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Biomedical subjects

H Weingartner

Publications and source records attributed to H Weingartner.

At least 55 records · Page 3Linked to original sources
PubMed1987

Effects of diazepam on cognitive processes in normal subjects.

The effects of 10 mg orally-administered diazepam on various aspects of cognition were examined in ten male subjects. Diazepam produced a subjective sense of cognitive impairment and impaired auditory vigilence, immediate recognition of twice presented words, and context-dependent free recall. There was a trend for a significant proportion of subjects to show impairment in delayed recognition of twice-presented words. There was no impairment of context-independent semantic memory, or of subjects' ability to judge how well they had performed on the free recall task. In fact, subjects' subjective sense of cognitive impairment was correlated with their performance on context-dependent memory tasks.

Adult↗
PubMed1987

Diazepam-induced amnesia: a neuropharmacological model of an "organic amnestic syndrome".

Diazepam has well-known amnestic properties. These effects, however, are selective for certain psychobiologically distinct memory functions. In this study, incremental doses of diazepam administered to 10 normal volunteers selectively impaired anterograde episodic memory and attention while totally sparing access to information in long-term memory (semantic or knowledge memory). This pattern of disruption mimics that seen in patients with organic amnesias and is in sharp contrast to the pattern seen in patients with dementia. These findings provide a framework for defining specific psychobiological determinants of cognitive failure.

Adult↗
PubMed1987

Dementia of the Alzheimer type: clinical and family study of 22 twin pairs.

We studied 22 twin pairs in which one or both twins had dementia of the Alzheimer type (DAT). In four twins, diagnosis was confirmed by autopsy. Seven monozygotic (MZ) pairs were concordant for DAT; 10 MZ pairs were discordant. Two dizygotic (DZ) pairs were concordant for DAT, and 3 DZ pairs were discordant. The current concordance rate was 41% for MZ twins and 40% for DZ twins. The study supports the belief that, etiologically, DAT cannot be entirely accounted for by a single autosomal dominant gene. The data also suggest that in certain genetic circumstances, disease expression may be delayed in females.

Aged↗
PubMed1987

Ethanol intoxication and memory. Recent developments and new directions.

A qualitative description of the acute effects of ethanol intoxication on learning and memory is presented. Mechanisms underlying the acquisition impairments observed in intoxicated subjects are discussed. Recent studies on retroactive facilitation are also considered. The importance of considering changes in attention, arousal, and mood in any account of the effects of ethanol on higher mental functions is emphasized. In the future, studies are needed in which the effects of ethanol are compared and contrasted with those of other agents. Such studies will not only improve our knowledge about ethanol's effects but will also enhance our understanding of cognition.

Alcoholic Intoxication↗
PubMed1986

Effortful and automatic cognitive processes in depression.

Ten patients with major depression and ten age- and sex-matched normal controls were presented with two contrasting cognitive tasks: one required sustained effort and information processing, and the other required only superficial information processing that could be accomplished automatically, with little effort. Depressed patients performed more poorly only on the effort-demanding cognitive task.

Cognition↗
PubMed1986

Benzodiazepine sensitivity in normal human subjects.

Increasing intravenous doses of diazepam or placebo were administered to ten healthy normal volunteers, and the changes in saccadic eye velocity, self-rated sedation and anxiety, and plasma cortisol and growth hormone concentrations were measured. Diazepam administration (4.4 to 140 micrograms/kg, cumulative dose) resulted in a dose-dependent decrease in saccadic eye velocity and plasma cortisol level as well as a dose-dependent increase in self-rated sedation and plasma growth hormone level. Self-rated anxiety was unaffected in these relatively nonanxious subjects. The diazepam-induced changes in saccadic eye velocity, sedation, and growth hormone and cortisol levels were highly correlated with each other and with increasing plasma diazepam concentration. These results are consistent with a benzodiazepine receptor-mediated action of diazepam. The highly quantifiable and dose-dependent decrease in saccadic eye velocity by benzodiazepines should make this a useful measure of benzodiazepine receptor sensitivity in humans.

Adult↗
PubMed1986

Naloxone and Alzheimer's disease. Cognitive and behavioral effects of a range of doses.

