Spinal root and plexus hypertrophy in chronic inflammatory demyelinating polyneuropathy. (1/157)

MRI was performed on the spinal roots, brachial and lumbar plexuses of 14 patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Hypertrophy of cervical roots and brachial plexus was demonstrated in eight cases, six of whom also had hypertrophy of the lumbar plexus. Of 11 patients who received gadolinium, five of six cases with hypertrophy and one of five without hypertrophy demonstrated enhancement. All patients with hypertrophy had a relapsing-remitting course and a significantly longer disease duration. Gross onion-bulb formations were seen in a biopsy of nerve from the brachial plexus in one case with clinically evident nodular hypertrophy. We conclude that spinal root and plexus hypertrophy may be seen on MRI, particularly in cases of CIDP of long duration, and gadolinium enhancement may be present in active disease.  (+info)

Three pathways between the sacroiliac joint and neural structures. (2/157)

BACKGROUND AND PURPOSE: Despite ongoing clinical suspicion regarding the relationship between sacroiliac joint (SIJ) dysfunction and lower extremity symptoms, there is a paucity of scientific literature addressing this topic. The purpose of this study was to describe patterns of contrast extravasation during SIJ arthrography and postarthrography CT in patients with lower back pain and to determine whether there are pathways of communication between the SIJ and nearby neural structures. METHODS: Fluoroscopically guided SIJ arthrography was performed on 76 SIJs. After the injection of contrast medium, anteroposterior, lateral, and oblique radiographs as well as 5-mm contiguous axial and direct coronal CT images were obtained. Contrast extravasation patterns were recorded for each joint. These observations included a search for contrast extravasation from the SIJ that contacted nearby lumbosacral nerve roots or structures of the plexus. RESULTS: Sixty-one percent of all joints studied revealed one of five contrast extravasation patterns. Three of these observed patterns show a pathway of communication between the SIJ and nearby neural structures. These included posterior extravasation into the dorsal sacral foramina, superior recess extravasation at the sacral alar level to the fifth lumbar epiradicular sheath, and ventral extravasation to the lumbosacral plexus. CONCLUSION: Three pathways between the SIJ and neural structures exist.  (+info)

The posterior sacral foramina: an anatomical study. (3/157)

The vascular and nervous structures and their relations with the spinal nerve roots were examined in the 2nd, 3rd and 4th posterior sacral foramina in relation to percutaneous needle insertion for neuromodulation. A foraminal branch provided by the lateral sacral artery to each foramen entered the inferior lateral quadrant of each foramen, adjacent to the nerve root medially. Facing the posterior sacral aperture and around the sacral nerves, there was no venous plexus. A venous plexus was sometimes present near the median line, and always around the proximal part of the spinal ganglion. The sacral nerve roots, especially the 3rd, had a long extradural course in the foramen, presenting a potential risk of nerve lesions during procedures involving needle insertion.  (+info)

Biomechanical response in the ankle to stimulation of lumbosacral nerve roots with spiral cuff multielectrode--preliminary study. (4/157)

Biomechanical response in the ankle to tetanic stimulation of the lumbosacral root was investigated to assess the potential for lower limb functional neurostimulation. Myotomal response in the leg was measured as the three-dimensional isometric torque in the ankle after extradural tetanic stimulation of the L3-S1 roots exposed surgically for herniated disc removal in five patients. The cuff multielectrode was employed to investigate functional topography of the roots by monopolar, bipolar, and tripolar electrode configurations. Four response patterns in the direction of three-dimensional torque vectors were observed. The L-5 and S-1 roots had the same response pattern, but S-1 roots produced stronger torques. Dorsiflexion torque was not obtained by stimulation of L-5 roots despite coactivation of the tibial anterior and peroneal muscles. Dorsiflexion torques were produced only by stimulating the L-4 roots. More selective bipolar and tripolar stimulations recruited force at higher thresholds and less gain. Additionally, some muscles were not activated by tripolar stimulation of the same root. In one L-4 root, the torque at lower electrical threshold was replaced by inverse torque at higher threshold, providing indirect evidence that different muscles may have motoneuron populations that differ in diameter or location within the root. Although dorsiflexion and plantarflexion torques are functional per se, they are accompanied by foot inversion and leg rotation torques (as well as proximal muscle contractions). Further experimental investigations on direct extradural stimulation of lumbosacral roots, either single or in combination, are recommended to explore the potential of lumbosacral nerve root stimulation for restoration of leg function.  (+info)

Sacral neural crest cells colonise aganglionic hindgut in vivo but fail to compensate for lack of enteric ganglia. (5/157)

