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PubMed2001

Delayed loss of spinal motoneurons after peripheral nerve injury in adult rats: a quantitative morphological study.

The existence of retrograde cell death in sensory dorsal root ganglion (DRG) cells after peripheral nerve injury is well established. However, with respect to retrograde motoneuron death after peripheral nerve injury, available data are conflicting. This may partly be due to the cell counting techniques used. In the present study, quantitative morphometric methods have been used to analyse retrograde motoneuron death induced by spinal nerve injury in adult rats. For comparison, DRG cells were also included in the study. The C7 spinal nerve was transected about 10 mm distal to the DRG and exposed to the fluorescent tracer fast blue in order to retrogradely label the spinal motoneurons and DRG cells of the C7 segment. At 1-16 weeks postoperatively, the nuclei of fast-blue-labelled C7 motoneurons and DRG cells were counted in consecutive 50-microm-thick serial sections. For comparison, the physical disector technique and measurements of neuronal density were also used to calculate motoneuron number. The counts of fast-blue-labelled motoneurons revealed a delayed motoneuron loss amounting to 21% and 31% after 8 and 16 weeks, respectively (P<0.001). The remaining motoneurons exhibited 20% (P<0.05) soma atrophy. Using the physical disector technique, the motoneuron loss was 23% (P<0.001) after 16 weeks. Calculations of neuronal density in Nissl-stained sections failed to reveal any motoneuron loss, although after correction for shrinkage of the ventral horn a 14% (P<0.001) motoneuron loss was found. The fast-blue-labelled DRG neurons displayed 51% (P<0.001) cell loss after 16 weeks, and the remaining cells showed 22% (P<0.001) soma atrophy. In summary, cervical spinal nerve injury induces retrograde degeneration of both motoneurons and DRG cells. However, to demonstrate the motoneuron loss adequate techniques for cell counts have to be employed.

Animals↗
PubMed1993

The response of central glia to peripheral nerve injury.

Microglial and astroglial cells undergo prompt responses to peripheral motor and sensory axon injury. These responses include proliferation of microglial cells as well as hypertrophy and increased levels of glial fibrillary acidic protein around the axotomized motoneurons and in the central projection territories of peripherally axotomized sensory ganglion cells. Proliferating microglial cells migrate towards reacting motoneurons, however, without directly apposing their cell membrane. Astroglial cells, on the other hand, increase their structural interrelationship with reacting motoneurons, seemingly at the expense of some presynaptic terminals. In sensory projection areas, microglial cells phagocytose degenerating axons and terminals. Beyond these observations, the functional role of the central glial cell response to peripheral nerve injury is obscure.

Animals↗
PubMed2004

Systemic lidocaine in pain due to peripheral nerve injury and predictors of response.

OBJECTIVE: To investigate the effects of IV lidocaine on spontaneous and evoked pain (allodynia and hyperalgesia) due to peripheral nerve injury (postherpetic neuralgia or nerve trauma) using quantitative sensory testing. METHOD: The authors randomized 22 patients to receive lidocaine 5 mg/kg IV during 30 minutes or placebo in a double-blind crossover design and 16 patients subsequently received mexiletine on an open basis titrated from 400 to 1,000 mg per day (mean 737 mg/day). RESULTS: Lidocaine induced a significant decrease in ongoing pain for up to 6 hours with a peak effect 60 to 120 minutes postinjection. The drug also decreased mechanical dynamic allodynia and static (punctate) mechanical allodynia/hyperalgesia, but not thermal allodynia and hyperalgesia. The effects of lidocaine and mexiletine on spontaneous pain intensity were significantly higher in patients with concomitant mechanical allodynia in comparison with those without allodynia. CONCLUSIONS: These data indicate modality-specific antihyperalgesic effects of IV lidocaine in patients with peripheral nerve injury. Patients with mechanical allodynia may be good candidates for treatment with local anesthetic-like drugs and possibly with other sodium-channel blockers.

Adult↗
PubMed1985

Thermographic imaging of cutaneous sensory segment in patients with peripheral nerve injury. Skin-temperature stability between sides of the body.

Sensory examination based on the patient's subjective assessment of symptoms may raise difficult questions about whether the individual's expressed complaint is based on organic nerve damage, psychogenic factors, or even malingering. A prototype computerized telethermograph has allowed clinical quantification of peripheral nerve injury. The system makes possible mapping and imaging of the damaged area, as well as skin temperature measurements. In normal persons, the skin temperature difference between sides of the body was only 0.24 degree +/- 0.073 degree C. In contrast, in patients with peripheral nerve injury, the temperature of the skin innervated by the damaged nerve deviated an average of 1.55 degrees C (p less than 0.001). The new technique requires further refinement, but it appears that use of this method may be cost-effective in helping to resolve medicolegal conflicts concerning peripheral nerve injury.

Adolescent↗
PubMed1988

Changes in neurotransmitter uptake in the spinal cord following peripheral nerve injury.

