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The Novelty of Bupropion As a Dopaminergic Antidepressant for the Treatment of Adult Attention Deficit Hyperactive Disorder

Deang KT, Sidi H, Zakaria H, Adam RL, Das S, Hatta NH, et al.

Curr Drug Targets, 2019;20(2):210-219.
PMID: 28494748 DOI: 10.2174/1389450118666170511145628

Attention deficit hyperactive disorder (ADHD), a hyperactivity disorder prevalent among children may continue as an adulthood attention deficit. To date, treating an individual with an adult ADHD may be an arduous task as it involves numerous challenges, which include a need for high index of suspicion to diagnose this medical condition. Many psychiatric disorders masquerade as ADHD and delay the necessary assessment and proper treatment for this debilitating medical disorder. Adult ADHD is often misdiagnosed (or under diagnosed) due to the fact that this medical condition is being masked by the patients' high level of intellectual achievement. As the ADHD in adult persists, it may end-up with impairment in the personal-social-occupational function in which the management becomes a great challenge. The treatment of ADHD can be optimized by using various drugs targets agents like norepinephrine-dopamine reuptake inhibitor (NDRI), with or without psycho stimulants like methylphenidate, which is marketed as Ritalin. Bupropion, an NDRI has a novel effect on ADHD as the molecule exerts its effects by modulating the reward-pleasure mesolimbic dopaminergic system and at the same time regulates the elevating mood dimension of the noradrenergic neurotransmission. The role of Bupropion in the neural and psychopharmacological perspective treatment of ADHD was deliberated. The present review highlights the novel effects of Bupropion in ADHD treatment, together with the help of other successful bio-psycho-social measures. This may be of immense benefit to the psychiatrists for treating their patients.
Subduing the Green-eyed Monster: Bridging the Psychopharmacological and Psychosocial Treatment Perspective in Understanding Pathological Jealousy

Samad FDA, Sidi H, Kumar J, Das S, Midin M, Hatta NH

Curr Drug Targets, 2019;20(2):201-209.
PMID: 28675999 DOI: 10.2174/1389450118666170704142708

Human being is not spared from a broad-ranged emotional state, including being jealous. Jealousy has both affective-cognitive and behavioural-evaluative dimension where the person perceives, or experiences a real threat on a valued relationship. As this complex emotion becomes irrational and not amenable to reason, it later transforms into a dangerously 'green-eyed monster'. This perilous situation which is viewed as pathological jealousy is a form of delusion, which is maintained by a fixed and false reasoning in an originally entrusted intimate relationship. Pathological jealousy is equally prevailing among both gender, and with a greater ubiquity among the geriatric population. The role of dopamine hyperactivity in the fronto-parietal-temporal region was implicated, with the anatomical mapping of the ventromedial prefrontal cortex (vmPFC), cingulate gyrus (CG), and amygdala involvement in the context of the disease's neurobiology. The etiology of pathological jealousy includes major psychiatric disorders, i.e. delusional disorder, schizophrenia, mood disorder, organic brain syndrome, and among others, the drug-induced psychosis. The role of relationship issues and psychodynamic perspective, i.e. psychological conflicts with dependence on a romantic partner, and low self-esteem are involved. Pathological jealousy inherits high-risk forensic psychiatry entanglement, which may warrant intensive intervention, including hospital admission and antipsychotic treatment. Treatment options include an early recognition, managing underlying neuropsychiatric disorders, psycho education, cognitive psychotherapy, and choosing an effective psychopharmacological agent. The management strategy may also resort to a geographical intervention, i.e. separation between both persons to complement the biological treatment.
Hypersexuality As a Neuropsychiatric Disorder: The Neurobiology and Treatment Options

Asiff M, Sidi H, Masiran R, Kumar J, Das S, Hatta NH, et al.

Curr Drug Targets, 2018;19(12):1391-1401.
PMID: 28325146 DOI: 10.2174/1389450118666170321144931

Hypersexuality refers to abnormally increased or extreme involvement in any sexual activity. It is clinically challenging, presents trans-diagnostically and there is extensive medical literature addressing the nosology, pathogenesis and neuropsychiatric aspects in this clinical syndrome. Classification includes deviant behaviours, diagnosable entities related to impulsivity, and obsessional phenomena. Some clinicians view an increase in sexual desire as 'normal' i.e. psychodynamic theorists consider it as egodefensive at times alleviating unconscious anxiety rooted in intrapsychic conflicts. We highlight hypersexuality as multi-dimensional involving an increase in sexual activity that is associated with distress and functional impairment. The aetiology of hypersexuality is multi-factorial with differential diagnoses that include major psychiatric disorders (e.g. bipolar disorder), adverse effects of treatments (e.g. levodopatreatment), substance-induced disorders (e.g. amphetamine substance use), neuropathological disorders (e.g. frontal lobe syndrome), among others. Numerous neurotransmitters are implicated in its pathogenesis, with dopamine and noradrenaline playing a crucial role in the neural reward pathways and emotionally- regulated limbic system neural circuits. The management of hypersexuality is determined by the principle of de causa effectu evanescent, if the causes are treated, the effect may disappear. We aim to review the role of pharmacological agents causing hypersexuality and centrally acting agents treating the associated underlying medical conditions. Bio-psycho-social determinants are pivotal in embracing the understanding and guiding management of this complex and multi-determined clinical syndrome.
Alcohol Addiction- Metabotropic Glutamate Receptor Subtype 5 and its Ligands: How They All Come Together?

Kumar J, Ismail Z, Hatta NH, Baharuddin N, Hapidin H, Get Bee YT, et al.

