Reaction to topical capsaicin in spinal cord injury patients with and without central pain

Central neuropathic pain is a debilitating and frequent complication to spinal cord injury (SCI). Excitatory input from hyperexcitable cells around the injured grey matter zone is suggested to play a role for central neuropathic pain felt below the level of a spinal cord injury. Direct evidence for this hypothesis is difficult to obtain. Capsaicin, activating TRPV1 receptors on small sensory afferents, induces enhanced cellular activity in dorsal horn neurons and produces a central mediated area of secondary hyperalgesia. We hypothesized that sensory stimuli and capsaicin applied at and just above the level of a spinal cord injury which already is hyperexcitable, would cause enhanced responses in patients with central pain at the level of injury compared to patients without neuropathic pain and healthy controls. Touch, punctuate stimuli, cold stimuli and topical capsaicin was applied above, at, and below injury level in 10 SCI patients with central pain below a thoracic injury, in 10 SCI patients with a thoracic injury but without neuropathic pain, and in corresponding areas in 10 healthy control subjects. The study found increased responses to touch at injury level compared to controls (p = 0.033) and repetitive punctuate stimuli above and at injury level compared to controls and pain-free SCI patients (p < 0.04) but not an increased response to capsaicin in patients with central pain. These results suggest that SCI patients with below-level pain have increased responses to some but not all sensory input at the level of injury.     

Ketamine for acute neuropathic pain in patients with spinal cord injury

Ketamine, an N-methyl-d-aspartic acid (NMDA) receptor antagonist, may be useful for treating neuropathic pain, which is often difficult to control. We report a prospective study of 13 patients with acute neuropathic pain due to spinal cord injury (SCI) treated with ketamine. All underwent a test challenge with 5 mg ketamine. Patients with satisfactory responses were then treated intravenously and subsequently perorally with ketamine. Pre- and post-treatment pain was recorded on a visual analogue scale. All 13 patients responded positively to the ketamine test challenge and underwent continued ketamine administration. At the cessation of treatment and alter at final follow up, pain was decreased by 74.7% and 96.8%, respectively. The average administration period was 17.2 days; it was longer (59 days) in one patient treated in the subacute phase. All patients suffered allodynia-type pain and experienced 30% or less of their original pain intensity upon test challenge. Side effects were noted in five patients, although their severity did not require treatment cessation. In patients with SCI, ketamine reduced allodynia. Particularly good results were obtained in patients treated in the acute phase and these patients did not experience post-treatment symptom recurrence. Our results suggest that in patients with SCI, ketamine is useful for treating neuropathic pain in the acute phase.     

Diagnostic spinal anaesthesia in chronic spinal cord injury pain.

In a double blind study, 21 patients with chronic spinal cord injury (SCI) pain underwent placement of a lumbar subarachnoid catheter and injection of placebo and lidocaine. The effects on pain intensity, distribution, altered sensations and sensory level of anaesthesia were monitored. Four patients responded briefly to placebo, while 13 demonstrated a mean reduction of pain intensity of 37.8 +/- 37% for a mean duration of 123.1 +/- 95.3 minutes in response to lidocaine. The pain response to subarachnoid lidocaine differed significantly (p less than 0.01) from placebo. Spinal anaesthesia was also associated with changes in pain distribution and altered sensation. A spinal anaesthetic-induced sensory level could not be achieved cephalad to the sensory level of neurological injury in 5 patients who presented with spinal canal obstruction. This study has demonstrated that response to diagnostic spinal anaesthesia in chronic SCI pain is complex, requiring individual interpretation in each patient and consideration of the following factors; symptomatology, etiology, pain perception, spinal canal anatomy, CSF chemistry and local anaesthetic pharmacology.     

Oesophageal trauma in patients with spinal cord injury.

