Neurophysiological markers of central and peripheral involvement of the nervous system in HIV-infection.

Peroneal motor and sural sensory conduction velocities (MNCVs/SNCVs), somatosensory evoked potentials to median nerve stimulation (MN-SEPs) and motor evoked potentials (MEPs) to transcranial stimulation were examined in 138 HIV-infected patients (in the different stages of the disease), 20 seronegative intravenous drug abusers (IVDAs), and 20 healthy subjects. Findings of peroneal MNCV slowing in patients ranged from 16% (asymptomatic HIV patients) to 63% (AIDS) and of sural SNCV slowing from 13% to 40%. Altered MN-SEPs ranged from 10% to 30%, and MEPs ranged from 44% to 72%, mostly due to a prolongation of the central motor conduction time (CMCT). All seronegative IVDAs showed patterns within the normal range. Electrophysiological techniques were helpful in demonstrating early and subclinical alterations in HIV patients.     

Multimodality evoked potentials in motor neuron disease

We performed median and tibial nerve somatosensory evoked potentials (SEPs), pattern-shift visual evoked potentials (PSVEPs), and brain-stem auditory evoked potentials (BAEPs) on 27 patients with motor neuron disease (MND). Median and tibial nerve SEPs were abnormal in 8 (30%) of 27 and 3 (14%) of 21 patients tested, respectively. Central and peripheral abnormalities were recorded in the absence of spondylosis. As a group, patients with MND and no evidence of cervical spondylosis had normal conduction to Erb's point following median nerve stimulation, but conduction times beyond this point were prolonged. The PSVEPs and BAEPs were within normal limits in all patients, excluding abnormalities attributable to other disease, but the group P100 latency was significantly prolonged in the group with MND. The BAEPs were normal in the group with MND. This study provides neurophysiological evidence of sensory system involvement in MND.     

The value of ulnar somatosensory evoked potentials (SEPs) in cervical myelopathy

In 57 patients with clinical signs and surgical documentation of compressive myelopathy, ulnar nerve somatosensory evoked potentials (SEPs) were more sensitive (with 74% abnormal) than either median or tibial nerve SEPs. The most frequent abnormalities were reduced or absent neck evoked responses and prolonged central conduction time. All subjects who had an SEP abnormality were identified by combined tibial and ulnar SEPs. Median nerve SEP added no additional information. Normal ulnar and tibial nerve SEPs were also able to exclude major cord damage in patients with cervical radiculopathy but little evidence of myelopathy.     

Neurophysiological evaluation of central-peripheral sensory and motor pudendal fibres

Extensive neurophysiological investigations were carried out in 18 healthy volunteer subjects, and 6 patients with neurological disease. The tests consisted of spinal and scalp somatosensory evoked potentials (SEPs) to stimulation of the dorsal nerve of penis/clitoris, motor evoked potentials (MEPs) from the bulbocavernosus muscle (BC) and anal sphincter (AS) in response to scalp and sacral root stimulation, and measurement of sacral reflex latency (SRL) from BC and AS. In the control subjects, the mean sensory total conduction time (sensory TCT), as measured at the peak of the scalp P40 wave was 40.9 msec (range: 37.8-44.2). The mean sensory central conduction time (sensory CCT = spine-to-scalp conduction time) was 27.0 msec (range: 23.5-30.4). Transcranial brain stimulation was performed by using a magnetic stimulator both at rest and during voluntary contraction of the examined muscle. Sacral root stimulation was performed at rest. Motor total conduction times (motor TCT) to BC and AS muscles were respectively 28.8 and 30.0 msec at rest, and 22.5 and 22.8 msec during contraction. Motor central conduction times (motor CCT) to sacral cord segments controlling BC and AS muscles were respectively 22.4 and 21.2 msec at rest, and 15.1 and 12.4 msec during contraction. The mean latencies of SRL were respectively 31.4 msec in the bulbocavernosus muscle and 35.9 msec in the anal sphincter. Combined or isolated abnormalities of SEPs, MEPs and SRL were found in a small group of patients with neurological disorders primarily or secondarily affecting the genito-urinary tract.     

