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Biomedical subjects

M Swash

Publications and source records attributed to M Swash.

At least 199 records · Page 11Linked to original sources
PubMed1985

Tetrabenazine induces acute dystonic reactions.

Four patients suffered acute dystonic reactions caused by tetrabenazine. Because dystonic reactions have previously been reported only after dopamine receptor blockade and not with dopamine depletion, it is likely that the ability of tetrabenazine to induce acute dystonia is due to its dopamine receptor blocking properties. Because tetrabenazine can induce acute dystonia even when combined with alpha-methyl-p-tyrosine, presynaptic dopamine stores may not be necessary for these reactions to occur.

Acute Disease↗
PubMed1985

Electrophysiological and manometric assessment of the pelvic floor in the solitary rectal ulcer syndrome.

Fifteen of twenty patients with the solitary rectal ulcer syndrome, eighteen of whom were women, had evidence of reinnervation in the external anal sphincter muscle as demonstrated by single fibre EMG and nine of these patients had an increased pudendal nerve terminal motor latency. In ten patients there was paradoxical puborectalis muscle activity on straining, but damage to the innervation of the external anal sphincter muscle was correlated with a history of straining, and with excessive perineal descent, rather than with paradoxical puborectalis activity. We suggest that this syndrome does not have a single cause.

Adult↗
PubMed1985

Neonatal spinal muscular atrophy presenting as respiratory distress: a clinical variant.

Respiratory distress from diaphragmatic and intercostal muscular weakness was the presenting feature of two neonates with progressive spinal muscular atrophy, leading to death in the first 2 months of life. This atypical feature provides evidence of heterogeneity within the commonly used clarification of type 1 spinal muscular atrophy.

Diagnosis, Differential↗
PubMed1985

The effect of continuous voluntary activation on neuromuscular transmission: a SFEMG study of myasthenia gravis and anterior horn cell disorders.

In normal subjects the neuromuscular jitter does not increase during continuous voluntary activation. In patients with myasthenia gravis, spinal muscular atrophy and motor neurone disease we have found that the neuromuscular jitter may increase during recordings of several minutes of continuous voluntary activation at steady innervation rates. In some units this led to impulse blocking, and in other units an initially normal jitter increased beyond the normal range. Measurement of jitter during continuous voluntary activation at steady innervation rates provides relevant information in the evaluation of neuromuscular transmission and fatigue in these disorders.

Adult↗
PubMed1985

Damage to the innervation of the pelvic floor musculature in chronic constipation.

Constipation and defecation straining have been implicated in the pathogenesis of anorectal incontinence. We have studied 24 women with chronic constipation and 20 age- and parity-matched control subjects. Electrophysiologic techniques were used to study the innervations of the puborectalis and external anal sphincter muscles. The results show that damage can occur to the nerve supply of both these muscles in chronic constipation, and that this probably is due to perineal descent during defecation straining.

Adult↗
PubMed1985

Adult onset acid maltase deficiency. Distribution and progression of clinical and pathological abnormality in a family.

The adult onset form of acid maltase deficiency (Type IIb) clinically affects only skeletal muscle. Proximal weakness is more severe in legs than arms and involvement of respiratory muscles is prominent in about a third of the cases. In three siblings with the disease, the severity of limb weakness was related to age and duration of disease. Respiratory muscle involvement was a feature in two of the patients. The pathological abnormality was more marked in quadriceps than deltoid, and was strikingly patchy in distribution within these muscles. In one case, vacuolar change was not evident by light microscopy in two quadriceps biopsies taken 2 years apart. There is thus a spectrum of clinical and pathological expression of the disorder even in a single sibship.

Biopsy↗
PubMed1985

Recognition memory in Alzheimer's disease.

Recognition memory for several types of stimulus material was examined in patients clinically diagnosed as having early Alzheimer's disease and in normal elderly controls. Although performance deficits were demonstrated for verbal and abstract stimuli (geometric shapes and histology slides), memory for faces was relatively intact in the patient group. Patients made more false positive responses than controls, but this could not be accounted for by a general disinhibition of responding. It is suggested that a contextual processing deficit may explain the pattern of false positive responding and this is discussed in relation to previous findings of drug studies in Alzheimer's disease.

Alzheimer Disease↗
PubMed1985

Perineal nerve damage in genuine stress urinary incontinence. An electrophysiological study.

Twelve patients with genuine stress incontinence of urine were investigated using manometric and electrophysiological techniques. All were shown to have slowed conduction in the perineal branch of the pudendal nerve which innervates the periurethral striated sphincter muscle. The mean perineal nerve terminal motor latency in these patients was 3.9 +/- 0.8 (ms) and in 20 age and parity matched control subjects was 2.0 +/- 0.2 (ms) (P less than 0.001). These results are consistent with a neurogenic factor in patients with genuine stress incontinence of urine which may have implications regarding selection of patients for surgery to restore urethral competence.

