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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.

Study Design: The 5 year review of patients referred to one center., Objective: To report spinal cord infarction secondary to vascular occlusion from disease in a lower thoracic intervertebral foramen., Method: The clinical and imaging findings of two cases with acute spinal cord dysfunction are presented., Setting: Midlands Centre for Spinal Injuries, England., Results: The CT and MR imaging features revealed lower thoracic unilateral foraminal occlusion due to acute facet joint septic arthritis in a diabetic patient, and secondary to chronic hypertrophic osteophytes in a second hypertensive individual. The presumed mechanism of infarction was occlusion of the artery of Adamkiewicz., Conclusion: Foraminal disease in the lower thoracic levels needs to be entertained in cases of unexplained nontraumatic acute spinal cord dysfunction.

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.

We have conducted a long-term study of spinal cord morphology and motor function recovery in rats that have undergone lumbar spinal demyelination induced by the B-fragment of cholera toxin (CTB)-saporin. We found that, after the initial demyelination and paraplegia, motor function recovered and was stable for up to 9 months, after which there occurred a slow deterioration of motor function accompanied by loss of motoneurons and loss of spinal white matter. A striking morphological feature was the appearance of large spheroids of calcium in the ventral and dorsal horns and occasionally in the white matter. Motor performance deterioration occurred earlier and was more severe in rats that had been exercised on a treadmill, but the same morphological changes occurred in both exercise- and nonexercise-treated animals. Rats given treadmill exercise starting 3 weeks after toxin injection had a mean motor deficit score of 3.0 (i.e., paraplegia) at perfusion, whereas the nontreadmill-treated rats had a mean score of 1.8 (SD 0.38; n = 6; P <.05). These findings suggest that, in addition to the acute effects of the toxin-induced demyelination from which there is recovery of motor function, there are chronic irreversible effects of the toxin, or the initial demyelination, that cause a slow progressive degeneration of the spinal cord. This model might therefore be useful in studying the long-term effects of spinal insult of the type associated with conditions such as postpolio syndrome., (Copyright 2004 Wiley-Liss, Inc.)

Previous reports showed the therapeutic effect of transplants of bone marrow stromal cells (BMSC) after incomplete traumatic spinal cord lesions. We studied the effect of this form of therapy in chronically paraplegic Wistar rats due to severe spinal cord injury (SCI). Rats were subjected to weight-drop impact causing paraplegia, and BMSC or phosphate buffered saline (PBS) was injected into spinal cord 3 months after injury. Functional outcome was measured using the Basso-Beattie-Bresnehan score until sacrifice of the animals, 4 weeks after transplantation. At this time, samples of spinal cord tissue were studied histologically. The results showed a clear and progressive functional recovery of the animals treated with BMSC transplantation, compared to controls. Grafted BMSC survived into spinal cord tissue, forming cell bridges within the traumatic centromedullary cavity. In this tissue, cells expressing neuronal and astroglial markers can be seen, together with a marked ependymal proliferation, showing nestin-positivity. These findings suggest the utility of BMSC transplantation in chronically established paraplegia., (Copyright 2004 Lippincott Williams and Wilkins)

Study Design: A case report., Objectives: To present and discuss some of the difficulties in the diagnosis of brucellar spondylitis., Setting: Ankara University, Ibni Sina Hospital, Turkey., Methods: We report a patient with paraplegia, misdiagnosed as having a malignancy or tuberculosis who actually suffered from brucellar spondylitis. Diagnosis was established by her history and a compatible clinical picture together with a standard tube agglutination (Wright test) titer of > or =1/160 of antibodies for brucellosis. The patient was treated with oral doxycycline, rifampicin, and ciprofloxacin combination., Results: At the end of the treatment, the blood Brucella Wright and anti-human globulin T titer levels decreased. Her lower limb weakness improved. She could walk, and climb stairs with the help of a cane. Urinary retention and fecal incontinence also resolved., Conclusion: Brucellosis is a systemic infection involving the musculoskeletal and nervous systems. Spondylitis frequently occurs in elderly patients. An early diagnosis of brucellar spondylitis can often be difficult. In endemic regions, as in the case of our country, brucellar spondylitis should always be considered in the differential diagnosis of older patients with back pain and constitutional symptoms. An early diagnosis will help to prevent the development of more severe complications such as spinal cord compression.

Experimental allergic encephalomyelitis (EAE) serves as an animal model for certain neuroinflammatory diseases of the central nervous system, in particular multiple sclerosis (MS). EAE is accompanied by transient weakness or paralysis of hind limbs. We have investigated the effect of partial and transient conduction failure in the central nervous system on skeletal muscle function. At approximately 2.5 days after development of maximal clinical signs, body and medial gastrocnemius muscle mass were lower (by approximately 21 and 33%, respectively; P < 0.05) in EAE rats compared with controls. Fiber cross-sectional area was lower by 40-50% in all fiber types. Maximal force and power were substantially lower (by 58% and 73%) in EAE rats, as was the force normalized for muscle mass (35%). However, no such weakness was found when lower stimulation frequencies were used. Generation of similar submaximal forces was attributable to a slower relaxation in EAE muscles. This advantage for the EAE muscles was lost during repeated exercise. While fatigability was similar, the difference in relaxation rate between EAE and control disappeared in fatigue. Our data suggest that, as a result of central neuroinflammatory diseases, maximal performance of skeletal muscle is impaired but submaximal performance is relatively well maintained.

