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.     

Familial paroxysmal exercise-induced dyskinesia and benign epilepsy: a clinical and neurophysiological study of an uncommon disorder

We report a family with 6 members affected by a long-lasting paroxysmal exertion-induced dyskinesia. Fasting and stress were precipitating factors. All the patients of this family had also epileptic seizures mainly of generalised type with a favourable outcome. All patients were submitted to a neurophysiological study which included somatosensory evoked potentials by median nerve stimulation (MN-SEPs), somatosensory evoked potentials by posterior tibial nerve stimulation (PTN-SEPs), brainstem auditory evoked potentials (BAEPs), visual evoked potentials (VEPs), motor evoked potentials (MEPs) by magnetic transcranial cortical stimulation (TCS) and electromyography (EMG). The neurophysiological findings suggest a hyperexcitability at the muscular and brain membrane levels, probably due to an ion channel disorder. Received: 2 February 2000 / Accepted in revised form: 16 June 2000     

Short latency somatosensory evoked potentials in patients with neurological lesions

Short latency somatosensory potentials following median nerve stimulation were recorded in patients grouped according to anatomic location of neurological lesion. Patients with cerebral lesions causing severe sensory deficit lacked a major positive wave of cortical origin that in normal subjects peaked at a mean latency of 20.5 ms. Patients with severe cervical spinal cord disease lacked all of the normal somatosensory response except for the earliest component attributed to peripheral nerve activity. Patients with brain-stem lesions showed delayed latencies of later waves and prolonged interwave latencies. However, auditory evoked potentials measured in the group with brain-stem lesions were more helpful in localization. Analysis of short latency somatosensory potentials can discriminate between peripheral nerve, spinal cord, brain-stem, and cerebral lesions. Further experience and refinement of technique of measurement should increase the value of this procedure.     

Vibration and muscle contraction affect somatosensory evoked potentials

We recorded potentials evoked by specific somatosensory stimuli over peripheral nerve, spinal cord, and cerebral cortex. Vibration attenuated spinal and cerebral potentials evoked by mixed nerve and muscle spindle stimulation; in one subject that was tested, there was no effect on cutaneous input. Presynaptic inhibition of Ia input in the spinal cord and muscle spindle receptor occupancy are probably the responsible mechanisms. In contrast, muscle contraction attenuated cerebral potentials to both cutaneous and muscle spindle afferent volleys; central mechanisms modulating neurons in the dorsal columns nuclei, thalamus, or cerebral cortex are probably responsible.     

Evoked potentials in spinal muscular atrophy

Visual evoked potentials, brainstem evoked responses, and somatosensory evoked potentials were evaluated in 22 children with spinal muscular atrophy, types I and II. Eleven of the children had the severe form of spinal muscular atrophy (type I) and 11 children had the intermediate form (type II). The results of visual evoked potentials, brainstem evoked responses, and somatosensory evoked potentials were compared with those obtained in a control group. Statistical analysis showed abnormalities in the different sensory modalities. A significant increase in the visual evoked potential latencies was observed and was found more often in patients with spinal muscular atrophy type I. Alterations of the somatosensory thalamocortical responses were also observed, as well as a delay in the central conduction time. Although spinal muscular atrophy is usually considered to be a purely motor disorder involving neurons of the spinal anterior horn and nuclei of the lower cranial nerves, lesions of the posterior roots, spinal ganglia, ascending tracts, lateral geniculated corpus, and thalamus have been reported. Our results suggest that sensory neuron degeneration occurs more commonly in spinal muscular atrophy than previously thought and that this process probably develops more slowly than motoneuron degeneration. Such degeneration may be associated with brain atrophy.     

运动诱发电位联合体感诱发电位监测在脊髓髓内肿瘤手术中的应用

目的 探讨全静脉麻醉下运动诱发电位(MEP)联合体感诱发电位(SEP)术中监测应用于脊髓髓内肿瘤手术的优越性、可靠性及临床应用价值.方法 对72例脊髓髓内肿瘤患者术中行SEP和MEP联合监测,参照McCormick评分标准对术前、术后脊髓功能的改变和诱发电位变化之间的关系进行统计分析.结果 14例脊髓神经功能改善,18例术后脊髓神经功能下降者与诱发电位监测结果具有一致性(P＜0.05).结论 对脊髓髓内肿瘤手术进行SEP与MEP监测有利于避免"假阴性/假阳性"结果及术后神经功能障碍的发生.     

