PubMed Health⌕ Search

Biomedical subjects

D W Hommer

Publications and source records attributed to D W Hommer.

At least 37 records · Page 2Linked to original sources
PubMed1993

A developmental study of smooth pursuit eye movements in normal children from 7 to 15 years of age.

OBJECTIVE: To examine age-related changes in smooth pursuit tracking. METHOD: Using infrared occulography, smooth pursuit eye movements are examined in 53 normal 7- to 15-year-old children during 6 degrees and 12 degrees/second visual pursuit. In addition to smooth pursuit gain and saccadic frequency, measures of mean amplitude per second are introduced to facilitate comparison across age and target speed. RESULTS: The 6 degrees/second task is found to be easier than the 12 degrees/second task. Age is correlated with smooth pursuit system performance but not saccadic system performance during 12 degrees/second pursuit. No measure correlates with age during 6 degrees/second pursuit. CONCLUSIONS: Eye movements improve as children age. The future use of smooth pursuit eye movements to study children and adolescents with and at risk for schizophrenia must control for developmental changes.

Adolescent↗
PubMed1992

A quantitative analysis of saccades and smooth pursuit during visual pursuit tracking. A comparison of schizophrenics with normals and substance abusing controls.

The eye movements of schizophrenic patients are characterized by decreased smooth pursuit gain and an increased frequency of saccades. However, the nature of these saccades and their function during smooth pursuit has not been clearly defined. To address this issue we examined the eye movements of 22 schizophrenic patients, 20 substance abusing patients (primarily alcohol; some with concomitant cocaine and/or cannabis abuse), and 17 normal controls during a visual pursuit task using infra-red oculography. A computerized pattern recognition algorithm divided pursuit eye movements into two basic components: smooth pursuit and saccadic eye movements. The algorithm also determined eye position error and velocity error before and after each saccade. Schizophrenic patients had lower smooth pursuit gain (p less than 0.02) and made more saccades during smooth pursuit (p less than 0.02) than either comparison group. When saccades were assigned to subcategories based on direction and position error, only the frequency of 'catch-up' saccades differentiated schizophrenic patients from the comparison groups (p less than 0.05). Smooth pursuit gain was negatively correlated with saccadic frequency among all three subject groups. Eye velocity preceding saccades was significantly lower among the schizophrenic patients, but pre or post saccadic position error did not differ among the three groups. Discrete analysis of the fine structure of visual pursuit tracking may lead to a better understanding of eye movement abnormalities in schizophrenia.

Adult↗
PubMed1992

Response to diazepam in sons of alcoholics.

Alcohol exerts several of its actions via the chloride channel associated with the central GABA-benzodiazepine receptor complex. To explore a possible role for this receptor complex in risk for alcoholism, and to determine whether risk for alcoholism is associated with risk for benzodiazepine abuse, the authors administered intravenous diazepam to 18 sons of male alcoholics (SOAs) and 18 control subjects. Four logarithmically increasing doses of diazepam and matched volumes of placebo were given in randomized order on separate days about 1 week apart. SOAs were significantly more likely than controls to report euphoric responses to diazepam. At some diazepam doses, SOAs were more likely to report feeling "high" and "intoxicated." SOAs and controls did not differ in feeling "drugged." SOAs and controls may differ in expectations regarding the subjective effects of drugs and/or in the function of the central GABA-benzodiazepine receptor complex. These findings also add further evidence for increased pleasurable effects, and thus possibly increased risk for benzodiazepine abuse, in a subgroup of SOAs.

Adolescent↗
PubMed1991

Maladaptive anticipatory saccades in schizophrenia.

