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At least 1,351 records · Page 75Linked to original sources
PubMed1982

Olivopontocerebellar atrophy. A review of 117 cases.

Fifty-four cases of familial OPCA (FOPCA) and sixty-three cases of sporadic OPCA (SOPCA) have been gathered from the literature. The data concerning age at onset, duration of the disease, frequency of symptoms and the various localizations of lesions have been evaluated. In comparison with SOPCA, the disease begins earlier in FOPCA and lasts longer (P less than 0.001). The differences in the percentages of clinical manifestations and associated lesions are also significant with regard to the greater frequency in FOPCA of abnormal movements, ophthalmoplegia, spinal symptoms and lesions located in the dentate nucleus and spinal cord, except for the pyramidal tract. The clinical signs and symptoms are reviewed, special emphasis being given to dysphagia and urinary incontinence, their relevance having been underestimated in previous studies. After a critical analysis of the classifications in current use, I conclude that that of Greenfield (1954) remains the most appropriate.

Atrophy↗
PubMed1989

Total manifestations of amyotrophic lateral sclerosis. ALS in the totally locked-in state.

We report 4 cases of amyotrophic lateral sclerosis (ALS) in the totally locked-in state (TLS); 2 of the cases were autopsied. The clinical and pathological findings of ALS reported previously were essentially included in those studied here. In all cases reported in this paper, the voluntary muscles, including the oculomotor muscles, deteriorated rapidly, resulting in respiratory failure within 1.5 years. Successive observation of the 4 cases confirmed that ontogenetically old motor functions, including oculomotor functions, were preserved in the advanced stage, and that the main lesions in the oculomotor system were supranuclear. The 2 autopsied cases showed widespread pathological lesions other than those of the pyramidal tract and motoneurons commonly seen in ALS. We review these findings, and discuss them from an ontogenetical aspect in terms of the development of motor functions and anatomical myelination, and compare them with clinico-pathological findings of progressive supranuclear palsy (PSP) and anatomical structures of the supranuclear oculomotor system in monkeys.

Adult↗
PubMed1989

Type IIa hyperlipoproteinemia masquerading as cerebrotendinous xanthomatosis.

We describe an adult patient with type IIa hyperlipoproteinemia, presenting with Achilles tendon xanthomas, cataracts, dementia, ataxia, pyramidal tract signs, and peripheral neuropathy, which are commonly seen in cerebrotendinous xanthomatosis (CTX). However, the diagnosis of CTX was excluded on the basis of the cholestanol level and the normal cholestanol/cholesterol ratio in his serum and tendon. The pathomechanism for some of the clinical manifestations in type IIa hyperlipoproteinemia and CTX might be caused by a common biochemical disturbance.

Aged↗
PubMed1991

Muscular changes in the guinea pig caused by chronic ascorbic acid deficiency.

The present study was undertaken in order to decide whether chronic ascorbic acid (AA) deficiency only causes myopathy in the guinea pig or whether it also causes central nervous system pathology. Juvenile male animals, fed an optimally balanced, purified diet with minimal amounts of AA, developed a nutritional myopathy complicated by trauma, arthrogenic factors and defective repair. The absence of changes in the spinal pyramidal tracts, the anterior horn cells and peripheral nerve agrees with the absence of neurogenic changes in muscle specimens as target, targetoid, or small angulated fibers, group atrophy, type grouping, or changes in the distribution pattern of fibers. We conclude that chronic AA deficiency in the guinea pig cannot serve as an animal model of human amyotrophic lateral sclerosis.

Amyotrophic Lateral Sclerosis↗
PubMed1991

Autopsy report of HTLV-I-associated myelopathy presenting with ALS-like manifestations.

We report an autopsy case of HTLV-I-associated myelopathy (HAM) showing clinical features indistinguishable from amyotrophic lateral sclerosis (ALS). A Japanese man developed bulbar palsy and generalized neurogenic muscular atrophy with symmetrical hyperreflexia at the age of 57 and died 4.5 years after the onset. He had an increased titer of anti-HTLV-I antibodies in serum and CSF. At autopsy, the leptomeninges were thickened and infiltrated with inflammatory cells. The brain and spinal cord were atrophic. The pyramidal tracts and anterior horn cells of spinal cord were severely degenerated but degenerative changes were also found in the basal ganglia, thalamus, brainstem tegmentum, and the dorsal columns of spinal cord. In all degenerative areas, prominent infiltrations of inflammatory cells were found. The present case indicates that HAM may produce clinical features indistinguishable from ALS.

