Hypothermic neuroprotection of peripheral nerve of rats from ischaemia-reperfusion injury. (1/363)

Although there is much information on experimental ischaemic neuropathy, there are only scant data on neuroprotection. We evaluated the effectiveness of hypothermia in protecting peripheral nerve from ischaemia-reperfusion injury using the model of experimental nerve ischaemia. Forty-eight male Sprague-Dawley rats were divided into six groups. We used a ligation-reperfusion model of nerve ischaemia where each of the supplying arteries to the sciatic-tibial nerves of the right hind limb was ligated and the ligatures were released after a predetermined period of ischaemia. The right hind limbs of one group (24 rats) were made ischaemic for 5 h and those of the other group (24 rats) for 3 h. Each group was further divided into three and the limbs were maintained at 37 degrees C (36 degrees C for 5 h of ischaemia) in one, 32 degrees C in the second and 28 degrees C in the third of these groups for the final 2 h of the ischaemic period and an additional 2 h of the reperfusion period. A behavioural score was recorded and nerve electrophysiology of motor and sensory nerves was undertaken 1 week after surgical procedures. At that time, entire sciatic-tibial nerves were harvested and fixed in situ. Four portions of each nerve were examined: proximal sciatic nerve, distal sciatic nerve, mid-tibial nerve and distal tibial nerve. To determine the degree of fibre degeneration, each section was studied by light microscopy, and we estimated an oedema index and a fibre degeneration index. The groups treated at 36-37 degrees C underwent marked fibre degeneration, associated with a reduction in action potential and impairment in behavioural score. The groups treated at 28 degrees C (for both 3 and 5 h) showed significantly less (P < 0.01; ANOVA, Bonferoni post hoc test) reperfusion injury for all indices (behavioural score, electrophysiology and neuropathology), and the groups treated at 32 degrees C had scores intermediate between the groups treated at 36-37 degrees C and 28 degrees C. Our results showed that cooling the limbs dramatically protects the peripheral nerve from ischaemia-reperfusion injury.  (+info)

Responses of sympathetic outflow to skin during caloric stimulation in humans. (2/363)

We previously showed that caloric vestibular stimulation elicits increases in sympathetic outflow to muscle (MSNA) in humans. The present study was conducted to determine the effect of this stimulation on sympathetic outflow to skin (SSNA). The SSNA in the tibial and peroneal nerves and nystagmus was recorded in nine subjects when the external meatus was irrigated with 50 ml of cold (10 degrees C) or warm (44 degrees C) water. During nystagmus, the SSNA in tibial and peroneal nerves decreased to 50 +/- 4% (with baseline value set as 100%) and 61 +/- 4%, respectively. The degree of SSNA suppression in both nerves was proportional to the maximum slow-phase velocity of nystagmus. After nystagmus, the SSNA increased to 166 +/- 7 and 168 +/- 6%, respectively, and the degree of motion sickness symptoms was correlated with this SSNA increase. These results suggest that the SSNA response differs from the MSNA response during caloric vestibular stimulation and that the SSNA response elicited in the initial period of caloric vestibular stimulation is different from that observed during the period of motion sickness symptoms.  (+info)

Motor nerve conduction velocity in spinal muscular atrophy of childhood. (3/363)

The ulnar and posterior tibial conduction velocities were measured in 29 children with spinal muscular atrophy, 14 of whom had the servere form of the disease. The ulnar nerve velocity was slow in 12 of the 14 severely affected infants, but normal or fast in 11 of 14 children less severely affected. The corresponding results for the posterior tibial nerve were slow velocities in 11 of 12 infants in the severe group and normal or fast in all 11 infants less severely affected. The difficulty in distinguishing infantile spinal muscular atrophy from peripheral neuropathy is emphasized.  (+info)

Relationships between lead absorption and peripheral nerve conduction velocities in lead workers. (4/363)

The motor sensory, and mixed nerve conduction velocities of median and posterior tibial nerves were measured in 39 lead workers whose blood lead (PbB) concentrations ranged from 2 to 73 mug/100 g with anaverage of 29 mug/100 g. The PbB concentrations significantly correlated with the maximal motor nerve conduction velocities (MCV) and mixed nerve conduction velocities (MNCV) of the median nerve in the forearm and with the MCV of the posterior tibial nerve. Erythrocyte delta-aminolevulinic acid dehydratase (ALAD) activity correlated similarly with the MCV and MNCV of the median nerve in the forearm, and the 24-hour urinary lead excretion following the intravenous administration of CaEDTA (20 mg/kg) (lead mobilization test) correlated with the MNCV. But no parameter correlated with the sensory nerve conduction velocities. By multiple regression analysis, a combination of the three parameters of lead absorption was found to correlate significantly with the MCV and MNCV of the median nerve in the forearm. The MCVs of the median and posterior tibial nerves in lead workers were significantly delayed in the PbB range of 29-73 mug/100 g (mean 45), in the lead mobilization test range from 173 to 3,540 mug/day (mean 973), and the ALAD activity range from 4.4 to 19.4 u. (mean 14.0), respectively.  (+info)

Modality-specific hyper-responsivity of regenerated cat cutaneous nociceptors. (5/363)

