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MR imaging of the cauda equina in hereditary motor sensory neuropathies: correlations with sural nerve biopsy.

BACKGROUND AND PURPOSE: Although spinal root abnormalities are known to occur, spinal MR examination is seldom performed in hereditary motor and sensory neuropathies (HMSN). The following work was undertaken to assess the MR imaging spectrum of lumbosacral spinal nerve root abnormalities and determine whether intradural nerve root involvement could be related to any biopsy feature. METHODS: Ten consecutive patients (eight male, two female; age range, 28-65 yrs) with Charcot-Marie-Tooth (CMT) (type I = 5, type II = 2) and Déjèrine-Sottas disease (DSD) (n = 3) underwent a contrast-enhanced lumbosacral MR examination. Sural nerve biopsy was performed in all patients. Atypical clinical features were present in two patients. The MR scans of each patient were reviewed for possible causes of myeloradiculopathy, spinal nerve root and ganglia dimensions, signal change, and abnormal enhancement. RESULTS: In the seven patients with CMT, abnormal MR findings were intradural nerve root hypertrophy (n = 2), signal abnormalities (n = 2), and enhancement (n = 3). Two of three patients with DSD had the abnormal MR finding of intradural nerve root enhancement. In both patients with atypical clinical features, MR imaging showed nerve root hypertrophy and enhancement. Both findings were related to an increased number of onion bulbs at sural nerve biopsy. Inflammatory infiltrates were not observed in any patients. CONCLUSION: In patients with HMSN enhancement of intradural spinal nerve roots, whether or not associated with marked thickening, may be found on lumbosacral MR examinations. Spinal nerve root thickening may be responsible for atypical symptoms, and its visibility on MR images represents a useful adjunct to diagnosis. Lumbosacral spinal nerve root abnormalities were related to an extremely high number of onion bulbs (indicating active demyelination) at sural nerve biopsy. Nerve root enhancement does not seem to be related to inflammatory infiltrates.

Adult↗

Nerve root ischemia and pain secondary to spinal stenosis syndrome: technical and clinical considerations.

Spinal stenosis is a loosely used term meaning different things to different people. A clinical picture of episodic sciatic pain and a normal physical examination usually confronts the physician. Various anatomic lesions can produce traction and compression of spinal nerve roots. The pathophysiology of the compression and the resultant ischemia of spinal nerve roots is discussed. Accurate diagnosis may allow conservative care, including manipulation, to be utilized prior to surgical consideration.

Chiropractic↗

Reinnervation of avulsed brachial plexus using the spinal accessory nerve.

The use of the accessory nerve as a donor is one of the possibilities for the reinnervation of the brachial plexus in cases of paralysis due to root avulsion. In this paper, an analysis of the reinnervation of the musculocutaneous or axillary nerve using the spinal accessory nerve is made on 13 cases, 8 of total and 5 of upper partial avulsion. In all cases, Allieu's technique was used, but in seven cases reinnervation was supplemented by upper intercostal nerves when there was total avulsion and/or by the medial pectoral nerve when there was partial avulsion. The methods are discussed and compared with the intercostobrachial anastomosis.

Accessory Nerve↗

[Anatomicosurgical comments on the importance of the spinal accessory nerve].

The preserved integrity of the spinal accessory nerve plays an extremely important role in cervico-facial surgery since the majority of surgical approaches involve this nervous structure. Following a short historical outline of the surgical method, the Authors illustrate the anatomo-topographical aspects and anatomo-surgical problems. A number of points emerge from a review of the literature which are vital to isolate the spinal accessory nerve: 1) the transversal apophysis of the atlas is particularly prominent in the retrostyloid space and lies half-way across an imaginary horizontal segment connecting the mastoid process with the angle of the mandible; 2) the posterior edge of the sternocleidomastoid muscle at approximately six centimetres from the mastoid process; 3) the nervous point of Erb located at the point where the superficial branches of the cervical plexus emerge from the posterior edge of the sternocleidomastoid muscle (the nerve generally emerges from the posterior edge of the sternocleidomastoid muscle two centimetres above this point and two centimetres below it the nerve meets the anterior edge of the trapezius). This is followed by an analysis of the possible complications deriving from lesions to this vital nervous structure. The resection of the spinal accessory nerve leads to the so-called "shoulder syndrome" mainly due to the denervation of the trapezius. This syndrome is characterised by the onset of regional pain, the typical deformation of the shoulder joint and functional deficit. The deformation is provoked by the decreased muscular strength of the superior and middle portion of the trapezius manifested as the rocking of the shoulder and a higher superointernal angle.(ABSTRACT TRUNCATED AT 250 WORDS)

Accessory Nerve↗

Surgical outcomes of 111 spinal accessory nerve injuries.

