Biomedical subjects

J L Ingles

Publications and source records attributed to J L Ingles.

8 recordsLinked to original sources

PubMed2001

Effectiveness of attention rehabilitation after an acquired brain injury: a meta-analysis.

The efficacy of attention rehabilitation after an acquired brain injury was examined meta-analytically. Thirty studies with a total of 359 participants met the authors' selection criteria. Studies were categorized according to whether training efficacy was evaluated by comparing pre- and posttraining scores only or included a control condition as well. Performance improved significantly (using the d+ statistic) after training in pre-post only studies but not in pre-post with control studies. Further analyses showed that specific-skills training significantly improved performance of tasks requiring attention but that the cognitive-retraining methods included in the meta-analysis did not significantly affect outcomes. These findings demonstrate that acquired deficits of attention are treatable using specific-skills training. Implications of these results for rehabilitation theory and future research are discussed.

Adult↗

PubMed1999

Fatigue after stroke.

OBJECTIVE: To determine the frequency and outcome of fatigue, its impact on functioning, and its relationship with depression in patients 3 to 13 months poststroke. DESIGN: Survey. SETTING: Community. PARTICIPANTS: Eighty-eight individuals from a pool of 181 consecutive patients previously admitted to an acute stroke service who were willing and able to complete the self-report questionnaires, and 56 elderly controls living independently in the community. MAIN OUTCOME MEASURES: Fatigue Impact Scale (a self-report measure of the presence and severity of fatigue and its impact on cognitive, physical, and psychosocial functions) and the Geriatric Depression Scale. RESULTS: The frequency of self-reported fatigue problems was greater in the stroke group (68%) than in the control group (36%, p < .001) and was not related to time poststroke, stroke severity, or lesion location. Forty percent of the stroke group reported that fatigue was either their worst or one of their worst symptoms. Patients attributed more functional limitations to their fatigue than did control subjects with fatigue. Although the presence of fatigue was independent of depression, the impact of fatigue on functional abilities was strongly influenced by depression. CONCLUSION: Fatigue can contribute to functional impairment up to 13 months after stroke, and its recognition and treatment are important for maximizing recovery.

Activities of Daily Living↗

PubMed1996

Evidence for multiple routes of speech production in a case of fluent aphasia.

A case study is reported of a 24-year old woman who developed fluent aphasia with superior reading relative to auditory comprehension following herpes simplex encephalitis. Her language disturbance showed exceptional features: oral reading, repetition and naming to confrontation were severely impaired and yet her spontaneous speech recovered to be relatively intact. These features are not consistent with Wernicke's aphasia, pure word deafness or any classic aphasic syndromes. These findings indicate the presence of several routes for phonological output that may be differentially impaired.

Adult↗

PubMed1994

Picolinic acid blocks the neurotoxic but not the neuroexcitant properties of quinolinic acid in the rat brain: evidence from turning behaviour and tyrosine hydroxylase immunohistochemistry.

Previous results suggest that the tryptophan metabolite, picolinic acid may have the unusual properties of antagonizing the neurotoxic but not the neuroexcitant effects of another tryptophan metabolite, quinolinic acid in the central nervous system. The present experiments tested this possibility utilizing behavioural and tyrosine hydroxylase immunohistochemical techniques. In the first series of experiments, rats received injections of relatively high concentrations of 6-hydroxydopamine (12 micrograms in 1 or 2 microliters), quinolinic acid (120 nmol in 0.5 microliters), picolinic acid (480 nmol in 0.5 microliters) or co-treatments (0.5 microliters) with quinolinic (120 nmol) plus picolinic acid (480 nmol) into the region of the substantia nigra. Results revealed that 6-hydroxydopamine and quinolinic acid alone produced a large loss of tyrosine hydroxylase-positive cells in the pars compacta of the substantia nigra. Behavioural results for all 6-hydroxydopamine (n = 10) and for some quinolinate-treated rats (n = 5) revealed ipsi- and contraversive circling following amphetamine (1 mg/kg, i.p.) and apomorphine (0.5 mg/kg, s.c.), respectively, consistent with unilateral loss of dopamine cells in the substantia nigra. The remaining quinolinate-treated rats (n = 9) circled ipsiversively following either stimulant suggesting damage to the pars reticulata. Groups treated with picolinic acid alone (n = 6) or co-injected (n = 6) showed no loss of tyrosine hydroxylase-positive cells in the substantia nigra and no circling response to the stimulants. In the second series of experiments, low concentrations of quinolinic acid (2.5, 5.0, 7.5 nmol), picolinic acid (10, 20, 30 nmol), or the two together (7.5 plus 30 nmol, respectively) were microinjected (0.5 microliter) into the dorsal striatum and circling behaviour evaluated. These results revealed dose-dependent contralateral circling with either quinolinate or picolinate; co-injection of the two tryptophan metabolites also produced contralateral circling. It was concluded that picolinic acid blocks the neurotoxic but not the neuroexcitant effects of quinolinic acid.

Animals↗

PubMed1994

Mnemonic deficits in the double Y-maze are related to the effects of nucleus basalis injections of ibotenic and quisqualic acid on choline acetyltransferase in the rat amygdala.