Oesophageal perforations associated with cervical fractures occur from a variety of injuries. Fractures of the cervical spine, blunt trauma and penetrating injuries such as gunshot wounds, knives and missiles, perforate the cervical oesophagus. This retrospective study consists of 24 patients with an oesophageal perforation and cervical fracture. Motor vehicle accidents were responsible for 54% of the oesophageal perforations. The other oesophageal injuries were related to anterior spine surgery, gunshot wounds and sports-related activities. The clinical features related to these injuries included the obvious signs of an oesophageal perforation as well as fever of unknown origin, leukocytosis and unexplained persistent tachycardia. A variety of techniques was used to establish the diagnosis. All the patients had treatment for the cervical fracture and 20 patients required surgical repair of the oesophagus. The most common oesophageal complications were stricture of the oesophagus (54%) and oesophageal diverticulum (10%). The other complications were atelectasis, pneumonia, tracheobronchitis, pulmonary embolism, cervical osteomyelitis, cervical abscess, mediastinitis, septicemia and cervical fistulae. These patients have a serious life-threatening illness that may be difficult to diagnose and treat.     

Prediction of central neuropathic pain in spinal cord injury based on EEG classifier

Objectives

To create a classifier based on electroencephalography (EEG) to identify spinal cord injured (SCI) participants at risk of developing central neuropathic pain (CNP) by comparing them with patients who had already developed pain and with able bodied controls.

Fire and phantoms after spinal cord injury: Na+ channels and central pain

Neuropathic pain and phantom phenomena occur commonly after spinal cord injury (SCI) but their molecular basis is not yet fully understood. Recent findings demonstrate abnormal expression of the Nav1.3 Na(+) channel within second-order spinal cord dorsal horn neurons and third-order thalamic neurons along the pain pathway after SCI, and suggest that this change makes these neurons hyperexcitable so that they act as pain amplifiers and generators. Delineation of molecular changes that contribute to hyperexcitability of pain-signaling neurons might lead to identification of molecular targets that will be useful in the treatment of neuropathic pain after SCI and related nervous system injuries.     

Septic ischial bursitis in patients with spinal cord injury.

Septic ischial bursitis is described in 4 patients with spinal cord injury. In these patients a pre-existing ischial bursitis probably became secondarily infected. Because these patients lack sensation, diagnosis may be difficult. The disease process in one patient with a prolonged fever was only recognized after a leucocyte scan detected an abscess extending to the thigh. At surgery it was found that the infection extended from the ischial bursa to the upper lateral thigh. Infection in these patients was due to beta hemolytic streptococcus, S. aureus, and S. epidermidis. The patients all responded well to local drainage and excision of the bursa.     

Evoked potentials and quantitative thermal testing in spinal cord injury patients with chronic neuropathic pain

ObjectiveNeuropathic pain (NP) is a common symptom following spinal cord injury (SCI). NP may be associated with altered processing of somatosensory pathways in dermatomes rostral to the injury level. To explore this possibility, the characteristics of contact heat evoked potentials (CHEPs) and quantitative thermal testing (QTT) were studied at and above the lesion level in SCI patients with NP. The goal was to determine processing abnormalities correlated with data from clinical evaluations.MethodsThirty-two subjects with chronic NP, 22 subjects without NP and 16 healthy control subjects were studied. Warm and heat pain thresholds were determined both at and above SCI level. CHEPs were recorded above SCI level and subjects rated their perception of evoked heat pain using a numerical rating scale.ResultsCHEPs were not different between the three groups. Evoked pain perception in SCI subjects with NP was significantly higher than in SCI subjects without NP and healthy controls. Heat pain threshold was significantly lower in subjects with NP in comparison to both groups.ConclusionsOur findings indicate that processing of somatosensory inputs from dermatomes rostral to the injury level is abnormal in SCI subjects with NP.SignificanceSCI somatosensory processing alteration may contribute to the understanding of the mechanisms underlying NP and secondary changes to NP in SCI.     

