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Metabolic Syndrome and Its Effect on the Brain: Possible Mechanism

Arshad N', Lin TS, Yahaya MF

CNS Neurol Disord Drug Targets, 2018;17(8):595-603.
PMID: 30047340 DOI: 10.2174/1871527317666180724143258

BACKGROUND & OBJECTIVE: Metabolic syndrome (MetS) is an interconnected group of physiological, biochemical, clinical and metabolic factors that directly increase the risk of cardiovascular disease, type 2 diabetes mellitus (T2DM) and mortality. Rising evidence suggests that MetS plays a significant role in the progression of Alzheimer's disease and other neurodegenerative diseases. Nonetheless, the factors linking this association has not yet been elucidated. As we are facing an increasing incidence of obesity and T2DM in all stages of life, understanding the association of MetS and neurodegenerative diseases is crucial to lessen the burden of the disease.
CONCLUSION: In this review, we will discuss the possible mechanisms which may relate the association between MetS and cognitive decline which include vascular damages, elevation of reactive oxygen species (ROS), insulin resistance and low-grade inflammation.

Matched MeSH terms: Brain/physiopathology*
Fulltext Epilepsy with myoclonic absences

Manonmani V, Wallace SJ

Arch Dis Child, 1994 Apr;70(4):288-90.
PMID: 8185360

The cases are described of eight children, five of them girls, who had epilepsy with myoclonic absences. The mean age of onset was 4.9 years. Brief episodes of loss of awareness with bilateral clonic jerking of the upper limbs were associated with rhythmic 3 cycles/second spike-wave discharges on electroencephalogram. Generalised tonic-clonic or astatic seizures, or both, also occurred in seven patients. All now have learning difficulties, and seven have behavioural problems. Conventional treatment for absences was effective in only two children. Of six patients treated with lamotrigine, five have improved substantially, but only one is in sustained complete remission. One recently diagnosed patient continues to have frequent myoclonic absences. As the response to treatment and long term outcome are much poorer, it is important to differentiate myoclonic absences from typical childhood absence epilepsy.

Matched MeSH terms: Brain/physiopathology
Modeling Parkinson's Disease in Zebrafish

Najib NHM, Nies YH, Abd Halim SAS, Yahaya MF, Das S, Lim WL, et al.

CNS Neurol Disord Drug Targets, 2020;19(5):386-399.
PMID: 32640968 DOI: 10.2174/1871527319666200708124117

Parkinson's Disease (PD) is one of the most common neurodegenerative disorders that affects the motor system, and includes cardinal motor symptoms such as resting tremor, cogwheel rigidity, bradykinesia and postural instability. Its prevalence is increasing worldwide due to the increase in life span. Although, two centuries since the first description of the disease, no proper cure with regard to treatment strategies and control of symptoms could be reached. One of the major challenges faced by the researchers is to have a suitable research model. Rodents are the most common PD models used, but no single model can replicate the true nature of PD. In this review, we aim to discuss another animal model, the zebrafish (Danio rerio), which is gaining popularity. Zebrafish brain has all the major structures found in the mammalian brain, with neurotransmitter systems, and it also possesses a functional blood-brain barrier similar to humans. From the perspective of PD research, the zebrafish possesses the ventral diencephalon, which is thought to be homologous to the mammalian substantia nigra. We summarize the various zebrafish models available to study PD, namely chemical-induced and genetic models. The zebrafish can complement the use of other animal models for the mechanistic study of PD and help in the screening of new potential therapeutic compounds.

Matched MeSH terms: Brain/physiopathology*
Behavioral effects of deep brain stimulation of different areas of the Papez circuit on memory- and anxiety-related functions

Hescham S, Jahanshahi A, Meriaux C, Lim LW, Blokland A, Temel Y

Behav Brain Res, 2015 Oct 1;292:353-60.
PMID: 26119240 DOI: 10.1016/j.bbr.2015.06.032

Deep brain stimulation (DBS) has gained interest as a potential therapy for advanced treatment-resistant dementia. However, possible targets for DBS and the optimal stimulation parameters are not yet clear. Here, we compared the effects of DBS of the CA1 sub-region of the hippocampus, mammillothalamic tract, anterior thalamic nucleus, and entorhinal cortex in an experimental rat model of dementia. Rats with scopolamine-induced amnesia were assessed in the object location task with different DBS parameters. Moreover, anxiety-related side effects were evaluated in the elevated zero maze and open field. After sacrifice, we applied c-Fos immunohistochemistry to assess which memory-related regions were affected by DBS. When comparing all structures, DBS of the entorhinal cortex and CA1 sub-region was able to restore memory loss when a specific set of stimulation parameters was used. No anxiety-related side effects were found following DBS. The beneficial behavioral performance of CA1 DBS rats was accompanied with an activation of cells in the anterior cingulate gyrus. Therefore, we conclude that acute CA1 DBS restores memory loss possibly through improved attentional and cognitive processes in the limbic cortex.

