Displaying publications 1 - 20 of 142 in total

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  1. Multiple sclerosis. The neuropathology of a case with a plea
    Arumugasamy N
    Med J Malaya, 1969 Sep;24(1):45-8.
    PMID: 4243843
    Matched MeSH terms: Brain/pathology*
  2. Intracranial hypoglossal neurinomas. A report of two cases
    Arumugasamay N, Sarvananthan K, Rudralingam V, Pillay RP
    Med J Malaya, 1972 Mar;26(3):168-72.
    PMID: 5031011
    Matched MeSH terms: Brain/pathology
  3. First case of schistosomiasis in Malaysia
    Murugasu R, Por P
    Southeast Asian J. Trop. Med. Public Health, 1973 Dec;4(4):519-23.
    PMID: 4787654
    Matched MeSH terms: Brain/pathology
  4. An epizootic of bovine malignant catarrh in Malaysia
    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: Brain/pathology
  5. Pathologic activity of Plasmodium berghei prevented but not reversed by dexamethasone
    Franz DR, Lim TS, Baze WB, Arimbalam S, Lee M, Lewis GE
    Am J Trop Med Hyg, 1988 Mar;38(2):249-54.
    PMID: 3281490
    Dexamethasone has recently been shown to block the production of cachectin (implicated in the pathogenesis of cerebral malaria) if administered prior to endotoxin induction of mouse macrophages. Using the hamster cheek pouch-cerebral malaria model, we tested the hypothesis that dexamethasone is effective as a therapeutic agent in severe malaria if given before some yet undefined trigger point in the disease. Infected hamsters were treated with dexamethasone (0.7 mg/kg) daily on days 7-12, 4-12, or 1-12 post-challenge. When treatment was started on day 1, whole body oxygen consumption (used as a measure of erythrocyte transport to sites of diffusion) on day 12 was greater than (P less than 0.05) that of infected control animals, though the degree of anemia was no different in treated and untreated groups. Furthermore, treatment produced a reduction in monocyte accumulation, capillary malfunction, and monocyte/red blood cell aggregate formation observable in the cheek pouch in vivo and a similar reduction in monocyte presence, capillary pathologic change, and multifocal hemorrhage in the brain on postmortem. These data suggest that mediator(s), whose production can be blocked by pretreatment with dexamethasone, are involved in the pathogenesis of disease leading to death of the Plasmodium berghei infected hamster.
    Matched MeSH terms: Brain/pathology
  6. Neurological disorders in sheep during signal grass (Brachiaria decumbens) toxicity
    Abdullah AS, Noordin MM, Rajion MA
    Vet Hum Toxicol, 1989 Apr;31(2):128-9.
    PMID: 2929118
    Severe neurological dysfunction was observed in sheep 4 weeks after grazing on Signal grass (Brachiaria decumbens). These neurological disorders included the stamping of forelegs, star-gazing, incoordination, head-pressing against the fence and circling movements. Histologically, numerous vacuolations of various sizes were observed in the white matter of the brain giving rise to a spongy appearance.
    Matched MeSH terms: Brain/pathology*
  7. Fulltext Occurrence of human rabies in peninsular Malaysia
    Ganesan J, Sinniah M
    Med J Malaysia, 1993 Jun;48(2):194-9.
    PMID: 8350795
    The occurrence of a case of human rabies in Peninsular Malaysia is reported. Despite the various control measures taken, sporadic cases of rabies have continued to occur in Peninsular Malaysia, especially in the northern states. Clinical awareness of the occurrence of rabies is therefore important and effective post-exposure prophylaxis should be instituted as soon as possible to prevent the possible occurrence of this dreaded disease.
    Matched MeSH terms: Brain/pathology
  8. Brain calcification in patients with cerebral lupus
    Raymond AA, Zariah AA, Samad SA, Chin CN, Kong NC
    Lupus, 1996 Apr;5(2):123-8.
