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 Table of Contents  
Year : 2020  |  Volume : 37  |  Issue : 3  |  Page : 101-109

Cutaneous silent period: A literature review

1 Department of Neurology, Cerrahpasa Medical Faculty, IUC, Turkey
2 Department of Neurology, Cerrahpasa Medical Faculty, IUC; Department of Neurology, Yedikule Chest Diseases and Chest Surgery Training and Research Hospital, İstanbul, Turkey

Date of Submission05-Apr-2020
Date of Decision05-May-2020
Date of Acceptance18-May-2020
Date of Web Publication16-Sep-2020

Correspondence Address:
Ayşegül Gunduz
Department of Neurology, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, İstanbul
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/NSN.NSN_38_20

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Cutaneous silent period (CSP) is the temporary suppression of voluntary muscle contraction by sensory stimulation. Here, we aimed to summarize the effect of physiological and pathological conditions on CSP and to reappraise its clinical utility in daily practice. We performed a literature search using the term “cutaneous silent period.” The search included all articles published in English in the PubMed, Cochrane Library, Google Scholar, and MEDLINE databases until October 2018. We have analyzed all articles covering CSP to collect the work on physiological conditions such as temperature, recording site, stimulus intensity, nonpharmacological interventions, and different medications or pathological conditions. Temperature, gender, recording site, stimulus duration, and stimulus intensity affect the parameters related to CSP. CSP onset latency is mainly affected by interventions affecting A-delta fibers. CSP shows changes in entrapment neuropathies and polyneuropathies. CSP is mainly mediated by A-delta fibers with contribution of large-diameter fibers. It is a spinal inhibitory response. It should be recorded under optimum temperature. Its clinical use in the diagnosis or assessment of neuropathic pain is limited. It is sometimes used to show functions of A-delta fibers.

Keywords: A-delta fibers, cutaneous silent period, pathological disorders, temperature

How to cite this article:
Gunduz A, Aydın &, Kızıltan ME. Cutaneous silent period: A literature review. Neurol Sci Neurophysiol 2020;37:101-9

How to cite this URL:
Gunduz A, Aydın &, Kızıltan ME. Cutaneous silent period: A literature review. Neurol Sci Neurophysiol [serial online] 2020 [cited 2023 May 29];37:101-9. Available from: http://www.nsnjournal.org/text.asp?2020/37/3/101/295179

  Introduction Top

Sensory (low-intensity or high-intensity, noxious electrical) stimulation may provide a temporary suppression in the electromyographic (EMG) activity during voluntary muscle contraction.[1],[2],[3] When obtained after a noxious electrical stimulation of a pure cutaneous nerve, it is called the cutaneous silent period (CSP), whereas silent period obtained after low-intensity stimulation is called cutaneomuscular response. Three separate phases of EMG modulation are distinguished in CSP: a first inhibitory phase (I1), an excitatory phase, and a second inhibitory phase (I2). I1 is the partial inhibitory phase, whereas total inhibition occurs in the second inhibitory phase (I2). The excitatory phase interrupting the periods of inhibition is suggested to contain a transcortical so-called long-loop reflex (LLR). The excitatory phase after the I2 is postinhibition excitatory phase.

Together with withdrawal reflexes, which are also generated by applying noxious, CSPs are mostly protective responses. CSP is mediated by a spinal inhibitory reflex that is subject to supraspinal descending control.[4] Studies suggest that inhibitory reflexes (CSP) and excitatory responses (withdrawal reflexes) share the same spinal circuitry.[2] CSP is mainly activated by slow-conducting, high-threshold A-delta-type nociceptive fibers.[3],[5],[6] The hypothesis was that CSP was generated at the level of corticospinal tract neurons, inhibitory interneurons, or spinal motoneurons. Different authors recorded motor-evoked potentials (MEPs), H-reflexes, or F-waves during recordings of CSPs. Leis et al.[7] studied H-reflexes and F-waves during CSPs and found that spinal motoneurons remained excitable throughout the CSP, suggesting a prominent role of presynaptic inhibition in the generation of CSPs,[7] whereas there was a similar temporal change of H-reflexes and MEPs during the CSP in the study of Manconi et al.[8] Thus, the latter study attributed the primary mechanism underlying a CSP to the postsynaptic inhibition of motoneurons.[8]

