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Biomedical subjects

S Craft

Publications and source records attributed to S Craft.

At least 55 records · Page 3Linked to original sources
PubMed1997

Visual attention in children with prenatal cocaine exposure.

Previous studies have reported that developmental disruption of dopaminergic systems results in lateralized deficits in visual attention (Posner et al., 1991; Craft et al., 1992). Infants who were prenatally exposed to cocaine were hypothesized to have increased reaction times to targets in the right visual field on measures of visual attention compared with infants who were not exposed to cocaine. Seventeen children without prenatal exposure to cocaine and 14 children who were exposed to cocaine (age range from 8-40 months) completed a visual attention task, the Mental Development Index of the Bayley Scales of Infant Development, Second Edition; and the Preschool Language Scale, Third Edition. Cocaine-exposed children were slower to orient to stimuli in the right visual field after repeated trials, especially after attention was first cued to the left visual field. They were also less likely to orient to the right when given a choice. Results suggest that the left hemisphere visual attention system is disproportionately affected by prenatal exposure to cocaine.

Attention↗
PubMed1997

Memory and insulin dependent diabetes mellitus (IDDM): effects of childhood onset and severe hypoglycemia.

Previous studies of the neuropsychological consequences of insulin dependent diabetes mellitus (IDDM) have had mixed and often contradictory results, possibly due to the heterogeneity of the samples and neuropsychological measures, and a lack of specific hypotheses. In order to address this problem, we focused on the effect of severe hypoglycemia on memory functioning in a relatively homogeneous sample of childhood-onset IDDM patients. Given the deleterious effects of hypoglycemia on medial temporal lobe structures (e.g., hippocampus) and the relationship between medial temporal damage and declarative memory functioning, we hypothesized that those patients who had experienced severe hypoglycemia would demonstrate impaired declarative memory and spared nondeclarative memory functioning. Results of the study were generally consistent with this hypothesis, although some impact of hypoglycemia was observed on perceptual priming ability.

Adult↗
PubMed1997

Associative learning in children with perinatal brain injury.

Associate learning for visual nonverbal and auditory verbal items was examined in 21 children with spastic diplegic cerebral palsy (SDCP) and 28 healthy children using four paired associate tasks. SDCP children showed poorer performance than the comparison group for learning pairs that required visual nonverbal responses, regardless of the stimulus modality. Within the SDCP group, lesion severity was assessed in 17 of the children. Lesion severity was related to the level of performance on paired associate tasks requiring visual nonverbal responses; lesion severity did not reach statistical significance for tasks requiring auditory verbal responses. The study suggests: (1) periventricular white matter regions are important for the development of basic learning processes, such as associative learning, and (2) learning of visual nonverbal material is disproportionately affected following white matter injury early in life.

Adolescent↗
PubMed1996

Impact of recent antecedent hypoglycemia on hypoglycemic cognitive dysfunction in nondiabetic humans.

To test the hypothesis that glycemic thresholds for hypoglycemic cognitive dysfunction, like those for neuroendocrine responses to and symptoms of hypoglycemia, shift to lower plasma glucose concentrations after recent antecedent hypoglycemia, 16 healthy young adult subjects (7 women and 9 men) were studied on two separate occasions in random sequence, once with hyperinsulinemic hypoglycemia (2.6 +/- 0.1 mmol/l, 47 +/- 1 mg/dl) and once with otherwise identical hyperinsulinemic euglycemia (4.8 +/- 0.1 mmol/l, 86 +/- 5 mg/dl) between 1430 and 1630. Neuroendocrine, symptomatic, and cognitive responses to hyperinsulinemic stepped hypoglycemic (4.7, 4.2, 3.6, 3.0, 2.8, 2.5, and 2.2 mmol/l; 85, 75, 65, 55, 50, 45, and 40 mg/dl) clamps were quantitated the following morning on both occasions. Cognitive function tests included measures of information processing (Serial Addition), attention (Stroop Arrow Word), pattern recognition and memory (Delayed Non-Match to Sample), and declarative memory (Paragraph Recall). As expected, plasma glucagon (P = 0.0094), epinephrine (P = 0.0063), and pancreatic polypeptide (P = 0.0046) responses to stepped hypoglycemia were reduced significantly, and symptomatic responses tended to be reduced after afternoon hypoglycemia. Performance on the cognitive function tests deteriorated (P < 0.0001) during stepped hypoglycemic clamps, but there were no significant overall effects of antecedent hypoglycemia on hypoglycemic cognitive dysfunction. Although deterioration was reduced (P < 0.05) from the 2.8 mmol/l (50 mg/dl) to the 2.5 mmol/l (45 mg/dl) steps on the Serial Addition and Delayed Non-Match to Sample tasks after afternoon hypoglycemia, comparable differences were not found on the Stroop Arrow Word or Paragraph Recall tasks. Thus, glycemic thresholds for hypoglycemic cognitive dysfunction, unlike those for neuroendocrine responses to and symptoms of hypoglycemia, do not seem to shift to substantially lower plasma glucose concentrations after recent antecedent hypoglycemia in nondiabetic humans.