高颈段脊髓电刺激促醒颅脑创伤昏迷一例并文献复习

目的 研究高颈段脊髓电刺激对颅脑创伤昏迷的促醒作用.方法 观察1例重型颅脑创伤患者高颈段脊髓电刺激术后清醒时间、脑电图、诱发电位及脑血流的变化.结果 患者术后2个月逐渐清醒,脑电图逐渐转为正常α节律,诱发电位潜伏期延长逐渐改善,脑血流明显增加.结论 高颈段脊髓电刺激可能通过增加脑血流、恢复正常的神经电生理活动促醒颅脑创伤昏迷患者.

Abstract：

Objective To study the awoking effect of high cervical spinal cord stimulation on comatose patients with traumatic brain injury.Methods Recovery time,electroencephalogram(EEG),evoked patentials,cerebral blood perfusion after cervical spinal cord stimulation in a comatose patient were investigated.Results The patient emerged form conla at 2 months after spinal cord stimulation treatment.EEG gradually turned into a normal(rhythm,evoked potentials latency improved,and cerebral blood perfusion increased significantly.Conclusions High cervical spinal cord stimulation exerts its beneficial effects to comatose patients with traumatic brain injury by increasing cerebral blood perfusion and restoring normal cerebral electrical activity.     

Cerebral cortical contributions to sensory evoked potentials: hydranencephaly

The contribution of the cerebral cortex to the generation of sensory evoked potentials was studied in an infant with hydranencephaly. On CT scan no tissue above the thalamus was noted. Long-latency potentials to auditory stimuli were absent whereas the short-latency or brain-stem auditory evoked potentials and some of the components of the middle latency auditory evoked potentials (No and Po) were present. To visual stimulation only the electroretinogram was detected. To somatosensory stimulation only the spinal cord potentials could be detected. The absence of long-latency components in each of the sensory modalities supports the concept that these potentials require intact cerebral hemispheres in man.     

Effects of halothane dose and stimulus rate on canine spinal, far-field and near-field somatosensory evoked potentials

Evidence that canine spinal, far-field and near-field somatosensory evoked potentials resemble those recorded in humans and other species has been presented, and the vulnerability of each component to varying depths of halothane anesthesia is reported. Lumbar spinal peak latencies are not affected by halothane dose, but the negative peak is significantly prolonged by rapid rates of stimulation. Elevated stimulus rates and halothane doses reduce lumbar spinal cord potential amplitudes. Early far-field cephalic components are refractory to halothane. Late far-field components and near-field cortical potentials are substantially altered by increments in halothane dose. Both near-field and far-field responses are more readily identified in vertex-neck than vertex-brow derivations. Early far-field somatosensory evoked potentials recorded from vertex to neck, together with lumbar spinal cord potentials, may be the preferred monitoring technique when the use of halothane anesthesia is desired. Rapid rates of stimulation may facilitate earlier recognition of cord dysfunction, but supplement rather than replace baseline recordings at slow stimulus rates.     

Median nerve somatosensory evoked potentials recorded with cephalic and noncephalic references in central and peripheral nervous system lesions.

Somatosensory evoked potentials (SSEP) to electrical stimulation of the median nerve by using cephalic and noncephalic references were studied to detect the generator sources of short latency evoked potentials in 29 patients with cerebral, brainstem, spinal and peripheral nerve lesions. Patients were divided into six groups according to the localization of their lesions: group 1: cortical and subcortical lesions, group 2: basal ganglion lesions, group 3: pons and mesencephalon lesions, group 4: diffuse cerebral lesions, group 5: cervical cord lesions, group 6: brachial plexus lesions. Potentials were recorded using cephalic and noncephalic references after median nerve stimulation. Evidence obtained from patients suggested the following origins for these short latency SSEPs: P9 may arise in brachial plexus, P11 in dorsal basal ganglions or dorsal column, P13 and P14 in the nucleus cuneatus and lemniscal pathways, N16 in subthalamic structures and most likely mid and lower pons, N18 from the thalamus and thalamocortical tract, and N20 from primary somatosensory cortex.     

