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Introduction: Chronic immune polyradiculopathies (sensory, motor, and mixed) are uncommon., Methods: In this single-center, retrospective study, the inclusion criteria for participants were progressive sensory ataxia and/or areflexic limb weakness; tibial somatosensory evoked potential (SSEP) abnormalities of the N22 and P40 potentials with normal sensory and motor nerve conduction studies or root involvement, according to magnetic resonance imaging (MRI); and albuminocytological dissociation., Results: Eight patients were included in our study. Two had weakness, two had sensory ataxia, and four had both weakness and ataxia. Patients with weakness had abnormal SSEPs and patients with sensory ataxia also had absent F waves. Electromyography showed chronic denervation. MRI scans confirmed thickening and enhancement of roots. The patients responded to corticosteroid treatment., Discussion: The overlapping clinicoelectrophysiological findings and similarities in radiological and therapeutic responses suggest that these entities are clinical variants of the same disease. The terms CIS(m)P, CI(s)MP, and CISMP (for chronic immune sensory motor polyradiculopathy) could be used to denote the predominant clinical involvement., (© 2020 Wiley Periodicals LLC.)

Introduction: We investigated the feasibility of motor unit number index (MUNIX) in quantitatively assessing motor root lesions and tracking different treatment outcomes in lumbosacral radiculopathy (LR)., Methods: Bilateral MUNIX was recorded from the abductor hallucis, extensor digitorum brevis, and tibialis anterior in 44 normal controls and 108 patients with LR, and this was repeated approximately 12 months after treatment in 60 patients with LR., Results: More abnormalities were observed when side-to-side differences of MUNIX measurements were used to evaluate LR (P < .05). Motor unit number index measurements worsened without progression of muscle weakness after conservative treatment, and MUNIX measurements improved with or without increased muscle strength after surgical treatment (P < .05)., Discussion: Motor unit number index may identify a specific L5 or S1 motor root lesion even before muscle weakness occurs, especially when side-to-side differences are used. Changes in MUNIX were larger than those in motor function measures after treatments for LR., (© 2020 Wiley Periodicals, Inc.)

Background: Radiculopathies caused by spinal stenosis in the upper lumbar spinal canal (L1/2, L2/3, L3/4) have not been comprehensively investigated., Methods: This retrospective study reviewed 14 patients from a tertiary hospital outpatient clinic. The inclusion criteria were upper lumbar stenosis seen on MRI and radiculopathies with active denervation confirmed on electromyography. Patients with any other conditions that could explain the clinical or electrophysiological manifestations were excluded., Results: Neurogenic findings were predominantly observed in L5 or S1 myotomes on electromyography. Abnormal spontaneous activity was observed in distal muscles in all patients and in proximal muscles in eight patients. Axonal involvement was bilateral in 10 patients and unilaterally in 4 patients. MRI showed redundant nerve roots in 13 patients with chronic reinnervation on electromyography., Conclusions: Upper lumbar spinal stenosis usually causes L5 or S1 radiculopathies with diverse patterns. This discrepancy may cause diagnostic confusion., (© 2020 Wiley Periodicals, Inc.)

Introduction: The rat tail exhibits functional impairment after cauda equina injury. Our goal was to better understand the innervation and roles of muscles that control the tail., Methods: Adult rats received either: (1) ventral root injury; (2) caudales nerve injury; or (3) mapping of sacrococcygeal myotomes. Activation of small muscles within the tail itself (intrinsics) was compared with that of larger lumbosacral muscles acting on the tail (extrinsics). Behavioral testing of tail movement was done 1 week later., Results: Rats that received ventral root injury exhibited multiple behavioral deficits, whereas rats with injury to caudales nerves maintained more fully preserved tail movement. Mapping studies revealed much broader overlap of myotomes for extrinsic muscles., Conclusions: Extrinsic tail muscles play a greater role in tail movement in the rat than their intrinsic counterparts and are innervated by multiple neurological segments. These findings have major implications for future research on cauda equina injury., (© 2014 Wiley Periodicals, Inc.)