Adolescent↗
PubMed1995

Working memory following improvements in articulation rate in children with cerebral palsy.

It has been postulated that rehearsal rate is the primary determinant of working memory capacity for verbal material (Baddeley et al., 1975). A previous study of normal control children and children with spastic diplegic cerebral palsy (SDCP) suggested that covert rather than overt rehearsal rate determines working memory capacity (White et al., 1994). In the current study, a subset of SDCP children who received a surgical treatment to relieve spasticity were retested on measures of articulation rate and memory span. A subset of control children from the original study were also retested. The SDCP group showed improvements in articulation rate at follow-up, though memory span did not change and was again equivalent to that of controls. These findings indicate that increases in articulation rate are not necessarily accompanied by improvements in memory span, and provide additional evidence that working memory capacity may be determined by covert rather than overt articulatory rehearsal.

Articulation Disorders↗
PubMed1995

Changes in cognitive performance in children with spastic diplegic cerebral palsy following selective dorsal rhizotomy.

Children with cerebral palsy who receive selective dorsal rhizotomy (SDR) for treatment of spasticity may show suprasegmental changes in upper limb function and control of speech musculature. Anecdotal reports suggest that supra-segmental effects may extend to cognitive functions such as attention and language. This study examined the performance of 16 children with spastic diplegic cerebral palsy on tests of visual attention and other cognitive functions 1 day prior to and 6 months following SDR. Children undergoing SDR were compared with 9 children with spastic diplegia, matched for severity of cerebral palsy and amount of therapy, who did not receive SDR, and 24 age- and sex-matched normal children tested at initial and 6-month follow-up sessions. Children with cerebral palsy treated with SDR showed disproportionately greater improvement in specific attentional and cognitive operations than either of the other groups. These results document cognitive changes following SDR which heretofore were reportedly anecdotally. This improvement may be due to improved mood, reduced physical discomfort, increased therapeutic intervention, or possible cortical effects of SDR.

Attention↗
PubMed1994

Interhemispheric transfer in children with early-treated phenylketonuria.

Phenylketonuria (PKU) is a genetic disorder of amino acid metabolism that is associated with brain catecholamine depletion and deficient myelination. Although neuropsychological deficits have been documented in children with early-treated PKU (ETPKU), no study to date has examined possible effects of impaired myelination in this population. In the present study, interhemispheric transfer time was assessed for 14 children with ETPKU, 22 children with attention deficit-hyperactivity disorder, and 48 normal children, using a manual reaction time paradigm previously validated with callosal agenesis patients (Milner, 1982). Children with ETPKU demonstrated slowed interhemispheric transfer from the left to the right hemisphere as compared with the two other groups. The magnitude of slowing was correlated with age and phenylalanine levels at birth. Results support the hypothesis that abnormal myelination disrupts the development of interhemispheric connections in ETPKU, and suggest that left hemisphere projections may be particularly susceptible to such disruption.

Adolescent↗
PubMed1994

Glucocorticoid-induced impairment in declarative memory performance in adult humans.

