Myelopathy in AIDS. A clinical and electrophysiological study of 23 Danish patients

In a cross-sectional population study of Danish patients with AIDS 16 of 23 had clinical signs of neurological disease with muscle weakness or ataxia of the lower limbs as the dominant manifestation. Tibial and median nerve conduction was mildly slowed in a few patients and 15 had widening of cerebral ventricles at CT. However, all had prolonged latency of cortical evoked response following tibial nerve stimulation mainly due to slowing through the spinal cord. The prolongation of the latency of the evoked cortical responses was most pronounced in patients with lower limb ataxia and/or paresis. It is concluded that affection of the long tracts of the spinal cord are closely associated with the human immunodeficiency virus infection.     

Spinal somatosensory evoked potentials in infants and children with spinal cord lesions

Spinal somatosensory evoked responses to peroneal nerve stimulation were examined in 23 control subjects and 8 patients with pathological lesions of the spinal cord or peripheral nerve. In the control subjects, the response was found as a triphasic potential increasing in latency rostrally at the lumbar spinous recording location. Another negative potential following this triphasic potential appeared at the L1 to T10 spinous recording locations, which might reflect synaptic and/or post-synaptic activity in the spinal cord. This negative response then progressively increased in latency rostrally. The spinal conduction velocity was higher at the upper thoracic leads than at the lower leads. Three patients with spinal cord atrophy showed disappearance of the spinal evoked potential at the spinous recording location corresponding to the pathological lesion. However, since the triphasic potential at the lumbar spinous lead was undetectable in the patients with lesions of the peripheral nerve or cauda equina, the spinal cord function could not be estimated well in these patients.     

Somatosensory evoked potentials in syringomyelia.

The two types of upper limb somatosensory evoked potential abnormality observed in nine patients with syringomyelia were reduced amplitude or absent cervical potentials and an abnormal central conduction time. Although this pattern of abnormalities resembles that observed in other intrinsic spinal cord lesions, it differs from peripheral nerve diseases and cervical radiculopathy in which the central conduction time is normal.     

Developmental and aging changes in somatosensory, auditory and visual evoked potentials

To assess developmental and aging changes in human sensory systems, components of short-latency somatosensory, brain-stem auditory and pattern-reversal visual evoked potentials, thought to originate in specific structures of these systems, were recorded in 286 normal subjects ranging in age from 4 to 95 years. Analysis was primarily restricted to peak and interpeak latencies; visual evoked potential amplitudes were also analyzed. Major results and conclusions are: (1) 'Developmental' changes (that is, decreases in latency attributable to decreased conduction time in younger subjects) were not seen in the median nerve, in brain-stem auditory pathways, or in some portions of visual cortex. Small developmental changes were seen in the somatosensory afferent pathway from the cervical spinal cord to thalamus, and large changes were seen in somatosensory and visual cortex. Cortical developmental changes appeared not to be complete until 17 years of age or later. (2) 'Aging' changes (that is, increases in latency attributable to increased conduction time in older subjects) were observed in the median nerve, cervical spinal cord, brain-stem auditory pathways, and somatosensory and visual cortex. (3) Visual evoked potential amplitudes tended to decrease with age, particularly during development; amplitude and latency effects were dissimilar for most components. (4) Males tended to show larger aging effects than females. (5) The results suggest that age-related changes in human sensory systems are not uniform, but rather are different in specific portions of these systems, different at particular epochs of the life span, and stronger in males than in females.     

