Spinal stretch reflex and cortical evoked potential amplitudes versus muscle stretch amplitude in the monkey arm

While investigating operant conditioning of the primate spinal stretch reflex (SSR), we studied SSR amplitude and cortical somatosensory evoked potential (SEP) amplitude as stretch amplitude changed in the monkey arm. Initial muscle length and background EMG activity remained constant. With change in stretch amplitude (and proportional change in stretch velocity and acceleration), changes in SSR and SEP amplitudes were respectively 0.75 and 0.66 as great. The lesser change in SSR amplitude may reflect saturation of Ia afferents, while that in SEP amplitude may also reflect participation of other peripheral receptors.     

Inhibitory processes in the flash evoked potential of the monkey.

Flash visual evoked potentials (VEP) and concurrent multiple unit activity (MUA) were recorded from closely spaced intracortical sites in unanesthetized monkeys before and after intracortical injection of the GABAA antagonist bicuculline. Laminar VEP profiles were subjected to current source density (CSD) analysis to localize the transmembrane current flows contributing to the generation of the field potentials. Before bicuculline, the first large VEP component, N40, was generated principally within the parvocellular thalamorecipient sublamina 4Cb. After bicuculline injection, the current sinks associated with N40 spread throughout lamina 4, consistent with a release of intracortical inhibition mediated by GABA. A subsequent component, P65, believed to represent recurrent inhibitory activity within 4Cb, was greatly diminished in size after bicuculline injection. The laminar pattern of current sources and sinks coincident with this component was more complicated after bicuculline, reflecting the summation of current flows associated with disinhibited lamina 4 activity. Bicuculline also altered the responses of neuronal elements in laminae 3 and 5, evidenced by large increases in MUA in these laminae that began approximately 50 msec after stimulation. Finally, bicuculline diminished the degree of intracortical ocular dominance, implicating GABAergic mechanisms in the maintenance and refinement of ocular input segregation within cortical columns.     

Spinal evoked potential in man: a maturational study.

Summated evoked potentials to peroneal nerve stimulation which arise in the cauda equina and spinal cord afferent pathways were recorded from surface electrodes placed over the spine of 95 infants, children and adults. The conduction velocity of these potentials from lumbar to cervical recording sites was calculated. Additionally, segmental conduction velocities over peroneal nerve, caudal and rostral spinal cord were determined. In all age groups the speed of conduction up the spine was non-linear. It was slower over caudal spinal cord segments than over peripheral nerve or rostral cord. All these velocities were about half adult values in the newborn and progressively increased with age. The conduction velocity over peripheral nerve was within the adult range by 3 years of age. The speed of conduction over the spinal cord did not reach adult values until the 5th year. This suggests that spinal cord afferent pathways mature at a slower rate than peripheral nerve fibers.     

体感诱发电位在脊髓损伤后药物疗效观察中的应用

目的观察大鼠脊髓损伤后药物对体感诱发电位（ＳＥＰ）的影响。方法４８只Ｗｉｓｔａｒ大鼠脊髓损伤术后立即给小檗胺或尼莫地平１次，术后２、４、８小时各给同样药１次，以后每日２次给药，至术后２周。分别于术前及术后４周在麻醉状态下进行ＳＥＰ检查。结果脊髓损伤后４周各组实验动物的ＳＥＰ潜伏期都有一定程度的延长，脊髓传导速度明显下降。大剂量小檗胺组与对照组相比其潜伏期及损伤部位的传导时间均明显缩短，损伤部位的传导速度明显加快，与对照组相比差异有极显著性意义（Ｐ＜０．０１）。结论ＳＥＰ能客观评价脊髓的神经传导功能，对脊髓损伤后药物疗效观察有一定的客观意义。     

Attenuation of the early anterior negativity of median nerve somatosensory evoked potential in the MPTP-treated monkey

Median nerve somatosensory evoked potentials (SEP) were recorded in 7 Cynomolgus monkeys, before and after the administration of N-Methyl 1,4 Phenyl 1,2,3,6 tetrahydropiridine (MPTP), a neurotoxin which induces a parkinsonian syndrome in primates. Following MPTP administration, the amplitude of the negative component recorded at 15 ms over the frontal derivations (N15) decreased by 70% or more. This amplitude reduction was not modified by administration of dopamine precursors. These findings shed light on recent findings in human parkinsonian patients.     

Spinal projections from the midbrain in monkey.

