Multiple sclerosis and other neurological disorders

Current Opinion in Psychiatry

Volumn 11, Issue 3, 1998, Pages 311-314

  Foong, Jacqueline ^a   Ron, Maria ^a  

^a UNIVERSITY COLLEGE LONDON   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

AMYOTROPHIC LATERAL SCLEROSIS; COGNITIVE DEFECT; HUMAN; MEDICAL RESEARCH; MENTAL DISEASE; MULTIPLE SCLEROSIS; NEUROFIBROMATOSIS; NEUROLOGIC DISEASE; NEUROPSYCHIATRY; NEUROPSYCHOLOGY; SHORT SURVEY; STROKE; SYMPTOM;

EID: 0031946490     PISSN: 09517367     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001504-199805000-00013     Document Type: Short Survey

References (20)

1. Kujala P, Portin R, Ruutiainen J. Memory deficits and early cognitive deterioration in multiple sclerosis. Acta Neurol Scand 1996; 93:329-335.
2. Basso MR, Beasonhazen S, Lynn J, Rammohan K. Borstein RA. Screening for cognitive function in multiple sclerosis. Neurology 1996; 53:980-984.
3. Losseff NA, Wang L, Lai HM, Yoo DS, Gawne-Cain ML, McDonald, et al. • Progressive cerebral atrophy in multiple sclerosis. A serial MRI study. Brain 1996; 119:2009-2019. This study detected progressive cerebral atrophy in a group of multiple sclerosis patients who were examined over an 18-month period, which was correlated with deterioration in physical disability.
4. Kujala P, Portin R, Ruutiainen J. The progress of cognitive decline •• in multiple sclerosis-a controlled 3 year follow-up. Brain 1997; 120:289-297. This study illustrates the natural progression of cognitive deficits in multiple sclerosis patients and indicates that progressive cognitive deterioration is a feature in multiple sclerosis. Patients with mild cognitive impairment had deteriorated after 3 years but those who were cognitively intact remained stable.
5. Foong J, Rocewicz L, Quaghebeur G, Davie CA, Kartsounis L, Thompson •• AJ, et al. Executive function in multiple sclerosis: the role of frontal lobe pathology. Brain 1997; 120:15-26. This study has further characterized executive deficits in multiple sclerosis patients and, more importantly, has highlighted the difficulty in attributing specific neuropsychological deficits to focal brain pathology in a widespread disease such as multiple sclerosis.
6. Foong J, Rocewicz L, Quaghebeur G, Thompson AJ, Miller DH. Ron MA. Neuropsychological deficits following acute relapse in multiple sclerosis. J Neurol Neurosurg Psychiatry 1997 (in press).
7. North KN, Riccardi V, Samagosprouse C, Ferner R, Moore B, Legius E, • et al. Cognitive function and academic performance in neurofibromatosis 1: consensus statement from the NF1 cognitive disorders task force. Neurology 1997; 48:1121-1127. This review article discusses the current understanding and future research of the clinical aspects and pathophysiological mechanisms in cognitive impairment in neurofibromatosis.
8. Said SMA, Yeh TL, Greenwood RS, Whitt JK, Tupler LA, Krishnan KRR, • MRI morphometric analysis and neuropsychological function in patients with neurofibromatosis. NeuroReport 1996; 7:1941-1944. Cerebral gray and white matter volumes were measured in 22 children with neurofibromatosis. Compared with control individuals, patients had increased brain volumes, particularly in white matter. Performance on two visuospatial tasks were positively correlated with right hemisphere gray matter volume. The authors suggested that this is a result of a failure of growth control leading to aberrant neurodevelopment.
9. Zoller M, Rembeck B, Backman L. Neuropsychological deficits in adults • with neurofibromatosis type 1. Acta Neurol Scand 1997; 95:225-232. One of the few studies examining cognitive deficits in adults with neurofibromatosis. Seventy patients were assessed and the pattern of cognitive deficits detected was similar to that reported in subcortical dementia.
