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Biomedical subjects

J P Ballantyne

Publications and source records attributed to J P Ballantyne.

At least 19 recordsLinked to original sources
PubMed2002

A clinical neurological, neurophysiological, and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides.

OBJECTIVES: To classify clinical diseases of the subjects with abnormal indices of peripheral neuropathy identified in field studies of sheep farmers and dippers exposed to organophosphate pesticides. To explore what neuropsychological profiles, if any, may be associated with neurophysiological damage in these subjects. METHODS: A case-control study (79 subjects) nested within the cross sectional study (685 subjects) of sheep farmers from the field study. Three groups with no, possible, and probable or definite neuropathy according to field studies were recruited. Investigations comprised symptoms of neuropathy, neurologial signs, motor and sensory nerve conduction, electromyography, quantitative sensory testing, and neuropsychological tests. RESULTS: The incidence of clinical neuropathy increased from 7% in the no neuropathy group to 52% in the probable or definite neuropathy group based on nerve conduction measurements or presence of neurological signs. Sensory abnormalities were found more often than motor deficits. Small diameter nerve fibres were also affected more than large fibres. CONCLUSIONS: The neuropathy is predominantly sensory and is characteristic of distal, chronic neuropathy with no acute features. Small fibre populations are affected more than large fibre populations. Increasing severity of neuropathy was associated with anxiety and depression as measured in the neuropsychological tests.

Adolescent↗
PubMed2000

Complex regional pain syndrome with selective emotional sudomotor failure.

We report a patient with sympathetically maintained pain following a mild limb injury. Only emotional sudomotor failure was found in the painful limb. Thermoregulatory vasomotor function was intact. However, the patient had other target-specific sympathetic lesions, including thermoregulatory vasomotor failure in a different limb, not associated with pain. We hypothesize that the sympathetic failure preceded the symptoms and that the mild injury may have provoked collateral sprouting of emotional sudomotor fibres, coupling them with somatic sensory fibres to cause continuous pain.

Adolescent↗
PubMed1997

Selective defect of baroreflex blood pressure buffering with intact cardioinhibition in a woman with familial aniridia.

We report a symptomatic failure of the baroreceptor blood pressure (BP) buffering mechanism in a woman with familial aniridia. Her baseline BP oscillated at 0.1 Hz, the frequency of Mayer waves, with increased amplitude on standing without orthostatic hypotension. Although sudomotor function was normal, cutaneous thermoregulatory function and BP response to Valsalva's maneuver were abnormal. The defective BP buffer mechanism suggests Mayer waves could be a sympathetic mediated cardiovascular resonance. Baroreceptor cardioinhibition was intact. We presume that the lesion is in the rostral aspect of the dorsal medulla oblongata.

Adult↗
PubMed1989

Cerebral cortical potentials to pure non-painful temperature stimulation: an objective technique for the assessment of small fibre pathway in man.

In six healthy subjects cortical potentials were evoked by rapidly changing heating or cooling stimuli to the hand. Recordings were made from the contralateral scalp area overlying the sensori-motor cortex, referred to a frontal reference. The potential averaged from 25 stimuli comprised a large positive wave with a mean amplitude of 9.2, SD 1.1 microV for heat and 8.8 SD 1.2 micro V for cold stimulation. The heat evoked potentials had longer peak latencies (range: 280-350 ms) than those elicited by cold stimuli (range: 178-200 ms). A lower amplitude positive wave of a longer latency was also recorded to both modes of stimulation over the corresponding ipsilateral cortex. Cortical thermal evoked potentials were absent in two patients, one with severe selective small fibre neuropathy and the other with syringomyelia, both of whom had high thermal thresholds demonstrated by the technique of Jamal et al. Cerebral potentials evoked by thermal stimuli may represent an alternative approach to the investigation of the central projections of the human small fibre system with both clinical and research potential.

Adult↗
PubMed1988

The localization of the lesion in patients with acute ophthalmoplegia, ataxia and areflexia (Miller Fisher syndrome). A serial multimodal neurophysiological study.

Results of comprehensive serial neurophysiological tests from onset to full recovery in 3 patients with the Miller Fisher syndrome (acute ophthalmoplegia, ataxia and areflexia) are presented. These included EMG and nerve conduction, late response (H and F wave) and direct facial motor and blink reflex studies, computerized motor unit number estimation, automated quantitative sensory threshold measurements, quantitative pupillometric and pupillopharmacological studies and multimodality evoked potential (VEP, SEP and BAEP) and EEG recordings. The results provided unequivocal evidence of peripheral nerve dysfunction. Improvement of the peripheral neurophysiological parameters accompanied or followed clinical recovery in all 3 patients. No abnormality in the CNS pathways investigated by these tests was found. The findings support the conclusion that this syndrome is to be included within the spectrum of acute inflammatory polyneuropathy. The value of serial measurements in detecting milder peripheral nerve lesions is emphasized.

Acute Disease↗
PubMed1987

Nifedipine in the treatment of myotonia in myotonic dystrophy.

Abnormal calcium transport may be implicated in the membrane defect in myotonic dystrophy. A single blind crossover trial of placebo (t.i.d.), nifedipine 10 mg (t.i.d.) and nifedipine 20 mg (t.i.d.), was performed in 10 patients with myotonic dystrophy. The severity of myotonia was assessed by measuring finger extension time after maximum voluntary finger flexion. A significant improvement in myotonia, after nifedipine, was recorded by this technique and supported by a subjective improvement in 50% of patients and clinical improvement of greater than 20% in five patients. Initial grip strength and muscle fatiguability measured by grip strength ergometry were not significantly altered.

