Lateral spread response elicited by double stimulation in patients with hemifacial spasm

In patients with hemifacial spasm (HFS), a lateral spread response (or abnormal muscle response) is recorded from facial muscles after facial nerve stimulation. The origin of this response is not completely understood. We studied the lateral spread responses elicited by double stimulation in 12 patients with HFS during microvascular decompression. The response was recorded from the mentalis muscle by electrical stimulation of the temporal branch of the facial nerve or from the orbicularis oculi muscles by stimulation of the marginal mandibular branch. The interstimulus intervals (ISIs) of double stimulation ranged from 0.5 to 7.0 ms. R1 was defined as the response elicited by the first stimulus, and R2 as the response elicited by the second stimulus. R1 had a constant latency and amplitude regardless of the ISI, whereas R2 appeared after a fixed refractory period without facilitation or depression in a recovery curve of latency and amplitude. From these findings, we consider that the lateral spread response is due to cross-transmission of facial nerve fibers at the site of vascular compression rather than arising from facial nerve motor neurons.     

Characteristics of habituation of the sympathetic skin response to repeated electrical stimuli in man.

OBJECTIVES: To study the effect of repeating electrical peripheral nerve stimulation on latency, duration and amplitude of the sympathetic skin response (SSR). METHODS: SSRs were elicited in all limbs by median and peroneal nerves stimuli. In 10 subjects, 20 stimuli were applied at random time intervals (15-20 s). Another test was performed in 7 subjects using the same protocol, but switching the stimulation site every 5 or 10 stimuli without warning. RESULTS: The mean amplitude of right palmar response to right peroneal nerve stimulation decreased from 5.05+/-0.76 (SEM) mV at the first stimulus to 1.23+/-0.42 mV at the 20th stimulus (P<0.001). The latency did not change significantly (1473+/-82 to 1550+/-90 ms, P>0.1), while the duration increased (1872+/-356 to 3170+/-681 ms, P<0.001). Stimulation and recording at other sites showed similar trends. Changing the stimulation site failed to alter the adaptation process in terms of amplitude, latency or duration. CONCLUSIONS: Changes in amplitude and duration of the SSRs to repeated electrical stimuli can occur in presence of constant latency and appear to be independent of the source of sensory input. Peripheral sweat gland mechanisms may be involved in the loss of amplitude and increase in duration of the SSR during habituation.     

Primary hemifacial spasm: a neurophysiological study.

A series of 53 cases of primary hemifacial spasm have been evaluated by means of blink reflexes and their results compared with a normal control group. Reflex responses were obtained by percutaneous electrical stimulus of both the supraorbital nerve (trigemino-facial reflex), and the facial nerve at the stylo-mastoid region (facio-facial reflex). The R2 response was considered abnormal when its latency was shortened (hyperactivity) or delayed (hypoactivity). Thirty-six out of 53 cases with primary hemifacial spasm showed abnormal responses, with a combination of facial nerve impairment (delayed R2 in the facio-facial reflex) and trigeminal-facial hyperactivity (shortened R2 in the trigemino-facial reflex). Five cases showed hyperactivity in both the trigemino-facial reflex and the facio-facial reflex reflexes. These results suggest a state of hyperexcitability, probably at the level of the facial nucleus, combined with a peripheral facial nerve involvement in a high proportion of patients with primary hemifacial spasm.     

Mechanically and electrically evoked somatosensory potentials in humans: effects of stimulus presentation rate

Somatosensory evoked potentials were recorded in response to: (1) electrical stimulation of the median nerve at the wrist; (2) electrical stimulation of the index finger; (3) mechanical stimulation of the index fingernail. Stimuli were presented at rates of 2, 4, 8, 16 and 32/sec, and the effects of presentation rate on components of the evoked potentials were evaluated. The effect of varying the duration of the mechanical stimulus was also observed. The findings suggest that stimulus rates of up to 8/sec can be used without significant loss in detectability of most of the components. The potentials recorded in response to a short duration mechanical stimulus were essentially identical to those evoked by the long duration stimulus. The findings of this study are consistent with a peripheral nerve generator for the Erb's point recorded component, a postsynaptic generator for the upper neck recorded component, and in general with a larger number of synapses leading to the generators of the later components than to earlier ones.     

