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The case of a 57-year-old woman with a primary melanoma of the cauda equina is reported. The peculiarity of the case is the very rare clinical presentation mimicking a subarachnoid hemorrhage. The patient underwent surgical excision of the mass. The clinicopathological and neuroradiological features are summarized.

Study Design: Case report., Objective: To report a rare cause of spinal cord compression., Setting: University Hospital, Wales, UK., Case Report: A 67-year-old gentleman on oral anticoagulation for atrial fibrillation presented with a 4-h history of progressive loss of sensation and weakness in both legs; there was no history of trauma. On examination, he had a flaccid paraplegia with altered sensation in the L1,2,3 dermatomes and complete anaesthesia in the L4,5 distribution. Knee and ankle jerk reflexes were absent, plantars were equivocal and anal sphincter tone was reduced. The patient's international normalized ratio (INR) was 4.1. An MR scan showed an extensive intradural haematoma compressing the cauda equina. The anticoagulation was reversed and an urgent T12-L2 laminectomy was performed; findings were a circumferential haematoma at L1 extending in the anterior canal between T10 and L3. The patient had an uneventful postoperative course generally, but at 1 week there was no neurological recovery., Conclusion: This case highlights that anticoagulation even when well controlled is not without risk. This is particularly of concern as the number of patients receiving long-term anticoagulation therapy has doubled between 1993 and 1998.

Thirteen patients with Schistosoma mansoni myelopathy are reported. Neurologic syndromes included acute areflexic flaccid paraplegia (three), thoracic myelopathy with hyperreflexia and Babinski sign (six), and a cauda equina syndrome (four). Inflammatory granulomas and a schistosome worm in a leptomeningeal vein of the spinal cord were observed in the one patient coming to necropsy.

Object: The purpose of this study was to analyze therapeutic possibilities and clinical outcomes in patients with lumbosacral plexus injuries to develop surgical concepts of treatment., Methods: In a retrospective investigation 10 patients with injuries to the lumbosacral plexus were evaluated after surgery. The patients were assessed clinically, electrophysiologically, and based on the results of magnetic resonance imaging and computerized tomography myelography. In most patients a traction injury had occurred due to severe trauma that also caused pelvic fractures. In most cases the roots of the cauda equina of the lumbosacral plexus had ruptured. In cases of spinal root ruptures repair with nerve grafts were performed. In cases in which proximal stumps of the plexus could not be retrieved palliative nerve transfers by using lower intercostals nerves or fascicles from the femoral nerve were performed., Conclusions: Lesions of the proximal spinal nerves and cauda equina occur in the most serious lumbosacral plexus injuries. Patients with such injuries subjected to reconstruction of spinal nerves, repair of ventral roots in the cauda equina, and nerve transfers recovered basic lower-extremity functions such as unsupported standing and walking.

A 55-year-old man with acute myeloid leukemia in second relapse presented 4 months after haploidentical CD34+-selected hematopoietic stem cell transplantation (HSCT) with symmetric, progressive neurological deficits of the lower extremities. Although there was no molecular evidence for drug resistance in the cerebral-spinal fluid, antiviral combination therapy failed to control the rapidly progressing CMV polyradiculopathy (PRP) and encephalitis, which were confirmed by autopsy studies. Late CMV PRP as an unusual manifestation of CMV disease should be kept in mind in patients with suggestive neurological symptoms after HSCT.