Conventionally, CSP is known to reflect the function of small-diameter fibers, i.e., A-delta fibers, however, it was not superior to laser evoked potentials in assessing the functions of nociceptive pathway in patients with neuropathic pain.[9] Concomitant studies also suggested contribution of other fibers [10] or startle response [11] and modulatory influence of suprasegmental pathways on CSP.[12] Therefore, we aimed to reappraise the utility of CSP in pain and in other disorders. In this review article, we have analyzed the articles covering CSP to collect the work on the effect of physiological conditions such as temperature, stimulus intensity, and different medications or pathological conditions upon CSP. By this way, we will be able to summarize the required optimum conditions to obtain CSP and its clinical use.

  Data Source and Methodology Top

We performed a literature search using the term “cutaneous silent period.” The search included all articles published in English in the PubMed, Cochrane Library, Google Scholar, and MEDLINE databases until October 2018 that analyzed CSP in healthy subjects or in groups of different disorders. We only included research articles and studies in humans. The studies in languages other than English, reviews or case reports, and studies of recordings only on facial muscles were excluded.

This review examined the details of physiological conditions under which the CSP was recorded, and the details of clinical and electrophysiological examinations. The clinical and demographic characteristics of the patients population (age, number of subjects, and disease duration), if included, their clinical data and assessment, the study design, details of pharmacological interventions or other intervention methods, measured electrophysiological parameters (duration, onset or end latencies, index of suppression, LLR amplitude, LLR latency), parameters related to other electrophysiological studies if performed were extracted. Various studies used different methods such as duration, onset latency, or end latency of total CSP, I1, or I2 phase. First, we analyzed which one was chosen in this specific article. In the second, step, we analyzed the change of the parameter in this specific condition. When calculating suppression index, the mean EMG amplitude was divided by mean baseline EMG amplitude and multiplied by 100. Suppression indices of CSP, I1, and I2 were calculated correspondingly by dividing either mean EMG amplitude during CSP, during I1 or during I2 by mean baseline EMG amplitude, respectively.

While searching the databases, we observed that we were able to group all studies under three headlines: physiological conditions, pharmacological/nonpharmacological interventions, and pathological conditions.

  Results Top

By a search using the term “cutaneous silent period,” we have determined 93 articles. After excluding review articles and case reports on the subject, we have included 75 articles in this review.

We classified articles under the headings of studies analyzing the effects of physiological conditions, pharmacological and nonpharmacological interventions, or pathological conditions. Although we classified the studies covering modulation of CSP by sensory or visceral stimulation [11],[13],[14] under the heading of changes by different physiological conditions, we grouped the two studies exploring the effects of transcutaneous electrical nerve stimulation (TENS)[15] or vibration [16] under the heading of pharmacological and nonpharmacological interventions because the former is used for the antinociceptive strategy and the latter is used for the effect on large fibers.

To determine EMG suppression periods, multiple (at least 10) consecutive recordings are done. Subsequently, all recordings are rectified and averaged. Conventionally, CSP is recorded on the distal muscles of upper extremities, for example, first dorsal interosseus or abductor pollicis brevis muscles and we have found studies performing CSPs over lower limb,[6],[14],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26] one of which recorded CSPs over a proximal muscle (rectus femoris).[26] Most of the studies used duration and onset latency of CSP. However, various parameters have been measured on a given CSP,[15],[27] each was suggested to develop secondary to several physiological factors. They may be listed as follows:

  • Mean baseline EMG amplitude during a 120 ms period preceding the stimulus
  • Onset latency, end latency, duration, and suppression index of the entire CSP
  • Duration and suppression index of I1;
  • Onset latency, end latency, duration, and area of LLR, as well as absolute LLR amplitude and amplitude relative to mean baseline EMG amplitude
  • Duration and suppression index of I2
  • Post-CSP EMG rebound
  • Afferent conduction time of CSP.