Matched MeSH terms: Brain/physiopathology*
Fulltext Electrical stimulation alleviates depressive-like behaviors of rats: investigation of brain targets and potential mechanisms

Lim LW, Prickaerts J, Huguet G, Kadar E, Hartung H, Sharp T, et al.

Transl Psychiatry, 2015;5:e535.
PMID: 25826110 DOI: 10.1038/tp.2015.24

Deep brain stimulation (DBS) is a promising therapy for patients with refractory depression. However, key questions remain with regard to which brain target(s) should be used for stimulation, and which mechanisms underlie the therapeutic effects. Here, we investigated the effect of DBS, with low- and high-frequency stimulation (LFS, HFS), in different brain regions (ventromedial prefrontal cortex, vmPFC; cingulate cortex, Cg; nucleus accumbens (NAc) core or shell; lateral habenula, LHb; and ventral tegmental area) on a variety of depressive-like behaviors using rat models. In the naive animal study, we found that HFS of the Cg, vmPFC, NAc core and LHb reduced anxiety levels and increased motivation for food. In the chronic unpredictable stress model, there was a robust depressive-like behavioral phenotype. Moreover, vmPFC HFS, in a comparison of all stimulated targets, produced the most profound antidepressant effects with enhanced hedonia, reduced anxiety and decreased forced-swim immobility. In the following set of electrophysiological and histochemical experiments designed to unravel some of the underlying mechanisms, we found that vmPFC HFS evoked a specific modulation of the serotonergic neurons in the dorsal raphe nucleus (DRN), which have long been linked to mood. Finally, using a neuronal mapping approach by means of c-Fos expression, we found that vmPFC HFS modulated a brain circuit linked to the DRN and known to be involved in affect. In conclusion, HFS of the vmPFC produced the most potent antidepressant effects in naive rats and rats subjected to stress by mechanisms also including the DRN.

Matched MeSH terms: Brain/physiopathology*
Fulltext A Review on the Relationship between Tocotrienol and Alzheimer Disease

Chin KY, Tay SS

Nutrients, 2018 Jul 09;10(7).
PMID: 29987193 DOI: 10.3390/nu10070881

Alzheimer’s disease (AD) is plaguing the aging population worldwide due to its tremendous health care and socioeconomic burden. Current treatment of AD only offers symptomatic relief to patients. Development of agents targeting specific pathologies of AD is very slow. Tocotrienol, a member of the vitamin E family, can tackle many aspects of AD, such as oxidative stress, mitochondrial dysfunction and abnormal cholesterol synthesis. This review summarizes the current evidence on the role of tocotrienol as a neuroprotective agent. Preclinical studies showed that tocotrienol could reduce oxidative stress by acting as a free-radical scavenger and promoter of mitochondrial function and cellular repair. It also prevented glutamate-induced neurotoxicity in the cells. Human epidemiological studies showed a significant inverse relationship between tocotrienol levels and the occurrence of AD. However, there is no clinical trial to support the claim that tocotrienol can delay or prevent the onset of AD. As a conclusion, tocotrienol has the potential to be developed as an AD-preventing agent but further studies are required to validate its efficacy in humans.

Matched MeSH terms: Brain/physiopathology
Focal epilepsy recruiting a generalised network of juvenile myoclonic epilepsy: a case report

Khaing M, Lim KS, Tan CT

Epileptic Disord, 2014 Sep;16(3):370-4.
PMID: 25166001 DOI: 10.1684/epd.2014.0672

We report a patient with juvenile myoclonic epilepsy who subsequently developed temporal lobe epilepsy, which gradually became clinically dominant. Video telemetry revealed both myoclonic seizures and temporal lobe seizures. The temporal lobe seizures were accompanied by a focal recruiting rhythm with rapid generalisation on EEG, in which the ictal EEG pattern during the secondary generalised phase was morphologically similar to the ictal pattern during myoclonic seizures. The secondary generalised seizures of the focal epilepsy responded to sodium valproate, similar to the myoclonic epilepsy. In this rare case of coexistent Juvenile Myoclonic Epilepsy and Temporal lobe epilepsy, the possibility of focal epilepsy recruiting a generalised epileptic network was proposed and discussed.

