A 54-year-old female presented with spontaneous thoracic spinal cord herniation manifesting as chronic progressive motor weakness in both legs. Spastic paraparesis (4/5) and pathological reflexes such as ankle clonus were noted. She also had mild bladder dysfunction but no bowel dysfunction. She had no sensory disturbance, including tactile and pinprick sense. Magnetic resonance (MR) imaging revealed that the atrophic spinal cord was displaced into the ventral extradural space at the T4-5 intervertebral level with markedly dilated dorsal subarachnoid space. Computed tomography obtained after myelography showed no evidence of intradural spinal arachnoid cyst. She underwent surgical repair of the spinal cord herniation via laminectomy, and spinal cord herniation through the ventral dural defect was confirmed. Postoperative MR imaging revealed improvement of the spinal cord herniation, but her symptoms were not improved. Spontaneous spinal cord herniation is a rare cause of chronic myelopathy, occurring in the upper and mid-thoracic levels, and the spinal cord is usually herniated into the ventral extradural space. Early differential diagnosis from intradural spinal arachnoid cysts is important for a satisfactory outcome. (+info)
A longitudinal study of abnormalities on MRI and disability from multiple sclerosis.
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BACKGROUND: In patients with isolated syndromes that are clinically suggestive of multiple sclerosis, such as optic neuritis or brain-stem or spinal cord syndromes, the presence of lesions as determined by T2-weighted magnetic resonance imaging (MRI) of the brain increases the likelihood that multiple sclerosis will develop. We sought to determine the relation between early lesion volume, changes in volume, and long-term disability. METHODS: Seventy-one patients in a serial MRI study of patients with isolated syndromes were reassessed after a mean of 14.1 years. Disability was measured with the use of Kurtzke's Expanded Disability Status Scale (EDSS; possible range, 0 to 10, with a higher score indicating a greater degree of disability). RESULTS: Clinically definite multiple sclerosis developed in 44 of the 50 patients (88 percent) with abnormal results on MRI at presentation and in 4 of 21 patients (19 percent) with normal results on MRI. The median EDSS score at follow-up for those with multiple sclerosis was 3.25 (range, 0 to 10); 31 percent had an EDSS score of 6 or more (including three patients whose deaths were due to multiple sclerosis). The EDSS score at 14 years correlated moderately with lesion volume on MRI at 5 years (r=0.60) and with the increase in lesion volume over the first 5 years (r=0.61). CONCLUSIONS: In patients who first present with isolated syndromes suggestive of multiple sclerosis, the increases in the volume of the lesions seen on magnetic resonance imaging of the brain in the first five years correlate with the degree of long-term disability from multiple sclerosis. This relation is only moderate, so the volume of the lesions alone may not be an adequate basis for decisions about the use of disease-modifying treatment. (+info)
Mechanisms of central nervous system viral persistence: the critical role of antibody and B cells.
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Contributions of humoral and cellular immunity in controlling neurotropic mouse hepatitis virus persistence within the CNS were determined in B cell-deficient J(H)D and syngeneic H-2(d) B cell+ Ab-deficient mice. Virus clearance followed similar kinetics in all mice, confirming initial control of virus replication by cellular immunity. Nevertheless, virus reemerged within the CNS of all Ab-deficient mice. In contrast to diminished T cell responses in H-2(b) B cell-deficient muMT mice, the absence of B cells or Ab in the H-2(d) mice did not compromise expansion, recruitment into the CNS, or function of virus-specific CD4+ and CD8+ T cells. The lack of B cells and lymphoid architecture thus appears to manifest itself on T cell responses in a genetically biased manner. Increasing viral load did not enhance frequencies or effector function of virus-specific T cells within the CNS, indicating down-regulation of T cell responses. Although an Ab-independent antiviral function of B cells was not evident during acute infection, the presence of B cells altered CNS cellular tropism during viral recrudescence. Reemerging virus localized almost exclusively to oligodendroglia in B cell+ Ab-deficient mice, whereas it also replicated in astrocytes in B cell-deficient mice. Altered tropism coincided with distinct regulation of CNS virus-specific CD4+ T cells. These data conclusively demonstrate that the Ab component of humoral immunity is critical in preventing virus reactivation within CNS glial cells. B cells themselves may also play a subtle role in modulating pathogenesis by influencing tropism. (+info)
A combination of gabapentin and morphine mediates enhanced inhibitory effects on dorsal horn neuronal responses in a rat model of neuropathy.