Paraplegia, which develops after operation on aorta, represents a real catastrophe for the patient and for the surgeon. The aim of the present work was to investigate the light microscopy picture of this complication and consequently better understand related processes. Twenty one adult dogs, cross breeds of both sexes, weight 18-25 kg, were divided into four groups: 1. Controls (n = 3); 2.30-min ischemia induced by occlusion of thoracic aorta by a tourniquet, followed for 30 min survival (n = 6); 3.30-min ischemia and 72 h of survival (n = 6); 4) 30-min ischemia and 6 days of survival (n = 6). All these manipulations were made in sterile conditions under general anesthesia. As soon as the planned time of survival passed, the animals were flushed out, in deep pentobarbital anesthesia, with 3,000 ml of sodium chloride and fixed with 3,000 ml of 10% neutral formaldehyde. Sections, 30 microns thick, from L3-S1 medulla segments were processed in the laboratory of Neurobiological Institute by the method of Nauta for light microscopy examination. Neurohistological picture was characterized by a marked damage of the medulla neurons. The changes proved to be irreversible and resulted, in the course of six days of survival, to death of the cells, characterized by their disintegration. The results indicate that the only rational procedure in conditions of threatening ischemic-reperfusion injury of medulla is to prevent it.

Complete spinal cord injury (SCI) is characterized, in part, by reduced fatigue-resistance of the paralyzed skeletal muscle during stimulated contractions, but the underlying mechanisms are not fully understood. The effects of complete SCI on skeletal muscle Na(+),K(+)-adenosine triphosphatase (ATPase) concentration, and fiber type distribution were therefore investigated. Six individuals (aged 32.0 +/- 5.3 years) with complete paraplegia (T4-T10; 1-19 years since injury) participated. There was a significantly lower Na(+),K(+)-ATPase concentration in the paralyzed vastus lateralis (VL) when compared to either the subjects' own unaffected deltoid or literature values (from our laboratory, utilizing the same methodology) of VL Na(+),K(+)-ATPase concentration for the healthy able-bodied (141.6 +/- 50.0, 213.4 +/- 23.9, 339 +/- 16 pmol/g wet wt., respectively; P < 0.05). There was also a significant negative correlation between the Na(+),K(+)-ATPase concentration in the paralyzed VL and years since injury (r = -0.75, P < 0.05). These findings are clinically relevant as they suggest that reductions in Na(+),K(+)-ATPase contribute to the fatigability of paralyzed muscle after SCI. Unexpectedly, the VL muscles of our subjects had a higher proportion of their area represented by type I fibers compared to literature values for the VL of the healthy able-bodied (52.6 +/- 25.3% vs. 36 +/- 11.3%, respectively; P < 0.05). As all our subjects had upper motor neuron injuries and, therefore, experienced muscle spasticity, our findings warrant further investigation into the relationship between muscle spasticity and fiber type expression after SCI.

Study Design: Case report., Objective: To report complete recovery after paraplegia in an elderly patient after removal of meningioma at C7-T1 level., Setting: Department of Neurosurgery, Reggio Calabria, Italy., Methods: An 82-year-old lady with 48 months of progressive weakness and numbness was admitted with complete paraplegia lasting 15 days. Investigations (magnetic resonance imaging (MRI)) demonstrated a meningioma at C7-T1. The tumour compressed the extremely thinned spinal cord. MRI after surgery showed no evidence of residual tumour and the spinal cord was of normal dimensions. The patient recovered fully and locomotion was restored., Conclusion: Surgical decompression gave an excellent result. The result raises the possibility of neuronal plasticity.

To determine the body composition differences across age, 133 men with chronic spinal cord injury (SCI) (66 with tetraplegia, 67 with paraplegia) were compared with an age-, height-, and ethnicity-matched able-bodied male reference population (n = 100) using two different dual-energy X-ray absorptiometry densitometers. The effects of duration of injury, level, and completeness of lesion were analyzed in the SCI population. Independent of age, total body and regional lean mass were lower and fat mass was higher in persons with SCI compared with controls. The SCI group was 13 +/- 1% (means +/- SE) fatter per unit of body mass index (kg/m2) compared with the control group (P < 0.0001). Advancing age was strongly associated with less lean mass and greater adiposity in those with SCI, whereas it was mildly related in the controls. Total body and regional arm and trunk, but not leg, lean tissues were lower in subjects with SCI, across all ages, than in the controls. In summary, persons with SCI were fatter for any body mass index and demonstrated significantly less lean and more adipose tissues for any given age compared with controls.

