Biomedical subjects

R F White

Publications and source records attributed to R F White.

At least 55 records · Page 3Linked to original sources

PubMed1995

Neurobehavioral effects of acute and chronic mixed-solvent exposure in the screen printing industry.

This 2-year prospective study examined the neurobehavioral effects of acute and chronic exposure to mixed solvents in workers in a screen printing business. A total of 30 subjects participated in the study in two field testings over a 12 month period. Each subject completed a detailed medical and occupational questionnaire, had a neurological examination, and underwent a battery of neuropsychological tests. Industrial hygiene investigation identified the following chemical exposures as present: toluene, methyl ethyl ketone, mineral spirits, beta-ether, methylene chloride, and acetic acid. Different departments and jobs had varying degrees of exposure to these chemicals, the highest exposures being in the ink mix area and the screen washroom area. However, all exposure levels were below recommended threshold limit values. Persons categorized as having higher acute exposure demonstrated significantly impaired test performance on tasks involving manual dexterity, visual memory, and mood. Those with higher chronic exposure demonstrated significantly poorer performance on visual memory tasks and mood. Results suggest that the mixed solvents used in the screen printing industry have an effect on central nervous system functioning in the absence of obvious clinical disease.

Adult↗

PubMed1995

Time-related changes in myeloperoxidase activity and leukotriene B4 receptor binding reflect leukocyte influx in cerebral focal stroke.

In previous studies, we have used histological methods to characterize cellular changes, and validated the use of the myeloperoxidase (MPO) activity assay to quantitate increased neutrophil infiltration in ischemic stroke. We also identified increased leukotriene B4 (LTB4) binding sites as a potential marker for neutrophil infiltration into focal ischemic tissue. However, these studies were conducted at only one time-point, 24 h after ischemia. In the present study, we examined the full time-course of MPO activity and LTB4 receptor binding following middle cerebral artery occlusion (MCAO) made permanently (PMCAO) or transiently (160 min followed by reperfusion; TMCAO) in spontaneously hypertensive rats, and compared the results to previously characterized histologic changes in these models. Ischemic and contralateral (control) cortical tissue samples were assayed for MPO (U/g wet wt) and [3H]LTB4 receptor binding (fmol/mg protein). Following PMCAO, MPO activity significantly increased as early as 12 h and continued to increase over the next 5 d (p < 0.05). Following TMCAO, MPO activity was significantly elevated already after only 6 h of reperfusion and also continued to increase over the next 5 d of reperfusion (p < 0.05). LTB4 receptor binding and MPO activity were highly correlated during periods when both measures increased together (i.e., 0.5-5 d; p <0.01). However, by 15 d post-MCAO, LTB4 receptor binding remained elevated after MPO activity levels had returned to normal. This persistent LTB4 binding was associated with the significant gliosis that was characterized previously to persist in these models. The time-course of increased MPO activity and initially increased LTB4 binding post-MCAO correspond very well to our previous histological data that characterized the time-course for leukocyte infiltration under these conditions. Therefore, the increased MPO activity over time was associated with initial neutrophil and later mononuclear cell infiltration into ischemic tissue in these models. In addition, the present studies utilized histochemical analysis to demonstrate peroxidase activity in macrophages within the cerebral infarct following MCAO, thus validating that MPO activity originates from the later infiltrating mononuclear cells in addition to the early infiltrating neutrophils that had been previously characterized in the same manner. TMCAO produces a significantly larger and earlier increase in ischemic cortex MPO activity and a similar later increase in MPO activity compared to PMCAO treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗

PubMed1995

Transforming growth factor-beta 1 exhibits delayed gene expression following focal cerebral ischemia.