Long lasting excitability changes in human peripheral nerve

When pairs of equal but submaximal electrical stimuli are delivered to a peripheral nerve, the second stimulus does not always excite the same number of fibers as the first. The number of fibers responding to the second stimulus depends on the interstimulus interval; the refractory period, a well-defined period of hypoexcitability, is followed by longer lasting and less well-characterized periods of hyper- and hypoexcitability. These cycles last at least 200 ms after the initial stimulus. We have carefully studied these cycles of excitability in human peripheral nerve in 12 normal subjects. The magnitude of excitability changes were found to be much greater in motor fibers than in mixed nerve; under some conditions, the motor response was reduced by more than 80% at interstimulus intervals of 40 ms, while the mixed nerve response never varied by more than 20%. In addition, the amplitude of the excitability changes varied as a function of the stimulus strength, so that stimuli that were near threshold or evoked near maximal responses were associated with smaller excitability changes than stimuli evoking midrange responses. Given that the excitability fluctuations are of large magnitude and occur at interresponse intervals easily achieved during physiological firing, it is suggested that they may be important modifiers of firing rate under experimental or physiological conditions. © 1994 John Wiley & Sons, Inc.     

Release of substance P from peripheral sensory nerve terminals

It is postulated that release of SP from peripheral terminals of sensory neurons contributes to neurogenic inflammation and possibly mediates, in part, the inflammatory response in a variety of diseases. This review addresses the Ca2+-dependent release of SP from peripheral nerve terminals in response to antidromic electrical stimulation of peripheral nerves and noxious thermal and chemical stimuli. Initial studies suggested that SP release is induced via an axon reflex, which involves antidromic impulses travelling along the peripheral nerve terminal. Further investigation indicated that SP release is also induced via direct depolarization of the terminals and, possibly, via a chemically-mediated mechanism which is independent of electrical excitation. Multiple transduction mechanisms, involved in SP release, seem to differ depending on the type of stimulus. These multiple mechanisms may account for the different routes of Ca2+ influx, which occurs via both voltage-dependent calcium channels and receptor-operated channels. It is also emerging that SP release is modulated by endogenous factors which either enhance or inhibit release, making it apparent that the mechanism(s) underlying the release of SP from peripheral nerve terminals is more complex than initially proposed.     

The R3 component of the blink reflex in man: a reflex response induced by activation of high threshold cutaneous afferents

Ten successive experiments were carried out in 10 volunteers to compare the physiological properties of R2 and R3 components of the blink reflex. The electrical activation threshold of the R3 component was found to be significantly higher than that of the R2 response and was more susceptible to anaesthetic blocking of the peripheral afferents. This result suggests that the R3 component is induced by the activation of a different population of peripheral afferents from the R2 component. A recovery cycle study performed using a double stimulus showed that R3 is inhibited to a greater extent and for a longer time than R2. The temporal relationship of R3 to the voluntarily produced blink demonstrates that R3 is not a voluntary response to electrical stimulation. In conclusion, these experiments support the existence of an independent R3 component and its relationship with the activation of small diameter and higher threshold afferent fibres, perhaps nociceptive ones.     