Matched MeSH terms: Brain/physiopathology*
Periodic lateralized epileptiform discharges in neuropsychiatric lupus: association with cerebritis in magnetic resonance imaging and resolution after intravenous immunoglobulin

Lim KS, Cheong KL, Tan CT

Lupus, 2010 May;19(6):748-52.
PMID: 20133346 DOI: 10.1177/0961203309351539

A 13-year-old girl with a known diagnosis of systemic lupus erythematosus presented with seizures and psychosis. An electroencephalogram (EEG) revealed continuous, non-evolving periodic lateralized epileptiform discharges (PLEDs) in the left temporal region, which did not resolve with benzodiazepine. A magnetic resonance imaging (MRI) brain scan demonstrated a focal hyperintensity in the left medial temporal and left occipital lobes, left thalamus and bilateral cerebellar white matter, with evidence of vasculitis in the magnetic resonance angiography. Intravenous immunoglobulin was given because of failed steroid therapy, which resulted in a full resolution of clinical, EEG and MRI abnormalities. Lupus cerebritis should be considered as a possible aetiology in PLEDs, and immunoglobulin can be effective in neuropsychiatric lupus.

Matched MeSH terms: Brain/physiopathology
48-hour video-EEG monitoring for epilepsy presurgical evaluation is cost-effective and safe in resource-limited setting

Lim KS, Fong SL, Thuy Le MA, Ahmad Bazir S, Narayanan V, Ismail N, et al.

Epilepsy Res, 2020 05;162:106298.
PMID: 32172144 DOI: 10.1016/j.eplepsyres.2020.106298

INTRODUCTION: Video-EEG monitoring is one of the key investigations in epilepsy pre-surgical evaluation but limited by cost. This study aimed to determine the efficacy and safety of a 48-hour (3-day) video EEG monitoring, with rapid pre-monitoring antiepileptic drugs withdrawal.
MATERIAL AND METHODS: This is a retrospective study of epilepsy cases with VEM performed in University Malaya Medical Center (UMMC), Kuala Lumpur, from January 2012 till August 2016.
RESULTS: A total of 137 cases were included. The mean age was 34.5 years old (range 15-62) and 76 (55.8 %) were male. On the first 24 -h of recording (D1), 81 cases (59.1 %) had seizure occurrence, and 109 (79.6 %) by day 2 (D2). One-hundred and nine VEMs (79.6 %) were diagnostic, in guiding surgical decision or further investigations. Of these, 21 had less than 2 seizures recorded in the first 48 h but were considered as diagnostic because of concordant interictal ± ictal activities, or a diagnosis such as psychogenic non-epileptic seizure was made. Twenty-eight patients had extension of VEM for another 24-48 h, and 11 developed seizures during the extension period. Extra-temporal lobe epilepsy and seizure frequency were significant predictors for diagnostic 48 -h VEM. Three patients developed complications, including status epilepticus required anaesthetic agents (1), seizure clusters (2) with postictal psychosis or dysphasia, and all recovered subsequently.
CONCLUSIONS: 48-h video EEG monitoring is cost-effective in resource limited setting.

Matched MeSH terms: Brain/physiopathology
Neuroimaging in refractory epilepsy. Current practice and evolving trends

Ramli N, Rahmat K, Lim KS, Tan CT

Eur J Radiol, 2015 Sep;84(9):1791-800.
PMID: 26187861 DOI: 10.1016/j.ejrad.2015.03.024

Identification of the epileptogenic zone is of paramount importance in refractory epilepsy as the success of surgical treatment depends on complete resection of the epileptogenic zone. Imaging plays an important role in the locating and defining anatomic epileptogenic abnormalities in patients with medically refractory epilepsy. The aim of this article is to present an overview of the current MRI sequences used in epilepsy imaging with special emphasis of lesion seen in our practices. Optimisation of epilepsy imaging protocols are addressed and current trends in functional MRI sequences including MR spectroscopy, diffusion tensor imaging and fusion MR with PET and SPECT are discussed.