Introduction: Sensory neuronopathy (SNN) mimics distal sensory axonopathy. The conventional H-reflex elicited by tibial nerve stimulation (tibial H-reflex) is usually abnormal in both conditions. We evaluated the proximally evoked soleus H-reflex in response to S1 nerve root stimulation (S1 foramen H-reflex) in SNN., Methods: Eleven patients with SNN and 6 with distal sensory axonopathy were studied. Tibial and S1 foramen H-reflexes were performed bilaterally in each patient., Results: Tibial and S1 foramen H-reflexes were absent bilaterally in all patients with SNN. In the patients with distal sensory axonopathy, tibial H-reflexes were absent in 4 and demonstrated prolonged latencies in 2, but S1 foramen H-reflexes were normal., Conclusions: Characteristic absence of the H-reflex after both proximal and distal stimulation reflects primary loss of dorsal root ganglion (DRG) neurons and the distinct non-length-dependent impairment of sensory nerve fibers in SNN., (Copyright © 2013 Wiley Periodicals, Inc.)

Peripheral nervous system involvement is common in Sjögren's syndrome (SS); however, polyradiculopathy has been reported rarely in association with SS, and predominantly chronic forms have been described. We describe a patient with clinical, cerebrospinal fluid, neurophysiological, and neuroradiological evidence of subacute inflammatory polyradiculopathy in whom Sjögren's syndrome was diagnosed after the onset of neurological symptoms. Our case suggests that SS should be included in the differential diagnosis of subacute inflammatory polyradiculopathy.

A detailed understanding of injury mechanisms in peripheral nerve fibers will help guide successful design of therapies for peripheral neuropathies. This study was therefore undertaken to examine the ionic mechanisms of Ca2+ overload in peripheral myelinated fibers subjected to chemical inhibition of energy metabolism. Myelinated axons from rat dorsal roots were co-loaded with Ca2+-sensitive (Oregon Green BAPTA-1) and Ca2+-insensitive (Alexa Fluor 594) dextran-conjugated fluorophores and imaged using confocal laser scanning microscopy. Axoplasmic regions were clearly outlined by the Ca2+-insensitive dye, from which axonal Ca2+-dependent fluorescence changes (FCa.ax) were measured. Block of Na+-K+ ATPase (ouabain), opening of Na+ channels (veratridine), and inhibiting energy metabolism (iodoacetate + NaN3) caused a rapid rise in FCa.ax to 96% above control after 30 min. Chemical ischemia (iodoacetate + NaN3) caused a more gradual increase in FCa.ax (54%), which was almost completely dependent on bath Ca2+, indicating that most of the Ca2+ accumulation occurred via influx across the axolemma. Na+ channel block (tetrodotoxin) reduced ischemic FCa.ax rise (14%); however, inhibition of L-type Ca2+ channels (nimodipine) had no effect (60%). In contrast, Na+-Ca2+ exchange inhibition (KB-R7943) significantly reduced ischemic FCa.ax rise (18%). Together our results indicate that the bulk of Ca2+ overload in injured peripheral myelinated axons occurs via reverse Na+-Ca2+ exchange, driven by axonal Na+ accumulation through voltage-gated tetrodotoxin-sensitive Na+ channels. This mechanism may represent a viable therapeutic target for peripheral neuropathies.

The patterns of normal daily activity that are required to maintain normal skeletal muscle properties remain unknown. The present study was designed to determine whether spinal cord isolation can be used as a reliable experimental model of neuromuscular inactivity, that is, as a baseline for the absence of activity. Electromyograms (EMGs) were recorded from selected hindlimb muscles of unanesthetized rats over 24-hour periods before and 7, 30, 60, and 90 days after surgical isolation of the lumbar spinal cord. Our data indicate that some rat slow muscle fibers pre-surgery were activated for less than 3 hours per day. Spinal cord isolation (SI) reduced the mean daily integrated EMG (IEMG) and daily EMG duration in the primary slow extensor muscle (soleus) to <1% of control, and in the primary fast extensor muscles [medial gastrocnemius (MG) and vastus lateralis (VL)] to <2% of control. These parameters were decreased to <8% and 3% of control, respectively, in a primary fast flexor muscle, the tibialis anterior (TA). From 30 to 90 days post-SI, the mean amplitudes of the spontaneous EMG bursts were relatively normal in the soleus, increased approximately 2-fold in the MG and VL, and increased approximately 4-fold in the TA. Some evidence of the normal antagonistic flexor-extensor relationship was apparent in the brief periods of recorded activity post-SI. These results indicate that SI eliminates nearly all of the normal EMG activity in the hindlimb muscles in the presence of relatively normal muscle innervation and functional intraspinal neural circuitry.