There have been conflicting reports on the effects of naloxone hydrochloride in patients with dementia of the Alzheimer type (DAT). In addition, none of the naloxone studies in DAT used doses of 2.0 mg/kg or more, the amount necessary to produce reliable cognitive and behavioral changes in young normal subjects. In a randomized, double-blind, placebo-controlled study, 12 patients with DAT were administered naloxone hydrochloride in doses of 5 micrograms/kg, 0.1 mg/kg, and 2.0 mg/kg, with detailed evaluation of its behavioral and cognitive effects using measures selected for their potential relevance to DAT and the known effects of blockade of endogenous opiate systems. None of the measures of motor performance, attention, memory, learning, or recognition showed improvement with naloxone. Increased inappropriate verbal productions were noted after 0.1 mg/kg of naloxone hydrochloride. Patients became irritably activated after this dose, which may account for the altered verbal behavior in this study and also for some of the changes suggesting cognitive improvement in prior studies. Differences in the sensitivity and dose dependency of the behavioral effects in patients with DAT compared with prior studies in young normal subjects merit further investigation.

Adult↗
PubMed1986

A psychobiologic analysis of cognitive failures. Structure and mechanisms.

Impairments in memory, learning, and related cognitive functions can vary in most psychiatric or neuropsychiatric disorders. Although many methods have been used to measure the presence and severity of cognitive symptoms, little progress has been made in defining and contrasting possible determinants of cognitive dysfunction. We propose a theoretical framework that describes impairments of higher mental functions in terms of both "extrinsic" noncognitive processes and "intrinsic" cognitive processes. The latter include effort (capacity) demanding processes; automatic processes; episodic (recent biographical) memory; and processes involved in accessing previously acquired knowledge. Noncognitive processes include sensitivity to reinforcement, activation, sensorimotor function, and mood. Each of these processes can be expressed at the time of information acquisition or retrieval from memory. Findings from clinical studies of patients suffering amnestic disorders, progressive dementias, and mood disorders illustrate the utility of such a model for understanding some of the determinants of cognitive dysfunction, for developing diagnostic tools, and for considering therapeutic strategies that may be useful in treating cognitive dysfunctions.

Alcohol Amnestic Disorder↗
PubMed1986

Hemispheric lateralization of functions related to emotion.

We have reviewed the evidence that processes and functions related to perception and expression of emotions are represented asymmetrically in the cerebral hemispheres. The literature describes three possible aspects of emotional lateralization: that emotions are better recognized by the right hemisphere; that control of emotional expression and related behaviors takes place principally in the right hemisphere; and that the right hemisphere is specialized for dealing with negative emotions, while the left is specialized for dealing with positive emotions. Evidence for the three hypotheses derives from methodologically diverse studies in unimpaired, brain-lesioned, and mood-disordered populations. Relatively little of the work has been precisely replicated, and conclusions rest on parallel lines of evidence from diverse sources. The present level of knowledge suggests a model of emotional control based on interactive inhibition between a right negatively biased and left positively biased hemisphere. However, the details of such a model, including the precise conditions under which emotion-related functions are lateralized, and the mechanisms of such lateralization have yet to be elucidated.

Brain↗
PubMed1986

Pharmacologic modelling of Alzheimer's disease.

Evidence pointing to the central role of the cholinergic system in normal human memory function and disorders such as Alzheimer's disease has grown tremendously in recent years. Anticholinergic and non-cholinergic agents have been found to create transient memory impairments in young adults which mimic the changes associated with normal aging or amnesia. The rationale for using scopolamine, a centrally active anticholinergic agent, as a pharmacologic probe of memory function is reviewed using data from studies in animals and humans. The cognitive functioning of normal elderly controls given scopolamine is compared to the baseline functioning of patients with Alzheimer's disease, followed by a discussion of the use of scopolamine as a modelling agent for dementia.

Adult↗
PubMed1986

Design and interpretation of opiate antagonist trials in dementia.

In view of the reports of possible beneficial effects of naloxone in dementia, rationales and strategies for studying endogenous opiate systems are reviewed. Important considerations in the design and interpretation of clinical investigations using naloxone are also reviewed. The nature and distribution of endogenous opiate systems are summarized from an historical perspective. Endogenous opiate systems are distributed throughout the central nervous system and play important roles in a variety of brain functions, including memory and learning. In view of this, several rationales are evident for studying endogenous opiate systems in dementia, since it is a syndrome in which structures known to contain opiate systems are disturbed, functions modulated by opiate systems are disturbed, and other neurotransmitter systems (functionally linked to endogenous opiate systems) are disturbed. Different strategies for studying endogenous opiate systems are reviewed, including examination of body fluids and pharmacologic challenge studies. Naloxone hydrochloride, a competitive opiate receptor antagonist, is a commonly used pharmacologic agent. The design of a multidose naloxone study of 12 dementia patients is discussed, with reference to the pharmacokinetics, pharmacodynamics, and specificity of naloxone as well as to the nature of the dependent measures selected for this study. No cognitive benefit was observed in this study. Behavioral arousal was observed at naloxone doses, with more evident psychomotor retardation at higher doses. These findings are contrasted with the results of naloxone challenges in other studies. The varying effects of naloxone within and across populations can be conceptualized in terms of the basic and clinical considerations previously discussed. The importance of dose-finding studies is stressed for this and other drug trials.