Injuries to the cauda equina of the spinal cord result in autonomic and motor neuron dysfunction. We developed a rodent lumbosacral ventral root avulsion injury model of cauda equina injury to investigate the lesion effect in the spinal cord. We studied the retrograde effects of a unilateral L5-S2 ventral root avulsion on efferent preganglionic parasympathetic neurons (PPNs) and pelvic motoneurons in the L6 and S1 segments at 1, 2, 4, and 6 weeks postoperatively in the adult male rat. We used Fluoro-Gold-prelabeling techniques, immunohistochemistry, and quantitative stereologic analysis to show an injury-induced progressive and parallel death of PPNs and motoneurons. At 6 weeks after injury, only 22% of PPNs and 16% of motoneurons remained. Furthermore, of the neurons that survived at 6 weeks, the soma volume was reduced by 25% in PPNs and 50% in motoneurons. Choline acetyltransferase (ChAT) protein was expressed in only 30% of PPNs, but 80% of motoneurons remaining at 1 week postoperatively, suggesting early differential effects between these two neuronal types. However, all remaining PPNs and motoneurons were ChAT positive at 4 weeks postoperatively. Nuclear condensation and cleaved caspase-3 were detected in axotomized PPNs and motoneurons, suggesting apoptosis as a contributing mechanism of the neural death. We conclude that lumbosacral ventral root avulsions progressively deplete autonomic and motor neurons. The findings suggest that early neuroprotection will be an important consideration in future attempts of treating acute cauda equina injuries., (Copyright 2003 Wiley-Liss, Inc.)

Although rare, direct infiltration of the cauda equina by non-Hodgkin's lymphoma (NHL) must be considered as a potential cause of subacute onset paraplegia. We present two cases of lymphomatous involvement of the cauda equina presenting with subacute paraplegia, each associated with a palsy of an oculomotor nerve. We highlight the need to use gadolinium-enhanced magnetic resonance imaging (MRI) when investigating potential cauda equina lesions, since it is crucial in detecting and outlining the extent of disease. Differential diagnoses and treatment options for NHL involving the cauda equina are also discussed.

Study Design: Case report., Objective: To describe the clinical presentations, radiological features and clinical progress of a rare case of chondroblastoma of the lumbar spine., Setting: Regional Hospital, Hong Kong, China., Method: A 54-year-old male patient presented with low back pain and left sciatica. X-ray and MRI revealed tumour infiltration of the fifth lumbar vertebrae and left paraspinal muscles, which was found to be a chondroblastoma by repeated open biopsies. The tumour was removed surgically by combined anterior and posterior approaches, followed by spinal fusion and instrumentation., Results: The anterior tricortical bone graft was complicated with fracture and nonunion. Surgical re-exploration confirmed local recurrence of tumour macroscopically and histologically. The patient developed symptoms and signs of cauda equina syndrome gradually despite repeated surgery and irradiation. The patient eventually died of complications of local recurrence and neurological deficit at 3 years and 8 months after the first operation., Conclusion: This is the first case report of chondroblastoma of the lumbar spine. The clinical profile of this patient and the evidence from the literature review suggests that spinal chondroblastoma has a very aggressive behaviour with high recurrence and mortality rate.

Three patients with a remote history of Hodgkin's disease treated with total or subtotal lymphoid radiation 17 to 24 years earlier developed lumbosacral polyradiculopathy associated with nodular meningeal enhancement of the conus medullaris and cauda equina on MRI. None had evidence of recurrent Hodgkin's disease or second malignancy, and the MRI findings may be sequelae of radiation therapy.

Bilateral acute foot drop is reported in a 30-year-old healthy male. He presented with a 7-day history of sudden severe backache, radiating to both the lower limbs and 1-day history of sudden bilateral ankle weakness that progressed to bilateral foot drop within 6 hours. He also developed retention of urine. Investigations revealed a large central disc prolapse at L3-4 with significant canal stenosis at that level. Following surgery the patient had progressive improvement.

Spinal hydatid cyst is a rare but serious condition. An 8-year-old boy presented with back pain, progressive weakness and numbness in both legs. Magnetic resonance imaging (MRI) of the lumbar region showed a cystic lesion with regular contour located in extradural space. There was cerebrospinal fluid- (CSF-) like signal intensity on T1- and T2-weighted images. The lesion had excessively compressed the dural sac and caudal roots, and expanded to the L3 and L4 neural foramina. The case was explored with L2, L3, L4 laminectomy and the hydatid cyst was removed totally. The clinical presentation, diagnosis and surgical treatment of this rare case of spinal hydatid disease is discussed, and all available cases of primary extradural hydatid cyst reported in the literature are presented.

