Displaying publications 1 - 20 of 23 in total

  1. Arumugasamy N
    Med J Malaya, 1969 Sep;24(1):45-8.
    PMID: 4243843
    Matched MeSH terms: Spinal Cord/pathology*
  2. Pallie W, Manuel JK
    Med J Malaya, 1968 Dec;23(2):96-7.
    PMID: 4240828
    Matched MeSH terms: Spinal Cord/pathology*
  3. Vanselow BA
    Vet Rec, 1980 Jul 05;107(1):15-8.
    PMID: 7434536
    A severe epizootic of bovine malignant catarrh occurred from November 1976 until June 1977 in cattle at an agricultural institute in peninsular Malaysia. In a group of 82 Kedah-Kelantan cattle the morbidity rate was 47.6 per cent with a fatality rate of 89.7 per cent. In a group of 43 local Indian dairy cattle the morbidity rate was 23.3 per cent with a fatality rate of 100 per cent. Although evidence suggested that sheep acted as a common source of infection, the disease occurred in one animal which had no contact with sheep but had contact with infected cattle and carcases.
    Matched MeSH terms: Spinal Cord/pathology
  4. El Beltagi AH, Swamy N, Dashti F
    Neuroradiol J, 2013 Apr;26(2):213-7.
    PMID: 23859245
    The widespread use of MRI in the assessment of low back pain has led to increased detection of degenerative cysts of the spine, which was essentially a surgical diagnosis earlier. The awareness of degenerative cysts, the significance of their role in the etiology of radicular and back pain and their effective management is evolving. We describe a case of bilateral, gas-filled lumbar facet synovial/ ganglion cysts causing focal arachnoid inflammation and lateral lumbar canal stenosis.
    Matched MeSH terms: Spinal Cord/pathology
  5. Chai CH, Yuki N, Nor HM, Goh KJ, Shahrizaila N
    Pract Neurol, 2012 Oct;12(5):328-31.
    PMID: 22976064 DOI: 10.1136/practneurol-2011-000205
    Matched MeSH terms: Spinal Cord/pathology
  6. Yusof MI, Hassan E, Abdullah S
    Surg Radiol Anat, 2011 Mar;33(2):109-15.
    PMID: 20658232 DOI: 10.1007/s00276-010-0704-7
    Posterior translation of the spinal cord occurs passively following laminoplasty with the presence lordotic spine and availability of a space for the spinal cord to shift. This study is to predict the distance of posterior spinal cord migration after expansive laminoplasty at different cervical levels based on measurement of posterior translation of the spinal cord in normal cervical morphometry.
    Matched MeSH terms: Spinal Cord/pathology*
  7. Chong HT, Ramli N, Lee KH, Kim BJ, Ursekar M, Dayananda K, et al.
    Can J Neurol Sci, 2006 Feb;33(1):95-100.
    PMID: 16583730
    Magnetic resonance imaging (MRI) of the brain is the most important paraclinical diagnostic test in multiple sclerosis (MS). The appearance of MRI in Asians with MS is not well defined. We retrospectively surveyed the first brain and spinal cord MRI in patients diagnosed to have MS, according to Poser's criteria in seven regions throughout Asia to define the MRI changes among Asians with MS. There were 101 patients with first brain, and 86 with first spinal cord MRI, 66 of whom had both. The brain MRI showed a mean of 17 lesions per patient in T2 weighted images, mostly asymptomatic. Almost all the lesions were in the white matter, particularly in the juxtacortical, deep and periventricular white matter. A third of the lesions were greater than 5 mm, 14% enhanced with gadolinium. There were more supratentorial than infratentorial lesions at a ratio of 7.5: 1. Ninety five percent of the spinal cord lesions were in cervical and thoracic regions, 34% enhanced with gadolinium. The lesions extended over a mean of 3.6 +/- 3.3 vertebral bodies in length. Fifty (50%) of the brain and 54 (63%) of the spinal MRI patients had the optic-spinal form of MS. The MRI of the optic-spinal and classical groups of patients were similar in appearance and distribution, except that the optic-spinal MS patients have fewer brain but longer and more severe spinal cord lesions. In conclusion, the brain and spinal cord MRI of Asian patients with MS was similar to that of the West, although, in this study, Asian MS patients had larger spinal cord lesions.
    Matched MeSH terms: Spinal Cord/pathology*
  8. Anjum A, Yazid MD, Fauzi Daud M, Idris J, Ng AMH, Selvi Naicker A, et al.
    Int J Mol Sci, 2020 Oct 13;21(20).