Transforming growth factor-beta 1 (TGF-beta 1) is a pleiotropic peptide growth factor. The expression of TGF-beta 1 mRNA in the focal ischemic cortex of rats was studied by means of Northern hybridization. A moderately low level of constitutively expressed TGF-beta 1 mRNA was detected following sham-surgery or in the contralateral (nonischemic) cortex. A significant increase of TGF-beta 1 mRNA level in the ischemic cortex was observed at 2 days (3.2-fold increase compared to sham-operated animals, p < 0.01, n = 4) following permanent occlusion of the middle cerebral artery (PMCAO). The elevated TGF-beta 1 mRNA expression was plateaued for up to 15 days (3.6-fold increase, p < 0.01) following PMCAO. This temporal profile for TGF-beta 1 mRNA expression in focal stroke was significantly delayed compared to that of TNF-alpha, IL-1 beta and IL-6 mRNA expressions as demonstrated previously which peaked at 12 h and decreased to almost basal levels by 5 days following PMCAO. Interestingly, the TGF-beta 1 mRNA expression profile was remarkably parallel with that of monocyte/macrophage accumulation in the ischemic cortex, as well as with the increased formation of extracellular matrix in the focal ischemic brain. These data suggest that TGF-beta 1 may play a role in anti-inflammatory process and in tissue remodeling following ischemic brain injury.

Analysis of Variance↗

PubMed1995

A behavioral evaluation of PCE exposure in patients and dry cleaners: a possible relationship between clinical and preclinical effects.

Long-term deficits in visuospatial function and memory and disturbances in mood have been clinically identified and followed in four patients occupationally exposed to perchloroethylene (PCE). A frontal/limbic hypothesis is offered as the site of pathology. A separate study among 65 dry cleaners was conducted to provide similar evidence of impairment, suggesting a continuum between clinical and preclinical effects. Three exposure zones were identified for the counter clerks, pressers, and operators corresponding to air levels of 11.2, 23.2, and 40.8 ppm. Decrements were found for visual reproductions (14.4%), the number correct (6.7%) and the latency (10%) for pattern memory, and the number correct (3.9%) for pattern recognition. Chronic, life-long deficits appear below 50 ppm and require at least 3 years of exposure. A reexamination of the OSHA standard is recommended and shows that behavioral testing can be used as an early indicator of more serious clinical effects.

Adult↗

PubMed1995

Milestone development in infants exposed to methylmercury from human milk.

Breastfeeding seems to confer an advantage to the infant with regard to neurobehavioral development, possibly in part due to essential nutrients in human milk. However, human milk may be contaminated by environmental neurotoxicants, such as methylmercury. At the Faroe Islands where maternal consumption of pilot whale meat and blubber may well cause a considerable transfer of these neurotoxicants into human milk, 583 infants were followed by district health nurses during the first 12 months after birth. Three developmental milestones that are usually reached between between 5 and 12 months of age, i.e., sitting, creeping and standing, were examined. Infants who reached milestone criteria early had significantly higher mercury concentrations in the hair at 12 months of age. This association is contrary to what would be expected from possible neurotoxic effects of mercury. However, early milestone development was clearly associated with breastfeeding which was again related to increased hair-mercury levels. Milestone development was not associated with indicators of prenatal methylmercury exposure, such as the maternal hair-mercury concentration at parturition. The relationship between early milestone development and high hair-mercury levels in the infant therefore seems to be due to confounding caused by the duration of breastfeeding. No other potential confounder played any role in this regard. This study therefore suggests that, if methylmercury exposure from human milk had any adverse effect on milestone development in these infants, the effect was compensated for or overruled by advantages associated with nursing.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

PubMed1995

The endothelin receptor antagonist SB 217242 reduces cerebral focal ischemic brain injury.

Previously, we demonstrated that cerebral focal ischemic tissue exhibits a significant increase in immunoreactive endothelin (ET). Because increased ET might exacerbate the consequences of cerebral ischemia, we evaluated the effects of the orally active ETA/B receptor antagonist SB 217242 on middle cerebral artery occlusion (MCAO) in the spontaneously hypertensive rat (SHR). SHRs were treated b.i.d. with vehicle or with 3 or 15 mg/kg SB 217242 p.o. for 7 days. Permanent MCAO was performed on day 7 and animals were sacrificed on day 8. Forebrains were stained and the extent of cerebral (i.e., cortical) infarction was determined using image analysis. Hemispheric swelling (%), hemispheric infarct (%), and infarct volume (mm3) were quantitated for each animal. SB 217242 treatment produced a significant decrease in ischemic brain injury. Hemispheric infarction and infarct volume were reduced after the 15 mg/kg treatment (12.0 +/- 1.1% and 69 +/- 6 mm3) compared to vehicle (17.3 +/- 1.5% and 99 +/- 8 mm3) (p < 0.05). No significant effects on hemispheric swelling were observed. This is the first demonstration of an ET receptor antagonist exhibiting efficacy in cerebral focal ischemia. The fact that a 30% reduction in ischemic brain injury can be demonstrated after oral administration of SB 217242 suggests that ET antagonists may be of therapeutic utility in focal stroke.

