Search PubMed⌕ Search

Biomedical subjects

Bruce H Price

Publications and source records attributed to Bruce H Price.

12 recordsLinked to original sources
PubMed2006

Brain imaging and cognitive dysfunctions in Huntington's disease.

Recent decades have seen tremendous growth in our understanding of the cognitive dysfunctions observed in Huntington's disease (HD). Advances in neuroimaging have contributed greatly to this growth. We reviewed the role that structural and functional neuroimaging techniques have played in elucidating the cerebral bases of the cognitive deficits associated with HD. We conducted a computer-based search using PubMed and PsycINFO databases to retrieve studies of patients with HD published between 1965 and December 2004 that reported measures on cognitive tasks and used neuroimaging techniques. Structural neuroimaging has provided important evidence of morphological brain changes in HD. Striatal and cortical atrophy are the most common findings, and they correlate with cognitive deficits in attention, working memory and executive functions. Functional studies have also demonstrated correlations between striatal dysfunction and cognitive performance. Striatal hypoperfusion and decreased glucose utilization correlate with executive dysfunction. Hypometabolism also occurs throughout the cerebral cortex and correlates with performance on recognition memory, language and perceptual tests. Measures of presynaptic and postsynaptic dopamine biochemistry have also correlated with measurements of episodic memory, speed of processing and executive functioning. Aided by the results of numerous neuroimaging studies, it is becoming increasingly clear that cognitive deficits in HD involve abnormal connectivity between the basal ganglia and cortical areas. In the future, neuroimaging techniques may shed the most light on the pathophysiology of HD by defining neurodegenerative disease phenotypes as a valuable tool for knowing when patients become "symptomatic," having been in a gene-positive presymptomatic state, and as a biomarker in following the disease, thereby providing a prospect for improved patient care.

Brain↗
PubMed2006

Asperger syndrome revisited.

Asperger syndrome (AS) is a disorder on the continuum of autistic spectrum disorders characterized by a lack of social reciprocity and empathy, and severe difficulties in social integration. Controversy remains as to what constitutes AS and whether it should be declared a separate disease or higher-functioning autism. This review discusses the contributions made by Hans Asperger and Leo Kanner in first delineating the condition, and examines the syndrome's incidence, prevalence, and etiologies. Recent studies using neuroimaging are described, along with current diagnostic and treatment options.

Affective Symptoms↗
PubMed2006

Mechanisms of Mind: Highlights of the 17th Annual Meeting of the American Neuropsychiatric Association, February 18-21, 2006, San Diego, CA.

Points of interest from the 17th Annual American Neuropsychiatric Association are reviewed, including several cognitive neuroscience frameworks that have been proposed to account for the neural basis of moral cognition. Also discussed are the brain mechanisms behind creative innovation, and an overview is presented of several of this year's outstanding contributions to clinical and basic neuroscience.

Brain↗
PubMed2005

Mild traumatic brain injury in psychiatric inpatients.

The purpose of this study was to compare psychiatric inpatients with and without mild traumatic brain injury (MTBI) on the variables of length of stay (LOS), number of psychiatric admissions, and change from admission to discharge on Global Assessment of Functioning (GAF). The study sample included 54 psychiatric inpatients, 18 to 65 years old, with a history of MTBI and 52 comparison psychiatric inpatients absent histories of MTBI, matched on age, sex and diagnostic category. LOS was longer for those with MTBI than for those without MTBI. This difference was statistically significant, after adjustment for matching. When adjusted for baseline GAF, this LOS difference remained statistically significant. The number of prior psychiatric admissions was 19% higher for participants with MTBI than for comparison participants, and when the LOS analysis was adjusted for this factor, it remained statistically significant. GAF change-from-baseline did not differ between the MTBI and comparison groups. Data from this study suggest that psychiatric inpatients with a history of MTBI may differ in frequency and length of hospitalization from otherwise similar inpatients without MTBI history.

Adolescent↗
PubMed2003

Cerebral metabolic correlates as potential predictors of response to anterior cingulotomy for treatment of major depression.

OBJECT: Neurosurgical procedures are a viable intervention for severe, treatment-refractory major depression, although they have been associated with only modest rates of efficacy. The purpose of this study was to identify possible neuroimaging predictors of treatment response to anterior cingulotomy in patients with major depression. METHODS: Thirteen patients underwent stereotactic anterior cingulotomy for treatment-refractory major depression. Symptom severity was measured using the Beck Depression Inventory (BDI) both before and approximately 12 months after surgery. The authors performed [18F]fluorodeoxyglucose-positron emission tomography (PET) studies in all patients preoperatively. Statistical parametric mapping methods were used to test for loci of significant correlation between preoperative regional cerebral metabolism and postoperative reduction in BDI scores. The mean (+/- standard deviation) change in the BDI score from the preoperative period (43.7 +/- 7.8) to the postoperative period (30.5 +/- 21.3) was 33.1 +/- 45.4%. Two loci--the left subgenual prefrontal cortex and left thalamus--were identified as sites at which preoperative metabolism was significantly correlated with subsequent improvement in depressive symptom severity following cingulotomy. Specifically, higher preoperative rates of metabolism at these loci were associated with better postoperative results. CONCLUSIONS: Possible PET scanning predictors of treatment response were identified in patients with major depression who had undergone anterior cingulotomy. Further research will be necessary to determine the reproducibility of this finding. If confirmed, the availability of an index for noninvasively predicting a patient's response to cingulotomy for the treatment of major depression would be of great clinical value.

Adult↗
PubMed2002

Magnetic resonance imaging-guided stereotactic limbic leukotomy for treatment of intractable psychiatric disease.

