Some comments concerning the status of research activities of clinical psychologists in the Veterans Administration.
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Humans↗
Biomedical subjects
N Butters
Publications and source records attributed to N Butters.
Comparison of rate of annual change of mental status score in four independent studies of patients with Alzheimer's disease.
Longitudinal studies of subjects with autopsy-proven Alzheimer's disease in one skilled nursing home and of clinically diagnosed cases (NINCDS/ADRDA criteria) in three community cohorts are compared with regard to the annual rate of change in the error score of the Blessed information-memory-concentration test (IMC) in which the maximum number of errors possible is 33. The four cohorts differed significantly from each other in regard to age, education, sex, and the degree of dementia as measured by the initial IMC score. Subjects spanned the age range of 52 to 96 years and had 2 to 20 years of education. The rate of change in error score per year was similar whether the initial error score was 0 to 7, 8 to 15, or 16 to 23; however, the rate was reduced when the initial error score was 24 or above, due to a ceiling effect of the test. Among subjects with initial IMC scores less than 24, the annual rate of change varied considerably. However, the mean annual rate of change, 4.4 errors (SD +/- 3.6, SEM +/- 0.3) per year, was independent of residence in a nursing home, location of the study site, and of the patient's sex or education. Of particular importance was the finding that the rate of change in mental test score was independent of age. It can be concluded that the rate of cognitive deterioration in patients with Alzheimer's disease is quite variable among individuals and is independent of the patient's age and whether the patient resides in the community or in a nursing home.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Priming semantic relations in patients with Huntington's disease.
To investigate the hypothesis that Huntington's Disease involves a breakdown in the organization of the lexico-semantic representational system, mildly and moderately demented patients with Huntington's Disease and age-matched normal control subjects were given a brief battery of language tests and a semantic priming free association task. Results of the language tests provided suggestive, but confounded, evidence for a semantic deficit in Huntington's Disease. Less equivocal evidence was yielded by results of the priming task, which showed a decline in the effect of association strength of primed stimulus-target word pairs on target hit rates. This finding was interpreted as a disruption in the system of spreading activation in a lexico-semantic network. This breakdown was contrasted with the more severe language deficits found in dementias which are primarily cortical in origin.
Dementia↗
Associative encoding and retrieval in Alzheimer's and Huntington's disease.
The associative encoding and retrieval abilities of patients with dementia of the Alzheimer type (DAT) and patients with Huntington's disease (HD) were investigated using an encoding specificity paradigm. When compared to age- and education-matched intact control subjects, both patient groups were severely (and equally) impaired on overall memory for word lists. However, the HD and DAT patients showed differential improvement in recall performance with the introduction of associated cues during stimulus presentation and recall. Although the HD patients, like intact subjects, were able to benefit from semantic retrieval cues (strong and weak) which were present during input, the performance of the patients with DAT improved only with the introduction of strong cues at output, regardless of whether the cues were present or absent during initial presentation. These findings suggest that patients with DAT failed to encode the semantic relationship between the to-be-recalled and cue words and simply generated free associations to the cue words during retrieval. Similarities between the performances of the patients with DAT and alcoholic Korsakoff patients are noted and discussed with regard to the neuropathological basis of the disorders.
Aged↗
Remote memory in a patient with circumscribed amnesia.
It has been suggested that extensive and severe remote memory loss is not a component of a circumscribed amnesic syndrome but may be attributable to problem solving and retrieval deficiencies associated with the frontal lobe damage which is present in some amnesic patients. In order to assess this notion, retrograde amnesia was studied in a patient, W.H., who had no apparent cortical damage revealed by radiological examination, and who evidenced no major cognitive deficiency other than amnesia. Regardless of whether remote memory was measured by recall or recognition procedures, patient W.H. exhibited impaired memory for information from the 1960s, 1970s, and 1980s, but was unimpaired in retrieving information from the 1940s and 1950s. These results demonstrate that retrograde amnesia can occur in patients who have a circumscribed memory deficit.
Amnesia↗
Impaired learning of a motor skill in patients with Huntington's disease.