Matched MeSH terms: Brain/physiopathology
Fulltext Functional dyspepsia

Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ

Lancet, 2020 11 21;396(10263):1689-1702.
PMID: 33049222 DOI: 10.1016/S0140-6736(20)30469-4

Dyspepsia is a complex of symptoms referable to the gastroduodenal region of the gastrointestinal tract and includes epigastric pain or burning, postprandial fullness, or early satiety. Approximately 80% of individuals with dyspepsia have no structural explanation for their symptoms and have functional dyspepsia. Functional dyspepsia affects up to 16% of otherwise healthy individuals in the general population. Risk factors include psychological comorbidity, acute gastroenteritis, female sex, smoking, use of non-steroidal anti-inflammatory drugs, and Helicobacter pylori infection. The pathophysiology remains incompletely understood, but it is probably related to disordered communication between the gut and the brain, leading to motility disturbances, visceral hypersensitivity, and alterations in gastrointestinal microbiota, mucosal and immune function, and CNS processing. Although technically a normal endoscopy is required to diagnose functional dyspepsia, the utility of endoscopy in all patients with typical symptoms is minimal; its use should be restricted to people aged 55 years and older, or to those with concerning features, such as weight loss or vomiting. As a result of our incomplete understanding of its pathophysiology, functional dyspepsia is difficult to treat and, in most patients, the condition is chronic and the natural history is one of fluctuating symptoms. Eradication therapy should be offered to patients with functional dyspepsia who test positive for Helicobacter pylori. Other therapies with evidence of effectiveness include proton pump inhibitors, histamine-2 receptor antagonists, prokinetics, and central neuromodulators. The role of psychological therapies is uncertain. As our understanding of the pathophysiology of functional dyspepsia increases, it is probable that the next decade will see the emergence of truly disease-modifying therapies for the first time.

Matched MeSH terms: Brain/physiopathology*
Incremental benefits of EEG informed fMRI in the study of disorders related to meso-corticolimbic dopamine pathway dysfunction: A systematic review of recent literature

Syed Nasser N, Ibrahim B, Sharifat H, Abdul Rashid A, Suppiah S

J Clin Neurosci, 2019 Jul;65:87-99.
PMID: 30955950 DOI: 10.1016/j.jocn.2019.03.054

Functional magnetic resonance imaging (fMRI) is a non-invasive imaging modality that enables the assessment of neural connectivity and oxygen utility of the brain using blood oxygen level dependent (BOLD) imaging sequence. Electroencephalography (EEG), on the other hands, looks at cortical electrical impulses of the brain thus detecting brainwave patterns during rest and thought processing. The combination of these two modalities is called fMRI with simultaneous EEG (fMRI-EEG), which has emerged as a new tool for experimental neuroscience assessments and has been applied clinically in many settings, most commonly in epilepsy cases. Recent advances in imaging has led to fMRI-EEG being utilized in behavioural studies which can help in giving an objective assessment of ambiguous cases and help in the assessment of response to treatment by providing a non-invasive biomarker of the disease processes. We aim to review the role and interpretation of fMRI-EEG in studies pertaining to psychiatric disorders and behavioral abnormalities.

Matched MeSH terms: Brain/physiopathology
Electroencephalography-detected neurophysiology of internet addiction disorder and internet gaming disorder in adolescents - A review

Sharifat H, Suppiah S

Med J Malaysia, 2021 05;76(3):401-413.
PMID: 34031341

INTRODUCTION: Internet Addiction Disorder (IAD) is an umbrella term for various types of Internet-based behavioural addiction, whereas Internet Gaming Disorder (IGD) addresses a specific type of IAD that is postulated to be due to a lack of control in impulse inhibition. IGD is an area of concern in the Diagnostic and Statistics Manual of Mental Disorders (DSM-5), which can be objectively assessed by dysfunctional behaviour and the increasing time of being online, particularly during the COVID-19 pandemic. Electroencephalography (EEG) identifies amplitude changes in the evoked response potential (ERP) among IGDs, correlated with underlying comorbidities.
MATERIALS AND METHODS: A scoping review was performed to elaborate on the research regarding resting-state EEG and task-based EEG, particularly for Go/No-go paradigms pertaining to subjects with IAD or specifically IGD. The role of EEG was identified in its diagnostic capability to identify the salient changes that occurred in the response to reward network and the executive control network, using restingstate and task-based EEG. The implication of using EEG in monitoring the therapy for IAD and IGD was also reviewed.
RESULTS: EEG generally revealed reduced beta waves and increased theta waves in addicts. IGD with depression demonstrated increased theta and decreased alpha waves. Whereas increased P300, a late cognitive ERP component, was frequently associated with impaired excessive allocation of attentional resources of the IAD towards addiction-specific cues. IGD had increased whole brain delta waves at baseline, which showed significant reduction post therapy.
CONCLUSION: EEG can identify distinct neurophysiological changes among Internet Addiction Disorder and Internet Gaming Disorder that are akin to substance abuse disorders.