Adult↗
PubMed1985

Faecal incontinence due to external anal sphincter division in childbirth is associated with damage to the innervation of the pelvic floor musculature: a double pathology.

The commonest cause of external anal sphincter division is injury during childbirth. We have studied 20 patients with anterior external anal sphincter division using physical and electrophysiological techniques. There was evidence of pudendal nerve damage in 60% of these patients. This finding suggests that damage to the innervation of the external anal sphincter often co-exists with direct injury to the muscle; in these patients pelvic floor surgery may be required, in addition to sphincter repair itself.

Adult↗
PubMed1985

Anorectal incontinence and rectal prolapse: differential assessment of the innervation to puborectalis and external anal sphincter muscles.

The innervation of the puborectalis and external anal sphincter muscles was studied in 32 patients with idiopathic (neurogenic) faecal incontinence, 12 of whom also had complete rectal prolapse, using transcutaneous spinal stimulation, transrectal pudendal nerve stimulation, single fibre EMG, anorectal manometry, and measurement of perineal descent. Fourteen normal subjects served as controls. Significant increases in the spinal motor latencies from L1 to the puborectalis and external anal sphincter muscles were shown in all 32 incontinent patients (p less than 0.01). The single fibre (EMG) fibre density was increased in the puborectalis muscle in 60% and in the external anal sphincter in 75% of patients. An increased pudendal nerve terminal motor latency was found in 68% of patients; 69% had an abnormal degree of perineal descent and all had reduced anal canal contraction pressures. These data show that the different innervations of the puborectalis and external anal sphincter muscles are both damaged in patients with anorectal incontinence.

Adult↗
PubMed1985

Motor conduction velocity in the human spinal cord: slowed conduction in multiple sclerosis and radiation myelopathy.

Transcutaneous electrical stimulation of the central nervous system was used to measure motor conduction velocity in the human spinal cord in 21 subjects aged 22 to 75 years (mean 55 years), none of whom had neurological disease. The motor conduction velocity between the sixth cervical (C6) and first lumbar (L1) vertebral levels was 67.4 +/- 9.1 m/s. This probably represents conduction velocity in the corticospinal tracts. In these subjects the motor conduction velocity in the cauda equina, between the first lumbar (L1) and fourth lumbar (L4) vertebral levels, was 57.9 +/- 10.3 m/s. In four of five patients with multiple sclerosis, all with corticospinal signs in the legs, motor conduction velocity between C6 and L1 was slowed (41.8 +/- 16.8 m/s), but cauda equina conduction was normal (55.8 +/- 7.8 m/s). Similar slowing of spinal cord motor conduction was found in a patient with radiation myelopathy. This method should provide a relevant, simple clinical test in patients with spinal cord disease.

Adenocarcinoma↗
PubMed1985

Cerebellar degeneration in dominantly inherited spastic paraplegia.

The clinical features of five affected members in three generations of a family with dominantly inherited Strumpell's spastic paraplegia are described, together with the pathological findings in two cases. The late presentation and slow progression of the disease encompass features of the types I and II of other authors illustrating the heterogeneous expression of the disorder. Cerebellar involvement was evident clinically and pathologically.

Cerebellar Ataxia↗
PubMed1985

Morbidity and mortality in motor neuron disease: comparison with multiple sclerosis and Parkinson's disease: age and sex specific rates and cohort analyses.

The cause of motor neuron disease (MND) remains unknown although recent reports have suggested a possible rise in mortality rate. The present account describes age-specific patterns in morbidity rate and cross-sectional and cohort analyses of mortality rate, and compares these with those in multiple sclerosis and Parkinson's disease. First hospital admission rate for motor neuron disease (a proxy for incidence rates) rose steadily with age in males and females until the age of 75 years or more, but then fell, but only in females. This irregular pattern suggested the possibility of an environmental effect on certain older birth cohorts. The validity of the results was supported by a similar pattern in the two hospital regional authorities studied and the difference between this pattern and that found in multiple sclerosis and Parkinson's disease. Age-specific mortality rates of motor neuron disease between 15 and 64 years for males and females in England and Wales from 1940 to 1982 rose steadily with age. Mortality rates after the age of 65 fell in all female cohorts studied, but only in the earlier male cohorts. Unlike Parkinson's disease there was no strong birth cohort effect. However an analysis of Office of Population Censuses and Surveys (Registrar General) reports has revealed a slight increase in the age-specific mortality rate in both males and females aged 65 and over for successive birth cohorts born since 1900. Neither changes in ICD coding or in diagnostic habits could account for this pattern, which differed from that seen in Parkinson's disease. No such effect was seen in multiple sclerosis.

Adult↗