Clinical Trials as Topic↗
PubMed1986

Myotonic dystrophy. A reassessment by conventional and more recently introduced neurophysiological techniques.

A series of complementary neurophysiological investigations was carried out on 24 patients with myotonic dystrophy to determine the extent of nervous system involvement. Conventional electromyography and nerve conduction studies, computerized motor unit number estimation and motor unit potential analysis, vibration threshold studies and a recently introduced technique for heat and cold threshold estimations were undertaken in all patients. The results provide unequivocal evidence of widespread nervous system dysfunction. In many patients there is significant involvement of peripheral large diameter motor and sensory fibres and of small diameter sensory fibres either peripherally and/or centrally. In the light of these results and others reviewed in the literature, the concept of myotonic dystrophy as a pure myopathy can no longer be sustained.

Action Potentials↗
PubMed1985

An improved automated method for the measurement of thermal thresholds. 1. Normal subjects.

Clinical tests of thermal sensation are poorly quantified and not strictly modality specific. Previous automated thermal testing systems have had limited usefulness with high intra-and inter-individual variability. This paper describes an automated thermal system (Glasgow system) which is an extensive modification of previous techniques to answer these criticisms. It comprises a microprocessor-driven Peltier element and utilises the forced choice method of psychophysical analysis to determine the thresholds to thermal stimulation. In a control group of 106 healthy subjects the mean heat threshold for the wrist was found to be 0.23 degree C (SD = 0.06 degree C) and the mean cold threshold 0.15 degree C (SD = 0.05 degree C). Repeated determinations showed a maximum of 5% intra-individual variation in comparison to previously reported values of up to 150%.

Adolescent↗
PubMed1985

An improved automated method for the measurement of thermal thresholds. 2. Patients with peripheral neuropathy.

Thermal thresholds were determined by a new technique, at wrists and ankles in 143 patients with peripheral neuropathies of diverse aetiologies. Ninety-nine percent of patients (141/143) had abnormalities of one or both thresholds. In only two patients with mild/early Friedreich's ataxia were thermal thresholds normal. Electromyography was performed and fastest motor nerve conduction velocities and sensory nerve action potential parameters were measured in all the patients using conventional techniques in ulnar, median and sural nerves. Eighty-nine percent of patients (127/143) had one or more abnormalities on these electrophysiological studies. However, 39 of 40 patients with completely normal sensory nerve studies had an abnormality of one or more thermal thresholds. Eighty-six percent of 48 patients with normal sural nerve studies had abnormal thermal thresholds at the ankle. Sixty percent of 70 patients with normal sensory median and ulnar nerve studies had abnormal wrist thermal thresholds. This improved technique for the determination of thermal thresholds reveals that disturbances of thermal sensibility are present in the majority of peripheral neuropathies irrespective of aetiology. In some patients disturbances of thermal thresholds antedate the appearance of abnormalities on conventional electrophysiological investigation. The findings suggest that this technique has considerable usefulness in the detection of small nerve fibre dysfunction in the context of generalised neuropathy.

Adolescent↗
PubMed1985

Sensory involvement in motor neuron disease: further evidence from automated thermal threshold determination.

Thermal thresholds were determined in 40 patients with motor neuron disease and in 40 age- and sex-matched healthy subjects. The thermal thresholds were estimated on the skin of wrist and ankle using an automated microprocessor controlled system and the "two alternative forced-choice method" of psycholphysical analysis. Abnormalities of thermal thresholds (greater than or equal to 99th percentile) were seen in 80% of the motor neuron disease patients. The results are in agreement with reports of sensory pathway involvement in the literature. Thermal threshold abnormalities are common in motor neuron disease and indicate the involvement of the small fibre afferent pathways.

Adult↗
PubMed1982

Anterior horn cell dysfunction in Alzheimer's disease.

Electrophysiological studies were undertaken on 29 patients with Alzheimer's Disease. A reduction in the number of functioning motor units was found in the extensor digitorum brevis muscle. The electrophysiological parameters of the motor unit potentials were increased compared to control values. Four of seven muscle biopsies showed abnormalities ranging from mild to severe. The results suggest dysfunction in the lower motor neurone in this disease.

Aged↗
PubMed1982

A quantitative assessment of reinnervation in the polyneuropathies.

The severity of denervation and the extent of compensatory reinnervation in a number of neuromyopathies was investigated using our computer-assisted motor unit counting and subtraction techniques. Patients with the chronic neuropathies of diabetes mellitus, renal failure and alcoholism, the acute neuropathy of the Guillain-Barré syndrome, and the neuronopathies of motor neuron disease and Alzheimer's disease were studied. Reinnervation in the uremic and alcoholic neuropathies was poor, and considerably less than that found in diabetic neuropathy. In general, the neuronopathies showed better reinnervation than the chronic neuropathies. In the acute neuropathy of the Guillain-Barré syndrome, reinnervation continued over periods of up to 7 years from the onset of the illness. Within this group some patients showed poor reinnervation, whereas in others we found that all of the electrophysiological parameters studied returned to normal, with concomitant remodeling of previously large motor units to normal size as reinnervation progressed.

Alzheimer Disease↗