A study of cognitive dysfunction in patients having carotid endarterectomy performed with regional anesthesia.

Background: In previous studies, we found that approximately 25% of patients having carotid endarterectomy with general anesthesia (CEA general) develop cognitive dysfunction compared with a surgical control Group 1 day and 1 mo after surgery. In this study, we tested the hypothesis that patients having CEA with regional anesthesia (CEA regional) will develop significant cognitive dysfunction 1 day after surgery compared with a control group of patients receiving sedation 1 day after surgery. We did not study persistence of dysfunction.

Prescription opioid abuse and dependence among physicians: hypotheses and treatment.

Physician impairment is a serious public health issue affecting physicians as well as their families, colleagues, and patients. Though physicians generally display healthier habits than members of the general population, overall rates of impairment are similar among both groups, and prescription drug abuse (including prescription opioids) is particularly problematic among physicians. The current review focuses mainly on prescription opioid abuse and dependence among physicians.

Methamphetamine causes microglial activation in the brains of human abusers.

Methamphetamine is a popular addictive drug whose use is associated with multiple neuropsychiatric adverse events and toxic to the dopaminergic and serotonergic systems of the brain. Methamphetamine-induced neuropathology is associated with increased expression of microglial cells that are thought to participate in either pro-toxic or protective mechanisms in the brain. Although reactive microgliosis has been observed in animal models of methamphetamine neurotoxicity, no study has reported on the status of microglial activation in human methamphetamine abusers.

Psychiatric research: psychoproteomics, degradomics and systems biology.

While proteomics has excelled in several disciplines in biology (cancer, injury and aging), neuroscience and psychiatryproteomic studies are still in their infancy. Several proteomic studies have been conducted in different areas of psychiatric disorders, including drug abuse (morphine, alcohol and methamphetamine) and other psychiatric disorders (depression, schizophrenia and psychosis). However, the exact cellular and molecular mechanisms underlying these conditions have not been fully investigated.

Psychoproteomic analysis of rat cortex following acute methamphetamine exposure.

Methamphetamine (METH) is recognized as one of the most abused psychostimulants in the United States. METH is an illicit drug that is known to exert neurotoxic effects on both dopaminergic and serotonergic neural systems both in vivo and in vitro. Our laboratory and others have been studying the biochemical mechanisms underlying METH-induced neurotoxicity.

Methadone- and heroin-related deaths in Florida.

Methadone is a potent synthetic opioid used for treatment of opioid dependence and chronic pain. Florida Department of Law Enforcement data were analyzed to examine trends in deaths related to or caused by methadone and/or heroin between 2001-2006. Results demonstrated that mortalities associated with methadone use increased steadily as mortalities associated with heroin decreased steadily.

Performance enhancing, non-prescription use of Ritalin: a comparison with amphetamines and cocaine.

Ritalin, known under chemical name methylphenidate (MPH), is a psychostimulant prescribed to treat attention-deficit/hyperactivity disorder (ADHD) and other conditions. Psychotropic effects and pharmacological pathways evoked by MPH are similar, but not identical to those produced by amphetamines and cocaine. Although not completely understood in detail, MPH psychostimulation is mediated by the increase of central dopamine (DA) and possibly norepinephrine (NE) and serotonin (ST) due to decrease of their re-uptake via binding to and inhibition of DA, NE, and ST transporters.

A marked increase in cocaine-related deaths in the State of Florida: precursor to an epidemic?

The history of cocaine misuse includes a destructive epidemic during the 1980s. While recent surveys suggest cocaine use is stable or decreasing, we have observed increasing trends of cocaine-related death through analysis of medical examiner data collected by the Florida Department of Law Enforcement (FDLE). Florida's per capita cocaine-related death rates nearly doubled from 2001 to 2005.

Changes in leptin, ghrelin, growth hormone and neuropeptide-Y after an acute model of MDMA and methamphetamine exposure in rats.

Club drug abuse is a growing problem in the United States. Beyond addiction and toxicity are endocrine effects which are not well characterized. Specifically, the changes in appetite following exposure to drugs of abuse are an interesting but poorly understood phenomenon.

Calpain and caspase proteolytic markers co-localize with rat cortical neurons after exposure to methamphetamine and MDMA.

Abuse of the club drugs Methamphetamine (Meth) and Ecstasy (MDMA) is an international problem. The seriousness of this problem is the result of what appears to be programmed cell death (PCD) occurring within the brain following their use. This follow up study focused on determining which cell types, neurons and/or glial cells, were affected in the brains of drug-injected rats.

The effects of buprenorphine on fentanyl withdrawal in rats.

Rationale: Fentanyl is a potent mu-opioid receptor agonist that is widely used for the treatment of severe chronic pain. Discontinuation of fentanyl administration has been shown to induce a negative emotional state.

Objectives: The aim of the present studies was to investigate the effects of the partial mu-opioid receptor agonist buprenorphine on the negative emotional state associated with precipitated and spontaneous fentanyl withdrawal in rats.

Opiate prescription medication dependence and pain perceptions.

Our study showed that the perception of pain lessens with detoxification from chronic prescription opiate medications. Thus, removal of opiates resulted in less pain, and chronic administration of opiates actually increased pain perceptions. The underlying pathophysiology of increased pain sensitivity from chronic administration is not well understood.

Comorbidity and "self-medication".

Comorbidity is the rule rather than the exception for substance use disorders, especially when they involve drugs other than alcohol. A common reaction of physicians to comorbidity is to attribute the substance use of addicted people to "self-medicating" with drugs of abuse. When an individual uses an abused drug nonmedically, he or she is seeking brain reward, not treatment.

Tobacco and psychiatric dual disorders.

Smoking is a leading cause of morbidity and premature mortality in the United States. The relationship between tobacco smoking and several forms of cancer, heart disease, stroke, chronic lung disease, and other medical diseases is well recognized and accepted. Recent epidemiological studies are now focusing on the link between tobacco use and psychiatric diseases.

Caffeine content of decaffeinated coffee.

Caffeine is the most widely consumed drug in the world with coffee representing a major source of intake. Despite widespread availability, various medical conditions necessitate caffeine-restricted diets. Patients on certain prescription medications are advised to discontinue caffeine intake.

Ecstasy toxicity: a comparison to methamphetamine and traumatic brain injury.

Ecstasy use is a growing problem in the United States. Techniques to demonstrate and characterize the toxicity associated with its use have been limited and employed infrequently. In this study, we compare the deleterious effects of ecstasy use in rats with that of methamphetamine and traumatic brain injury.

Dexmedetomidine does not increase the incidence of intracarotid shunting in patients undergoing awake carotid endarterectomy.

Systemic administration of dexmedetomidine (DEX) decreases cerebral bloodflow (CBF) via direct alpha-2-mediated constriction of cerebral blood vessels and indirectly via its effect on the intrinsic neural pathway modulating vascular smooth muscle. Reduction in CBF without a concomitant decrease in cerebral metabolic rate has raised concerns that DEX may limit adequate cerebral oxygenation of brain tissue in patients with already compromised cerebral circulation (e.g.