We present three cases of dropped head syndrome that occurred as a complication of mantle field (i.e., lymph nodes of the neck, axillae, and mediastinum) or whole-body radiation therapy for Hodgkin's disease. These cases are characterized by a late onset (2-27 years after radiation treatment), fibrosis, and contraction of the anterior cervical muscles, and atrophy of the posterior neck and shoulder girdle. This report adds to the increasing literature about the late neurological complications of radiation therapy and describes a previously unrecognized cause of dropped head syndrome.

In the belief that changes in the adductor reflex (AR) may be helpful in evaluating lumbar root and plexus lesions, expression of the AR was studied in 43 healthy human subjects. ARs elicited with an electronic reflex hammer were recorded from the inner side of the proximal thigh using needle and surface electrodes, and patellar reflexes (PRs) were recorded simultaneously. These reflexes were obtained by tapping the ipsilateral medial aspect of the knee, the contralateral patellar tendon, the ipsilateral and contralateral anterior superior iliac spines, and the Achilles tendon. The H reflex of the obturator nerve was also evaluated in 17 cases. ARs were evoked consistently by tapping the ipsilateral medial aspect of the knee and by contralateral patellar tap, and by tapping ipsilateral and contralateral anterior superior iliac spines when a needle recording electrode was used. Sometimes an Achilles tendon tap also elicited the AR ipsilaterally. By contrast, the PR could only be elicited by a tap to the ipsilateral patellar tendon. ARs have somewhat different features than other well-known tendon reflexes such as the PR and are recorded consistently when a needle electrode is used, being elicited from both distal and proximal areas of the legs by tapping the Achilles tendon or anterior superior iliac spines unilaterally or bilaterally. Their role in evaluating lumbar root disease and monitoring adductor spasticity merits investigation.

Neoplastic lumbosacral plexopathy occurs with some abdominal and pelvic malignancies. Patients present with severe pain radiating from the low back down to the lower extremities, and this progresses to weakness. Neoplastic lumbosacral plexopathy is virtually always associated with known malignancy or obvious pelvic metastatic disease. Uncommonly, prostate cancer can present as a lumbosacral plexopathy occurring through direct pelvic spread. We describe two cases of lumbosacral radiculoplexopathy from infiltrative prostate cancer without evidence of other pelvic or extraprostatic spread. The probable etiology of tumor spreading along prostatic nerves into the lumbosacral plexus (i.e., perineural spread) is discussed as are the potential mechanisms for this unusual mode of cancer dissemination.

Two patients with multiple sclerosis developed symptomatic chronic inflammatory demyelinating polyneuropathy with massive spinal or cranial nerve hypertrophy revealed by neuroimaging. Sural nerve biopsy in one showed only moderate demyelination, axonal loss, and onion-bulb formation, illustrating dichotomy between severe proximal and milder distal nerve involvement. Patients with coexistent central and peripheral demyelination usually are symptomatic from dysfunction at one site or the other, but not from both. Our patients showed minimal response to steroids, intravenous immunoglobulin, or azathioprine. These cases suggest that the mechanism of disease in symptomatic central and peripheral demyelination may differ from that of disease in only one region, and that optimal therapy in this situation must be explored further.

Root conduction time (RCT), defined as the time difference between M-wave latency by cervical magnetic stimulation (CMS) and the total peripheral motor conduction time calculated from the shortest F-wave latency, was investigated in patients with inflammatory demyelinating neuropathies (IDP) and amyotrophic lateral sclerosis (ALS). The minimal threshold for CMS also was studied. In the IDP patients, conduction in the proximal motor root segment was considered abnormal in 52% by the RCT and in 47% by the minimal threshold for CMS, whereas both were normal in 85% of the ALS patients. These findings suggest that the RCT and minimal threshold for CMS might be additional parameters for evaluating motor nerve conduction in IDP., (Copyright 2002 Wiley Periodicals, Inc.)