The authors describe a case of arachnoiditis ossificans (AO) of the cauda equina. The lesion is a rare pathological entity usually confined to the thoracic and high lumbar regions that can cause progressive spinal cord and cauda equina compression, inducing severe neurological deterioration. The authors analyze the clinical symptoms, radiological features, histological data, and treatment options relating to this case and 13 others described in the literature; additionally, they consider the possible mechanisms responsible for ossification of the leptomeninges. Although clustered arachnoidal cells are usually implicated in its pathogenesis, an environment induced by arachnoiditis and disturbed cerebrospinal fluid flow appears to be a more important factor. A therapeutic strategy is proposed for AO for which no effective treatment currently exists.

Purpose: To report bilateral corneal endotheliitis caused by a vesicular virus (family Rhabdoviridae)., Methods: Case report of a 49-year-old man with a complaint of sudden onset of decreased vision in both eyes had diffuse corneal stromal edema with extensive folds in Descemet's membrane and was diagnosed as having bilateral viral endotheliitis. Virologic investigations were performed using aqueous humor from the right eye., Results: An ether- and chloroform-sensitive cytopathic agent was isolated in Vero and BHK-21 cell lines from the aqueous humor. It was identified as a vesicular virus belonging to the family Rhabdoviridae by electron microscopy. Neutralizing antibody was demonstrated at a titer greater than 1 in 4,096 dilutions in the convalescent serum. Neurologic complications included loss of hearing and postinfectious polyradiculopathy affecting both lower limbs. Best-corrected visual acuity was 20/120 OD and 20/20 OS. Six months later, he developed glaucoma in the right eye. Trabeculectomy with intraoperative application of 5-fluorouracil was performed., Conclusion: This is the first report of bilateral endotheliitis caused by a vesicular virus and confirmed by virus isolation from the aqueous humor of the affected eye.

1. The aim of the present study is to map the incipient phase of Fos expression in the sacral spinal cord neuronal pools of multiple cauda equina constrictions canine model. 2. Fos-positive neurons were found bilaterally in the lateral portion of superficial dorsal horn layers (Laminae I-III) and along the lateral edge of the dorsal horn accompanied by the lateral collateral pathway, fibers of Lissauer's tract, terminating at the sacral parasympathetic nucleus. Similarly, high Fos expression was detected in the ventral portion of the dorsal sacral commissure and in the dorsomedial portion of the anterior horns at S1-S3 segment level. Finally, a clearly expressed Fos-positivity was disclosed bilaterally in the neuropil of the nucleus Y in the anterior horn. 3. Data from the present study show that continuous stimulation of the central fibers of sacral dorsal root ganglia neurons, i.e., fibers of sacral primary afferents, unlike those using various stimulations of the peripheral fibres offers an unusual pattern of Fos-like immunoreactivity.

A 55 year old man presented with features of cauda equina syndrome. Magnetic resonance imaging (MRI) showed a well demarcated intradural extramedullary tumour at L2 vertebra. At surgery it was found to be well encapsulated and had no attachment to spinal cord or root. Histopathology including immunohistochemistry confirmed it to be a low grade astrocytoma.

Study Design: The case reports of three pregnant patients with lumbar disc herniation causing cauda equina syndrome or severe neurologic deficits are presented to illustrate that disc surgery during gestation is a safe method of management., Objective: To emphasize the importance of recognizing and definitively treating lumbar disc displacement causing neurologic deficits during pregnancy., Summary of Background Data: The advent of magnetic resonance imaging and modern surgical techniques for treatment of lumbar disc displacement allows safe management of this condition at any stage of gestation. A review of the literature on the risks of nonobstetric surgery and the risks of delaying disc surgery until delivery shows that operating at any stage during gestation for severe neurologic deficit secondary to lumbar disc displacement is justified., Methods: A review of the literature on the use of magnetic resonance imaging scan and nonobstetric surgery during pregnancy was performed. Three case reports of the authors' patients who had lumbar disc displacement with cauda equina syndrome or severe neurologic deficit are presented. Patients were placed prone on a four-poster frame, and an epidural anesthetic agent was administered. A one-level hemilaminectomy, partial facetectomy, and disc excision were performed in all three cases., Results: The methods used for diagnosis and surgical treatment of three patients with disc herniation during pregnancy resulted in a satisfactory outcome for both mother and child. The medical literature supports surgical intervention in pregnant patients with cauda equina syndrome and severe and/or progressive neurologic deficit(s) from lumbar disc displacement at any state of gestation., Conclusion: Although extremely rare, cauda equina syndrome and severe and/or progressive neurologic deficit caused by lumbar disc displacement can occur during pregnancy. The prevalence of symptomatic lumbar disc herniation during pregnancy may be on the increase because of the increasing age of patients who are becoming pregnant. These cases showed, and the literature confirms, that pregnancy at any stage is no contraindication to magnetic resonance imaging scan, epidural and/or general anesthesia, and surgical disc excision.