They were defined in previous reports.[15],[27] Afferent conduction time of CSP was calculated as follows: CSP latency-root MEP latency.[28]

Some of the studies also included other types of electrophysiological measurements, which were;

  • MEPs
  • Withdrawal reflex (RIII)
  • F-wave (latency and duration)
  • Cutaneomuscular response
  • Compound muscle action potential
  • H reflex and H/M ratio
  • Sympathetic skin response
  • Motor unit potentials.

  Studies Analyzing the Effects of Physiological Conditions Top

Several parameters such as recording site, stimulus intensity, stimulus type, stimulus location, muscle force, limb temperature, and gender of participants may have an influence on CSP.

CSPs were accepted as robust responses because there are not huge differences between different types of stimulation or recording site.

To obtain a CSP, the stimulus should be noxious and high in intensity.[6] By this way, it is possible to trigger high-threshold sensory fibers. In general, twenty times the sensory threshold is used to evoke an inhibitory period.[1],[2],[27] Low-threshold stimuli (1 or 2 × sensory threshold) can also induce an inhibitory response restricted to the distal muscles.[10] Thus, the authors claimed contribution of low-threshold afferents in the production of the CSP in the upper limbs. However, to us, these responses resemble cutaneomuscular responses and are beyond our topic in this review.

Different studies investigated the effects of changes in stimulus intensity or duration on CSP. The CSP duration increased, and suppression index decreased with increasing stimulus intensity, from 10, 15, up to 20 times the sensory threshold.[29] However, another study showed higher intensities varying between 40 and 80 mA did not change the CSP duration. Similarly, stimulus durations varying between 0.2 and 1.0 ms did not change CSP duration, either.[30] These authors recommend to use an electrical stimulus with a minimum stimulus intensity of 40 mA and with a minimum stimulus duration of 0.2 ms. The onset latency, on the hand, shortened as stimulation intensity increased.[6]

Stimulus other than the electrical one may also evoke CSP. One recent study showed laser evoked CSP, in which 8 Hz laser pulses were applied to palm and reflex was recorded on first dorsal interosseous muscle.[31] The onset latency and duration of CSP evoked by laser stimulation were longer compared to those evoked by electrical stimulation. However, there was no response after laser stimulation of the hand dorsum although electrical stimulation of both the dorsum and the palm or laser stimulation of palm evoked a CSP.[32]

The recording site, as we mentioned, is mostly distal muscles of upper extremities, for example, first dorsal interosseus or abductor pollicis brevis muscles. After stimulation of one cutaneous nerve, CSP is evoked in different limb and cranial muscles, and it occurs synchronously in antagonist muscles.[3] One study analyzed CSPs over seven muscles (proximal and distal) in upper extremities after noxious finger stimulation which showed existence of CSP over both flexor and extensor muscles. Distal muscles of the upper limb presented with the earliest reflex onset times, longest reflex duration, and lowest level of EMG suppression when compared to the more proximal muscles, regardless of extensor/flexor role.[33] In some studies, noxious lower extremity stimulation was able to trigger CSPs over the distal muscles of lower extremities [6],[19] or over quadriceps femoris muscle.[26] However, to elicit CSP over quadriceps femoris muscle,[26] the authors used a train of five electrical pulses. There are no side differences in a given individual.[34] Kofler and Poustka also studied contralateral recordings of CSP after noxious digital stimulation and found no crossed inhibition over contralateral thenar muscles.[2]

Regarding muscle contraction, average EMG amplitudes prior to stimulus and during the CSP increased with the increasing amount of voluntary muscle contraction (20%, 40%, and 60% of maximum value).[29],[35] The CSP onset and end latency, and CSP duration, are not influenced by voluntary muscle contraction ranging from 10% to 50% of the maximum. Kofler et al. found no change in the magnitude of EMG suppression.[35]

Temperature is an important external factor affecting CSPs. In cold limbs (15°C cold water for 20 min), CSP onset and end latencies were delayed, which was even more prominent than distal and proximal median nerve motor and sensory latencies, whereas CSP duration was not affected. In warm limbs (42°C warm), smaller changes, which were opposite to cold, were reported.[35]

