SUMMARY Clinical tests of thermal sensation are poorly quantified and not strictly modality specific. Previous automated thermal testing systems have had limited usefulness with high intraand 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°C (SD = 0.06°C) and the mean cold threshold 0 15°C (SD = 0.05°C). Repeated determinations showed a maximum of 5% intra-individual variation in comparison to previously reported values of up to 150%. through the element to maintain background skin temperature, allowing the heat pumping capacity of the thermode to be reserved exclusively for the test studies.6Simple measurements of thresholds were superseded by the "Marstock method" where the temperature interval between the perceptual thresholds for warm and cold stimuli was defined as the most sensitive index of neural abnormality.79 In this interval, the "warm-cold difference limen", no thermal sensation is appreciated. These short-term studies were repeated over periods of minutes but longer term studies repeated over days showed an unsatisfactory intra-individual variation of up to 150% between estimations.'0 This variability was attributed to central processing mechanisms although variation due to patient bias and reaction time had not been excluded.The most recent studies have used automated control systems to operate the Peltier element and
Barwick, 1974;Lenman and Ritchie, 1976), the increase in motor unit muscle fibre densities (Stalberg et al., 1975) and anatomical territories (Erminio et al., 1959) are the electrophysiological signs of a relentlessly progressive denervation of the somatic musculature. Active reinnervation from surviving motor units is evident but inadequate to prevent the clinical and electrophysiological deterioration of the patient.The electrophysiological literature provides copious qualitative but little quantitative information on the electrophysiological changes in motor neurone disease. The purpose of the present paper is to present the results of the application of our computer assisted electrophysiological techniques Address for correspondence: Dr J. P. Ballantyne, Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF. Accepted 9 May 1978 for the quantitation of the number of motor units in the extensor digitorum brevis (EDB) muscle (Ballantyne and Hansen, 1974a) along with the measurements of the parameters of the surviving and electrically evoked motor unit potentials (MUPs) in the same muscle by a computer subtraction method (Ballantyne and Hansen, 1974b MethodsThe composition and placement of the surface recording electrodes over the EDB muscle, the properties of the stimulating electrodes over the anterior tibial nerve at the ankle, and the details of the rate and strength of stimulation used to evoke motor unit potentials have been described (Ballantyne and Hansen, 1974a
We have applied our technique for the measurement of thermal thresholds to 25 patients referred with symptoms and signs of small fiber peripheral neuropathy in whom conventional electrophysiological indices were individually within the range of normal values for our laboratory. Vibration threshold determinations were also within normal range. Significant abnormalities of thermal thresholds were noted in all patients. The results indicate that the technique provides an accurate, easily performed and reproducible index of function in small A delta and C groups of nerve fibers.
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.
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