Biomedical subjects

Duncan Clark

Publications and source records attributed to Duncan Clark.

3 recordsLinked to original sources

PubMed2004

Human herpesvirus type 6 and multiple sclerosis.

The aetiology of multiple sclerosis (MS) is unknown, but is probably the result of an interaction between predisposing genetic and environmental factors. The potential role of an infectious agent in MS aetiology stems from evidence of a geographical risk component, with disease being more prevalent in temperate regions. Also, several epidemics of MS have been recorded, suggesting a transmittable element to the disease. Although no one particular virus has been implicated as a causative factor, several herpesviruses have been incriminated due to their neurotropism, ubiquitous nature and ability to establish latency. The majority of evidence supporting a link between MS and human herpesvirus-6 (HHV-6) comes from case control studies comparing the presence of HHV-6 in brain tissue, cerebrospinal fluid (CSF) and peripheral blood mononuclear cells (PBMCs) in patients with and without MS. HHV-6 was detected in a high proportion of individuals without MS, indicating that HHV-6 polymerase chain reaction (PCR) positivity in itself is not sufficient for its causality in the development of MS. Studies of the association between HHV-6 and MS have been contradictory and the International Herpes Management Forum (IHMF) recommends that any future studies should use validated, sensitive methods and that masked samples should undergo independent analyses. If therapy trials are indicated, it is recommended that drugs with improved activity against HHV-6 are evaluated.

Herpesvirus 6, Human↗

PubMed2003

Alcohol and psychiatric comorbidity.

Comorbid psychiatric disorders and drug use disorders (DUDs) are common among alcoholics (Regier, Farmer, Rae, Locke, Keith, Judd, & Goodwin, 1990; Kessler, McGonagle, Zhao, Nelson, Hughes, Eshleman, Wittchen, & Kendler, 1994). These comorbid disorders often predict a shorter time to relapse of alcoholism (Greenfield, Weiss, Muenz, Vagge, Kelly, Bello, & Michael, 1998). However, despite the prevalence and the adverse effects of this comorbidity, few controlled treatment studies have been conducted involving this dual diagnosis population (Litten & Allen, 1999). To date, most of these few studies of alcoholics with comorbid disorders have been restricted to studies of alcoholics with either comorbid major depression or comorbid anxiety disorders (Litten & Allen, 1995). The results of these trials suggest efficacy for SSRI antidepressants and tricyclic antidepressants for treating alcoholics with comorbid major depression and suggest efficacy for buspirone for treating alcoholics with comorbid anxiety disorders (Mason, Kocsis, Ritvo, & Cutler, 1996; Cornelius, Salloum, Ehler, Jarrett, Cornelius, Perel, Thase, & Black, 1997; Kranzler, Burleson, Del Boca, Babor, Korner, Brown, & Bohn, 1994). However, controlled treatment studies involving alcoholics with other comorbid disorders are almost totally lacking. Consequently, to date, no empirically proven treatment exists for most of these comorbid disorders.

Alcoholism↗

PubMed2003

Neurobehavioral disinhibition in childhood predicts early age at onset of substance use disorder.

OBJECTIVE: This longitudinal study had three aims: 1) determine the extent to which boys at high average risk and low average risk for substance use disorder differ on a construct of neurobehavioral disinhibition, 2) evaluate the capacity of neurobehavioral disinhibition to predict substance use frequency at age 16, and 3) demonstrate the utility of neurobehavioral disinhibition in predicting substance use disorder. METHOD: The authors derived an index of neurobehavioral disinhibition from measures of affect, behavior, and cognition. The neurobehavioral disinhibition score was used to discriminate youth at high and low average risk for substance use disorder and to predict substance use frequency after 4-6 years and substance use disorder after 7-9 years. RESULTS: The neurobehavioral disorder score significantly discriminated boys at high average risk from those at low average risk at ages 10-12. Neurobehavioral disinhibition at age 16, in conjunction with substance use frequency and risk status group, predicted substance use disorder at age 19 with 85% accuracy and accounted for 50% of the variance in Drug Use Screening Inventory overall problem density score. Neurobehavioral disinhibition was a stronger predictor of substance use disorder (odds ratio=6.83) than substance consumption frequency (odds ratio=3.19). CONCLUSIONS: Cross-sectional and longitudinal analyses indicated that neurobehavioral disinhibition is a component of the liability to early age at onset of substance use disorder.

Adolescent↗