Significance of sensory evoked potentials in the diagnosis of polyneuropathy

In 172 patients suffering from neuropathies of different aetiologies (diabetic, uraemic, inflammatory, hereditary, alcoholic, cryptogenic) the SEP findings (cortical median and sural nerve SEP, cervical median nerve SEP, Erb's point potential) were compared with the results of conventional sensory and motor electroneurography (ENG) and with clinical signs. SEP's yielded a high percentage of abnormalities. Thus in 5 of the 6 groups the sural nerve SEP presented an unequivocal latency prolongation in 55 to 75% of the patients, in HMSN-I-patients even in 100%. Also well over 50% of the median nerve evoked potentials were outside the normal range. In many cases the delay of the SEP's simply reflected the impairment of conduction within the peripheral nerve fibres as documented by ENG; here the ENG was naturally even more sensitive in detecting slight distal conduction disturbance, which did not shift the SEP latency outside the normal range. However, in a certain percentage that varied in the different aetiological groups, the SEP's demonstrated an impairment of conduction within the proximal segments of the sensory system not accessible to conventional ENG technique. Thus, in 15 to 25% of the patients with diabetic, uraemic, inflammatory and cryptogenic neuropathies, pathological SEP findings were combined with normal results of the ENG examination. In no case this "proximal" conduction disturbance affected the "central conduction" between the cervical spinal cord and the cortex. A more detailed differentiation was often impossible: A prolonged conduction time between brachial plexus and cervical cord could not be subdivided further due to the lack of the SEP component representing the "spinal entry of the afferent volley". SEP's--especially the cortical SEP's--can be reliably recorded even if a peripheral sensory nerve action potential is lacking; in these cases the extent of the conduction disturbance is documented only by the--practically always demonstrable--delay of the SEP. Nearly without exception, pronounced latency prolongations were seen only in cortical SEP's because in these cases the subcortical components could no longer be identified. Two types of considerably delayed cortical SEP's could be distinguished: Potentials of abnormal shape, where the complete extinction of the initial complex had to be assumed: the latency prolongation cannot be equated with the actual conduction delay. Completely normal-shaped potentials whose latency times evidently reflected the real delay.(ABSTRACT TRUNCATED AT 400 WORDS)     

Peripheral and segmental spinal abnormalities of median and ulnar somatosensory evoked potentials in Hirayama's disease

OBJECTIVES: To investigate the origin of juvenile muscle atrophy of the upper limbs (Hirayama's disease, a type of cervical myelopathy of unknown origin). SUBJECTS: Eight male patients were studied; data from 10 normal men were used as control. METHODS: Median and ulnar nerve somatosensory evoked potentials (SEP) were recorded. Brachial plexus potentials at Erb's point (EP), dorsal horn responses (N13), and subcortical (P14) and cortical potentials (N20) were evaluated. Tibial nerve SEP and motor evoked potentials (MEP) were also recorded from scalp and spinal sites to assess posterior column and pyramidal tract conduction, respectively. RESULTS: The most important SEP findings were: a very substantial attenuation of both the EP potentials and the N13 spinal responses; normal amplitude of the scalp N20; and normal latency of the individual peaks (EP-N9-N13-P14-N20). Although both nerves were involved, abnormalities in response to median nerve stimulation were more significant than those in response to ulnar nerve stimulation. There was little correlation between the degree of alterations observed and the clinical state. Latencies of both spinal and cortical potentials were normal following tibial nerve stimulation. The mean latency of cervical MEP and the central conduction time from the thenar eminence were slightly but significantly longer in patients than in controls. CONCLUSIONS: The findings support the hypothesis that this disease, which is clinically defined as a focal spinal muscle atrophy of the upper limb, may also involve the sensory system; if traumatic injury caused by stretching plays a role in the pathogenesis, the damage cannot be confined to the anterior horn of the spinal cord.     

Electrophysiological localization of central somatosensory lesions in patients with multiple sclerosis.

Somatosensory evoked potentials (SEPs) and selected indices of peripheral nerve function were compared in 30 multiple sclerosis (MS) patients and 15 normal controls. A high incidence of delayed SEP onset was observed in the MS patients, correlating with sensory loss--particularly of joint position and vibration sense. Using a method for deriving an indirect estimate of spinal cord conduction velocity, the longitudinal level of the sensory disturbance could in many cases be localized either to the spinal or to the supraspinal segment (or both) of the somatosensory pathway. Abnormally low spinal conduction velocity correlated with clinical judgements of spinal cord malfunction, but abnormalities were encountered also in some cases with no clinical evidence of myelopathy. Electrophysiological studies can contribute to the assessment of patients with suspected MS by demonstrating conduction abnormalities in specific segments of the somatosensory pathway.     

Assessment of intraspinal and intracranial conduction by P30 and P39 tibial nerve somatosensory evoked potentials in cervical cord, brainstem, and hemispheric lesions.

