MSA. MATERIALS a) 12 cases with MSA, b) 16 cases with autosomal dominant (AD) form of spinocerebellar degeneration (SCD): AD form of OPCA 5 cases, Joseph disease 4 cases, AD-dentatorubropallidoluysian atrophy (Naitoh & Oyanagi's form) 6 cases, AD-spastic ataxia (Brown) 1 case, c) 4 cases with autosomal recessive (AR) form of SCD: AR form of OPCA 1 case, myoclonic epilepsy with ragged-red fibers (MERRF) 1 case, complicated form of spastic paraplegia 2 cases, d) 6 cases with non-hereditary SCD including intoxications: late cortical cerebellar atrophy 1 case, alcoholic cerebellar degeneration 2 cases, phenytoin-induced cerebellar degeneration 1 case, neuroleptic malignant syndrome 1 case, and e) 27 cases with other neuropsychiatric diseases: Alzheimer disease 20 cases, progressive supranuclear palsy 5 cases, schizophrenia 2 cases. METHOD We examined 10 mu-thick paraffin sections stained with HE, Kluver-Barrera, Bodian, Holzer, Gallyas, and Bielschowski methods. RESULTS AI in pontine neurons were found only in two cases of MSA. Interestingly no AI could be detected even in cases with AD form of OPCA showing mild degeneration in the pontocerebellar system. On the other hand, GCIs were found in all cases with MSA irrespective of the degree of degeneration in the olivo-ponto-cerebellar or striato-nigral system. However, there was no GCIs in cases with other form of SCD and other neuropsychiatric diseases. Gallyas stain was the best method for detecting GCIs. GCIs were widely distributed in the CNS except for superficial layers of the cerebral cortex, the cerebellar cortex, and the dorsal column of the spinal cord. There were also many GCIs in the putamen, pontine base, and cerebellar white matter, even though these sites were well preserved.