Study Design: A retrospective analysis of records and radiographs in five patients who developed acute cauda equina syndrome after surgery for lumbar disc herniation., Objectives: To postulate as a possible pathophysiologic mechanism the venous congestion caused by preexisting spinal stenosis and to present a management plan: extended decompression within 48 hours., Summary of Background Data: Cauda equina syndrome is reported as a sequela in 0.2%-1% of the surgeries for lumbar disc herniation. There is, however, no consensus on the possible pathophysiologic mechanism to the complication or to its management., Methods: Preoperative investigations consisted of magnetic resonance imaging, or myelography and computed tomography. There was a good correlation between clinical appearance and radiographic findings in all patients. When the complication became apparent in four of the patients, they were investigated with magnetic resonance imaging and reoperated on within 48 hours with wide decompressions., Results: The index operation was reported uneventful in all patients. Postoperative magnetic resonance imaging did not show the cause of the cauda equina syndrome, nor could this be established at the reoperation. Before surgery, all five patients had preexisting narrowing of the spinal canal. In no case was the lumbosacral disc the index level. Two patients recovered fully, whereas the other three experienced varying degrees of residual symptoms. There was no correlation between the end result and the delay until secondary decompression., Conclusion: Relative spinal stenosis may contribute to the development of cauda equina syndrome after surgery for lumbar disc herniation. A venous congestion can be triggered by postoperative edema, leading to nerve root ischemia. The treatment of choice seems to be extended decompression within 48 hours.

Study Design: Three cases of idiopathic epidural lipomatosis are reported., Objectives: Description of the relationship between spinal pathologic overgrowth of fat tissue and neurologic symptoms., Summary of Background Data: Idiopathic epidural lipomatosis is a very rare condition; it is usually secondary to chronic steroid therapy or endocrinopathic diseases., Methods: Three men with a mean age of 58.5 years, who experienced intermittent claudication, bilateral radicular pain in both legs, and urinary dysfunction with hypoesthesia in the perineal region, were evaluated by plain radiography and magnetic resonance imaging, the results of which demonstrated a pathologic overgrowth of fat tissue in the spinal canal with a marked impingement of the dural sac. Obesity, endocrinopathic diseases, and chronic steroid therapy were excluded for all patients. Surgical treatment was performed by wide multilevel laminectomies, fat debulking, and instrumented posterolateral fusion., Results: After surgery there was a gradual improvement in symptoms and signs so that 2 years later the patients returned to daily activities and were neurologically normal., Conclusions: Spinal epidural lipomatosis can be a cause of back pain but rarely radicular impingement. Magnetic resonance imaging is the procedure of choice. The treatment must be performed early by wide surgical decompression.

Gas production as a part of disk degeneration can occur, but it rarely causes clinical nerve compression syndromes. A rare case of gaseous degeneration in a prolapsed lumbar intervertebral disk causing acute cauda equina syndrome is described. Radiologic features and intraoperative findings are reported. A 78-year-old woman with severe lumbar canal stenosis had acute cauda equina syndrome. Magnetic resonance imaging revealed a large disk protrusion, and she underwent an urgent operation for this. Surgery confirmed the severe lumbar canal stenosis, but the disk prolapse contained gas that had caused the nerve compression.

