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PubMed1999

Morphological alterations induced by sodium valproate on somites and spinal nerves in rat embryos.

The antiepileptic drug valproic acid is a well-known teratogenic agent; its main target organ is the neural tube, though skeletal malformations have also been described. In our recent work, respecifications of vertebrae were described in rat fetuses after treatment with 400 mg/kg of sodium valproate at specific somitogenic stages. The observed malformations were stage-dependent. Morphological segmental respecification was observed at the level of segments in formation at the moment of exposure and at the level of more posterior segments. Recently, specific alterations in the development of cranial nerves and ganglia were described in mouse embryos after in vitro exposure to VPA. The aim of the present work was to analyze dysmorphogenetic effects of VPA on embryonic metameric structures: somites, spinal and cranial nerves, and ganglia. Sodium valproate (400 mg/kg) was subcutaneously injected at specific gestational times corresponding to embryonic stages: presomitic or at about 2, 6, 10, 14, 18, or 22 somites. Females were sacrificed on the day 12 post coitum, and embryos were examined. Morphological examination of somites was performed by staining with acridine orange. Morphological examination of nerves and ganglia was performed by immunostaining, using monoclonal antibodies to the 160-kD neurofilament protein. No abnormalities were observed in the cranial nerves and ganglia. Specific and stage-dependent alterations were observed both at the level of the somites and at the level of the spinal nerves. The following characteristic malformations were observed: fusions, duplications, and reductions of somites and corresponding spinal nerves and ganglia. Our morphological data suggest a morphogenetic action of VPA at the level of the axial segments, with a possible respecification of the identity of the interested segments and their derivatives.

Animals↗
PubMed2006

Antisense knock down of TRPA1, but not TRPM8, alleviates cold hyperalgesia after spinal nerve ligation in rats.

Patients with neuropathic pain frequently experience hypersensitivity to cold stimulation. However, the underlying mechanisms of this enhanced sensitivity to cold are not well understood. After partial nerve injury, the transient receptor potential ion channel TRPV1 increases in the intact small dorsal root ganglion (DRG) neurons in several neuropathic pain models. In the present study, we precisely examined the incidence of cold hyperalgesia and the changes of TRPA1 and TRPM8 expression in the L4 and L5 DRG following L5 spinal nerve ligation (SNL), because it is likely that the activation of two distinct populations of TRPA1- and TRPM8-expressing small neurons underlie the sensation of cold. We first confirmed that L5 SNL rats developed cold hyperalgesia for more than 14 days after surgery. In the nearby uninjured L4 DRG, TRPA1 mRNA expression increased in trkA-expressing small-to-medium diameter neurons from the 1st to 14th day after the L5 SNL. This upregulation corresponded well with the development and maintenance of nerve injury-induced cold hyperalgesia of the hind paw. In contrast, there was no change in the expression of the TRPM8 mRNA/protein in the L4 DRG throughout the 2-week time course of the experiment. In the injured L5 DRG, on the other hand, both TRPA1 and TRPM8 expression decreased over 2 weeks after ligation. Furthermore, intrathecal administration of TRPA1, but not TRPM8, antisense oligodeoxynucleotide suppressed the L5 SNL-induced cold hyperalgesia. Our data suggest that increased TRPA1 in uninjured primary afferent neurons may contribute to the exaggerated response to cold observed in the neuropathic pain model.

Animals↗
PubMed1995

Variations in the lumbosacral ligament and associated changes in the lumbosacral region resulting in compression of the fifth dorsal root ganglion and spinal nerve.

Sixty-five lumbosacral regions from adult cadavers were dissected and the position and relations of the lumbosacral ligament noted. The lumbosacral ligament was present in all specimens; in 22 (34%) it extended medially across the ventral ramus of the fifth lumbar nerve, and in six (9%) of these the underlying nerve was compressed and visibly flattened. On two of these specimens the nerve, together with its dorsal root ganglion, was removed, processed, and stained with Masson's trichrome. The compressed nerve showed increased thickness of endoneurial and perineurial connective tissue, and the cells of the dorsal root ganglion were smaller and surrounded by increased connective tissue, particularly at the periphery of the ganglion. Observation of the lumbosacral ligament and surrounding anatomical structures suggests that anatomical variation in this region may be attributed to the health of the lumbosacral articular elements. In those specimens showing compression of the fifth lumbar spinal nerve there was also narrowing of the lumbosacral interspace. In these the disc itself was compressed and showed degenerative changes. The articular processes at the lumbosacral joint were irregular, with thinning and fissuring of the artiuclar cartilage. It is suggested that the processes which lead to the further development of the ligament, by the formation of additional fibrous bands, are mechanical in nature and result from instability at the lumbosacral region itself. Instability subsequently leads to the initiation of a chain of degenerative changes, involving pathology at the lumbosacral disc and zygapophyseal joints.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

[Neurinoma of the L3 spinal nerve root as a cause of stress-induced lumbo-ischialgias].