The electromyographic silent period produced by supramaximal electrical stimulation in normal man

The electromyographic silent period produced by supramaximal electrical stimulation of the median nerve was recorded in the abductor pollicis brevis muscle of four normal subjects during maximal isometric voluntary contraction. Except for an inconstant F response, electrical silence could usually be induced in the muscle from the twitch potential until the reappearance of uninterrupted voluntary activity. The silent period produced by stimulation at the wrist was approximately 25 msec longer than that produced by stimulation at the elbow and was independent of muscle tension. Further shortening of the muscle during the twitch contraction did not significantly alter the length of the silent period. A silent period in the abductor pollicis brevis muscle was also obtained after stimulation of the ulnar nerve, at the wrist and at the elbow. The onset of this period of silence was delayed, but it ended at the same time after the stimulus as the corresponding silent periods produced by median nerve stimulation. It is concluded that the end point of the silent period produced by supramaximal electrical stimulation of a mixed peripheral nerve is determined by an inhibitory spinal reflex, afferent impulses travelling in slowly-conducting fibres that are directly activated by the stimulus. Under these conditions the length of the silent period gives no indication of spindle activity in the muscle.     

Physiologic and anatomic basis for contralateral R1 in blink reflex

We studied the rate of appearance and mechanism of contralateral R1 responses in normal subjects. Contralateral R1 could be produced by facilitating maneuvers such as a gentle contraction of the orbicularis oculi and conditioning stimulus of the median nerve. In addition, changing the position of the stimulating anode to the midline evoked these responses that were abolished by blocking the contralateral supraorbital nerve, confirming its peripheral origin. We conclude that crossed trigeminofacial pathways probably exist in normal subjects, but in some instances contralateral peripheral trigeminal ophthalmic sensory fibers may be stimulated, giving rise to a contralateral R1 response.     

Further evidence for a central reorganisation of synaptic connectivity in patients with hypoglossal-facial anastomosis in man

In normal subjects, electrical stimulation of trigeminal mucosal afferents (lingual nerve - V3) can elicit a short latency (12.5+/-0. 3 ms; mean+/-S.D.) reflex response in the ipsilateral genioglossus muscle (Maisonobe et al., Reflexes elicited from cutaneous and mucosal trigeminal afferents in normal human subjects. Brain Res. 1998;810:220-228). In the present study on patients with hypoglossal-facial (XII-VII) nerve anastomoses, we were able to record similar R1-type blink reflex responses in the orbicularis oculi muscles, following stimulation of either supraorbital nerve (V1) or lingual nerve (V3) afferents. However, these responses were not present in normal control subjects. Voluntary swallowing movements produced clear-cut facilitations of the R1 blink reflex response elicited by stimulation of V1 afferents. In a conditioning-test procedure with a variable inter-stimulus interval, the R1 blink reflex response elicited by supraorbital nerve stimulation was facilitated by an ipsilateral mucosal conditioning stimulus in the V3 region. This facilitatory effect was maximal when the two stimuli (conditioning and test) were applied simultaneously. This effect was not observed on the R1 component of the blink reflex in the normal control subjects. These data strongly suggest that in patients with XII-VII anastomoses, but not in normal subjects, both cutaneous (V1) and mucosal (V3) trigeminal afferents project onto the same interneurones in the trigeminal principal sensory nucleus. This clearly supports the idea that peripheral manipulation of the VIIth and the XIIth nerves induces a plastic change within this nucleus.     

Differential activation and block of peripheral nerve fibers by magnetic fields

The ability to noninvasively and reversibly block conduction in peripheral nerves would have several clinical applications. As an initial step in this direction, we investigated the possibility of magnetically generating and differentially blocking activity in mammalian peripheral nerve fibers in vitro. Compound action potentials at each end of individual explanted phrenic nerves were recorded in response to currents induced at the midpoint of the nerve with an externally placed magnetic coil. Current in the coil was then reversed and the recordings repeated. In all cases, the area under the compound action potential on the virtual anode side of the magnetic stimulus was reduced (mean of 18.2 +/- 8.8%) in comparison to the area on the virtual cathode side. This indicates that peripheral nerve activity can be differentially induced by magnetic stimulation. Extension of this effect to the point of generating unidirectional action potentials in vivo may prove clinically useful in a number of contexts, such as reducing contractures secondary to spasticity and generating magnetically induced anesthesia in limbs. Further investigations of this effect seem warranted.     