The relations between long-latency reflexes in hand muscles, somatosensory evoked potentials and transcranial stimulation of motor tracts

In 15 normal subjects the latency of electrically elicited long-latency reflexes (LLRs) of thenar muscles was compared with somatosensory evoked potentials (SEPs) after median nerve stimulation and with the latencies of thenar muscle potentials after transcranial stimulation (TCS) of the motor cortex. Assuming a transcortical reflex pathway the intracortical relay time for the LLR was calculated to be 10.4 +/- 1.9 msec (mean +/- S.D.) or 8.1 +/- 1.6 msec depending on the experimental conditions. The duration of the cortical relay time is not correlated with the peripheral or central conduction times, with body size or arm length. If the LLRs of hand muscles are conducted transcortically the long duration of the cortical relay time suggests a polysynaptic pathway.     

Neuromuscular consequences of prolonged hunger strike: an electrophysiological study.

OBJECTIVES: The purpose of this study was to determine the electrophysiological consequences of neuromuscular and central nervous system involvement in a group of patients presented with the neurological complications of a long-term hunger strike (HS). METHODS: Motor and sensory nerve conduction (NCV), F wave, somatosensory evoked potential (SEP) and motor evoked potential (MEP) studies were performed in 12 male and 3 female patients (mean age: 29.4) following HS. RESULTS: All patients whose weight loss was 11-31 (mean: 22.8) kg after 69-day HS, had neurological findings consistent with Wernicke's encephalopathy or Wernicke-Korsakoff syndrome. Abnormally prolonged latency and/or low amplitude sensory nerve action potentials were found in 7 patients. The amplitudes of compound muscle action potentials were significantly reduced in ulnar, median and tibial motor NCV studies as compared to the controls. F waves elicited by median nerve stimulation at wrist and muscle responses evoked by cervical and lumbar magnetic stimulation had significantly prolonged latencies. MEPs recorded from the lower extremities showed a slight prolongation in central conduction times. The cortical response latencies were prolonged in tibial SEPs. CONCLUSIONS: The most prominent finding in this patient group was the low amplitude of CMAPs elicited in motor NCV studies which was concluded to be resulted from the reversible muscular changes. The other electrophysiological findings suggested that peripheral nerves and long central nervous system pathways were also mildly involved.     

Nerve, spinal cord and brain somatosensory evoked responses: a comparative study during electrical and magnetic peripheral nerve stimulation.

Somatosensory evoked potentials (SEPs) and compound nerve action potentials (cNAPs) have been recorded in 15 subjects during electrical and magnetic nerve stimulation. Peripheral records were gathered at Erb's point and on nerve trunks at the elbow during median and ulnar nerve stimulation at the wrist. Erb responses to electrical stimulation were larger in amplitude and shorter in duration than the magnetic ones when 'electrical' and 'magnetic' compound muscle action potentials (cMAPs) of comparable amplitudes were elicited. SEPs were recorded respectively at Cv7 and on the somatosensory scalp areas contra- and ipsilateral to the stimulated side. SEPs showed a statistically significant difference in amplitude only for the brachial plexus response and for the 'cortical' N20-P25 complex; differences were not found between the magnetic and electrical central conduction times (CCTs) or for the peripheral nerve response latencies. Magnetic stimulation preferentially excited the motor and proprioceptive fibres when the nerve trunks were stimulated at motor threshold intensities.     

Central motor and sensory conduction in X-linked recessive bulbospinal neuronopathy.

Central conduction was studied in 12 patients with X-linked recessive bulbospinal neuronopathy (XBSN) using percutaneous electrical cortical, cervical and lumbar stimulation and somatosensory evoked potentials (SEPs). The central motor conduction time from the motor cortex to the cervical and lumbar segments of the spinal cord was normal in XBSN. SEPs, however, were abnormal or central sensory conduction time was prolonged in patients with XBSN. These results are consistent with the clinicopathological findings of XBSN in which the primary sensory neurons are involved as well as the lower motor neurons in the CNS, whereas the upper motor neurons are well preserved.     

Time course of frontal somatosensory evoked potentials. Relation to L-dopa plasma levels and motor performance in PD.

