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Biomedical subjects

E K Tan

Publications and source records attributed to E K Tan.

At least 55 records · Page 3Linked to original sources
PubMed2004

Dysphagia as a side effect of botulinum toxin injection.

Dysphagia is a known adverse effect of botulinum toxin injection into the cervical region for dystonia. We present an unusual case of dysphagia arising from injection into the orbicularis oculi muscle, which has hitherto not been described. We postulate that her dysphagia was caused by distant side effects of botulinum toxin due to repeated injections. We recommend that clinicians should restrict the frequency of injections to as few life-time doses of the toxin as possible for adequate management of spasm. The practice of re-injecting patients routinely every three months, or at the first return of mild spasms should be discouraged.

Blepharospasm↗
PubMed2003

Cortical excitability changes associated with musical tasks: a transcranial magnetic stimulation study in humans.

Neuroimaging studies have suggested differences in cortical activation in human vocalization and musical tasks. However, functional neurophysiological evidence on cortical excitability changes is lacking. We utilized transcranial magnetic stimulation to demonstrate changes in cortical excitability during overt humming and singing tasks. The findings complement those from neuroimaging and support the existence of separate bilateral deep-seated neural networks, as distinct from those for vocalization.

Adult↗
PubMed2003

Spinocerebellar ataxia type 3 presenting as an L-DOPA responsive dystonia phenotype in a Chinese family.

The clinical spectrum of spinocerebellar ataxia 3 (SCA 3) disease is wide and varied. We describe a Chinese patient with a mutation at the SCA 3 locus with clinical features of levodopa-responsive dystonia. The family history was suggestive of being autosomally dominant. Levodopa responsiveness though rare has been described in families with features of parkinsonism. Noteworthy is the relatively late onset of disease (>40 years) possibly explained by the low number of affected alleles at 59, the usual range being from 62 to 86, with the lowest recorded number at 56. This expands the wide and varied phenotypic manifestations of SCA 3, and highlights the observation that features suggestive of levodopa-responsive dystonia (DRD) such as focal dystonia, gait difficulty with diurnal fluctuation of symptoms, and a marked response to low doses of levodopa can be presenting features of SCA 3. SCA 3 should be considered a differential diagnosis in adult patients who present with DRD phenotype and with a positive family history.

Adult↗
PubMed2003

Monoamine oxidase B polymorphism, cigarette smoking and risk of Parkinson's disease: a study in an Asian population.

Cigarette smoking is associated with reduced monoamine oxidase B (MAO B) activity. Polymorphisms of the MAO B gene may modify the relationship between smoking and Parkinson's Disease (PD). We examined the association of MAO B intron 13 G/A polymorphism and risk of PD, and the modulation of the polymorphism on smoking and PD in an Asian study population in Singapore. Two hundred and thirty PD patients (mean age 66.0 +/- 9.4 years, 63% men) and 241 age, gender, and race matched controls (mean age 64 +/- 9.2 years, 58.9% males) were studied. The frequency of G and A alleles in PD and controls was; 66/315 (21.0%) vs. 73/340 (21.5%) and 249/315 (79.0%) vs. 267/340 (78.5%). For women, the genotype frequency in PD and controls was; GG: 7/85 (8.2%) vs. 8/99 (8.1%); GA: 25/85 (29.4%) vs. 27/99 (27.3%); AA: 53/85 (62.4%) vs. 64/99 (64.6%). For men, allele frequency in PD and controls was; A: 118/145 (81.4%) vs. 112/142 (78.9%) and G: 27/145 (18.6%) vs. 30/142 (21.1%). The allele and genotype frequencies were not significantly different between young and late onset PD. The frequency of "ever" smokers in PD and controls was 31/230 (13.5%) vs. 52/241 (21.6%), P = 0.02. A stepwise logistic regression analysis did not reveal any interaction of smoking and the G allele and risk of PD. The MAO B G/A genotype frequency in our Asian population was quite different from Caucasians suggesting that ethnicity specific effects need to be considered in evaluating gene-environmental interaction.

