Displaying publications 21 - 34 of 34 in total

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  1. Maximal respiratory pressures in adult Chinese, Malays and Indians
    Johan A, Chan CC, Chia HP, Chan OY, Wang YT
    Eur Respir J, 1997 Dec;10(12):2825-8.
    PMID: 9493668
    Maximal static inspiratory and expiratory mouth pressures (PI,max and PE,max, respectively) enable the noninvasive measurement of global respiratory muscle strength. The aim of this study was primarily to obtain normal values of PI,max and PE,max for adult Chinese, Malays and Indians and, secondarily, to study their effect on lung volumes in these subjects. Four hundred and fifty two healthy subjects (221 Chinese, 111 Malays, 120 Indians) were recruited. Measurements of PI,max from residual volume (RV), PE,max from total lung capacity (TLC) and forced vital capacity (FVC) were obtained in the seated position. There were significant ethnic differences in PI,max and PE,max measurements obtained in males, and FVC measurements in both males and females. Chinese males had higher PI,max values (mean (+/-SD) 88.7+/-32.5 cmH2O) and higher PE,max values (113.4+/-41.5) than Malay males (PI,max 74.0+/-22.7 cmH2O, PE,max 94.7+/-23.4 cmH2O). Chinese males had higher PE,max than Indian males (PI,max = 83.7+/-30.0 cmH2O, PE,max 98.4+/-29.2 cmH2O). There were no significant differences among Chinese females (PI,max 53.6+/-2.3 cmH2O, PE,max 68.3+/-24.0 cmH2O), Malay females (PI,max 50.7+/-18.3 cmH2O, PE,max 63.6+/-21.6 cmH2O) and Indian females (PI,max 50.0+/-15.2 cmH2O, PE,max 60.7+/-20.4 cmH2O). In both sexes, the Chinese had a higher FVC compared with Malays and Indians. After adjusting for age, height and weight, race was still a determinant for PE,max in males, and FVC in both sexes. The FVC only correlated weakly with PI,max and PE,max in both sexes. Ethnic differences in respiratory muscle strength, and lung volumes, occur among Asians. However, respiratory muscle strength does not explain the differences in lung volumes in healthy Asian subjects.
    Matched MeSH terms: Muscle Weakness/ethnology*
  2. Fulltext Follicular thyroid carcinoma in a patient with myasthenia gravis and thymoma: a rare association
    Ni H, Htet A
    Ecancermedicalscience, 2012;6:274.
    PMID: 23074376 DOI: 10.3332/ecancer.2012.274
    Myasthenia gravis (MG) is an autoantibody-mediated disorder affecting the neuromuscular junction causing characteristic fatigable muscle weakness. Though it can be associated with tumours of the thymus as well as thyroid disorders, it is rare for both to coexist. The exact prevalence of thyroid carcinoma in MG with thymoma is not known but only about a dozen cases have been reported in the literature. We report a case of a 38-year-old Myanmar lady who presented with weakness and breathlessness due to MG with neck swelling. On examination, she had fatigable proximal muscle weakness and thyroid enlargement with no obvious features of hyperthyroidism. Mediastinal widening and an enlarged thyroid gland were noted on her chest X-ray and chest CT. A subtotal thyroidectomy and thymectomy were done. The histology showed follicular carcinoma of the thyroid and benign thymoma. The majority of the reported cases of thyroid carcinoma in association with MG were papillary carcinoma. Follicular carcinoma thyroid associated with MG has not yet been reported in the literature.
    Matched MeSH terms: Muscle Weakness
  3. Fulltext A case of persistent hyponatraemia due to reset osmostat
    Rohana AG, Norasyikin AW, Suehazlyn Z, Ming W, Norlela S, Norazmi MK
    Med J Malaysia, 2006 Dec;61(5):638-40.
    PMID: 17623970 MyJurnal
    We report a case of a 65 year old Malay lady with long-standing diabetes mellitus, who presented to our institution with a one month history of worsening neck pain and progressive upper and lower limb weakness. She was stable despite severe hyponatraemia which was initially treated as syndrome of inappropriate anti-diuretic hormone (SIADH). This was consistent with her underlying illness which was concluded as cervical tuberculosis (TB) with spinal cord compression. She underwent decompression and bone grafting. Despite continuous treatment her serum sodium levels remained low. There were no other problems with her adrenals or thyroid. A water loading and hypertonic saline perfusion test was performed and supported the diagnosis of reset osmostat. Her serum sodium remained below the normal range and she was discharged well.
