Changes In Nerve Conduction Velocity Research Articles

PERIPHERAL NEUROPATHY IN SYSTEMIC LUPUS ERYTHEMATOSUS ‐ A LONGITUDINAL STUDY

Objective ‐ Peripheral neuropathy (PN) is reported to occur in 5–27% of patients with systemic lupus erythematosus (SLE) mostly as a length‐dependent sensorimotor axonopathy. Studies over time have not been performed. Design ‐ Longitudinal study. Subjects and methods ‐ Thirty‐three Caucasian SLE patients consented to participate in the study and were subjected to clinical examination, laboratory tests, and nerve conduction velocity (NCV) studies. At the follow‐up 7 years later, 7 patients (21%) were dead, 4 refused to participate, and 2 did not want to perform NCV studies. Twenty patients were thus available for longitudinal study. Results ‐ When all SLE patients were considered on a group basis at follow‐up, 8 (33%) out of 24 NCV parameters showed significant deterioration despite correction for time, while 16 (67%) were unchanged. Analysis of change from baseline showed that, except for F ‐responses, several NCV changes were highly dependent (negative regression coefficients) on baseline levels at start of study. No demographic, laboratory, or disease associated quantitative factor was associated with these changes in NCV parameters over time. Nor was a consistent effect on NCV parameters from any qualitative demographic or disease associated factor confirmed by Repeated Measures ANOVA analyses. Conclusions ‐ A modest progressive neuropathic process exists in patients with SLE. Important is also the finding that, over time, the abnormalities of NCV parameters fluctuate in the individual patients, and the impairments are not necessarily irreversible. This study also shows no association to medication, demographic‐, or other disease associated factors.

Acetyl-L-Carnitine (Levacecarnine) in the Treatment of Diabetic Neuropathy

To assess the efficacy and tolerability of acetyl-L-carnitine (levacecarnine; LAC) versus placebo in the treatment of diabetic neuropathy, mainly by evaluating the effects of treatment on electrophysiological parameters and pain symptoms. This was a multicentre (n = 20), randomised, double-blind, placebo-controlled, parallel-group study. 333 patients meeting clinical and/or neurophysiological criteria for diabetic neuropathy were enrolled. Patients were randomised to treatment with LAC or placebo. LAC (or placebo) was started intramuscularly at a dosage of 1000 mg/day for 10 days and continued orally at a dosage of 2000 mg/day for the remainder of the study (355 days). MAIN OUTCOME PARAMETERS AND RESULTS: The main efficacy parameter was the effect of treatment on 6- and 12-month changes from baseline in nerve conduction velocity (NCV) and amplitude in the sensory (ulnar, sural and median) and motor (median, ulnar and peroneal) nerves. The effect of treatment on pain was also evaluated by means of a visual analogue scale (VAS). Among the 294 patients with impaired electrophysiological parameters at baseline, those treated with LAC showed a statistically significant improvement in mean NCV and amplitude compared with placebo (p < 0.01). The greatest changes in NCV (at 12 months) were observed in the sensory sural nerve (7 m/sec in the LAC group vs +1.0 m/sec in the placebo group), sensory ulnar nerve (+2.9 vs +0.1 m/sec, respectively) and motor peroneal nerve (+2.7 vs -0.2 m/sec), whereas the greatest changes in amplitude were recorded in the motor peroneal nerve (+2.2 vs +0.1 mV). After 12 months of treatment, mean VAS scores for pain were significantly reduced from baseline by 39% in LAC-treated patients (p < 0.0 vs baseline) compared with 8% in placebo recipients. LAC was well tolerated over the study period. LAC was effective and well tolerated in improving neurophysiological parameters and in reducing pain over a 1-year period. LAC is, therefore, a promising treatment option in patients with diabetic neuropathy.

Peripheral neuropathy in systemic lupus erythematosus--a longitudinal study.