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。     

Anorectal functions in patients with spinal cord injury

We wished to establish anorectal functions in patients with spinal cord lesions, related to the level of lesion and its completeness. We also wished to determine the value of neurophysiological tests for completeness of transsections in comparison with manometry and visceral sensory testing. In 32 patients (31.5 +/- 14.1 years, 25 males) with spinal trauma, completeness of transsection was assessed clinically. In 16 of these patients (30 +/- 15.6 years, nine males), a neurological work-up included recording of somatosensory evoked potentials (SEP) and motor evoked potentials (MEP) from the pudendal nerve within the first week after trauma. Also, anal sphincter EMG and pudendal nerve terminal motor latency (PNTML) were assessed. All patients also underwent conventional anorectal manometry and visceral sensory testing. Of all 32 patients, 15 were judged as 'complete' based on their clinical signs. Of those 16 tested neurologically, seven were labelled 'complete' since no MEP or SEP were detectable; one had pudendal SEP and MEP present, while SEP were present but delayed (47.0 +/- 8.8 msec) in the remaining patients. In four of these patients, also MEP were recorded (27.9 +/- 5.2 msec) and normal. PNTML was present in 12/16 patients independent of the completeness of lesion, and was rated normal in nine and delayed in three patients. EMG was normal in five, and pathological in 11 cases. In 5/15 cases of those judged as 'complete' (in 3/7 evaluated neurologically), visceral sensory testing revealed a minimal threshold for rectal perception of distension of 44 mL (range: 10-130), which sometimes was also perceived as urge to defecate. In a further case, manometry showed major voluntary action of the anal sphincter. These patients had lesions at all levels of the spinal column, ranging from cervical (C4,C6,C7) via thoratical (2 x T7,T8,T12) to lumbar segments. Anorectal function testing, and specifically visceral sensory testing may be superior to neurological assessment of 'completeness' of spinal cord lesions. It may be that visceral afferent pathways others than spinothalamic tract are involved in rectal perception that are less accessible to conventional neurophysiological diagnostic work-up.     

Assessment of autonomic dysreflexia in patients with spinal cord injury.

OBJECTIVES AND METHODS: To assess the impairment of supraspinal control over spinal sympathetic centres and the occurrence of autonomic dysreflexia in patients with spinal cord injury. Autonomic dysreflexia is caused by the disconnection of spinal sympathetic centres from supraspinal control and is characterised by paroxysmal hypertensive episodes caused by non-specific stimuli below the level of the lesion. Therefore, patients with spinal cord injury were examined clinically and by different techniques to assess the occurrence of autonomic dysreflexia and to relate disturbances of the sympathetic nervous system to episodes of autonomic dysreflexia. RESULTS: None of the paraplegic patients, but 59% (13/22) of tetraplegic patients (91% of the complete, 27% of the incomplete patients) presented signs of autonomic dysreflexia during urodynamic examination. Only 62% of the tetraplegic patients complained about symptoms of autonomic dysreflexia. Pathological sympathetic skin responses (SSRs) of the hands were related to signs of autonomic dysreflexia in 93% of cases. No patient with preserved SSR potentials of the hands and feet showed signs of autonomic dysreflexia, either clinically or during urodynamic examination. Ambulatory blood pressure measurements (ABPMs) indicated a loss of circadian blood pressure rhythm (sympathetic control) but preserved heart rate rhythm (parasympathetic regulation) only in patients with complete tetraplegia. Pathological ABPM recordings were seen in 70% of patients with symptoms of autonomic dysreflexia. CONCLUSIONS: The urodynamic examination was more sensitive in indicating signs of autonomic dysreflexia in patients with spinal cord injury, whereas SSR allowed the assessment of the degree of disconnection of the sympathetic spinal centres from supraspinal control. Using ABPM recordings the occurrence of episodes of autonomic dysreflexia over 24 hours and the effectiveness of therapeutical treatment can be assessed.     

Recurrent inhibition is increased in patients with spinal cord injury.

Mechanisms underlying the development of spasticity after spinal cord injury are not understood. One spinal interneuron likely to be affected is the Renshaw cell, which acts to produce recurrent inhibition in motor neurons as well as inhibiting Ia interneurons. Descending pathways exert both excitatory and inhibitory control over Renshaw cell activity. We studied Renshaw cell activity in normal subjects and in patients with varying levels of spasticity after spinal cord injury using the conditioned H-reflex technique of Pierrot-Deseilligny and Bussel. A submaximal stimulus to the tibial nerve is presented prior to a supramaximal stimulus so that action potential collision permits an H reflex (H') to be elicited in response to the supramaximal stimulus. The amplitude of this H' reflex is affected by activity in recurrent inhibitory pathways. Patients with both complete and partial spinal cord lesions were studied; date of injury ranged from 1 month to 216 months prior to evaluation. In the 18 patients in whom H reflexes could be recorded, H' reflexes were absent in 13, in contrast to their uniform presence in normal subjects. We conclude that recurrent inhibition via Renshaw cell activity is increased in spinal cord injury, and that measures of recurrent inhibition may correlate well with some clinical measures of spasticity.