    PMID: 33066029 DOI: 10.3390/ijms21207533
    Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. Many therapeutic strategies have been proposed to overcome neurodegenerative events and reduce secondary neuronal damage. Efforts have also been devoted in developing neuroprotective and neuro-regenerative therapies that promote neuronal recovery and outcome. Although varying degrees of success have been achieved, curative accomplishment is still elusive probably due to the complex healing and protective mechanisms involved. Thus, current understanding in this area must be assessed to formulate appropriate treatment modalities to improve SCI recovery. This review aims to promote the understanding of SCI pathophysiology, interrelated or interlinked multimolecular interactions and various methods of neuronal recovery i.e., neuroprotective, immunomodulatory and neuro-regenerative pathways and relevant approaches.
    Matched MeSH terms: Spinal Cord/pathology
  9. Mustafa M, Subramanian N
    Int Orthop, 1996;20(6):383-4.
    PMID: 9049770
    We describe a patient with acute compression of the spinal cord by a spontaneous extra-dural haematoma. This rare condition is often misdiagnosed. We believe that an urgent MRI scan is indicated in patients presenting with progressive neurological deficit following spinal trauma. This allows the diagnosis of extra-dural haematoma to be made rapidly and for prompt decompression of the cord.
    Matched MeSH terms: Spinal Cord/pathology
  10. Schee JP, Viswanathan S
    Mult Scler, 2019 07;25(8):1189-1195.
    PMID: 29771191 DOI: 10.1177/1352458518775912
    We identified five female patients retrospectively with relapsing short-segment partial myelitis whose clinical and paraclinical features were suggestive of cord involvement of multiple sclerosis (MS)-type albeit not rigidly fulfilling the 2017 McDonald criteria. Notably, these patients had not developed any typical MS-like brain lesions despite repeated neuroimaging assessments over years. Comprehensive work-up for differential diagnoses of MS and other causes of transverse myelitis particularly neuromyelitis optica spectrum disorders had been consistently negative on longitudinal follow-up. Thus, we postulate a possible entity of pure spinal MS which may represent a novel forme fruste within the MS disease spectrum.
    Matched MeSH terms: Spinal Cord/pathology*
  11. Marza AD, Jesse Abdullah FF, Ahmed IM, Teik Chung EL, Ibrahim HH, Zamri-Saad M, et al.
    Microb Pathog, 2017 Mar;104:340-347.
    PMID: 28126667 DOI: 10.1016/j.micpath.2017.01.031
    Lipopolysaccharide (LPS) of P. multocida B:2, a causative agent of haemorrhagic septicaemia (HS) in cattle and buffaloes, is considered as the main virulence factor and contribute in the pathogenesis of the disease. Recent studies provided evidences about the involvement of the nervous system in pathogenesis of HS. However, the role of P. multocida B:2 immunogens, especially the LPS is still uncovered. Therefore, this study was designed to investigate the role of P. multocida B:2 LPS to induce pathological changes in the nervous system. Nine eight-month-old, clinically healthy buffalo calves were used and distributed into three groups. Calves of Group 1 and 2 were inoculated orally and intravenously with 10 ml of LPS broth extract represent 1 × 10(12) cfu/ml of P. multocida B:2, respectively, while calves of Group 3 were inoculated orally with 10 ml of phosphate buffer saline as a control. Significant differences were found in the mean scores for clinical signs, post mortem and histopathological changes especially in Group 2, which mainly affect different anatomic regions of the nervous system, mainly the brain. On the other hand, lower scores have been recorded for clinical signs, gross and histopathological changes in Group 1. These results provide for the first time strong evidence about the ability of P. multocida B:2 LPS to cross the blood brain barrier and induce pathological changes in the nervous system of the affected buffalo calves.
    Matched MeSH terms: Spinal Cord/pathology
  12. Mitra NK, Goh TE, Bala Krishnan T, Nadarajah VD, Vasavaraj AK, Soga T
    Int J Clin Exp Pathol, 2013;6(8):1505-15.
    PMID: 23923068
    Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease of idiopathic etiology. Glutamate excitotoxicity is one of the proposed hypotheses causing progressive death of motor neurons. We aimed to develop an experimental animal model of this disease to enhance the knowledge of pathophysiological mechanism of ALS. Male Wistar rats were infused with Kainic acid (KA) intra-cisternally for 5 days at the dosage of 50 fmol/day and 150 fmol/day. Locomotor activity, sensory function and histological changes in cervical and lumbar sections of spinal cord were evaluated. Glial Fibrillary Acidic Protein (GFAP) and Neurofilament Protein (NFP) were used as immunohistochemical marker for reactive astrogliosis and neuronal damage respectively. Specific Superoxide Dismutase (SOD) activity of spinal cord was estimated. The locomotor activity in the parameter of observed mean action time remained reduced on 14(th) day after administration of KA. Spinal motor neurons under Nissl stain showed pyknosis of nucleus and vacuolation of neuropil. GFAP expression increased significantly in the lumbar section of the spinal cord with high dose of KA treatment (p<0.05). NFP was expressed in axonal fibres around the neurons in KA-treated rats. A significant increase in specific SOD activity in both cervical and lumbar sections of the spinal cord was found with low dose of KA treatment (p<0.05). This study concludes that spinal cord damage with some features similar to ALS can be produced by low dose intra-cisternal administration of KA.