Peripheral neuropathy (PN) is reported to occur in 5-27% of patients with systemic lupus erythematosus (SLE) mostly as a length-dependent sensorimotor axonopathy. Studies over time have not been performed. Design - Longitudinal study. Thirty-three Caucasian SLE patients consented to participate in the study and were subjected to clinical examination, laboratory tests, and nerve conduction velocity (NCV) studies. At the follow-up 7 years later, 7 patients (21%) were dead, 4 refused to participate, and 2 did not want to perform NCV studies. Twenty patients were thus available for longitudinal study. When all SLE patients were considered on a group basis at follow-up, 8 (33%) out of 24 NCV parameters showed significant deterioration despite correction for time, while 16 (67%) were unchanged. Analysis of change from baseline showed that, except for F-responses, several NCV changes were highly dependent (negative regression coefficients) on baseline levels at start of study. No demographic, laboratory, or disease associated quantitative factor was associated with these changes in NCV parameters over time. Nor was a consistent effect on NCV parameters from any qualitative demographic or disease associated factor confirmed by Repeated Measures ANOVA analyses. A modest progressive neuropathic process exists in patients with SLE. Important is also the finding that, over time, the abnormalities of NCV parameters fluctuate in the individual patients, and the impairments are not necessarily irreversible. This study also shows no association to medication, demographic-, or other disease associated factors.

Experimental disc herniation: evaluation of the natural course.

Changes in L7 nerve root conduction velocity and changes in appearance on magnetic resonance study of the L6-L7 intervertebral disc in the dog were assessed for 2-6 months after an experimental disc herniation was performed. To assess the time-related changes of nerve conduction velocity and magnetic resonance changes of the intervertebral discs. It is known that nucleus pulposus may induce nerve root morphologic and functional changes when applied epidurally. However, it is not known whether such changes are reversible. The spinal canal was opened by laminotomy of the upper part of the L7 lamina and the lower part of the L6 lamina on the left side. The L7 nerve root was gently retracted (sham) or the disc was punctured and injected with saline to produce herniation of the nucleus pulposus during the retraction time (herniation). After 1 day to 2 months, nerve root conduction velocity was determined by local electrical stimulation. Six dogs had the herniation or the sham procedure, and the L6-L7 disc was studied by magnetic resonance imaging at various times up to 6 months after the procedure. Decrease in nerve conduction velocity reached a maximum after 7 days and recovered to baseline level fully within 2 months. Although there was a clear reduction-recovery pattern, the difference in conduction velocity compared with that of the sham group was statistically significant after only 7 days. Disc degeneration started in the herniated discs within 7 days after the herniation procedure. However, none of the experimentally induced disc herniations were visualized by magnetic resonance imaging 7 days after the procedure. In no case was there subsequent nerve root compression. In one case, disc protrusion was visible 6 months after the herniation procedure. The results demonstrate for the first time that nucleus pulposus-induced nerve root injury reverses in 2 months and that it may be present without simultaneous nerve root compression, as confirmed by findings in magnetic resonance imaging. The previously described nucleus pulposus-induced nerve root changes may therefore be of clinical importance, and experimental studies of these mechanisms will probably be relevant for expanded understanding of the pathophysiologic mechanism behind sciatica that is caused by disc herniation.

The effect of 8 years of strict glycaemic control on peripheral nerve function in IDDM patients: the Oslo Study

We have investigated the effect of long-term strict glycaemic control on peripheral and autonomic nerve function in 45 IDDM patients (age 18–42 years, diabetes duration 7–23 years) without clinical signs of neuropathy or other neurological disease. They were randomly assigned to treatment either with continuous insulin infusion, multiple injections (4–6 times daily), or conventional treatment (twice daily) for 4 years and followed prospectively for 8 years. Motor and sensory nerve conduction velocities were measured at the start and after 8 years. Autonomic nerve function tests were performed only once, after 8 years. A significant reduction of nerve conduction velocity was observed during 8 years in patients with mean HbA1 more than 10% (n=12, group mean 10.9%, range 10.1–13.2%) compared to patients with HbA1 less than 10% (n=33, group mean 9.0%, range 7.5–9.9%). Change of motor nerve conduction velocity in the peroneal nerve was: −4.8±4.9 (SD) vs −2.2±5.3 m/s (p<0.01). Change of motor nerve conduction velocity in the posterior tibial nerve was: −6.8±5.7 vs −3.9±5.1 m/s (p<0.05). No significant changes were observed in the ulnar nerve. Change of sensoric nerve conduction velocity in the sural nerve was: −8.9±8.0 vs −4.6±5.3 m/s (p<0.05). Multiple regression analysis showed that a change in HbA1 of 1% resulted in a 1.3 m/s change in nerve conduction velocity during 8 years. A significantly lowered heart-rate variation during deep breathing (p<0.05) and heart-rate response to standing (p<0.01) was found in patients with HbA1 more than 10% compared to patients with HbA1 less than 10%. This study confirms that the long-term lowering of blood glucose retards the deterioration in nerve conduction velocity observed in the diabetic nerve.