Curr Drug Targets, 2018;19(8):907-915.
PMID: 28494749 DOI: 10.2174/1389450118666170511144302

In the past decade, many studies have highlighted the role of metabotropic glutamate receptor subtype 5 (mGlu5) modulators in attenuating alcohol-related biological effects such as alcohol consumption, alcohol-seeking and relapse-like behaviors. Taken together, these findings suggest that pharmacological agents acting at mGlu5 could be promising tools in curbing inebriation. mGlu5s are present abundantly in brain regions known to be involved in emotion regulation, motivation and drug administration. On a cellular level, they are primarily located at the postsynaptic part of the neuron where the receptor is functionally linked to various downstream proteins that are involved in cell signaling and gene transcription that mediate the alcohol-induced neuroplasticity. As well, the discovery of a functional link between mGlu5 and a specific isozyme, Protein Kinase C epsilon (PKCε) in mediating the attenuating effects of selective negative allosteric modulators of mGlu5 such as methyl- 6(phenylethynyl)pyridine (MPEP) and 3-((2-methyl-4-thiazolyl)ethynyl)pyridine (MTEP) has sparked interesting speculations. In this article, we shall review the following: the effects of acute and chronic alcohol intake on mGlu5 signaling; the effects of mGlu5 ligands on alcohol-related neurobehavioral changes that are currently being studied both at pre-clinical and clinical stages; and the mechanisms underlying the pharmacological effects of these drugs.
Fulltext How Much Do We Know about the Biopsychosocial Predictors of Glycaemic Control? Age and Clinical Factors Predict Glycaemic Control, but Psychological Factors Do Not

Abdullah MFILB, Sidi H, Ravindran A, Gosse PJ, Kaunismaa ES, Mainland RL, et al.

J Diabetes Res, 2020;2020:2654208.
PMID: 32455131 DOI: 10.1155/2020/2654208

Objective: Diabetes mellitus is one of the most common noncommunicable diseases in Malaysia. It is associated with significant complications and a high cost of treatment, especially when glycaemic control is poor. Despite its negative impact on health, data is still lacking on the possible biopsychosocial predictors of poor glycaemic control among the diabetic population. This study is aimed at determining the prevalence of poor glycaemic control as well as its association with biopsychosocial factors such as personality traits, psychiatric factors, and quality of life (QOL) among Malaysian patients with diabetes.
Methods: A cross-sectional study was conducted at the Universiti Kebangsaan Malaysia Medical Centre (UKMMC) using outpatient population diabetic patients. Demographic data on social and clinical characteristics were collected from participants. Several questionnaires were administered, including the Beck Depression Inventory-II (BDI-II) to measure depressive symptoms, the Generalized Anxiety Disorder-7 (GAD-7) to assess anxiety symptoms, the Big Five Inventory (BFI) to evaluate personality traits, and the WHO Quality of Life-BREF (WHOQOL-BREF) to assess QOL. Multivariate binary logistic regression was performed to determine the predictors of poor glycaemic control.
Results: 300 patients with diabetes mellitus were recruited, with the majority (90%) having type 2 diabetes. In this population, the prevalence of poor glycaemic control (HbA1C ≥ 7.0%) was 69%, with a median HbA1C of 7.6% (IQR = 2.7). Longer duration of diabetes mellitus and a greater number of days of missed medications predicted poor glycaemic control, while older age and overall self-perception of QOL protected against poor glycaemic control. No psychological factors were associated with poor glycaemic control.
Conclusion: This study emphasizes the importance of considering the various factors that contribute to poor glycaemic control, such as duration of diabetes, medication adherence, age, and QOL. These findings should be used by clinicians, particularly when planning a multidisciplinary approach to the management of diabetes.
Fulltext Depression, anxiety, and associated factors in patients with diabetes: evidence from the anxiety, depression, and personality traits in diabetes mellitus (ADAPT-DM) study

Woon LS, Sidi HB, Ravindran A, Gosse PJ, Mainland RL, Kaunismaa ES, et al.

BMC Psychiatry, 2020 05 12;20(1):227.
PMID: 32397976 DOI: 10.1186/s12888-020-02615-y

BACKGROUND: Depression and anxiety are common psychiatric complications affecting patients with diabetes mellitus. However, data on the prevalence of depression, anxiety, and associated factors among Malaysian diabetic patients is scarce. The Anxiety, Depression, and Personality Traits in Diabetes Mellitus (ADAPT-DM) study aimed to determine the prevalence of depression and anxiety, and their associated factors in the Malaysian diabetic population.
METHODS: This cross-sectional study recruited 300 diabetic patients via convenience sampling from the Endocrine outpatient clinic of Universiti Kebangsaan Malaysia Medical Centre, a tertiary referral healthcare facility in Kuala Lumpur. Socio-demographic characteristics and clinical history were obtained from each participant. The Generalised Anxiety Disorder-7 (GAD-7) was administered to assess anxiety symptoms, the Beck Depression Inventory (BDI) to assess depressive symptoms, the Big Five Inventory (BFI) to evaluate personality traits, and the World Health Organization Quality of Life-BREF (WHOQOL-BREF) to measure quality of life (QOL). Stepwise multiple logistic regression analyses were performed to determine the association between various factors, and depression and anxiety.
RESULTS: The prevalence of depression was 20% (n = 60) while anxiety was 9% (n = 27). Co-morbid depression (adjusted odds ratio [OR] = 9.89, 95% confidence interval [CI] = 2.63-37.14, p = 0.001) and neuroticism (adjusted OR = 11.66, 95% CI = 2.69-50.47, p = 0.001) increased the odds of developing anxiety, while conscientiousness (adjusted OR = 0.45, 95% CI = 0.23-0.80, p = 0.004) and greater psychological-related QOL (adjusted OR = 0.47, 95% CI = 0.29-0.75, p = 0.002) were protective. Co-morbid anxiety (adjusted OR = 19.83, 95% CI = 5.63-69.92, p