On the development of optical peripheral nerve interfaces

Limb loss and spinal cord injury are two debilitating conditions that continue to grow in prevalence. Prosthetic limbs and limb reanimation present two ways of providing affected individuals with means to interact in the world. These techniques are both dependent on a robust interface with the peripheral nerve. Current methods for interfacing with the peripheral nerve tend to suffer from low specificity, high latency and insufficient robustness for a chronic implant. An optical peripheral nerve interface may solve some of these problems by decreasing invasiveness and providing single axon specificity. In order to implement such an interface three elements are required:(1) a transducer capable of translating light into a neural stimulus or translating neural activity into changes in fluorescence,(2) a means for delivering said transducer and(3) a microscope for providing the stimulus light and detecting the fluorescence change. There are continued improvements in both genetically encoded calcium and voltage indicators as well as new optogenetic actuators for stimulation. Similarly, improvements in specificity of viral vectors continue to improve expression in the axons of the peripheral nerve. Our work has recently shown that it is possible to virally transduce axons of the peripheral nerve for recording from small fibers. The improvements of these components make an optical peripheral nerve interface a rapidly approaching alternative to current methods.     

Comparison of single motor unit responses to transcranial magnetic and peroneal nerve stimulation in the tibialis anterior muscle of patients with amyotrophic lateral sclerosis

Responses of single tibialis anterior motor units to transcranial magnetic stimulation and to a synchronized la volley evoked by peripheral nerve electrical stimulation were obtained in amyotrophic lateral sclerosis (ALS) patients and normal controls. Whereas the units of normal subjects exhibited rather stereotyped short-latency spike density peaks in response to both types of stimulus, the responses of ALS patient units were much less uniform. All ALS patient units exhibited a response to the synchronized la volley indistinguishable from that of normal subjects, indicating that the investigated spinal motoneurons are capable of normal excitatory responses in ALS patients. More than half of the ALS patient units responded to the transcranial magnetic stimulus with prolonged spike-density peaks appearing at a latency consistent with the notion that these pathological peaks are evoked by some relatively hyperexcitable structures presynaptic to the corticomotoneurons.     

ISP and PAP4 peptides promote motor functional recovery after peripheral nerve injury

Both intracellular sigma peptide(ISP) and phosphatase and tensin homolog agonist protein(PAP4) promote nerve regeneration and motor functional recovery after spinal cord injury. However, the role of these two small peptides in peripheral nerve injury remains unclear. A rat model of brachial plexus injury was established by crush of the C6 ventral root. The rats were then treated with subcutaneous injection of PAP4(497 μg/d, twice per day) or ISP(11 μg/d, once per day) near the injury site for 21 successive days. After ISP and PAP treatment, the survival of motoneurons was increased, the number of regenerated axons and neuromuscular junctions was increased, muscle atrophy was reduced, the electrical response of the motor units was enhanced and the motor function of the injured upper limbs was greatly improved in rats with brachial plexus injury. These findings suggest that ISP and PAP4 promote the recovery of motor function after peripheral nerve injury in rats. The animal care and experimental procedures were approved by the Laboratory Animal Ethics Committee of Jinan University of China(approval No. 20111008001) in 2011.     

Patterns of conduction impairment in experimental allergic neuritis. An electrophysiological and histological study.

Electrophysiological and histological studies of peripheral nerve were performed in 24 Lewis rats with experimental allergic neuritis (EAN) in which disease had been induced by a single myelin and adjuvant inoculation in one footpad. Demyelination was demonstrated in transverse nerve sections from ventral roots, proximal sciatic nerves and also in distal plantar nerves. Histological and electrophysiological assessments showed that injected limbs were more affected than uninjected limbs. Neurophysiological studies demonstrated two distinct patterns of conduction failure based upon proximal/distal compound muscle action potential (CMAP) amplitude ratios in both uninjected and injected limbs. Slightly more than half of all nerve trunks showed a mildly reduced distal CMAP amplitude irrespective of stimulus origin. The rest displayed a more severe reduction of distal amplitude that was length-dependent, becoming smaller with proximal stimulation. Histological lesions in plantar nerves were often more severe than those in proximal sciatic nerves or ventral roots. Axonal degeneration was an uncommon finding. This study has demonstrated patterns of peripheral nerve conduction impairment similar to those reported in patients with inflammatory demyelinating neuropathy. Moreover, it has shown that a low distal CMAP amplitude may result from demyelination of distal motor nerve segments and not necessarily from axonal degeneration.     