Effect of a prostaglandin I 2 derivative (Iloprost) on peripheral neuropathy of diabetic rats

PGE 1 has been found to improve the symptoms of diabetic neuropathy. We considered that a PGI 2 derivative may also have a similar action and therefore studied its effect in diabetic rats. Iloprost was administered intraperitoneally to streptozotocin-induced diabetic rats at a dose of 10 μg/kg/day for a month. The changes in nerve conduction velocity (NCV) were measured in the tail. One day after the last dose of iloprost, both sciatic nerves were removed from each rat, homogenized, and extracted with 6% TCA. The sorbitol and myo-inositol concentrations were determined by a combination of HPLC and an enzymatic method. Cyclic AMP (cAMP) levels were determined by RIA, and Na +, K + ATPase activity was assessed by the enzyme cycling method of Greene and Lattimer. Iloprost was found to improve the NCV in the diabetic rats. The sorbitol content was not affected by iloprost, but the myo-inositol content was higher in the iloprost group than in the untreated group, although the difference was not statistically significant. The Na +, K + ATPase activity and cAMP content were significantly higher in the iloprost group than in the untreated group. These findings suggest the possibility that the cAMP-dependent protein kinase (A-kinase) system has an important influence on improvement in Na +, K + ATPase activity.

A comparison of magnetic and electrical stimulation of peripheral nerves

We compared magnetic stimulation using different coil designs (2 rounded coils and a butterfly-prototype coil) with electrical stimulation of the median and ulnar nerves in 5 normal subjects. Using magnetic stimulation we were able to record technically satisfactory maximal sensory and motor responses only with the butterfly coil. Submaximal electrical stimuli preferentially activated sensory rather than motor axons, but submaximal magnetic stimuli did not. The onset latency, amplitude, area and duration of responses elicited electrically or magnetically with the butterfly coil during routine sensory and motor nerve conduction studies were similar, and motor and sensory conduction velocities were comparable when studied over long segments of nerve. However, the motor conduction velocities with magnetic and electrical stimulation differed by as much as 18 m/sec in the across-elbow segment of ulnar nerve. Thus, recent developments in magnetic stimulator design have improved the focality of the stimulus, but the present butterfly coil design cannot replace electrical stimulation for the detection of focal changes in nerve conduction velocity at common entrapment sites, such as in the across-elbow segment of the ulnar nerve.

Distal Sensory Latencies of the Ulnar Nerve in Long Distance Bicyclists: Pilot Study

* This article is adapted from a paper written in partial fulfillment of the requirement for the Master of Science Degree, Duke University, Durham, NC 27710. Ulnar neuropathy, an overuse compression syndrome injury of the ulnar nerve at the wrist, is frequently associated with bicycling. Previous studies have shown that after severe compression injury to the ulnar nerve there is a change in nerve conduction velocity. The purpose of this study was to determine if long distance bicyclists have altered nerve conduction velocities due to repeated sustained compression of the ulnar nerve. This study compares the distal sensory latency period of the ulnar nerve in 15 controls and 10 long distance cyclists. The controls bicycled less than 10 miles per week on the average and the long distance cyclists bicycled an average of more than 100 miles per week. Results showed that there was a statistically significant difference (p < 0.002) in distal sensory latencies between long distance cyclists and the control group. However, there was no significant correlation (p > 0.10) between distance bicycled and latency. Results of this study lead to the belief that there may be adaptive changes in long distance cyclists which could account for changes in sensory nerve conduction velocity of the ulnar nerve.J Orthop Sports Phys Ther 1988;9(11):370-374.

An experimental study on nerve conduction velocities and biochemical parameters in lead-administered rats.