Glucocorticoids (GCs) have a variety of effects on the brain including site-preferential, inhibitory effects on hippocampal neurons. In the case of dexamethasone (DEX), extended rather than single-dose treatment in vivo may be required for binding to brain rather than peripheral (e.g., pituitary) GC receptors and for maximizing other biologic effects in hippocampus (e.g., GC receptor downregulation, inhibition of glucose transport). Based on the contributory role of hippocampal neurons in declarative memory performance, we investigated the cognitive consequences of DEX treatment in normal adult human subjects, hypothesizing a decrease in declarative memory performance after extended but not overnight treatment. Double-blind, placebo-controlled treatment with DEX was given at 2300 hr for four consecutive days (0.5, 1, 1, 1 mg, respectively). Plasma sampling (0800 and 1600 hr) and cognitive testing (1600 hr) were performed on study days 0 (baseline), 1, and 4, and 7 d posttreatment. Repeated-measures ANOVA found a significant interaction between study day and treatment condition for correct recall during a paragraph recall task [F(3,51) = 3.52, p = 0.02]. DEX (n = 10) in comparison to placebo (n = 9) treatment decreased correct paragraph recall on study day 4 [F(1,17) = 5.01, p = 0.04] and study day 11 [F(1,17) = 5.82, p = 0.03], with the lowest level of performance occurring on day 4 followed by a return toward baseline performance level by day 11. In the placebo-treated subjects, correct paragraph recall improved over the course of treatment, consistent with practice.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Neuropsychologic effects of stroke in children with sickle cell anemia.

We examined the nature and extent of neuropsychologic impairment in children with sickle cell anemia (SCA) with or without stroke. Twenty-nine children with SCA received cranial magnetic resonance imaging. Strokes were classified into three groups: diffuse cortical stroke (n = 11), anterior stroke (n = 6), or none (n = 12). Children with SCA and 20 age-matched sibling control subjects then received a neurologic examination and a neuropsychologic battery of tests that included motor, verbal, spatial, attentional, and memory measures. Tests of spatial function showed that children with diffuse cortical strokes were impaired, whereas children with anterior lesions had intrusions of irrelevant material during list recall. There were no significant differences between children with stroke and sibling control subjects on motor, verbal, or memory measures. Six children had evidence of stroke on magnetic resonance imaging without any history of a damaging neurologic event. These children had impaired neuropsychologic performance relative to that of sibling control subjects in a pattern similar to that of children with overt stroke. Children with SCA without stroke did not differ from sibling control subjects on any measure. Our results indicate that overt and silent strokes result in lesion-specific neuropsychologic deficits in children with SCA.

Adolescent↗
PubMed1993

Effects of hyperglycemia on memory and hormone levels in dementia of the Alzheimer type: a longitudinal study.

The effect of hyperglycemia on hormone levels, metabolite levels, and memory performance was examined in 22 subjects with very mild and mild probable dementia of the Alzheimer type (DAT) and in 12 normal elderly adults. Subjects were tested in 3 plasma glucose conditions (fasting baseline, 175 mg/dl, and 225 mg/dl) at initial and 18-month follow-up sessions. Initially, adults with very mild DAT showed memory facilitation and elevations in plasma insulin in the 225-mg/dl glucose condition relative to baseline. At follow-up, very mild DAT patients whose dementia had progressed showed significant decreases in insulin and hyperglycemic memory facilitation. Changes in basal insulin and cortisol levels over time were correlated with memory changes for DAT subjects. These results suggest that glucoregulatory abnormalities may contribute to the pathophysiology of DAT.

Aged↗
PubMed1993

Hypoglycemia-associated autonomic failure in insulin-dependent diabetes mellitus. Recent antecedent hypoglycemia reduces autonomic responses to, symptoms of, and defense against subsequent hypoglycemia.