Sudomotor nerve conduction velocity and central processing time of the skin conductance response.

OBJECTIVE: To estimate the sudomotor nerve conduction velocity (CV), the central processing time (CPT) and habituation of the skin conductance response (SCR). METHODS: SCRs in response to a single deep inspiratory breath, an electrical stimulus and a sound click were obtained from the fingers and toes of 30 healthy adults. Sudomotor nerve conduction velocities were determined after measuring extremity length and latency differences. CPT was estimated by subtracting the efferent time and the known afferent times and neuroeffector times from the onset latency. RESULTS: The inspiratory SCR habituated slower than the auditory or electrical SCRs. CVs of the 3 modalities did not differ statistically and their mean was 1.07 m s(-1) (95% CI: 1.01-1.13). The inspiratory SCR arrived at the fingers 1.26+/-0.09 s after the onset of chest wall movement. Electrical and auditory SCR onset latencies at the fingers were 1.60+/-0.03 and 1.75+/-0.04 s, respectively. Their CPTs were 140 and 160 ms, estimated from the electrical and auditory SCR onset latencies to the fingers. The CPT for inspiratory SCR was estimated to occur during the inspiratory CPT after the inspiratory decision and before chest movement. CONCLUSIONS: In contrast to the SCR following an electrical or auditory stimulus, initiation of deep inspiratory SCR occurs before the inspiratory act, precluding any possible input from respiratory afferent receptors and implicating a central generator. SIGNIFICANCE: This study provides new insights into the origin of the SCR following inspiration.     

The refractory period of fast conducting corticospinal tract axons in man and its implications for intraoperative monitoring of motor evoked potentials.

OBJECTIVE: To determine the absolute and relative refractory period (RRP) of fast conducting axons of the corticospinal tract in response to paired high intensity (HI or supramaximal) and moderate intensity (MI or submaximal) electrical stimuli. The importance of the refractory period of fast conducting corticospinal tract axons has to be considered if repetitive transcranial electrical stimulation (TES) is to be effective for eliciting motor evoked potentials (MEPs) intraoperatively. METHODS: Direct (D) waves were recorded from the epidural space of the spinal cord in 14 patients, undergoing surgical correction of spinal deformities. To assess the absolute and RRPs of the corticospinal tract, paired transcranial electrical stimuli at interstimulus intervals (ISI) from 0.7 to 4.1 ms were applied. Recovery of conditioned D wave at short (2 ms) and long (4 ms) ISI was correlated with muscle MEP threshold. The refractory period for peripheral nerve was tested in comparison to that for the corticospinal tract. In four healthy subjects sensory nerve action potentials of the median nerve were studied after stimulation with paired stimuli. RESULTS: HI TES revealed a mean duration of 0.82 ms for the absolute refractory period of the corticospinal tract, while MI stimulation resulted in a mean refractory period duration of 1.47 ms. Stimuli of HI produced faster recovery of D wave amplitude during the RRP. Furthermore, short trains of transcranial electrical stimuli did not elicit MEPs when D wave showed incomplete recovery. A similar influence of stimulus intensity on recovery time was found for the refractory period of peripheral nerve. CONCLUSIONS: The recovery of D wave amplitude is dependent upon stimulus intensity. High intensity produces fast recovery. This is an important factor for the generation of MEPs. When HI TES is used to elicit MEPs, short and long ISIs are equally effective. When MI TES is used to elicit MEPs, only a long ISI of 4 ms is effective.     

Facilitation of motor evoked potentials by somatosensory afferent stimulation.