An experimental study was carried out to clarify the relationships between lead exposure and the changes in nerve conduction velocities or in por-phyrin metabolism in rats. The rats in Groups A, B and C received intraperitoneal lead injections in respective doses of 0, 0.2 and 2.0 mg/kg of lead, once a week for 22 weeks. During the experiment, all rats grew normally, and there was no signi-ficant difference in the group mean body weights. Lead concentrations in the blood and organs increased in these groups as the lead dose increased. Significant changes in nerve function and in biochemical indices relating to porphyrin metabolism were observed only in Group C treated with 2.0 mg/kg of lead, and not in the other groups. In Group C, urinary coproporphyrin and free erythrocyte protoporphyrin increased from an early stage, 4-6th week, of the lead administration, and urinary δ-aminolevulinic acid increased from the 8th week. Slight but significant slowing of conduction velocity in motor nerves appeared from the 10th week, when the rats had received lead injection 9 times in total. The change in distal motor latency occurred from the 16th week. No functional change in sensory nerves was ob-served in this study.

Electrophysiological Studies of Nerve Function in Patients on CAPD over Long Periods

The authors studied electrophyhsiological parameters in 29 patients (23 non-diabetics, six diabetics, mean age 47.9, range 16–74 yr.), who had been on CAPD for three to five years. The parameters studied were: motor nerve conduction velocities of the median, ulnar, and peroneal nerves, and sensory nerve conduction velocities of the median and ulnar nerves. These parameters were measured before or within the first month of CAPD and every six months thereafter. The changes in nerve conduction velocities were studied using simple linear regression analysis, and calculating the differences of the slopes from zero. Comparison of the mean values of the conduction velocities in non-diabetics at the beginning of CAPD and in age - matched, non uremic patients showed significantly (p &lt; 0.001) lower values in all parameters measured. The initial nerve conduction velocities in diabetic patients were significantly (p &lt; 0.01) slower than in non-diabetics except sensory conduction velocity of the ulnar nerve. The slopes of nerve conduction velocities plotted against time were not significantly different from zero for any nerve in both non-diabetics and diabetic patients. In conclusion, no significant change in peripheral nerve function was seen after long term CAPD in either diabetic or non-diabetic patients.

Acute and chronic implantation of coiled wire intraneural electrodes during cyclical electrical stimulation

The posterior tibial nerves of 18 rabbits were intraneurally implanted with coiled wire electrodes for up to 9 weeks to evaluate their usefulness for neuromuscular electrical stimulation. In one group an electrode was implanted and removed in one leg while the other leg was chronically implanted. A second group was chronically implanted without electrical stimulation in one leg and implanted with cyclical electrical stimulation applied through the electrode in the other leg. No significant changes in nerve conduction velocities between the time of implantation and up to 9 weeks post-implantation were observed in either the stimulated or the non-stimulated nerves. Little change in motor current threshold was observed beyond 10 days post-implantation. The nerves showed little or no histologic demyelination or denervation in most specimens, although in about 40% of the nerves, a bulbous formation of connective tissue was observed at electrode entry and exit sites with some demyelination in these regions. The spinal cords showed no histologic abnormalities in either group. The gastrocnemius and soleus muscles showed only occasional signs of denervation. One cat was implanted in both the posterior tibial and peroneal nerves of each leg for a 4-year period. Threshold current showed very little change during the implantation period. The nerves showed minimal focal demyelination at the electrode site and the muscles showed normal fibers.

Vitesses de conduction nerveuse motrice chez l'enfant: Valeurs normales et applications a quelques cas pathologiques

Nerve conduction velocity (NCV), according to age, was studied in normal children. Motor distal ulnar NCV (in 63 children, from 1 day to 4 years of age), motor distal tibial NCV (in 93 children, from birth to 15 years of age), proprioceptive tibial NCV (in 59 children, from birth to 5 years of age) and proximal CV (in 133 children from birth to 15 years of age), as well as VIIth superior branch CV (in 67 children) and XIIth CV (in 56 children) from birth to 3 years of age, were measured. These measurements showed that NCV changes were similar; NCV was 45-50% of the adult value during the first month of life. Then NCV increased very quickly, the progression being 90% of the first month's value during the first 18 months of life. The adult value was reached between 2 and 5 years of age. Proprioceptive NCV was 8-13 m/sec higher than motor NCV; proximal NCV was also 10-13 m/sec higher than distal motor tibial NCV. Ulnar NCV remained higher than tibial NCV, although changes in velocity as a function of age remained parallel. These NCV measurements proved significant in some diseases. The were useful for diagnosis of Krabbe's disease or of metachromatic leucodystrophy and to calculate the degree of disturbance in toxic polyneuritis, polyradiculoneuritis and some cranial nerve injuries; they were also useful in following up children undergoing chronic haemodialysis. In each case, NCV was only one aspect of a more complete neurophysiological study.