Neurons descending from the midbrain to the spinal cord in the monkey were identified with the retrograde horseradish peroxidase technique. Beginning in the caudal midbrain and extending anteriorly beneath the superior colliculus, large numbers of neurons of the nucleus cuneiformis and lateral central gray were found to project ipsilaterally to the spinal cord. In the posterolateral superior colliculus, neurons of the intermediate and deep layers, stratum griseum intermediale and stratum griseum profundum, were found to give rise to contralateral projections to the upper cervical spinal segments. An ipsilateral tectospinal projection from the anteromedial part of the collicus may also exist. In the red nucleus, neurons of the magnocellular division were shown to give rise to a somatotopically organized projection to the upper cervical cord and spinal enlargements. No neurons of the parvocellular red nucleus were labeled from the spinal cord. In the anterior midbrain, neurons of the interstitial nucleus of Cajal, nucleus of Darkschewitsch, and the adjacent dorsomedial and ventromedial midbrain tegmentum were found to give rise to an extensive ipsilateral descending spinal projection. Neurons located in various midline nuclei including the supratrochlear nucleus, oculomotor nucleus, Edinger-Westphal nucleus, and the ventral part of the central gray were also labeled from the spinal cord. These findings indicate that the primate midbrain is the origin of an extensive system of descending spinal pathways, some of which are likely to be involved in mediating descending influences involved in complex motor and sensory behavior.     

Visual 'cognitive' evoked potentials in the behaving monkey.

Using a visual 'oddball' paradigm we studied ERPs in monkeys trained in a 'go' 'no-go' discrimination task. The stimuli were 2.5 cpd sinusoidal gratings differing only in orientation (0 degrees or 25 degrees). Monkeys released a lever during 1 of 2 response windows (RW), 480-1762 or 740-1672 msec, following target stimulus onset. Target stimulus presentation probabilities were 1.0, 0.5 and 0.3. The primary evoked potentials recorded to either the target or non-target stimulus were similar in all monkeys. P3 signals progressively emerged in the monkeys only to the target stimulus. P3 recorded at Cz, P3, and P4 had similar mean latencies and amplitudes. Eye movements showed no relationship to P3 potentials. Neither the primary visual potentials nor P3 changed significantly as a function of RW. P3 amplitude was inversely related to target probability. When the target stimulus was presented 100% of the time (P = 1.0) P3 disappeared over 4-5 blocks of trials, while the primary evoked potentials remained consistent.     

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.     

Spinal and early scalp-recorded components of the somatosensory evoked potential following stimulation of the posterior tibial nerve

Somatosensory evoked potentials (SEPs) were elicited by stimulation of the posterior tibial nerve (PTN) in 12 normal adults. Recording using both cephalic and non-cephalic references were obtained from multiple electrodes placed over the spine and scalp. Following PTN stimulation, the fastest recorded potentials of the afferent sensory volley proceeds up the spinal cord at constant velocity. After arrival of the volley at cervical cord levels, 3 widely distributed waves, P28, P31 and N34, are recorded from scalp electrodes. These 'far-field' potentials are followed by a localized positivity (P38) which has a peak voltage either at the vertex or just laterally toward the side of stimulation. A contralateral negativity (N38) was present in most individuals. We propose that P28 arises from medial lemniscus; that P31 is generated by ventrobasal thalamus; and that N34 is probably the result of further activity in thalamus and/or thalamocortical radiations. The P38/N38 complex represents the primary cortical response to PTN stimulation. Its most consistent characteristic is a positivity at the vertex or immediately adjacent scalp areas ipsilateral to the stimulated leg. The topography of the P38/N38 potential varies slightly from individual to individual in a manner consistent with a functional dipole situated in the leg and foot area on the mesial aspect of the postcentral gyrus, whose exact location and orientation changes in accordance with known variations in the location of the leg area.     

Spinal evoked potential in the cat: effects of asphyxia, strychnine, cord section and compression.

Averaged evoked potentials to sciatic nerve stimulation and to direct stimulation of the cervical spinal cord were recorded from the dura and skin over the spinal cord and cauda equina in bipolar and common reference leads in cats and compared. Response waveform and conduction characteristics are described. The effects of increasing stimulus intensity, asphyxia and strychnine on these potentials are related. Alterations in these potentials produced by spinal cord at one or two levels are also described. These potentials are compared to similar potentials which have been recorded in man and the possible clinical application of some of these methods is discussed.     

Cortico-striatal evoked potentials in the monkey (Macaca mulatta).