OBJECTIVE: To verify whether the change in L-dopa plasma levels after a single dose of carbidopa/L-dopa 50/200 (controlled-release) transiently modifies frontal components of somatosensory evoked potentials (SEPs) in patients with PD in parallel with improvement of motor performance. BACKGROUND: Apomorphine, a potent dopamine-agonist drug, transiently increases frontal SEP components, which may be depressed in PD; however, relationships between clinical status, frontal SEPs, and therapy are still unclear. METHODS: Nineteen PD patients (mean age 65.9 years, range 52 to 77, responders to L-dopa therapy, were studied in the same day at times T0 (baseline predose level), T1 (presumed L-dopa peak time), and T2 (end of dose-induced motor response). The following were monitored: L-dopa plasma concentration, tapping test, reaction times, peak latency (with central conduction times), and amplitude of cervical, subcortical, as well as cortical parietal and frontal SEP components elicited by median nerve stimulation of the more clinically affected arm. RESULTS: The average amplitude of frontal components of PD patients was significantly reduced at T0 with respect to control subjects. A significant and transient amplitude increase of frontal SEPs was found at T1, in parallel with the L-dopa peak concentration and improvement in motor performance (tapping and reaction times), without significant changes in amplitude of parietal SEP waves. No latency shifts were observed in brain and spinal waves. CONCLUSIONS: L-Dopa may influence the responsiveness of the parkinsonian brain as assessed by frontal somatosensory evoked potentials. The time course of these modifications coincides with that of the clinical response in the motor performance.     

Antiepileptic drug effects on somatosensory evoked potentials

Some evoked potential changes have been documented in chronic phenytoin (PHT), valproate (VPA), or benzodiazepine therapy, whereas other studies have suggested little change with carbamazepine (CBZ) or phenobarbital (PB). We recorded median and posterior tibial nerve somatosensory evoked potentials (SEPs) in complex partial seizure patients taking PHT, CBZ, or VPA in monotherapy with stable therapeutic serum levels and no toxic symptoms. Ten patients each were studied with PHT, CBZ, and VPA and were compared with age-matched controls. Median nerve responses were recorded at Erb's point, cervical spine, and contralateral cerebral sites; tibial nerve evoked potentials were recorded from popliteal fossa, lumbar, cervical spine, and midline scalp electrodes. Epileptic patients and controls did not differ in SEP latency, amplitude, or central condition time. PHT prolonged Erb's point and popliteal fossa latencies, but not central conduction time. CBZ had no effect on latencies or amplitudes. Evoked potential amplitudes were reduced by VPA, and cortical response latencies were minimally prolonged. Chronic antiepileptic therapy without toxicity had little effect on SEPs. PHT may have a slight effect on peripheral nerve conduction, and VPA may have an effect on amplitude of cerebral responses.     

Central vs peripheral nerve conduction. Before and after treatment of subacute combined degeneration

Central and peripheral nerve conduction was studied in two patients with subacute combined degeneration by using the short-latency somatosensory evoked potentials and the peripheral nerve conduction study during treatment with cyanocobalamin. Before the treatment, somatosensory evoked potentials with median nerve stimulation were normal, but those with peroneal nerve stimulation revealed prolonged central conduction indicating dysfunction within the posterior column. Peripheral sensory and motor nerve action potentials were reduced with normal or slightly reduced conduction velocity. After treatment, marked shortening of the central conduction time (by 24% and 31%, respectively) was observed with mild or no recovery of peripheral nerve action potentials. These physiologic findings suggest that the main pathologic changes in the central nervous system may be demyelination in the posterior column in addition to axonal degeneration in the peripheral nerve. The former was responsive to treatment but the latter was poorly responsive to treatment. Sensory symptom in subacute combined degeneration appears to be, at least partially, attributed to the spinal cord lesion.     

Retrograde effects of digital nerve severance on somatosensory evoked potentials in man

To determine if retrograde conduction changes might occur long after injury of the most distal peripheral nerves, short-latency somatosensory evoked potentials (SEPs) to median or ulnar nerve stimulation at the wrist were studied in 10 subjects who had sustained traumatic digit amputation 4 months to 15 years previously. SEPs were recorded from Erb's point (N9), the cervical region (N13), and the contralateral scalp hand area (N20). While N9 latency was slightly delayed or not affected, the amplitude was either markedly reduced or undetectable. For N13 and N20 components, latency prolongation and amplitude reduction were mild to moderate, but the central conduction time (N13–N20) remained normal. The present data indicate that even the most distal nerve injury may have profound long-term retrograde effects on parental nerve function which are presumed mainly due to an axonopathy. © 1994 John Wiley & Sons, Inc.     