N-Hexane-induced changes in nerve conduction velocities and somatosensory evoked potentials.

Fifteen women from a shoe factory were examined clinically and their cerebral evoked responses to 256 electrical stimulations of the median nerve were averaged. Neurophysiological investigations included maximal motor (MCV) and distal sensory (dSCV) nerve conduction velocity measurement on ulnar, median, and peroneal nerves. A referent group was composed of 15 age-matched women without exposure to neurotoxic chemicals. MCVs and dSCVs of the exposed workers were significantly reduced vs referents, while P15 and N20 components of the somatosensory evoked potentials (SEP) showed an increased latency. A negative linear relationship was found between dSCV and P15 latency. However, two subjects with an abnormally low dSCV showed normal SEP latency, and two other subjects displayed abnormal SEP latency, while their dSCV was in the normal range. Therefore, SEP investigation may give additional information on nervous system function, even in subjects with peripheral neuropathy. The later SEP components were much flatter in the exposed than in the referent group, suggesting some neurotoxic effects of n-hexane on the central nervous system too.

Changes in nerve conduction velocity after six weeks of glucoregulation with portable insulin infusion pumps

Changes in nerve conduction velocity after six weeks of glucoregulation with portable insulin infusion pumps

A neurological and biochemical study of early lead poisoning.

ABSTRACT Changes in nerve conduction velocity were found in 94 workers exposed to lead in a battery factory compared with 94 age-matched controls. There was no clinical evidence of nerve damage in the lead workers. The mean blood lead concentration in the 94 lead workers was 2·9 μmol/l (60 μg/100 ml) and their length of exposure to lead ranged from 6 months to 33 years. All mean maximum motor nerve conduction velocities (MMCV) measured were highly statistically significantly lower in the lead-exposed group when compared with their age-matched controls. Thus mean ulnar MMCV was 53·4 m/s in lead workers and 55·6 m/s in control subjects (p The amplitude of the muscle action potential produced by proximal stimulation of a nerve was expressed as a percentage of the amplitude of the muscle action potential produced by distal stimulation and the percentage amplitude thus obtained used as an indicator of the conduction velocity of slower fibres (SFCV). Peroneal nerve percentage amplitude of lead workers was statistically significantly lower (p There was no statistically significant correlation to indicate that progressive slowing of nerve conduction (MMCV and SFCV) was associated with increasing exposure to lead (as indicated by blood and urine lead concentrations) or with the commonly measured biochemical changes associated with disturbed haemopoiesis in lead exposure (δ-aminolaevulinic acid dehydrase; free erythrocytc protoporphyrin; haemoglobin and urinary δ-aminolaevulinic acid). MMCV of the ulnar nerve was the only conduction velocity statistically significantly correlated with length of exposure to lead. Increased length of exposure to lead was associated with a decrease in the ulnar MMCV. Only 13 of the subjects had been exposed to lead for two years or less and in none of them had the blood lead ever risen above 3·9 μmol/l (80 μg/100 ml) in three-monthly tests (mean blood lead concentration at time of testing: 2·8 μmol/l). In these subjects the MMCV of ulnar, radial, and peroneal nerves and the peroneal percentage amplitude were statistically significantly reduced. The results from this group suggest that the onset of nerve conduction changes occurs within two years and at concentrations of lead in blood of less than 3·9 μmol/l (80 μg/100 ml).

Effect of acute and chronic misonidazole administration on peripheral-nerve electrophysiology in mice.

I.p. administration at several dose levels over periods of up to 12 weeks, or continuous i.v. infusion of high doses of misonidazole (MISO) for 15 h, produced no significant change in peripheral nerve conduction velocity (NCV) and did not prevent the normal increase in NCV as the animals matured from 12 to 24 weeks of age. Peripheral NCV (sural nerve) was reduced in both MISO-treated and control mice with hind-limb tumour implants, presumably owing to physical pressure due to tumour growth. In addition, neither the medial nerves nor the tibial nerve in the normal limbs of the tumour-implanted, drug-treated animals showed any change. Consequently our earlier and present studies do not confirm the recent reports of changes in NCV following either acute or chronic MISO administration to mice.