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BACKGROUND: Peripheral nerve damage can result in severe, long-lasting pain accompanied by sensory deficits. This neuropathic pain remains a clinical problem, and effective morphine analgesia is often limited by intolerable side effects. The antiepileptic gabapentin has recently emerged as an alternative chronic pain treatment. Improved management of the diverse symptoms and mechanisms of neuropathic pain may arise from combination therapy, based on multiple pharmacologic targets and low drug doses. METHODS: The authors used the Kim and Chung rodent model of neuropathy to induce mechanical and cold allodynia in the ipsilateral hind paw. In vivo electrophysiologic techniques were subsequently used to record evoked dorsal horn neuronal responses in which the effects of systemic morphine and gabapentin were investigated, both individually and in combination. RESULTS: Morphine (1 and 4 mg/kg) inhibited neuronal responses of control rats but not after neuropathy. Gabapentin (10 and 20 mg/kg) inhibited neuronal responses in nerve injured rats and to a lesser extent in sham rats but not in naive rats. In the presence of gabapentin (ineffective low dose of 10 mg/kg), morphine (1 and 3 mg/kg) mediated significant inhibitory effects in all experimental groups, with the greatest inhibitions observed in spinal nerve-ligated and sham-operated rats. After neuropathy, inhibitions mediated by morphine were significantly increased in the presence of gabapentin compared with morphine alone. CONCLUSIONS: After spinal nerve ligation, the inhibitory effects of systemic morphine on evoked dorsal horn neuronal responses are reduced compared with control, whereas the effectiveness of systemic gabapentin is enhanced. In combination with low-dose gabapentin, significant improvement in the effectiveness of morphine is observed, which demonstrates a clinical potential for the use of morphine and gabapentin combinational treatment for neuropathic pain. (+info)
We present the MRI findings in a case of a 24-year-old woman with spinal hemangioblastoma, causing neural foraminal widening by producing a dumbbell mass in the lower cervical region. Hemangioblastomas can very rarely present as an intradural extramedullary lesions and this case is another exceptional pathology which should be considered among the differential diagnosis of enlarged intervertebral foramen due to neoplastic processes. (+info)
Ventral cervical fusion at multiple levels using free vascularized double-islanded fibula - a technical report and review of the relevant literature.
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Reconstruction of the cervical spine using free vascularized bone flaps has been described in the literature. The reports involve either one level or, when multiple levels, they describe en bloc resection and reconstruction. Stabilization of different levels with a preserved intermediate segment with a single vascularized flap has not been described. We report on the case of a 55-year-old man, who had been operated several times using conventional techniques for cervical myelopathy and instability, who presented to us with severe neck pain. Diagnostic procedures showed pseudarthrosis of C3/4 and stress-overload of the C3/4 and C5/6 segments. The C4/5 fusion was adequately rigid, but avascular. We performed anterior cervical fusion at the C3/4 and C5/6 levels with a vascularized fibula flap modified as a double island. The rigidly fused C4/5 block was preserved and vascularized with the periosteum bridging the two fibular islands. The method and technique are described in detail. Fusion was adequate. Donor site morbidity was minimal and temporary. The patient is symptom free to date (25 months). The suggested method provides the possibility of vertebral fusion at different levels using a single vascularized flap. The indications for this procedure are (1) repeated failure of conventional methods, (2) established poor bone healing and bone non-union with avascular grafts and (3) a well-fused or preserved intermediate segment. The relevant literature is reviewed. (+info)
Human T cell leukaemia virus type I associated neuromuscular disease causing respiratory failure.
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Polymyositis and inclusion body myositis have rarely been described in association with human T cell leukaemia virus type I (HTLV-I) infection. Most of such patients have coexisting HTLV-I associated myelopathy (HAM). Two patients with HTLV-I infection, myopathy, and respiratory failure are described. The muscle biopsy specimen of the first patient bore the histological features of inclusion body myositis and there was no evidence of concurrent myelopathy. The second patient had HAM, and her muscle biopsy showed non-specific myopathic and neuropathic changes. Both patients developed respiratory muscle weakness over eight years after diagnosis of myopathy, leading to hypercapnic respiratory failure requiring mechanical ventilatory support. Respiratory failure as a complication of HTLV-I associated myopathy has not previously been described. (+info)
Myelopathy from intracranial dural arteriovenous fistula.
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Dural arteriovenous fistulas arising intracranially are an uncommon cause of progressive myelopathy. This report is of a patient in whom the diagnosis of the condition was confounded by coexisting small vessel cerebrovascular disease. (+info)