PS1 mutations are associated with classic Alzheimer's disease (AD); however, some families develop AD and spastic paraplegia (SP) with brain pathology characterized by Abeta cotton wool plaques. The authors report a variant AD family with the E280Q PS1 mutation. The fact that the same PS1 mutation can be found in patients with either variant or classic AD argues in favor of the presence of a genetic modifier. The authors have excluded that this modifier effect originates from coding sequence variations in three SP genes or from a second mutation in the other AD genes.

The purpose of this study was to investigate the effect of N-acetylcysteine (NAC) on spinal cord ischemia-reperfusion (I-R) in rabbits. Thirty rabbits were divided into five equal groups, group I (sham-operated, no I-R), group II (control, only I-R), group III (I-R+NAC), group IV (I-R+hypothermia), group V (I-R+NAC+hypothermia). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Forty-eight hours postoperatively, the motor function of the lower limbs was evaluated in each animal according to Tarlov Score. Spinal cord samples were taken to evaluate the histopathological changes. The sham-operated rabbits (group I) showed no neurologic deficit (Score=4). Paraplegia (Score=0) developed in all rabbits in the control group (group II). Administration of 50 mg/kg of NAC (group III) resulted in significant reduction of motor dysfunction (Score=3.1+/-1.3, p=0.002). Application of hypothermia alone (group IV) showed significant recovery of motor functions (Score=3.0+/-1.1, p=0.002), and combination of hypothermia and 50 mg/kg of NAC (group V) showed complete recovery of lower limb motor function (Score=4, p=0.001). Histologic examination of the spinal cord in rabbits with paraplegia revealed several injured neurons. The cords of animals with no motor function deficits showed only minimal cellular infiltrates in the gray matter, and there was good preservation of nerve cells. NAC showed protective effects of the spinal cord. Moderate hypothermia alone also showed protective effects. Combined use of NAC and hypothermia resulted in highly significant recovery of spinal cord function.

A 55-year-old woman presented first episode of paraplegia at D6 level with a marked improvement of neurological signs, but relapse occurred five months later. Hashimoto's thyroiditis with euthyroidism was found. Long-term 9 months treatment with oral corticosteroids was applied. Also she was able to walk with help. Two years after the second palsy she developed a new paraplegia at D6 level with a severe residual deficit five months later in spite of oral corticosteroids. Thyroid antibodies remained positive. Devic's disease without optica neuritis associated with thyroiditis or spinal cord localisation of Hashimoto's encephalopathy was discussed.

Implications: Our case report describes the electrophysiological features associated with the development of a spinal epidural hematoma during surgery of the lumbar spine. It stresses the importance of the evaluation of nonsurgical factors, which can potentially affect intraoperative evoked potentials; in this case, epidural local anesthetic or epidural hematoma.

Unlabelled: In the present study, we sought to elucidate the temporal profile of the reaction of microglia, astrocytes, and macrophages in the progression of delayed onset motor dysfunction after spinal cord ischemia (15 min) in rabbits. At 2, 4, 8, 12, 24, and 48 h after reperfusion (9 animals in each), hind limb motor function was assessed, and the lumbar spinal cord was histologically examined. Delayed motor dysfunction was observed in most animals at 48 h after ischemia, which could be predicted by a poor recovery of segmental spinal cord evoked potentials at 15 min of reperfusion. In the gray matter of the lumbar spinal cord, both microglia and astrocytes were activated early (2 h) after reperfusion. Microglia were diffusely activated and engulfed motor neurons irrespective of the recovery of segmental spinal cord evoked potentials. In contrast, early astrocytic activation was confined to the area where neurons started to show degeneration. Macrophages were first detected at 8 h after reperfusion and mainly surrounded the infarction area later. Although the precise roles of the activation of microglia, astrocytes, and macrophages are to be further determined, the results indicate that understanding functional changes of astrocytes may be important in the mechanism of delayed onset motor dysfunction including paraplegia., Implications: Microglia and macrophages play a role in removing tissue debris after transient spinal cord ischemia. Disturbance of astrocytic defense mechanism, breakdown of the blood-spinal cord barrier, or both seemed to be involved in the development of delayed motor dysfunction.

We report two cases of spinal cord compression by AL amyloid deposits in the setting of multiple myeloma. The first patient, a 57 year old man, had a surgical procedure late in his course, when his neurological status worsened despite medical treatment. The second patient, a 61 year old man, had surgical treatment as soon as vertebral body collapse and epiduritis were diagnosed and spinal amyloidosis revealed a non secretory myeloma. Neurological recovery was significant in both cases and neither developed manifestations of systemic amyloidosis 4 years later.