Amyotrophic Lateral Sclerosis↗
PubMed1992

Pathological changes in skeletal muscle in HTLV-I-associated myelopathy.

The main lesion site of HTLV-I-associated myelopathy or tropical spastic paraparesis (HAM/TSP) is the pyramidal tract. In some HAM patients, clinical symptoms and findings indicate neuromuscular involvement, such as muscular atrophy, fasciculation, elevated serum creatine kinase (CK) or significant electrophysiological data. Cases of HAM/TSP complicated with polymyositis or motor neuron disease have been reported. But no investigation has been directed to muscular pathology in many patients of HAM/TSP. We conducted muscle biopsies on 13 HAM patients. Four patients showed neurogenic changes. Six patients showed histological findings indicative of inflammatory myopathy. We investigated surface marker of invading cells in these 6 patients. In all patients, T lymphocytes were more predominant than B lymphocytes and in three of them T helper/inducer cells were more predominant than T suppressor cells. In 2 patients, only slight myopathic change could be seen, such as variation in fiber diameter and increase in the number of internal nuclei. In 1 patient, type 2 fiber atrophy was seen, and was possibly the result of disuse. Disturbance of secondary motor neurons or inflammatory myopathy is thus shown to be possibly associated with HAM/TSP.

Adult↗
PubMed1992

Extrapyramidal system involvement in motor neuron disease.

Three cases of motor neuron disease (MND), in which neuropathological findings were atypical, are reported. The first case manifested widespread and severe degeneration of the spinal cord, as in spinal fibrosis. Case 2 revealed severe degeneration of the pyramidal tract with many spheroids, which made it difficult to differentiate from primary amyotrophic lateral sclerosis. The last case revealed degeneration of the nigro-pallido-luysian system, even though no clinical manifestation of extrapyramidal and/or cerebellar symptoms had been noted throughout the clinical course. In MND, degeneration might occur in various locations other than the motor system.

Aged↗
PubMed1993

Involvement of the frontotemporal lobe and limbic system in amyotrophic lateral sclerosis: as assessed by serial computed tomography and magnetic resonance imaging.

The present paper concerns serial examinations of computed tomography (CT) and magnetic resonance imaging (MRI) in 22 patients with sporadic amyotrophic lateral sclerosis (ALS). Supranuclear ophthalmoplegia developed in 13 and dementia in 3 patients. The investigations showed gradually progressive atrophy, first in the frontal and anterior temporal lobes then in the precentral gyrus, and later in the postcentral gyrus, anterior part of the cingulate gyrus, corpus callosum and brain stem tegmentum. MRI revealed high intensity signals on T2-weighted images in the precentral and adjacent gyri, frontotemporal white matter and pyramidal tract as well as rarely in the globus pallidus and thalamus. These neuroradiological changes were not related to the duration of the clinical course or to the degree of the motor impairment. These alterations may play a critical role in the supranuclear ophthalmoplegia seen in ALS patients. The dementia of ALS probably reflects involvement of both the frontotemporal lobes and limbic system.

Adult↗
PubMed1995

Onuf's nucleus is frequently involved in motor neuron disease/amyotrophic lateral sclerosis.

Involvement of Onuf's nucleus (ON) in 28 cases of amyotrophic lateral sclerosis/motor neuron disease (MND/ALS) with different clinical syndromes is reported. Although significant neuronal loss was absent, all cytoskeletal abnormalities typical of alpha-motor neurons in MND/ALS were found in ON. Spheroids were detected in 53.5% of cases; 0.6-4.5% of ON neurons contained Bunina bodies, which were present in 42.8% of cases. Ubiquitin-reactive inclusions (UBRI) of filamentous and hyaline type were found in 57.1% of cases and in 1.2-10.7% of ON neurons. Cases with pyramidal tract involvement (ALS) were involved by UBRI in 76.5%, whereas cases with progressive spinal muscular atrophy revealed the same inclusions in only 27.2%. No similar inclusions were present in sacral parasympathetic intermediolateral nucleus. It can be concluded, therefore, that ON belongs to the somatic motor system and is principally vulnerable to MND/ALS, albeit to a lower degree.

