scholarly journals Brugada Pattern Electrocardiogram Unmasked with Cocaine Ingestion

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
M. Chadi Alraies ◽  
Mohammed A. R. Chamsi-Pasha ◽  
Motaz Baibars ◽  
Abdul Hamid Alraiyes ◽  
Khaldoon Shaheen
Keyword(s):  
Myocardial Infarction ◽  
Central Nervous System ◽  
Nervous System ◽  
Cardiac Arrest ◽  
Ventricular Tachycardia ◽  
Psychomotor Agitation ◽  
Paranoid Ideation ◽  
Generalized Seizures ◽  
Electrocardiogram Ecg ◽  
Brugada Pattern

Cocaine is considered a leading cause of drug-related deaths. This is usually sudden, unwitnessed, and without prodromal features. It has been reported that in-hospital mortality is close to 2%. Cocaine has powerful central nervous system effects1and acute cocaine overdose has been associated with hyperthermia, agitation, paranoid ideation, status epilepticus, ventricular fibrillation, ventricular tachycardia, and myocardial infarction (MI). The mechanisms of cocaine-related death remain poorly understood. We report a patient who survived massive cocaine ingestion with psychomotor agitation and generalized seizures followed by asystolic cardiac arrest and transient Brugada pattern on electrocardiogram (ECG).

Neuropathologic Findings in a Child with a Novel Variant of TBCK-Related Encephaloneuronopathy

2019 ◽  
Vol 18 (03) ◽  
pp. 148-156
Author(s):  
Sonja Chen ◽  
Fouad Zakka ◽  
Salwa Khedr ◽  
Shamlal Mangray ◽  
Lauren Massingham ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
White Matter ◽  
Developmental Delays ◽  
Cerebral White Matter ◽  
Heterozygous Mutation ◽  
Generalized Seizures ◽  
Novel Variant ◽  
White Matter Development ◽  
Venous Angiomas

AbstractA 3-year-old girl with developmental delays, hypotonia, and generalized seizures was diagnosed with a novel variant of a heterozygous mutation in the TBC1 domain containing kinase (TBCK) gene. Postmortem findings revealed severe hypotrophy of cerebral white matter, hypogenesis of the corpus callosum with reduced myelination and oligodendrocyte populations, and reactive gliosis, and venous angiomas of the cerebrum, brainstem, and cerebellum white matter. This report is the first to link a TBCK gene mutation to impaired white matter development with the targeting of central nervous system myelin and oligodendrocytes. The mechanism may involve inhibition of signaling through (mTORC1).

THROMBOCYTOSIS, CENTRAL NERVOUS SYSTEM DISEASE, AND MYOCARDIAL INFARCTION PATTERN IN INFANCY

PEDIATRICS ◽  
1966 ◽  
Vol 38 (4) ◽  
pp. 629-636
Author(s):  
Shyamal K. Sanyal ◽  
Richard B. Yules ◽  
Arthur I. Eidelman ◽  
Norman S. Talner
Keyword(s):  
Myocardial Infarction ◽  
Central Nervous System ◽  
Blood Flow ◽  
Nervous System ◽  
Coronary Blood Flow ◽  
Central Nervous System Disease ◽  
Neurological Symptoms ◽  
Nervous System Disease ◽  
System Disease

Two infants with thrombocytosis and significant neurological symptoms are presented. The electrocardiographic and vectorcardiographic findings in both suggested apical myocardial infarction. The isoenzyme studies done in one infant, however, did not support this diagnosis. This observation raises the possibility that the electrocardiographic and vectorcardiographic abnormalities may be due to associated central nervous system disease rather than due to a compromised coronary blood flow.

scholarly journals Scavenging superoxide selectively in mouse forebrain is associated with improved cardiac function and survival following myocardial infarction

2009 ◽  
Vol 296 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
Timothy E. Lindley ◽  
David W. Infanger ◽  
Mark Rishniw ◽  
Yi Zhou ◽  
Marc F. Doobay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Central Nervous System ◽  
Nervous System ◽  
Gene Transfer ◽  
Cardiac Function ◽  
Myocardial Function ◽  
Critical Role ◽  
Coronary Artery Ligation ◽  
Control Vector

