GENERAL COGNITIVE-ABILITY FOLLOWING UNILATERAL AND BILATERAL FETAL VENTRAL MESENCEPHALIC TISSUE-TRANSPLANTATION FOR TREATMENT OF PARKINSONS-DISEASE

Citation
Kj. Sass et al., GENERAL COGNITIVE-ABILITY FOLLOWING UNILATERAL AND BILATERAL FETAL VENTRAL MESENCEPHALIC TISSUE-TRANSPLANTATION FOR TREATMENT OF PARKINSONS-DISEASE, Archives of neurology, 52(7), 1995, pp. 680-686
Citations number
40
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00039942
Volume
52
Issue
7
Year of publication
1995
Pages
680 - 686
Database
ISI
SICI code
0003-9942(1995)52:7<680:GCFUAB>2.0.ZU;2-X
Abstract
Objective: To contrast the neuropsychological profiles of Parkinsonian patients, before and after fetal ventral mesencephalic tissue transpl antation. Design: Case series of personally examined patients. Setting : Patients were evaluated by neurologists, neurosurgeons, and neuropsy chologists as outpatients at a university hospital. Patients: Fetal me sencephalic tissue was implanted in the right caudate nucleus of three patients and both nuclei of one patient. These patients were evaluate d prior to surgery and at 12, 24, and 26 months postoperatively. Resul ts: Factor analysis of the test battery identified four statistically orthogonal test clusters. No statistically significant changes were id entified postoperatively for clusters assessing verbal cognitive abili ty, nonverbal cognitive ability, and information-processing speed. An improvement of verbal memory cluster index was observed 12 months afte r surgery, and the improvement reached the level of statistical signif icance at 24 months after surgery. However, the verbal memory of all p atients declined between 24 and 36 months after surgery. Conclusions: Fetal tissue transplantation to one or both caudate nuclei did not per manently arrest cognitive dysfunction. Although there is some evidence of improved cognitive ability after transplantation, it is improbable that normal cognitive function can be restored by this procedure beca use the impairments of cognitive ability associated with Parkinson's d isease do not appear to originate solely from dopamine deficiency.