The effect of an electrically induced peripheral afferent volley upon electrical and magnetic motor evoked potentials (MEPs) from muscles of the upper and lower extremities was studied in 16 healthy volunteers. A standard conditioning-test (C-T) paradigm was employed whereby the test stimulus (transcranial electric or magnetic) was applied at random time intervals, from 10 msec prior to 90 msec after the conditioning stimulus (peripheral nerve stimulus). MEP amplitude facilitation was observed for the majority of the upper extremity muscles tested at two distinct periods, one occurring at short, and the other at long C-T intervals. This bimodal trend of MEP facilitation was found to be equally as prominent in the lower extremity muscles tested. The period of short C-T interval facilitation is consistent with modifications in the spinal excitability of the segmental motoneuron pool. On the other hand, the period of long C-T interval facilitation is suggested to be due to alterations in excitability of the motor cortex as a result of the arrival of the orthodromic sensory volley. Although most pronounced in muscles innervated by the nerve to which the conditioning stimulus was applied, this bimodal facilitatory effect was also observed in adjacent muscles not innervated by the stimulated nerve. Qualitatively, the conditioned MEPs from the upper and lower extremities responded similarly to both electrical and magnetic trans-cranial stimulation. In addition, our study demonstrates that the C-T paradigm has potential for use in the assessment of spinal and cortical sensorimotor integration by providing quantitative information which cannot be obtained through isolated assessment of sensory and/or motor pathways.(ABSTRACT TRUNCATED AT 250 WORDS)     

高压电烧伤后周围神经损害的调查研究

目的探讨高压电烧伤病例周围神经的损害情况。方法采用回顾性研究,收集2012-01—2016-10因"高压电烧伤"入我院治疗的病例资料,所有患者均接受过神经传导测试(NCSs),收集受伤侧及正常侧数据并进行分析。结果 30例患者(42侧肢体)纳入研究,其中56.7%的患者从事电工维修职业,其余主要为意外触电所致。52.5%的患者正中神经至少出现一项参数异常;44.7%的患者出现尺神经的异常,未发现脱髓鞘的证据;12例患者行正常侧的NCSs检测,复合肌肉动作电位及神经传导速度显著高于患侧(P0.05);25例随访显示复合肌肉动作电位及神经传导速度均显著改善(P0.05)。结论高压电烧伤后主要造成患者的周围神经损害而非脱髓鞘病变。虽伤后NCSs检测结果正常,患者仍可能存在外周神经损害;对侧肢体的对照及后续的随访对于周围神经损害的确切评价具有重要意义。     

Deafness alters auditory nerve fibre responses to cochlear implant stimulation

Here we characterized the relationship between duration of sensorineural hearing loss and the response of the auditory nerve to electrical stimulus rate. Electrophysiological recordings were made from undeafened guinea pigs and those ototoxically deafened for either 5 weeks or 6 months. Auditory neuron survival decreased significantly with the duration of deafness. Extracellular recordings were made from auditory nerve fibres responding to biphasic, charge-balanced current pulses delivered at rates of 20 and 200 pulses/s via a monopolar scala tympani stimulating electrode. The response to 20 pulses/s electrical stimulation of the deafened cochlea exhibited a decrease in spike latency, unaltered temporal jitter and unaltered dynamic range (of nerve firing rate against stimulus current), and a reduction in threshold after 6 months of deafness. The response to a 200-pulse/s stimulus was similar except that the dynamic range was greater than with 20 pulses/s and was also greater in deafened animals than in undeafened animals. Deafness and pulse rate are related; in deaf animals spike recovery appears to be complete between successive stimulus pulses at a low rate (20 pulses/s), but incomplete between pulses at a moderate pulse rate (200 pulses/s). These results suggest that changes in the function of individual auditory nerve fibres after deafness may affect clinical responses during high-rate stimulation such as that used in contemporary speech processing strategies, but not during lower rate stimulation such as that used to record evoked potentials.