Many researchers have reported that the magnitude of decrease in cortical choline acetyltransferase (ChAT) following excitotoxic lesions of the nucleus basalis magnocellularis (nbm) is unrelated to the degree of cognitive impairment. Recently, an explanation has been offered for this lack of correlation: different excitotoxins, when injected into the nbm, differentially affected cholinergic projections to the cortex and amygdala, and those excitotoxins previously reported to produce the greatest mnemonic deficits produced the largest decreases in amygdaloid ChAT. The present study evaluated the role of amygdalofugal cholinergic projections in memory by comparing the effects of intra-nbm ibotenic and quisqualic acid on cortical and amygdaloid ChAT and on mnemonic performance in the double Y-maze. Rats were trained in the double Y-maze until working and reference memory choice accuracy stabilized to a criterion of > or = 78% correct. Rats then were given either bilateral quisqualic acid (60 nmol in 0.5 microliter), bilateral ibotenic acid (50 nmol in 0.5 microliter), or sham (0.9% saline in 0.5 microliter) lesions of the nbm, and again were tested on the maze. Quisqualate produced a selective impairment of working memory, a large (51%) decrease in cortical ChAT and a small (17%) decrease in amygdaloid ChAT; ibotenate, on the other hand, produced a greater impairment of working memory, an impairment of reference memory, a similar (51%) decrease in cortical ChAT, but a greater (30%) decrease in amygdaloid ChAT. These results suggest that the cholinergic projections from the nbm to the cortex and amygdala play an important role in memory. They suggest that excitotoxins producing greater depletions of amygdaloid ChAT produce greater mnemonic deficits.

Amygdala↗

PubMed1993

Scopolamine injected into the rat amygdala impairs working memory in the double Y-maze.

Recent neurochemical results suggest the hypothesis that the nucleus basalis magnocellularis (nbm) cholinergic projection to the amygdala may play a role in memory. The present study investigated the effects of intra-amygdaloid injections of the cholinergic antagonist scopolamine on working and reference memory in the double Y-maze. Rats were pretrained until working and reference memory choice accuracy stabilized to a criterion of > or = 86% correct. Bilateral cannulae were then surgically implanted in the basolateral amygdaloid complex. Rats (n = 9) received scopolamine in doses of 8.0, 24.0, and 72.0 micrograms/0.5 microliter and saline (0.5 microliter) in a counterbalanced order with retraining to criterion between injections. Intra-amygdaloid scopolamine produced a dose-dependent and differential impairment of working and reference memory. A dose of 24.0 micrograms impaired working memory without significantly affecting reference memory; doses of 8.0 micrograms and 72.0 micrograms affected neither and both types of memory, respectively. Results implicate amygdaloid acetylcholine in memory.

Amygdala↗

PubMed1992

Muscimol injections into the nucleus basalis magnocellularis of rats: selective impairment of working memory in the double Y-maze.

Anatomical and neurochemical results suggest that the cortico- and amygdalopetal cholinergic neurons of the nucleus basalis magnocellularis (NBM) may receive GABAergic inputs. The present experiments were undertaken to evaluate the possible influence of intra-NBM injections of the GABAA agonist, muscimol, on memory. In two experiments, rats were chronically implanted with guide cannulae placed bilaterally into the NBM. Rats were trained to a criterion of at least 83% correct on each component in a double Y-maze task that allowed a dissociation of working and reference memory. The task began with placement into one of the two end arms of the first Y-maze and the reference memory task was to go to the stem for food. Access to the second Y was then given and the working memory task was to go to the goal arm opposite the arm in the first maze from which that trial began. In experiment 1, pre-trained rats (n = 7) received muscimol (0.5 microliter) in doses of 0, 0.01, 0.1 and 1.0 microgram in a counterbalanced order with re-training to criterion between injections. In experiment 2, pre-trained rats (n = 8) received saline, muscimol (0.1 microgram), the GABAA antagonist, bicuculline (0.01 microgram), and muscimol + bicuculline. Results of experiment 1 revealed that intra-NBM muscimol produced a dose-dependent and differential impairment of working and reference memory. A dose of 0.1 microgram impaired working memory without significantly affecting reference memory; doses of 0.01 microgram and 1.0 microgram affected neither and both types of memory, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Scopolamine differentially affects memory of 8- and 16-month-old rats in the double Y-maze.

The present study investigated the effects of scopolamine on working and reference memory in the same rats at 8 and 16 months of age. Rats were trained in the double Y-maze until a criterion of > or = 88% correct was reached on both memory components. Doses of scopolamine (0.1, 0.4, 0.8 mg/kg for rats at 8 months; 0.05, 0.1, 0.4 mg/kg for rats at 16 months) were administered in a counterbalanced order 30 min before test sessions which also included delays of 0, 5, or 30 s prior to both memory components. Results showed that at both ages the 0.1 mg/kg scopolamine dose selectively impaired working memory, whereas higher doses impaired both working and reference memory. Delays selectively decreased working memory choice accuracy and enhanced the effect of scopolamine. Rats at 16 months performed less well on both reference and working memory and showed greater impairments with scopolamine and delays. The present findings support the hypothesis that a decrease in cholinergic neurotransmission contributes to age-related memory deficits.

Aging↗