OBJECTIVE: Iatrogenic injury to the spinal accessory nerve is not uncommon during neck surgery involving the posterior cervical triangle, because its superficial course here makes it susceptible. We review injury mechanisms, operative techniques, and surgical outcomes of 111 surgical repairs of the spinal accessory nerve. METHODS: This retrospective study examines clinical and surgical experience with spinal accessory nerve injuries at the Louisiana State University Health Sciences Center during a period of 23 years (1978-2000). Surgery was performed on the basis of anatomic and electrophysiological findings at the time of operation. Patients were followed up for an average of 25.6 months. RESULTS: The most frequent injury mechanism was iatrogenic (103 patients, 93%), and 82 (80%) of these injuries involved lymph node biopsies. Eight injuries were caused by stretch (five patients) and laceration (three patients). The most common procedures were graft repairs in 58 patients. End-to-end repair was used in 26 patients and neurolysis in 19 patients if the nerve was found in continuity with intraoperative electrical evidence of regeneration. Five neurotizations, two burials into muscle, and one removal of ligature material were also performed. More than 95% of patients treated by neurolysis supported by positive nerve action potential recordings improved to Grade 4 or higher. Of 84 patients with lesions repaired by graft or suture, 65 patients (77%) recovered to Grade 3 or higher. The average graft length was 1.5 inches. CONCLUSION: Surgical exploration and repair of spinal accessory nerve injuries is difficult. With perseverance, however, these patients with complete or severe deficits achieved favorable functional outcomes through operative exploration and repair.

Accessory Nerve↗

Organization of the motor nuclei in the cervical spinal cord of salamanders.

The distribution and cytoarchitecture of motor nuclei of the cervical spinal cord were studied by using HRP techniques (whole mounts and sections) in 22 species of salamanders (families Hynobiidae, Dicamptodontidae, Ambystomatidae, Salamandridae, and Plethodontidae) representing a wide variety of life histories and functional modes of feeding. The nucleus of the first spinal nerve extends from the level of, or slightly caudad to, the root of the tenth cranial nerve, almost to the ventral root of the second spinal nerve. Approximately one-half of this nucleus is situated in the brainstem. This anterior extension is longest in bolitoglossine plethodontids. The nucleus of the second spinal nerve extends from the root of the first spinal nerve to the dorsal root of the second spinal nerve. The nuclei of the first and second spinal nerves in all species except bolitoglossines have motor neurons arranged in two columns: a lateral one containing large spindle-shaped cells and a medial one containing pear-shaped or polygonal smaller cells. The primary dendrites of these lateral and medial cells are parallel and their arborization is relatively narrow. In contrast, bolitoglossines lack the lateral motor column. The nucleus of the first spinal nerve consists only of a medial band of pear-shaped and sometimes polygonal cells, and the nucleus of the second spinal nerve is a wider band of pear-shaped and polygonal cells which are always situated inside the periventricular gray matter. The arrangement of the somata in bolitoglossines is less organized and the primary dendrites are less parallel and have a broader arborization than in other salamanders. In all species, cells in the second spinal nucleus are arranged in a less orderly manner than those in the first. All salamanders studied possess a spinal accessory nerve whose motor neurons are located in the cervical spinal cord; the axons leave the brainstem with fibers of the vagus nerve. The rostrocaudal extent of this nucleus differs markedly among species. In bolitoglossines the nucleus is more or less restricted to the region of the nucleus of the second spinal nerve. In all other species studied, the accessory nucleus extends from the obex to the caudal end of the nucleus of the third spinal nerve. In the tribe Plethodontini the cytoarchitecture of the accessory nucleus is similar to that of the second spinal. In desmognathine and hemidactyliine plethodontids as well as in all nonplethodontid species studied the nucleus consists of pear-shaped and cone-shaped cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Accessory Nerve↗

Focal conduction block in the dorsal root ganglion in experimental allergic neuritis.