    Matched MeSH terms: Muscle Weakness
  4. Prolonged Exercise Test in Patients With History of Thyrotoxicosis
    Tan HT, Tan CY, Teong CS, Ratnasingam J, Goh KJ
    J Clin Neurophysiol, 2020 Aug 05.
    PMID: 32773648 DOI: 10.1097/WNP.0000000000000766
    PURPOSE: Thyrotoxic periodic paralysis is characterized by recurrent episodes of reversible, severe proximal muscle weakness associated with hypokalemia and hyperthyroidism. Prolonged exercise test is an easy, noninvasive method of demonstrating abnormal muscle membrane excitability in periodic paralyses. Although abnormal in thyrotoxic periodic paralysis patients, the effects thyroid hormone levels in non-thyrotoxic periodic paralysis thyrotoxicosis patients have not been well studied. The study aims to evaluate thyrotoxicosis patients (regardless of thyrotoxic periodic paralysis history) with prolonged exercise test and correlate it with their thyroid status.

    METHODS: This is a prospective, cross-sectional study of consecutive thyrotoxicosis patients seen at the endocrine clinic of a tertiary medical center. Thyroid status was determined biochemically before prolonged exercise test. Compound muscle action potential (CMAP) amplitudes postexercise were compared against pre-exercise amplitudes and recorded as percentage of mean baseline CMAP amplitude. Comparisons of time-dependent postexercise CMAP amplitudes and mean CMAP amplitude decrement were made between hyperthyroid and nonhyperthyroid groups.

    RESULTS: Seventy-four patients were recruited, 23 (31%) men, 30 (41%) Chinese, and the mean age was 48.5 ± 16.8 years. Of 74 patients, 32 (43%) were hyperthyroid and 42 (57%) were nonhyperthyroid viz. euthyroid and hypothyroid. Time-dependent CMAP amplitudes from 10 to 45 minutes after exercise were significantly lower in hyperthyroid patients compared with nonhyperthyroid patients (P < 0.01). Mean CMAP amplitude decrement postexercise was significantly greater in hyperthyroid than nonhyperthyroid patients (23.4% ± 11.4% vs. 17.3% ± 10.5%; P = 0.02).

    CONCLUSIONS: Compound muscle action potential amplitude declines on prolonged exercise test were significantly greater in hyperthyroid patients compared with nonhyperthyroid patients. Muscle membrane excitability is highly influenced by thyroid hormone level. Thyrotoxic periodic paralysis occurs from increased levels of thyroid hormone activity in susceptible patients.

    Matched MeSH terms: Muscle Weakness
  5. Fulltext Occupational risk factors for carpal tunnel syndrome among nurses in medical
    Anuar Ithnin, Kong, Dinnee, Venkataraman, Saraswathy
    Int J Public Health Res, 2012;2(2):137-143.
    MyJurnal
    Carpal tunnel syndrome (CTS) is a hand disorder which indicates the presence of symptoms such as pain, numbness, and muscle weakness among the patient. CTS is an occupational related disorder which can occur in any profession. However, it can be prevented and managed. The aims of the research were to determine the prevalence of acquiring CTS among nurses who worked in the wards and occupational risk factors involving the upper limbs during nursing tasks performance. The specific aims were to determine the relationship between the prevalence of acquiring CTS and individual factors (age, gender, race, educational level, duration of work and medical history), relationship between the prevalence of acquiring CTS and occupational risk factors in nursing tasks. Nurses profession was chosen as they are performing multitask involving upper limbs especially the wrist joints. Boston Carpal Tunnel Syndrome Questionnaire (BCTQ) was used to determine the level of severity in CTS. Occupational risk factors were assessed by using the Rapid Upper Limb Assessment (RULA). This research was a cross sectional mode which was carried out at a government university medical centre from November through December 2010. Eighty nurses were involved in the research. The respondents were required to fill in the socio-demographic information sheet. Those having CTS were required to fill in the BCTQ. Assessments were performed by observing of the job activity through RULA. The results showed that the prevalence for nurses acquiring CTS is 7.5%. The RULA assessment also indicated that the risk factor was in the highest level with a score of 7. No relationship was shown between the prevalence of CTS and race, gender, educational level and medical history. Significant relationship was indicated by the prevalence of CTS and occupational risk factors. In conclusion, a significant prevalence of CTS related to age of more than 30 years old, Malay races compared to Indian, working experience of more than 10 years and respondents with right hand dominant. Occupational risk factors also indicated among the active nurses. Therefore, it is important for us to modify the work environment, work flow, work methodology and ergonomic factors in order to prevent the nurses from acquiring CTS. Furthermore, education about the condition of CTS should be implemented and reinforced especially among the higher risk nurses.