Changes in neurotransmitter systems of the spinal cord were studied in response to peripheral nerve injury. The uptake and compartmentalization of radiolabeled spinal cord neurotransmitters and transmitter precursors were examined as a function of time following unilateral sciatic nerve crush in adult mice. Accumulation of transmitter was measured within synaptosomally enriched fractions prepared using combinations of differential and density gradient centrifugations. The amount of transmitter substance recovered from these fractions was strongly dependent upon the amount of time following nerve injury and on the specific transmitter or precursor being examined (GABA, glutamate, glycine, and choline chloride). However, for each of these substances, uptake values returned to control levels within nine to twelve days after nerve crush. Localization of GABA changes postcrush revealed reciprocal differences between ipsilateral and contralateral sides of the spinal cord, as well as differences between segmental levels. Altered GABA uptake may reflect changes in the postcrush microchemical environment present during tissue processing, but may also be related to direct changes in the synaptic binding, transport, and compartmentalization of transmitter substance. The time course, magnitude, and direction of these neurochemical changes follow those observed neurophysiologically, and may thus underlie injury-induced short-term (days) alterations reported in primary afferent depolarizations, cross cord responses, and other spinal mechanisms.

Aminooxyacetic Acid↗
PubMed2000

Dorsal column-thalamic pathway is involved in thalamic hyperexcitability following peripheral nerve injury: a lesion study in rats with experimental mononeuropathy.

A total of 68 neurons were recorded from the ventro-postero-lateral nucleus of thalamus (VPL) in rats with a unilateral chronic constriction injury (CCI) of the sciatic nerve (n=20), sham operation (n=24) and naive rats (n=24), and effects of the lesion of dorsal column (DC) pathway [DC lesion or DC+gracile nucleus lesions] on VPL nucleus neuronal activities were studied. In the VPL nucleus contralateral to the CCI (receiving input from the injured nerve), response latencies of low threshold mechanoreceptive (LTM) and wide dynamic range (WDR) neurons to electrical stimulation of the sciatic nerve were significantly longer than that in the contralateral VPL nucleus receiving input from the sham-operated side (P<0.05). In contrast, response latencies of LTM and WDR neurons to DC stimulation were not different between the sham operated and CCI sides (0.05). Background activity of WDR neurons was significantly higher in the VPL nucleus contralateral to the CCI side when compared to neurons in the VPL nucleus contralateral to the sham operated side and in naive animals. Responses of LTM and WDR neurons to innocuous mechanical stimulation of the receptive fields were significantly decreased after DC and DC+gracile nucleus lesions in all animals. However, the responses of WDR neurons to noxious stimuli were selectively reduced only in rats with CCI by DC and DC+gracile nucleus lesions (P<0.05). The decrease in noxious stimulus-evoked responses of WDR neurons in the VPL nucleus contralateral to the CCI side after DC and DC+gracile nucleus lesions was greater than that in the VPL nucleus contralateral to the sham operated side and naive animals. These results indicated that DC and DC+gracile nucleus lesions produced selective and stronger effect on noxious responses of VPL nucleus WDR neurons receiving input from the site of nerve injury. The findings suggest that the gracile nucleus-thalamic pathway conveys, or modulates, nociceptive information to the VPL nucleus following peripheral nerve injury, resulting in an increase in VPL nucleus response to noxious stimuli that contributes to the development of mechanical hyperalgesia.

Animals↗
PubMed2001

Endogenous galanin is required for the full expression of central sensitization following peripheral nerve injury.

The neuropeptide galanin is known to be involved in nociceptive sensory processing in the spinal cord. We have attempted to better characterise the function of endogenous galanin in nociceptive signalling by examining a mouse strain carrying a loss of function mutation in the galanin gene (gal-/-). Galanin expression is significantly up-regulated following damage to a peripheral nerve. To address what effect this up-regulation has on spinal cord excitability we have examined wild type (gal+/+) and gal-/- mice 3 days after complete transection of the sciatic nerve using an electrophysiological paradigm, the flexor withdrawal reflex. We demonstrate that the up-regulation of galanin has no direct effect on basal spinal excitability after nerve injury. However, galanin is shown to be a crucial neuromodulator involved in the development of the central sensitization as both windup and the facilitation of spinal reflexes following conditioning stimulation are significantly impaired in gal-/- mice following peripheral nerve injury.

Action Potentials↗
PubMed2003

Does cortical motor neuron excitability change in peripheral nerve injury?