    Matched MeSH terms: Spinal Cord/pathology
  13. Harreld JH, Mohammed N, Goldsberry G, Li X, Li Y, Boop F, et al.
    AJNR Am J Neuroradiol, 2015 May;36(5):993-9.
    PMID: 25614472 DOI: 10.3174/ajnr.A4221
    Postoperative intraspinal subdural collections in children after posterior fossa tumor resection may temporarily hinder metastasis detection by MR imaging or CSF analysis, potentially impacting therapy. We investigated the incidence, imaging and clinical features, predisposing factors, and time course of these collections after posterior fossa tumor resection.
    Matched MeSH terms: Spinal Cord/pathology*
  14. Mitra NK, Bindal U, Eng Hwa W, Chua CL, Tan CY
    Int J Clin Exp Pathol, 2015;8(10):12041-52.
    PMID: 26722389
    Out of the minor myelin proteins, most significant one is myelin oligodendrocyte glycoprotein (MOG). Mesenchymal stem cells (MSCs) have proven immunoregulatory capacity. The objective of this study was to investigate the effects of syngeneic MSCs on mouse model of experimental autoimmune encephalomyelitis (EAE) through observation of locomotion by footprint analysis, histological analysis of spinal cord and estimation IL-17. C57BL/6 mice (10 weeks, n = 16) were immunized with 300 µg of MOG35-55 and 200 µL of complete Freund's adjuvant (CFA) to produce EAE model. Sham-treated control (n = 8) were injected with CFA. Half of immunized mice were given 100 µL of PBS (n = 8) and next half (n = 8) received 1 × 10(5) MSCs on day 11 through the tail veins. Clinical scoring showed development of EAE (loss of tonicity of tail and weakness of hind limb) on day 10. Following MSC treatment, clinical scores and hindlimb stride length showed significant improvement on day 15 onwards, compared to day 10 (P < 0.05). Under LFB staining, while PBS-treated group of EAE mice showed pale and degenerated axons in anterolateral white column of lumbar spinal cord, MSC-treated group showed numerous normal-looking axons. H&E staining showed normal axons in anterolateral white column and reduction of macrophages in MSC-treated EAE mice group. A lower level of IL-17 was observed in MSC treated EAE mice, compared to PBS-treated EAE mice. Our results suggest that Intravenous MSC has the potential to improve the locomotion and regeneration of axons in spinal cord in MOG-induced EAE model.
    Matched MeSH terms: Spinal Cord/pathology
  15. Wazir NN, Kareem BA
    Singapore Med J, 2011 Jan;52(1):47-9.
    PMID: 21298241
    Cervical spondylotic myelopathy (CSM) represents a spectrum of pathologies with progressive compression of the spinal cord. The clinical signs and symptoms play a key role in diagnosis. The characteristic hand myelopathy signs are of significant clinical importance. The aim of this descriptive study was to report a relatively easy to elicit new hand myelopathy sign. The basis for this is finger and wrist flexor disinhibition, which is used for the spinal specificity of cord compression at or above the C5/6 level.
    Matched MeSH terms: Spinal Cord/pathology
  16. Wolf NI, Toro C, Kister I, Latif KA, Leventer R, Pizzino A, et al.
    Neurology, 2015 Jan 20;84(3):226-30.
    PMID: 25527264 DOI: 10.1212/WNL.0000000000001157
    To describe the expanding clinical spectrum of a recently described hereditary leukoencephalopathy, hypomyelination with brainstem and spinal cord involvement and leg spasticity, which is caused by mutations in the aspartyl tRNA-synthetase encoding gene DARS, including patients with an adolescent onset.
    Matched MeSH terms: Spinal Cord/pathology
  17. Prow NA, Setoh YX, Biron RM, Sester DP, Kim KS, Hobson-Peters J, et al.
    J Virol, 2014 Sep 1;88(17):9947-62.
