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At least 631 records · Page 35Linked to original sources
PubMed1985

Initial agonist burst duration changes with movement amplitude in a deafferented patient.

Changes in the duration of the initial agonist burst were studied in a deafferented human. The patient had been functionally deafferented for five years, having no touch, vibration, pressure or kinesthetic sensation nor any tendon reflexes in the four limbs. Pain and temperature sensation were intact and motor fibres were unaffected. The subject made visually guided step-tracking movements using flexion/extension movements about the elbow. Initial agonist burst duration increased with movement amplitude. Burst duration was approximately 65 ms in small movements (6-12 deg) increasing to 136 ms in intermediate (36 deg) and 200 ms in large (54 and 60 deg) movements. Similar changes in initial burst duration with movement amplitude were seen when the subject made non-visually guided movements. It is concluded that the duration of the initial agonist burst is centrally determined.

Adult↗
PubMed1995

Amyotrophic lateral sclerosis with marked neurological asymmetry: clinicopathological study.

We attempted to correlate the marked neurological asymmetry observed in two amyotrophic lateral sclerosis patients with their histopathological lesions. Patient 1, a 52-year-old man, developed dysarthria and dysphagia, followed by muscle weakness in the left arm and then of the left leg. Patient 2, a 44-year-old man, developed muscle weakness in the left hand, left leg, tongue with left-sided predominance, right hand and right leg in that order of progression. Both patients exhibited moderate to marked left-sided predominant involvement of the lower motor neuron system, accompanied by retained or hyperactive deep tendon reflexes on the left side in the early stage of their illness. Most of the asymmetry in the lower motor neuron system involvement persisted until the death of the patients. Histopathological examinations, including semiquantitative analysis, revealed that both patients exhibited left-sided predominant degeneration of the lower motor neuron system at those spinal cord levels where the neurological asymmetry was of a moderate to marked degree. In addition left-sided predominant degeneration of the lateral corticospinal tracts was seen in both patients and right-sided predominant involvement of Betz cells in the leg area of the motor cortex of patient 1. This pattern of both the neurological and histopathological asymmetry suggested the probable existence of an intimate somatotopically related linkage between the upper motor neuron system degeneration and lower motor neuron system degeneration in both patients.

Amyotrophic Lateral Sclerosis↗
PubMed1995

Influence of age on symptoms and signs in lumbar disc herniation.

In a prospective and consecutive study we evaluated the prevalence of pain-related symptoms, the results of the straight leg raising (SLR) test and neurological disturbances by age group in a total of 150 patients operated on due to lumbar disc herniation. On admission, all patients were interviewed, and pain at rest, at night and on coughing was recorded. Walking capacity was recorded under four categories: > 5 km, 1-5 km, 0.5-1 km and < 0.5 km. Results of the SLR test were also registered as category data: positive 0-30 degrees, positive 30-60 degrees, positive > 60 degrees or negative. Findings from examination of tendon reflexes and power of the extensor hallucis longus (EHL) muscle were registered, as were sensory disturbances. The above mentioned parameters were analysed separately for five different age groups: 20-29 years, 30-39 years, 40-49 years, 50-59 years and above 60 years of age. There was an age-related change in the prevalence of certain parameters. Highly restricted positive SLR test results and pain on coughing was most commonly found in the youngest patient group. With increasing age there was a decreasing prevalence of highly restricted positive SLR test results, while the prevalence of severe reduction of walking capacity increased. In short, the youngest patient group showed the most obvious clinical picture of disc herniation and, with increasing age, the clinical picture gradually changed towards the picture associated with spinal stenosis.

Adult↗
PubMed1992

Perivascular siderophages in skeletal muscle from a patient with diabetic neuropathy.

Hemosiderin deposition in skeletal muscle histiocytes is uncommon but has been occasionally noted in hemochromatosis, hemosiderosis and Waldenstrom's macroglobulinemia. The purpose of this report is to describe the light microscopic and ultrastructural characterization of this abnormality in a patient with diabetes mellitus. A 56-year-old diabetic male presented with paresthesias and intermittent diffuse lower extremity myalgias. Neurologic examination was remarkable only for diminished vibratory sense in the toes, diminished deep tendon reflexes, and ankle-level stocking distribution hypalgesia. There was no clinical evidence of hemochromatosis and laboratory studies ruled out Waldenstrom's macroglobulinemia. Muscle biopsy showed modest variability in myofiber diameter with a few scattered angular atrophic type II fibers. There were numerous collections of granular pigment-containing histiocytes in endomysial and perimysial perivascular areas and marked thickening of blood vessels walls. The histiocytic pigment was bright blue with the Prussian blue stain. No pigment was seen in the myofibers. Ultrastructural examination revealed numerous perivascular histiocytes filled with hemosiderin containing granules of variable size and density and marked thickening of capillary walls with striking reduplication of basement membranes. A modest number of subsarcolemmal paracrystalline mitochondrial inclusions were present. X-ray dispersion analysis of the histiocytic pigment material confirmed the presence of iron in the lysosomal granules.