    Matched MeSH terms: Muscle Weakness
  6. Fulltext Four nucleotide deletions of exon 47 in Dystrophin gene: a case report of a Kelantanese Duchenne Muscular Dystrophy patient
    Fatimah Azman, Rose Adzrianee Adnan, Norhafizah Che Abdul Razak, Nazihah Mohd Yunus, Sarina Sulong, Rozita Abdullah, et al.
    Journal of Biomedical and Clinical Sciences, 2017;2(202):11-13.
    MyJurnal
    Muscular dystrophy is a group of diseases that result in progressive muscle weakness and atrophy. Duchenne Muscular Dystrophy (DMD) is classified as dystrophinopathy and is an X-linked recessive disease. It is caused by alterations in the dystrophin gene at Xp21.2 encoding 79 exons [1]. It is characterised by progressive muscle wasting that begins at 3 to 5 years, delay in motor development and eventually wheelchair confinement followed by premature death at about 30 years from cardiac or respiratory complications [2]. Genetic etiology of cases of DMD in Malaysia are still scarcely reported. Here, we report the genetic cause in the case of an 11-year-old Kelantanese Malay boy who has progressive muscle weakness since 5 years old. He has difficulty in getting up from sitting and supine position also in climbing up stairs until 1st floor. He has a strong family history of DMD and musculoskeletal problems. His younger brother was diagnosed with DMD by molecular analysis and his maternal uncle died at the age of 16 with musculoskeletal problems but was never investigated. Physical examination revealed no dysmorphic features, positive Gower sign with absent tounge fasciculation. On neurological examination, tendon reflexes and muscle tone for limbs were normal. Muscle power for bilateral upper limbs were normal, however, bilateral lower limbs showed slight reduction in muscle power with calf hypertrophy.
    Matched MeSH terms: Muscle Weakness
  7. Fulltext Expression profiling of genes involved in the development and function of skeletal muscles in ts1cje mouse model of Down Syndrome
    Pike-See Cheah, Usman Bala, King-Hwa Ling
    Malaysian Journal of Medicine and Health Sciences, 2018;14(101):12-19.
    MyJurnal
    Introduction: Down syndrome (DS) is caused by trisomy of human chromosome 21 (HSA21). Motor dysfunction due to hypotonia has limited labour productivity and have significant effects on socio-economic status in DS individuals. Ts1Cje, a mouse model of DS that exhibits muscle weakness was employed, to investigate the expression profile of selected trisomic and disomic genes involved in skeletal muscle structure and function. Methods: Quadriceps and triceps were harvested from the Ts1Cje (C57BL/6) postnatal day 60-70 mice and corresponding wild-type littermates. Total RNA extracted from these tissues was subjected for quantitative expression profiling of three trisomic genes (Itsn1, Synj1 and Rcan1) involved in neurotransmission and six disomic genes (Lamc1, Leprel1, Myl6b, Msn, Pgm5 and Tmod1) essential for maintenance of muscle structure and function. Real-time quantitative PCR method was used for the profiling. Results: Differential gene expression in DS is reflected by 1.5-fold or more increase in the level of expression as predicted by the gene dosage imbalance hypothesis. The analysis showed no significant changes in the expression level of trisomic genes (Itsn1, Synj1 and Rcan1). On contrary, disomic genes, Leprel1 and Pgm5, were upregulated for more than 1.5-fold in DS quadriceps whereas Lamc1, Myl6b and Pgm5 were upregulated for more than 1.5 fold in DS triceps as compared to the wild-type group. Conclusions: Our findings suggest that the dysregulation of Lamc1, Leprel1, Myl6b and Pgm5 genes is associated to muscle weakness seen in Ts1Cje and may play a role in molecular pathogenesis of muscle weakness in DS.
