Here are the results of a MEDLINE search on the above topics as
requested.
 
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<c:\dlink\parkneon.txt>
 
 
 
HIP FRACTURES IN PARKINSON'S DISEASE
 
 
 1/L/1
DIALOG(R)File 154:MEDLINE(R)
(c) format only 1995 Knight-Ridder Info. All rts. reserv.
 
06541945 88186945
  Prosthetic replacement of the femoral head for fracture of the
femoral
neck in patients who have Parkinson disease.
  Staeheli JW; Frassica FJ; Sim FH
  Department of Orthopedics, Mayo Clinic, Rochester, Minnesota 55905.
  J Bone Joint Surg [Am] (UNITED STATES) Apr 1988, 70 (4) p565-8,
ISSN
0021-9355 Journal Code: HJR
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 8807
  Subfile: AIM; INDEX MEDICUS
  A retrospective study was performed of forty-nine patients
(fifty
fractures of the femoral neck) who had Parkinson disease and who had had
an
endoprosthetic replacement of the femoral head. The average age of
the
patients was seventy-four years (range, forty-seven to ninety-two
years).
All of the fractures were Garden Stage III or IV. An anterolateral
surgical
approach was used in twenty-five hips; a posterior approach, in
twenty
hips; and a transtrochanteric approach, in five hips. An adductor
tenotomy
was required in five patients to release an adduction contracture.
Ten
patients died by the sixth postoperative month. The remaining
thirty-nine
patients were followed for a minimum of two years (average, 7.3
years).
Common postoperative complications were infection of the urinary tract
(20
per cent) and pneumonia (10 per cent). There was only one dislocation.
At
the time of writing, nineteen (80 per cent) of the surviving patients
could
walk.
  Tags: Female; Human; Male
  Descriptors: *Femoral Neck Fractures--Surgery--SU; *Hip
Prosthesis;
*Parkinson Disease--Complications--CO; Aged; Femoral Neck
Fractures
--Complications--CO; Hip Dislocation--Prevention and Control--PC; Hip
Joint
--Physiopathology--PP; Locomotion; Middle Age; Parkinson
Disease
--Physiopathology--PP; Postoperative Complications--Etiology--ET;
Retrospec
tive Studies
 
 
============================================================
 
NEONATAL MOVEMENT DISORDERS
 
 3/L/3
DIALOG(R)File 154:MEDLINE(R)
(c) format only 1995 Knight-Ridder Info. All rts. reserv.
 
09152699 95082699
  Pregnancy and movement disorders.
  Golbe LI
  Department of Neurology, University of Medicine and Dentistry of
New
Jersey, Robert Wood Johnson Medical School, New Brunswick.
  Neurol Clin (UNITED STATES) Aug 1994, 12 (3) p497-508, ISSN
0733-8619
Journal Code: NEU
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
  JOURNAL ANNOUNCEMENT: 9503
  Subfile: INDEX MEDICUS
  The concurrence of pregnancy and movement disorders is an uncommon
event
in a general neurologic practice. Even at specialized movement
disorder
referral centers, there is insufficient experience to adequately
guide
management of pregnancy, except perhaps in the case of WD. The
questions
posed most urgently by patients regard the safety of medication, an
issue
on which there is insufficient data, and their ability to care for a
child
for at least the next decade, an issue that differs by disease and
social
situation. The author's formulation of efficacy and toxicity suggests
that
certain medications commonly used in movement disorders should
 be
discontinued before pregnancy, if possible. These medications
include
neuroleptics, amantadine, diazepam, primidone, selegiline, and
reserpine.
Pregnancy may unmask a pre-existing potential for chorea (i.e.,
chorea
gravidarum) and frequently has a mild exacerbating effect on symptoms
of
PD; however, it has little effect on other movement disorders.
Severe
generalized dystonia would probably interfere with vaginal delivery,
but
the scant existing data suggest minimal effect of movement disorders
on
pregnancy, childbirth, and neonatal health. (40 Refs.)
  Tags: Female; Human
  Descriptors: *Movement Disorders--Etiology--ET; *Pregnancy
Complications
--Etiology--ET; Antiparkinson Agents--Administration and
Dosage--AD;
 Antiparkinson Agents--Adverse Effects--AE; Diagnosis,
Differential;
Infant, Newborn; Movement Disorders--Therapy--TH; Neurologic
Examination
--Drug Effects--DE; Parkinson Disease--Etiology--ET; Parkinson
Disease
--Therapy--TH; Pregnancy; Pregnancy Complications--Therapy--TH
  CAS Registry No.: 0 (Antiparkinson Agents)
 
 3/L/4
DIALOG(R)File 154:MEDLINE(R)
(c) format only 1995 Knight-Ridder Info. All rts. reserv.
 