The ability of patients with Huntington's disease (HD), patients with dementia of the Alzheimer's type (DAT), and amnesic patients (AMN) to acquire the motor skills underlying a pursuit rotor task was assessed. Differences between groups in initial levels of performance were minimized by adjusting the rotation speed of the disk. The HD and DAT groups were also administered a verbal recognition span test. The results showed that the DAT, AMN, and intact control groups all significantly improved their time on target over six test blocks whereas the HD group was severely impaired in the acquisition of this motor skill. On the verbal recognition span test, the DAT and HD groups were significantly and equally impaired, but the HD group evidenced better immediate and delayed recall than did the DAT group. These results provide further evidence that the basal ganglia are critically involved in the acquisition of motor skills.
Alzheimer Disease↗
Lexical and semantic priming deficits in patients with Alzheimer's disease.
Two experiments utilizing priming procedures examined the status of semantic memory in demented and amnesic patients. In the first investigation, lexical priming was assessed in patients with dementia of the Alzheimer type (DAT), Huntington's Disease (HD), alcoholic Korsakoff's syndrome (KS), and in intact control subjects. Subjects were first exposed to a list of words in a rating task and then required to complete three-letter stems with the "first word that comes to mind". Half of the stems could be completed with the previously presented words and the other half were used to assess baseline guessing rates. Recall and recognition of incidentally exposed words was also assessed. Although all three patient groups were impaired on tests of recall and recognition, only the DAT patients exhibited a priming deficit on the stem-completion task. In the second experiment, DAT, HD, and intact control subjects were administered a semantic priming test which required the subject to "free associate" to the first words of previously presented semantically associated word pairs. The results for this association task showed that DAT patients were significantly less likely to produce the second word of the semantically related pair than were the other subject groups. The results of these two experiments suggest that the memory capacities of DAT patients are characterized by a breakdown in the structure of semantic memory and that this impairment is evident on some "automatic" as well as "effortful" processing tasks.
Adult↗
Subcortical signal hyperintensities in bipolar patients detected by MRI.
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Adult↗
Procedural learning in a patient with amnesia due to hypoxia.
It has been claimed that procedural learning on a broad range of perceptuomotor and cognitive tasks is normal in amnesic patients whose severe deficits in acquiring declarative knowledge can be well documented. To evaluate the generality of this proposition we studied procedural learning on three different tasks in an amnesic patient who displayed no signs of intellectual deterioration including problem-solving difficulty. The patient showed normal improvement in learning to read transformed script and normal within-session improvement on a mirror-reading task. However, his retention of the mirror-reading skill from one day to the next was impaired, and he learned the Tower of Hanoi puzzle more slowly than normal. This patient's performance demonstrates that even amnesics without problem-solving difficulties do not perform normally on all tasks that are said to measure procedural learning. In the absence of a clear operational definition of procedural learning the usefulness of the concept remains heuristic.
Amnesia↗
Neuropsychologic deficits and the risk for alcoholism.
The importance of genetic factors in alcoholism has prompted a search for trait or vulnerability markers of a predisposition toward this disorder. Responding to the diverse and at times persistent neuropsychologic impairments observed in alcoholics, several laboratories have documented possible neurocognitive deficits in young men with alcoholic biologic fathers. This paper begins with a review of this complex, and at times contradictory, literature and then presents original data comparing 24 sons of alcoholic fathers with 24 control subjects matched on demography and drinking histories. Among the present sample of students and working men aged 18 to 25 years, the sons of alcoholics demonstrated no significant levels of impairment on the Category Test, the Trail Making Test Part B, Body Sway, Word REcall, or the Missing Digit Test. Taken together with the literature, these negative findings call into question whether any specific array of neurocognitive or psychomotor test results will in the near future prove to be clinically relevant general markers of a risk for alcoholism.
Adult↗
Remote memory in a patient with amnesia due to hypoxia.
