Displaying all 7 publications

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  1. Dang YL, Hor JY, Chia YK, Lim TT, Eow GB
    Acta Neurol Belg, 2014 Sep;114(3):239-41.
    PMID: 23757110 DOI: 10.1007/s13760-013-0217-3
    Matched MeSH terms: Tuberculosis, Central Nervous System/physiopathology*
  2. Wong KT, Munisamy B, Ong KC, Kojima H, Noriyo N, Chua KB, et al.
    J. Neuropathol. Exp. Neurol., 2008 Feb;67(2):162-9.
    PMID: 18219253 DOI: 10.1097/nen.0b013e318163a990
    Previous neuropathologic studies of Enterovirus 71 encephalomyelitis have not investigated the anatomic distribution of inflammation and viral localization in the central nervous system (CNS) in detail. We analyzed CNS and non-CNS tissues from 7 autopsy cases from Malaysia and found CNS inflammation patterns to be distinct and stereotyped. Inflammation was most marked in spinal cord gray matter, brainstem, hypothalamus, and subthalamic and dentate nuclei; it was focal in the cerebrum, mainly in the motor cortex, and was rare in dorsal root ganglia. Inflammation was absent in the cerebellar cortex, thalamus, basal ganglia, peripheral nerves, and autonomic ganglia. The parenchymal inflammatory response consisted of perivascular cuffs, variable edema, neuronophagia, and microglial nodules. Inflammatory cells were predominantly CD68-positive macrophage/microglia, but there were a few CD8-positive lymphocytes. There were no viral inclusions; viral antigens and RNA were localized only in the somata and processes of small numbers of neurons and in phagocytic cells. There was no evidence of virus in other CNS cells, peripheral nerves, dorsal root autonomic ganglia, or non-CNS organs. The results indicate that Enterovirus 71 is neuronotropic, and that, although hematogenous spread cannot be excluded, viral spread into the CNS could be via neural pathways, likely the motor but not peripheral sensory or autonomic pathways. Viral spread within the CNS seems to involve motor and possibly other pathways.
    Matched MeSH terms: Central Nervous System/physiopathology
  3. George R, Liam CK, Chua CT, Lam SK, Pang T, Geethan R, et al.
    PMID: 3238469
    Four recent cases of dengue fever with severe, unusual clinical manifestations are described. Two of these cases had features of fulminant hepatitis and encephalopathy; one of these cases was fatal. The two remaining cases showed hepatitis with renal impairment. The significance and importance of these unusual manifestations of dengue disease are discussed.
    Matched MeSH terms: Central Nervous System/physiopathology
  4. Kimura K, Yokoyama K, Sato H, Nordin RB, Naing L, Kimura S, et al.
    Ind Health, 2005 Apr;43(2):285-94.
    PMID: 15895843
    We examined the effects of pesticides on the central and peripheral nervous system in the setting of a tobacco farm at a developing country. Maximal motor and sensory nerve conduction velocities (MCV and SCV, respectively) in the median, sural and tibial nerves, postural sway, and brain-evoked potentials (auditory event-related and visual-evoked potentials) were measured in 80 male tobacco farmers and age- and sex-matched 40 controls in Kelantan, Malaysia. Median SCV (finger-wrist) in farmers using Delsen (mancozeb, dithiocarbamate fungicide), who showed significant decrease of serum cholinesterase activities, were significantly lower compared with the controls. Sural SCV in farmers using Fastac (alpha-cypermethrin, pyrethroid insecticide) and median MCV (elbow-wrist) in farmers using Tamex (butralin, dinitroaniline herbicide) were significantly slowed compared with their respective controls. In Delsen (mancozeb, dithiocarbamate) users, the power of postural sway of 0-1 Hz was significantly larger than that in the controls both in the anterior-posterior direction with eyes open and in the right-left direction with eyes closed. The former type of sway was also significantly increased in Tamaron (methamidophos, organophosphorus insecticide) users. In conclusion, nerve conduction velocities and postural sway seem to be sensitive indicators of the effects of pesticides on the central and peripheral nervous system.