Acute experimental allergic neuritis was induced in Lewis rats by inoculation with bovine intradural root myelin and adjuvants. In terminal experiments, sensory conduction was assessed in rats with hindlimb ataxia and weakness by stimulating the exposed sciatic nerve and recording directly from the exposed L-4 spinal nerve, dorsal root ganglion, dorsal root, and dorsal root entry zone. Focal conduction block was present in a high proportion of large-diameter fibers in the dorsal root ganglion. In contrast, nerve conduction in the peripheral nerve and spinal nerve was essentially normal apart from probable conduction block in some fibers in the proximal spinal nerve in a minority of rats. The afferent volley arriving at the dorsal root entry zone of the spinal cord was greatly reduced, as a consequence of the conduction block in the dorsal root ganglion and probable conduction block in the dorsal root. The M wave recorded from the fourth dorsal interosseus muscle of the hindfoot was normal in amplitude but slightly prolonged in latency and the H reflex was absent. These electrophysiological findings correlated well with the histological findings of inflammation and prominent demyelination in the dorsal root ganglia and dorsal roots with minimal involvement of the proximal spinal nerve and no involvement of the sciatic nerve. It is concluded that the hindlimb ataxia in rats with this form of acute experimental allergic neuritis is due to demyelination-induced nerve conduction block in the dorsal root ganglia and probably in the dorsal roots.

Afferent Pathways↗

The anatomy of the lumbar intervertebral disc syndrome.

Four elements of the nervous system may be involved in the production of the lumbar intervertebral disc syndrome. These are the lumbosacral nerve roots, the spinal nerves, the dorsal rami and the sinuvertebral nerves. Each nerve is associated with a particular group of pathological conditions which may irritate the nerve and produce symptoms. The anatomy of each nerve determines which particular conditions may irritate it. Moreover, one or both of two mechanisms may be involved in symptom production. The type of nerve irritated determines which mechanism is involved. In the first mechanism, low back pain and referred lower limb symptoms are produced when afferent fibres from dorsal and ventral rami are stimulated where they pass in common through spinal nerves or nerve roots. In the second mechanism, dorsal rami or sinuvertebral nerves are stimulated. This directly produces low back pain, but referred pain is produced by reflex mechanisms in the spinal cord.

Back Pain↗

Neurotization via the spinal accessory nerve in complete paralysis due to multiple avulsion injuries of the brachial plexus.

The authors report their experience with 21 cases of neurotization via the spinal accessory nerve for multiple nerve root avulsion injuries of the brachial plexus associated with total paralysis of the upper limb. They performed microneuroanastomoses with interposed cable nerve grafts between the spinal accessory nerve taken in the supraclavicular fossa and the musculocutaneous nerve at its entrance into the biceps muscle. Surgical indications depend on the accurate diagnosis of spinal nerve root avulsion, especially C5. The anatomicosurgical basis of this technique is as precise as are the indications. As many as two-thirds of the patients with a neurotized musculocutaneous nerve can be expected to achieve strength of at least Grade 3 on late muscle testing. Nevertheless, these results are always inferior to those obtainable when grafting is performed with carefully selected unavulsed C5 or C6 spinal nerve root fibers in the intervertebral foramina. Therefore, neurotization via donor nerves extrinsic to the plexus should only be considered as a second-choice intervention.

Adult↗

Variations in the surface anatomy of the spinal accessory nerve in the posterior triangle.

Iatrogenic injury to the spinal accessory nerve has been widely documented and can have medico-legal implications. The resulting syndrome of pain, paralysis and winging of the scapula are often the source of considerable morbidity. This paper researches the degree of accuracy achievable in mapping the surface anatomy of the spinal accessory nerve in the region of the posterior triangle with a view to creating a cartographical aid to surgical procedures. The necks of 25 adult cadavers were dissected bilaterally to expose the spinal accessory nerve. Variations in the course and distribution of the spinal accessory nerve in the posterior triangle were recorded along with its relationship to the borders of sternocleidomastoid and trapezius. Considerable variation was seen in the surface and regional anatomy of the nerve and in the contribution of the cervical plexus to the spinal accessory nerve in the posterior triangle. Measurements of the running course and exit point of the nerve into and from the posterior triangle differed significantly from those previously recorded. Delineation of an accurate surface anatomy was not possible. Creating a map to define the surface anatomy of the spinal accessory nerve in the posterior triangle is an unrealistic goal given its wide variations in man. Avoidance of damage to the spinal accessory nerve cannot be achieved by slavishly adhering to surface markings given in textbooks, but only by cautious dissection during operations on the posterior triangle.

Accessory Nerve↗

Reconstruction of spinal accessory nerve after radical neck dissection.

Resection of the spinal accessory nerve in cases of radical neck dissection often causes considerable damage to the function of the shoulder girdle; it leads to limitation of the motion of the upper limb and pain in the shoulder girdle. It seems a sensible compromise to reconstruct the spinal accessory nerve in one-stage operation with radical neck dissection, which can often prevent extensive atrophy of the trapezius muscle, with a resultant improvement in the chance of successful rehabilitation. The technique of the operation is described: after completion of radical neck dissection, in one-stage operation an autogenous nerve transplant from the n. auricularis magnus is sewn onto the central and peripheral stumps of the spinal accessory nerve, which are protected by a "vein-muff" and the fascia of the muscle. After such spinal accessory nerve reconstruction, subjective complaints and objective symptoms were much milder in 6 patients than in the control group, which consisted of 10 patients who underwent a similar operation but without spinal accessory nerve reconstruction.