During partial dorsal rhizotomy (PDR), intraoperative dorsal rootlet stimulation often evokes nonreflex, rather than reflex, motor responses that are due to costimulation of adjacent ventral roots. Intraoperative areflexia typically predicts that motor responses evoked by dorsal rootlet stimulation are nonreflexive. The cause of areflexia during PDR is in part due to anesthesia, but other mechanisms are likely to play a role as well. In this study of three consecutive patients undergoing lumbosacral neurosurgery, soleus H-reflexes evoked by tibial nerve stimulation at the popliteal fossa were found to suddenly decline in amplitude following retraction and gentle dissection of the S-1 dorsal root. In one areflexic patient, dorsal rootlet stimulation proximal to the main site of dissection evoked soleus H-reflexes, although they could not be evoked by tibial nerve stimulation. We conclude that the gentle retraction and dissection of dorsal rootlets that occurs during PDR can induce conduction block of reflex afferents. High-intensity dorsal rootlet stimulation distal to the site of conduction block may then evoke not reflex responses, but rather nonreflex motor responses, due to the costimulation of adjacent ventral roots., (Copyright 2001 John Wiley & Sons, Inc.)

We describe two cases of neuralgic amyotrophy with electrophysiological evidence of conduction block across the lower trunk of the brachial plexus. Low-output impedance stimulation of the cervical spinal roots in combination with collision was used to accurately demonstrate the conduction block. Complete electrophysiological recovery of the conduction block occurred within 3 months. Early clinical and electrophysiological recovery in both patients suggests that, in some cases, demyelination may predominate early in the course of neuralgic amyotrophy., (Copyright 2001 John Wiley & Sons, Inc.)

We reviewed the electrophysiologic data and the etiology of lumbosacral plexopathy in 22 consecutive patients with pelvic trauma referred for electromyography (EMG). Most (68%) patients had sacral fractures or sacroiliac joint separation, 14% had acetabular fractures, and 9% had femoral fractures. Lumbosacral plexopathy was significantly more common (P = 0.0026) among patients with sacral fractures (incidence of 2.03%) than among the entire population of patients with pelvic and acetabular fractures (overall incidence 0. 7%). Patients with acetabular and femoral fractures may have suffered injury to multiple proximal nerves originating from the plexus rather than injury to the plexus, as confirmed by magnetic resonance imaging (MRI) neurogram in select cases., (Copyright 2000 John Wiley & Sons, Inc.)

The double crush hypothesis has not been rigorously evaluated in humans. We therefore analyzed cases of C6, C7, and C8 radiculopathy and exploited the fact that the median sensory response is of C6/C7 origin and the median motor response is primarily of C8 origin. We hypothesized that C6 and/or C7 cases would demonstrate an increased frequency of median mononeuropathy by sensory criteria, and C8 cases would demonstrate an increased frequency of median mononeuropathy by motor criteria. We also hypothesized that median sensory and motor response parameters among these same groups would be altered in ways consistent with a proximal influence on distal nerve conduction studies. Although median mononeuropathy was unexpectedly common (22.1%) among cases of cervical radiculopathy (which may explain the clinical acceptance of the double crush hypothesis), none of the hypotheses was supported. This study identified no evidence to support a neurophysiological explanation for the double crush hypothesis.

The anatomy and pathophysiology of radiculopathies are reviewed, and the electrodiagnostic approaches used in evaluating patients with suspected root lesions are discussed. Such electrophysiologic procedures include motor and sensory nerve conduction studies, late-response studies, somatosensory and motor evoked potentials, nerve root stimulation, and needle electromyography. The value and limitations of these different procedures are considered. At the present time, needle electromyography is the single most useful approach. The findings in patients with radiculopathies at different levels are summarized.

Cervical spondylytic myelopathy (CSM) is common. Magnetic resonance imaging (MRI), although sensitive, often reveals extensive and sometimes clinically irrelevant findings. The purpose of this study was to investigate the usefulness of central motor conduction studies in localizing the rostral level of cord involvement in 6 patients with CSM. Central motor conduction was assessed using high-voltage stimulation for the spinal roots and magnetoelectrical stimulation for the motor cortex, recording from "marker muscles" innervated by successively higher cervical cord segments. Abnormal central motor conduction affected all subjects at C8-T1, 5 subjects at C7, but none at the C5-C6 levels. The MRI showed abnormalities at multiple levels as high as C4. Our results suggest that central motor conduction studies are helpful in localizing the clinically relevant levels of spinal cord compression in CSM and correlate well with motor abnormalities on clinical examination.