In routine recordings of tibial nerve somatosensory evoked potentials (SEPs), a global central conduction time is evaluated by measuring the interval between the segmental spinal N22 potential, recorded in the lumbar region, and the cortical P39 potential. In this study, we tested the reliability of the scalp far-field P30 potential, which originates in the vicinity of the cervico-medullary junction, in order to evaluate separately intraspinal and intracranial conduction in normal subjects and patients with cervical cord and intracranial lesions. P30 and cortical P39 potentials were studied in 23 healthy subjects and in 70 patients with cervical cord (n = 47), brainstem (n = 11) or hemispheric lesions (n = 12) selected on the basis of neuroimaging--computed tomography (CT) or magnetic resonance (MR)--findings. Median nerve SEPs were also recorded in all patients. Of the several montages tested to obtain the P30 potential, the Fpz-Cv6 derivation gave the highest signal-to-noise ratio; it permitted to obtain a P30 potential that peaked at 29.2 +/- 1.6 ms in all normal subjects. P30 abnormalities were observed only in patients with cervical or cervico-medullary lesions; these were associated with a normal P39 in only two of 33 abnormal recordings. Conversely, P30 was consistently normal in lesions situated above the cervico-medullary junction whether associated with normal, delayed, or reduced P39. P30 abnormalities were subclinical in 42% of abnormal recordings. All patients with normal tibial and median nerve SEPs on both sides had normal touch, joint, and vibration sensation in the four limbs. There was a strong correlation between tibial nerve P30 and median nerve P14 data in the whole series of patients; both potentials behaved similarly in all cases of intracranial supramedullary lesions. Combined abnormalities of P30 and P39 potentials thus indicate that conduction is impaired at the spinal level and proved to be particularly informative for detecting spinal cord dysfunction in patients with neuroimaging evidence of a narrowed cervical canal. Recording of abnormal N13, P14, or P30 potentials provided evidence of a cervical cord dysfunction in 66% of patients who had a suspected spondylotic myelopathy. Recording of tibial nerve P30 potential has proven to give reliable and useful information when a separate assessment of intraspinal and intracranial somatosensory conduction is needed; it merits inclusion, as does the upper limb N13 potential, in the evaluation of patients whose MR image indicates cervical canal narrowing.     

脊髓病变的运动诱发电位研究及其应用探讨

采用经颅和椎骨的电刺激技术检查19位脊髓病变患者上、下肢的运动诱发电位(MEP)反应。结果表明:对锥体束产生压迫和(或)破坏的病变,可造成运动诱发电位潜伏时和中枢运动传导时间的延长、波幅降低。下肢异常比上肢明显。异常改变在肢体的分布与病变部位密切相关。对运动诱发电位在脊髓病变方面的应用进行初步探讨。     

Indirect estimation of spinal cord conduction velocity in man.

A method is described for deriving an indirect estimate of the velocity of impulse propagation in the spinal cord of intact man. The estimate is computed from measurements of motor and sensory nerve conduction velocity in the limbs, F-wave latencies, and the latencies of somatosensory evoked potentials. The mean estimated spinal cord conduction velocicy in normal subjects was found to be 55.1 m/sec, with a standard deviation of 9.9. This method appears to have potential application in the electrophysiological evaluation of patients with myelopathic disorders.     

N10 potential as an antidromic motor evoked potential in a median nerve short-latency somatosensory evoked potential study.

When stimulating the mixed nerve to record evoked potential, both sensory and motor fibers are activated before entering the spinal cord. The N10 potential has been described as an antidromic motor evoked potential based on results obtained by recording at the anterior midneck. In the present study, we examined the changes in latencies of Erb's potential, N10, and N13 by stimulating the median nerve distally at the wrist and proximally at the elbow. The conduction velocity of N10 calculated by the difference between N10 latencies at the two stimulation points was consistent with motor conduction velocity, although N13 conduction velocity estimated by the same method reflected a sensory conduction velocity. A positive relation was also observed between the indirect latency from the stimulation point to the anterior root as calculated using the equation (F - M - 1) / 2 (ms) and the direct latency to the negative peak of the N10 potential. Our data support the notion that N10 represents antidromic motor potential originating in the spinal entry zone of the anterior root.     