Accessory Nerve↗

Early onset of spontaneous activity in uninjured C-fiber nociceptors after injury to neighboring nerve fibers.

Ligation and transection of the L5 spinal nerve in the rat lead to behavioral signs of pain and hyperalgesia. Discharge of injured nociceptors has been presumed to play a role in generating the pain. However, A fibers, but not C fibers, in the injured L5 spinal nerve have been shown to develop spontaneous activity. Moreover, an L5 dorsal root rhizotomy does not reverse this pain behavior, suggesting that signals from other uninjured spinal nerves are involved. We asked if abnormal activity develops in an adjacent, uninjured root. Single nerve fiber recordings were made from the L4 spinal nerve after ligation and transection of the L5 spinal nerve. Within 1 d of the lesion, spontaneous activity developed in approximately half of the C fiber afferents. This spontaneous activity was at a low level (median rate, seven action potentials/5 min), originated distal to the dorsal root ganglion, and was present in nociceptive fibers with cutaneous receptive fields. The incidence and level of spontaneous activity were similar 1 week after injury. The early onset of spontaneous activity in uninjured nociceptive afferents could be the signal that produces the central sensitization responsible for the development of mechanical hyperalgesia. Because L4 afferents comingle with degenerating L5 axons in the peripheral nerve, we hypothesize that products associated with Wallerian degeneration lead to an alteration in the properties of the adjacent, uninjured afferents.

Action Potentials↗

Lumbar-spinal somatosensory evoked potentials in the rat after stimulation of the tibial nerve.

Spinal somatosensory evoked potentials after stimulation of the tibial nerve were recorded from the lumbospinal cord of rats. Their components and the respective latencies recorded over L5/6 and L1/2 in 40 normal animals are described. Using this method exact statements concerning lesions particularly of the proximal segment of the peripheral nerves and their roots can be made.

Animals↗

Extraforaminal ligament attachments of human lumbar nerves.

STUDY DESIGN: An anatomic study of the extraforaminal attachments of the lumbar spinal nerves was performed using human lumbar spinal columns. OBJECTIVES: To identify and describe the existence of ligamentous structures at each lumbar level that attach lumbar spinal nerves to structures at the level of the extraforaminal region. SUMMARY OF BACKGROUND DATA: During the last 120 years, several mechanisms to protect the spinal nerve against traction have been described. All these structures involved are located in the spinal canal, proximal to the intervertebral foramen. METHODS: Five embalmed human lumbar spines (T12-S1) were used. Bilaterally, the extraforaminal region was dissected to describe and measure anatomic structures and their relationships. Histology was performed with staining on the sites of attachment and along the ligament. RESULTS: The levels T12-L2 show bilaterally 2 ligaments, a superior extraforaminal ligament and an inferior extraforaminal ligament. The superior extraforaminal ligament emerges from the joint capsule of the facet joints and inserts in both, the intervertebral disc and the ventral crista of the intervertebral foramen, passing the spinal nerve laterally. In one specimen on level L2-L3, the superior extraforaminal ligament is not attached to the spinal nerve. The inferior extraforaminal ligament emerges from the intervertebral disc, passing the nerve medially and attaching the spinal nerve. At the levels L2-L5, the inferior extraforaminal ligaments are only attached to the intervertebral disc, not to the joint capsule. Histologically, the ligaments consisted of mainly collagenous structures. CONCLUSION: Ligamentous connections exist between lumbar extraforaminal spinal nerves and nearby structures.

Aged, 80 and over↗

Development of purinergic sensitivity in sensory neurons after peripheral nerve injury in the rat.