Adult↗
PubMed1994

Benign monomelic amyotrophy of lower limb: a rare entity with a characteristic muscular CT.

Six patients presented with amyotrophy confined to a single lower limb and characterized by insidious onset, slow progression and later stabilization. Wasting was out of proportion with disability and there were no sensory, pyramidal tract or bulbar signs. All cases were sporadic, and there was no history of poliomyelitis. CK, anti-ganglioside antibodies, motor and sensory conductions were normal. Quantitative EMG and muscle biopsy revealed neurogenic features also in clinically unaffected limbs. Muscular CT showed selective or predominant, asymmetrical involvement of posterior leg muscles and caput longus of biceps femoris. Monomelic amyotrophy of lower limb is a clinically localized variant of spinal muscular atrophy with a particularly benign course. Although in the early stage there are no clinical or laboratory findings which allow differential diagnosis with other motor neuron diseases, the history of an amyotrophy clinically localized for more than 3 years to a lower single limb and the characteristic muscular CT pattern suggest the diagnosis since the first observation and indicate a favorable prognosis.

Adult↗
PubMed1994

A single report of hemiplegic arm stretching related to yawning: further investigation using apomorphine administration.

We observed a stroke patient with an infarct of the internal capsule interrupting the pyramidal tract who stretched his hemiplegic arm during spontaneous and apomorphine-induced yawning. The putative mechanism by which yawning can induce the paradoxical motor response of the plegic arm in the patient might be the functional efficiency of a pathway projecting directly from the stimulated basal ganglia to lower motor systems in the brainstem.

Apomorphine↗
PubMed1995

Mortality from motor neuron disease in Japan, 1950-1990: association with radioactive fallout from atmospheric weapons testing.

Motor neuron disease (MND) is a progressive and invariably fatal disease affecting the nuclei of the pyramidal tract and anterior horn cells. Despite intensive research into environmental agents associated with the onset or course of the disease, there is no single factor that can be confidently linked over time with regional, national or international variations in mortality rates. However, unusual variations in MND mortality rate in Japan from 1950-1990 were found to correlate highly significantly with variations in radioactive fallout released by atmospheric weapons testing in the Pacific. This association could be explained by the ingestion of alpha-emitting radionuclides acting upon a pre-existing susceptible subpopulation, a hypothesis which is consistent with recent research on the epidemiology and pathology of MND. However, it is likely that radiation is only one of many factors that act singly or in combination to accelerate the condition in subpopulations susceptible to MND.

Adult↗
PubMed1995

A new familial disorder presenting with amyotrophic lateral sclerosis-like manifestation: a clinicopathological study.

We studied a family in which three siblings had an identical clinical feature indistinguishable from familial amyotrophic lateral sclerosis (ALS), consisting of progressive generalized neurogenic muscular atrophy with hyporeflexia and normal sensations beginning in the fourth decade. The duration of illness was about 4 years in all affected members. Autopsy of one patient revealed multiple foci of spongy degeneration in the white matter of the spinal cord, brain stem, cerebellum, and the thalamus, characterized by vacuoles of various size, foamy macrophages and degenerating swollen axons. These changes were most marked in the spinal cord, where there was neither pyramidal tract involvement nor neuronal loss in the anterior horn. The pathological findings were different from those of ALS. A similar disease affected the siblings' mother, suggesting an autosomal dominant inheritance. The disease in the kindred, therefore, appears to be a unique hereditary disorder.

Amyotrophic Lateral Sclerosis↗
PubMed1984

Recent physiological and pathophysiological aspects of Parkinsonian movement disorders.

Deficits in the neural control of limb movements constitute a major part of Parkinsonian symptoms and are linked to a decay of dopaminergic neurotransmission. In animal models, Parkinsonian-like hypokinesia is consistently reproduced with large nigrostriatal dopamine depletions, while tremor and rigidity are less readily obtained. Lesions leading to a less than 70% striatal dopamine depletion are largely compensated by an increased activity of dopamine terminals. With more important lesions, supersensitivity of striatal non-adenylate cyclase-linked dopamine receptors occurs. Electrophysiological studies in Parkinsonian patients demonstrate increased reaction times and a reduced build-up of movement-related muscular activity underlying hypokinesia and provide circumstantial evidence for a central origin of tremor and rigidity. Single cell activity in unlesioned, behaving monkeys shows an increasingly direct relationship to movements when following the neural connections from mid-brain dopamine cells via striatum, globus pallidus, thalamus to pyramidal tract neurons of motor cortex. These data corroborate experimentally the concept that Parkinsonian hypokinesia is due to a failure of basic behavioral activating mechanisms.