自体肋间神经联合酸性成纤维细胞生长因子移植治疗高位脊髓损伤

背景：酸性成纤维细胞生长因子具有调节细胞增殖、移行、分化和生存的作用,也可以下调已知轴突再生的抑制因子如蛋白聚糖等,帮助轴突克服这些抑制因子,对神经纤维再生有重要作用。 目的：观察酸性成纤维细胞生长因子联合周围神经移植治疗大鼠高位脊髓损伤的可行性及效果。 方法：健康成年雌性SD大鼠108只随机抽签法分为自体神经组、自体神经联合生长因子组、高位脊髓横断组。咬除大鼠T8~10棘突、椎板,显露硬膜囊,水平切断高位脊髓并切除3 mm,显微镜下确认无神经纤维相连。自体神经组、自体神经联合生长因子组取双侧第8~10对肋间神经各2 cm,将肋间神经交叉移植入高位脊髓缺损处(近端白质与远端灰质、远端白质与近端灰质),分别以纤维蛋白凝胶、含有酸性成纤维细胞生长因子的纤维蛋白凝胶固定植入的肋间神经,缝合硬膜。高位脊髓横断组断端间旷置。术后90 d,行体感诱发电位及运动诱发电位检测观察神经电生理恢复情况。术后76 d,生物素葡聚糖胺顺行神经示踪观察运动传导束恢复情况。术后60 d,后肢BBB运动功能评分观察肢体运动恢复情况。 结果与结论：高位脊髓横断组大鼠均未引出体感及运动诱发电位波形。自体神经组、自体神经联合生长因子组均可引出体感及运动诱发电位,自体神经联合生长因子组体感诱发电位及运动诱发电位的平均潜伏期和波幅、BBB评分均明显优自体神经组(P < 0.01)。自体神经组和自体神经联合生长因子组在损伤区有较多生物素葡聚糖胺标记阳性神经纤维通过,明显多于高位脊髓横断组(P < 0.01),自体神经联合生长因子组多于自体神经组(P < 0.01)。提示自体周围神经移植酸性成纤维细胞生长因子能更好地恢复高位脊髓损伤后大鼠肢体运动功能。     

Short latency somatosensory evoked potentials: studies in patients with focal neurological disease

In non-cephalic reference recordings, the scalp recorded short latency evoked potentials to median nerve stimulation in normal subjects consist of 3 positive potentials followed by a negative potential. The sources of these potentials have not been precisely defined. Therefore, these potentials were recorded in 31 patients with focal lesions of the nervous system. Recordings were evaluated for (a) the presence or absence of these potentials and (b) peak latency differences between components. The results were compared with similar data obtained on 25 normal control subjects. Only the first positive potential was recorded with stimulation ipsilateral to the lesion in one patient with unilateral C5-T1 root avulsion. This indicates that this potential arises in stimulated peripheral nerve fibers. The second potential, although not consistently recorded in normal subjects, had an abnormally prolonged interpeak latency in 2 patients with cervical cord and medullary lesions. Therefore, it seems that it arises in the central nervous system, either in spinal cord or lower brain stem. The third potential was absent in 2 patients with medullary lesions and its interpeak latency was prolonged in 2 patients with brain stem lesions. It was recorded in 3 patients with thalamic lesions in whom subsequent potentials were absent. This suggests that this potential arises primarily in brain stem pathways. The negative potential was absent in 2 patients with cerebral lesions which did not appear to involve the thalamus which suggests that it arises in the thalamocortical radiations or cerebral cortex. Short latency evoked potential abnormalities correlated more with impairment of proprioception than with disturbances in appreciation of pain and temperature.     

