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CURRENT SCIENCE REVIEWS By Joe Bruman October 1998 Page 1 of 3 Plotnik M et al; J Neur N'surg Psych 1998;65:328-337: Old people and PD patients are substantially slower to modify a movement underway. PD patients also are less able to process simultaneous movement responses to two different stimuli. Warner T, Schapira A: J Neur N'surg Psych 1998;64:378-379: Upon discovery two years ago, in a large cluster of autosomal- dominant PD (the Contursi kindred) and two other families, of a mutant gene for alpha-synuclein, the authors tested 70 other patients with sporadic PD for that mutation but found none. There still may be a genetic factor: In a recent study, 26% of supposedly sporadic PD patients turned out to have an affected first- or second-degree relative. JAMA, 19 Aug 1998;594 (new item): National Institute of Neurological Disorders and Stroke (NINDS) scientists moved a step closer to creating an unlimited source of transplantable nerve cells for such disorders as PD. Cultured cells from rat embryos, transplanted into rats with induced PD, have continued to improve motor symptoms for nearly three months. Presumably the technique may be used to culture human cells as well. Lancet, 29 Aug 1998;666 (editorial): Because of genetic closeness to humans, tissue from pig embryos may become a source of transplant material for PD and several other disorders. But porcine endogenous retroviruses may infect recipients and spread to the human population. All trials so far show no such infection, but researchers are still worried. Chen S et al; Arch Neur 1998;55:1075-1080: Pursuing an unusual suspicion that PD might have an autoimmune factor, they extracted IgG (gamma globulin) from serum of 5 PD patients and 10 non-PD controls, and injected it into the substantia nigra of rats. Sure enough, the PD immunoglobulin killed nearly 3 times as many SN neurons as the non-PD IgG. Adler C et al; Arch Neur 1998;55:1089-1095: In one more trial, in 215 patients at the fluctuating stage of PD, tolcapone (Tasmar) was well tolerated, increased "on" time, decreased "off" time, and reduced the requirement for levodopa. Masterman D et al; Arch Neur 1998;55:1201-1208: In 32 PD patients without dementia, unilateral posteroventral pallidotomy improved motor performance and daily functioning without adverse effect on cognition or behavior. Sethi I et al; Arch Neur 1998;55:1211-1216: In a 6-month extension of a prior study, Ropinirole was effective and well tolerated as monotherapy in new PD patients. Mizuno Y (ed); Neur 1998;51:Supp 2: The second International Symposium On Treatment Of PD was held at Kobe, Japan in 1997 (The first was at Tokyo in 1996). The 7 contributed review articles were cited last month, in the CSR for September 1998. Interestingly, author O. Hornykiewicz was also an original co-discoverer of the relation of dopamine to PD, in 1960. A long career. CURRENT SCIENCE REVIEWS By Joe Bruman October 1998 P. 2 of 3 Olanow C (ed); Ann Neur 1998;44:Supp 1: Review articles contributed at the symposium Neuroprotection In Parkinson's Disease, Cannes, France, 31 Oct 97-2 Nov 97: Too numerous (25) to include here, papers were reviewed in a separate posting. They are divided into sections: Introduction, Etiology, Pathogenesis, Apoptosis, and Neuroprotection. Fellows S et al; Brain 1998;121:1771-1784: In a standardized grasp-and-lift task, PD patients were impaired in sensorimotor processing and control. Pfann K et al; Neur 1998;51:796-803: Nine fluctuating patients were tested for bradykinesia before and after pallidotomy. All were much slower in the "on" phase than early-stage patients or healthy controls, but despite great improvement in the "off" phase, "on" phase bradykinesia was unaffected by the operation. So bradykinesia seems due to a different mechanism than other motor impairment symptoms of PD. Antonini A et al; Neur 1998;51:803-810: PET study of 8 PD patients having resting tremor and 8 without showed that the tremor group had distinctly more activity of the thalamo-motor cortical projections, a clue to possible therapy. Goetz C et al; Neur 1998;51:811-814: Comparing 12 PD patients who developed hallucinations within 3 months of starting dopaminergic treatment with 58 others whose hallucinations were delayed a year or more, they found that all the early-onset group had disorders other than PD; mostly DLBD or AD, and some with pre-existing psychiatric illness. Olanow C et al; Neur 1998;51:825-830: Contrary to reports from a large UK study, meta-analysis of mortality among subjects of 5 different controlled trials of selegiline showed no increase, whether those subjects also received levodopa or not. Kumar R et al; Neur 1998;51:850-855: Double-blind clinical study of 7 advanced PD patients at 6 and 12 months after implantation of Deep-Brain Stimulation (DBS) electrode in the sub-thalamic nucleus (STN) showed marked extension of "on" time and reduction of dyskinesia, as well as several other significant benefits. Mori H et al; Neur 1998;51:890-892: Autopsy of a patient with autosomal-recessive juvenile parkinsonism (AR-JP) linked to chromosome 6q showed no Lewy bodies, but some previously unreported signs not typical of idiopathic PD; neurofibrillary tangles and argyrophilic astrocytes in the cerebral cortex and brainstem nuclei. Assal F et al; Lancet, 19 Sep 1998:958: Tolcapone is a most welcome addition to PD therapy, but is not without risk, in rare cases, of fatal liver failure. The product information leaflet mentions one such incident, and authors here describe another, somewhat complicated by abrupt withdrawal of amantadine when Tolcapone was started. Others have reported (CSR Jul 98) that such withdrawal has caused acute delirium and other psychoses. CURRENT SCIENCE REVIEWS By Joe Bruman October 1998 Page 3 of 3 Mamelak A et al; J Neurosurg 1998;89:592-598: A fairly routine bilateral fetal tissue transplant in a PD patient developed a large cyst, which killed 23 months later by compression of the brainstem. Eskandar E et al; J Neurosurg 1998;89:630-634: Unilateral pallidotomy, guided by macrostimulation but not by microrecording, in two patients with advanced PD led only to transient improvement of symptoms. But repeating the procedure with the target site only a few mm away from the first provided lasting improvement. McKenzie R et al; JAMA 1998;280:1061-1066: Although many (nearly all?) PWP complain of constant and often disabling fatigue, it's a mistake to call it Chronic Fatigue Syndrome (CFS). CFS is not related to PD at all, but is associated with a dysregulated hypothalamic-pituitary adrenal axis and hypocortisolemia. Authors here did a randomized controlled trial in 70 people with CFS, of low-dose oral hydrocortisone. It improved symptoms somewhat, but the degree of adrenal suppression precludes its practical use. In contrast, I believe the condition associated with PD has been referred to as "pseudo-fatigue". JAMA 1998;280:1084 (editorial): Discusses the relatively poor understanding of Chronic Fatigue Syndrome despite many decades of research. Among other possibilities, a viral origin is thought to be likely. -- J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks, CA 91403-5013