CURRENT SCIENCE REVIEWS    By Joe Bruman   March 1997   p. 1 of 3

Morrish K et al;Brain 1996;119:2097-2103:
Careful FD/PET scans of 15 PD patients and 6 controls revealed that
the progression of PD affects only the dorsal putamen in the early
and preclinical phase, spreading to the ventral putamen later on.

Kulisevsky J et al;Brain 1996;119:2121-2132:
The role of dopaminergic systems in cognitive defects of PD, and
cognitive effects of levodopa, are controversial. Neuropsychologic
tests of 10 PD patients having stable response to levodopa and 10
having a wearing-off effect showed that levodopa generally improved
performance, but in demanding executive function tests the stable-
response patients did better.

Obeso J et al;J Neur N'surg Psych 1997;62:2-8:
History and status of stereotactic surgery techniques in PD.

de Rijk M et al;J Neur N'surg Psych 1997;62:10-15:
To learn prevalence and age distribution of PD in 5 European
populations, 14,636 visitors, 65 or older, at various clinics were
surveyed. Overall incidence of parkinsonism was 2.3 per 100, and
of PD, 1.6 per 100. 25% of the PD cases were newly detected by the
surveys.

Olanow C et al;Ann Neur 1996;40:841-845:
Refutation of the British study a year ago that raised a scare about
shortened life-span of PD patients given selegiline.

Frey K et al;Ann Neur 1996;40:873-884:
The state of presynaptic monoaminergic vesicles is an important
indicator of the progression of PD. Authors found that PET scans
using the marker 11-C-dihydrotetrabenazine (DTBZ) offer an
objective, noninvasive, diagnostic tool.

Pezzoli G et al;Ann Neur 1996:40:922-925:
A woman worked in a leather-goods factory 10 yr, followed by 10 yr
of piecework at home, and developed rapidly progressive
parkinsonism, confirmed as PD by PET scan, response to levodopa and other
PD drugs, and later autopsy. She died of aspirative pneumonia
69 months after stopping work. Authors believe the PD was caused by
chronic exposure to a mixture of hydrocarbons present in the glue
that was used, mainly n-hexane and halogenated compounds.

Maki-Ikola O et al;Ann Neur 1996;40:946-949:
Attack on methodology of the DATATOP study (to evaluate selegiline),
followed by reply from representatives of the study.

Rajput A;Ann Neur 1996;40:950:
Comment on earlier paper, which reported use of PET scan to trace
the origin of alcohol-responsive essential tremor to the cerebellum
and the inferior olivary nuclei, followed by reply from authors.

Science, 24 Jan 1997:473 (news item):
In a possible setback for PD surgery, a British panel cautiously
approved "research" on transplantation of pig organs to humans,
but not "clinical trials", and the government set up a new bureau
to oversee any work in the field.



CURRENT SCIENCE REVIEWS   by Joe Bruman     March 1997  P. 2 of 3

Bucher S et al;Ann Neur 1997;41:32-40:
Essential Tremor (ET) afflicts 0.3% to 1.7% of the population (7.2%
of those over 50) but is poorly understood. Authors used passive
wrist motion to simulate ET in 12 patients and 15 controls, and
functional MRI to compare activity in various areas of the brain.
They found ET associated mainly with overactivity in the cerebellar
pathway, cerebellum, red nucleus, and globus pallidus, but not the
olivary nuclei.

Vingerhoets J et al;Ann Neur 1997;41:58-64:
Looking for clinical signs which best correlate with the
nigrostriatal deficit of PD, authors applied various
neuropsychological tests, along with fluorodopa PET scans, to 35 PD
patients. They conclude that the Purdue pegboard score and the
bradykinesia subscale of the modified Columbia score offer the most
reliable clinical signs of PD.

Boeker H et al;Ann Neur 1997;41:108-111:
Authors used PET scans (with H2O-15 as marker) to evaluate effect
of stereotactic VIM thalamotomy on 2 PD patients with refractory
tremor. The surgery reduced the tremor, but impaired activation of
the ipsilateral sensorimotor cortex, premotor cortex, and parietal
area.

Johkura K et al;Ann Neur 1997;41:133:
Abrupt withhdrawal of the anticholinergic trihexyphenidyl (Artane)
in a patient with mild PD caused a coma and other alarming signs,
not reversible until dosage was resumed.