Conduction characteristics of somatosensory evoked potentials to peroneal, tibial and sural nerve stimulation in man

Lumbar spine and scalp short latency somatosensory evoked potentials (SSEPs) to stimulation of the posterior tibial, peroneal and sural nerves at the ankle (PTN-A, PN-A, SN-A) and common peroneal nerve at the knee (CPN-K) were obtained in 8 normal subjects. Peripheral nerve conduction velocities and lumbar spine to cerebral cortex propagation velocities were determined and compared. These values were similar with stimulation of the 3 nerves at the ankle but were significantly greater with CPN-K stimulation. CPN-K and PTN-A SSEPs were recorded from the L3, T12, T6 and C7 spines and the scalp in 6 normal subjects. Conduction velocities were determined over peripheral nerve-cauda equina (stimulus-L3), caudal spinal cord (T12-T6) and rostral spinal cord (T6-C7). Propagation velocities were determined from each spinal level to the cerebral cortex. With both CPN-K and PTN-A stimulation the speed of conduction over peripheral nerve and spinal cord was non-linear. It was greater over peripheral nerve-cauda equina and rostral spinal cord than over caudal cord segments. The CPN-K response was conducted significantly faster than the PTN-A response over peripheral nerve-cauda equina and rostral spinal cord but these values were similar over caudal cord. Spine to cerebral cortex propagation velocities were significantly greater from all spine levels with CPN-K stimulation. These data show that the conduction characteristics of SSEPs over peripheral nerve, spinal cord and from spine to cerebral cortex are dependent on the peripheral nerve stimulated.     

Spinal somatosensory evoked potentials in juvenile diabetes

Spinal somatosensory evoked potentials to stimulation of the peroneal nerves in the popliteal fossa were recorded from 46 insulin-dependent neurologically normal patients with juvenile diabetes. Conduction velocities of these potentials were determined over proximal peroneal nerve, cauda equina, and spinal cord and were compared with those obtained from 46 age-matched control subjects. Mean values for overall spinal conduction velocity (L3-C7 spines) and conduction velocity over rostral spinal cord (T6-C7 spines) and peroneal nerve-cauda equina (stimulus to L3 spine) were lower in the diabetic group (p less than 0.001). Peripheral nerve conduction velocity alone was slow in 5 patients, and spinal conduction velocity was slow in 8; in 2 patients both peripheral and spinal velocities were slow. This study suggests that in addition to impairment of peripheral nerve function, patients with juvenile diabetes without clinical evidence of neurological involvement can have a defect in spinal afferent transmission.     

Evoked potentials in HIV infection]

The study of the literature data on the multimodal evoked potentials in HIV infected patients shows many abnormalities as well in asymptomatic subjects without AIDS as in AIDS subjects with or without neurological signs. Visual evoked potentials (VEPs) reveal prolonged P100 wave latency in 22% of HIV asymptomatic subjects and in 26% of HIV symptomatic subjects; brainstem auditory evoked potentials (BAEPs) reveal an increase of the interpeak latency I-V in 16% of asymptomatic subjects and in 32% of symptomatic subjects; somatosensory evoked potentials (SEPs) by median nerve stimulation reveal prolonged central conduction time in 6% of asymptomatic subjects and in 11% of symptomatic subjects; somatosensory evoked potentials (SEPs) by tibial nerve stimulation reveal prolonged central conduction time in 4% of asymptomatic subjects and in 45% of symptomatic subjects; motor evoked potentials (MEPs) by magnetic stimulation reveal prolonged central motor conduction time in 46% of asymptomatic subjects.     

Age-related changes in peripheral and central nerve conduction in man

Somatosensory evoked potential (SEP) latencies, motor and sensory nerve conduction velocities (CVs), and F-wave latenies were measured in 15 elderly normal subjects (mean age 74.1 years), and the results were used to derive indirect estimates of spinal cord CVs. These measurements were compared to those from 15 younger normal adults (mean age 31.6 years), and the nerve conduction characteristics of all 30 subjects were analyzed with respect to age. Peripheral motor and sensory CVs slowed progressively, and the onset latencies of F-waves and SEPs increased gradually with advancing age. Spinal cord CVs showed little change until approximately age 60, and declined sharply thereafter. In addition, the latencies of F-waves and SEPs were positively associated with height. Human clinical and experimental studies utilizing SEP and F-wave measurements must allow for morphologic differences between individuals, and for the systematic changes which accompany normal aging.     