We compared the saccades made by 8 neuroleptic-treated and 7 drug-free schizophrenic inpatients with those made by 11 normal controls during two eye movement tasks. The first task was designed to elicit visually guided but not internally guided saccades. The second task was designed so that optimal performance required saccades be guided on the basis of an internal representation of target behavior. During the first task, schizophrenics made visually guided saccades that were as accurate as those made by control, but both drug-free and neuroleptic-treated schizophrenics made intrusive saccades at a significantly higher rate than control subjects. Most of these maladaptive saccades appeared to be premature attempts to anticipate target jump. During the second eye movement task, which for optimal performance required use of an internal representation to guide eye movements, most patients learned to anticipate target jump as well as controls. However, neuroleptic-treated patients made significantly smaller adaptive anticipatory saccades than either drug-free schizophrenic patients or normal subjects. These finding are discussed as they relate to the prefrontal cortex-basal ganglia circuits involved in the regulation of behavior by representational knowledge and the idea that the abnormal anticipatory saccades we observed represent a failure in the sensorimotor gating of information derived from internal representations.

Adult↗
PubMed1991

Smooth pursuit and saccadic eye movements and neurological soft signs in obsessive-compulsive disorder.

Patients with obsessive-compulsive disorder (OCD) demonstrate an increased number of neurological soft signs as well as neuroanatomic abnormalities detected with modern imaging techniques. Quantitative analysis of eye movements has proved fruitful in investigations of other neuropsychiatric disorders with similar findings. Therefore, we studied the smooth pursuit and saccadic eye movements of 8 OCD patients and 12 normal controls using infrared oculography and computerized pattern recognition software. We also measured neurologic soft signs using a standardized rating instrument. Despite having an increased number of neurological soft signs, OCD patients' performance on a variety of measures of eye movement was not significantly impaired. Neither the severity of obsessions or compulsions nor the number of neurologic soft signs correlated with any of the parameters of eye movement function. We conclude that OCD patients do not have prominent oculomotor dysfunction and that eye movement dysfunction and neurologic soft signs are not inextricably linked.

Adult↗
PubMed1991

Correlation of Wisconsin Card Sorting Test performance with eye tracking in schizophrenia.

The authors studied the relationship between performance on the Wisconsin Card Sorting Test and on the Trailmaking-B test and measures of smooth pursuit eye movements in 12 patients with chronic schizophrenia and 12 normal volunteers. They found that performance on the Wisconsin Card Sorting Test was significantly correlated with measures of smooth pursuit eye movements in schizophrenic patients but not in normal subjects. Trailmaking-B scores, however, were unrelated to smooth pursuit eye movements in either group.

Adult↗
PubMed1989

Smooth pursuit eye movements in schizophrenia: effects of neuroleptic treatment and caffeine.

Abnormal smooth pursuit eye movement (SPEM) has been proposed as a trait marker in schizophrenia. We utilized high resolution infra-red oculography to measure SPEM in 11 neuroleptic-treated schizophrenic patients, 10 drug-free schizophrenic patients, and 11 normals. The most characteristic abnormality was a significant increase in saccadic intrusions during SPEM in schizophrenic patients (p less than .001). SPEM gain was reduced in schizophrenic patients (p less than .005). No significant effects of neuroleptic treatment on SPEM were found, including analysis of seven patients in whom paired data was available. We also measured SPEM prior to and after caffeine ingestion (10 mg/kg) in 10 normals. We found reduced saccadic interruptions as a result of caffeine ingestion compared with placebo (p less than .05). As caffeine has been shown to selectively increase dopaminergic neurotransmission in mesocortical neurons, further study utilizing dopamine agonists during SPEM in schizophrenic patients is warranted.

Adult↗
PubMed1989

Attenuating effects of diazepam on the electroretinogram of normal humans.

