Experimental trigeminal neuralgia (the concept of the generator mechanism of the pain syndrome)

Крыжановский, Г. Н.; Igonʼkina, S. I.; Grafova, V. N.; Danilova, E. I.

doi:10.1007/bf00804343

Cited by 7 publications

(7 citation statements)

References 10 publications

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“…The present article reports an extensive analysis of spontaneous behavior and of responses to mechanical stimulation of the face observed after CC1 to the ION. Previous reports on behavioral consequences of trigeminal nerve injury (Anderson et al, 197 1;Burchiel, 1980), as well as studies of the behavioral responses to chemical irritation of the trigeminal nucleus caudalis (King et al, 1956;King and Bamett, 1957;King, 1970;Black, 1974;Kryzhanovsky et al, 1974;Sakai et al, 1979), both in rats and in cats, have described the occurrence of recurrent attacks of ipsilateral face grooming together with hyperresponsiveness to light mechanical stimulation of the ipsilateral side of the face. Experimental studies of acute trigeminal pain in rats commonly report ipsilateral face grooming as the most obvious behavioral response to noxious stimulation of the face (Rosenfeld et al, 1978;Morris et al, 1982;Ramabadran and Bansinath, 1986;Clavelou et al, 1989;Cahusac et al, 1990).…”

Section: Video Recordingsmentioning

confidence: 98%

Behavioral evidence of trigeminal neuropathic pain following chronic constriction injury to the rat's infraorbital nerve

1994

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Video recordings of free behavior and responses to mechanical facial stimulation were analyzed to assess whether chronic constriction injury (CCI) to the rat's infraorbital nerve (IoN) results in behavioral alterations indicative of neuropathic pain. A unilateral CCI was produced by placing loose chromic gut ligatures around the IoN. After CCI to the IoN, rats exhibited changes in both non-evoked and evoked behavior. Behavioral changes developed in two phases. Early after CCI (postoperative days 1–15), rats showed increased face-grooming activity with face-wash strokes directed to the injured nerve territory, while the responsiveness to stimulation of this area was decreased. Later after CCI (postoperative days 15–130), the prevalence of asymmetric face grooming was reduced but remained significantly increased compared to control rats. The early hyporesponsiveness was abruptly replaced by an extreme hyperresponsiveness: all stimulus intensities applied to the injured nerve territory evoked the “maximal” response (brisk head withdrawal, avoidance behavior plus directed face grooming). This response was never observed in control rats. Concurrently, IoN ligation rats showed a limited increase in the responsiveness to stimulation of the contralateral IoN territory, and around postoperative days 30–40 the responsiveness to stimulation of facial areas outside the IoN territories also increased. The hyperresponsiveness to stimulation of the ligated IoN territory slightly decreased from 60 d postoperative. Throughout the study, IoN ligation rats showed decreased exploratory behavior, displayed more freezing-like behavior, had a slower body weight gain, and a higher defecation rate, compared to control rats. The behavioral alterations observed after CCI to the IoN are indicative of severe sensory disturbances within the territory of the injured nerve: mechanical allodynia develops after a period of relative hypo- /anesthesia during which behavioral signs of recurrent spontaneous, aversive (possibly painful) sensations (paresthesias/dysesthesias) are maximal.

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Section: Video Recordingsmentioning

confidence: 98%

Behavioral evidence of trigeminal neuropathic pain following chronic constriction injury to the rat's infraorbital nerve

1994

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“…In group 1 rats, an agar plate [2] (6xl.5x2 mm) containing 25000 U/ml penicillin sodium chloride salt was applied to the DS of lumbar segments of spinal cord exposed under ether anesthesia. The wound was sutured, and the animals were observed during the development of pain syndrome.…”

Section: Methodsmentioning

confidence: 99%

“…We have shown that application of convulsants (tetanotoxin, penicillin, and strychnine)to various subdivisions of the noeiceptive system provokes pain syndromes [ 1,2,5]. In this work our aim was to study the pathophysiological mechanisms of spinal pain syndrome caused by application of penicillin to the dorsal surface (DS) of the spinal cord lumbar segments and to analyze the characteristic features of electrical activity both in the penicillin-affected primary nocieeptive relay (dorsal horn, DH) and in the corresponding area of the sensorimotor cortex.…”