We hypothesize that in patients with insulin-dependent diabetes mellitus (IDDM), recent antecedent iatrogenic hypoglycemia is a major cause of hypoglycemia-associated autonomic failure, a disorder distinct from classical diabetic autonomic neuropathy (CDAN), and that hypoglycemia-associated autonomic failure, by reducing both symptoms of and defense against developing hypoglycemia, results in recurrent iatrogenic hypoglycemia, thus creating a vicious cycle. We used the hyperinsulinemic (12.0 pmol.kg-1.min-1) stepped hypoglycemic clamp technique to assess autonomic and symptomatic responses to hypoglycemia and the insulin infusion test (4.0 pmol.kg-1.min-1) to assess defense against hypoglycemia on mornings before and after clamped afternoon hypoglycemia (approximately 2.8 mmol/liter) and hyperglycemia (approximately 11.1 mmol/liter) in patients with IDDM. Compared with nondiabetic subjects, IDDM with or without CDAN exhibited reduced epinephrine (P = 0.0222 and 0.0040) and pancreatic polypeptide (P = 0.0083 and 0.0056) responses to hypoglycemia. After afternoon hypoglycemia, lower plasma glucose concentrations were required to elicit autonomic and symptomatic responses during morning hypoglycemic clamps in patients without CDAN. At the 2.8 mmol/liter step, mean (+/- SE) epinephrine levels were 1,160 +/- 270 and 2,040 +/- 270 pmol/liter (P = 0.0060), pancreatic and total symptom scores were 22 +/- 3 and 41 +/- 7 (P = 0.0475) after afternoon hypoglycemia and hyperglycemia, respectively. During morning insulin infusion tests after afternoon hypoglycemia, nadir plasma glucose concentrations were 2.6 +/- 0.2 mmol/liter compared with 3.3 +/- 0.3 mmol/liter (P < 0.001) at the corresponding time points after afternoon hyperglycemia. Thus, we conclude: (a) elevated glycemic thresholds for autonomic responses to hypoglycemia are a feature of IDDM per se, not classical diabetic autonomic neuropathy; and (b) a single episode of afternoon hypoglycemia results in both elevated glycemic thresholds for autonomic and symptomatic responses to hypoglycemia and impaired physiological defense against hypoglycemia the next morning in IDDM.

3-Hydroxybutyric Acid↗
PubMed1993

Mechanism of awareness of hypoglycemia. Perception of neurogenic (predominantly cholinergic) rather than neuroglycopenic symptoms.

We sought 1) to determine which symptoms of hypoglycemia are reproducible, 2) to pharmacologically distinguish neurogenic (autonomic) from neuroglycopenic symptoms, and 3) to test the hypothesis that awareness of hypoglycemia is the result of perception of neurogenic rather than neuroglycopenic symptoms. Awareness of hypoglycemia and 19 symptoms were quantitated in 10 normal, young adults, each studied on four occasions in random sequence, during 1) clamped euglycemia (approximately 5 mM), 2) clamped hypoglycemia (approximately 2.5 mM), 3) clamped hypoglycemia with combined alpha- and beta-adrenergic blockade (phentolamine and propranolol), and 4) clamped hypoglycemia with pan-autonomic blockade (phentolamine, propranolol and atropine). Significant (ANOVA, P < 0.001) treatment effects on the awareness of hypoglycemia ("blood sugar low") were noted. No change occurred in the score for this during euglycemia, but the mean +/- SE increase was 2.1 +/- 0.4 during hypoglycemia. This increase was not reduced significantly by adrenergic blockade (1.6 +/- 0.5), but was reduced significantly and substantially (approximately 70%) by pan-autonomic blockade (0.6 +/- 0.3). Significant neurogenic symptoms included shaky/tremulous (P < 0.001), heart pounding (P < 0.001), and nervous/anxious (P = 0.002), all adrenergic; and sweaty (P < 0.001), hungry (P < 0.001), and tingling (P = 0.009), all cholinergic. Significant neuroglycopenic symptoms, those produced by hypoglycemia but not reduced by pan-autonomic blockade, included warm (P < 0.001), weak (P = 0.011), difficulty thinking/confused (P = 0.004), and tired/drowsy (P = 0.003). We conclude that muscarinic cholinergic mechanisms mediate an important and previously uncharacterized component of the neurogenic symptoms of hypoglycemia and awareness of hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1992

Lateralized deficits in visual attention in males with developmental dopamine depletion.