Study Design: Longitudinal study among patients with acute and chronic spinal cord injuries (SCI)., Objectives: To compare total gastrointestinal transit times (GITT) and segmental colorectal transit times (CTT) in SCI patients with acute and chronic lesions to those of healthy volunteers. Furthermore, to examine the impact of time elapsed since injury on GITT and CTT, and finally to compare the pattern of colorectal dysfunction in patients with supraconal versus conal/cauda equina lesions., Setting: Surgical Research Unit and Department of Neurosurgery, University Hospital of Aarhus, Denmark., Methods: Patients took 10 radioopaque markers on six consecutive days and an abdominal X-ray was taken on day 7. GITT and CTTs were computed from the number of markers in the entire colorectum and in each colorectal segment respectively. We studied 26 patients with acute spinal cord lesions (15 supraconal and 11 conal/cauda equina lesions; time since injury=11 - 24 days) and 18 patients were available for follow-up 6 - 14 months later. Results were compared to 24 healthy volunteers., Results: In patients with acute supraconal or conal/cauda equina lesions GITT and CTTs of the ascending, transverse, and descending colon were significantly prolonged, but rectosigmoid transit time was only significantly prolonged in patients with conal/cauda equina lesions. In patients with chronic supraconal lesions GITT and CTTs of the transverse colon and the descending colon were significantly prolonged. In patients with chronic conal/cauda equina lesions GITT and CTT of the transverse, the descending colon and the rectosigmoid were significantly prolonged. Thus, supraconal SCI resulted in generalized colonic dysfunction whereas chronic conal/cauda equina lesions resulted in severe rectosigmoid dysfunction., Conclusion: SCI results in severely prolonged colonic transit times both in the acute and chronic phase. However, the type of colorectal dysfunction depends on the level of SCI.

Objective: To determine whether microscopic vasculitis explains the clinical and pathologic features of diabetic lumbosacral radiculoplexus neuropathy (DLSRPN)., Background: DLSRPN is usually attributed to metabolic derangement or ischemic injury, but microscopic vasculitis as the sole cause needs consideration., Methods: We prospectively studied the clinical, laboratory, and EMG features as well as the pathology of distal cutaneous nerve biopsy specimens of patients with DLSRPN., Results: Study of DLSRPN nerve biopsy specimens (n = 33) compared with those from healthy controls (n = 14) and those with diabetic polyneuropathy (n = 21) provided strong evidence for ischemic injury (axonal degeneration, multifocal fiber loss, focal perineurial necrosis and thickening, injury neuroma, neovascularization, and swollen fibers with accumulated organelles), which we attribute to microscopic vasculitis (epineurial vascular and perivascular inflammation, vessel wall necrosis, and evidence of previous bleeding). Segmental demyelination was significantly associated with multifocal fiber loss., Conclusions: 1) This severe, debilitating neuropathy begins with symptoms unilaterally and focally in the leg, thigh, or buttock and spreads to involve the other regions of the same and then opposite side and is due to multifocal involvement of lumbosacral roots, plexus, and peripheral nerve (i.e., diabetic lumbosacral radiculoplexus neuropathy). 2) Motor, sensory, and autonomic fibers are all involved. 3) Ischemic injury explains the clinical features and pathologic abnormalities of nerve. 4) The proximate cause of the ischemic injury appears to be microscopic vasculitis. 5) The segmental demyelination is probably secondary to ischemic axonal dystrophy, thus providing a unifying hypothesis for both axonal degeneration and segmental demyelination.

A 22 year old woman with recently diagnosed systemic lupus erythematosus presented with subacute progressive areflexic paraparesis, electrophysiologically identified as a pure axonal polyradiculopathy. Sural nerve biopsy disclosed necrotising vasculitis. A striking radiological feature was marked enhancement of the cauda equina with gadolinium.