    PMID: 8743125 DOI: 10.1177/096120339600500207
    Cerebral lupus (CL) is a common cause of morbidity and mortality in patients with SLE. The brain CTs of 27 consecutive adult patients with SLE and various neurological presentations were reviewed. The median age and duration of neurological symptoms at the time of the brain CT were 30 years (range = 14-51 years) and six days (range = 1 day-22 years), respectively. Eleven patients (41%) had normal CTs. The abnormalities in the remaining patients could be divided into six categories: (a) cerebral atrophy alone (two patients); (b) calcification alone (three patients); (c) infarct(s) alone (five patients); (d) cerebral atrophy and calcification (three patients); (e) cerebral atrophy and infarct(s) (one patient) and (f) cerebral atrophy, calcification and infarct(s) (two patients). Altogether eight patients (30%) (age range = 17-47 years) had intracerebral calcification: the globus pallidus was involved in all, putamen in two, head of the caudate nucleus in one, thalamus in one, centrum semiovale in two and cerebellum in three patients. Two patients had extensive calcifications of most of the basal ganglia, centrum semiovale and cerebellum. There was no relationship between the presence/degree of calcification and age of patients/duration or type of neurological presentation. The pathogenesis of cerebral calcification in CL is unknown. Cerebral lupus must now be included in the differential diagnosis of intracerebral calcification.
    Matched MeSH terms: Brain/pathology
  9. Incidence of tumours suitable for radiosurgery in a developing country like Malaysia: retrospective study done before the decision to start a radiosurgery programme
    Abdullah J, Ridzuan MY
    Stereotact Funct Neurosurg, 1997;69(1-4 Pt 2):152-5.
    PMID: 9711749
    This is a descriptive epidemiologic study that was done retrospectively for the years 1990-1996. The objective was to determine whether tumours less than 4 cm in diameter are common and thereafter suitable for radiosurgical treatment. The results showed that the incidence of brain tumours less than 4 cm in diameter was 73.3% and about 20% were situated in the eloquent area.
    Matched MeSH terms: Brain/pathology
  10. Video-EEG telemetry: apparent manifestation of both epileptic and non-epileptic attacks causing potential diagnostic pitfalls
    Raymond AA, Gilmore WV, Scott CA, Fish DR, Smith SJ
    Epileptic Disord, 1999 Jun;1(2):101-6.
    PMID: 10937139
    Video-EEG telemetry is often used to support the diagnosis of non-epileptic seizures (NES). Although rare, some patients may have both epileptic seizures (ES) and NES. It is crucially important to identify such patients to avoid the hazards of inappropriate anticonvulsant withdrawal. To delineate the electroclinical characteristics and diagnostic problems in this group of patients, we studied the clinical, EEG and MRI features of 14 consecutive patients in whom separate attacks, considered to be both NES and ES were recorded using video-EEG telemetry. Only two patients were drug-reduced during the telemetry. Most patients had their first seizure (ES or NES) in childhood (median age 7 years; range: 6 months-24 years); 8/14 patients were female. Brain MRI was abnormal in 10/14 patients. Interictal EEG abnormalities were present in all patients; 13/14 had epileptiform and 1/14 only background abnormalities. Over 70 seizures were recorded in these 14 patients: in 12/14 patients, the first recorded seizure was a NES (p < 0.001), and 7 of these patients had at least one more NES before an ES was recorded. Only 3/14 patients had more than 5 NES before an ES was recorded. Recording a small number of apparently NES in an individual by no means precludes the possibility of additional epilepsy. Particular care should be taken, and multiple (> 5) seizure recording may be advisable, in patients with a young age of seizure onset, interictal EEG abnormalities, or a clear, potential aetiology for epilepsy.
    Matched MeSH terms: Brain/pathology
  11. Trailing a virus
    Gibbs WW
    Sci. Am., 1999 Aug;281(2):80-7.
    PMID: 10443039
    Matched MeSH terms: Brain/pathology
  12. The neurological manifestations of Nipah virus encephalitis, a novel paramyxovirus
    Lee KE, Umapathi T, Tan CB, Tjia HT, Chua TS, Oh HM, et al.
    Ann Neurol, 1999 Sep;46(3):428-32.