Blood Vessels↗
PubMed1981

Peroneal muscular atrophy with ataxia and partial myoclonic epilepsy.

Two brothers, 17 and 11 years old, presented with pes cavus, absence of deep tendon reflexes, péripheral vibratory sensory loss, ataxia, tremor, nystagmus, dysarthria and partial myoclonic epilepsy. Electromyography showed severe slowing of motor conduction velocity in the lower extremities and increased distal latencies. A peroneal nerve biopsy showed absence of myelin sheath in most fibres resulting in numerous demyelinated nerve fibres. The father and seven uncles on the paternal side had pes cavus, hammer toes and moderate vibratory peripheral sensory loss. Three of seven siblings had slow motor conduction velocities on EMG. None had EEG abnormalities. Epilepsy started at an early age in both patients with myoclonic jerks of the right arm especially during sleep. EEG recordings were characterized by focal or diffuse epileptiform discharges. In the elder brother a partial motor epileptic status occurred with adversive seizures involving the right side of the body. He died of a broncopneumonia after 3 days of this epileptic status. Histopathological examination showed a severe demyelination of dentato-rubral pathways in the cerebellum and a partial degeneration of Goll and Burdach's tracts in the cervical spinal cord. The nosological classification of this syndrome is discussed and an autosomal dominant inheritance with incomplete penetrance or variable expressivity is suggested.

Adolescent↗
PubMed1984

The Guillain-Barré syndrome: clinical and electroneuromyographic studies.

Clinical and electrophysiological studies were carried out on 39 patients with the Guillain-Barré syndrome to evaluate which elements were of prognostic value during the acute phase. Residual clinical signs such as motor weakness and absent patellar tendon reflexes were found in 16 (52%) of those patients who had had a preceding illness. Persistence of deficit was significantly correlated to age at onset, the degree of quadriparesis and loss of deep sensation in the acute phase. Of the 10 patients who showed a reduction in motor nerve conduction velocity (MCV) in the early stage, 8 (80%) revealed significantly residual clinical symptoms at follow-up. There was a tendency for the incidence of residual signs to be more common in the patients with slowing of mixed nerve conduction velocity, and prolonged latency of H-wave and the residual latency. Nerve conduction studies, especially measurement of MCV, were of value as a reliable prognostic indicator in this syndrome.

Adolescent↗
PubMed1984

Leigh's syndrome in an adult.

A 55-year-old man with a subacute onset of slurred speech, ataxia, nystagmus, extrapyramidal rigidity, decreased tendon reflexes, vomiting, bilateral optic atrophy, and clonic jerks died of bronchopneumonia and respiratory failure. Neuropathological examination showed lesions characteristic of subacute necrotizing encephalopathy. Clinicopathological observations of reported cases of Leigh's syndrome in the adult are reviewed.

Brain↗
PubMed1990

A manifesting carrier of Duchenne muscular dystrophy with severe myocardial symptoms.

A 42-year-old so-called manifesting carrier of Duchenne muscular dystrophy (DMD), whose first complaints were severe myocardial symptoms, is described. Immunohistochemical study using anti-dystrophin anti-serum and analysis of cloned segments of X chromosome DNA were performed. Her two sons and one of her brothers appear to have had the same disease. She was admitted to the hospital complaining of dyspnoea, back pain and palpitations and was first diagnosed as having myocardial infarction. However, this diagnosis was excluded. The echocardiogram showed diffuse abnormalities of myocardial function. Serum enzymes were increased. Minimal weakness and decreased deep tendon reflexes were detected in her left lower extremity. Muscle biopsy revealed a small number of necrotic fibres. Immunohistochemical study using anti-dystrophin antiserum showed a mosaic pattern of the surface membrane. Analysis of cloned segments of X chromosome DNA from the patient and her son showed the XmnI(Asp) alleles of pERT 87-15 and the TaqI alleles of pERT 87-8 in both patients.