OBJECTIVE: To assess the efficacy and complication rates of magnetic resonance imaging-guided stereotactic limbic leukotomy for the treatment of intractable major depressive disorder (MDD) and obsessive-compulsive disorder (OCD). METHODS: We conducted preoperative evaluations and postoperative follow-up assessments of efficacy and complications for 21 patients who underwent limbic leukotomy. Efficacy was based on physician- and patient-rated global assessments of functioning, as well as evaluations using disease-specific rating scales commonly used in studies of MDD and OCD. RESULTS: The mean time from limbic leukotomy to follow-up assessment was 26 months. On the basis of standard outcome measures, 36 to 50% of patients were considered to be treatment responders. Although permanent surgical morbidity was rare, there were reports of postoperative sequelae, including apathy, urinary incontinence, and memory complaints, which occurred in a substantial minority of cases. CONCLUSION: For this cohort of 21 patients with chronic severe MDD or OCD, who had experienced failure with an exhaustive array of previous treatments, limbic leukotomy was associated with substantial benefit for 36 to 50%. This rate is comparable to those of previous studies of limbic system surgery and indicates that limbic leukotomy is a feasible treatment option for severe, treatment-refractory MDD or OCD. Adverse consequences associated with the procedure included affective, cognitive, and visceromotor sequelae, which were generally transient.

Adult↗
PubMed2002

EEG abnormalities during treatment with typical and atypical antipsychotics.

OBJECTIVE: Clozapine produces EEG abnormalities and dose-dependent risk of epileptic seizures. Much less is known about EEG effects of newer antipsychotics. The present study therefore examined the risk of EEG abnormalities associated with various antipsychotic drugs. METHOD: EEG recordings from 323 hospitalized psychiatric patients (293 treated with antipsychotics, 30 who did not receive any antipsychotic treatment) were graded blind to diagnosis and treatment for type and severity of EEG abnormalities. Drug type, dose, and clinical factors were evaluated for association with EEG abnormalities by multivariate logistic regression. RESULTS: EEG abnormalities occurred in 56 subjects (19.1%) treated and four (13.3%) not treated with antipsychotics. EEG abnormality risk among antipsychotic agents varied greatly (clozapine=47.1%, olanzapine=38.5%, risperidone=28.0%, typical neuroleptics=14.5%, quetiapine=0.0%). Significant risk factors in order of influence were hypertension, use of an atypical antipsychotic, bipolar diagnosis, and older age; benzodiazepine cotreatment lowered risk. Unassociated with risk were sex, treatment response, length of hospital stay, drug potency, daily dose (in mg or mg/kg), drug exposure time, or cotreatments. CONCLUSIONS: EEG abnormality risk varied widely among specific antipsychotics. Risk was particularly high with clozapine and olanzapine, moderate with risperidone and typical neuroleptics, and low with quetiapine. Comorbid hypertension, bipolarity, and older age-but not dose or clinical response-were associated with risk.

Adolescent↗
PubMed2002

Prospective long-term follow-up of 44 patients who received cingulotomy for treatment-refractory obsessive-compulsive disorder.

OBJECTIVE: Long-term outcome associated with cingulotomy for obsessive-compulsive disorder (OCD) was prospectively assessed. Findings are reported for 18 patients previously described in 1995 and for 26 new patients. METHOD: An open preoperative and follow-up assessment was conducted at multiple time points for 44 patients undergoing one or more cingulotomies for treatment-refractory OCD. The patients were assessed by using the Structured Clinical Interview for DSM-III-R preoperatively and with the Yale-Brown Obsessive Compulsive Scale, the Beck Depression Inventory, and the Sickness Impact Profile both preoperatively and at all follow-up assessments. The patients completed clinical global improvement scales at all follow-up assessments. RESULTS: At mean follow-up of 32 months after one or more cingulotomies, 14 patients (32%) met criteria for treatment response and six others (14%) were partial responders. Thus, 20 patients (45%) were at least partial responders at long-term follow-up after one or more cingulotomies. Few adverse effects were reported. CONCLUSIONS: Thirty-two percent to 45% of patients previously unresponsive to medication and behavioral treatments for OCD were at least partly improved after cingulotomy. Cingulotomy remains a viable treatment option for patients with severe treatment-refractory OCD.

Adolescent↗
PubMedDate not supplied

Long-term neuropsychiatric consequences of "ecstasy" (MDMA): a review.

The recreational drug "ecstasy" (3,4-methylenedioxymethamphetamine, or MDMA) is widely used by young people throughout the world. Experimental studies indicate that MDMA damages serotonergic neurons in animals and possibly in humans. Repeated use may induce long-term neurotoxic effects, with cognitive and behavioral implications. We reviewed both the preclinical and the clinical literature to assess the evidence for persistent neuropsychiatric sequelae in humans. We focused on studies of chronic recreational use and reports of presence or absence of neurological, psychiatric, and psychological problems related to MDMA exposure. These investigations show repeated use of ecstasy to be associated with sleep, mood, and anxiety disturbances, elevated impulsiveness, memory deficits, and attention problems, which may persist for up to 2 years after cessation. In a subset of humans, particularly adolescents, depletion of serotonin by MDMA use may hasten or enhance vulnerability to a wide array of neuropsychiatric problems. Together, the studies reviewed provide substantial evidence that MDMA causes neuronal damage in animals and humans. Additional research is necessary to determine whether the MDMA-induced destruction of serotonergic neurons can have long-term and possibly permanent neuropsychiatric consequences in humans.

Cognition Disorders↗