Animals↗
PubMed1982

Inspiratory onset or termination induced by electrical stimulation of the brain.

In anesthetized cats, electrical stimulation of the cerebral cortex and subcortical structures with short trains could induce onset or termination of activity of the phrenic nerve. Onset of phrenic discharge was obtained following stimulation of the primary sensory areas of the cerebral cortex, the periaqueductal gray, the ponto-mesencephalic reticular formation, the parabrachial nucleus, the vestibular nucleus, and the fastigial nucleus. When these structures were stimulated by repetitive trains at frequencies of 1-5 Hz, the respiratory rhythm was entrained to these same frequencies. The phrenic discharge during these repetitive stimulations exhibited a decrementing pattern similar to that during thermal polypnea. Termination of phrenic activity was obtained upon stimulation of the motor and visceral cortices, the internal capsule, the pyramidal tract, the red nucleus, the rubrospinal tract and the motor nucleus of the trigeminal nerve. Stimulation of these latter structures by repetitive trains resulted in a temporary or permanent arrest of phrenic discharge. These results are discussed in the context of the possible roles of medullary respiratory neurons in the onset or termination of inspiratory activity.

Animals↗
PubMed1987

Treatment of experimental spinal cord injury with TRH, naloxone, and dexamethasone.

Comparison of thyrotropin-releasing hormone (TRH), naloxone, and dexamethasone treatments in experimental spinal cord injury was studied in albino rats. Animals were made paraplegic by the application clip method of Rivlin and Tator. Treatment was administered intraperitoneally as a bolus injection in two doses at 45 and 120 minutes each after the injury. Animals were allocated randomly to one of four experimental treatment groups: (1) TRH (0.6 mg of TRH per dose) (2) naloxone (0.8 mg per dose), (3) dexamethasone (0.6 mg per dose), and (4) saline. Neurologic recovery was assessed by the inclined plane method, and cavitation size of the cord and of the pyramidal tract was examined under the light microscope. Results show that TRH and naloxone are therapeutically beneficial in the treatment of spinal cord injury, and that dexamethasone is ineffective.

Animals↗
PubMed1992

Idiopathic hemiparetic parkinsonism, a syndrome distinct from idiopathic parkinsonism.

Two women had a syndrome of progressive parkinsonism with ipsilateral rigidity, mild resting tremor, paresis, hyperreflexia, and an extensor plantar response. Symptoms had started 24 and 3 months after a surgical procedure in the affected limb. Neuroimaging studies were unhelpful. Both the parkinsonian features and the pyramidal tract signs responded well to dopaminergic drug treatment. We propose that the syndrome be called "idiopathic hemiparetic parkinsonism".

Adult↗
PubMed1979

Sets of neurons in somatic cerebral cortex of the cat and their ontogeny.

The process of set formation is briefly reviewed and five monothetic schemes for classification of neurons in the somatic cerebral cortex are described. Criteria for evaluation of neuronal sets are presented and applied to the five different monothetic classification schemes. Classification by size and distribution of peripheral receptive fields orders existing data on cortical neurons better than classification by possession of an axon in the pyramidal tract, by modality, by lability of receptive field, or by 'lemniscal properties'; however, no monothetic scheme orders all the data. A useful polythetic scheme, using s and m terminology is suggested. The ontogeny of the cerebral cortex is reviewed in detail. It is suggested that sa neurons are Golgi type II neurons while m neurons are Golgi type I neurons. The hypothesis is presented that wide-field or m neurons develop and are recognizable before small-field or sa neurons in ontogeny. Evidence regarding this hypothesis is indirect, often conflicting, but suggestive that the hypothesis may be correct. The idea that m neurons may also be phylogenetically older than sa neurons is presented and shown to be consistent with ontogenetic data and interpretations.

Animals↗