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.     

Examination of motor function in lesions of the spinal cord by stimulation of the motor cortex

Electrical stimulation of the motor cortex was performed in 3 patients with cervical cord trauma and in 3 with cervical myelopathy caused by cervical spondylosis. Abnormal conduction in central motor tracts was demonstrated in 5 of the 6 patients; yet in 4 of these, cortical somatosensory evoked potentials from the same limb were of normal latency. In the remaining patient who had normal motor latencies, the somatosensory evoked potentials were delayed on one side. Electrophysiological examination of the motor pathways by cortical stimulation may therefore be of considerable value in the assessment and management of patients with traumatic and compressive disease of the spinal cord.     

The diagnostic value of sensory evoked potentials in pediatric Wilson disease

We studied the sensory evoked potentials in pediatric Wilson disease to verify their subclinical neurologic involvement and to elucidate the role of cirrhosis in abnormal evoked potentials in non-neurologic Wilson disease. Thirty children (17 male, 13 female), diagnosed with Wilson disease before 18 years, were enrolled. The mean age during studies was 15.8 +/- 6.3 years, and disease duration since diagnosis was 3.0 +/- 3.3 years. In 12 neurologic Wilson disease cases, there were prolonged interpeak latencies of brainstem auditory evoked potentials III-V, I-V, somatosensory evoked potentials N13-N20 (P < 0.01 vs controls and non-neurologic cases), and P100 latency (P < 0.01 vs controls). All 12 patients had at least one abnormal evoked potential, including 91.7% brainstem auditory, 58.3% somatosensory, and 25% visual evoked potentials. In 18 non-neurologic Wilson disease cases, there were still prolonged interpeak latencies for brainstem auditory evoked potentials I-V and somatosensory evoked potentials N13-N20 (P < 0.05 vs controls), with 27.8% of them having at least one abnormal evoked potential, including 16.6% brainstem auditory, 5.6% somatosensory, and 11.1% visual evoked potentials. In those with non-neurologic Wilson disease, there were no significant differences in all the evoked potential parameters between the cirrhotic and non-cirrhotic patients.     

Spinal cord potentials in traumatic paraplegia and quadriplegia.

Cortical, cervical and lumbar somatosensory evoked potentials were recorded following median and tibial nerve stimulation in patients with traumatic paraplegia and quadriplegia. The isolated cord was able to produce normal potentials even during spinal shock if the vertical extent of the lesion did not involve the generator mechanisms. The cervical potentials showed subtle changes in paraplegia at Th5 levels and below. In high cervical lesions the early cervical potentials may still be present but the later potentials were absent or, in partial lesions, delayed.     

Spinal evoked potential in the monkey

Computer-averaged evoked potential responses (EPs) to stimulation of the sciatic nerve and cervical spinal cord were recorded from the dura and skin over the cauda equina and spinal cord in seven monkeys, three with chronic spinal cord lesions. Sciatic EPs consisted of predominantly negative triphasic propagated potentials recorded at all spinal levels and greatest in amplitude over the cauda equina and caudal spinal cord. The conduction velocity of this EP was faster over the cauda equina and rostral spinal cord than over caudal cord segments. Triphasic potentials were succeeded by small negative potentials over the cauda equina and larger negative potentials over the lumbar enlargement. Sciatic EPs over the upper lumbar and thoracic cord were more sensitive to asphyxia than the initial triphasic potentials recorded over cauda equina and caudal cord but resisted changes from increasing the rate of stimulation up to 100 per second. Propagated thoracic EPs were preceded by nonpropagated potentials. The longer latency negative potentials occurring locally over the cauda equina and lower lumbar enlargement were abolished at levels of asphyxia and were attenuated at rates of stimulation that did not affect the preceding triphasic potentials. Following complete spinal cord transection, nonpropagated sciatic EPs were recorded in leads rostral to the section. In preparations with chronic partial cord hemisection involving dorsal and lateral quadrants, ipsilateral sciatic EPs had increased latency, reduced amplitude, and poor definition in the vicinity of and rostral to the lesion. Direct cervical cord stimulation elicited caudally propagated potentials which were followed by large, broad potentials over the lumbar enlargement.     

