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CURRENT SCIENCE REVIEWS   By Joe Bruman   April 1998   Page 1 of 3

Pol S et al; J Neur N'surg Psych 1998;64:164-171:
The motor nerve system contains numerous redundant pathways which
permit a 'detour' to compensate for failure, as in PD, of the
primary pathway. Using electromyography and artificial stimulation
of wrist muscle in 45 PD patients and 23 controls, authors
confirmed that cervical premotor neurons become more active when
serving as a secondary pathway in PD.

Mahieux F et al; J Neur N'surg Psych 1998;64:178-183:
To look for predictors of future dementia in later-stage PD,
they gave a battery of neuropsychological tests to 89 new patients,
and again about 3.5 years later. The most prominent indicators
were impairment of visuospatial judgement and difficulty
inhibiting irrelevant stimuli.

Heberlein I et al; J Neur N'surg Psych 1998;64:262-266:
Pursuing the idea of a non-motor PD syndrome, they compared
personality traits and mood in 15 twin pairs discordant for PD
and 17 unrelated healthy controls. The differences suggest that
there is a genetic component for some personality features in PD.

Hua S et al; J Neur N'surg Psych 1998;64:273-276:
Essential tremor and PD tremor are clearly different, but
recording of thalamic activity during thalamotomy for ET had not
been done, so they did that, confirming importance of the
thalamus in ET.

J Neurosurg 1998;88(3)(ad):
The current (March 1998) issue has full-page ads with good
pictures of the refined Leksell stereotactic frame and one of
its competitors.

Counihan T et al; J Comp Neur 1998;390:91-101:
Evidence is growing that the neurotoxic effect of the
neurotransmitter glutamate is important in PD. To test the
hypothesis that the difference in vulnerability of dopamine
neurons in the substantia nigra is due to selective expression
of N-methyl-D-aspartate receptors (NR), they examined postmortem
tissue from subjects without known neurological disorder, but
the distribution doesn't agree with the characteristic pattern
of neurodegeneration in PD.

Nakao N et al; Brain Res 1997;777:202-209:
Pretreatment of dopaminergic neurons in vitro with an inhibitor
of mitochondrial Complex I augmented the toxic effect of L-dopa.
The selective toxic effect was blocked by antioxidants but not
by glutamate antagonists. Since mitochondrial damage is known
to occur in PD, they suspect that long-term L-dopa treatment
may accelerate the progress of PD.

Dorozynski A; BMJ;28 Feb 1998:648:
According to a French (where else?) study of 34,000 middle-aged
men, 2 to 3 glasses of wine a day reduced overall mortality in
the following 10-15 years by 30%. Drinking 4 to 7 glasses a day
reduced mortality by 24%, but above that, the risk grew. Whee!




CURRENT SCIENCE REVIEWS  By Joe Bruman   April 1998  P. 2 of 3

Muthane U et al; Ann Neur 1998;43:283-287:
PD incidence varies widely with age and race. Estimated at 280
per 100,000 in U.S. whites, 196 in U.S. blacks, 59 in Nigeria,
44 in China, 14 to 27 in India. But in one ethnic group of
western India it's 328/100,000. They counted pigmented neurons
of the SN and found 40% fewer in Indians than in people of the
UK, despite the lower prevalence of PD. Further, Indians don't
seem to lose melanized nigral neurons with advancing age.

Schneider J et al; Ann Neur 1998;43:311-317:
In MPTP monkeys, the nicotinic acetylcholine receptor agonist
SIB-1508Y alone was of little help, but together with levodopa/
benserazide improved both cognitive and motor function, using
only 1/3 to 1/6 the dose of levodopa/benserazide needed alone.
(A much later report of encouraging human trials is in the
Winter '98 issue of the NPF Report.)

Parkinson Study Group; Ann Neur 1998;43:318-325:
Still following the 800 patients of the DATATOP trial 10 years
ago; mortality, either as a whole or associated with various
options of Deprenyl and Vitamin E, was no different from that
of a normal population.

Brownell A et al; Ann Neur 1998;43:387-390:
In parkinsonian rats, they grafted either dopaminergic neurons
or non-DA cells, and proved by PET scans that only the former
resulted in functional recovery.