The axonal distribution of voltage-dependent Na+ channels was determined during inflammatory demyelinating disease of the peripheral nervous system. Experimental allergic neuritis was induced in Lewis rats by active immunization. In diseased spinal roots Na+ channel immunofluorescence at many nodes of Ranvier changed from a highly focal ring to a more diffuse pattern and, as the disease progressed, eventually became undetectable. The loss of nodal channels corresponded closely with the development of clinical signs. Electrophysiological measurements and computations showed that a lateral spread of nodal Na+ channels could contribute significantly to temperature sensitivity and conduction block. During recovery new clusters of Na+ channels were seen. In fibers with large-scale demyelination, the new aggregates formed at the edges of adhering Schwann cells and appeared to fuse to form new nodes. At nodes with demyelination limited to paranodal retraction, Na+ channels were often found divided into two symmetric highly focal clusters. These results suggest that reorganization of Na+ channels plays an important role in the pathogenesis of demyelinating neuropathies.

The purpose of this study was to determine whether paraspinal and other major proximal and distal muscle spontaneous activity (SA) is related to cervical radiculopathy (CR) symptom duration. A multivariate analysis of 124 (retrospectively identified) electrodiagnostically confirmed CRs was used to test these hypotheses. The results showed no evidence of correlation between SA and symptom duration for any of the upper limb muscles analyzed.

We previously reviewed the presentation, initial clinical course, and electrodiagnostic features of children with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We now report the long-term follow-up of 12 children with idiopathic CIDP, and compare these to 62 adults with idiopathic CIDP. Children often had more rapidly fluctuating courses than adults. A relapsing course was significantly more common in children than in adults. The recovery of children from each episode of deterioration was usually excellent, and better, on average, than in adults. Ventilatory support was never required for children with slowly evolving illness; only 2 children with a precipitous onset clinically resembling Guillain-Barré syndrome required ventilatory support. Prednisone, plasma exchange, and intravenous immunoglobulin (IVIg) usually were effective in children. Multiple courses of IVIg could be given with continued efficacy. Treatment often could be discontinued in children with relapsing courses. The prognosis for children was excellent. Adults demonstrated a good, but more variable, outcome.

Magnetic cervical nerve root stimulation was performed in 9 patients with plexopathies secondary to suspension (SP) and in 12 cases with neurogenic thoracic outlet syndrome (NTOS). The findings were compared with those of the previously reported case groups: n-hexane polyneuropathy (HPNP), inflammatory demyelinating polyneuropathy (IDP), and motor neuron disease (MND). Muscle responses elicited by magnetic stimulation had very high rates of amplitude and area loss in the neck-axilla segments of the 6 SP patients. This, along with the other electrophysiological findings, suggested the presence of segmentally demyelinating plexus lesions. In NTOS patients, magnetic stimulation findings were not significantly different from those of the controls. Neck-axilla segment amplitude and are reduction rates in SP and IDP patients were significantly higher than those found in NTOS, HPNP, and MND groups, implying that magnetic nerve root stimulation may have a role in the demonstration of segmentally demyelinating lesions involving proximal nerve segments.

The pathological basis of nerve inexcitability in Guillain-Barré syndrome has not been established with certainty. We report the clinicopathological findings in a 67-year-old patient with fulminant Guillain-Barré syndrome who died 18 days after onset. Three serial electrophysiological studies revealed nerve inexcitability. Antibodies to Campylobacter jejuni were present but there was no antiganglioside reactivity. Spinal root sections revealed extensive and almost pure macrophage-associated demyelination with occasional presence of T lymphocytes and neutrophil leukocytes. Conversely, in femoral, median, and sural nerves the outstanding lesion was axonal degeneration, with some denuded axons remaining. Unmyelinated fibers, posterior root ganglia, and dorsal columns were preserved. Endoneurial postcapillary venules showed plump endothelial cells with loss of their tight junctions. We conclude that both primary demyelination and axonal degeneration secondary to inflammation account for nerve inexcitability. Our findings lend support to the hypothesis of increased endoneurial pressure as the cause of wallerian degeneration in nerve trunks.

Motor conduction velocity is expected to be normal or nearly normal in amyotrophic lateral sclerosis (ALS). Some studies have suggested that pathology may be present in the proximal axons. Indeed, some investigators have shown a decrease in the proximal conduction velocity in ALS by using motor conduction velocity measurements and H-reflex and F-response recordings, but they could not delineate the precise region of the conduction pathology. In this study, unlike the ones carried out previously, the most proximal segment has been studied in 11 patients with ALS, 13 normal controls, and 5 patients with sequel of poliomyelitis (SPM) by recording sensory and motor spinal root potentials. While no conduction pathology, H-reflex, or F-response abnormalities were found in ALS patients compared to normal subjects, it was shown that conduction velocity decreased in the proximal segment of the lower motor neuron of the ventral root. Despite motor neuron pathology in SPM, there was no proximal motor conduction slowing compared with that in normal subjects.