Gender may also affect CSP. Interestingly, females tended to have shorter CSP onset latencies, longer CSP duration, and a smaller index of suppression, resulting in a larger overall suppression.[34]

In paired stimulus experiments, used to study the recovery cycle of the CSP, neither low- nor high-intensity conditioning stimuli delivered 100–500 ms before the test stimulus changed test CSPs.[1],[3] It also did not habituate after trains of 5 Hz stimuli.[3] At shorter interstimulus intervals (60-, 80-, and 100-ms), however, CSP onset latencies were delayed and durations were shorter whereas there were no significant differences in the latencies and durations between test and conditioning CSPs beyond 120 ms.[36]

Several researches studied the modulation of CSP during or after heterotopic stimulations or visceral changes. An interesting study explored the effects of heterotopic painful and nonpainful stimulation on CSP in healthy adults.[13] The study found no change in CSP by nonpainful stimulation whereas CSP duration was shorter, and its onset latency was longer during painful stimulation of opposite hand. There was no difference during painful stimulation of opposite foot.[13]

Low-intensity sensory conditioning (prepulse) stimulus did not influence CSP onset and end latency, CSP duration, and the degree of EMG suppression, whereas prepulse stimuli significantly reduced EMG activity after CSP.[11]

Modulatory effect of descending pathways and viscero-somatic interactions were explored through investigating effect of bladder filling on CSPs, nociceptive withdrawal reflex and H reflex in healthy subjects.[14] In this study, there was no interaction of CSP and bladder filling.

A different approach used probability-based and frequency-based analyses simultaneously to examine CSP. In this method, motor unit potentials were monitored through wire electrodes during shocks of strong electrical stimuli.[37] The authors were able to induce CSP in all motor units tested and based on their results; the authors suggested that the strong electrical stimuli induce longer lasting inhibitory currents than the previous opinion. By this analysis, they also suggested the postinhibition excitatory phase appeared to be a continuation of the CSP because all IPSPs appeared synchronously and generated a sizable peak.

  Studies Analyzing the Effects of Pathological Conditions Top

Interestingly, CSP has been analyzed in almost all disorders of nervous system, including both peripheral and central nervous system disorders. Among these disorders, polyneuropathies, pain syndromes, restless legs syndrome (RLS), and different types of parkinsonism syndromes comprise most of the studies.

Latency and duration of CSP have been measured in cases with carpal tunnel syndrome (CTS).[23],[38],[39],[40],[41],[42],[43] There was no change in end latency, whereas onset latency was prolonged in some.[23],[41] However, two studies showed no abnormal CSP findings.[38],[41] CSP duration did not correlate with the presence or severity of pain in CTS.[43] Kofler et al. investigated CSP in various entrapment neuropathies and found preserved CSP in some patients similar to a subsequent study.[39] There was no association of clinical symptomatology and CSP, whereas longer latencies correlated with severity of CTS.[42]

In meralgia paresthetica, CSP recorded on vastus medialis after stimulating anterolateral side of the thigh had delayed-onset latency and shorter duration compared to healthy controls. There was a mild correlation between disease duration and onset latency.[26]