We have recently mapped a new rare form of spastic paraplegia complicated by bilateral cataracts, gastroesophageal reflux with persistent vomiting, and amyotrophy to chromosome 10q23.3-q24.2. This locus, named SPG9, is located in an interval spanning about 12 cM of genomic DNA, between markers D10S536 and D10S603, where different neurological disorders have been mapped. In particular, a gene for partial epilepsy has been assigned to a 3 cM interval between markers D10S185 and D10S577, which is completely included in the SPG9 critical region. A few families affected with spastic paraplegia and epilepsy have been reported; in the present study, we tested a pedigree with concurrence of spastic paraplegia, epilepsy, and mental retardation inherited as an autosomal dominant trait, using markers located in the SPG9 interval. Haplotype reconstruction excluded the linkage to 10q23.3-q24.2. In addition, the seven different loci so far reported to be associated with autosomal dominant pure forms of spastic paraplegia have been tested and excluded by linkage analysis and haplotype reconstruction, including SPG4 on chromosome 2p22-p21, where a familial form of spastic paraplegia associated with dementia and epilepsy has been mapped. These data confirm genetic heterogeneity in familial spastic paraplegia with epilepsy and suggest a specific locus for the family here analyzed., (Copyright 2003 Wiley-Liss, Inc.)

Spinal cord abscess is an unusual cause of progressive paraplegia. We report the case of a 75-year-old man who presented Chlamydia pneumoniae bronchopulmonary infection with secondary spinal cord localization. Little clinical improvement was observed with antibiotic therapy, but the neuroradiological course was favorable.

Extramedullary haemopoiesis causing spinal cord compression is a rare manifestation of thalassemia. We describe a 17 year old male with thalassemia intermedia who presented with progressive paraplegia and sphincter disturbance. Magnetic resonance imaging revealed an epidural lesion extending from T5 to T8 compressing the spinal cord. The patient recovered completely after surgical decompression with postoperative radiation therapy. Histological examination of the lesion confirmed the diagnosis of extramedullary haemopoiesis. Clinical awareness of this phenomenon with early treatment is essential for optimizing the neurological outcome., (Copyright 2002 Published by Elsevier Science Ltd.)

Peripheral and central nervous system lesions can induce reorganization within central somatosensory and motor body representations. We report changes in brain activation patterns during movements of non-affected body parts in paraplegic patients with spinal cord injury (SCI). Nine SCI patients and 12 healthy controls underwent blood oxygen level dependent signal functional MRI during sequential finger-to-thumb opposition, flexion and extension of wrist and of elbow, and horizontal movements of the tongue. Single subject and group analyses were performed, and the activation volumes, maximum t values and centres of gravity were calculated. The somatotopical upper limb and tongue representations in the contralateral primary motor cortex (M1) in the SCI patients were preserved without any shift of activation towards the deefferented and deafferented M1 foot area. During finger movements, however, the SCI patients showed an increased volume in M1 activation. Increased activation was also found in non-primary motor and parietal areas, as well as in the cerebellum during movements of the fingers, wrist and elbow, whereas no changes were present during tongue movements. These results document that, in paraplegic patients, the representation of the non-impaired upper limb muscles is modified, though without any topographical reorganization in M1. The extensive changes in primary and non-primary motor areas, and in subcortical regions demonstrate that even distant neuronal damage has impact upon the activation of the whole sensorimotor system.

A 53 year old male underwent total excision of a large sphenoidal wing meningioma. Patient was treated with cephalosporins and phenytoin for postoperative meningitis. Three weeks after surgery, a follow up lumbar puncture was done. The patient became paraplegic over a few hours. Imaging of the dorsolumbar spine and other investigations demonstrated a large intraspinal hematoma caused by thrombocytopenia which was probably drug induced. After normalising the platelet count surgical evacuation of the spinal subarachnoid hematoma was done. Relevant literature is reviewed.

Ossified ligamentum flavum is increasingly appreciated as an important cause of thoracic myeloradiculopathy. Fifteen patients with age ranging from 30-61 years were studied. Fourteen presented with spastic paraparesis, and radiculopathy was the only complaint in one patient. Routine skiagrams and myelograms showed non-specific changes. Baseline CT and CT myelogram, however, documented the ossification of ligamentum flavum comprehensively. MRI was done in three patients. Multiple levels of the disease were seen in two cases. Four patients had ossified posterior longitudinal ligament. Thickened ligamentum flavum should be considered as an important cause of thoracic cord compression.

This pilot study examined the effects of composite implants of cultured embryonal nerve cells and laser irradiation on the regeneration and repair of the completely transected spinal cord. Embryonal spinal cord nerve cells dissociated from rat fetuses and cultured on biodegradable microcarriers and embedded in hyaluronic acid were implanted in the completely transected spinal cords of 24 adult rats. For 14 consecutive post-operative days, 15 rats underwent low power laser irradiation (780 nm, 250 mW), 30 min daily. Eleven of the 15 (73%) showed different degrees of active leg movements and gait performance, compared to 4 (44%) of the 9 rats with implantation alone. In a controlgroup of seven rats with spinal cord transection and no transplantation or laser, six (86%) remained completely paralyzed. Three months after transection, implantation and laser irradiation, SSEPs were elicited in 69% of rats (p = 0.0237) compared to 37.5% in the nonirradiated group. The control group had no SSEPs response. Intensive axonal sprouting occurred in the group with implantation and laser. In the control group, the transected area contained proliferating fibroblasts and blood capillaries only. This suggests: 1. These in vitro composite implants are a regenerative and reparative source for reconstructing the transected spinal cord. 2. Post-operative low power laser irradiation enhances axonal sprouting and spinal cord repair.