Section: Abstract: Dorsal Horns; Sensorimotor Cortex Generator Of Pmentioning

confidence: 99%

Electrical activity in dorsal horns of the spinal cord and in sensorimotor cortex in rats with the spinal pain syndrome

et al. 1998

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In rats with the spinal pain syndrome caused by penicillin application to the dorsal surface of lumbar segments of the spinal cord, the following changes in evoked potentials were observed in the dorsal horn in L S segment at the side of penicillin application: a marked increase in primary response and disappearance of the secondary hyperpolarization wave with its replaument by a high-amplitude and long depolarizing wave. In addition to these changes, repetitive spontaneous burst discharges were recorded in the corresponding region of the sensorimotor cortex. Thus, the pathogenic basis of the pain syndrome is a pathological algetie system formed of altered structures that belong to nociceptive apparatus in dorsal horn and higher subdivisions of. the pain sensory system. Key Words: dorsal horns; sensorimotor cortex, generator of pathologically enhanced excitation; pathological algetic system; spinal pain syndrome; penicillinWe have shown that application of convulsants (tetanotoxin, penicillin, and strychnine)to various subdivisions of the noeiceptive system provokes pain syndromes [ 1,2,5]. In this work our aim was to study the pathophysiological mechanisms of spinal pain syndrome caused by application of penicillin to the dorsal surface (DS) of the spinal cord lumbar segments and to analyze the characteristic features of electrical activity both in the penicillin-affected primary nocieeptive relay (dorsal horn, DH) and in the corresponding area of the sensorimotor cortex. MATERIALS AND METHODSThe study was carried out on 24 male Wistar rats weighing 270-320 g in accordance to regulations for experimental pain investigations in animals [9] and to the principles of work with animals in neuroInstitute of General Pathology and Pathophysioiogy0 Russian Academy of Medical Sciences, Moscow physiological studies [10]. In group 1 rats, an agar plate [2] (6xl.5x2 mm) containing 25000 U/ml penicillin sodium chloride salt was applied to the DS of lumbar segments of spinal cord exposed under ether anesthesia. The wound was sutured, and the animals were observed during the development of pain syndrome.In group 2 rats, electrical activity was recorded in penicillin-affected DH and in the corresponding region of the sensorimotor cortex. Measurements were performed when the pain syndrome reached the maximum in group 1 rats. The rats were anesthetized by intraperitoneal urethane (1400 mg/kg), placed in a stereotaxic apparatus with rigid fixation of the head and spine, trepanized, laminectomized, immobilized with a muscle relaxant (Myo-Relaxin, 50 mg/kg intramuscularly), and artificially ventilated. Muscle tissue, skin, and the vertebral spinous processes in the stereotaxic fixation points were treated with 0.5% procaine. Evoked potentials (EP) in DH of the spinal cord and in the sensorimotor cortex were recorded

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“…It was previously reported that penicillin application to the dorsal surface of the spinal cord induces central spinal pain syndrome (CSPS) [1,3]. The development of CSPS is associated with the formation of a generator of pathologically enhanced excitation in the spinal dorsal horns, presented by a cluster of sensitized neurons with self-sustained activity [3,4].…”

Section: Abstract: Akatinol; Central Spinal Pain Syndrome" Penicillmentioning

confidence: 99%

“…The development of CSPS is associated with the formation of a generator of pathologically enhanced excitation in the spinal dorsal horns, presented by a cluster of sensitized neurons with self-sustained activity [3,4]. In the mechanisms underlying the neurogenic pain syndromes (in particular, CSPS) an important role is played by the release of excitatory amino acids from central terminals of the primary sensory neurons.…”

Section: Abstract: Akatinol; Central Spinal Pain Syndrome" Penicillmentioning

confidence: 99%

Effect of akatinol (Memantine) in central spinal pain syndrome

et al. 2000

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On the model of central spinal pain syndrome in rats induced by application of penicillin to the dorsal surface of the lumbar spinal cord, akatinol injected intraperitoneally at the peak of syndrome or applied locally simultaneously with penicillin produced a dose-dependent analgesic effect. Intraperitoneal injection of akatinol at the peak of pain syndrome inhibited neuronal activity in spinal dorsal horn: the amplitude of total evoked neuronal response significantly decreased and the duration of action potentials returned to normal. It is concluded that activation of NDMA receptors plays a significant role in the development of central spinal pain syndrome, in particular spontaneous pain attacks, hyperalgesia, and tactile allodynia. Akatinol can be an essential component of the complex pathogenetic therapy of central pains.

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Experimental trigeminal neuralgia (the concept of the generator mechanism of the pain syndrome)

Cited by 7 publications

References 10 publications

Behavioral evidence of trigeminal neuropathic pain following chronic constriction injury to the rat's infraorbital nerve

Behavioral evidence of trigeminal neuropathic pain following chronic constriction injury to the rat's infraorbital nerve

Electrical activity in dorsal horns of the spinal cord and in sensorimotor cortex in rats with the spinal pain syndrome

Effect of akatinol (Memantine) in central spinal pain syndrome

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