Animals↗

PubMed1994

Reperfusion following focal stroke hastens inflammation and resolution of ischemic injured tissue.

Previously, we described cellular changes following Permanent Middle Cerebral Artery Occlusion (PMCAO) in spontaneously hypertensive rats. Ischemic changes following PMCAO included a time-related focal pan necrosis, inflammatory cell infiltration, gliosis, and eventual loss of necrotic tissue post PMCAO. We have now characterized changes which occur after Temporary Middle Cerebral Artery Occlusion (TMCAO; 80 or 160 min) followed by reperfusion and compared these changes to those which occur following PMCAO. TMCAO with reperfusion results in cortical infarcts which vary in size in an occlusion-time-dependent manner. After 1 h of reperfusion, ischemic changes were observed histologically, including microhemorrhages and the beginning of a slight inflammatory infiltration in and around the meningeal vasculature. This infiltrate consisted primarily of neutrophils, which by 6 h of reperfusion was significant with infiltration from deep blood vessels into brain tissue, including the presence of some monocytes adhering within blood vessels. Neutrophil infiltration occurred sooner and to a greater extent in reperfused tissues than in permanently occluded tissues, where it only began at 12 h post PMCAO. As occurred following PMCAO, increased Glial Fibrillary Acidic Protein (GFAP) immunoreactivity indicating astrogliosis was first observed at 12 h postTMCAO. Over 1-3 days of reperfusion, a heavy macrophage infiltrate was observed in the reperfused tissues in addition to a continued influx of neutrophils. Following 5 days of reperfusion, the lesion was completely replaced with inflammatory cells, of which macrophages predominated. Unlike PMCAO, which resulted in focal spots of neutrophil accumulation, neutrophils were more distributed throughout the infarcted cortex following TMCAO.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Endothelin levels increase in rat focal and global ischemia.

Endothelin-1, a peptide exhibiting extremely potent cerebral vasoactive properties, is elevated in the cerebrospinal fluid after hemorrhagic stroke and implicated in cerebral vasospasm. The purpose of this study was to determine changes in endothelin in ischemic rat brain by assaying endothelin tissue and extracellular levels. Immunoreactive endothelin levels in ischemic brain tissue following permanent or transient focal ischemia produced by middle cerebral artery occlusion was determined. In addition, endothelin levels were assayed in striatal extracellular fluid collected by microdialysis before, during, and after global ischemia produced by two-vessel occlusion combined with hypotension. Twenty-four hours after the onset of permanent middle cerebral artery occlusion, the ischemic cortex level (0.58 +/- 0.27 fmol/mg protein) of immunoreactive endothelin was significantly (p < 0.05) increased, by 100%, over that in the nonischemic cortex (0.29 +/- 0.13 fmol/mg protein). Transient artery occlusion for 80 min with reperfusion for 24 h also resulted in a similar significant (p < 0.05) increase, 78%, in immunoreactive endothelin in the ischemic zone. Global forebrain ischemia significantly (p < 0.05) increased the level of immunoreactive endothelin collected in striatal microdialysis perfusate, from a basal level of 14.6 +/- 6.7 to 26.5 +/- 7.7 and 26.2 +/- 7.4 amol/microliters (i.e. 82 and 79%). These changes reflect the relative picomolar extracellular concentration increases during ischemia and following reperfusion, respectively. This is the first demonstration of elevated levels of endothelin in focal ischemic tissue and in the extracellular fluid in global ischemia and suggests a role of the peptide in ischemic and postischemic derangements of cerebral vascular function and tissue injury.

Animals↗

PubMed1994

Neuropsychological effects of exposure to naphtha among automotive workers.