The vagal neural crest is the origin of majority of neurons and glia that constitute the enteric nervous system, the intrinsic innervation of the gut. We have recently confirmed that a second region of the neuraxis, the sacral neural crest, also contributes to the enteric neuronal and glial populations of both the myenteric and the submucosal plexuses in the chick, caudal to the level of the umbilicus. Results from this previous study showed that sacral neural crest-derived precursors colonised the gut in significant numbers only 4 days after vagal-derived cells had completed their migration along the entire length of the gut. This observation suggested that in order to migrate into the hindgut and differentiate into enteric neurons and glia, sacral neural crest cells may require an interaction with vagal-derived cells or with factors or signalling molecules released by them or their progeny. This interdependence may also explain the inability of sacral neural crest cells to compensate for the lack of ganglia in the terminal hindgut of Hirschsprung's disease in humans or aganglionic megacolon in animals. To investigate the possible interrelationship between sacral and vagal-derived neural crest cells within the hindgut, we mapped the contribution of various vagal neural crest regions to the gut and then ablated appropriate sections of chick vagal neural crest to interrupt the migration of enteric nervous system precursor cells and thus create an aganglionic hindgut model in vivo. In these same ablated animals, the sacral level neural axis was removed and replaced with the equivalent tissue from quail embryos, thus enabling us to document, using cell-specific antibodies, the migration and differentiation of sacral crest-derived cells. Results showed that the vagal neural crest contributed precursors to the enteric nervous system in a regionalised manner. When quail-chick grafts of the neural tube adjacent to somites 1-2 were performed, neural crest cells were found in enteric ganglia throughout the preumbilical gut. These cells were most numerous in the esophagus, sparse in the preumbilical intestine, and absent in the postumbilical gut. When similar grafts adjacent to somites 3-5 or 3-6 were carried out, crest cells were found within enteric ganglia along the entire gut, from the proximal esophagus to the distal colon. Vagal neural crest grafts adjacent to somites 6-7 showed that crest cells from this region were distributed along a caudal-rostral gradient, being most numerous in the hindgut, less so in the intestine, and absent in the proximal foregut. In order to generate aneural hindgut in vivo, it was necessary to ablate the vagal neural crest adjacent to somites 3-6, prior to the 13-somite stage of development. When such ablations were performed, the hindgut, and in some cases also the cecal region, lacked enteric ganglionated plexuses. Sacral neural crest grafting in these vagal neural crest ablated chicks showed that sacral cells migrated along normal, previously described hindgut pathways and formed isolated ganglia containing neurons and glia at the levels of the presumptive myenteric and submucosal plexuses. Comparison between vagal neural crest-ablated and nonablated control animals demonstrated that sacral-derived cells migrated into the gut and differentiated into neurons in higher numbers in the ablated animals than in controls. However, the increase in numbers of sacral neural crest-derived neurons within the hindgut did not appear to be sufficiently high to compensate for the lack of vagal-derived enteric plexuses, as ganglia containing sacral neural crest-derived neurons and glia were small and infrequent. Our findings suggest that the neuronal fate of a relatively fixed subpopulation of sacral neural crest cells may be predetermined as these cells neither require the presence of vagal-derived enteric precursors in order to colonise the hindgut, nor are capable of dramatically altering their proliferation or d  (+info)

Sacral neural crest cell migration to the gut is dependent upon the migratory environment and not cell-autonomous migratory properties. (6/157)

Avian neural crest cells from the vagal (somite level 1-7) and the sacral (somite level 28 and posterior) axial levels migrate into the gut and differentiate into the neurons and glial cells of the enteric nervous system. Neural crest cells that emigrate from the cervical and thoracic levels stop short of the dorsal mesentery and do not enter the gut. In this study we tested the hypothesis that neural crest cells derived from the sacral level have cell-autonomous migratory properties that allow them to reach and invade the gut mesenchyme. We heterotopically grafted neural crest cells from the sacral axial level to the thoracic level and vice versa and observed that the neural crest cells behaved according to their new position, rather than their site of origin. Our results show that the environment at the sacral level is sufficient to allow neural crest cells from other axial levels to enter the mesentery and gut mesenchyme. Our study further suggests that at least two environmental conditions at the sacral level enhance ventral migration. First, sacral neural crest cells take a ventral rather than a medial-to-lateral path through the somites and consequently arrive near the gut mesenchyme many hours earlier than their counterparts at the thoracic level. Our experimental evidence reveals only a narrow window of opportunity to invade the mesenchyme of the mesentery and the gut, so that earlier arrival assures the sacral neural crest of gaining access to the gut. Second, the gut endoderm is more dorsally situated at the sacral level than at the thoracic level. Thus, sacral neural crest cells take a more direct path to the gut than the thoracic neural crest, and also their target is closer to the site from which they initiate migration. In addition, there appears to be a barrier to migration at the thoracic level that prevents neural crest cells at that axial level from migrating ventral to the dorsal aorta and into the mesentery, which is the portal to the gut.  (+info)