We report a 72-year-old woman who died of respitory failure. History included onset of diabetes mellitus at the age of 67 years and hypertension at the age of 72 years. The patient had been in good health otherwise until 2000, when she had onset of numbness or tingling of the bilateral lower limbs. On December 3, 2000, she was admitted to a hospital in the vicinity of her home because of the above-mentioned complaints. Neurological examinations revealed progressive paraplegia. Symptoms and signs suggested Guillain-Barré syndrome. Examinations of cerebrospinal fluids revealed cell count of 338/3 (mono 72%, poly 18%) and protein value of 100 mg/dl. Later the patient course deteriorated. On December 15, 2000, she was admitted to Hakujikai Memorial Hospital for the second time. Ten days later, MRI examination showed diffuse swelling of the spinal cord from the cervical (C 3/4) level to the thoracic level. Gd-enhanced T 1-weighted MRI performed 22 days later showed a partially enhanced lesion at the thoracic (Th 5/6) level of the spinal cord. The patient was treated with steroid therapy (methylprednisolone 500 mg/dl). She died of respiratory failure on January 6, 2001. The patient was presented in a neurological CPC. Neurological and imaging findings suggested a transverse myelopathy. However, there were several points in this case that were unusual for a typical transverse myelopathy, such as total sensory loss below spinal segments of thoracic level (Th 5) and motor weakness of the upper limbs of upper segment of the same level. A clinical neurologist concluded that the patient had subacute transverse myelopathy with fused multiple pathy pathologic lesions. We discussed whether this case was a transverse myelopathy or multiple sclerosis. Post mortem examination revealed acute necrotic myelopathy affecting the spinal cord from the second cervical to the tenth thoracic vertebrae, with conspicuous infiltration of CD 68-positive macrophages involving both gray and white matter, partially necrotic associated with scattered UCHL-1 dominants lymphocytic infiltration of T cells around vessels. There were relatively older lesions with demyelinating features in the spinal roots that were particularly dominant in the anterior roots. No demyelinated plaques in the optic chiasm, tracts and nerves, or in the cerebero-cerebellar white matter were found. Systemic pathological diagnosis was lung edema with fresh hemorrhage, pancreatic atrophy consistent with diabetes mellitus and choleductlithiasis.

Spinal cord compression due to extramedullary hematopoiesis is a well-known complication in a number of hematological diseases. Most of the patients present with progressive paraparesis due to the slow expansion of the extramedullary hematopoietic tissue. The authors report a case of chronic myeloproliferative disorder with spinal extramedullary hematopoiesis presenting with acute paraplegia. Chronic myeloproliferative disorder is an uncommon cause of spinal cord compression, especially when associated with acute paraplegia. The authors discuss the pathomechanism of this unusual presentation.

Hereditary spastic paraplegia (HSP) is a group of clinically and genetically heterogeneous neurodegenerative disorders characterized by slowly progressive spasticity and weakness of the lower extremities. Among eight loci linked with autosomal-dominant (AD)-HSP, the SPG4 locus on chromosome 2p22 accounts for about 40% of all patients. Recently, mutations in a new member of the AAA protein family, called spastin, have been identified as responsible for SPG4-linked AD-HSP. Here, we describe a novel missense mutation (c.1031T>A; I344K) in exon 7 of the SPG4 gene identified in a Korean family with typical clinical features of pure AD-HSP. The mutation affects the third amino acid of the highly conserved AAA cassette domain, which is the most fore part of the domain altered by a missense mutation reported so far. Clinical presentations of affected individuals carrying the I344K mutation were not different from those of pure AD-HSP with SPG4 mutations reported previously. However, it is noteworthy that neither urinary dysfunction nor involvement of upper extremities was noticed in this family. To our knowledge, this is the first report of genetically confirmed AD-HSP in Korea.

Multiple intercostals nerve neuromas are surgically implanted in the lesioned spinal cord by bridging transaction lesions at T6 or T8 by removing one centimeter of spinal cord. In these experiments one to four intercostals nerves with origin proximal to the transection and the distal stumps, the neuroma was implanted distal to the transection. These procedures plus rehabilitation resulted in enhancing of regeneration of axons in the spinal cord lesion and dogs developed standing, stepping and reflex walking locomotion. Surgical resection of the implanted nerve resulted in paraplegia. Multiple nerve implants bridging the transaction of 34 mature female dogs. A pattern of neurological deficits developed when a sequence of resection of the implanted nerves were performed. If four nerves were implanted and one nerve resected usually no deficits were observed. When the second nerve was resected certain deficits were observed. When three nerves were resected some dogs became paraplegic, and some dogs showed increased sign of paraplegia but were not completely paralyzed and showed hind limb movements but no weight bearing. When four nerves were resected full paraplegia was observed.

