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CURRENT SCIENCE REVIEWS By Joe Bruman January 1999 Page 1 of 3 Rinne U et al; Neur 1998;51:1309-1314: In a 6-month formal trial on 171 PD patients at the fluctuation, or wearing-off, stage, entacapone (Comtan in U.S., Comtess elsewhere) was safe and effective, prolonging duration of response to levodopa, irrespective of reducing the levodopa dose. The most commonly reported adverse event was diarrhea. Valldeoriola F et al; Neur 1998;51:1315-1320: An unexpected startling noise, combined with the visual "go" signal, shortens reaction time in normal subjects and patients having idiopathic PD or Multiple System Atrophy (MSA), but not in those with Progressive Supranuclear Palsy (PSP). Ziv I et al; Neur 1998;51:1583-1586: Enhanced motor fatigue in PD is one of the most often reported disabling symptoms, but poorly understood. They tested 17 PD patients and 10 controls, finding that fatigue is much more prominent in PD but that it quickly improves after an oral dose of levodopa. It's part of the spectrum of PD symptoms. Agundez J et al; Neur 1998;51:1587-1592: They studied 121 unrelated sporadic-PD patients and 121 healthy controls, for mutations of the gene for arylamine N-acetyl transferase (NAT2), finding it significantly more frequent in those patients with early-onset PD. Baker K et al; Neur 1998;51:1592-1598: Electromyographic (EMG) study of the thyroarytenoid muscle, whose weakness in aging and PD causes hypophonia. Uitti R et al; Neur 1998;51:1755-1757: In 41 consecutive PD patients who had microelectrode guided unilateral posteroventral pallidotomy, motor function improved and the efficacy of levodopa therapy was sustained. Parsian A et al; Neur 1998;51:1757-1759: They screened additional cases of familial PD for the mutant alpha-synuclein gene of the Contursi PD kindred, but found none. Mendez E et al; J Neur N'surg Psych 1998;65:921-923: Checking a suggestion that a deficit in timing might account for the sensory disturbances reported in PD, they did neuropsycho- logical tests on PD patients and healthy controls both young and old. Time discrimination in PD patients was normal and didn't slow the initial steps of visual processing. Lucotte G et al; J Neur N'surg Psych 1998;65:948-949: Following the dramatic announcement (see CSR DEC 96) by a U.S. team of a mutant gene for alpha-synuclein in a large Italian kindred of PD patients, these authors looked for it in both sporadic and familial French PD patients, and didn't find it. Roche Labs Inc.; Tolcapone (Tasmar) original leaflet:1998: After 53 days taking tolcapone, a patient developed diarrhea, followed in 4 days by jaundice, and died on day 60. Although no liver function tests were done, evidently it looked enough like fulminant liver failure that the leaflet also advised monthly testing of tolcapone users, and quitting if the enzyme level reaches more than 5 times upper limit of normal range. CURRENT SCIENCE REVIEWS By Joe Bruman January 1999 P. 2 of 3 Lancet; 28 February 1998:653 (news item): In a single ward of an Italian hospital, 7 out of 15 patients suddenly died of fulminant liver failure due to hepatitis B, 9 to 10 weeks after suspected exposure by a 2-day stay of a patient (who died later from other causes) with hepatitis B. Virus-induced liver failure is said to be indistinguishable from that induced by a drug, and the long incubation period is strikingly similar to that of some drug-induced cases. Assal F et al; Lancet; 19 September 1998:958: (cited earlier in CSR OCT 98) Nine weeks after starting tolcapone, a PD patient entered the hospital with jaundice and encephalopathy. Hepatic enzymes had been checked repeatedly and were normal, but on admission her ALT level was over 8 times the upper limit of normal range. She died in hepatic coma 2 weeks later, but the family's refusal to permit necropsy prevented more complete study. Bjero K et al; Lancet; 3 October 1998:1119: A patient with no history of liver disease and with normal levels of liver enzymes started on the antiepileptic drug topiramate, with dosage increased over 4 months to 300mg/day. She entered the hospital with intermittent lapses of consciousness and alanine aminotransferase (ALT) level about 4 times upper limit of normal, rising in 12 hours to 29 times ULN. After a liver allograft she recovered, and the removed tissue showed extensive necrosis. BMJ, 21 November 1998:1408: Reporting an entire recent issue of JAMA devoted to "alternative medicine": Last year, 40% of Americans used one of its many forms. They spent an estimated 27 $billion, but only 40% of them told their doctors. Kulisevsky J et al; Clin Neuropharm 1998;21:358-362: To rectify a lacuna, they did a 6-month open-label (except to the UPDRS rater) comparison of pergolide (Permax) vs. levodopa (Sinemet) in 10 newly diagnosed PD patients each, finding both overall benefits and adverse effects of each about equal. Swedlow R et al; Ann Neur 1998;44:873-881: One reason hereditary PD has been hard to prove is that it may be carried in mitochondrial DNA, rather than the chromosomal DNA. Authors found a family where three generations are affected with PD through exclusively maternal lines, and lab results support the hypothesis of mitochondrial DNA mutation. Hattori N et al; Ann Neur 1998;44:835-941: Autosomal-recessive juvenile parkinsonism is a specific variant of PD, that responds to levodopa. Authors found mutations of a particular gene in affected Japanese individuals. Volksmann J et al; Ann Neur 1998;44:953-961: They followed 9 bilateral deep-brain-stimulation (DBS) implant recipients for up to a year, and found that chronic DBS of the internal globus pallidus is neurologically safe and highly effective treatment for "off" symptoms, dyskinesias, and motor fluctuations in advanced stages of PD. CURRENT SCIENCE REVIEWS By Joe Bruman JANUARY 1999 P. 3 of 3 Counsell C; Aaltonen H et al; BMJ, 5 December 1998:1586-1587: Analysis and debate over mortality statistics from trials of selegiline added to levodopa go on and on, with no conclusion as yet of significant risk from selegiline. Ruottinnen H, Rinne U; Jour Neur 1998:245 Supp 3:25-34: Reviews benefits in PD of the catechol-O-methyltransferase (COMT) inhibitors tolcapone (Tasmar) and entacapone (Comtan). COMT is a natural enzyme that destroys levodopa, so a COMT inhibitor conserves it, permitting lower medication dosage to obtain the desired effect, which in turn delays the onset of levodopa-induced dyskinesia and end-of-dose fluctuations. -- J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks, CA 91403-5013