A systematic study has been made of topographic organization in the striatum of evoked potentials elicited by stimulation of the cerebral cortex in unanesthetized, comatose monkeys (Macaca mulatta). Stimulation of the dorsal field of the prefrontal convexity elicited potentials primarily in rostral portions of the caudate, while stimulation of the ventral field of the prefrontal convexity elicited potentials in ventromedial areas of the putamen. Stimulation of different points on the precentral and postcentral gyri revealed a distinct somatopic organization of evoked responses in the putamen, although responsive zones in the putamen to precentral and postcentral stimulation showed almost total overlap. An overlap of responsive zones to stimulation of the dorsal prefrontal convexity and the premotor area (area 6) was found in the dorsolateral part of the rostral caudate, while a zone of overlap of responses to stimulation of the ventral prefrontal convexity and "hand" motor area of the precentral gyrus was found in the ventromedial area of the putamen near the commissural level.     

Visual evoked potential

Under the pathological conditions, the VEP may show changes in amplitude, latency, or waveform in one or more of its components. The major advantage of the pattern reversal VEP over the flash VEP lies in smaller variability in the waveform and latency of its components in the healthy population. The flash VEP is, however, particularly useful to infants and newborns. The variation in the waveform of the flash VEP was evaluated, and Type V was abnormal waveform. Subsequently, patients with various CNS diseases were examined. Acute hemiplegic patients showed high amplitude or increased latency patterns. In 45 percent of the West syndrome cases, VEP showed abnormal responses. The patients with asphyxia, respiratory distress syndrome and mental retardation showed increased latency. Latency was decreased in hypoglycemia and hypocalcemia of newborns, and it was increased or decreased in autism and epilepsy. In our study, it was concluded that the rhythmic after-discharge is a true response. This assumption is supported by the following observations: (1) the after-discharge of VEP appeared before the occurrence of the alpha-wave in EEG; (2) the frequency of the after-discharge was generally higher than that in EEG; and (3) the frequency of the after-discharge did not change between the conditions of the resting state and hyperventilation. There was no after-discharge in VEP in patients with a history of encephalitis even when their IQs were normal, and the latency was increased in pattern reversal VEP.     

Cortical evoked potential changes in a rat model of acute ischemic stroke Detection of somatosensory evoked potential and motor evoked potential

BACKGROUND:Studies have shown that latency changes of some elements in a somatosensory evoked potential (SEP) and motor evoked potential (MEP) can reflect electrical activity of cerebral cortical neurons and conduction of white matter nerve fibers. However, there is a paucity of information regarding the dynamic observation of SEP and MEP following cerebral ischemic injury. OBJECTIVE:To explore SEP and MEP changes following acute ischemic stroke, and investigate the role of evoked potentials in monitoring brain function in stroke. DESIGN, TIME AND SETTING:A randomized, controlled, animal experiment was performed at the Chongqing Key Laboratory of Neurology, Affiliated Hospital of Chongqing Medical University from September 2007 to August 2008.MATERIALS:Hydrogen blood flow detector was purchased from Soochow University Medical Instrument Co., China, and Power lab system was purchased from AD Instruments, Inc., USA. METHODS:A total of 36 healthy, adult, male, Sprague Dawley rats were randomly assigned to four groups (n = 9), including three ischemia groups (12, 24 and 72 hours of ischemia) and a sham-surgery group. The rat model of acute ischemic stroke was established by middle cerebral artery occlusion (MCAO) in the left hemisphere.MAIN OUTCOME MEASURES:SEP and MEP of the left limbs were detected, and cerebral blood flow was measured by the hydrogen cleaning method.RESULTS:The latency of positive wave 1 (P1), negative wave 1 (N1) and positive wave 2 (P2) waves in SEP, and latency of negative wave 1, 2 (N1, N2) waves in MEP were significantly prolonged with increasing ischemic duration following MCAO (P < 0.01), but cerebral blood flow was significantly decreased (P < 0.05, or P < 0.01).CONLUSION:Ischemic stroke prolongs the latency of SEP waves (P1, N1, P2) and MEP waves (N1, N2), and cerebral cortical evoked potential may correlate with cerebral blood flow changes. This indicates that SEP and MEP can be used to evaluate brain function following acute ischemic stroke.     