Dermatomal and segmental somatosensory evoked potentials (SEPs) have been reported to be of diagnostic utility in unilateral/unilevel L5 and S1 radiculopathies. This investigation employs history, physical examination, imaging studies, and electrodiagnostic medicine evaluations to clearly define unilateral/unilevel L5 or S1 nerve root compromise. Inclusion criteria require all of the preceding diagnostic methods to corroborate a specific nerve root lesion. Regression equation analysis for cortical P1 latencies evaluating age and height based on comparable patient and control reference populations reveals segmental and dermatomal sensitivities for L5 radiculopathies to be 70% and 50%, respectively, at 90% confidence intervals. Similar sensitivities are obtained for 2 standard deviation mean cortical P1 latencies. Side-to-side cortical P1 latency difference data reveal segmental and dermatomal sensitivities for S1 radiculopathies to be 50% and 10%, respectively, at two standard deviations. The clinical utility of both segmental and dermatomal SEPs are questionable in patients with known unilateral/unilevel L5 and S1 nerve root compromise.

During partial lumbosacral dorsal rhizotomy (PDR), intraoperative dorsal rootlet stimulation (drs) evokes motor responses, presumed to be reflexes, which are used to select rootlets for section. However, dr stimuli may also costimulate ventral root (vr) and evoke an M rather than a reflex response, the two being distinguishable only by comparison of response latencies after drs at two separate sites. In 15 consecutive spastic cerebral palsy patients undergoing PDR, we asked whether reflex and M responses were distinguishable on the basis of stimulus intensity (SI). For soleus H reflexes evoked by percutaneous tibial nerve stimulation, the SI for reflex afferents was usually subthreshold for exciting motor fibers. Similarly, for nerve roots, reflexes were evoked by drs at SIs generally less than that for M responses evoked by vr stimulation (vrs). In contrast, M responses evoked by drs required SIs that were on average 20 times greater. Finally, costimulation of contralateral vr after ipsilateral vrs occurred at SIs shown to evoke M responses after drs. We conclude that: (1) reflex and M responses evoked by drs are distinguishable on the basis of the required SI; and (2) drs employing SIs greater than required for vrs evokes M rather than reflex responses due to costimulation of ipsilateral and contralateral vr.

In the Lewis rat, acute experimental autoimmune encephalomyelitis (EAE) induced by inoculation with myelin basic protein (MBP) and adjuvants is characterized by tail and hindlimb weakness that resolves spontaneously after several days. In rats with neurological signs of this form of EAE (MBP-EAE) we have previously demonstrated demyelination and nerve conduction block in the proximal peripheral nervous system (PNS) and in the central nervous system (CNS). The present study was performed to assess conduction in the PNS and CNS, after recovery from acute MBP-EAE, using direct recordings from surgically exposed spinal roots and spinal cord dorsal columns. The study revealed that 1-2 weeks after clinical recovery from tail paralysis there was almost complete restoration of conduction in the sacral spinal roots but persistent severe conduction abnormalities in the dorsal columns. Significant restoration of conduction through the dorsal columns occurred over the following 2 weeks. These findings indicate that PNS conduction block due to a demyelinating polyradiculitis is a major cause of the neurological signs of acute MBP-EAE in the Lewis rat.

In traumatic brachial plexus injuries a thorough neurological, electrodiagnostic, and radiological examination is essential to determine treatment and prognosis. The most important diagnostic question concerns the presence or absence of a preganglionic nerve root lesion. Electromyography and motor and sensory conduction studies were performed in 17 patients with traumatic plexus injuries who had myelographic evidence of nerve root avulsion; in 8 of these clinical and electrophysiological features confirmed the X-ray findings. However, in 9 cases there was a discrepancy between myelographic and neurophysiological data regarding the actual number and sites of roots avulsed. Thus, in 2 cases myelography showed avulsion of one more root than did conduction studies and EMG; in 2 others, there was discordance as to the specific roots avulsed; in 4 cases fewer nerve roots seem to be avulsed radiologically than predicted clinically, and in 1, none at all, although clinical and electrophysiological data were compatible with avulsion of four roots. In 6 cases recovery showed that avulsions indicated by clinical and electrophysiological considerations could not have occurred. When both EMG and myelography are misleading, surgical exploration should be considered.