Clinical and electrophysiological studies of human immunodeficiency virus-seropositive men without AIDS

Motor weakness and ataxia of lower limbs and abnormalities of somatosensory evoked potentials occur in many patients with the acquired immunodeficiency syndrome (AIDS). We studied 15 human immunodeficiency virus-seropositive subjects without AIDS and found no clinical neurological abnormalities. The mean latency of the brainstem auditory evoked potential (peak V) was increased, suggesting a central defect. Despite normal peripheral nerve conduction along the tibial nerve, the mean latency of the spinal cord potential of the twelfth thoracic vertebra was increased compared with normal, possibly indicating an incipient conduction defect at or near the spinal root ganglion or lumbar spinal cord.     

Somatosensory evoked potentials in chronic acquired demyelinating peripheral neuropathy

We recorded somatosensory evoked potentials (SEPs) over the scalp in eight patients with chronic acquired demyelinating peripheral neuropathy. They were obtained from 15 nerves in which sensory nerve action potentials (SNAPs) were absent or not more than 1 microV, but from which motor responses could be elicited. Motor and sensory (SEP-derived) conduction velocity was determined from the difference in response latency with wrist and elbow stimulation. In 11 nerves, afferent conduction velocity was slowed. In 10, there was relatively equal slowing in sensory and motor axons, whereas in 1 there was disproportionate slowing in afferent fibers. In four nerves, afferent conduction velocity was within the normal range despite slowing of motor conduction. We conclude that SEPs may be useful in evaluating peripheral sensory conduction in the absence of SNAPs, but can provide misleadingly normal data, presumably because of central amplification of an attenuated response arising from a few axons that conduct normally.     

Multimodal evoked potentials in human immunodeficiency virus infection

We have studied 95 HIV seropositive patients (77 males and 18 females; mean age: 31 years): 67 had no neurological symptoms or signs, 28 had various neurological symptoms and signs. This study included a full multimodal evoked potentials (MEP) assessment: visual evoked potentials by flash and reversal checkerboard; brainstem auditory evoked potentials; somatosensory evoked potentials obtained by stimulation of the median nerve. Patient evaluation further included: electroencephalography, electromyography with measurement of conduction velocities and neuroimaging (brain CT scan and/or MRI). We found abnormal MEP for all modalities. The prevalence of abnormal results was high in neurological symptomatic patients; in non neurological ones, the changes tended to be more frequent with the progression of the HIV infection. Whatever the stage of the disease, the various modes were equally affected. MEP were abnormal in 54.7 p. 100 of the cases: in 41.8 p. 100 (28/67) of patient without neurological signs (in 4/12 of fully asymptomatic subjects, 11/34 ARC patients and 13/21 AIDS patients) vs 85.7 p. 100 of neurological symptomatic patients. In neurological asymptomatic patients, a similar proportion of abnormal MEP was found in asymptomatic and ARC patients, while the evolution into AIDS was associated with a higher prevalence of abnormal MEP. In the latter group, MEP changes were nearly as frequent as in neurological symptomatic patients. Comparison between MEP and other electrophysiological procedures (EEG, EMG) and with neuroimaging techniques (CT Scan, MRI) showed the high sensitivity of the MEP technique at all stages of the disease. EMG was a sensitive method and complementary to MEP. The EEG and neuroimaging techniques showed abnormalities principally at the neurological symptomatic stage. Previous studies could not be properly compared.(ABSTRACT TRUNCATED AT 250 WORDS)     

Multimodality evoked potentials in progression of metachromatic leukodystrophy

A 2-yr-3-mo-old girl with metachromatic leukodystrophy (MLD) was examined using serial multiple electrophysiological procedures. Sensory nerve conduction velocity was delayed earlier and more severely than motor nerve conduction velocity. Visual evoked potentials (VEPs) showed prolonged latency of wave IV. Auditory brainstem responses (ABRs) showed prolonged latency of waves I and V, and the I-V interval. As to the interpeak latency of somatosensory evoked potentials (SEPs), the P9-P14 and the P14-N20 intervals were prolonged on admission. Two months later, both intervals were more prolonged, but the prolongation of the P9-P14 interval was the most prominent. The demyelination in our case may have started in the cerebral white matter, progressed to the peripheral nerves, and at last via the spinal root reached the brainstem. An electrophysiological follow-up study may be valuable in the understanding of the progressive pathological changes and in the evaluation of therapeutic measures.     