Response/log I curves were obtained under conditions of dark-and light-adaptation in seven normal male volunteers. For each subject, a baseline electroretinogram (ERG) was recorded. In the same afternoon, a second ERG was obtained after 0.05 mg/kg diazepam, and a third ERG was recorded following 0.10 mg/kg diazepam. Under conditions of dark-adaptation, the following dose-dependent changes were identified: 1) Diazepam attenuated the rod b-wave peak amplitude and increased its implicit time; 2) The dark-adapted longer wavelength cone a-wave and 'blue cone' b-wave showed an increased implicit time; 3) All oscillatory potentials showed an increased implicit time. Under conditions of light-adaptation, dose-dependent decreases in peak amplitude and delays in implicit time were observed for the a- and b-waves. The effects of diazepam on the human ERG were more profound under conditions of light- than dark-adaptation.

Adult↗
PubMed1988

Preferential effects of caffeine on limbic and cortical dopamine systems.

In this study, we investigated the effects of acute caffeine administration on the activity of midbrain dopamine neurons. Caffeine significantly depressed the firing rates of dopamine neurons in the ventral tegmental area (A10 group), but had no significant effect on the firing rates of dopamine neurons in the substantia nigra zona compacta (A9 group). The action of caffeine in A10 was completely blocked by pretreatment with the adenosine agonist L-phenyl-isopropyl-adenosine (L-PIA), confirming numerous lines of evidence that caffeine and other xanthines act as competitive antagonists at adenosine receptors. The dopamine antagonist haloperidol also antagonized the effects of caffeine. This finding is consistent with a mechanism of caffeine-induced depression of dopamine neuron activity involving dopamine release, similar to that observed during amphetamine administration. Finally, the benzodiazepine diazepam also antagonized the dopaminergic effects of caffeine. It appears that, in the rat, caffeine administration inhibits mesolimbic and mesocortical projecting dopamine neurons, but has no effect on dopamine neurons that project to the striatum.

Animals↗
PubMed1987

Differential effects of an anxiogenic beta-carboline on single unit activity in the locus coeruleus and substantia nigra of the rat brain.

The firing rates of single units in the substantia nigra pars reticulata, substantia nigra pars compacta and the locus coeruleus were recorded during the intravenous administration of beta-carboline-3-carboxylic acid ethyl ester (beta CCE). beta-Carboline-3-carboxylic acid produced a dose-dependent excitation in all units tested in the substantia nigra pars reticulata and a small inhibitory effect on some units in the substantia nigra pars compacta. It had no effect on the firing rates of single units in the locus coeruleus, but did prove effective in reversing inhibition induced by diazepam in this nucleus. The relevance of the findings to the anxiogenic effects of beta-carboline-carboxylic acid ethyl ester are discussed.

Animals↗
PubMed1987

Electrophysiological evidence for a non-opioid interaction between dynorphin and GABA in the substantia nigra of the rat.

Interactions between neuronal responses mediated by dynorphin A1-8 and GABA were investigated in the substantia nigra zona reticulata. Extracellular recordings and microiontophoresis were performed using five-barrel microelectrodes in chloral hydrate-anesthetized male rats. When iontophoresed alone, dynorphin A1-Q significantly inhibited the firing of 22% of the neurons tested. The inhibition was rapid in onset and recovery and was dose-dependent. In another 22% of the cells, iontophoretic dynorphin produced an increase in the baseline firing rate which was slow in both onset and offset; the remaining 56% were unaffected by dynorphin. When GABA and dynorphin A1-8 were applied in conjunction, the inhibitory action of GABA was attenuated in 61% of the cells; whereas, when dynorphin and GABA were ejected simultaneously onto the cells that were inhibited by dynorphin A1-8, the respective inhibitory effects of dynorphin and GABA appeared to be additive. The kappa antagonist, MR-2266, failed to block the ability of dynorphin A1-8 to attenuate the action of GABA. In addition, the non-opiate peptide des-tyr-dynorphin A2-17, produced effects similar to that of dynorphin A1-8. The role of dynorphin in the basal ganglia and its interaction with the other major transmitter in the substantia nigra zona reticulata, GABA, is discussed.