OBJECTIVE: To investigate changes in cortical motor neuron excitability after peripheral nerve injury, evoked spinal cord potentials (ESCPs) following hemispheric transcranial magnetic stimulation (TMS) were recorded in awake patients with unilateral brachial plexus injury. METHODS: ESCPs following hemispheric TMS were recorded in 6 patients with unilateral complete type brachial plexus injury. Studies were performed within 6 months from the time of injury. ESCPs were recorded from posterior epidural space using catheter electrodes. Hemispheric TMS was applied on the motor cortex using a figure-of-8 coil. The threshold of ESCPs following hemispheric TMS was measured. The number, latency, and amplitude of ESCPs following high stimulus hemispheric TMS were measured and compared. RESULTS: No significant change was observed in the threshold of ESCPs following TMS contra-lateral to the injured upper limb compared to that following TMS contra-lateral to the intact upper limb. Several ESCP components were recorded following high stimulus hemispheric TMS. No significant changes were observed in comparison with number, latency and amplitude of ESCPs following high stimulus TMS contra-lateral to the injured upper limb and those following TMS contra-lateral to the intact upper limb. CONCLUSIONS: From a study of ESCPs following single TMS, no evidence was obtained that cortical motor neuron excitability changes in patients with traumatic unilateral brachial plexus injury at relatively early stages. We investigated the changes of cortical motor neuron excitability in patients with brachial plexus injury from the ESCPs following TMS. In single TMS, our data gave no evidence for cortical excitability changes at relatively early stages.

Adolescent↗
PubMed1999

Effects of peripheral nerve injury on alpha-2A and alpha-2C adrenergic receptor immunoreactivity in the rat spinal cord.

Neuropathic pain resulting from peripheral nerve injury can often be relieved by administration of alpha-adrenergic receptor antagonists. Tonic activation of alpha-adrenergic receptors may therefore facilitate the hyperalgesia and allodynia associated with neuropathic pain. It is currently unclear whether alpha2A- or alpha2c-adrenergic receptor subtypes are involved in the pro-nociceptive actions of alpha-adrenergic receptors under neuropathic conditions. We therefore investigated the effects of peripheral nerve injury on the expression of these subtypes in rat spinal cord using immunohistochemical techniques. In addition, neuropeptide Y immunoreactivity was examined as an internal control because it has previously been shown to be up-regulated following nerve injury. We observed a decrease in alpha2A-adrenergic receptor immunoreactivity in the spinal cord ipsilateral to three models of neuropathic pain: complete sciatic nerve transection, chronic constriction injury of the sciatic nerve and L5/L6 spinal nerve ligation. The extent of this down-regulation was significantly correlated with the magnitude of injury-induced changes in mechanical sensitivity. In contrast, alpha2c-adrenergic receptor immunoreactivity was only increased in the spinal nerve ligation model; these increases did not correlate with changes in mechanical sensitivity. Neuropeptide Y immunoreactivity was up-regulated in all models examined. Increased expression of neuropeptide Y correlated with changes in mechanical sensitivity. The decrease in alpha2A-adrenergic receptor immunoreactivity and the lack of consistent changes in alpha2C-adrenergic receptor immunoreactivity suggest that neither of these receptor subtypes is likely to be responsible for the abnormal adrenergic sensitivity observed following nerve injury. On the contrary, the decrease in alpha2A-adrenergic receptor immunoreactivity following nerve injury may result in an attenuation of the influence of descending inhibitory noradrenergic input into the spinal cord resulting in increased excitatory transmitter release following peripheral stimuli.

Animals↗
PubMed1998

Spontaneous release of immunoreactive neuropeptide Y from the central terminals of large diameter primary afferents of rats with peripheral nerve injury.

Microprobes bearing immobilized antibodies to the C-terminus of neuropeptide Y were used to measure the release of this neuropeptide in the spinal cords of rats with a unilateral peripheral neuropathy and in sham-operated animals. All neuropathic animals showed the characteristic behavioural syndrome and were studied at 14 days postsciatic nerve loose-ligation. An extensive spontaneous release of immunoreactive neuropeptide Y was detected in the spinal cords of the neuropathic rats and, compared to sham-operated rats, a new zone of release was found in the deep dorsal horn. Electrical stimulation of large diameter primary afferents proximal to the nerve ligature produced widespread release of neuropeptide Y in the dorsal horn which persisted for up to 1 h poststimulation. It is possible that ectopic impulses arising in the injured nerve were responsible for the spontaneous central release of neuropeptide Y and this neuropeptide may play a role in the central response to peripheral nerve injury.

Animals↗
PubMed1995

Paradoxical clinical consequences of peripheral nerve injury: conduction of nerve impulses does not occur across the site of injury immediately following nerve division and repair.

The occasional apparent clinical phenomenon of the immediate although transient return of peripheral nerve function after nerve division and primary repair has been previously reported. Electrophysiological findings from the sciatic nerve of the rabbit have been previously presented in support of the concept of the transmission of nerve impulses across a freshly divided and repaired peripheral nerve for a short period until the onset of Wallerian degeneration. This paper presents experimental evidence to show that these findings were misinterpreted and that a compound action potential cannot be transmitted across a surgically repaired division in a peripheral nerve. Observations from previous experimental research in neurophysiology are discussed which confirm these conclusions. The claim that failure to diagnose a peripheral nerve injury at presentation can be explained in some circumstances by "jump transmission" is not based on sound evidence and the concept of "jump transmission" cannot be accepted as a defence for clinicians who fail to diagnose a peripheral nerve injury.

Action Potentials↗