Dietary myo-inositol intake and peripheral nerve function in diabetic neuropathy

The effect of variations in dietary myo-inositol intake upon plasma myo-inositol concentrations, urinary myo-inositol excretion, motor nerve conduction velocities in the median and peroneal nerves, and sensory nerve conduction velocities in the median and sural nerves was studied in six nondiabetic subjects and in twenty patients with symptomatic distal symmetrical diabetic polyneuropathy. Diets were developed which provided either a low, a normal, or a high intake of myo-inositol. In control subjects, the low- myo-inositol diet was found to decrease, while the high- myo-inositol diet increased both the preprandial plasma myo-inositol concentrations and the daily urinary excretion of myo-inositol. These diets had little effect upon measured nerve function in the control subjects, although the high- myo-inositol diet appeared to slightly reduce the median sensory nerve conduction velocity in this group. In the neuropathic diabetics, the low- and high- myo-inositol diets were found to have similar effects upon the plasma myo-inositol concentrations and urinary myo-inositol excretion, but did not affect the plasma glucose concentrations. When analyzed by groups, no statistically significant changes were observed in any of the measured nerve conduction velocities in the diabetic patients. However, when the change in nerve conduction velocity was analyzed, it was found that the ingestion of the high- myo-inositol diet resulted in a statistically significant increase in the median sensory (+1.92 m/sec, p < 0.001) and the sural sensory nerve conduction velocity (+6.67 m/sec, p < 0.001). In contrast, ingestion of the low- myo-inositol diet produced a statistically significant decrease in the median motor (−2.35 m/sec, p < 0.001) and the peroneal motor nerve conduction velocity (−1.18 m/sec, p < 0.001). Thus, ingestion of a diet enriched in myo-inositol may have a salutory effect upon peripheral nerve function in the patient with symptomatic diabetic neuropathy and appears to be without significant side effects in this patient group.

Changes in nerve conduction velocity in the mouse after acute and chronic administration of nitroimidazoles

The effect of the nitroimidazoles misonidazole, Ro-05-9963, RGW-608 and metronidazole on nerve conduction velocity (NCV) were measured in the anaesthetized mouse. The compounds were administered by i.p. injection either as a single dose of 1 mg/g (only 0.5 mg/g for RGW-608) or in 36 fractions of 0.15 mg/g over 18 days (only 4 fractions in 2 days for RGW-608). After single doses a reduction in nerve conduction velocity was seen with all the compounds except metronidazole, which had no significant effect. During chronic exposure, a reduction in NCV occurred towards the end of the course of injections. All compounds produced an effect, although RGW-608 was the most neurotoxic, giving the largest reduction in NCV after only 4 injections. After the end of chronic exposure to misonidazole, Ro-05-9963 and metronidazole, recovery to normal took 2-3 weeks.

Nerve Conduction Velocity

To the Editor. —The article, Nerve Conduction Velocity in the Assessment of Hypertension by Viskoper, Chaco, and Aviram (Arch Intern Med 128:574-575, 1971) concluded that conduction velocity can provide us with an objective measurable index of the severity of hypertension. Although one might think that this could be done more easily with a sphygmomanometer, the article does present an interesting attempt to correlate decreases in nerve conduction velocity with increases in blood pressure. However, I am concerned that two factors, which alter nerve conduction and which might play a role in changes in nerve conduction velocity in hypertensive patients, were not taken into account. First, it is well documented that nerve conduction velocity decreases with a decrease in nerve temperature. Henriksen 1 found that conduction velocity is reduced approximately 2.4 meters per second for each degree centigrade drop in temperature. Other investigators have reported a decrease in conduction velocity

Idiopathic polyneuritis: serial studies of nerve and immune functions

The clinical features of idiopathic polyneuritis in 22 patients admitted to the University of Kentucky Medical Center between July 1965 and June 1970 are described. Serial studies of peripheral nerve function in 12 patients followed to clinical recovery showed changes in nerve conduction velocity, distal motor latency, and/or muscle action potential amplitude. Six children and one adult, showing a change in all three parameters, exhibited a strong correlation between the degree of slowing and the shortness of their illness. Assessment of immune status, by quantitative measurement of cerebrospinal fluid immunoglobulin G(11 patients) and by the degree of lymphocyte transformation on exposure to specific brain protein and/or a homogenate of sciatic nerve (10 patients), bore no consistent relation to the severity or course of the illness. A double-blind trial of short-term, high dose adrenocorticotrophic hormone has yielded no valid evidence to date for or against the effectiveness of such therapy in this illness.