Action Potentials↗
PubMed1987

Innervation of substantia nigra neurons by cholinergic afferents from pedunculopontine nucleus in the rat: neuroanatomical and electrophysiological evidence.

Dopaminergic neurons of the substantia nigra pars compacta are excited by nicotine and acetylcholine, and possess both high-affinity nicotine binding sites and intense acetylcholinesterase activity, consistent with a cholinoceptive role. A probable source of cholinergic afferents is the pedunculopontine nucleus, which forms part of a prominent group of cholinergic perikarya located caudal to the substantia nigra in the tegmentum. Although pedunculopontine efferents, many of them cholinergic, project to the substantia nigra pars compacta, it has not been established whether they terminate in this structure. In the first experiment, which combined retrograde tracing with immunohistochemical visualization of cholinergic neurons, cholinergic cells in and around the pedunculopontine nucleus were found to send projections to the substantia nigra. This projection was almost completely ipsilateral. Subsequent experiments employed anaesthetized rats; kainate was microinfused into tegmental sites in order to stimulate local cholinergic perikarya, and concurrently, extracellular recordings were made of single dopaminergic neurons in the substantia nigra. Consistent with our anatomical findings, unilateral microinfusion of kainic acid in or near the pedunculopontine nucleus increased the firing rate of dopaminergic neurons situated remotely in the ipsilateral substantia nigra. The kainate-induced excitation of nigral dopaminergic neurons was dose-related and was prevented by intravenous administration of the centrally-acting nicotinic cholinergic antagonist mecamylamine. These results suggest that cholinergic perikarya in the vicinity of the pedunculopontine tegmental nucleus innervate dopaminergic neurons in the substantia nigra pars compacta via nicotinic receptors.

Action Potentials↗
PubMed1987

Attenuating actions of diazepam on the photomyoclonic reflex.

The photomyoclonic reflex (PMR), consisting of a one- or two-component blink reflex associated with the flash electroretinogram (ERG), is sensitive to the acute effect of intravenously administered diazepam. In the 29% (two of seven) of normal volunteers who had a PMR, diazepam reduced it to a nonobservable level. Diazepam also had a significant attenuating effect on the a- and b-waves of the ERG; the magnitude of attenuation in normal volunteers, however, probably would not alter a clinical diagnosis based on ERG. These two findings together predict that individuals known to have a marked PMR may have the diagnostic risk associated with these specious artifacts reduced by receiving diazepam before clinical ERG studies are begun.

Adult↗
PubMed1987

Effect of pimozide on positive and negative symptoms in schizophrenic patients: are negative symptoms state dependent?

In a double-blind, placebo-controlled trial of treatment with the neuroleptic pimozide, negative symptoms improved in schizophrenic patients who showed an antipsychotic response. Furthermore, there was a significant positive correlation between changes in positive and negative symptoms for the group as a whole, including both pimozide responders and nonresponders. In our patient sample, neuroleptic treatment did not exert a differential effect on the positive and negative symptoms of schizophrenia. It is conceivable that negative symptoms are state dependent and may become neuroleptic nonresponsive over time just as positive symptoms do in some chronic patients.

Adolescent↗
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

Neuroleptic responsivity of negative and positive symptoms in schizophrenia.

The authors prospectively examined the effects of double-blind, placebo-controlled neuroleptic withdrawal and administration on ratings of negative and positive symptoms in 19 young patients with chronic schizophrenia. Negative symptoms were significantly reduced by neuroleptic treatment, and negative and positive symptoms demonstrated similar patterns of reduction and exacerbation during neuroleptic treatment and withdrawal, respectively. The changes in negative and positive symptoms induced by neuroleptic treatment and withdrawal were not significantly correlated, however. The negative and positive symptom profiles of individual patients were significantly altered by neuroleptic treatment, indicating limitations to the cross-sectional classification of patients on the basis of predominance of one or the other symptom group. The authors discuss implications for the neurobiological underpinnings of negative and positive symptoms.

Adult↗