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)