Background Context: Lumbar nerve root blocks and epidural steroid injections are frequently employed in the management of degenerative conditions of the lumbar spine, but relatively few papers have been published that address the complications associated with these interventions. Serious complications include epidural abscess, arachnoiditis, epidural hematoma, cerebrospinal fluid fistula and hypersensitivity reaction to injectate. Although transient paraparesis has been described after inadvertent intrathecal injection, an immediate and lasting deficit has not been previously described as sequelae of a nerve root block., Purpose: We present three cases in which either persisting paraplegia or paraparesis occurred immediately after administration of a lumbar nerve root block and propose a mechanism for this devastating but previously unreported complication., Study Design/setting: Case reports of three patients., Patient Sample: Three patients, two women and one man ranging in age from 42 to 64 years, underwent three procedures performed at three different facilities, in the hands of two different injectionists. In each instance, penetration of the dura was not thought to have occurred. In two procedures the needles were placed transforamenally, one at L3-4 on the left and one at L3-4 on the right, and in the third the needle tip was placed immediately lateral to the S1 nerve root., Outcome Measures: Patient follow-up data from medical office records., Methods: In each case, needle placement was verified with injection of a contrast media in conjunction with either computerized tomography or biplanar fluoroscopy. No backbleeding or cerebrospinal fluid was encountered upon aspiration in any of the procedures. Magnetic resonance imaging (MRI) was performed within 48 hours of injury in all patients., Results: In each patient, paraplegia suddenly ensued after instillation of the steroid solution and, in each instance, postprocedure MRI revealed increased signal in the low thoracic spinal cord on T2-weighted imaging consistent with edema. The sudden onset of neurological deficit and the imaging changes noted in the spinal cord point to a vascular explanation for these injuries. We postulate that in these patients the spinal needle either penetrated or caused injury to an abnormally low dominant radiculomedullary artery, a recognized anatomical variant. This vessel, also known as the artery of Adamkiewicz, in 85% of individuals arises between T9 and L2, usually from the left, but in a minority of people may arise from the lower lumbar spine and rarely even from as low as S1. The artery of Adamkiewicz travels with the nerve root through the neural foramen and irrigates the anterior spinal artery. Injury of it or injection of particulate matter into it, as what may happen with the commonly used epidural steroid injectates, may result in infarction of the lower thoracic spinal cord, producing the clinical and imaging findings seen in these three patients., Conclusions: We present the cases of three patients who had lasting paraplegia or paraparesis after the performance of a nerve root block. We propose that the mechanism for this rare but devastating complication is the concurrence of two uncommon circumstances, the presence of an unusually low origin of the artery of Adamkiewicz and an undetected intraarterial penetration of the procedure needle.

Objectives: To investigate the morphological aspects of blood microvasculature of the skin and subcutaneous tissues in subjects with paraplegia with heterotopic ossification (HO)., Methods: In two patients with traumatic spinal cord injury and HO, punch biopsies of skin and hypodermic soft tissue in the region of HO near the hip were studied with histological and ultrastructural methods., Results: Alterations of endothelial cell and basement membrane of capillaries and small vessels were observed. Hyperactive endothelium, thickening and reduplication of the basement membrane, changes of the perivascular connective tissues and microcalcifications in the subcutaneous fat tissue were also seen., Conclusions: This present study indicates microvascular changes in the skin and subcutaneous tissue in the region of HO near the hip of two subjects with paraplegia. In our opinion the described vascular changes may induce hypoxiemic alterations of the soft para-articular tissues leading metabolic changes which may contribute to the development of HO. Therefore, it cannot be concluded whether these changes are directly responsible for HO induction.

Hereditary Spastic Paraplegias (HSPs) are heterogeneous neurodegenerative disorders whose etiopathogenesis is still unclear. The identification of pathogenic mutations in a gene (SPG7) encoding a mitochondrial metalloprotease suggested that oxidative phosphorylation (OXPHOS) alterations might underlie HSP in a subgroup of patients. We performed clinical, morphological, biochemical, and molecular genetic studies in six HSP patients and in six sporadic patients to investigate OXPHOS in muscle biopsies. Complicated and pure forms were included in our study. Morphological alterations of the type seen in OXPHOS-related disorders were found in three patients. Five patients showed an isolated defect of complex I activity. No mutations in the SPG7 gene were detected. Our results suggest that OXPHOS defects in HSP patients are more common than previously believed.

Objective: The purpose of this study was to investigate the effect of regional infusion of carnitine on spinal cord ischemia--reperfusion (I--R) in rabbits., Methods: The 36 rabbits were divided into four equal groups, group I (sham operated, no I--R injury), group II (control, only I--R), group III (I--R+intraaortic lactated Ringer's, LR, during aortic occlusion), group IV (I--R+LR plus 100mg/kg carnitine). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. The spinal cord function of all animals was assessed clinically 24h after aortic declamping. Spinal cord samples were taken to measure the levels of tissue malondialdehyde (MDA) and to evaluate the histopathological changes., Results: We found significant increases in the levels of MDA in groups II and III compared with group I (P<0.01), and elevation of MDA in group IV was insignificant. In group II, all animals (100%) were paraplegic with Tarlov's score of 0 and in group III, eight animals (88%) were paraplegic with Tarlov's score of 0 or 1. None of the animals (0%) from group IV was paraplegic. Histologic examination of spinal cords from group IV animals revealed that the appearance of the spinal cord was relatively preserved, whereas spinal cords from groups II and III had evidence of acute neuronal injury., Conclusion: The results suggest that regional infusion of carnitine during aortic clamping reduces spinal cord injury and prevents neurologic damage in rabbit spinal cord I--R model.

