Introduction: A sudden loss of consciousness followed by abnormal movements can be ictal or syncopal in origin. Transient response by the brain to sudden decrease of blood flow may cause sudden loss of consciousness followed by abnormal movements that mimic seizure. Dysrhythmia is one of the important and critical reasons of such events that should be differentiated from seizure.
Case Presentation: In this case report we describe a 55 year-old woman admitted to our emergency department first with the impression of seizure. Eventually, it was realized that she had suffered from brain hypo-perfusion secondary to hypokalemia induced arrhythmia. Her arrhythmia was managed by unsynchronized biphasic shock in acute phase and also potassium replacement. She was then admitted to the CCU (Coronary Care Unit) where she received further care for medical management and drug dose adjustment and was discharged 4 days later.
Conclusions: Syncope from arrhythmia most commonly results from ventricular tachycardia, which accounts for 11% of all cases of syncope. Torsades de point is a unique type of ventricular tachycardia, characterized by QRS complexes of changing amplitude proceeded by prolonged QT intervals and almost often followed by loss of consciousness and also seizure like movements. Prolonged QT interval which is an important provocative factor for torsades de point commonly results from interactions between drug therapy, myocardial ischemia, and electrolyte disturbances such as hypokalemia or hypomagnesaemia. Changes in the extracellular potassium level have predominant and profound influences on the function of the cardiovascular system that may provoke fatal demonstrations such as QT prolongation, ventricular arrhythmia and even cardiac arrest. Electrolyte assessment is particularly important in certain patient populations, such as the elderly in whom a variety of pathological states or conditions like dehydration or renal failure are more common. Early identification and correction of these disturbances are necessary to control either seizures or seizure-like movements and prevent permanent brain damage, as anticonvulsants alone are generally ineffective.
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http://dx.doi.org/10.5812/traumamon.12016 | DOI Listing |
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Alamiri, MD, ABPN, ScD, Al-Manara CAP Centre, Kuwait Centre for Mental Health (KCMH), Shuwaikh, State of Kuwait.
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Institute of Pharmaceutical Pharmacology, School of Pharmacy, University of South China, Hengyang 421001, China.
Neurodegenerative diseases (NDDs), mainly including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), and Alzheimer's disease (AD), are sporadic and rare genetic disorders of the central nervous system. A key feature of these conditions is the slow accumulation of misfolded protein deposits in brain neurons, the excessive aggregation of which leads to neurotoxicity and further disorders of the nervous system.
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Department of Theory and Bio-Systems, Max Planck Institute of Colloids and Interfaces, 14476, Potsdam, Germany.
Neurodegeneration in Huntington's disease (HD) is accompanied by the aggregation of fragments of the mutant huntingtin protein, a biomarker of disease progression. A particular pathogenic role has been attributed to the aggregation-prone huntingtin exon 1 (HTTex1), generated by aberrant splicing or proteolysis, and containing the expanded polyglutamine (polyQ) segment. Unlike amyloid fibrils from Parkinson's and Alzheimer's diseases, the atomic-level structure of HTTex1 fibrils has remained unknown, limiting diagnostic and treatment efforts.
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