Aged↗
PubMed2003

Increased cortical excitability in human deception.

Deception is a cognitive process in humans and animals which is not well understood. Most studies on lie detection have focused on emotional components associated with deception. We employed transcranial magnetic stimulation of the motor cortex in conjunction with a constrained question answer protocol for the first time to show increased cortical excitability in generating deceptive responses, in contrast with truthful responses. This may be due to increased cognitive activity in the motor and premotor connections. Our findings corroborate functional imaging studies and may have future implications in evaluating lie detection.

Adult↗
PubMed2003

Levodopa-induced oromandibular dystonia in progressive supranuclear palsy.

Levodopa-induced dyskinesias have been reported in Parkinson's disease and multiple system atrophy. Cranial dystonias are rare in patients with progressive supranuclear palsy (PSP). In this report we describe an unusual case of reversible levodopa-induced Oromandibular dystonia (OMD) in a PSP patient to highlight the importance of recognizing this drug related complication in the management of PSP, and discuss the possible underlying pathophysiology.

Aged↗
PubMed2003

Autosomal dominant spinocerebellar ataxias: an Asian perspective.

Autosomal dominant cerebellar ataxias, frequently referred to as spinocerebellar ataxias (SCAs) have been under intense scientific research limelight since expansions of coded CAG trinucleotide repeats were demonstrated to cause several dominantly inherited SCAs. The number of new SCA loci has expanded dramatically in recent years. At least ten genes have been identified for SCAs 1, 2, 3, 6, 7, 8, 10, 12, 17, dentatorubral-pallidoluysian atrophy (DRPLA), and six loci responsible for SCAs 4, 5, 11,13, 14, and 16 have been mapped. Genetic testing is essential for diagnosis due to the overlapping and varied phenotypic features of the different SCAs. While there is no effective treatment available, genetic counseling is important for addressing the many ethical, social, legal, and psychological issues facing SCA patients. Researchers have recently provided valuable information on the pathogenesis of the disease and hopefully a cure will be available in the near future.

Asian People↗
PubMed2003

Piribedil and bromocriptine in Parkinson's disease: a single-blind crossover study.

INTRODUCTION: Clinicians switch from one dopamine agonist to another for various reasons. However, each change may inadvertently result in certain potential risks such as decreased medication efficacy or new side-effects. OBJECTIVE: We evaluated the tolerability of a switch of bromocriptine to piribedil using two conversion ratios as a primary outcome measure, with motor function as a secondary outcome measure, in patients with mild to moderate Parkinson's disease (PD). METHODS: Twenty consecutive patients with mild to moderate PD (Hoehn and Yahr, stage II-III) on treatment with stable doses of bromocriptine and levodopa were randomized to two groups of 10 patients each, to receive piribedil based on 1:5 or 1:10 conversion ratios. Blinded evaluations were performed: 1) United Parkinson's Diseased Rating Scale (UPDRS) scores both in 'on' and 'off', 2) Open-ended interviews for adverse events, 3) Epworth Sleepiness Scale, 4) Purdue Pegboard assessment during 'on' and 'off', 5) Hand-arm movement test during 'on' and 'off', and 6) Walking test during 'on' and 'off'. RESULTS: Major adverse events included 'sleep attacks' in one patient and minor side-effects included giddiness, nausea, hallucinations, sleepiness and lethargy. However, these were mild and 19 (95%) of the 20 patients completed the study. There was a significant improvement in both the UPDRS 'off' total and motor scores at 1 month compared with baseline for the group on 1:10 ratio. The walking times during the 'off' state at 1 and 2 months were significantly better compared with baseline in the 1:5 group. There were otherwise no significant differences in the rating tests during both 'off' and 'on' states before and after the bromocriptine switch. CONCLUSIONS: We demonstrated that patients with mild to moderate PD who were on relatively low doses of bromocriptine can be safely switched to piribedil based on a conversion ratio of either 1:5 or 1:10. However, the higher conversion ratio has to be carried out with caution in patients with daytime somnolence.