10. Massman PJ, Sims J, Cooke N. Haverkamp LJ, Appel V, Appel SH. • Prevalence and correlates of neuropsychological deficits in amyotrophic lateral sclerosis. J Neurol Neurosurg Psychiatry 1996; 61:450-455. Comprehensive neuropsychological testing was conducted in a large sample of ALS patients and approximately one-third of patients were found to have significant cognitive impairment. Patients with dysarthria were found to be more impaired than were nondysarthric patients.
11. Abe K, Fujimura H, Toyooka K, Sakoda S. Yorifuji S, Yanagihara T. Cognitive function in amyotrophic lateral sclerosis. J Neurol Sci 1997; 148:95-100.
12. Abrahams S, Goldstein LH, Alchalabi A, Pickering A. Morris RG, •• Passingham RE, et al. Relation between cognitive dysfunction and pseudobulbar palsy in amyotrophic lateral sclerosis. J Neurol Neurosurg Psychiatry 1997; 62:464-472. Tests of executive function were used to provide further evidence of frontal lobe dysfunction in ALS patients. Executive deficits appeared to be more prominent in patients with pseudobulbar palsy.
13. Abrahams S. Goldstein LH, Kew JJM, Brooks DJ, Lloyd CM, Frith CD, • Leigh PN. Frontal lobe dysfunction in amyotrophic lateral sclerosis - a PET study. Brain 1996; 119:2105-2120. This study assessed regional cerebral blood flow on positron emission tomography to explore frontal lobe dysfunction in ALS. An activation paradigm of verbal fluency (an executive frontal lobe test) was compared with word generation and repetition. Cognitively impaired ALS patients were impaired on executive tests and displayed significantly impaired activation of cortical and subcortical regions, including dorsal-lateral prefrontal cortex, compared with nondemented patients and control individuals.
14. House A. Depression associated with stroke. J Neuropsychiatry Clin Neurosci 1996: 8:453-457.
15. Morris PLP, Robinson RG, Raphael B, Hopwood MJ. Lesion location and •• post stroke depression. J Neuropsychiatry Clin Neurosci 1996; 8:399-403. This study supports previous research findings that the location of stroke lesion is important in poststroke depression. Results indicated that there was an increased frequency of depression in patients with lesions involving left hemisphere prefrontal and basal ganglia regions compared with patients with lesions in other areas of the left hemisphere or with right hemisphere lesions.
16. Lauterbach EC, Jackson JG, Price ST, Wilson AN, Kirsh AD, Dever GEA. • Clinical, motor and biological correlates of depressive disorders after focal subcortical lesions. J Neuropsychiatry Clin Neurosci 1997; 9:259-266. In a small sample of patients, depression after focal subcortical lesions was reported to be mainly associated with pallidal lesions implicating pallidothalamic pathways to the frontal lobe. The authors suggest that these patients should be closely monitored for depression and especially if accompanied by symptoms of parkinsonism or dystonia.
17. Phillips NA, Matekole CC. Cognitive deficits in peripheral vascular disease: •• a comparison of mild stroke patients and normal control subjects. Stroke 1997; 28:777-784. In this study, patients with peripheral vascular disease were examined and neuropsychological deficits were detected, particularly in patients with severe peripheral vascular disease. The pattern of cognitive impairment was similar to that is patients with cerebrovascular disease (unilateral atherothrombotic brain infarctions). Brain imaging would have been of interest but was not performed in this study. The findings suggest the presence of early vascular related brain dysfunction and therefore longitudinal studies should be conducted in view of the clinical implications.
18. Pohjasvaara T, Erkinjuntti T, Vataja R, Kaste M. Dementia three months after stroke: baseline frequency and effect of different definitions of dementia in the Helsinki Stroke Aging Memory Study (SAM) cohort Stroke 1997; 28:782-792.
19. Desmond DW, Moroney JT, Sano M, Stern Y. Recovery of cognitive function after stroke. Stroke 1996; 27:1798-1803.
20. Bokura H. Robinson RG. Long term cognitive impairment associated with caudate stroke. Stroke 1997; 28:970-975.