In a 67-year-old patient, generalised stable muscular weakness preexisting for several years became rapidly progressive within a few weeks prior to hospitalisation. He died one month after admission from acute cardiocirculatory failure. There was no history of muscular pain, clinical examination showed weak or absent tendon reflexes, hyposensibility of the dorsa of his feet, fasciculations and myocloni of the muscles of the lower limbs as well as a generalised muscular atrophy. Polyneuropathy due to diabetes mellitus and monoclonal IGG-kappa-type gammopathy were preexisting. CSF examination showed inflammatory cerebral fluid changes and further investigations revealed inflammatory polyradiculopathy affecting mainly motor nerve fibres. There was evidence of a reactivated varicella-zoster infection in serum and in the cerebrospinal fluid samples. The search for a tumour, vasculitis or a drug-related cause for this syndrome remained negative. Neuropathological examination at autopsy showed subacute polyradiculitis accompanied by myelitis. The most probable cause of this disorder is immune-mediated polyradiculitis after varicella-zoster infection.

Clinical and electrophysiological features in 43 children with acute inflammatory demyelinating polyradiculoneuropathy (AIDP) were retrospectively studied. More than one-third of these children were less than 3 years old. Some distinctive clinical features specific to adults or to children were identified. Initial symptoms such as ataxia and severe limb or back pain were more frequent in children. By using the criteria suggested here, according to our neurophysiological findings, the diagnosis of AIDP could be proposed as early of the first days of illness in 90% of the children and is confirmed during the second week. The neurophysiological evolution was very similar in children and adults except that recovery occurred sooner in children. Prognosis was better in childhood (complete recovery in all but 2 patients with minor disabilities).

Neoplastic meningitis as the presentation of occult primitive neuroectodermal tumor (PNET) is occasionally described in children. We report the case of an 64 year old-man who presented a meningo-radiculopathy with progressive injury of the cauda equina and then the ocular motor nerves, revealing an occult medulloblastoma-PNET.

Study Design: The effect of epidural injection of betamethasone or bupivacaine was investigated in an animal model of lumbar radiculopathy., Objective: To investigate the effects of an epidural steroid (betamethasone) or a local anesthetic (bupivacaine) in an animal model of radiculopathy produced by nerve root irritation., Summary of Background Data: Epidural injections are commonly used for the treatment of low back pain and sciatica. However, efficacy remains controversial, and there is a paucity of basic information to support clinical use or the injections., Methods: Fifty-one rats were used. The left L4 and L5 nerve roots were loosely ligated with chromic gut, and either betamethasone, bupivacaine, betamethasone in combination with bupivacaine, or saline was injected using an epidurally placed catheter. The effects of epidural injection were evaluated using response to noxious stimuli and immunohistochemical methods., Results: In betamethasone-treated rats (either alone or in combination with bupivacaine), thermal hyperalgesia was significantly less (P < 0.010 after surgery than that in saline- or bupivacaine-treated groups, in which the hyperalgesia was maximum at 2-3 postoperative weeks before resolving 5 weeks after surgery. Immunohistochemical analysis did not correlate with these results., Conclusions: Epidural steroid injection has a significant effect on the thermal hyperalgesia produced in a model of radiculopathy, which may provide clinical support for advocates of epidural steroids.

Patients with AIDS can present clinical involvement of the peripheral nervous system due to different causes. In the present work, it was studied the histopathological changes in sural nerve biopsy of fifteen patients with AIDS with this clinical involvement. It was observed the presence of a polyarteritis nodosa-like vasculitis of small arteries with fibrinoid necrosis in the sural nerve of 3 patients, one of them associated to polyradiculitis due to cytomegalovirus infection (CMV). Six patients presented mild axonal loss by light microscopy. Three other patients had a more important axonal neuropathy with myelin ovoids by teasing. By the electron microscopy in these patients were observed some fibers with axonal damage. The other three patients had normal sural nerves. We concluded that sural nerve biopsy may be important in peripheral neuropathies or myelo-radiculo-polyneuropathies in AIDS especially to search for nerve vasculitis, because it can change the therapeutic approach.

Patients with diabetic amyotrophy may have an inflammatory vasculopathy and may obtain reversal of neurological deficits with immunosuppression. We present a patient with NIDDM, subacute onset of painful asymmetric polyradiculopathy, and unilateral enhancement of lumbar nerve roots on MRI. Clinical improvement and resolution of nerve root enhancement occurred with immunosuppression. We suggest, therefore, that nerve biopsy and gadolinum-enhanced lumbosacral MRI be performed in all patients presenting with diabetic amyotrophy. If nerve root enhancement is present or if nerve biopsy shows perivascular infiltrates, we recommend a trial of immunosuppression.

