Multiple Deficit Research Articles

Specificity of Cognitive Impairment in Neurological Disease: A Methodological Critique of Parkinson’s Disease

Multiple cognitive deficits have been recognized in many neurological disorders but the specificity of the findings and the relationship to the underlying neuropathology remain obscure. Definitions of dementia have been proposed based on symptom profiles of the cognitive disorder and qualitative differences have been claimed between dementias of different aetiology. Some conditions have been claimed to show patterns of cognitive deficit that are distinguished from dementia and related to specific neuropathology or psychological processes, e.g. frontal lobe deficits in Parkinson's disease. Sometimes, a relationship has been established between certain cognitive deficits and particular neurochemical deficits which has led to the notion of specific drug treatment, e.g. cholinergic deficits and memory failure in Alzheimer's disease. However, these conclusions are often potentially flawed by methodological inadequacies. This critique presents some methodological issues relevant to the study of brain-behaviour and drug-behaviour relationships in syndromes of multiple cognitive deficit, using Parkinson's disease as the model. The following recommendations are made: rigid diagnostic criteria; representative patient groups; avoidance of arbitrary quantitative criteria to limit definitions of dementia; matching of groups for overall level of cognitive impairment in the search for qualitative cognitive differences related to neuropathology or effects of particular drugs; the use of suitable controls in patient groups, neuropsychological tests and treatment regimes; the use of specific quantitative tests of cognition, affect and motor disability; and longitudinal, compared with cross-sectional, study design.

The effects of imagery instructions on total congenital blind recall

Abstract Research on the performance of total congenital blind subjects in imagery tasks is of particular interest because it helps to evaluate the consequences of their lack of visual experience. The present paper examines some points which remained unclear in the preceding research on the effects of imagery instructions on the recall of blind subjects. In Experiment 1 it is shown that, in a free recall task of unrelated nouns, the blind may take advantage of imagery instructions, independently of the particular requirement to form either common or bizarre images. In Experiment 2 the multiple image processing deficit of the blind found by De Beni and Cornoldi (1988) was again observed, but the effect was not found when the same quantity of material had to be processed verbally. Results are interpreted as showing that, although the blind may follow imagery instructions, their visual handicap creates specific difficulties in creating interactive images involving several items at the same time.

Multiple retention deficit in passive avoidance in rats is eliminated by suprachiasmatic lesions

Rats with suprachiasmatic lesions, sham-operated rats, and intact rats were trained on a one trial step-through passive avoidance task and retested after 18-, 24-, or 30-hr intervals. In agreement with previous reports, intact and sham-operated rats showed a significant deficit in retention performance at 18 and 30 hr compared to the 24-hr training-test interval (TTI). For rats with suprachiasmatic lesions, retention performance was not significantly different at the TTIs used in this experiment. Since suprachiasmatic lesions abolish circadian rhythms in a broad spectrum of behavioral and physiological processes, these results suggest that multiple retention deficits in passive avoidance retention are based on endogenous circadian rhythms.

Serum and C.S.F. levels of transaminases in neurological disorders.

The levels of transaminases in the C.S.F. and the serum in forty cases of various neurological disorders were determined. In most of the cases of tuber-culous meningitis the C.S.F. levels of transaminases showed an increase corresponding to the rise in proteins and cell count. High levels were noted in cases with more severe involvement of the disease with multiple neurological deficit. Some of the cases of epilepsy showed increased contents of serum transaminases. In other cases of neurological disorders the values of C.S.F. and serum transaminases were within the normal limits or showed only a borderline elevation. It is apparent that the estimation of these enzymes in neurological disorders does not have any diagnostic value. It may, however, be possible to correlate the raised transaminase levels with brain damage and thus help to prognosticate the development of sequelae such as paralysis of the extremities and cranial nerves, spinal blocks, cerebral palsy, mental retardation, etc.