    Matched MeSH terms: Muscle Weakness
  8. Fulltext Cellular function of satellite cells does not play a role in muscle weakness of adult Ts1Cje mice
    Lim, Chai Ling, Usman Bala, Leong, Melody Pui-Yee, Johnson Stanslas, Rajesh Ramasamy, Ling, King-Hwa, et al.
    Neuroscience Research Notes, 2018;1(1):3-10.
    MyJurnal
    Down syndrome (DS) is a genetic condition resulting from triplication of human chromosome (HSA)21. Besides intellectual disability, DS is frequently associated with hypotonia. Satellite cells are the resident cells that provides robust and remarkable regenerative capacity to the skeletal muscles, and its population size has been reported to be disease-associated. However, little is known about the population size of satellite cells in DS and the association of its intrinsic cellular functionality and hypotonia seen in DS. Here, we studied the Ts1Cje mouse, a DS murine model displays the muscle weakness characteristic. Satellite cell populations were immunostained with Pax7 and myonuclei numbers in the Ts1Cje extensor digitorum longus muscle were assessed. Their cellular function was further determined via in vitro assay in high-serum conditioned medium. Subsequently, the in vitro self-renewal, proliferative, and differentiation activities of these myogenic precursor cells were assessed after 24, 48, and 72h using Pax7, MyoD, and Ki67 immunomarkers. Our results showed that the population and functionality of Ts1Cje satellite cell did not differ significantly when compared to the wildtype cells isolated from disomic littermates. In conclusion, our findings indicated that intrinsic cellular functionality of the satellite cells, do not contribute to muscle weakness in Ts1Cje mouse.
    Matched MeSH terms: Muscle Weakness
  9. Hypokalemic periodic paralysis due to Graves disease
    Drakaki A, Habib M, Sweeney AT
    Am J Med, 2009 Dec;122(12):e5-6.
    PMID: 19958876 DOI: 10.1016/j.amjmed.2009.06.016
    Hypokalemic thyrotoxic periodic paralysis is a potentially life-threatening complication of hyperthyroidism, defined by 3 characteristic features: thyrotoxicosis, hypokalemia, and acute painless muscle weakness. In this case, a 25-year-old Malaysian man presented with acute, painless lower extremity weakness immediately after a meal. His associated symptoms included palpitations, tremor, and anxiety. He also reported a 30-pound unintentional weight loss over the previous 18 months, dyspnea on exertion, and insomnia.
    Matched MeSH terms: Muscle Weakness/etiology
  10. Spectra of central nervous system melioidosis
    Muthusamy KA, Waran V, Puthucheary SD
    J Clin Neurosci, 2007 Dec;14(12):1213-5.
    PMID: 17964168
    Burkholderia pseudomallei infection of the central nervous system (CNS) is rare with less than 50 cases reported over the last 30 years. The retrospective melioidosis study at University Malaya Medical Centre has documented three cases of CNS melioidosis out of more than 160 cases of melioidosis since 1978. There were two patients with brain abscess and one with spinal epidural abscess. The predisposing factors were: one patient was an aboriginal farmer and the other two were diabetic. Their age ranged from 17 to 45 years. Prominent neurological features were limb weakness, cranial nerve palsy (6th and 7th) and visual disturbance. CT brain scan and MRI spine showed abscess formation, subdural collection, and spinal epidural collection, osteomyelitis of vertebra and occipital bone and also sagital sinus thrombosis. All these patients underwent surgical drainage leading to bacteriological diagnosis as well as appropriate long-term antibiotic therapy. All had good recovery at 6 months after completion of treatment.
    Matched MeSH terms: Muscle Weakness/etiology
  11. 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: Muscle Weakness/epidemiology
  12. Fulltext Transcriptomic profiling of skeletal muscle from the Ts1Cje mouse model of Down syndrome suggests dysregulation of trisomic genes associated with neuromuscular junction signaling, oxidative stress and chronic inflammation
    Leong, Melody Pui Yee, Usman Bala, Lim, Chai Ling, Rozita Rosli, Cheah, Pike-See, Ling, King-Hwa
    Neuroscience Research Notes, 2018;1(1):21-41.