We studied three patients with myelomeningoradiculitis caused by Borrelia burgdorferi, herpes zoster virus or cytomegalovirus infection. All patients underwent MRI of the spinal cord with gadolinium-DTPA and showed enhancing lesions of the spinal cord or nerve roots that correlated with clinical signs. Gadolinium-DTPA enhancement may visualize lesions that suggest an inflammation associated with blood-brain-barrier alteration and indicate the diagnosis before serological results are available.

Subclinical lumbar polyradiculopathy was present in the intradural dorsal and ventral nerve rootlets of 19 aged individuals of the following wild and exotic mammalian species: woodrat, raccoon, mink, lynx, reindeer, red deer, musk ox, scimitar-horned oryx, Arabian oryx, hybrid waterbuck, Persian onager, Przewalski's wild horse, Malayan sun bear, Asian elephant, East African river hippopotamus, vervet monkey and rhesus monkey. It was characterized by mild to severe multifocal ballooning of myelin sheaths. Occasionally, ballooned myelin sheaths contained thin strands of myelin and macrophages surrounding distorted axons. Additionally, a mild incidental lymphocytic polyneuritis was present in intradural nerve rootlets of the Malayan sun bear, and a moderate lymphocytic spinal ganglionitis in the East African river hippopotamus.

A technique of epidural catheterization in rabbits is described. Twelve albino rabbits received a totally implanted epidural catheter system. The system was implanted surgically, and the functioning of the system tested for a period of 3 months. X-ray examinations following epidural contrast injections showed a distribution up to Th4 following 1.5 ml and Th8-9 following 1.0 and 1.25 ml. Epidural injection of lidocaine throughout the study period proved the system to be functioning for all 3 months. Another 12 rabbits were included for the neurotoxicological examinations following epidural catheterization, without any injections (three rabbits), epidural injections of saline (four rabbits) and meptazinol (five rabbits) once a day for 14 days. Histopathological examinations showed a fibrous cocoon, at the tip of the catheter, in all rabbits. In the group of rabbits which did not receive any injections, the cocoon was slightly infiltrated with leukocytes and local depression of the spinal cord was observed in one rabbit. In the saline-injected group this infiltration was more pronounced and in one rabbit it extended into the meninges. Three rabbits showed local depression of the spinal cord and local myelopathy of the white matter in the area adjacent to the cocoon. In the group of rabbits receiving meptazinol, three out of five had local depression and myelopathy of the white matter. In this group these findings were more pronounced. In two rabbits the myelopathy extended transversely through the white matter into the grey matter of the spinal cord. The number of pathological changes in the group receiving meptazinol was significantly higher compared to the control and placebo groups.(ABSTRACT TRUNCATED AT 250 WORDS)

A 77-year-old man with T-cell lymphoma developed an acute fatal meningoradiculitis of cranial nerve roots and cauda equina, pathologically and virologically confirmed to be caused by varicella-zoster virus. This is the first report of fatal varicella-zoster virus-induced neurological disease in the absence of skin lesions. Varicella-zoster virus should be included in the differential diagnosis of acute radiculoneuropathy in the immunocompromised patient, particularly because antiviral treatment for varicella-zoster virus exists.

A 30 year-old male, with the acquired immune deficiency syndrome (AIDS) presented with rapidly progressive flaccid paraplegia and sphincter incontinence. Cerebrospinal fluid examination showed elevated protein and pleocytosis. Death occurred 2 months after the onset of neurological signs. Post-mortem examination showed inflammatory necrotic lesions, relatively sparing the axons and predominantly involving the roots of the cord. Numerous cytomegalovirus (CMV) inclusion bodies were found in the necrotic lesions, in the subarachnoid spaces and in Schwann cells. CMV encephalitis and involvement of the 3rd cranial nerves were also observed. Only 8 well-documented clinico-pathological cases of acute CMV myeloradiculitis, which all presented as progressive cauda equina syndrome, have been reported until now in AIDS patients.