Somatosensory perception and cortical evoked potentials in established paraplegia

In 66 patients who suffered severe spinal cord injury 7 months to 28 years previously, somatosensory cortical evoked potentials were recorded to electrical stimulation of the leg nerves and compared to clinical assessment of light touch, pain, position sense and two-point discrimination. The patients were separated into 4 categories according to the degree of disintegration of the somatosensory evoked potential waveform. A clear correlation was found between the impairment of somatosensory perception and the deterioration of the somatosensory evoked potential in each group. However, it was not possible to observe any direct correlation between the sensory score or impairment of a single modality and somatosensory evoked potential changes, or among the impairment of single modalities on a case by case basis. This study indicates that the somatosensory evoked potential can be used to provide electrophysiological information independent of the clinical examination on functions of the dorsal columns in the chronic stage of spinal cord injury.     

Cortical potentials evoked by epidural stimulation of the cervical and thoracic spinal cord in man

Scalp somatosensory evoked potentials (SEPs) were recorded after electrical stimulation of the spinal cord in humans. Stimulating electrodes were placed at different vertebral levels of the epidural space over the midline of the posterior aspect of the spinal cord. The wave form of the response differed according to the level of the stimulating epidural electrodes. Cervical stimulation elicited an SEP very similar to that produced by stimulation of upper extremity nerves, e.g., bilateral median nerve SEP, but with a shorter latency. Epidural stimulation of the lower thoracic cord elicited an SEP similar to that produced by stimulation of lower extremity nerves. The results of upper thoracic stimulation appeared as a mixed upper and lower extremity type of SEP. The overall amplitudes of SEPs elicited by the epidural stimulation were higher than SEPs elicited by peripheral nerve stimulation. In 4 patients the CV along the spinal cord was calculated from the difference in latencies of the cortical responses to stimulation at two different vertebral levels. The CVs were in the range of 45-65 m/sec. The method was shown to be promising for future study of spinal cord dysfunctions.     

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.     

Subpially recorded cervical spinal cord evoked potentials in syringomyelia.

Intraoperative spinal cord evoked potentials (SCEPs) to median nerve stimulation were detected subpially from the dorsal surface of the cervical spinal cord in 5 patients with cervical syringomyelia and were compared to normal SCEPs obtained from the unaffected side in 6 patients during intraoperative monitoring of dorsal root entry zone lesion. Normal SCEP began with a positive deflection P9 and a complex N11/N13 with several low amplitude short potentials superimposed on the N11/N13. The complex was followed by a second negative potential N2 and a late prolonged positivity, P. In the 4 patients in whom median nerve somatosensory evoked potentials (SEPs) were present preoperatively, SCEP consisted of the N11 potential and the following low amplitude short (LAS) potentials, while the N13 wave was missing. In the fifth patient, in whom the preoperative median nerve SEP was missing, SCEPs were of much lower amplitude and shorter duration than normal. The potentials N2 and P were not recorded in any of our 5 patients. Changes in N13 wave, N2 and P potentials noted in syringomyelia were presumed to be the result of destruction of the spinal cord dorsal horn neurons caused by spinal cord central cavitation.     

Use of evoked potentials for diagnosis of multiple sclerosis

The author discusses visual evoked potentials, brain stem auditory evoked potentials, somatosensory evoked potentials, motor evoked potentials, and MRI for the diagnosis of MS. Most patients with MS will eventually have an MRI scan. However, certain specific questions regarding function and anatomic regions are better studied with evoked potentials, especially those of optic nerve, brain stem, and spinal cord.