Choi-Lundberg D et al;Science, 7 Feb 97;838-841:
Glial cell-line-Derived Neurotrophic Factor (GDNF) supports growth
and survival of dopaminergic neurons in animal models of PD, when
delivered near the affected site (the substantia nigra) but it can
be toxic to nearby cells. Instead of GDNF itself, authors in rat
experiments used a benign virus, altered to carry the gene for expression
of human GDNF, which then infected nearby cells so that
they would generate the GDNF in vivo. This less-invasive delivery
scheme is safer but still effective against induced PD in the rats.

Holthoff-Detto V et al;Arch Neur 1997;54:145-150:
By PET scan and clinical tests on 20 probable PD patients having
varying disability, authors found that motor impairment originates
in the putamen, while memory impairment originates in the caudate.

Rinne U et al;Neur 1997;48:363-368:
In a double-blind trial, authors gave levodopa to 176 new PD
patients, and cabergoline, a potent D2 agonist with a half-life of
65 hr, to 175 others, for a year. They conclude that cabergoline
alone is virtually as effective as levodopa, and when levodopa
is eventually needed, it reduces the amount required.

Metman L et al;Neur 1997;48:369-372:
Authors used apomorphine to test dyskinetic effect of levodopa in
28 PD patients with varying susceptibility. From dopa-naive to
the severely fluctuating state, duration of apomorphine response
shortened, dose-response slope steepened, and the therapeutic
window narrowed. These results suggest that motor complications
arise downstream from the nigrostriatal dopaminergic synapses.

CURRENT SCIENCE REVIEWS    by Joe Bruman    March 1997  p.3 of 3

Leopold N, Kagel M;Neur 1997;48:373-375:
By fluoroscopic study of 71 PD patients (H-Y stages II-V),
authors found significant slowing and shortening of laryngeal
(swallowing) motion, and impaired control of vocal cords. They
suspect the deficits arise in the basal ganglia-medulla control pathways.

Louis E et al;Neur 1997;48:376-380:
While Lewy bodies are always present in PD, some consider PD to be
a distinct member of a family of Lewy-body diseases. Authors
believe, for example, that up to 88% of diffuse Lewy-body disease
(DLBD) cases are misdiagnosed as PD. To test the hypothesis, they
analyzed clinical signs of 31 pathologically (postmortem) verified
DLBD cases and 34 similarly studied PD cases. There were no
differences in rigidity, bradykinesia, dystonia, or gaze palsy,
but DLBD cases had older onset, more common myoclonus, less common
rest tremor, and less common response to or perceived need for
levodopa. Any one of the last 4 signs is 10 times more likely to
indicate DLBD.

Piccirilli M et al, Jacobs D et al:Neur 1997;48:546-547:
Pro and con on cognitive deficits as diagnostic precursors of
motor deficits and dementia in PD.

Golstein P: Science, 21 Feb 1997:1081-1082:
Ability of an individual cell to commit suicide (apoptosis) in a
well-regulated way is vital to health of any multicelled organism.
Malfunction of the process leads to disease (as suspected in PD).
Author comments on 4 other articles in the same issue, but details
unfortunately too abstruse for me. Apoptosis is a very complex
chain of events, and they're learning how it works and what may
go wrong.

Lees A et al;Ann Neur 1997;41:282-283:
Reply to critics by the British team that set off last year's
Eldepryl scare: They admit flaws in study but are unrepentant.

Conrad C et al;Ann Neur 1997;41:277-281:
Authors found a genetic marker associated with progressive
supraanuclear palsy (PSP) but not with Alzheimer's or with
Parkinson-dementia complex of Guam (PDG).

Wooten F et al;Ann Neur 1997;41:265-268:
Authors examined 32 PD patients who had a parent with PD. Eighteen
had younger onset than the mother with PD, but fourteen did not
have younger onset than the father with PD. They conclude from this
that at least some PD cases arise from inherited abnormalities of
mitochondrial DNA.

Piccini P et al;Ann Neur 1997;41:222-229:
Authors used FD/PET to study 32 asymptomatic relatives of PD
patients with known family linkage, and found 11 with preclinical
indication (reduced dopamine uptake) of PD.

Lancet, 15 Feb 1997:478 (news item):
PET scan and personality analysis of 24 subjects showed correlation
between lower density of D2 receptors in the putamen (associated
with PD) and personal detachment (cold, aloof, and vindictive).




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