It has been suggested that amnesic patients suffer a selective loss of episodic memory while semantic memory remains well preserved. To assess the validity of this idea we studied remote memory in an amnesic patient, (M.R.L.), using several different measures that differ in the extent to which they engage episodic or semantic memory. On two different versions of the Albert et al. (1979) remote memory battery M.R.L. displayed severe retrograde amnesia (RA) extending backwards in time for about 15 years with excellent preservation of older memories. With standard recall instructions his overall performance on the Crovitz test of autobiographical memory was impaired and all of M.R.L.'s specific, temporally dated memories were given from the first half of his life. When asked to reconstruct his past residential history in detail, M.R.L. provide specific and generally accurate information for residences occupied from his boyhood until 1970, but thereafter his memory became quite unreliable. On a test of knowledge of terms commonly employed in the surveying profession, in which he worked for the past 20 years, M.R.L.'s performance was also impaired. The consistent pattern of RA displayed by this patient on all of the tests of remote memory indicates that both episodic and semantic memory are impaired in amnesia.
Amnesia↗
Memory dysfunction and word priming in dementia and amnesia.
Memory performance of patients with the clinical diagnosis of Alzheimer's disease was compared with performance of patients with alcoholic Korsakoff's syndrome and patients with Huntington's disease. Although all patient groups exhibited impairment on tests of verbal memory, only patients with Alzheimer's disease exhibited impaired priming. Priming is an unconscious expression of recently encountered material, and it is intact even in severely amnesic patients. Because mildly demented patients with Alzheimer's disease exhibited impaired priming, damage to brain structures in addition to those damaged in the amnesic syndrome must occur at a relatively early stage of the disease process.
Aged↗
Episodic and semantic memory: a comparison of amnesic and demented patients.
Episodic (recall of passages) and semantic (letter and category fluency) memory tasks were administered to Alzheimer's Disease (early stages), Huntington's Disease (HD), and alcoholic Korsakoff patients matched for overall severity of dementia. Although all three patient groups were severely (and equally) impaired on memory for passages, only the Alzheimer and Korsakoff patients emitted numerous intrusion errors. On the fluency tasks, the performance of the mild Alzheimer patients was distinguishable from that of the other two patient groups. On both fluency tasks, the HD and Korsakoff patients demonstrated severe and moderate deficits, respectively, whereas the mild Alzheimer patients were impaired only on the category fluency task. As with the episodic memory test, the Alzheimer and Korsakoff patients made more perseverative errors than did the HD patients on letter fluency. These findings suggest that Alzheimer and HD patients' impairments on episodic and semantic memory tasks reflect different underlying processes. The performance of Alzheimer patients is affected by their language dysfunction and an increased sensitivity to proactive interference; the deficits of the HD patients appear due to a general retrieval problem. Similarities in the error patterns (i.e., perseveration errors) of Alzheimer and Korsakoff patients are discussed with regard to recent neuropathological findings.
Adult↗
The etiology and neuropathology of alcoholic Korsakoff's syndrome. Some evidence for the role of the basal forebrain.
Recent neuropsychological and neuropathological investigations with long-term alcoholics suggest that the etiology and neuropathology of the Wernicke-Korsakoff syndrome are more complex than previously believed. Although problem-solving and visuoperceptual deficits seem to develop slowly during decades of alcoholism, the amnesic symptoms associated with Korsakoff's syndrome may appear acutely when severe malnutrition and alcoholism are combined. Furthermore, the report that alcoholic Korsakoff patients, like patients with Alzheimer's disease, have endured a substantial neuronal loss in structures comprising the basal forebrain suggests a role for this brain region in the alcoholic patients' amnesic syndrome. Some initial demonstrations of similarities in the memory disorders of alcoholic Korsakoff and Alzheimer patients indicate that Korsakoff's syndrome may be accurately characterized as a "basal forebrain" as well as a "diencephalic" amnesia.
Alcohol Amnestic Disorder↗
Differential patterns of memory loss among patients with Alzheimer's disease, Huntington's disease, and alcoholic Korsakoff's syndrome.