    PMID: 10482278 DOI: 10.1002/1531-8249(199909)46:3<428::AID-ANA23>3.0.C
    A novel Hendra-like paramyxovirus named Nipah virus (NiV) was the cause of an outbreak among workers from one abattoir who had contact with pigs. Two patients had only respiratory symptoms, while 9 patients had encephalitis, 7 of whom are described in this report. Neurological involvement was diverse and multifocal, including aseptic meningitis, diffuse encephalitis, and focal brainstem involvement. Cerebellar signs were relatively common. Magnetic resonance imaging scans of the brain showed scattered lesions. IgM antibodies against Hendra virus (HeV) were present in the serum of all patients. Two patients recovered completely. Five had residual deficits 8 weeks later.
    Matched MeSH terms: Brain/pathology
  13. Nipah viral encephalitis or Japanese encephalitis? MR findings in a new zoonotic disease
    Lim CC, Sitoh YY, Hui F, Lee KE, Ang BS, Lim E, et al.
    AJNR Am J Neuroradiol, 2000 Mar;21(3):455-61.
    PMID: 10730635
    BACKGROUND AND PURPOSE: An epidemic of suspected Japanese encephalitis occurred in Malaysia in 1998-1999 among pig farmers. In neighboring Singapore, an outbreak occurred among pig slaughterhouse workers. It was subsequently established that the causative agent in the outbreak was not the Japanese encephalitis virus but a previously unknown Hendra-like paramyxovirus named Nipah virus.

    METHODS: The brain MR images of eight patients with Nipah virus infection were reviewed. All patients tested negative for acute Japanese encephalitis virus. Seven patients had contrast-enhanced studies and six had diffusion-weighted examinations.

    RESULTS: All patients had multiple small bilateral foci of T2 prolongation within the subcortical and deep white matter. The periventricular region and corpus callosum were also involved. In addition to white matter disease, five patients had cortical lesions, three had brain stem involvement, and a single thalamic lesion was detected in one patient. All lesions were less than 1 cm in maximum diameter. In five patients, diffusion-weighted images showed increased signal. Four patients had leptomeningeal enhancement and four had enhancement of parenchymal lesions.

    CONCLUSION: The brain MR findings in patients infected with the newly discovered Nipah paramyxovirus are different from those of patients with Japanese encephalitis. In a zoonotic epidemic, this striking difference in the appearance and distribution of lesions is useful in differentiating these diseases. Diffusion-weighted imaging was advantageous in increasing lesion conspicuity.

    Matched MeSH terms: Brain/pathology
  14. Infectious cDNA clone of attenuated Langat tick-borne flavivirus (strain E5) and a 3' deletion mutant constructed from it exhibit decreased neuroinvasiveness in immunodeficient mice
    Pletnev AG
    Virology, 2001 Apr 10;282(2):288-300.
    PMID: 11289811
    Forty-five years ago a naturally attenuated tick-borne flavivirus, Langat (LGT) strain TP21, was recovered from ticks in Malaysia. Subsequently, it was tested as a live attenuated vaccine for virulent tick-borne encephalitis viruses. In a large clinical trial its attenuation was confirmed but there was evidence of a low level of residual virulence. Thirty-five years ago further attenuation of LGT TP21 was achieved by multiple passages in eggs to yield mutant E5. To study the genetic determinants of the further attenuation exhibited by E5 and to allow us to manipulate the genome of this virus for the purpose of developing a satisfactory live attenuated tick-borne flavivirus vaccine, we recovered infectious E5 virus from a full-length cDNA clone. The recombinant E5 virus (clone 651) recovered from a full-length infectious cDNA clone was more attenuated in immunodeficient mice than that of its biologically derived E5 parent. Increase in attenuation was associated with three amino acid substitutions, two located in the structural protein E and one in nonstructural protein NS4B. Subsequently an even greater degree of attenuation was achieved by creating a viable 320 nucleotide deletion in the 3'-noncoding region of infectious full-length E5 cDNA. This deletion mutant was not cytopathic in simian Vero cells and it replicated to lower titer than its E5-651 parent. In addition, the E5 3' deletion mutant was less neuroinvasive in SCID mice than its E5-651 parent. Significantly, the deletion mutant proved to be 119,750 times less neuroinvasive in SCID mice than its progenitor, LGT strain TP21. Despite its high level of attenuation, the E5 3' deletion mutant remained highly immunogenic and intraperitoneal (ip) inoculation of 10 PFU induced complete protection in Swiss mice against subsequent challenge with 2000 ip LD50 of the wild-type LGT TP21.