Children with early treated phenylketonuria (ETPKU), a disorder associated with developmental dopamine depletion, were tested with a visual orienting paradigm to determine the existence of lateralized deficits in specific attentional operations. Male ETPKU subjects showed a right visual field impairment in disengaging attention, indicating left hemisphere dysfunction, and overall slowed reaction times. Female ETPKU and normal subjects did not differ. The results suggest that for males, dopamine depletion disrupts left hemisphere function. This finding has important implications for disorders with suspected developmental dopamine abnormalities, and may also illustrate how sex differences in functional lateralization develop in the normal brain.

Attention↗
PubMed1992

Glucose and memory in mild senile dementia of the Alzheimer type.

Glucose utilization appears to play a role in memory, and patients with Senile Dementia of the Alzheimer Type (SDAT) show particular abnormalities of the glucose system. The present study examined the effects of glucose administration on memory in subjects with mild SDAT and age-matched controls. SDAT subjects demonstrated greater overall increases in blood glucose levels following glucose administration. Normal subjects whose blood glucose levels returned to near baseline following glucose administration showed facilitated memory performance, whereas SDAT subjects whose blood glucose levels remained elevated showed significant improvement following glucose administration. The results suggest that impaired glucose regulation contributes to memory impairment in SDAT.

Aged↗
PubMed1991

Higher glycemic thresholds for symptoms during beta-adrenergic blockade in IDDM.

We tested the hypotheses that nonselective beta-adrenergic blockade does not cause absolute hypoglycemia unawareness but shifts the glycemic thresholds for symptoms to lower plasma glucose concentrations and that neither neuroglycopenic symptoms nor cognitive impairments during hypoglycemia are altered by beta-adrenergic blockade. To do so, we applied the euglycemic and stepped hypoglycemic clamp techniques to patients with moderately controlled insulin-dependent diabetes mellitus (IDDM) in the absence (n = 8) and presence (n = 9) of the nonselective beta-adrenergic antagonist propranolol. Compared with the corresponding euglycemic clamps, total symptom scores first increased at the 4.4-mM plasma glucose step (a higher level than that of 2.8 mM in nondiabetic subjects studied previously) in the absence of propranolol. Beta-adrenergic blockade did not produce absolute hypoglycemia unawareness. Indeed, at the frankly hypoglycemic step of 2.8 mM, total symptom scores tended to be higher in the presence than in the absence of propranolol. This was largely the result of greater (P less than 0.01) perception of diaphoresis. However, symptom scores did not increase until the 3.3-mM plasma glucose step during beta-adrenergic blockade. The perception of hunger, and perhaps that of tremulousness, was reduced by propranolol at the higher glucose steps. Neuroglycopenic symptoms were not reduced by propranolol. The cognitive function of memory, but not that of attention, was impaired, also starting at the 4.4-mM glucose step. This was not impaired further by propranolol. Thus, we formed the following conclusions. 1) Nonselective beta-adrenergic blockade does not cause absolute hypoglycemia unawareness but shifts the glycemic thresholds for symptoms to lower plasma glucose concentrations in patients with IDDM. 2) Beta-adrenergic blockade does not reduce neuroglycopenic symptoms, and it does not further impair cognitive function during hypoglycemia in IDDM patients.

Adult↗
PubMed1989

Contributions of clinical neuropsychology to the study of schizophrenia.

Clinical neuropsychological findings are examined with respect to competing hypotheses about localized neuropathology in schizophrenia. Two general models of structural and functional impairment are described. The first addresses deficits in cortical/subcortical processes concerned with arousal, attention, and higher cortical functions. The second addresses impairments in the balance of lateralized functions consistent with left hemisphere overactivation. Empirical data provide support for both models, and suggest that the explanatory power of these models may vary when they are applied to different subtypes of schizophrenia.

Cerebral Cortex↗