Matched MeSH terms: Brain/physiopathology*
Fulltext Management of acute intracerebral haemorrhage - an update

Law ZK, Appleton JP, Bath PM, Sprigg N

Clin Med (Lond), 2017 Apr;17(2):166-172.
PMID: 28365631 DOI: 10.7861/clinmedicine.17-2-166

Managing acute intracerebral haemorrhage is a challenging task for physicians. Evidence shows that outcome can be improved with admission to an acute stroke unit and active care, including urgent reversal of anticoagulant effects and, potentially, intensive blood pressure reduction. Nevertheless, many management issues remain controversial, including the use of haemostatic therapy, selection of patients for neurosurgery and neurocritical care, the extent of investigations for underlying causes and the benefit versus risk of restarting antithrombotic therapy after an episode of intracerebral haemorrhage.

Matched MeSH terms: Brain/physiopathology
Fulltext Alzheimer's disease-like perturbations in HIV-mediated neuronal dysfunctions: understanding mechanisms and developing therapeutic strategies

Jha NK, Sharma A, Jha SK, Ojha S, Chellappan DK, Gupta G, et al.

Open Biol, 2020 Dec;10(12):200286.
PMID: 33352062 DOI: 10.1098/rsob.200286

Excessive exposure to toxic substances or chemicals in the environment and various pathogens, including viruses and bacteria, is associated with the onset of numerous brain abnormalities. Among them, pathogens, specifically viruses, elicit persistent inflammation that plays a major role in Alzheimer's disease (AD) as well as dementia. AD is the most common brain disorder that affects thought, speech, memory and ability to execute daily routines. It is also manifested by progressive synaptic impairment and neurodegeneration, which eventually leads to dementia following the accumulation of Aβ and hyperphosphorylated Tau. Numerous factors contribute to the pathogenesis of AD, including neuroinflammation associated with pathogens, and specifically viruses. The human immunodeficiency virus (HIV) is often linked with HIV-associated neurocognitive disorders (HAND) following permeation through the blood-brain barrier (BBB) and induction of persistent neuroinflammation. Further, HIV infections also exhibited the ability to modulate numerous AD-associated factors such as BBB regulators, members of stress-related pathways as well as the amyloid and Tau pathways that lead to the formation of amyloid plaques or neurofibrillary tangles accumulation. Studies regarding the role of HIV in HAND and AD are still in infancy, and potential link or mechanism between both is not yet established. Thus, in the present article, we attempt to discuss various molecular mechanisms that contribute to the basic understanding of the role of HIV-associated neuroinflammation in AD and HAND. Further, using numerous growth factors and drugs, we also present possible therapeutic strategies to curb the neuroinflammatory changes and its associated sequels.

Matched MeSH terms: Brain/physiopathology
Cardiorespiratory findings in epilepsy: A recent review on outcomes and pathophysiology