Spinal segmental somatosensory evoked potentials in lumbosacral radiculopathies

We studied 21 patients with lumbosacral radiculopathy with segmental somatosensory evoked potentials (SEPs) recorded over both spine and scalp following saphenous, superficial peroneal, and sural nerve stimulation. Spinal SEPs were abnormal in 10 patients. In 3 patients, SEPs detected abnormalities not seen on EMG examination. With 1 exception, all anatomic levels of SEP abnormalities matched that of radiographic, EMG, or clinical abnormalities. SEPs were abnormal in 41% of nerve roots shown to be involved by other techniques. SEPs added to the clinical evaluation in 4 patients, but were less accurate than a combination of EMG and radiography in indicating the extent of nerve root involvement. We conclude that spinal SEPs following segmental sensory stimulation are useful in the evaluation of lumbosacral radiculopathies and complement information provided by the EMG. In contrast, scalp-recorded segmental SEPs rarely provide additional useful clinical information.     

Somatosensory evoked potential in neurosyphilis

Since the development of effective antibiotic therapy, the occurrence of neurosyphilis has become less frequent. The number of syphilitic patients is gradually increasing as a complication in acquired immunodeficiency syndrome, but the diagnosis of neurosyphilis sometimes is difficult. We describe six patients with neurosyphilis and an analysis of their tibial nerve somatosensory evoked potentials. Four of them, including two with no tabes dorsalis symptoms, had delayed P15-N21 or the absence of N21. These abnormalities were ameliorated by treatment for syphilis. Analysis of tibial nerve SEPs provides a useful tool for the diagnosis of neurosyphilis and the evaluation of the extent to which neurosyphilis has progressed. Received: 20 December 2001, Received in revised form: 15 March 2002, Accepted: 18 March 2002     

Long-latency corticocortical evoked responses in squirrel monkey frontal cortex

Early (5 to 15 msec) and late (120 to 180 msec) responses are evoked bilaterally in postarcuate cortex of unanesthetized squirrel monkeys by electrical stimulation of postcentral somatosensory cortex. Sectioning the precentral corpus callosum abolishes both early and late responses to contralateral stimulation and leaves unchanged the responses recorded at the same site to ipsilateral stimulation, suggesting that generation of the late response depends on generation of the early response in the same frontal lobe. Units in postarcuate cortex fire in relation to the early and late responses, but are silent in the period between them. Other investigators have suggested that late components of the direct cortical response and postinhibitory rebound of cortical neurons are dependent on input to cortex from the thalamus. Our data indicate, rather, that it is input to cortex from the mesencephalon, probably feeding through the thalamus, which is necessary. Late responses are selectively depressed or even abolished by bilateral lesions in and near the mesencephalic reticular formation (MRF) and by general anesthetic agents, but the convulsant stimulants, picrotoxin and pentylenetetrazol, can induce recovery of late responses after lesions or administration of anesthetic agents. The data are consistent with the interpretation that neurons in postarcuate cortex are excited to fire during the early surface response, undergo long-duration postsynaptic inhibition such as is generated in cortical neurons by activation of many cortical afferents, and then show postinhibitory rebound if input from the mesencephalic reticular formation has not been interrupted by lesions or anesthetic agents, or if the convulsants substitute for this input.     

Spinal evoked potential P2 wave elicited by C fiber input and depressed by analgesic factors

Spinal cord potentials were recorded from the surface of the spinal cord of rats. The effects of various treatments on a positive wave following the original P wave, which was evoked by strong electrical stimulation and named the P2 wave, were investigated. The results of this study demonstrate that capsaicin applied on to the sciatic nerve, intrathecal injection of morphine, electroacupuncture and noxious heat applied to the hindpaw contralateral to the recording side could suppress the P2 wave. These data suggest that P2 is mediated by C afferents and might be useful as a new indicator of spinal nociception.     

Spinal and cortical inhibition of intestinal motility in the squirrel monkey

Cortical control over intestinal motility was examined by stimulating the cerebral cortex and recording subsequent changes in gut volume in the chloralose-anesthetized squirrel monkey. Also, correlations were made between the cortical areas effecting changes in gut motility and those receiving sensory input from the bowel, by recording evoked potentials from the same areas following stimulation of the splanchnic nerve. It was found that: (a) intestinal motility is inhibited by stimulation of frontal polysensory cortex; (b) such inhibition does not occur following stimulation of primary sensory motor cortex; (c) visceral afferents carried in the splanchnic nerve converge with somatic inputs on the same frontal cortical area controlling gut motility; (d) the cortical control may act, at least in part, by modulation of the intestino-intestinal inhibitory reflex (I₃-R); and (e) the I₃-R in the squirrel monkey is similar to that previously described in carnivores.