Accidental B virus (Herpesvirus simiae) infection of human beings working with macaques is frequently fatal. However, the pathogenic potential of other similar simian alphaherpesviruses, such as the squirrel monkey virus Herpesvirus saimiri (HVS1), is virtually unknown. As part of an effort to develop a murine model for infections with these agents, Balb/c mice were inoculated intramuscularly in the left hindlimb with 10 to 10(6) plaque forming units (PFU) of HVS1. After observation for clinical signs of infection for 21 days, mice were killed and specimens collected for serology and histopathology. Mice receiving 510(3) PFU of HVS1 exhibited severe, pruritic, ulcerative skin lesions near the site of inoculation and developed unilateral or bilateral hindlimb paralysis with severe muscle atrophy. Histological lesions were characterized by a necrotizing dermatitis and folliculitis. Spinal cord lesions consisted of a non-suppurative myelitis affecting primarily the ipsilateral dorsal horn of the thoracolumbar spinal cord with occasional extension to ventral and contralateral spinal cord regions. Immunohistochemical labelling confirmed the presence of viral antigen within the lesions, and anti-HVS1 IgG concentrations were related to the occurrence of disease. HVS1 infection in some mice extended from the ipsilateral dorsal horn and funiculus into the ventral and contralateral grey and white matter, resulting in bilateral hindlimb paralysis. Thoracolumbar spinal cord lesions resolved without continued spread of the virus to cranial nervous system structures, i.e., cervical spinal cord and brain., (Copyright Harcourt Publishers Ltd.)

Heterotopic ossification is a benign, ectopic bone growth that develops in muscle and other soft tissue. The exact cause is poorly understood, but it is a rarely serious complication of soft tissue trauma. Its most common form, myositis ossifications traumatica, occurs as a secondary complication of direct muscle injury. However, other forms are less common and can result from specific pathologic conditions, such as spinal cord trauma and metabolic disorders. In patients who have had spinal cord injury and subsequent paraplegia, heterotopic ossification often results in ankylosis of the hip and a loss in range of motion. Ectopic ossification occurs below the injury site, and, although the specific muscle groups can vary, it usually involves those for which the origin and insertion involve the anterior pelvis and proximal femur. In dried bone, heterotopic ossification can appear as a smooth, irregularly shaped benign tumor of mature bone, extending from the surface but not invading the cortical bone. These tumors range in size from a few millimeters to several centimeters. Because heterotopic ossification is often associated with specific types of injuries, it has a unique anthropological use in forensic cases.

Neurotization of the brachial plexus is an established procedure in the upper limb. However, neurotization of the lower limb remains experimental. Brunelli reported the use of the ulnar nerve to neurotize the lower limb. Zhao et al reported the use of intercostals nerve to neurotize the lower limb in rats. The aim of the study was to determine the feasibility of using intercostals nerve to neurotize the femoral nerve in human cadavers and to ascertain the ideal intercostals nerve that has the anatomical course that suit this role. Six fresh cadaveric dissection were performed through an extensile midline incision in the postmortem room and the lower six (T7-T12) were identified and traced from their origin. Their length and course identified and charted. T9 and T10 intercostal nerve was thought to be the most suitable nerve as the donor nerve, and the T11 and T12 intercostal nerve could not be free from its intra-muscular course sufficiently to be use as donor.

Background: In recent years, experimental studies have sought some type of functional improvement in traumatic paraplegia by transplanting neural tissue into the injured spinal cord. The aim of this work is to study the possibility of functional recovery in chronic paraplegic rats after co-transplantation of fetal cerebral tissue and adult peripheral nerve tissue., Methods: Seventy adult female Wistar rats were subjected to spinal cord injury at the T6-T8 level, causing complete paraplegia. Three months later, in 50 rats (grafted group) the injured spinal cord tissue received a graft of fetal brain cortex associated with crushed adult peripheral nerve. All the animals (grafted and control groups) were subjected to daily rehabilitation procedures from the first week after the injury, and evaluated weekly for motor and sensory recovery. Statistical analysis of different behavioral data between control and grafted animals was performed using the Kruskal-Wallis ANOVA and the nonparametric Wilcoxon test., Results: Between 8 and 12 months after transplantation, progressive signs of functional recovery were observed in the grafted animals, associated with an increase in muscle mass in the lower extremities, findings that were significantly different from those in nongrafted animals (p < 0.05). At this time, donor cerebral tissue is integrated into previously injured spinal cord and results in formation of bundles of nerve fibers that emerge from the area of the transplant and surround the spinal cord beneath the lesion., Conclusions: Delayed co-transplantation of fetal cerebral tissue and peripheral nerve tissue can be used to achieve anatomical remodeling and long-term functional recovery in rats rendered paraplegic as result of severe spinal cord injury. These findings support the possibility of functional recovery after chronic traumatic paraplegia.