    MyJurnal
    Ts1Cje is a mouse model of Down syndrome (DS) with partial triplication of chromosome 16, which encompasses a high number of human chromosome 21 (HSA21) orthologous genes. The mouse model exhibits muscle weakness resembling hypotonia in DS individuals. The effect of extra gene dosages on muscle weakness or hypotonia in Ts1Cje and DS individuals remains unknown. To identify molecular dysregulation of the skeletal muscle, we compared the transcriptomic signatures of soleus and extensor digitorum longus (EDL) muscles between the adult Ts1Cje and disomic littermates. A total of 166 and 262 differentially expressed protein-coding genes (DEGs) were identified in the soleus and EDL muscles, respectively. The partial trisomy of MMU16 in Ts1Cje mice has a greater effect on gene expression in EDL. Top-down clustering analysis of all DEGs for represented functional ontologies revealed 5 functional clusters in soleus associated with signal transduction, development of reproductive system, nucleic acid biosynthesis, protein modification and metabolism as well as regulation of gene expression. On the other hand, only 3 functional clusters were observed for EDL namely neuron and cell development, protein modification and metabolic processes as well as ion transport. A total of 11 selected DEGs were validated using qPCR (disomic DEGs: Mansc1; trisomic DEGs: Itsn1, Rcan1, Synj1, Donson, Dyrk1a, Ifnar1, Ifnar2, Runx1, Sod1 and Tmem50b). The validated DEGs were implicated in neuromuscular junction signalling (Itsn1, Syn1), oxidative stress (Sod1, Runx1) and chronic inflammation processes (Runx1, Rcan1, Ifnar1, Ifnar2). Other validated DEGs have not been well-documented as involved in the skeletal muscle development or function, thus serve as interesting novel candidates for future investigations. To our knowledge, the study was the first attempt to determine the transcriptomic profiles of both soleus and EDL muscles in Ts1Cje mice. It provides new insights on the possible disrupted molecular pathways associated with hypotonia in DS individuals.
    Matched MeSH terms: Muscle Weakness
  13. Development of the clinical assessment scale in autoimmune encephalitis
    Lim JA, Lee ST, Moon J, Jun JS, Kim TJ, Shin YW, et al.
    Ann Neurol, 2019 03;85(3):352-358.
    PMID: 30675918 DOI: 10.1002/ana.25421
    OBJECTIVE: There is no scale for rating the severity of autoimmune encephalitis (AE). In this study, we aimed to develop a novel scale for rating severity in patients with diverse AE syndromes and to verify the reliability and validity of the developed scale.

    METHODS: The key items were generated by a panel of experts and selected according to content validity ratios. The developed scale was initially applied to 50 patients with AE (development cohort) to evaluate its acceptability, reproducibility, internal consistency, and construct validity. Then, the scale was applied to another independent cohort (validation cohort, n = 38).

    RESULTS: A new scale consisting of 9 items (seizure, memory dysfunction, psychiatric symptoms, consciousness, language problems, dyskinesia/dystonia, gait instability and ataxia, brainstem dysfunction, and weakness) was developed. Each item was assigned a value of up to 3 points. The total score could therefore range from 0 to 27. We named the scale the Clinical Assessment Scale in Autoimmune Encephalitis (CASE). The new scale showed excellent interobserver (intraclass correlation coefficient [ICC] = 0.97) and intraobserver (ICC = 0.96) reliability for total scores, was highly correlated with modified Rankin scale (r = 0.86, p

    Matched MeSH terms: Muscle Weakness/etiology; Muscle Weakness/physiopathology
  14. Patient with statin-associated immune-mediated necrotizing myopathy presenting with subcutaneous edema, persistent bulbar weakness and absent anti-HMGCR
    Ong SG, Ding HJ
    Int J Rheum Dis, 2017 Dec;20(12):2175-2178.
    PMID: 26692320 DOI: 10.1111/1756-185X.12814
    Matched MeSH terms: Muscle Weakness
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