Administration, Oral↗
PubMed2003

Piribedil-induced sleep attacks in Parkinson's disease.

'Sleep attacks', episodes of sudden onset of sleep without any prodromal symptoms, were initially described in patients with Parkinson's disease (PD) taking the newer dopamine agonists pramipexole and ropinirole. Piribedil, a nonergot agonist with both D2 and D3 agonist action, is an effective antiparkinsonian medication. However, there are very few reports of Piribedil-induced sleep attacks in PD. Among 50 PD patients seen at our Movement Disorder Clinic who had recently taken Piribedil, we identified three (6%) who satisfied the clinical description of sleep attacks. Here we provide details of the clinical characteristics of Piribedil-induced sleep attacks in these PD patients.

Antiparkinson Agents↗
PubMed2002

Restless legs syndrome in Parkinson's disease.

INTRODUCTION: Recent clinical and functional imaging data suggest impaired central dopaminergic transmission in restless legs syndrome (RLS). As RLS responds to dopaminergic medications, an etiologic link between RLS and Parkinson's disease (PD) has been proposed. However, few studies have examined this association. OBJECTIVE: To investigate the prevalence of RLS amongst PD outpatient population. METHOD: The prevalence of RLS was determined by the diagnostic criteria of the International Restless Legs Syndrome Study Group (IRLSSG). Consecutive PD patients (n=125) were prospectively evaluated in our clinic. RESULTS: There were 77 (61.6%) males and 48 (38.4%) females with a mean age of 65.1+/-9.3 (SD) years (range 34-83), and mean age of onset of disease at 59.6 years+/-10.7 (SD) years (range 30-81). Nineteen (15.2%) patients had motor restlessness. Of these, one (0.8%) patient had RLS-like symptoms closely correlated to wearing "off" effect of levodopa. None of the patients satisfied the IRLSSG diagnostic criteria of RLS. This was not significantly different compared to the 0.6% and 0.1% RLS prevalence in our general population and clinic population. CONCLUSIONS: Our study demonstrates that motor restlessness was present in 15.2% of our PD patients. However, prevalence of RLS in our PD patients was not significantly different from our general population or clinic population, suggesting that these two diseases may not share the same pathophysiologic mechanism.

Adult↗
PubMed2002

Evaluation of somnolence in Parkinson's disease: comparison with age- and sex-matched controls.

The authors found a significantly higher prevalence of daytime somnolence in 201 patients with PD compared with 214 age- and sex-matched healthy control subjects (Epworth Sleepiness Scale score 5.6 vs 4.6). The prevalence of "sleep attacks" (SA) was about seven times higher in patients with PD than in control subjects (13.9% vs 1.9%; p < 0.0005). Multivariate analysis demonstrated that a higher dose of levodopa and longer duration of disease significantly predicted for SA in patients with PD. Epworth Sleepiness Scale scores of > or =10 had 71.4% sensitivity and 88.4% specificity for SA.

Adult↗
PubMed2002

Evolving spectrum of movement disorders in extrapontine and central pontine myelinolysis.

Extrapontine (EPM) and central pontine myelinolysis (CPM) are rare and frequently related to rapid correction of hyponatremia. We describe a 60-year-old woman who developed an unusual evolving spectrum of movement disorders secondary to EPM and CPM following intravenous sodium replacement therapy for severe hyponatremia. She presented initially with confusion, generalized coarse postural limb tremor, myoclonic jerks and quadriparesis. Subsequently her mental state improved and her tremor and weakness resolved. Over the following months, she developed progressive painful dystonia of her facial musculature and lower limbs. This gradually became generalized and associated with choreoathethosis in her limbs. In addition, she had increasing bradykinesia and rigidity, which responded poorly to levodopa treatment. Our case illustrates that while the myelin destruction occurs during the initial insult of the osmotic demyelinating process, its delayed clinical effects resulting from ineffective reorganization of neuronal structures may be progressive, evolve with time, and difficult to treat.

Disease Progression↗