Degenerative diseases of the lumbar vertebral discs or the vertebral joints are the main causes of low back pain and sciatica following overstraining during sports activities. However, they are rarely seen in sportsmen engaged in competitive sports because these persons are mostly young and well-trained. Other neurological diseases are even rarer as possible causes of sciatica. That is why we report on a young athletic who is a short-distance hurdler (110m hurdle race) and has been suffering from a neurinoma of the spinal nerve root L3 with sciatica and pain in the knee as initial symptoms. Attention is drawn to the importance of neurological examinations as part of medical examinations conducted by sports physicians for the purpose of obtaining an overall guiding picture of the subjects' health status.

Adult↗
PubMed2002

The effect of intrathecal gabapentin on mechanical and thermal hyperalgesia in neuropathic rats induced by spinal nerve ligation.

Gabapentin decreases the level of glutamate and elevates that of alpha-amino-butyric acid in the central nervous system. Gabapentin was shown to have antinociceptive effects in several facilitated pain models. Intrathecal gabapentin was also known to be effective in reducing mechanical allodynia in animals with neuropathic pain. In this study, we investigated to see whether intrathecal gabapentin produces antihyperalgesic effects on thermal and mechanical hyperalgesia in neuropathic rats and whether its effects are associated with motor impairment. To induce neuropathic pain in Sprague-Dawley rats, left L5 and L6 spinal nerves were ligated. After a week, lumbar catheterization into subarachnoid space was performed. Then, paw withdrawal times to thermal stimuli and vocalization thresholds to paw pressure were determined before and up to 2 hr after intrathecal injection of gabapentin. Also, motor functions including performance times on rota-rod were determined. Intrathecal gabapentin attenuated significantly thermal and mechanical hyperalgesia in neuropathic rats, but did not block thermal and mechanical nociception in sham-operated rats. Intrathecal gabapentin of antihyperalgesic doses inhibited motor coordination performance without evident ambulatory dysfunction. This study demonstrates that intrathecal gabapentin is effective against thermal and mechanical hyperalgesia, in spite of moderate impairment of motor coordination.

Acetates↗
PubMedDate not supplied

[Differential diagnosis of the level of traumatic damage of cervical spinal nerves and brachial plexus].

In 80 patients with paresis or paralysis of the upper extremity due to injury to the brachial plexus or cervical roots, EMG with muscular test, skin thermometry and radiculography were done. The comparison of EMG investigations and Lovett's test with the diagram of segmental and peripheral innervation gave only an approximate determination of the level and extent of injury. Skin thermometry demonstrated vasomotór disturbances in 330 patients. Vasodilating activity was present, in the first place, in patients with complete paralysis of the extremity. These cases showed no significant improvement after rehabilitation management. Radiculography permitted to determine exactly the number of damaged spinal nerve pouches and this damage was found in 16 out of 18 patients. The character and location of pain in the upper extremity were without any significant diagnostic value in relation to the site and degree of injury.

Brachial Plexus↗
PubMed1975

Quantitative ultrastructural studies of the axon Schwann cell abnormality in spinal nerve roots from dystrophic mice.

Lumbo-sacral spinal roots and the nerve to the medial gastrocnemius muscle (NMG) from normal and dystrophic mice were examined by quantitative ultrastructural techniques. It was demonstrated that, although many axons at this level were totally devoid of Schwann cells, totatl axonal numbers were approximately normal. Some axons in these roots were surrounded by Schwann cells but their myelin sheaths were abnormally thin. In addition, cells resembling oligodendrocytes were observed in the dorsal roots of the dystrophic mice. In contrast, Schwann cells and myelin sheaths were normal in the more peripherally situated NMG and the regenerative response of these nerves to crush injury was not significantly different from that of control nerves. Thus, the main abnormality of neural morphology in dystrophic mice is a localized absence of Schwann cells. Such a deficiency does not appear to have influenced axonal growth or the capacity of these axons to regenerate when crushed distally.

Animals↗
PubMedDate not supplied

Spinal nerve enhancement with Gd-DTPA: MR correlation with the postoperative lumbosacral spine.