Using a formula for standard deviation and several assumptions, the potential benefit of electrophysiological recording (ER) during dorsal rhizotomy for cerebral palsy is calculated and expressed in a ratio, the electrophysiological recording benefit ratio (ERBR). ERBR is approximately 1.1 in most of the examples, but other factors may reduce this ratio. Severing an additional rootlet appears to be a viable alternative to ER in most of the examples. Advantages of dorsal rhizotomy without ER include reduced expense and operative time. Prospective studies are recommended to evaluate further the benefit of ER during dorsal rhizotomy. If stimulation of dorsal rootlets is abandoned during dorsal rhizotomy, stimulation of whole dorsal and ventral roots may still be necessary to prevent inadvertent severing of motor fibers.

H reflex studies were performed in ten spastic children with cerebral palsy who underwent partial dorsal rhizotomy (PDR). Under anesthesia prior to PDR, H reflex amplitude evoked by percutaneous peripheral nerve stimulation gradually declined in all patients and became unobtainable in five. Motor responses could still be evoked by apparent dorsal root stimulation in these five, but since it was shown that they were M responses and not reflexes, PDR was performed randomly. In the other five patients, in whom H reflexes were still evokable, dorsal root stimulation evoked motor responses which were true reflex responses, and PDR was performed "selectively." Compared to preoperative values, postoperative Hmax/Mmax ratios declined, but no more so in selective than in random PDR. We conclude that current intraoperative methods for selection of "abnormal" dorsal rootlets for section may be invalid and may have no bearing on successful outcome, since spasticity improves even with random PDR.

A 53-year-old man developed multifocal radicular pain. The diagnosis of Lyme neuroborreliosis was delayed until bifacial paresis and right lower abdominal wall weakness developed, prompting further evaluation. Cerebrospinal fluid (CSF) examination showed aseptic meningitis. Antibodies directed against Borrelia burgdorferi were present in the serum; higher titers were present in the CSF, indicating local antibody production. Electrophysiologic studies showed both an axonal polyradiculopathy as well as demyelinative facial palsy. Ceftriaxone therapy led to marked improvement in pain and facial palsies.

Excitability of rat dorsal root axons were studied 3 weeks after injury to the sciatic nerve. Whole nerve recordings were obtained from injured and control nerves in a sucrose gap chamber. Constant current depolarization pulses (30-200 ms) applied approximately 50% above the stimulus strength required for maximal amplitude compound action potentials (CAPs) evoked a burst of action potentials in the dorsal root which displayed spike adaptation. The depolarization-induced burst response of the dorsal roots was greatly reduced after crush or transection of the sciatic nerve. However, application of the potassium channel blocker, tetraethylammonium (TEA), restored the burst discharge in injured dorsal root axons. Brief tetanic stimulation of the dorsal root also induced an afterhyperpolarization (AHP) that was twice as large in the transection group as compared to the control group, and which was blocked by TEA. There were no changes seen in the amplitude of the compound action potential, frequency-following characteristics, refractory properties, or 4-AP sensitivity in the dorsal roots after peripheral nerve injury. These results suggest that there is enhanced spike adaptation that occurs at the same time as an increase in the sensitivity to the potassium channel blocker, TEA, in axon regions proximal to the site of nerve injury and have implications for the pathophysiology of nerve injury.

In the diagnosis of low back pain, the presence of a high percentage of false positive findings on radiologic imaging studies has lead to a more definitive role for electrodiagnosis as a confirmatory test. The paraspinal muscles are a crucial part of the electrodiagnostic examination for radiculopathy. To date, no technique for paraspinal evaluation has been validated. Based on previously documented anatomical techniques, we have designed a method of paraspinal examination termed "paraspinal mapping" (PM). Electromyographic (EMG) needles are placed in five carefully chosen locations and inserted in multiple directions. Individual scores for these insertions are added to determine a total PM sensitivity score. The first 50 studies using PM were compared to peripheral EMG, imaging studies, and pain drawings. Results indicate that the technique is easy to perform. Sensitivity scores relate well with these tests. In this limited and uncontrolled population, PM had higher sensitivity for abnormalities than either peripheral EMG or imaging studies. Because of the anatomical validity of PM, future studies may show it to be useful in localizing the level of radiculopathy independently from peripheral EMG, and to support clinical findings and imaging studies.