Akyüz E, Üner AK, Köklü B, Arulsamy A, Shaikh MF

J Neurosci Res, 2021 09;99(9):2059-2073.
PMID: 34109651 DOI: 10.1002/jnr.24861

Epilepsy is a debilitating disorder of uncontrollable recurrent seizures that occurs as a result of imbalances in the brain excitatory and inhibitory neuronal signals, that could stem from a range of functional and structural neuronal impairments. Globally, nearly 70 million people are negatively impacted by epilepsy and its comorbidities. One such comorbidity is the effect epilepsy has on the autonomic nervous system (ANS), which plays a role in the control of blood circulation, respiration and gastrointestinal function. These epilepsy-induced impairments in the circulatory and respiratory systems may contribute toward sudden unexpected death in epilepsy (SUDEP). Although, various hypotheses have been proposed regarding the role of epilepsy on ANS, the linking pathological mechanism still remains unclear. Channelopathies and seizure-induced damages in ANS-control brain structures were some of the causal/pathological candidates of cardiorespiratory comorbidities in epilepsy patients, especially in those who were drug resistant. However, emerging preclinical research suggest that neurotransmitter/receptor dysfunction and synaptic changes in the ANS may also contribute to the epilepsy-related autonomic disorders. Thus, pathological mechanisms of cardiorespiratory dysfunction should be elucidated by considering the modifications in anatomy and physiology of the autonomic system caused by seizures. In this regard, we present a comprehensive review of the current literature, both clinical and preclinical animal studies, on the cardiorespiratory findings in epilepsy and elucidate the possible pathological mechanisms of these findings, in hopes to prevent SUDEP especially in patients who are drug resistant.

Matched MeSH terms: Brain/physiopathology*
Fulltext Overlap of Bickerstaff brainstem encephalitis/Guillain-Barré syndrome simulating brain death

Tan CY, Ahmad SB, Goh KJ, Latif LA, Shahrizaila N

Neurol India, 2018 9 21;66(5):1475-1480.
PMID: 30233023 DOI: 10.4103/0028-3886.241342
Matched MeSH terms: Brain/physiopathology
Inter-hemispheric EEG coherence analysis in Parkinson's disease: assessing brain activity during emotion processing

Yuvaraj R, Murugappan M, Ibrahim NM, Sundaraj K, Omar MI, Mohamad K, et al.

J Neural Transm (Vienna), 2015 Feb;122(2):237-52.
PMID: 24894699 DOI: 10.1007/s00702-014-1249-4

Parkinson's disease (PD) is not only characterized by its prominent motor symptoms but also associated with disturbances in cognitive and emotional functioning. The objective of the present study was to investigate the influence of emotion processing on inter-hemispheric electroencephalography (EEG) coherence in PD. Multimodal emotional stimuli (happiness, sadness, fear, anger, surprise, and disgust) were presented to 20 PD patients and 30 age-, education level-, and gender-matched healthy controls (HC) while EEG was recorded. Inter-hemispheric coherence was computed from seven homologous EEG electrode pairs (AF3-AF4, F7-F8, F3-F4, FC5-FC6, T7-T8, P7-P8, and O1-O2) for delta, theta, alpha, beta, and gamma frequency bands. In addition, subjective ratings were obtained for a representative of emotional stimuli. Interhemispherically, PD patients showed significantly lower coherence in theta, alpha, beta, and gamma frequency bands than HC during emotion processing. No significant changes were found in the delta frequency band coherence. We also found that PD patients were more impaired in recognizing negative emotions (sadness, fear, anger, and disgust) than relatively positive emotions (happiness and surprise). Behaviorally, PD patients did not show impairment in emotion recognition as measured by subjective ratings. These findings suggest that PD patients may have an impairment of inter-hemispheric functional connectivity (i.e., a decline in cortical connectivity) during emotion processing. This study may increase the awareness of EEG emotional response studies in clinical practice to uncover potential neurophysiologic abnormalities.

Matched MeSH terms: Brain/physiopathology*
Fulltext On the analysis of EEG power, frequency and asymmetry in Parkinson's disease during emotion processing

Yuvaraj R, Murugappan M, Mohamed Ibrahim N, Iqbal M, Sundaraj K, Mohamad K, et al.

Behav Brain Funct, 2014;10:12.
PMID: 24716619 DOI: 10.1186/1744-9081-10-12

While Parkinson's disease (PD) has traditionally been described as a movement disorder, there is growing evidence of disruption in emotion information processing associated with the disease. The aim of this study was to investigate whether there are specific electroencephalographic (EEG) characteristics that discriminate PD patients and normal controls during emotion information processing.

Matched MeSH terms: Brain/physiopathology*
Emotion processing in Parkinson's disease: an EEG spectral power study

Yuvaraj R, Murugappan M, Omar MI, Ibrahim NM, Sundaraj K, Mohamad K, et al.

Int J Neurosci, 2014 Jul;124(7):491-502.
PMID: 24168328 DOI: 10.3109/00207454.2013.860527

Although an emotional deficit is a common finding in Parkinson's disease (PD), its neurobiological mechanism on emotion recognition is still unknown. This study examined the emotion processing deficits in PD patients using electroencephalogram (EEG) signals in response to multimodal stimuli.

Matched MeSH terms: Brain/physiopathology*

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