The association between exposure to naphtha and neurobehavioural measures was examined prospectively over one year among workers employed at an automotive plant that used naphtha to calibrate fuel injectors. The neurobehavioural tests included those that assess mood, basic intelligence, and functioning of the cerebral frontal lobes and limbic system and were designed so that acute, reversible, and chronic effects of solvent exposure could be assessed. Participants were 248 workers in June 1988, and the testing was repeated on 185 of these workers in 1989. Concentrations of naphtha at the plant ranged from six to 709 mg/m3, although exposure was greater in 1988 than in 1989. Duration of exposure for individual subjects ranged from 0.8 to 7.3 years. Cross sectional data analyses showed significant associations between level of exposure to naphtha and slower timed scores on trails A, and greater reports of negative affective symptoms on profile of mood states scales in 1988 but not 1989. Threshold model analyses of the 1989 data showed an association between score on visual reproductions immediate recall and daily exposure to naphtha at or above 1050 h x mg/m3. Models of chronic exposure showed no associations between chronic exposure and negative neurobehavioural outcome. Results suggest that naphtha produces mild acute reversible effects on function of the central nervous system at or above daily exposures of 540 h x mg/m3 (approximately 90 ppm/h).

Adult↗

PubMed1994

A case-control study of chronic neuropsychiatric disease and organic solvent exposure in automobile assembly plant workers.

A case-control study of chronic neurological and psychiatric disease and occupational exposure to solvents was carried out in eight automobile assembly plants. Cases included 299 subjects who were granted medical disability retirement in 1980-8. Two control groups were selected, the first from those granted retirement in the same period because of medical disability from causes unrelated to solvent exposure. The second included hourly employees from the plant population. In these facilities, solvent exposures tended to be short term and low level, although common: the average duration of exposure was 2.3 years; about 41% experienced at least one day of exposure. Of those exposed, 46% had less than one year of exposure. Results for all psychiatric disease combined (273 cases) suggested that cases had lower exposures than either control group, regardless of how exposure was expressed. Results could not be explained by conventional confounding exposures or characteristics or by usual manifestations of the healthy worker effect. By contrast, chronic neurological disease, and multiple sclerosis in particular, seemed to be associated with exposure, although few cases were identified and observed increases in risk were not statistically significant.

Adult↗

PubMed1994

Tumor necrosis factor-alpha expression in ischemic neurons.

BACKGROUND AND PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with diverse proinflammatory actions, including endothelial leukocyte adhesion molecule expression. Since leukocytes infiltrate into ischemic brain lesions, the present study was conducted to examine whether TNF-alpha messenger RNA (mRNA) and peptide are expressed in the brain after experimental focal stroke and before leukocyte accumulation. METHODS: TNF-alpha mRNA and protein expression were monitored in the ischemic and nonischemic cerebral cortex of rats after focal ischemia produced by permanent middle cerebral artery occlusion. The effect of TNF-alpha administered by microinjection into the brain cortex on leukocyte adherence to brain capillaries was also studied. RESULTS: Induction of TNF-alpha mRNA, normalized to a standard reference rat macrophage TNF-alpha mRNA, was detected as early as 1 hour after middle cerebral artery occlusion. TNF-alpha mRNA was elevated by 3 hours (29 +/- 6% versus 2 +/- 1% in sham-operated rats) only in the ischemic cortex, with peak expression at 12 hours (104 +/- 8%; P < .01). Five days after middle cerebral artery occlusion, TNF-alpha mRNA levels in ischemic cortex were still significantly elevated (38 +/- 5%; P < .05). Also, TNF-alpha mRNA expression was greater in the ischemic cortex of spontaneously hypertensive rats than in normotensive rats (P < .05). Double-labeling, immunohistochemical studies revealed the presence of TNF-alpha protein localized within nerve fibers in the evolving infarct at 6 and 12 hours after ischemia and further expression in the tissues immediately adjacent to the infarct 24 hours after ischemia. After 5 days, the neuronally localized peptide had diminished greatly, but macrophages located within the infarcted tissues were immunoreactive. Cortical microinjections of TNF-alpha (10 ng in 1 microL) produced a significant neutrophil adherence/accumulation in capillaries and small blood vessels 24 hours later. CONCLUSIONS: These results represent the first demonstration that focal cerebral ischemia in rats results in elevated TNF-alpha mRNA and protein in ischemic neurons. The neuronal expression of peptide appears to facilitate the infiltration of inflammatory cells that can further exacerbate tissue damage in cerebral ischemia and might contribute to increased sensitivity and risk in focal stroke.

Animals↗

PubMed1993

Cytokine-induced neutrophil chemoattractant mRNA expressed in cerebral ischemia.