    Matched MeSH terms: Brain/pathology
  15. Update on viral encephalitis
    Hinson VK, Tyor WR
    Curr. Opin. Neurol., 2001 Jun;14(3):369-74.
    PMID: 11371762
    Over 100 viruses have been associated with acute central nervous system infections. The present review focuses on some of the most common agents of viral encephalitis, as well as important emerging viral encephalitides. In this context, the initial detection of West Nile virus in the Western Hemisphere during the 1999 New York City outbreak, the first description of Nipah virus in Malaysia, and the appearance in Asia of a new neurovirulent enterovirus 71 strain that causes severe neurologic disease are highlighted. In addition, advances regarding diagnosis, neuroimaging and treatment of Japanese and herpes simplex encephalitis are presented.
    Matched MeSH terms: Brain/pathology
  16. Relapsed and late-onset Nipah encephalitis
    Tan CT, Goh KJ, Wong KT, Sarji SA, Chua KB, Chew NK, et al.
    Ann Neurol, 2002 Jun;51(6):703-8.
    PMID: 12112075
    An outbreak of infection with the Nipah virus, a novel paramyxovirus, occurred among pig farmers between September 1998 and June 1999 in Malaysia, involving 265 patients with 105 fatalities. This is a follow-up study 24 months after the outbreak. Twelve survivors (7.5%) of acute encephalitis had recurrent neurological disease (relapsed encephalitis). Of those who initially had acute nonencephalitic or asymptomatic infection, 10 patients (3.4%) had late-onset encephalitis. The mean interval between the first neurological episode and the time of initial infection was 8.4 months. Three patients had a second neurological episode. The onset of the relapsed or late-onset encephalitis was usually acute. Common clinical features were fever, headache, seizures, and focal neurological signs. Four of the 22 relapsed and late-onset encephalitis patients (18%) died. Magnetic resonance imaging typically showed patchy areas of confluent cortical lesions. Serial single-photon emission computed tomography showed the evolution of focal hyperperfusion to hypoperfusion in the corresponding areas. Necropsy of 2 patients showed changes of focal encephalitis with positive immunolocalization for Nipah virus antigens but no evidence of perivenous demyelination. We concluded that a unique relapsing and remitting encephalitis or late-onset encephalitis may result as a complication of persistent Nipah virus infection in the central nervous system.
    Matched MeSH terms: Brain/pathology
  17. Nipah virus infection, an emerging paramyxoviral zoonosis
    Wong KT, Shieh WJ, Zaki SR, Tan CT
    Springer Semin. Immunopathol., 2002;24(2):215-28.
    PMID: 12503066
    The Nipah virus outbreak represented one of several bat-derived paramyxoviruses that has emerged during the last decade to cause severe human and animal disease. The pathogenesis of Nipah infection is associated with its ability to infect blood vessels and extravascular parenchyma in many organs, particularly in the central nervous system. The clinical manifestations of acute Nipah infection range from fever and mild headache to a severe acute encephalitic syndrome in which there is a high mortality. Much remains to be understood about this new disease, including its intriguing ability to cause relapsing encephalitis in some survivors. This review provides an overview of the Nipah outbreak, focussing on what is presently known about it as an infectious disease, including the clinical aspects, pathology and pathogenesis.
    Matched MeSH terms: Brain/pathology
  18. Late clinical and magnetic resonance imaging follow up of Nipah virus infection
    Lim CC, Lee WL, Leo YS, Lee KE, Chan KP, Ling AE, et al.
    J Neurol Neurosurg Psychiatry, 2003 Jan;74(1):131-3.