Adult↗
PubMed1991

Intrafamilial phenotype variation in Friedreich's disease: possible exceptions to diagnostic criteria.

Three families are described which include members with "typical" Friedreich's disease (FD) and others who are ataxic but do not satisfy all the diagnostic criteria for that disease. In family A two patients have an early-onset, rapidly progressive FD, while two others have a late-onset, more benign form. In families B and C one member has "typical" FD, and another has a similar ataxic syndrome, except for preservation of knee jerks. Laboratory evaluation is consistent with the diagnosis of FD in all cases. FD diagnosis appears justified in secondary cases with late onset or preserved tendon reflexes, provided that the index case fulfils all diagnostic criteria. Whether the diagnosis of FD is tenable in sporadic "atypical" cases remains to be seen. Echocardiographic and neurophysiological examination may be valuable in classifying such cases.

Adolescent↗
PubMed1982

A case report of congenital hypomyelination.

A 3 year, 11 month-old Japanese male with congenital hypomyelination is described. Clinical features are delay of motor development, generalized muscle hypotonia and weakness, absent tendon reflexes due to peripheral neuropathy, and normal mental development. Electrophysiologically, nerve conduction velocities could not be measured. Histological examination of the right sural nerve revealed total of absence myelin of most of the myelinated fibers. Electronmicroscopically, there was a concentric network of lamellae formed by double-layered sheets of basement membranes with fragments of Schwann cell cytoplasm around the myelinated fibers, so called "onion-bulbs". These peculiar features were similar to those in the cases reported by Lyon, (1969); Kennedy et al., (1977); Karch et al., (1975); and Anderson et al. (1973).

Biopsy↗
PubMed1985

De Barsy syndrome--an autosomal recessive, progeroid syndrome.

We report two families with seven siblings with de Barsy syndrome. Characteristic features include severe mental retardation, hypermobility with athetoid movements, grimacing, muscular hypotonia, laxity of small joints and brisk deep tendon reflexes, progeroid aspect with cutis laxa, atrophy of skin with hyperpigmentation, isolated depigmentations, reduction of subcutaneous fatty tissue, translucent vein pattern, short stature, frontal bossing in the young child, large prominent ears with dysplastic helices and corneal clouding or cataracts. The syndrome probably has autosomal recessive inheritance.

Abnormalities, Multiple↗
PubMed1983

Periodic paralysis with cardiac arrhythmia.

In 1963, Klein et al. first described two girls with normokalemic periodic paralysis and cardiac arrhythmia. We have observed a 15-year-old girl with cardiac arrhythmia and normokalemia but with some features of hyperkalemic, periodic paralysis. The patient showed a waddling gait and Gower's sign. She had atrophy of the proximal muscles and deep tendon reflexes were reduced. Her ECG showed bigeminy with multifocal premature ventricular contractions. At the start of an episode of muscle weakness, the serum potassium concentration rose from 3.1 to 4.4 mEq/l. Muscle weakness was not provoked by intravenous administration of 45 g glucose or of 72 g glucose followed by 10 units of regular insulin. Muscle weakness was evoked by the ingestion of 4 g potassium chloride. During the provoked muscle weakness, the ECG showed normal sinus rhythm temporarily.

Adolescent↗
PubMed1977

Ring 11 chromosome (46,xx,r11(p15q25)).

A girl has a stable chromosome 11, which does not reveal loss of any chromosomal material. She demonstrates small stature, mild retardation, behavior problems, mild abnormal EEG, prominent sole furrow, increased deep tendon reflexes and hypothyroidism; this latter condition may have contributed to her retardation.

Child↗
PubMed1989

"Occult" hydrocephalus in children.

The authors describe 32 children between 2 and 15 years of age who had hydrocephalus that was only clinically manifest late in life. The clinical picture of these children did not suggest an obvious increase in intracranial pressure; instead, the presenting signs were rather nonspecific and included macrocrania, mild psychomotor retardation, unsteady gait, increased muscle tone and deep tendon reflexes in the lower limbs, impaired ocular movement, epilepsy, and endocrine dysfunction. Their histories suggest the possible causes of the ventricular dilation in about one third of the cases were: perinatal hemorrhage, leptomeningitis, neurofibromatosis, and untreated aneurysm of the great vein of Galen. In 20 patients, however, no positive anamnestic findings were reported. CT scan revealed triventricular dilation in more than half of the cases; tetraventricular dilation was present in 6 patients, and biventricular dilation in the remaining subjects. All children underwent CSF shunting, which resulted in complete recovery in all but 2 cases. The most frequently recorded surgical complication was post-operative subdural effusion (7 subjects), which required surgical treatment in only 2 cases.