The application of rapidly changing magnetic fields (magnetic stimulation) over the neck or lower back elicits EMG responses in the muscles of the arm or leg respectively. Such responses have stable onset latencies but their amplitudes vary depending on the position of the coil over the neck or lower back. Supramaximal responses could not be obtained. Comparison of onset latencies with estimates of peripheral conduction time using a conventional F-wave technique suggest that the site of excitation of the motor axons is about 1.3 msec conduction time distal to the cervical motoneurons and 3 msec distal to the lumbosacral motoneurons. Response configuration after paravertebral magnetic stimulation was similar to that of the standard electrically evoked M-wave in the small hand muscles but not in lower limb muscles. Responses in lower limb muscles after paravertebral magnetic stimulation may consist of additional F-wave and H-reflex components. The possible clinical role of paravertebral magnetic stimulation in the investigation of peripheral and central motor pathways is discussed in the light of these findings.

We reviewed the medical records of 233 patients having electrodiagnostic evidence of polyradiculopathy. Patients with polyneuropathy or incomplete diagnostic evaluation were excluded. A clinical diagnosis was secured in 92 of the 118 remaining patients. Patients were separated into three groups based upon the anatomic location of root involvement: extradural (55), intradural-extraaxial (23), and intraaxial (14). Collectively, patients with intradural-extraaxial disorders had earlier disease onset, shorter symptom duration, and a higher disability score compared with the intraaxial or extradural groups. Pain was an initial complaint in 50 of 55 patients with extradural lesions, 20 of 23 with intradural-extraaxial disease, but only in 4 of 14 with intraaxial involvement. CSF abnormalities and reduced compound muscle action potential amplitudes were more common in the intradural-extraaxial group. We conclude that the anatomic localization of root involvement in patients with polyradiculopathy can be suggested by a combination of clinical, laboratory, and electrodiagnostic features.

The evoked potentials in the ventral and dorsal roots were recorded independently by stimulating the sciatic nerve of both control and methylmercury-poisoned rats. Poisoned rats showed markedly decreased amplitudes but normal latencies of the potentials evoked in the dorsal roots. Potentials evoked in the ventral roots had normal latencies and amplitudes. Pathological correlates indicated acute axonal degeneration of the dorsal roots, with a significant decrease of the large and small myelinated fiber densities. The ventral roots were histologically unremarkable. Our pathological confirmation of the electrophysiologic changes in the methylmercury-poisoned rats enables us to substantially assess the pathophysiological aspects of acute lesions in the spinal roots.

A middle-aged man with lymphomatous meningitis developed acute cervical radiculopathy. Repetitive stimulation of an affected nerve revealed a "U-Shaped" decrement. The decrement was absent 10 days later. We hypothesize that the decrement was secondary to simultaneous denervation of many motor units and disappeared as denervation became complete in those motor units.

Variability of the lumbosacral somatosensory evoked potential (LSEP) in test/retest situations was assessed in 49 patients with nonprogressive neurological disorder and 20 healthy subjects. The average time of LSEP follow-up in the patients was 16.2 months. The first group of healthy subjects had a short test/retest period of between 2 days and 2 weeks, and the second group had a long period between tests, with a mean of 35.7 months. The R and S waves of the LSEP were analyzed separately for latency and amplitude. Test/retest differences were statistically compared. The average correlation coefficient for healthy subjects was 0.84 and for patients was 0.78. These results suggested a remarkable stability of LSEPs in both healthy subjects and patients with nonprogressive neurological disorders. Therefore, we propose that LSEPs can be used in follow-up both to screen for initial dysfunction of the sensory system and to detect any changes in present dysfunction.

Three patients with Guillain-Barré syndrome underwent electrophysiological examination prior to and during a period of rapid clinical recovery. In each case, improved strength of the abductor digiti minimi coincided with electrophysiologic evidence of a marked reversal of proximal conduction block. In contrast, the degree of distal conduction block remained relatively unchanged after stimulation at the wrist, elbow, axilla, and Erb's point. These findings indicate that rapid motor recovery, early in the course of Guillain-Barré syndrome, can result from reversal of proximal conduction block and explains the often noted dissociation between clinical improvement and conventional distal nerve conduction studies.