    PMID: 12486285
    The Nipah virus is a newly identified paramyxovirus responsible for an outbreak of fatal encephalitis in Malaysia and Singapore. This paper reports the follow up clinical and magnetic resonance imaging findings in 22 affected subjects. Of 13 patients with encephalitis, one died, one was lost to follow up, and seven recovered. Among the four remaining patients, one had residual sixth nerve palsy, another suffered from severe clinical depression, and a third patient had evidence of retinal artery occlusion. One patient with delayed onset Horner syndrome had a single lesion in the cervical spinal cord. The brain magnetic resonance findings were stable or improved in nine patients over 18 months of follow up. Among a second group of nine asymptomatic seropositive abattoir workers, magnetic resonance examination in seven subjects revealed discrete small lesions in the brain; similar to those detected in encephalitis patients. These findings suggest that in addition to encephalitis, the newly discovered Nipah virus affects the spinal cord and the retina. Late clinical and radiological findings can occur in Nipah virus infections as with other paramyxoviruses.
    Matched MeSH terms: Brain/pathology*
  19. Fulltext A golden hamster model for human acute Nipah virus infection
    Wong KT, Grosjean I, Brisson C, Blanquier B, Fevre-Montange M, Bernard A, et al.
    Am J Pathol, 2003 Nov;163(5):2127-37.
    PMID: 14578210 DOI: 10.1016/S0002-9440(10)63569-9
    A predominantly pig-to-human zoonotic infection caused by the novel Nipah virus emerged recently to cause severe morbidity and mortality in both animals and man. Human autopsy studies showed the pathogenesis to be related to systemic vasculitis that led to widespread thrombotic occlusion and microinfarction in most major organs especially in the central nervous system. There was also evidence of extravascular parenchymal infection, particularly near damaged vessels (Wong KT, Shieh WJ, Kumar S, Norain K, Abdullah W, Guarner J, Goldsmith CS, Chua KB, Lam SK, Tan CT, Goh KJ, Chong HT, Jusoh R, Rollin PE, Ksiazek TG, Zaki SR, Nipah Virus Pathology Working Group: Nipah virus infection: Pathology and pathogenesis of an emerging paramyxoviral zoonosis. Am J Pathol 2002, 161:2153-2167). We describe here a golden hamster (Mesocricetus auratus) model that appears to reproduce the pathology and pathogenesis of acute human Nipah infection. Hamsters infected by intranasal or intraperitoneal routes died within 9 to 29 days or 5 to 9 days, respectively. Pathological lesions were most severe and extensive in the hamster brain. Vasculitis, thrombosis, and more rarely, multinucleated endothelial syncytia, were found in blood vessels of multiple organs. Viral antigen and RNA were localized in both vascular and extravascular tissues including neurons, lung, kidney, and spleen, as demonstrated by immunohistochemistry and in situ hybridization, respectively. Paramyxoviral-type nucleocapsids were identified in neurons and in vessel walls. At the terminal stage of infection, virus and/or viral RNA could be recovered from most solid organs and urine, but not from serum. The golden hamster is proposed as a suitable model for further studies including pathogenesis studies, anti-viral drug testing, and vaccine development against acute Nipah infection.
    Matched MeSH terms: Brain/pathology
  20. Fulltext Acute disseminated encephalomyelitis: a report of six cases
    Thomas GST, Hussain IHMI
    Med J Malaysia, 2004 Aug;59(3):342-51.
    PMID: 15727380 MyJurnal
    Six children with Acute Disseminated Encephalomyelitis (ADEM) were seen at the Penang Hospital over a two year period (July 1999-June 2001). Diagnosis was based upon typical clinical features and characteristic findings on neuroimaging. Cerebrospinal fluid examination and other investigations were done, where appropriate, to rule out other causes of central nervous system disease. Three children had a prodromal illness. The most common presenting symptoms were fever, seizures, ataxia, focal neurological deficits and labile mood. Two children presented with status epilepticus. All children had an abnormal neurological examination. Brain magnetic resonance imaging revealed hyperintense signals on T2-weighted and FLAIR sequences in the subcortical and deep white matter regions of the frontal, parietal, and temporal lobes, as well as in the thalami, cerebellum and brainstem. One child had multiphasic disseminated encephalomyelitis (three episodes). The child with multiphasic disease had only one treated episode, and has suffered mild disability. Three children were treated with either methylprednisolone or immunoglobulins, and remain well. One child received both treatments but expired as a result of severe gastrointestinal bleeding from the use of methylprednisolone. The child who was not treated has severe disability.
    Matched MeSH terms: Brain/pathology*
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