    PMID: 24942584 DOI: 10.1128/JVI.01304-14
    The mosquito-borne West Nile virus (WNV) is responsible for outbreaks of viral encephalitis in humans, horses, and birds, with particularly virulent strains causing recent outbreaks of disease in eastern Europe, the Middle East, North America, and Australia. Previous studies have phylogenetically separated WNV strains into two main genetic lineages (I and II) containing virulent strains associated with neurological disease. Several WNV-like strains clustering outside these lineages have been identified and form an additional five proposed lineages. However, little is known about whether these strains have the potential to induce disease. In a comparative analysis with the highly virulent lineage I American strain (WNVNY99), the low-pathogenicity lineage II strain (B956), a benign Australian strain, Kunjin (WNVKUN), the African WNV-like Koutango virus (WNVKOU), and a WNV-like isolate from Sarawak, Malaysia (WNVSarawak), were assessed for neuroinvasive properties in a murine model and for their replication kinetics in vitro. While WNVNY99 replicated to the highest levels in vitro, in vivo mouse challenge revealed that WNVKOU was more virulent, with a shorter time to onset of neurological disease and higher morbidity. Histological analysis of WNVKOU- and WNVNY99-infected brain and spinal cords demonstrated more prominent meningoencephalitis and the presence of viral antigen in WNVKOU-infected mice. Enhanced virulence of WNVKOU also was associated with poor viral clearance in the periphery (sera and spleen), a skewed innate immune response, and poor neutralizing antibody development. These data demonstrate, for the first time, potent neuroinvasive and neurovirulent properties of a WNV-like virus outside lineages I and II.
    Matched MeSH terms: Spinal Cord/pathology
  18. Ong KC, Badmanathan M, Devi S, Leong KL, Cardosa MJ, Wong KT
    J. Neuropathol. Exp. Neurol., 2008 Jun;67(6):532-42.
    PMID: 18520772 DOI: 10.1097/NEN.0b013e31817713e7
    We describe a model of Enterovirus 71 encephalomyelitis in 2-week-old mice that shares many features with the human central nervous system (CNS) disease. Mice were infected via oral and parenteral routes with a murine-adapted virus strain originally from a fatal human case. The mice succumbed to infection after 2 to 5 days. Vacuolated and normal-appearing CNS neurons showed viral RNA and antigens and virions by in situ hybridization, immunohistochemistry, and electron microscopy; inflammation was minimal. The most numerous infected neurons were in anterior horns, motor trigeminal nuclei, and brainstem reticular formation; fewer neurons in the red nucleus, lateral cerebellar nucleus, other cranial nerve nuclei, motor cortex, hypothalamus, and thalamus were infected. Other CNS regions, dorsal root, and autonomic ganglia were spared. Intramuscular-inoculated mice killed 24 to 36 hours postinfection had viral RNA and antigens in ipsilateral lumbar anterior horn cells and adjacent axons. Upper cord motor neurons, brainstem, and contralateral motor cortex neurons were infected from 48-72 hours. Viral RNA and antigens were abundant in skeletal muscle and adjacent tissues but not in other organs. The distinct, stereotypic viral distribution in this model suggests that the virus enters the CNS via peripheral motor nerves after skeletal muscle infection, and spread within the CNS involves motor and other neural pathways. This model may be useful for further studies on pathogenesis and for testing therapies.
    Matched MeSH terms: Spinal Cord/pathology
  19. Paudel YN, Angelopoulou E, Piperi C, Othman I, Shaikh MF
    Pharmacol Res, 2020 06;156:104792.
    PMID: 32278047 DOI: 10.1016/j.phrs.2020.104792
    Amyotrophic lateral sclerosis (ALS) is a devastating and rapidly progressing neurodegenerative disorder with no effective disease-modifying treatment up to date. The underlying molecular mechanisms of ALS are not yet completely understood. However, the critical role of the innate immune system and neuroinflammation in ALS pathogenesis has gained increased attention. High mobility group box 1 (HMGB1) is a typical damage-associated molecular pattern (DAMP) molecule, acting as a pro-inflammatory cytokine mainly through activation of its principal receptors, the receptor for advanced glycation end products (RAGE) and toll-like receptor 4 (TLR4) which are crucial components of the innate immune system. HMGB1 is an endogenous ligand for both RAGE and TLR4 that mediate its biological effects. Herein, on the ground of pre-clinical findings we unravel the underlying mechanisms behind the plausible contribution of HMGB1 and its receptors (RAGE and TLR4) in the ALS pathogenesis. Furthermore, we provide an account of the therapeutic outcomes associated with inhibition/blocking of HMGB1 receptor signalling in preventing motor neuron's death and delaying disease progression in ALS experimental models. There is strong evidence that HMGB1, RAGE and TLR4 signaling axes might present potential targets against ALS, opening a novel headway in ALS research that could plausibly bridge the current treatment gap.
    Matched MeSH terms: Spinal Cord/pathology
  20. Silva JF
    Paraplegia, 1973 Aug;11(2):146-58.
    PMID: 4584434 DOI: 10.1038/sc.1973.19
    One hundred and forty-one patients with non-traumatic paraplegia were reviewed. The common causative factors and the problems arising were evaluated. Management of the clinical problems were described. The need for prevention and early treatment has been stressed.
    Matched MeSH terms: Spinal Cord/pathology
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