Cytokine-induced neutrophil chemoattractant (CINC), originally identified as a chemoattractant in rat kidney epithelial cells, is related to human 'gro' and murine 'KC'. The proteins encoded by these genes belong to the chemokine alpha superfamily, most of which have neutrophil chemotactic activity. Since brain chemokines may play a significant role in neutrophil accumulation in cerebral ischemia which can contribute to the extent of tissue injury in stroke, we examined the expression of CINC mRNA in the cerebral cortex of rats subjected to focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). Significant CINC mRNA expression was observed in the ipsilateral (ischemic) cortex from 6 h (17.3 +/- 3.7%, n = 6, P < 0.05) to 24 h (32.1 +/- 3.7%, n = 5, P < 0.01) with a peak at 12 h (43.9 +/- 3.7%, n = 6, P < 0.01) after MCAO. Five days post-MCAO, CINC mRNA levels were no longer elevated. No significant CINC mRNA expression was observed in the contralateral (control) cortex. These studies suggest that message for the neutrophil chemoattractant CINC is induced early in brain tissue subjected to ischemia, and therefore supports the possibility that brain-derived chemokines support the infiltration of circulating inflammatory cells following focal stroke.

Animals↗

PubMed1993

Neuron-specific enolase increases in cerebral and systemic circulation following focal ischemia.

Neuron-specific enolase (NSE) is an isoform of the glycolytic enzyme, enolase, and is found in neurons and neuroendocrine cells. We evaluated cerebral immunohistologic and plasma changes in NSE in rats from 2 h to 15 days following permanent or transient middle cerebral artery occlusion (MCAO). At 1-2 days post-MCAO, loss of NSE immunofluorescence from within neurons to the extracellular space was observed in the infarcted areas of all MCAO animals. NSE also was identified intravascularly throughout the brain following MCAO. NSE in plasma was determined by a specific radioimmunoassay. Plasma NSE following permanent or transient MCAO was increased significantly from that observed in controls (2.8 +/- 0.3 ng/ml) beginning at 2 h and persisting for 2.5 days post-MCAO (maximum levels of 8.8 +/- 0.9 to 9.6 +/- 0.5 ng/ml after 6-12 h; P < 0.05, n = 4-9). Quantified contralateral forelimb and hindlimb neurological deficits in these animals were significant and persisted for at least 15 days following MCAO but were not observed following sham surgery. These data suggest that MCAO-induced cortical infarction and neurological dysfunction is associated with neuronal depletion and vascular redistribution of brain NSE resulting in a measurable increase in plasma NSE. Such diffusion of NSE into the cerebral vasculature and systemic circulation from ischemic tissue can be expected to serve as a marker for the incidence of cerebral damage in acute and chronic ischemic brain infarcts.

Animals↗

PubMed1993

Trimethyltin encephalopathy.

A chemistry student was acutely exposed to vapors of an organotin compound. Seventy-two hours later, he exhibited delirium, spatial disorientation, perseveration, inappropriate affect, and memory defects. Five months later, he experienced episodes of complex partial seizures, which continue to require anticonvulsant medication after 7 years. Trimethyltin was identified in blood and urine samples taken 17 days after the accident; the blood level of trimethyltin was elevated 35 days after exposure. Serial electroencephalograms showed persistent left temporal paroxysmal epileptogenic potentials. Serial neuropsychological tests revealed persistent memory defects, cognitive dysfunction, and dysphoria 4 years after exposure. We review acute, resolving, and long-term residual neurotoxic effects of trimethyltin in man. We describe detailed clinical observations, serial neuropsychological test results, electroencephalographic findings, and exposure data in this patient, confirming the limbic system effects of trimethyltin and relating them to the known histopathologic pattern of this condition.

Accidents, Occupational↗

PubMed1993

Magnetic resonance imaging (MRI), neurobehavioral testing, and toxic encephalopathy: two cases.