CSP was also recorded in the vast majority of polyneuropathy syndromes such as hereditary sensory-autonomic neuropathy,[44] human immunodeficiency virus-related peripheral neuropathy,[24] and demyelinating and axonal polyneuropathies [28] or in patients with diabetes mellitus,[22],[45],[46] with Fabry disease,[25] undergoing hemodialysis,[47] or with hyperlipidemia.[48] In the demyelinating PNP group, the afferent CSP conduction time was significantly longer; in the axonal PNP group, CSP duration was shorter than the demyelinating group and healthy controls, whereas CSP parameters were not different between patients with and without neuropathic pain.[28] In human immunodeficiency virus-related peripheral neuropathy, CSP recorded over intrinsic hand muscles had significantly delayed onset latency, independent from the involvement of large fibers of upper extremities.[24] Hemodialysis led to longer onset latencies in association with large-fiber neuropathy.[47] CSP durations exhibited a bimodal distribution in patients with Fabry disease, including a subset of seven patients with durations shorter than all controls.[25] This subset also had a profound loss of thermal sensation in the feet, similar to some patients who had normal CSPs. Patients with shortened CSPs had modestly elevated vibration thresholds and reduced sensory potentials in comparison to patients with normal CSPs. Patients with hyperlipidemia who described symptoms suggestive of small-diameter fiber neuropathy underwent nerve conduction studies, CSP, and sympathetic skin response studies.[48] Patients had prolonged CSP latencies on upper extremities and shortened CSP duration on both upper and lower extremities, despite normal sympathetic skin response latencies and amplitude. In one study of generalized chronic pruritus, CSP onset latency in the upper and lower extremities was longer and duration was shorter in the patient group compared with the controls.[49] In patients with diabetes mellitus, the first study showed longer CSP onset latency than controls, however, the duration of CSP was similar between the two groups. The CSP latency of patients who were clinically diagnosed with small fiber neuropathy was not different than the latencies of patients without findings suggestive of small fiber neuropathy.[45] In a subsequent study, Onal et al. showed longer lower extremity CSP latency and shorter CSP duration in patients with diabetes than controls, more significantly in patients with neuropathic pain.[22] In another study, patients with diabetes, with large-fiber neuropathy, small-fiber neuropathy, or even asymptomatic patients had significantly prolonged onset latency, which also significantly correlated with the late responses in routine nerve conduction studies.[46] In pure sensory neuronopathy with absent sensory responses, CSPs were found to be preserved.[5]

There are several studies analyzing CSP in RLS.[18],[21],[50],[51] The first study, in this regard, used CSP to disclose any relationship between RLS and small fiber neuropathy which showed prolonged CSP duration on lower extremities in RLS and its normalization after dopaminergic treatment.[50] Subsequent studies did not replicate these results and disclosed conflicting findings: no difference of CSP duration or onset latency on lower or upper extremity [18] as well as shorter CSP duration and delayed onset latency on upper [21] or lower extremity.[18],[21]

Four studies analyzed CSPs in fibromyalgia or myofascial pain syndrome.[17],[20],[52],[53] Three of them determined longer CSP onset latency lower and upper extremities,[17],[20],[53] one of which also found shorter CSP duration although the other two studies did not show any change in duration. Interestingly, one study [52] revealed shorter CSP onset latency.

In some other peripheral nervous system disorders such as brachial plexopathy even with multiple root avulsions, the CSP was mostly preserved.[54] In cases with radiculopathy and cervical root avulsion, only a small portion of patients had absent CSPs.[54],[55] In patients with syringomyelia at the cervical spinal cord, mean SEP amplitude obtained on vertebral column was reduced whereas CSPs were absent in almost half of the patients on the symptomatic side.[56] Motor responses, MEPs and F-wave were normal. However, in chronic whiplash injury, CSP was abnormal in 90% of the cases despite normal MEPs and neuroimaging in almost 80% of the patients.[57] In assessing the type of pain in postburn scars, CSP was evaluated and was shown to have short duration.[58]

Although CSP onset latency was longer in patients with amyotrophic lateral sclerosis (ALS) than that in healthy controls and CSP duration was not different, there were no changes of CSP recorded over thenar and hypothenar muscles in ALS patients even in the presence of split-hand phenomenon.[59]

Regarding disorders involving mostly central nervous system, duration of CSP was longer in patients with Parkinson's disease,[60] with brachial dystonia [61] or with multiple system atrophy.[62] Onset and end latencies of CSP were also longer in patients with multiple system atrophy. Patients with brachial dystonia had longer CSP duration with no change in latency and suppression of EMG activity, very similar to that found in Parkinson's disease. Subsequent studies disclosed longer CSPs in patients with organic or psychogenic dystonia [63] or delayed CSP onset latencies with no different duration.[64] The patients in the latter study had generalized or cervical dystonia and were examined after pallidal deep brain stimulation. In a specific type of ataxia (cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome, CANVAS), CSP was absent in more than half of the patients with other abnormal electrophysiological findings (e.g., uniformly absent sensory nerve action potentials in all limbs, abnormal blink reflexes, abnormal masseter reflexes, absent tibial nerve H-reflexes and abnormal somatosensory evoked potentials).[65]

  Studies Analyzing the Effects of Pharmacological and Nonpharmacological Interventions Top

To date, tramadol, escitalopram, fentanyl, cetirizine, propranolol, baclofen, anesthetic nerve blockage, TENS, and vibration have been used mainly to understand and to reveal the neurotransmitters or type of fibers operating in CSP pathway.