Abnormalities of multimodality evoked potentials in amyotrophic lateral sclerosis

Thirty-two patients with amyotrophic lateral sclerosis were studied with somatosensory evoked potentials (SEPs), visual evoked potentials, and brain-stem auditory evoked potentials. H-reflexes were used to screen for abnormalities of peripheral nerve conduction. Nineteen patients (59%) showed an abnormality of lower extremity SEPs. In 13 patients (40%) the delay was of central origin, while in six patients (19%) peripheral conduction delay was possible. Abnormality of upper limb SEPs was seen in 11 patients (34%), all but two of whom had abnormal lower limb SEPs as well. Four patients (12%) had abnormal brain-stem auditory evoked potentials, all of whom had abnormal SEPs from upper and lower limbs. Four patients had abnormal visual evoked potentials, which in three patients were of minor degree. These results give physiologic evidence to suggest that abnormalities in amyotrophic lateral sclerosis occur outside the motor system.     

Somatosensory evoked potentials following nerve and segmental stimulation do not confirm cervical radiculopathy with sensory deficit.

Twenty eight patients with unilateral cervical radiculopathy were studied by somatosensory evoked potentials (SEPs) from nerve stimulation at the wrist and from skin stimulation at the first, third or fifth finger depending on the root involved. In order to evaluate the reliability of various "radicular SEP patterns" as described in the literature, absolute latencies and side-to-side differences of the brachial plexus component from the supraclavicular fossa (N9), the medullary component (N13) from the cervical vertebra Cv7, and the primary cortical component (N20, P25) were assessed. Side-to-side differences of the amplitudes of N20/P25 and of the conduction times across the intervertebral fossa (interval N9-N13) were analysed. After nerve stimulation, 68% of the patients had false negative findings on the symptomatic, while 36% had positive findings on the asymptomatic side. After segmental stimulation, 72% of the patients had false negative findings on the symptomatic, while 22% had positive findings on the asymptomatic side. It is concluded that SEPs following nerve and segmental stimulation do not reliably confirm clear-cut already established diagnoses of unilateral radiculopathy with sensory and motor deficit. Therefore, they will not be helpful in the electrophysiological investigation of cervicobrachialgias of unknown origin.     

Neurophysiological testing in anorectal disorders

The neurophysiological techniques currently available to evaluate anorectal disorders include concentric needle electromyography (EMG) of the external anal sphincter, anal nerve terminal motor latency (TML) measurement in response to transrectal electrical stimulation or sacral magnetic stimulation, motor evoked potentials (MEPs) of the anal sphincter to transcranial magnetic cortical stimulation, cortical recording of somatosensory evoked potentials (SEPs) to anal nerve stimulation, quantification of electrical or thermal sensory thresholds (QSTs) within the anal canal, sacral anal reflex (SAR) latency measurement in response to pudendal nerve or perianal stimulation, and perianal recording of sympathetic skin responses (SSRs). In most cases, a comprehensive approach using several tests is helpful for diagnosis: needle EMG signs of sphincter denervation or prolonged TML give evidence for anal motor nerve lesion; SEP/QST or SSR abnormalities can suggest sensory or autonomic neuropathy; and in the absence of peripheral nerve disorder, MEPs, SEPs, SSRs, and SARs can assist in demonstrating and localizing spinal or supraspinal disease. Such techniques are complementary to other methods of investigation, such as pelvic floor imaging and anorectal manometry, to establish the diagnosis and guide therapeutic management of neurogenic anorectal disorders.     

Electrophysiological evaluation of genito-sphincteric dysfunction in multiple system atrophy

Thirteen patients with multiple system atrophy underwent multimodality neurophysiological evaluation, including sphincteric needle electromyography (EMG), sacral reflexes, pudendal nerve terminal latency, pudendal (PSEPs) and tibialis posterior nerve somatosensory evoked potentials (TPSEPs), and perineal motor evoked potentials (PMEPs). EMG revealed denervation or neurogenic changes, with reduction in spontaneous tonic activity at rest and abnormal pudendal nerve terminal latency in 10 patients (76.9%); anal reflex was delayed in 7 patients (53.8%). TPSEPs scalp responses were clearly abnormal in 4 patients (30.7%), whereas PSEPs exhibited changes in 9 (69.2%): in 6 patients responses were delayed at lumbar level (46.2%), and in 5 over the scalp (38.4%). PMEPs showed an increase in latency with a mild prolongation of central motor conduction time (CMCT) in 2 cases (15.3%); 1 patient had prolonged latencies following both cortical and sacral stimulation, but a normal CMCT. Even if diagnostic yield is not improved using these investigations they provide evidence of multiple lesion sites other than Onuf's nucleus.