Detection and peripheral or central localization of sensory pathway involvement of the lower limbs by somatosensory evoked potentials

In the presence of more or less atypical sensory or sensorimotor symptoms the questions that arise most frequently concern the authenticity of the disorders and the precise level of the lesion. In this study, somatosensory evoked potentials (SEPs) to stimulation of the tibial nerve at the ankle were recorded at different levels in 35 healthy subjects and 32 patients with sensory disorders. Recording electrodes were placed at the popliteal fossa (peripheral sensory nerve conduction velocity), at the T12-L1 level (medullary potential: N21) and at the vertex (P40 wave). The spine to cortex time interval was measured. A systematic study of evoked responses to median nerve stimulation was performed. The 32 patients were divided into 4 groups: Group I (3 cases) had slowed sensory conduction velocity (SCV), similar delay in N21 latency and normal N21-P40: peripheral neuropathy. Group II (4 cases) had normal SCV, delayed N21 latency and normal N21-P40: radicular or conus medullaris injury. Group III (19 cases) had normal SCV, normal N21 latency and lengthened N21-P40 interval. A study of responses to median nerve stimulation made it possible to discriminate between spinal and cortical or subcortical impairment. Group IV (6 cases) had abnormalities from any two of the three groups defined above. In 24 out of 32 patients (75 p. 100), further investigations (myelography, MRI, EMG) confirmed the localization determined by evoked responses. In the other 8 patients (25 p. 100) whose clinical picture suggested a medullary or radicular impairment, SEPs alone clearly revealed an injury. SEPs can distinctly show a spinal impairment and determine the choice of further investigations.     

The role of somatosensory evoked potentials in the diagnosis of AIDS-associated myelopathy

BACKGROUND: Although AIDS-associated vacuolar myelopathy is detected in >50% of autopsy cases, it is often unrecognized during life. The clinical assessment is often difficult because of concurrent peripheral neuropathy and lack of specific diagnostic markers. Somatosensory evoked potentials (SEPs) have been successfully used to evaluate central conduction in a number of diseases involving the spinal cord. OBJECTIVES: To assess the diagnostic yield of SEPs in AIDS-associated myelopathy. METHODS: We recorded tibial and median nerve SEPs in 69 HIV-infected subjects referred for evaluation of lower extremity neurologic abnormalities. Stimulation of the peroneal nerve at the popliteal fossa was performed in patients with absent response to ankle stimulation. RESULTS: HIV-infected subjects had significantly delayed latencies of both peripheral and central potentials, suggesting a combination of peripheral and CNS abnormalities. Analysis of peripheral and central latencies allowed us to discriminate between neuropathy and myelopathy in individual patients. Abnormalities of tibial central conduction time (CCT) correlated with clinical diagnosis of myelopathy. There was no significant difference in median CCTs between patients and controls, suggesting that conduction abnormalities were restricted to the thoracolumbar spinal cord. A derived spinal conduction time was a sensitive indicator of central conduction abnormalities in AIDS patients with myelopathy. CONCLUSIONS: The combination of median, posterior tibial, and peroneal SEPs is a valuable tool in the diagnosis of AIDS-associated myelopathy, particularly when myelopathy and peripheral neuropathy coexist. The use of a derived spinal conduction time improves the diagnostic yield of SEPs in AIDS-associated myelopathy.     

Cerebral and spinal somatosensory evoked potentials in children with CNS degenerative disease

Spinal and cerebral somatosensory evoked potentials to peroneal nerve and median nerve stimulation were recorded in 17 children with CNS degenerative disease and compared with similar potentials obtained in a group of age-matched normal control subjects. Spinal potentials were increased in duration over caudal cord segments and were poorly defined or absent over the rostral cord in some patients. In 12 patients the conduction velocity of the spinal response was slow over spinal cord segments. However, conduction velocity over peripheral nerve and cauda equina was normal in all patients. The scalp recorded evoked potentials to both median and peroneal nerve stimulation which arise in neural structures rostral to the brain stem were absent in 14 patients. Cerebral responses and certain spinal potentials were greatly increased in amplitude in one patient with myoclonus. This study demonstrates that these methods permit an evaluation of the entire neuraxis from peripheral nerve to cerebral cortex and that they may be helpful in the evaluation of patients with diffuse or multifocal disease of the nervous system.