PURPOSE: To search for a probable source of the recurrent signs and symptoms associated with lumbosacral postsurgical syndrome on intravenous gadolinium-enhanced MR. METHODS: A retrospective study of 120 patients with recurrent symptomatology following lumbar disk surgery was carried out with spin-echo MR pre- and postenhancement with gadopentetate dimeglumine (0.1 mmol/kg). In addition, 10 asymptomatic subjects were evaluated at least 6 months postoperatively using the same imaging protocol. RESULTS: 21.6% of the symptomatic subjects (N = 26) had enhancement of one or more spinal nerve root. This enhancement was focal or multisegmental, and involved single or multiple nerve roots. The abnormal neural enhancement was associated with otherwise isolated epidural fibrosis in 88.5%, and with herniated nucleus pulposus in the remaining 11.5%. The overall clinical correlation of single root enhancement with a monoradiculopathy and multiroot enhancement with a polyradiculopathy was 95.7%. However, 21.7% of these same cases also showed additional nerve root enhancement that did not have an overt clinical correlation. All of these latter patients were imaged relatively early in the postoperative period (5 days to 8 months). The 10 patients in the asymptomatic group all manifested degrees of postoperative epidural scarring on MR, but no abnormal radicular enhancement or other associated pathology. CONCLUSION: In the chronic postoperative phase (more than 6 to 8 months), the presence of radicular enhancement on MR imaging in symptomatic individuals, and its absence in asymptomatic subjects, suggests that neural enhancement serves as a marker for active neural pathology that may in certain individuals be related temporally to the signs and symptoms associated with the lumbosacral postsurgical syndrome.

Adult↗
PubMed2006

Ewing's sarcoma in the spinal nerve root: a case report and review of the literature.

Ewing's sarcoma (ES) is a highly malignant tumor composed of uniform small round cells. Recently, a single biologic entity, Ewing's sarcoma family of tumors (ESFT) has been accepted. The entity includes ES, extraskeletal Ewing's sarcoma (EES) and primitive neuroectodermal tumor (PNET). ESFT cells have immunoreactivity for CD99, an antigen determined by the MIC2 gene. Most ESFT has the (11;22) (q24;q12) translocation. The translocation results in the fusion of the EWS gene with the transcription factor gene FLI1 which has been considered a hallmark of ESFT. We present an extremely unusual case with ESFT in a spinal nerve root mimicking a neurogenic dumbbell tumor. A male aged 20 years noticed pain in his right buttock. Magnetic resonance imaging (MRI) revealed a mass in the right L5/S intervertebral foramen and the lesions in the sacrum. Surgery was performed with a presumptive diagnosis of a nerve sheath tumor. At surgery, the tumor was located in the right L5 nerve root sleeve. The sacral lesions were observed closely. At one month after surgery, radiologically multiple lesions were detected in the pelvic bones. Microscopically the lesions from the root and ilium were composed of small round cells immunoreactive for CD99. Reverse transcription-polymerase chain reaction detected transcripts resulting from the fusion of the EWS gene with FLI1 genes in the iliac lesion. Immunoreactivity for CD99 and detection of the EWS-FLI1 hybrid transcripts are important for the correct diagnosis of ESFT arising in an unusual location.

Adult↗
PubMed2003

Increased sensitivity of injured and adjacent uninjured rat primary sensory neurons to exogenous tumor necrosis factor-alpha after spinal nerve ligation.

Tumor necrosis factor-alpha (TNF) is upregulated after nerve injury, causes pain on injection, and its blockade reduces pain behavior resulting from nerve injury; thus it is strongly implicated in neuropathic pain. We investigated responses of intact and nerve-injured dorsal root ganglia (DRG) neurons to locally applied TNF using parallel in vivo and in vitro paradigms. In vivo, TNF (0.1-10 pg/ml) or vehicle was injected into L5 DRG in naive rats and in rats that had received L5 and L6 spinal nerve ligation (SNL) immediately before injection. In naive rats, TNF, but not vehicle, elicited long-lasting allodynia. In SNL rats, subthreshold doses of TNF synergized with nerve injury to elicit faster onset of allodynia and spontaneous pain behavior. Tactile allodynia was present in both injured and adjacent uninjured (L4) dermatomes. Preemptive treatment with the TNF antagonist etanercept reduced SNL-induced allodynia by almost 50%. In vitro, the electrophysiological responses of naive, SNL-injured, or adjacent uninjured DRG to TNF (0.1-1000 pg/ml) were assessed by single-fiber recordings of teased dorsal root microfilaments. In vitro perfusion of TNF (100-1000 pg/ml) to naive DRG evoked short-lasting neuronal discharges. In injured DRG, TNF, at much lower concentrations, elicited earlier onset, markedly higher, and longer-lasting discharges. TNF concentrations that were subthreshold in naive DRG also elicited high-frequency discharges when applied to uninjured, adjacent DRG. We conclude that injured and adjacent uninjured DRG neurons are sensitized to TNF after SNL. Sensitization to endogenous TNF may be essential for the development and maintenance of neuropathic pain.

Animals↗