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CURRENT SCIENCE REVIEWS   by Joe Bruman  September 1996  p.1 of 2

Lancet, 27 Jul 1996:255 (news item):
Attention Deficit Hyperactivity Disorder (ADHD) in children  may be
related to dopamine deficiency in the brain. MRI studies of
children with ADHD suggest abnormalities of dopamine-using areas;
and genetic studies reveal unusually frequent anomaly of the
dopamine D4 receptor gene, associated with more severe ADHD.

Johnson M et al: Brain 1996;119:801-813:
Contrary to the idea that PD patients slow their movement to gain
better position control, tracking slowness is a true feature of PD,
responsive to levodopa. An error correction deficit is also present
but does not respond to levodopa.

Cunnington R et al; Brain 1996;119:815-822:
Transcranial magnetic stimulation slowed execution of intentional
movement in PD patients but not in controls, and only in early or
pre-movement stages but not in later stages of movement.

Fernandez A et al; Brain 1996;119:823-830:
In postmortem samples from PD patients, authors found decrease of
the neuropeptides Met-enkephalin and Leu-enkephalin, in brain
regions associated with PD and incidental Lewy body disease
(pre-clinical PD).

Litvan I et al; Neur 1996;47:1-9:
Presently Progressive Supranuclear Palsy (PSP or Steele-Richardson
-Olszewski syndrome) has no diagnostic marker and is often mis-
diagnosed as PD. An international workshop has proposed some
clinical diagnostic standards.

Golbe L et al; Neur 1996;47:148-154:
The cause of PSP is unknown and little studied. In a questionnaire
to 91 PSP patients and 104 controls on environment and lifestyle
factors, the only significant difference was that PSP patients
were less likely to have had 12 years of school.

Marder K et al; Neur 1996;47:155-160:
A life history study of 233 PD patients and 1458 of their first-
degree relatives showed that the relatives were 2.3 times as likely
as relatives of controls to develop PD, in both sporadic and
familial cases.

Ishikawa I, Tsuji S; Neur 1996;47:160-166:
A study of 17 patients having familial juvenile PD in 12 Japanese
families suggests autosomal-recessive inheritance, and that AR-JP
is a distinct clinical entity.

Herrero M et al; Neur 1996;47:219-224:
The expression of glutamic acid decarboxylase messenger RNA in the
internal pallidum was increased by nigrostriatal denervation in
MPTP monkeys, as well as in human PD subjects, and the increase was
reversed by L-dopa therapy.

Sandy M et al; Neur 1996;47:225-230:
The gene CYP2D6 is associated with higher risk of PD in older
people, but a study of 108 young-onset PD patients showed no
corresponding increase in risk.


CURRENT SCIENCE REVIEWS   By Joe Bruman   September 1996  p.2 of 2

Busenbark K et al; Neur 1996;47:264-265:
216 (67.7%) out of 319 ET patients reported positive family
history, but when first-degree relatives were contacted directly,
the ratio rose to 243 (96%) out of 253. ET is primarily hereditary.

(Book Review) Arch Neur 1996;51:721:
Ellenberg J, Koller W, Langston W (eds): Etiology of Parkinson's
Disease. Marcel Dekker Inc., New York, 1995: Despite decades of
effort, the cause of PD remains elusive.

Van Hilten I, Olanow C et al; Ann Neur 1996;40:266-269:
Latest round in debate on whether selegiline (Eldepryl) with
Sinemet really slows progression of PD or merely relieves symptoms.
Three letters about Olanow's article of Dec '95, together with his
replies. Competitors and skeptics mostly quibble about validity
of trial protocol, while Olanow & co. emphasize benefits, however
gained. The problem with any long-term clinical trial is, the more
stringent the protocol to ensure scientific validity, the more
likely that hardship will be imposed on the patient/volunteer
subjects.

Albin R et al; Neur 1996;47:462-466:
Six demented patients were studied by FD-PET, which can show local
distribution of dopamine metabolism, and CAT scan. Five of the six
showed some clinical signs of PD, and two who responded to levodopa
were so diagnosed. On autopsy later, all six were found to have
Diffuse Lewy Body Disease, a condition much more pervasive and
disabling than PD. Five of the six reported visual hallucinations,
and the two diagnosed with PD while living were distinct in having
"cognitive fluctuations". Despite past impression, apparently
FD-PET failed to distinguish DLBD from PD.

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