The studies covering tramadol, escitalopram, fentanyl, cetirizine, TENS, and vibration were carried out in healthy controls. Pujia et al. measured CSP duration over first dorsal interosseus muscle and noxious withdrawal flexor reflexes in the right biceps femoris muscle before, 30 min and each hour up to the 6th after administration of 100 mg oral tramadol to 11 healthy volunteers.[66] Tramadol lengthened the CSP duration, which paralleled the reduction in withdrawal reflexes and subjective pain perception. Similarly, CSPs in the first dorsal interosseous muscle of the right hand were longer 3 h after administration of a single, 20 mg oral dose of the selective serotonin reuptake inhibitor, escitalopram,[67] whereas there were no changes in CSP latency and subjective pain threshold. Placebo did not lead to any change in any of the parameters, either. Duration of CSP over the first dorsal interosseous muscle was also assessed before and 10 and 20 min after fentanyl injection, which caused no change in CSP duration whereas it suppressed RIII component of nociceptive reflex.[68] In the study of Kofler et al., the authors measured CSP onset and end latency as well as CSP duration and index of suppression before and 90, 180, and 360 min following intake of 10 mg cetirizine and showed no change in any of the parameters measured.[69]

Kofler studied the effects of 15-min high-frequency TENS on CSP.[15] CSP onset latency, CSP duration, index of suppression, LLR amplitude, and LLR latency were measured. CSP duration was shorter, whereas the index of suppression and LLR amplitude were lower. The increase in exteroceptive EMG inhibition was attributed to the concomitant suppression of transcortical LLRs. In the study analyzing the effect of vibration, CSP onset and end latencies, CSP duration, suppression index, and amplitude and latency of LLR were measured. The study reported reduced suppression during and shortly after vibration.[16]

In a study of CSP in neurologically normal patients prepared for surgery of hallux valgus, CSP onset latency was delayed and CSP duration was shorter after ultrasound-guided sciatic nerve popliteal anesthetic block, whereas no change in CSP end latency developed.[19] Other electrophysiological tests included sympathetic skin response, F-wave, and cutaneomuscular reflex. The amplitude of sympathetic skin response gradually reduced and latency of F-waves increased with reduced persistence. In a study of patients with essential tremor, prolonged CSP was normalized after the administration of low-dose propranolol for a month.[70] Levodopa did not normalize any of the abnormal CSP parameters in patients with multiple system atrophy [62] whereas, in patients with Parkinson's disease,[60] a single dose of levodopa or a treatment trial for 3 months provided shortening of CSP duration. There was no change of CSP onset latency. CSP duration of both upper and lower extremities was longer 1 week after the initiation of pramipexole (0.5 mg/day) in patients with RLS, in which condition the authors measured longer duration CSP over upper extremities and shorter duration in lower extremities compared to healthy controls prior to the treatment.[18] Another study among patients with RLS showed normalization of CSP duration after 1-month treatment with dopamine agonist.[50] The effect of baclofen on CSP was also investigated in patients with spasticity developed after spinal cord injury or progressive multiple sclerosis.[71] Intrathecal baclofen administered for spasticity did not change CSP latency and duration.