Purinoceptors are present in the cell bodies as well as in both peripheral and central terminals of many sensory neurons, where they may play a role in sensory transmission, including pain. After peripheral nerve injury at the spinal nerve level, some axotomized afferent neurons develop ongoing discharges (ectopic discharges) that originate in the dorsal root ganglion (DRG). In the present study, we attempted to determine whether or not purinergic sensitivity develops in injured sensory neurons which display ectopic discharges, as well as in silent units. The L(4) and L(5) spinal nerves were ligated in Sprague-Dawley rats. Four to 21 days after the surgery, the DRGs with attached dorsal roots and spinal nerves were removed and ectopic discharges were recorded from teased dorsal root fascicles using an in vitro recording set-up. The results showed that 75.6 and 65.1% of the chronically axotomized DRG neurons displaying ectopic discharges enhanced their activity after application of adenosine 5'-triphosphate (ATP, 1 mM) or alpha,beta-methylene ATP (mATP, 100 microM), respectively. In addition, application of these purinoceptor agonists evoked activity in 7 of 28 axotomized DRG neurons, which did not show ongoing discharges. In contrast, only 1 of 34 DRG neurons acutely isolated from normal rats (no previous spinal nerve ligation) responded to either mATP or ATP. In most of the tested units, mATP-induced enhancement of ectopic discharges was blocked by non-specific P2X receptor antagonists, PPADS or suramin. The data from the present study suggest that purinergic sensitivity develops in DRG neurons after chronic axotomy and that this purinergic sensitivity is likely to be mediated by P2X purinoceptors. This acquired purinergic sensitivity may play an important functional role in the enhancement of ectopic discharges and exacerbation of pain upon sympathetic activation in the neuropathic pain state.

Adenosine Triphosphate↗

Juvenile xanthogranuloma of peripheral nerve: a report of two cases.

As a rule, juvenile xanthogranuloma (JXG) is a cutaneous lesion most often occurring in infancy. An inflammatory process of unknown etiology, it is self-limited and benign in nature. The spectrum of JXG has expanded to include adult examples, multifocal lesions, and ones arising at extracutaneous locations. Although a variety of extracutaneous sites may be affected, few reported lesions have involved cranial or peripheral nerves. Solitary examples have been reported in trigeminal nerve and spinal nerve root; affected individuals were children or adolescents. An optic nerve lesion has also been described. We describe two additional cases of JXG of nerve. One patient developed multiple dorsal nerve root lesions, as well as skin involvement. The other case featured isolated involvement of the left radial nerve. Both patients were adults with no known underlying systemic disorder. These cases further expand the spectrum of extracutaneous JXG, and underscore its consideration in the differential of nerve "tumors."

Adult↗

Aberrant formation and clinical picture of brachial plexus from the point of view of a neurosurgeon.

UNLABELLED: Variations detected during surgery stimulated us to study the variations of the formation of the brachial plexus. METHODS: We examined 110 brachial plexus in 55 adult cadavers in order to determine the incidence of neural variations. We observed the contribution of the C4 root and possibly Th2 root as well as various anomalies in the origination of each plexiform root and its branches from the spinal cord, and variations of the formation of the neural trunks, fascicles and peripheral branches. We examined their course, anastomosis, thickness and possible absence. We observed the plexiform but not the spinal roots. We saw the pretruncal part of plexus including segment of spinal nerve in the sulcus spinal nerve and anterior branch of the spinal nerve. Motor innervation anomalies in relation to diagnostics are emphasized as well, apart from the anatomic variability. Attention focused on the mechanism and the morphologic reasons for particular types of injuries. RESULTS: The prefixed type was present in 26 cases (47.3%), and was postfixed in one case. We did not observe any anomaly in the formation of the plexus in 9 cases. We observed 143 anomalies in 46 cases (83.6%). There was one anomaly present in 11 cases and in 35 two or more anomalies were noted. The anomalies were present more frequently on the left side--in 60 cases (41.2%) and bilaterally in 48 cases (33.6%). The anomalies were usually anatomic and in the area of the formation of the terminal branches. The least number of anomalies was present in the area of neural roots. CONCLUSION: This study allowed us to find out and describe unusual and previously not described anatomic variations in the formation of neural roots, trunks, fascicles and terminal branches of the brachial plexus. The formation of the axillary nerve as a continuation of the posterior branch of the superior trunk was noted. (Tab. 4, Fig. 8, Ref. 10.).

Brachial Plexus↗

Leptomeningeal metastases from ethmoid sinus adenocarcinoma: clinico-radiological correlation.

A patient with sinonasal adenocarcinoma is presented with leptomeningeal metastases affecting multiple cranial nerves and spinal nerve roots. Head and neck cancer is known to be an extremely rare source for leptomeningeal metastatic spread. The cranial nerves, the spinal cord and roots and the cerebral hemispheres can be affected in case of leptomeningeal metastatic spread. Examination of the CSF is the hallmark of the diagnosis if leptomeningeal metastatic spread is suspected, but this case illustrates that the combination of specific clinical features on one hand and specific lesions on the Gd-enhanced T1-weighted MRI study on the other hand is reliable enough to make a presumed diagnosis if the CSF analysis remains negative. We suggest that in our patient direct leptomeningeal spread occurred through the cribriform plate to the CSF, followed by further spread in a gravity dependent way.

Adenocarcinoma↗