Study Design: The bone mineral density (BMD) in 22 male subjects with complete lesion paraplegia sustained 1.8 to 27 years previously was measured. The measurements were used in screening each subject for a research programme investigating the restoration of standing using functional electrical stimulation (FES)., Objectives: To assess the extent of bone loss in this group of subjects and correlation to age, time post-injury and level of lesion., Setting: District General Hospital in the UK., Methods: BMD was measured by dual energy X-ray absorptiometry (DEXA) in the lumbar spine and femoral neck and expressed as an indirect index to an age matched 'normal' population. Fracture risk was described from this score using published data indicating that the risk increased with each standard deviation difference from the 'normal' mean., Results: The bone density in the lumbar spine was better preserved than in the femoral neck. BMD in the lumbar spine was found to be greater than the mean from the age matched population in 57.1% of subjects. Bone loss at the femoral neck suggested that 81.8% of the subjects were at increased risk of fracture, but only 22.7% were at a high risk. No correlation was found between BMD at the lumbar spine or the femoral neck and age, lesion level or time post-injury., Conclusion: The study indicates that further investigation into baseline BMD values for the SCI population is required to improve information provided to patients and assessment of fracture risk on an individual basis.

A 6.5-year-old male rhesus macaque (Macaca mulatta) was presented with acute paraplegia following a surgical procedure. During surgery, he experienced an acute hypotensive episode that required 3 hours of supportive therapy before hemodynamic stability was restored. Paraplegia remained unchanged until euthanasia 72 hours later. At necropsy, spinal cord segments T10-S3 had acute, massive panmedullary necrosis, which involved most of the central and middle spinal cord, sparing the peripheral white matter. Additional lesions included arterial border zone necrosis of the brain, centrilobular hepatic necrosis, and proximal renal tubular necrosis. The histologic findings of central spinal cord necrosis with a preserved rim of white matter is consistent with severely decreased flow in the anterior spinal artery. Such lesions can result from episodes of generalized hypoperfusion. Possible factors contributing to the hypotensive episode in this case included the addition of xylazine to ketamine and atropine in the preanesthetic medication, positioning during anesthesia, and decreased blood pressure during surgery.

Remyelination of the CNS is necessary to restore neural function in a number of demyelinating conditions. Schwann cells, the myelinating cells of the periphery, are candidates for this purpose because they have more robust regenerative properties than their central homologs, the oligodendrocytes. Although the ability of Schwann cells to remyelinate the CNS has been demonstrated, their capacity to enter the adult spinal cord in large numbers and effect functional recovery remains uncertain. We used cholera toxin B-subunit conjugated to saporin to demyelinate the rat lumbar spinal cord, remove macroglia, and produce paraplegia. After the removal of oligodendrocyte and astrocyte debris by invading macrophages, there was a spontaneous entry of Schwann cells into the spinal cord, along with axonal remyelination and concomitant functional recovery from paraplegia occurring within 75 d. The Schwann cells appeared to enter the dorsal funiculi via the dorsal root entry zone and the lateral funiculi via rootlets that had become adherent to the lateral spinal cord after the inflammation. In the following weeks, Schwann cell myelin surrounding central axons was progressively replaced by oligodendrocyte myelin without lapse in motor function. Our results show that endogenous Schwann cells can reverse a severe neurological deficit caused by CNS demyelination and enable later oligodendrocyte remyelination.

Purpose: To evaluate residual activity in the sensorimotor cortex of the lower limbs in paraplegia., Methods: 5 patients suffering from a complete paralysis after traumatic medullar lesion (ASIA=A). Clinical evaluation of motility and sensitivity. 1. Control functional MR study of the sensorimotor cortex during simultaneous movements of hands, imaginary motor task and passive hands stimulation. 2. Concerning the lower limbs, 3 fMRI conditions: 1-patient attempts to move his toes with flexion-extension, 2-mental imagery task of the same movement, 3-peripheral passive proprio-somesthesic stimulation (squeezing) of the big toes., Results: Activations were observed in the primary sensorimotor cortex (M1), premotor regions and in the supplementary motor area (SMA) during movement and mental imaginary tasks in the control study and during attempt to move and mental imaginary tasks in the study concerning the lower limbs. Passive somesthesic stimulation generated activation posterior to the central sulcus for 2 patients., Conclusion: Activations in the sensorimotor cortex of the lower limbs can be generated either by attempting to move or mental evocation. In spite of a clinical evaluation of complete paraplegia, fMRI can show a persistence of sensitive anatomic conduction, confirmed by Somesthesic Evoked Potentials.