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Cord Pathology (cord + pathology)

Distribution by Scientific Domains
Medical Sciences85%

Kinds of Cord Pathology

  • spinal cord pathology
    		•

    Selected Abstracts

    Long-term outcome of tension-free vaginal tape for treating stress incontinence in women with neuropathic bladders

    BJU INTERNATIONAL, Issue 6 2010
    Ahmad Abdul-Rahman
    Study Type , Therapy (case series) Level of Evidence 4 OBJECTIVE To evaluate the long-term safety and efficacy of the tension-free vaginal tape (TVT) for the treatment of stress urinary incontinence (SUI) in women with neuropathic bladder dysfunction. PATIENTS AND METHODS Twelve women (mean age 53.3 years, range 41,80) with neuropathic bladder dysfunction and SUI confirmed by video-cystometrography (VCMG) were treated with a TVT in one institution by an expert neuro-urologist between November 1997 and December 2000. The patient's notes, clinical annual follow-up and VCMG after the procedure, and the incontinence impact questionnaire (IIQ) forms (Urinary Distress Inventory, and IIQ-7) were assessed during the long-term clinical follow-up for SUI, in addition to a health-related quality of life assessment. The cure of SUI was defined as no loss of urine on physical exercise, confirmed VCMG after the procedure, and by clinical assessment. RESULTS The mean (range) follow-up was 10 (8.5,12) years. Nine patients were using clean intermittent self-catheterization before the insertion of TVT and continued to do so afterward. At 10 years of follow-up, one patient had died (with failed TVT initially), and two were lost to follow-up at 5 years after surgery, but up to 5 years they did not complain of UI and VCMG did not show SUI. The remaining seven of the nine patients were completely dry, and two improved and were satisfied with using one or two pads/day. Two patients showed neurogenic detrusor overactivity confirmed on VCMG, with no evidence of SUI. One patient needed a transient urethral catheter for urinary retention after surgery, one had a bladder injury that required leaving the catheter for 5 days, but no urethral erosions were reported during the follow-up. CONCLUSIONS In women with neuropathic bladder dysfunction secondary to a variety of spinal cord pathologies, and who have SUI necessitating a definitive intervention, insertion of TVT should be considered a desirable treatment, with very good long-term outcomes. [source]

    Mycoplasma pneumoniae -associated myelitis: a comprehensive review

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2006
    S. Tsiodras
    Myelitis is one of the most severe central nervous system complications seen in association with Mycoplasma pneumoniae infections and both acute transverse myelitis (ATM) as well as acute disseminated encephalomyelitis (ADEM) have been observed. We reviewed all available literature on cases of Mycoplasma spp. associated ATM as well as ADEM with dominant spinal cord pathology and classified those cases according to the strength of evidence implicating M. pneumoniae as the cause. A wide range of data on diagnosis, epidemiology, immunopathogenesis, clinical picture, laboratory diagnosis, neuroimaging and treatment for this rare entity is presented. The use of highly sensitive and specific molecular diagnostic techniques may assist in clearly elucidating the role of M. pneumoniae in ATM/ADEM syndromes in the near future. Immunomodulating therapies may have a role in treating such cases. [source]

    Thoracic myelitis as a possible cause of myocardial infarction

    JOURNAL OF INTERNAL MEDICINE, Issue 6 2005
    K. T. LAPPEGÅRD
    Abstract. During the course of an inflammatory process in the thoracic part of the spinal cord, a previously healthy male suffered two myocardial infarctions in separate coronary territories. A coronary angiogram revealed only minor wall changes in one coronary artery. We hypothesize that the myocardial infarctions may have been caused by vasospastic reactions secondary to his spinal cord pathology, and present the case report and a review of the literature. [source]

    NAALADase (GCP II) inhibitors protect in models of amyotrophic lateral sclerosis (ALS)

    JOURNAL OF NEUROCHEMISTRY, Issue 2002
    A. G. Thomas
    Chronic glutamate toxicity is implicated in the pathogenesis of ALS. The neuropeptide N-acetyl-aspartyl glutamate (NAAG) appears to function both as a storage form for glutamate and as a neuromodulator at glutamatergic synapses. Catabolism of NAAG by N-acetylated-,-linked acidic dipeptidase (NAALADase; also termed glutamate carboxypeptidase II), yields N-acetyl aspartate (NAA) and glutamate. Since prior studies demonstrate an up-regulation of NAALADase in motor cortex and increased levels of NAA and glutamate in the CSF of ALS patients, we hypothesized that inhibition of NAALADase could protect against neuronal degeneration in ALS. Neuroprotective effects of two NAALADase inhibitors were assessed. 2-(Phosphonomethyl)pentanedioic acid (2-PMPA) decreased motor neuron loss and prevented loss of choline acetyltransferase (ChAT) activity in an in vitro model of ALS wherein chronic glutamate toxicity was induced by blocking glutamate transport. Gross morphology was preserved in 2-PMPA-treated cultures. In a SOD-1 transgenic mouse model of ALS, oral administration of a structurally different NAALADase inhibitor (GPI 5693) increased survival by 29 days and delayed onset of clinical symptoms by 17 days. Preliminary analysis of spinal cord pathology revealed severe neuronal depletion and astrocytosis with white matter changes in control mice. In mice treated with GPI 5693, normal neuronal populations with modest vacuolar changes were observed. These data suggest that NAALADase inhibition may provide an exciting therapeutic approach to the devastating disease, ALS. [source]

    Assessment of spinal cord pathology following trauma using early changes in the spinal cord evoked potentials: A pharmacological and morphological study in the rat

    MUSCLE AND NERVE, Issue S11 2002
    Hari Shanker Sharma PhD
    Abstract The possibility that spinal cord pathology following trauma can be assessed with early changes in the spinal cord evoked potentials (SCEPs) was examined in a rat model. Spinal cord injury (SCI) was produced in Equithesin-anesthetized (3 ml/kg, i.p.) rats through a longitudinal incision into the right dorsal horn at the T10,11 segments. The SCEPs were recorded with epidural electrodes placed over the T9 (rostral) segment of the cord. The SCEPs consisted of a small positive amplitude and a broad and high negative amplitude (NA). SCI resulted in an instant depression of the rostral NA that lasted for 1 h. However, the latency of NA continued to increase over time. At 5 h, spinal cord blood flow declined by 30% in the T9 segment, whereas the spinal cord water content and the permeability of the blood,spinal cord barrier (BSCB) were markedly increased. Damage to the nerve cells, glial cells, and myelin was quite common in the spinal cord, as seen by light and electron microscopy. Pretreatment with p -chlorophenylalanine, indomethacin, ibuprofen, and nimodipine attenuated the SCEP changes immediately after trauma and resulted in a marked reduction in edema formation, BSCB permeability, and blood flow changes at 5 h. However, pretreatment with cyproheptadine, dexamethasone, phentolamine, and propranolol failed to attenuate the SCEP changes after SCI and did not reduce the cord pathology. These observations suggest that early changes in SCEP reflect secondary injury-induced alterations in the cord microenvironment. Obviously, these changes are crucial in determining the ultimate magnitude and severity of cord pathology. © 2002 Wiley Periodicals, Inc. Muscle Nerve Supplement 11: S83,S91, 2002 [source]