1. Experiments were performed on anaesthetized cats to investigate the receptive properties of regenerated cutaneous tibial nerve nociceptors, and to obtain evidence for coupling between them and other afferent fibres as being possible peripheral mechanisms involved in neuropathic pain. These properties were studied 6-7 months after nerve section and repair. 2. Recordings were made from 25 regenerated nociceptors; 14 were A fibres and the remainder were C fibres. Their receptive field sizes and conduction velocities were similar to controls. There was no significant difference between their mechanical thresholds and those of a control population of nociceptors. 3. Regenerated nociceptors were significantly more responsive to suprathreshold mechanical stimuli than were uninjured control fibres. This increase in mechanical sensitivity occurred in both A and C fibres, although A fibres showed a greater increase in mechano-sensitivity than C fibres. Over half of the regenerated nociceptors (13/25) showed after-discharge to mechanical stimuli which was never seen in controls; the mean firing rate during this period of after-discharge was significantly related to both stimulus intensity and stimulus area. 4. There was no significant difference between the heat encoding properties of regenerated nociceptors and control nociceptors. Cold sensitivity was similarly unchanged. Thus, abnormal peripheral sprouting was unlikely to account for the increased mechanical sensitivity of the regenerated fibres. None of the regenerated nociceptors were found to be coupled to other fibres. 5. These results suggest that the clinical observation of mechanical hyperalgesia in patients after nerve injury may have a peripheral basis. Based on this model, other signs of neuropathic pain (i.e. tactile or thermal allodynia) are more likely to be due to altered central processing.  (+info)

Neurotoxic effects of 2,5-hexanedione on normal and neurofilament-deficient quail. (6/363)

The neurotoxic effects of 2,5-hexanedione (2,5-HD) were investigated using neurofilament (NF)-deficient (Quv) Japanese quail in comparison with normal Japanese quail. Both Quv and normal Japanese quail were inoculated intraperitoneally with 350 mg/kg/day 2,5-HD for 6 consecutive wk. The results of 2,5-HD exposure differed substantially between the 2 strains of Japanese quail. The 2,5-HD-exposed normal quail showed leg paralysis about 4 wk after initiation of dosing. Some treated normal quail fell into dysstasia and died of nutritional disturbances. Histologically, 2,5-HD-treated normal quail had NF-rich axonal swellings and degeneration in the distal parts of the peripheral nerves, spinal cord, and cerebellar peduncles. In contrast, 2,5-HD-injected Quv quail showed tonic convulsion, ataxia gait, severe quivering, and excitation about 2-3 days after administration. Some treated Quv birds died immediately after systemic tonic convulsion, probably because of asphyxia. Although all treated Quv quail showed neurologic signs, there were no recognizable 2,5-HD-induced lesions in the nervous system. After about 4-6 wk of dosing, 2,5-HD induced distal axonopathy in normal quail and acute neurotoxicity in Quv quail.  (+info)

Cutaneous reflexes of the human leg during passive movement. (7/363)

1. Four experiments tested the hypothesis that movement-induced discharge of somatosensory receptors attenuates cutaneous reflexes in the human lower limb. In the first experiment, cutaneous reflexes were evoked in the isometrically contracting tibialis anterior muscle (TA) by a train of stimuli to the tibial nerve at the ankle. The constancy of stimulus amplitudes was indirectly verified by monitoring M waves elicited in the abductor hallucis muscle. There was a small increase in the reflex excitation (early latency, EL) during passive cycling movement of the leg compared with when the leg was stationary, a result opposite to that hypothesized. There was no significant effect on the magnitude of the subsequent inhibitory reflex component (middle latency, ML), even with increased rate of movement, or on the latency of any of the reflex components. 2. In the second experiment, the two reflex components (EL and ML) elicited in TA at four positions in the movement cycle were compared with corresponding reflexes elicited with the limb stationary at those positions. Despite the markedly different degree of stretch of the leg muscles, movement phase exerted no statistically significant effect on EL or ML reflex magnitudes. 3. In the third experiment, taps to the quadriceps tendon, to elicit muscle spindle discharge, had no effect on the magnitude of ML in TA muscle. The conditioning attenuated EL magnitude for the first 110 ms. Tendon tap to the skin over the tibia revealed similar attenuation of EL. 4. The sural nerve was stimulated at the ankle in the fourth experiment. TA EMG reflex excitatory and inhibitory responses still showed no significant attenuation with passive movement. Initial somatosensory evoked potentials (SEPs), measured from scalp electrodes, were attenuated by movement. 5. The results indicate that there is separate control of transmission in Ia and cutaneous pathways during leg movement. This suggests that modulation of the cutaneous reflex during locomotion is not the result of inhibition arising from motion-related sensory receptor discharge.  (+info)

Sympathetic outflow to muscle in humans during short periods of microgravity produced by parabolic flight. (8/363)

We have investigated the changes in muscle sympathetic nerve activity (MSNA) from the tibial nerve during brief periods of microgravity (microG) for approximately 20 s produced by parabolic flight. MSNA was recorded microneurographically from 13 quietly seated human subjects with their knee joints extended in a jet aircraft simultaneously with the electrocardiogram, the blood pressure wave (measured with a Finapres), the respiration curve, and the thoracic fluid volume (measured by impedance plethysmography). During quiet and seated parabolic flight, MSNA was activated in hypergravity and was suppressed in microG phasically. At the entry to hypergravity at 2 G just before microG, the thoracic fluid volume was reduced by 3.2 +/- 3%, and the arterial blood pressure was lowered transiently and then gradually elevated from 89.5 +/- 1.7 to 100.2 +/- 1.7 mmHg, which caused the enhancement of MSNA by 91.4 +/- 14.2%. At the entry to microG, the thoracic fluid volume was increased by 3.4%, which lowered the mean blood pressure to 77.9 +/- 2.3 mmHg and suppressed the MSNA by 17.2%. However, this suppression lasted only approximately 10 s, followed by an enhancement of MSNA that continued for several seconds. We conclude that MSNA is suppressed and then enhanced during microG produced by parabolic flight. These changes in MSNA are in response not only to intrathoracic fluid volume changes but also to arterial blood pressure changes, both of which are caused by body fluid shifts induced by parabolic flight, and these changes are quite phasic and transient.  (+info)