09129687 95059687
  Differential postmorbidity mortality in observational studies of
risk
factors for neurologic disorders.
  Ellenberg JH
  National Institute of Neurological Disorders and Stroke, Bethesda,
Md.
20892.
  Neuroepidemiology (SWITZERLAND) 1994, 13 (5) p187-94, ISSN
0251-5350
Journal Code: NXY
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 9502
  Subfile: INDEX MEDICUS
  Selection bias may be introduced in case-control or
cross-sectional
studies, and the impact on the observed associations may be dramatic.
Many
authors have examined this issue primarily in the context of subject
source
(e.g. referral bias). The potential bias encountered when a risk
factor
associated with outcome is also associated with an increase in
mortality
among cases greater than that among those not developing the disease
(e.g.
selective survival) is examined here. The potential for selective
survival
bias arising in observational studies is demonstrated in studies of
the
etiology of neonatal seizures and Parkinson's disease.
  Tags: Female; Human; Male
  Descriptors: *Cause of Death; *Nervous System
Diseases--Mortality--MO;
Aged; Case-Control Studies; Cohort Studies; Cross-Sectional Studies;
Infant
; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature,
Diseases
--Etiology--ET; Infant, Premature, Diseases--Mortality--MO;
Models,
Statistical; Nervous System Diseases--Etiology--ET; Parkinson
Disease
--Etiology--ET; Parkinson Disease--Mortality--MO; Pregnancy; Risk
Factors;
Selection Bias; Smoking--Adverse Effects--AE;
Smoking--Mortality--MO;
Spasms, Infantile--Etiology--ET; Spasms,
Infantile--Mortality--MO;
Survival Analysis; Treatment Outcome
 
 3/L/6
DIALOG(R)File 154:MEDLINE(R)
(c) format only 1995 Knight-Ridder Info. All rts. reserv.
 
08709903 94024903
  Neonatal exposure to paraquat or MPTP induces permanent changes
in
striatum dopamine and behavior in adult mice.
  Fredriksson A; Fredriksson M; Eriksson P
  Department of Toxicology, Uppsala University, Sweden.
  Toxicol Appl Pharmacol (UNITED STATES) Oct 1993, 122 (2) p258-64,
ISSN 0041-008X Journal Code: VWO
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 9401
  Subfile: INDEX MEDICUS
  We have recently reported that environmental toxicants, such as
DDT,
PCBs, pyrethroids, and nicotine can induce permanent functional
and
neurochemical changes in adult mice when given to neonatal mice during
the
peak of rapid brain growth. In the present investigation the
neurotoxic
effects following neonatal exposure to paraquat
(N,N'-dimethyl-4,4'-bipyrid
ylium), a broad-spectrum herbicide with structural similarity to
the
1-methyl-4-phenylpyridium ion (MPP+), the active metabolite
 of
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) which can
induce
Parkinson's syndrome, and MPTP were studied. Five groups of mice were
given
paraquat or MPTP orally: group 1, vehicle; groups 2 and 3, MPTP 0.3 and
20
mg/kg; groups 4 and 5, paraquat 0.07 and 0.36 mg/kg when 10 and 11
days
old. Neonatal spontaneous motor activity was tested on Day 18 in mice
given
paraquat 0.36 mg/kg body wt. Adult spontaneous motor activity testing
was
performed at ages 60 and 120 days. On Day 125 the mice were decapitated
and
the contents of dopamine (DA), serotonin (5-HT), and metabolites
in
striatum were analyzed. The results may be summarized as follows: (1)
No
signs of acute toxicity or differences in weight gain were observed in
any
of the groups. Nor was any respiratory distress or motor
performance
dysfunction evident on Day 18 in mice given paraquat 0.36 mg/kg body
wt.
(2) The behavioral tests at 60 days of age showed a marked
hypoactive
condition in the mice given paraquat (at both doses) and MPTP (at
both
doses). (3) At the age of 120 days the hypoactive behavior persisted
and
appeared even more pronounced. (4) The high doses of MPTP and
paraquat--and
to a less extent the low doses--reduced the striatal content of DA
and
metabolites without affecting 5-HT. The altered behavior, together with
the
dose-dependent reduction of DA and metabolites in neostriata in this
study,
further demonstrates the susceptibility to low-dose exposure
 to
environmental pollutants during the neonatal period.
  Tags: Animal; Male; Support, Non-U.S. Gov't
  Descriptors: *Corpus Striatum--Drug Effects--DE;
*Dopamine--Metabolism
--ME; *Motor Activity--Drug Effects--DE;
*Paraquat--Toxicity--TO;
*1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine--Toxicity--TO; Animals,
Newbo
rn; Corpus Striatum--Growth and Development--GD; Corpus
Striatum
--Metabolism--ME; Mice; Mice, Inbred C57BL; Serotonin--Metabolism--ME
  CAS Registry No.: 28289-54-5
(1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridi
ne); 4685-14-7 (Paraquat); 50-67-9 (Serotonin); 51-61-6 (Dopamine)