    Matched MeSH terms: Central Nervous System/physiopathology*
  5. Aziz MNM, Kumar J, Muhammad Nawawi KN, Raja Ali RA, Mokhtar NM
    Nutrients, 2021 Aug 31;13(9).
    PMID: 34578939 DOI: 10.3390/nu13093061
    Patients with irritable bowel syndrome (IBS) are increasingly presenting with a wide range of neuropsychiatric symptoms, such as deterioration in gastroenteric physiology, including visceral hypersensitivity, altered intestinal membrane permeability, and gastrointestinal motor dysfunction. Functional imaging of IBS patients has revealed several abnormalities in various brain regions, such as significant activation of amygdala, thinning of insular and anterior cingulate cortex, and increase in hypothalamic gray matter, which results in poor psychiatric and cognitive outcomes. Interrelations between the enteric and central events in IBS-related gastrointestinal, neurological, and psychiatric pathologies have compelled researchers to study the gut-brain axis-a bidirectional communication that maintains the homeostasis of the gastrointestinal and central nervous system with gut microbiota as the protagonist. Thus, it can be disrupted by any alteration owing to the gut dysbiosis or loss of diversity in microbial composition. Available evidence indicates that the use of probiotics as a part of a balanced diet is effective in the management of IBS and IBS-associated neurodegenerative and psychiatric comorbidities. In this review, we delineate the pathogenesis and complications of IBS from gastrointestinal and neuropsychiatric standpoints while also discussing the neurodegenerative events in enteric and central nervous systems of IBS patients and the therapeutic potential of gut microbiota-based therapy established on clinical and preclinical data.
    Matched MeSH terms: Central Nervous System/physiopathology
  6. Loh WF, Hussain IMI, Soffiah A, Lim YN
    Med J Malaysia, 2000 Dec;55(4):459-63.
    PMID: 11221157
    In a cross-sectional study of 21 children with Systemic Lupus Erythematosus, 15 (71%) were found to have neuropsychiatric manifestations. The most common finding was generalised seizures (42.8%) followed by encephalopathy (19%) and hallucinations (19%). One child (4.76%) had hemichorea. In 3 children neurological manifestations were the first symptom of SLE. Computerised Axial Tomograms (CAT scans) showed cerebral atrophy in 7 of 12 scans available for review. Ten children had abnormal EEGs. Although none of the children had clinical evidence of a peripheral neuropathy, 8 had neurophysiological evidence of a neuropathy. One child died of intracranial haemorrhage. Six children had residual neuropsychiatric sequalae.
    Matched MeSH terms: Lupus Vasculitis, Central Nervous System/physiopathology
  7. Chua AS
    World J Gastroenterol, 2006 May 07;12(17):2656-9.
    PMID: 16718748 DOI: 10.3748/wjg.v12.i17.2656
    Dyspepsia itself is not a diagnosis but stands for a constellation of symptoms referable to the upper gastrointestinal tract. It consists of a variable combination of symptoms including abdominal pain or discomfort, postprandial fullness, abdominal bloating, early satiety, nausea, vomiting, heartburn and acid regurgitation. Patients with heartburn and acid regurgitation invariably have gastroesophageal reflux disease and should be distinguished from those with dyspepsia. There is a substantial group of patients who do not have a definite structural or biochemical cause for their symptoms and are considered to be suffering from functional dyspepsia (FD). Gastrointestinal motor abnormalities, altered visceral sensation, dysfunctional central nervous system-enteral nervous system (CNS-ENS) integration and psychosocial factors have all being identified as important pathophysiological correlates. It can be considered as a biopsychosocial disorder with dysregulation of the brain-gut axis being central in origin of disease. FD can be categorized into different subgroups based on the predominant single symptom identified by the patient. This subgroup classification can assist us in deciding the appropriate symptomatic treatment for the patient.
    Matched MeSH terms: Central Nervous System/physiopathology
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