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General Cognitive Ability Following Unilateral and Bilateral Fetal Ventral Mesencephalic Tissue Transplantation for Treatment of Parkinson's Disease

Kimberlee J. Sass, PhD; Cathleen P. Buchanan; Michael Westerveld, PhD; Kenneth L. Marek, MD; Anita Farhi, RN; Richard J. Robbins, MD; Frederick Naftolin, MD, DPhil; Timothy L. Vollmer, MD; Csaba Leranth, MD, PhD; Robert H. Roth, PhD; Lawrence H. Price, MD; Benjamin S. Bunney, MD; John D. Elsworth, PhD; Paul B. Hoffer, MD; D. Eugene Redmond, MD; Dennis D. Spencer, MD
Arch Neurol. 1995;52(7):680-686. doi:10.1001/archneur.1995.00540310050016.
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Objective:  To contrast the neuropsychological profiles of Parkinsonian patients, before and after fetal ventral mesencephalic tissue transplantation.

Design:  Case series of personally examined patients.

Setting:  Patients were evaluated by neurologists, neurosurgeons, and neuropsychologists as outpatients at a university hospital.

Patients:  Fetal mesencephalic tissue was implanted in the right caudate nucleus of three patients and both nuclei of one patient. These patients were evaluated prior to surgery and at 12, 24, and 26 months postoperatively.

Results:  Factor analysis of the test battery identified four statistically orthogonal test clusters. No statistically significant changes were identified postoperatively for clusters assessing verbal cognitive ability, nonverbal cognitive ability, and information-processing speed. An improvement of verbal memory cluster index was observed 12 months after surgery, and the improvement reached the level of statistical significance at 24 months after surgery. However, the verbal memory of all patients declined between 24 and 36 months after surgery.

Conclusions:  Fetal tissue transplantation to one or both caudate nuclei did not permanently 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 because the impairments of cognitive ability associated with Parkinson's disease do not appear to originate solely from dopamine deficiency.


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