Alzheimer Disease↗
PubMed1986

Alcoholic organic brain disease: nosology and pathophysiologic mechanisms.

Study of alcoholic chronic organic brain syndrome may have applicability to the large population of alcoholics with less severe cerebral dysfunction. Brain impairment in alcoholics may be conceptualized as two clinically and neuropathologically distinguishable organic brain syndromes: alcohol amnestic disorder or Korsakoff's psychosis (KP) and alcoholic dementia. Alcoholic organic brain disease may result from two interacting pathophysiological processes: nutritional (thiamine) deficiency and ethanol neurotoxicity. Subcortical periventricular lesions associated with KP result primarily from thiamine deficiency, whereas ethanol neurotoxicity and various secondary effects of alcoholism may contribute to the cortical neuropathological changes associated with alcoholic dementia. These two patterns of brain damage may be differentiable in individual alcoholics using cognitive tests and other measures of CNS function and, therefore, allow selection of a treatment strategy based on pathophysiological considerations. Studies in animals and humans suggest that a genetic predisposition to thiamine deficiency may contribute to alcoholism-associated dysfunction of brain and other organ systems and possibly have a causative role in the development of alcoholism.

Alcohol Amnestic Disorder↗
PubMed1986

Treatment of childhood hyperactivity with desipramine: plasma drug concentration, cardiovascular effects, plasma and urinary catecholamine levels, and clinical response.

Twenty-nine boys with attention deficit disorder/hyperactivity were randomly assigned to receive desipramine (DMI; n = 17) or placebo (n = 12) for 14 days in a noncrossover, double-blind study. There was immediate behavioral improvement with DMI at day 3 that was sustained for 2 weeks; behavioral improvement did not correlate with plasma concentrations of DMI, hydroxy-DMI, or their sum at either days 3 or 14. There were no untoward side effects; there was a drug-induced increase in pulse and diastolic blood pressure. During drug therapy, the urinary excretion of norepinephrine, vanillymandelic acid, and 3-methoxy-4-hydroxyphenylglycol (MHPG) was decreased at both days 3 and 14. The plasma MHPG level was decreased at days 3 and 14 and (standing) plasma NE levels increased at day 14. The decreases in both urinary and plasma MHPG levels showed significant correlations with behavioral improvement during the second week. These data corroborate previous findings on sympathomimetic effects of tricyclic antidepressants in children and support a noradrenergic mechanism in the mediation of drug effects on attention deficit disorder/hyperactivity.

Administration, Oral↗
PubMed1986

The effects of lateralized frontal lesions on mood regulation.

A group of Vietnam veterans with penetrating brain wounds to the orbitofrontal, dorsofrontal, and nonfrontal cortex were compared with a stratified control group of self-report and observed measures of mood state and cognition. In particular, hypotheses regarding the regulation of anxiety by frontal cortical mechanisms were evaluated. Results indicated that patients with right orbitofrontal lesions were prone to abnormally increased 'edginess'/anxiety and depression, whereas patients with left dorsofrontal lesions were prone to abnormally increased anger/hostility. A working model of mood state regulation is presented which represents the thesis that mood sensations are subject to numerous cognitive and biological influences that result in a variety of expressions of a particular mood disorder.

Adult↗
PubMed1986

Cognitive processing in anorexia nervosa. A disturbance in automatic information processing.

Anorexia nervosa patients were found to perform as well or better than control subjects on cognitive tasks that both require considerable cognitive effort and 'direct' the subject to the information that will be tested, but do more poorly than controls on tests that assess automatic or incidental processing of information. The implications of this particular pattern of cognitive alterations for theories concerning the etiology of anorexia nervosa are discussed.

Adult↗
PubMed1986

Consciousness and amnesia after penetrating head injury: neurology and anatomy.

Among 342 men who survived severe penetrating brain wounds, only 15% had prolonged unconsciousness and 53% had no or momentary unconsciousness after injury, emphasizing the focal nature of these wounds. The left (or language-dominant) hemisphere was dominant for the "wakefulness" component of consciousness. The areas most associated with unconsciousness included the posterior limb of the left internal capsule, left basal forebrain, midbrain, and hypothalamus. Left dominance was not seen for posttraumatic amnesia after elimination of the wakefulness variable, suggesting that wakefulness may be linked to the role of the left hemisphere in verbal memory.

Amnesia↗