Spinal cord lesions, although far less frequent than brain lesions, are not uncommon in AIDS. Almost all diffuse or multifocal pathological processes involving the central nervous system and/or leptomeninges may also affect the spinal cord. However, some of them involve it predominantly causing specific, clinically overt, myelopathic diseases. The most characteristic of these is vacuolar myelopathy which usually manifests as progressive spastic ataxia. Its incidence varies in different pathological series and its pathogenesis is still controversial. Acute meningomyeloradiculitis in AIDS patients presents a remarkably uniform and distinct clinical and cerebrospinal fluid profile although they might be due to various causes including cytomegalovirus infection, syphilis, mycobacterial infection or leptomeningeal malignancy. Tumoral focal syndromes have exceptionally been recorded due to epidural lymphomas, intraspinal gliomas or toxoplasma abscesses. Spinal cord ischemic lesions have been documented in two cases: they were related to inflammatory lesions of the blood vessels in one case and to diffuse intravascular coagulation in the other. An ascending myelitis syndrome, secondary to spinal cord infection by both herpes simplex virus type 2 and cytomegalovirus, without significant vasculitis has also been reported.

Denervated muscles due to lumbar radiculopathy, peroneal axonal neuropathy and hypoglossal neuropathy were studied with magnetic resonance imaging (MRI). Denervated muscle was clearly distinguished from normal muscle by its higher intensity signal. Comparison of the resulting signal intensity of the muscle using various imaging parameters suggests an alteration in water macromolecular binding. These preliminary findings indicate that MRI may be useful in the noninvasive in vivo diagnosis and study of the effects of denervation on muscle.

Patterns of demyelination are described in several autoimmune and virus-induced demyelinating diseases of the peripheral and central nervous system. Myelin can be destroyed by injuries that affect either the myelin-supporting cells and/or the myelin lamellae. After destruction of the supporting cells, the related disintegrating sheaths are stripped off axons by invading phagocytes. Virus-induced cytolysis can occur with or without participation of immune responses, as demonstrated in subacute sclerosing panencephalitis and progressive mutlifocal leukoencephalopathy, respectively. Autoimmune demyelination is characterized by disintegration of myelin sheaths in periventular, mononuclear cell infiltrates. Myelin lamellae rather than the myelin-supporting cells are the target of the allergic reaction. The lamellae are lysed in focal areas when in contact with presumably sensitized mononuclear cells. The damaged sheaths are then removed in a nonspecific manner by invading macrophages that strip the myelin remnant off the axons. This sequence of changes is best revealed in experimental and human autoimmune demyelination of peripheral nerves, ie, allergic neuritis and idiopathic polyneutris (the Guillain-Barré syndrome). Autoimmune demyelination triggered by virus infection is described in Marek's disease and postinfectious Theiler's virus myelitis. Changes in canine distemper are discussed with reference to both autoimmune and virus-induced demyelination. The observations are compared with lesions in multiple sclerosis, the most common human demyelinating disease of unknown etiology.

Crystalline inclusions were found in the muscle of a previously healthy 63 year old male with atypical postinfectious polyradiculoneuropathy. Approximately 12 days after the onset of the illness, biopsy of biceps femoris and vastus lateralis muscles revealed, in addition to changes consistent with early neurogenic atrophy, inclusions measuring 22 micronm in greatest dimensions. In plastic-embedded toluidine blue stained sections the translucent ovoid to angular inclusions were seen in a subsarcolemmal position, adjacent to nuclei. Ultrastructural examination revealed a crystalline structure consisting of parallel dense lines measuring approximately 70 A in diameter with an axial periodicity of 130 A. Unlike rods, the crystalline inclusions were not continuous with Z-discs; rather they displaced contractile and other cellular elements. Their appearance was similar to intramuscular crystals in diabetic amyotrophy and to vincristine-induced and naturally occurring intracytoplasmic crystalline structures. The nature of the crystalline inclusions and their relationship to the basic disease process was not established.