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Here are the results of a MEDLINE search on the above topics as requested. ----------------------------------------------------------------------- <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)