Patients with Huntington's disease (HD), alcoholic Korsakoff's syndrome (KS), and Alzheimer's disease (AD) were compared with normal control subjects on a task designed to assess recognition memory for different classes of stimuli: spatial, verbal, color, pattern, and facial. In addition, recall of verbal stimuli was assessed at two delay intervals. On recognition testing, AD and KS patients were impaired on each of the five stimulus conditions. However, HD patients, though impaired on four of the recognition conditions, were unimpaired when verbal stimuli were used. On recall testing, the AD, HD, and KS groups were equally impaired at the shorter delay (15 s). However, at the longer delay (two minutes), the KS and HD patients, though still impaired relative to the normal control group, performed significantly better than the AD group.
Adult↗
Further analysis of encoding in patients with Huntington's disease.
Arguments favoring the view that derangement of normal encoding processes contributes to the memory defects of patients with Huntington's disease (HD) are supported by the finding that HD patients do not learn highly imageable words more rapidly than they learn words that are difficult to image. But other data indicating that HD patients can use verbal mediators as mnemonic aids for picture recognition question the existence of important and general encoding deficits in HD. In the first of two experiments the influence of imagery on the acquisition and recall of 14-word lists was studied using a free-recall paradigm. Both HD patients and controls learned highly imageable words more quickly and retained them better than low imagery words over a 30-min delay. The impact of imagery on learning was apparent by the first trial. In the second experiment, a modified Brown-Peterson distractor paradigm was used to assess release from proactive interference (PI). It was found that both HD patients and controls exhibited comparable release from PI following a shift in taxonomic categories. The results of both experiments question the importance of encoding deficits in the memorial dysfunctions associated with HD.
Adult↗
An assessment of verbal recall, recognition and fluency abilities in patients with Huntington's disease.
Two investigations concerned with the memory deficits of patients with Huntington's Disease (HD) were performed. In the first experiment, early and advanced HD patients showed superior recognition memory than did alcoholic Korsakoff patients on modified recall and recognition forms of the Rey Auditory Verbal Learning Test. In contrast, on a letter fluency test (FAS) requiring the patients to search their semantic memories, both HD groups produced fewer correct words and perseveration errors than did the alcoholic Korsakoff group. In the second experiment, HD patients and Korsakoff patients were compared in their and recognition of short passages. While the HD and Korsakoff patients were equally impaired on recall tests, the HD patients evidenced significantly better recognition memory than did the amnesic group. As on the fluency test, the prose of the Korsakoff patients was characterized by intrusion (i.e., perseverative) errors. The results of the two experiments indicate that HD and Korsakoff patients' memory deficits are related to deficiencies in retrieval and an increased sensitivity to proactive interference, respectively.
Alcohol Amnestic Disorder↗
Patterns of memory failure after scopolamine treatment: implications for cholinergic hypotheses of dementia.
To test the idea that scopolamine provides a suitable pharmacological model of the memory defects associated with cortical or subcortical dementias, we assessed memory on a battery of tasks in healthy young normal subjects who received 0.5 mg scopolamine, 0.1-0.2 mg glycopyrrolate or physiological saline, once each on three separate occasions, and compared the pattern of memory failure induced by scopolamine to that observed on the same tasks in patients with Alzheimer's disease (AD) or Huntington's disease (HD). In agreement with previous reports, scopolamine impaired acquisition and delayed recall of a 14-word list and disrupted retention on the Brown-Peterson distractor task, whereas the peripherally active anticholinergic glycopyrrolate was without effect. However, under scopolamine the pattern of errors made on these memory tasks was quite different from that seen in patients with AD. Scopolamine did not increase the number of false positive errors on delayed recognition of the word list and also failed to increase the number of prior-item intrusions on the Brown-Peterson task. Also, scopolamine did not impair learning of a symbol-digit paired-associate task, and did not reduce the number of words retrieved or increase the number of words repeated on a standardized verbal fluency test. When the effects of scopolamine on memory were compared to the pattern of impairments observed in demented patients with HD, several differences were found. Although scopolamine clearly produces deficits on some measures of anterograde memory, the present findings question whether anticholinergic drugs adequately mimic the full range of memory impairments observed in cortical or subcortical dementias.
Adult↗