The objective of this investigation was to examine cerebral magnetic resonance imaging (MRI) pathology and functional deficits demonstrated by neuropsychological testing in cases of toxic encephalopathy. Two subjects, occupationally exposed to toxic chemicals, were studied. As part of their neurological assessment, MRI was done and each underwent a neuropsychological battery for patients with toxic exposures (White et al. Clin. Neuropharmacol. 13(5), 392-412, 1990). In Case 1, who was exposed to inorganic mercury, MRI showed mild central and cortical atrophy. Punctiform foci (T2) were noted in both frontal regions underlying the precentral gyri and in the subcortical myelin. Neuropsychological testing showed problems in cognitive flexibility, cognitive tracking, inhibiting perseveration, fine manual motor coordination, visuospatial analysis and organization, memory, and affect and personality. In Case 2, who was exposed to 2.6-dimethyl-4-heptanone, MRI showed multiple small foci in the white matter and pons. Neuropsychological testing indicated affective changes, deficits in manual motor speed, verbal fluency, visuospatial organization, and short-term memory. Lack of aphasia in patients with toxic encephalopathy indicates that neurotoxins probably affect subcortical and mesial temporal structures more than cortical gray matter. These MRI studies show subcortical sites of pathology.

Behavior↗

PubMed1993

Development of tissue damage, inflammation and resolution following stroke: an immunohistochemical and quantitative planimetric study.

Development and resolution of the lesion produced by occlusion of the middle cerebral artery (MCAO) was studied through quantitative planimetry and histologic/immunohistochemical techniques. MCAO, performed in spontaneously hypertensive rats (SHR), initially (1-3 days) produced large, consistent cerebral cortical infarctions and an increase in ipsilateral hemispheric size (i.e., swelling) quantitated by planimetry on 2,3,5-triphenyltetrazolium chloride (TTC)-stained gross tissue sections. These initial changes correlated well with changes identified from 2 h to 3 days using hematoxylin and eosin stained histologic tissue sections and immunohistochemical techniques including: the progressive development of a cortical area of pan necrosis, infiltration of neutrophils into infarcted tissues, and activation of astroglia. During the initial 2 days following MCAO, glial fibrillary acidic protein immunoreactive cells increased in number and became larger and more intensely fluorescent medial to the cortical infarct. At 5 to 15 days, both the infarct and the ipsilateral hemisphere decreased in size. These changes correlated with the presence of abundant macrophages, and cavitation of the lesion along its medial border. Also during this period, a loose connective tissue matrix formed along the superficial aspect of the infarct. This connective tissue contained fibroblasts, extracellular matrix immunoreactive for laminin and collagen, capillary buds indicating neovascularization, and abundant macrophages. By the final timepoint (30 days), necrotic tissue could no longer be detected in either gross or histologic tissue sections, the inflammatory infiltrate had resolved, and the connective tissue was removed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Microbial transformation of L-696,474, a novel cytochalasin as an inhibitor of HIV-1 protease.

The microbiological transformation of L-696,474 [1], a novel cytochalasin that is an inhibitor of HIV-1 protease, was investigated using Actinoplanes sp. ATCC 53771. Six hydroxylated metabolites 2-7 of 1 were isolated and purified using reversed-phase hplc. All six metabolites were found to have undergone hydroxylation at the C-16 methyl group (C-22) of 1. Three of the compounds, 3, 4, and 5, were further hydroxylated at the para (C-29), the meta (C-28), and both the para and the meta, positions of the phenyl ring, respectively. Metabolites 6 and 7 were shown to result from vicinal dihydroxylation on both C-16 and its attached Me (C-22). The metabolite 7 was further hydroxylated on the meta position of the phenyl ring. The structures of the metabolites were established using spectroscopic techniques including ms, 1H nmr, 13C nmr, and various 2D nmr spectroscopy experiments.

Actinomycetales↗

PubMed1993

The diagnostic utility of savings scores: differentiating Alzheimer's and Huntington's diseases with the logical memory and visual reproduction tests.

Recent research has demonstrated that patients with dementia of the Alzheimer type (DAT) evidence more rapid forgetting than do patients with Huntington's disease (HD). The present study focused on whether such group differences translated into measures with adequate sensitivity and specificity at different stages of these disorders. It was found that measures of forgetting (i.e., savings scores) based upon the Logical Memory and Visual Reproduction tests of the Wechsler Memory Scale--Revised had satisfactory to excellent sensitivity and specificity in differentiating DAT and HD patients from healthy control subjects. Savings scores also had good sensitivity and specificity in differentiating DAT from HD in the early stages of the diseases. However, unsatisfactory specificity may limit the utility of savings scores in differentiating among patients with moderate DAT and HD.

Aged↗