Postpartum lumbosacral plexopathy limited to autonomic and perineal manifestations: clinical and electrophysiological study of 19 patients. (7/157)

The objective was to describe perineal electrophysiological findings and to determine their diagnostic value in a type of lumbosacral plexopathy after vaginal delivery, which only involves the lower part of the plexus (S2-S4). Consecutive female patients referred to an outpatients' urodynamic clinic were the source. Nineteen previously healthy women, 13 multiparae and six para 1, were investigated. Mean age was 33.7 (SD 5.4) (range 28-41) years. All of them presented with urinary (stress incontinence 14, dysuria five), anorectal (faecal incontinence eight, dyskesia one), or sexual dysfunctions (hypoorgasmia or anorgasmia six) after vaginal delivery. No associated lower limb sensory or motor deficits were noted. All the patients had electrophysiological recordings (bulbocavernosus muscle EMG, measurements of the bulbocavernosus reflex latencies (BCRLs), somatosensory evoked potentials of the pudendal nerve (SEPPNs), and pudendal nerve terminal motor latencies (PNTMLs)). Cystometry and urethral pressure profile (UPP) were performed in the 14 patients with stress urinary incontinence. Perineal electrophysiological examination disclosed signs of denervation in the perineal muscles in all the cases, prolonged BCRLs in 17/19, and abolished BCRLs in 2/19, abnormal SEPPN in 1/19, and normal PNTMLs in all the patients. Urodynamic investigations disclosed low urethral closure pressure for age (< 50 cm H(2)O) in half of the patients. In conclusion, Lower postpartum lumbosacral plexopathy is evoked when perineal sensory disturbances whether or not associated with urinary or faecal incontinence persist after a history of a difficult vaginal delivery. Electrophysiological investigations precisely identify the site of the lesion and demonstrate distal innervation integrity.  (+info)

Lumbar plexus block reduces pain and blood loss associated with total hip arthroplasty. (8/157)

BACKGROUND: The usefulness of peripheral nerve blockade in the anesthetic management of hip surgery has not been clearly established. Because sensory afferents from the hip include several branches of the lumbar plexus, the authors hypothesized that a lumbar plexus block could reduce pain from a major hip procedure. METHODS: In a double-blind prospective trial, 60 patients undergoing total hip arthroplasty were randomized to receive general anesthesia with (plexus group, n = 30) or without (control group, n = 30) a posterior lumbar plexus block. The block was performed after induction using a nerve stimulator, and 0.4 ml/kg bupivacaine, 0.5%, with epinephrine was injected. General anesthesia was standardized, and supplemental fentanyl was administered per hemodynamic guidelines. Postoperative pain and patient-controlled intravenous morphine use were serially assessed for 48 h. RESULTS: The proportion of patients receiving supplemental fentanyl intraoperatively was more than 3 times greater in the control group (20 of 30 vs. 6 of 29, P = 0.001). In the postanesthesia care unit, a greater than fourfold reduction in pain scores was observed in the plexus group (visual analogue scale [VAS] pain score at arrival 1.3 +/- 2 vs. 5.6 +/- 3, P < 0.001), and "rescue" morphine boluses (administered if VAS > 3) were administered 10 times less frequently (in 2 of 28 vs. in 22 of 29 patients, P < 0.0001). Pain scores and morphine consumption remained significantly lower in the plexus group until 6 h after randomization (VAS at 6 h, 1.4 +/- 1.3 vs. 2.4 +/- 1.4, P = 0.007; cumulative morphine at 6 h, 5.6 +/- 4.7 vs. 12.6 +/- 7.5 mg, P < 0.0001). Operative and postoperative (48 h) blood loss was modestly decreased in the treated group. Epidural-like distribution of anesthesia occurred in 3 of 28 plexus group patients, but no other side-effects were noted. CONCLUSIONS: Posterior lumbar plexus block provides effective analgesia for total hip arthroplasty, reducing intra- and postoperative opioid requirements. Moreover, blood loss during and after the procedure is diminished. Epidural anesthetic distribution should be anticipated in a minority of cases.  (+info)

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