Dysregulation in central nervous system (CNS) signaling that results in chronic sympathetic hyperactivity is now recognized to play a critical role in the pathogenesis of heart failure (HF) following myocardial infarction (MI). We recently demonstrated that adenovirus-mediated gene transfer of cytoplasmic superoxide dismutase (Ad-Cu/ZnSOD) to forebrain circumventricular organs, unique sensory structures that lack a blood-brain barrier and link peripheral blood-borne signals to central nervous system cardiovascular circuits, inhibits both the MI-induced activation of these central signaling pathways and the accompanying sympathoexcitation. Here, we tested the hypothesis that this forebrain-targeted reduction in oxidative stress translates into amelioration of the post-MI decline in myocardial function and increase in mortality. Adult C57BL/6 mice underwent left coronary artery ligation or sham surgery along with forebrain-targeted gene transfer of Ad-Cu/ZnSOD or a control vector. The results demonstrate marked MI-induced increases in superoxide radical formation in one of these forebrain regions, the subfornical organ (SFO). Ad-Cu/ZnSOD targeted to this region abolished the increased superoxide levels and led to significantly improved myocardial function compared with control vector-treated mice. This was accompanied by diminished levels of cardiomyocyte apoptosis in the Ad-Cu/ZnSOD but not the control vector-treated group. These effects of superoxide scavenging with Ad-Cu/ZnSOD in the forebrain paralleled increased post-MI survival rates compared with controls. This suggests that oxidative stress in the SFO plays a critical role in the deterioration of cardiac function following MI and underscores the promise of CNS-targeted antioxidant therapy for the treatment of MI-induced HF.

Central nervous system tolerance to cardiac arrest during profound hypothermia

1975 ◽  
Vol 18 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Gary S. Kopf ◽  
David M. Mirvis ◽  
Ronald E. Myers
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cardiac Arrest ◽  
Profound Hypothermia

scholarly journals Cardiac Arrest/Cardiopulmonary Resuscitation Increases Anxiety-Like Behavior and Decreases Social Interaction

2004 ◽  
Vol 24 (4) ◽  
pp. 372-382 ◽  
Author(s):  
Gretchen N. Neigh ◽  
Julia Kofler ◽  
Jessica L. Meyers ◽  
Valerie Bergdall ◽  
Krista M. D. La Perle ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cardiac Arrest ◽  
Social Interaction ◽  
Cardiopulmonary Resuscitation ◽  
Organ Damage ◽  
Central Nervous System Damage ◽  
Sensorimotor Deficits ◽  
Peripheral Organs ◽  
Behavioral Impairments

Advances in medical technology have increased the number of individuals who survive cardiac arrest/cardiopulmonary resuscitation (CPR). This increased incidence of survival has created a population of patients with behavioral and physiologic impairments. We used temperature manipulations to characterize the contribution of central nervous system damage to behavioral deficits elicited by 8 minutes of cardiac arrest/CPR in a mouse model. Once sensorimotor deficits were resolved, we examined anxiety-like behavior with the elevated plus maze and social interaction with an ovariectomized female. We hypothesized that anxiety-like behavior would increase and social interaction would decrease in mice subjected to cardiac arrest/CPR and that these changes would be attributable to central nervous system damage rather than damage to peripheral organs or changes orchestrated by the administration of epinephrine. Mice that were subjected to cardiac arrest/CPR while the peripheral organs, but not the brain, were protected by hypothermia exhibited increased anxiety-like behavior and decreased social interaction, whereas mice with hypothermic brains and peripheral organs during cardiac arrest/CPR did not exhibit behavioral impairments. The present study demonstrates that central nervous system damage from cardiac arrest/CPR results in increased anxiety and decreased social interaction and that these behavioral changes are not attributed to underlying sensorimotor deficits, dynamics of arrest and CPR, or peripheral organ damage.

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