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Year : 2006  |  Volume : 54  |  Issue : 3  |  Page : 246--247

Cognitive substrates and their treatments in neurodegenerative diseases

Edward C Lauterbach 
 Department of Psychiatry and Behavioral Sciences, Mercer University School of Medicine, 655 First Street, Macon, Georgia - 31201, USA

Correspondence Address:
Edward C Lauterbach
Department of Psychiatry and Behavioral Sciences, Mercer University School of Medicine, 655 First Street, Macon, Georgia - 31201
USA




How to cite this article:
Lauterbach EC. Cognitive substrates and their treatments in neurodegenerative diseases.Neurol India 2006;54:246-247


How to cite this URL:
Lauterbach EC. Cognitive substrates and their treatments in neurodegenerative diseases. Neurol India [serial online] 2006 [cited 2023 Mar 27 ];54:246-247
Available from: https://www.neurologyindia.com/text.asp?2006/54/3/246/27142


Full Text

Neurodegenerative diseases with known neuropathologies provide a natural laboratory for the study of functional neural circuitry. Systematic cognitive probing of diseases of differing neuropathology offers the hope of understanding the contributions of select neural systems in mediating distinct cognitive processes. It can also reveal differential cognitive risks and morbidities imposed by specific diseases, important to the clinician.

In this issue of Neurology India , Krishnan and colleagues[1] report their observations on global and frontal cognition in three neuropathologically - different neurodegenerative disorders, progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and Parkinson's disease (PD). Their study incorporates several elegant methodological features, including the use of clinically - accepted diagnostic criteria, distinction between "possible" and "probable" diagnostic levels of certitude, systematic use of the Unified Parkinson's Disease Rating Scale (UPDRS) across diseases and probes of global vs. frontal cognitive function. These features allow inferences to be drawn about the impacts of disease severity and parkinsonism upon specific types of cognition.

Confirming previous results, both global and frontal impairments were most severe in PSP and global cognitive impairments were more severe in PD than in MSA. Newer findings observed by Krishnan et al include a lack of correlation of impairments with UPDRS scores in PSP, more severe frontal executive impairments in MSA than in PD and relations of frontal impairments to disease severity and UPDRS scores in MSA. One possible interpretation is that neurodegenerative effects are more potent than hypodopaminergic neurophysiological effects upon basal ganglia circuit functions, particularly in regard to frontal cognitive systems. Their finding of more trail-making test part B errors in PD than in MSA may, however, represent an artifact of sampling since their PD patients had more advanced disease and UPDRS scores (PD 50.6 17.4 vs. MSA 22.5 6.6). In a previous study that matched for parkinsonism severity, Soliveri and colleagues[2] found greater fluency impairment in MSA than in PD, adding to the list of MSA frontal impairments.

Krishnan et al consider that frontotemporal, pallidal, subthalamic and thalamic pathology in PSP and striatal pathology in MSA, in contrast with PD, may account for their findings. While MSA has been observed to be relatively free of dementia, the authors make the important clinical point that executive dysfunction in MSA may not be evident until the disease progresses, suggesting a clinical need for serial executive testing in MSA. Indeed, Pillon and colleagues[3] have previously documented the dysexecutive syndrome of striatonigral degeneration (MSA-P).

Specific neuropsychological and neuropsychiatric differences are slowly emerging in PSP, MSA and PD.[4] Future studies in these diseases may reveal more about the functional neuronal circuit routines of cognitive test components by fMRI imaging of the activity underlying their performance. Some day it may even be possible to select treatments based on specific neuropathologies or pathophysiologies. Robbins et al[5] demonstrated differing disease-specific mechanisms of executive and working memory impairment in PSP, MSA and PD. These authors also found differing disease-specific strategies employed by patients to compensate for these deficits. Understanding distinct plural pathophysiologies that underlie single functional deficits in different neurodegenerative diseases may ultimately generalize to allow selection of specific pharmacotherapeutic approaches for treating specific impairments across the diversity of neurological diseases.

References

1Krishnan S, Mathuranath PS, Sarma S, Kishore A. Neuropsychological functions in progressive supranuclear palsy, multiple system atrophy and Parkinson's disease. Neurol India 2006;54:268-72.
2Soliveri P, Monza D, Paridi D, Carella F, Genitrini S, Testa D, et al . Neuropsychological follow up in patients with Parkinson's disease, striatonigral degeneration type multisystem atrophy and progressive supranuclear palsy. J Neurol Neurosurg Psychiatry 2000;69:313-8.
3Pillon B, Gouider-Khouja N, Deweer B, Vidailhet M, Malapani C, Dubois B, et al . Neuropsychological pattern of striatonigral degeneration: Comparison with Parkinson's disease and progressive supranuclear palsy. J Neurol Neurosurg Psychiatry 1995;58:174-9.
4Lauterbach EC. The neuropsychiatry of Parkinson's disease and related disorders. Psychiatr Clin North Am 2004;27:801-25.
5Robbins TW, James M, Owen AM, Lange KW, Lees AJ, Leight PN, et al . Cognitive deficits in progressive supranuclear palsy, Parkinson's disease and multiple system atrophy in tests sensitive to frontal lobe function. J Neurol Neurosurg Psychiatry 1994;57:79-88.