Pallidal deep-brain stimulation for upper limb dystonia did not change the CSP.[64]

  Discussion Top

Most authors agree that the presence of a CSP is dependent on intact small-diameter A-delta fibers, while the efferent reflex arm is formed by the large-diameter alpha motoneurons.[19],[34],[72]

To obtain optimum investigation parameters, one should pay attention to the recording site, temperature of the extremity on which the recordings are done, the level of muscle contraction, the site of stimulation, as well as the stimulus intensity and duration. Cold should be avoided during recordings. Level of contraction may be between 20% and 60% of the maximum value. Stimulus should be applied on the same extremity as the recording site.[34] The stimulus intensity should be at least twenty times the sensory threshold, preferably above 40 mA and stimulus duration should be at least 0.2 ms.[30] Conventionally, the distal hand muscles are used, however, CSP may be generated on any extremity muscle [3],[33] and the recording site depends on the hypothesis. The normal values, on the other hand, changes according to the recordings site. Normal values also change according to the gender.[34]

The onset latency is generated by the small-diameter A-delta fibers.[20] According to Serrao et al., large diameter afferents provide a small contribution to the CSP maintaining the excitability of interneurons and probably providing an additional security for the protective reflex.[10] The effect of vibration in healthy controls also confirms large-diameter afferents operate in the depth of inhibition.[16] The CSP pathway is devoid of μ-opiate receptors since there is no effect of fentanyl.[68] Although it is an inhibitory spinal phenomenon, the circuit is not modulated by GABA-B receptors.[71] However, corticospinal projections modulate the excitability of CSP.[12]

Post-CSP EMG rebound activity is mainly accepted to be generated by the resynchronization of motoneurons. Some evidence also suggests that post-CSP EMG rebound activity may contain an excitatory reflex component, which, based on the latency and the nature of the underlying stimulus, is compatible with a somatosensory startle reflex.[11]

CSPs were primarily used to analyze the integrity and functioning of small-diameter fibers. Conventionally, CSP has been used to understand the contribution of small-fiber pathology in various disorders. Among them, in patients with diabetes mellitus who had large-fiber or small-fiber neuropathy or were asymptomatic, CSP onset latency was longer.[45],[46],[48] The abnormal CSP finding was more significant in patients with neuropathic pain in diabetes mellitus [22] whereas there was no relationship with neuropathic pain and abnormal CSP in other types of polyneuropathy syndromes.[28] Although CSP onset latency was longer in patients with hyperlipidemia or chronic pruritus, there was no association between small-fiber neuropathy in Fabry disease and CSP.[25]

Longer CSP latency in CTS was also attributed to the dysfunction and delayed conduction of A-delta fibers secondary to compression. However, normal CSP in other studies of CTS suggests other factors.[39],[42] Normal CSP in entrapment neuropathies may be used to determine residual intact fibers and fiber continuity.[39] Based on the absence of correlation between pain in these patients and abnormal CSP findings, the authors suggested CSP should not be used as an objective method in the evaluation of pain in entrapment neuropathies.[42] Despite the limited diagnostic value of CSP in most of the entrapment neuropathies, CSP may be used in diagnosing meralgia paresthetica. Because lateral femoral cutaneous nerve is a pure sensory nerve and is difficult to record in some patients, CSP may be obtained and longer onset latency suggests meralgia paresthetica.[26] CSPs were also studied in pathological conditions affecting more proximal parts of the lower motor neuron or spinal cord. However, there were conflicting results. CSP was helpful in chronic whiplash injury or some cases of syringomyelia, however, it was mostly preserved in radiculopathy or root avulsions limiting the clinical use in these conditions. In disorders, such as ALS, Parkinson's disease, or dystonia, it can be used for investigational purposes, not for diagnosis or follow-up. In RLS or myofascial pain syndrome, CSP findings were conflicting.

In assessing the origin of the pain in conditions with impaired integrity of skin such as postburn scars, the safety of CSP is unknown and recording CSP is not recommended.[73] Anyway, despite the role of A-delta fibers in the production of CSP, the suggestion was that it was not a good way to assess neuropathic pain.[9] However, this study only studied correlation between the duration of CSP and neuropathic pain. In a similar study, authors again only investigated correlation between CSP duration and pain in CTS.[43] Therefore, we think CSP latency and suppression index still warrant studying in painful conditions.

  Conclusion Top

CSP is mainly mediated by A-delta fibers with contribution of large-diameter fibers. It is a spinal inhibitory response. It should be recorded under optimum conditions. For now, its clinical use in the diagnosis or assessment of neuropathic pain is limited. It is sometimes used to show functions of A-delta fibers.

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Conflicts of interestb

There are no conflicts of interest.

  References Top

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