Farrer M et al; Ann Neur 1998;43:394-397:
Contrary to recent reports of a mutant alpha-synuclein gene
connected with autosomal-dominant PD, they studied several
other familial clusters of PD and related diseases, and found
no special variation of the gene.

Olanow C, Koller W; Neur 1998;50:Supp 3(separately bound):1-50:
Management of long-term diseases such as PD requires special
attention to timing and strategy. Here is a how-to-do-it
compendium of all you could ever wish to know about it, assembled
by two top authorities. Covers every imaginable problem in turn,
from constipation to freezing to hallucinations.

(Committee); Neur 1998;50:596-598(editorial):
Assisted suicide, euthanasia, and the neurologist: 3 pages of
dancing around semantic issues, ending in emphatic rejection.

Shultz C et al; Neur 1998;50:793-795:
They tried Coenzyme Q10, a potent mitochondrial antioxidant that
is deficient in PD, on 15 patients in a short trial. Complex I
activity increased but the UPDRS motor scores didn't improve.

Carpenter M et al; Neur 1998;50:796-798:
Seven ET patients who received successful VIM-STIM implants for
hand tremor enjoyed a reduction in voice tremor as well.

Goren J, Friedman J; Neur 1998;50:823:
A fairly typical PD patient on levodopa reports that he always
yawns before the most recent dose kicks in and he turns "on".
They wonder if yawning is mediated by dopamine.

CURRENT SCIENCE REVIEWS   By Joe Bruman   April 1998  P. 3 of 3

Gerlach M et al; Lancet, 21 Mar 1998:850-851:
N-methyl-(R)-salsolinol, an endogenous analog of the synthetic
MPTP, is suggested as a possible cause of PD. More work is needed.

Agid Y et al; Lancet, 21 Mar 1998:851-852:
A panel of 25 PD experts met in Paris to discuss whether adverse
effects ascribed to long-term use of levodopa are due to the
drug or to progression of the disease. They conclude, despite
some in vitro evidence of uncertain relevance, there is no cause
for concern over neurotoxicity. Motor complications such as
levodopa-induced dyskinesia represent sensitivity to levodopa
due to progression of PD, rather than the effect of long use.

Yenari M et al; Clin Neuropharm 1998;21:28-34:
Seeking a tolerable antagonist to the neurotoxin glutamate,
they tested the NMDA antagonist Selfotel (CGS 19755) on 32
ischemic-stroke surgery patients. Among the side effects were
hallucinations, agitated dreams, paranoia, ataxia and dizziness,
but at levels acceptable in view of the perceived benefits.

Kuno S et al; Clin Neuropharm 1998;21:35-40:
They compared effects of apomorphine with the novel ergoline-
derived dopamine agonist BAM-1110 on MPTP monkeys, finding good
antiparkinson properties and better tolerance of BAM-1110.

Krack P et al; Brain 1998;121:451-457:
The pioneer DBS team implanted devices in the internal globus
pallidus (GPi) of 5 PD patients and in the subthalamic nucleus
(STN) of 8 others, all confirmed by levodopa challenge. The STN
group had much better improvement in UPDRS score, particularly
in akinesia. The GPi group did better with levodopa-induced
dyskinesia (LID), but that was balanced by the reduced levodopa
requirement in the STN group.

Platz T et al; Brain 1998;121:505-514:
They assigned standardized aimed-movement tasks to 15 PD patients
(off medication) and 15 controls, finding that bradykinesia of
PD may be persistently reduced by practice and training.

Rascol O et al; Brain 1998;121:527-533:
Using single-proton-emission computed tomography (SPECT) to
map cerebral blood flow in 14 PD patients experiencing
L-dopa-induced dyskinesia (LID), 23 without LID, and 15 normal
controls, they conclude that hyperkinetic abnormal movement such
as LID is due to disinhibition of the primary and associated motor
cortex by excessive output of the pallidothalamocortical loop.

Monza D et al; Arch Neur 1998;55:372-378:
Seeking differential-diagnostic signs, they tested 14 PD patients,
19 with MSA, and 19 with PSP, and a group of comparable controls
for cognitive and complex motility function. All the patient groups
were worse than controls in motor function, but only the PSP and
MSA groups showed cognitive deficit.


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J. R. Bruman   (818) 789-3694
3527 Cody Road
Sherman Oaks, CA 91403-5013