Adolescent↗
PubMed1991

Follow-up study of sensory-motor polyneuropathy in type 1 (insulin-dependent) diabetic subjects after simultaneous pancreas and kidney transplantation and after graft rejection.

The influence of successful simultaneous pancreas and kidney transplantation on peripheral polyneuropathy was investigated in 53 patients for a mean observation period of 40.3 months. Seventeen patients were followed-up for more than 3 years. Symptoms and signs were assessed every 6 months using a standard questionnaire, neurological examination and measurement of sensory and motor nerve conduction velocities. While symptoms of polyneuropathy improved (pain, paraesthesia, cramps, restless-legs) and nerve conduction velocity increased, there was no change of clinical signs (sensation, muscle-force, tendon-reflexes). Following kidney-graft-rejection there was a slight decrease of nerve conduction velocity during the first year, which was not statistically significant. Following pancreas-graft rejection there was no change of nerve conduction velocity during the first year. Comparing the maximum nerve conduction velocity of the patients with pancreas-graft-rejection to the nerve conduction velocities of these patients at the end of the study, there was a statistically significant decrease of 6.5 m/s. In conclusion, we believe that strict normalization of glucose metabolism alters the progressive course of diabetic polyneuropathy. It may be stabilized or partly reversed after successful grafting even in long-term diabetic patients.

Adult↗
PubMed1983

Ganglioradiculitis in the dog. A clinical, light- and electron-microscopic study.

Facial hypalgesia, sensory ataxia, depression of tendon reflexes, and masticatory muscle wasting developed acutely to subacutely in three adult dogs. These deficits were correlated with craniospinal sensory ganglioradiculitis. CNS degeneration in the dorsal funiculus, spinal tract of the trigeminal nerve, and solitary tract was secondary to loss of primary sensory neurons. Megaesophagus, which occurred in two dogs appeared to be associated with loss of vagal primary afferent neurons; however, esophageal and gastric myenteric ganglionitis was also observed in one of these animals. In the three dogs changes in the sensory ganglia and roots included non-suppurative inflammation and degeneration and loss of neurons. Perivenular and perineuronal mononuclear infiltrates were prominent. EM study revealed that the satellite cells around degenerating and necrotic cell bodies were commonly invaded and displaced by lymphocytes and macrophages. It was not clear whether these mononuclear cells effected neuronal degeneration or merely responded to it. Although the pathogenesis remained undefined, the similarity of the clinical and pathologic findings in these dogs indicated a nosologic entity that had not been reported previously. This canine ganglioradiculitis was compared with inflammatory disorders of the cranial and spinal ganglia in man.

Animals↗
PubMed1998

Hypokalemic thyrotoxic paralysis: a rare cause of tetraparesis with acute onset in Europeans.

We describe a 21-year-old Italian male affected by hypokalemic tetraparesis with acute onset. In the emergency ward, the patient was agitated, with tachycardia (140/min) and systolic hypertension (180/70 mm Hg). He was not able to flex the lower extremities against a light resistance and furthermore, he was hypotonic and without tendon reflexes. One hour later he developed strength deficit of the upper extremities as well. Biochemical analyses revealed severe hypopotassemia (2.1 meg/l). After administration of 140 meq potassium phosphate, the patient began to improve, and 12 h after the onset he was able to walk normally. Successive investigations documented an undiagnosed case of Graves' disease. Thyrotoxic hypokalemic paralysis has been observed almost only in Asians, however, with this case and others reported, we believe that it should be considered as a cause of muscular paralysis also in Caucasians.

Acute Disease↗
PubMed1992

Prevalence of hereditary ataxias and spastic paraplegias in Molise, a region of Italy.

An epidemiological survey of hereditary ataxias and paraplegias was conducted in Molise, a region of Italy (335, 211 inhabitants on 1 January 1989). Total prevalence was 7.5 x 10(-5) inhabitants (95% confidence limits 4.8-11.1). There were 7 patients with Friedreich's disease, 5 with early onset cerebellar ataxia with retained tendon reflexes, 4 with ataxia-telangiectasia, 9 with hereditary spastic paraplegias (2 autosomal dominant and 7 autosomal recessive cases). There was no patient with autosomal dominant cerebellar ataxia.

Adolescent↗