Part One of a MEDLINE on PD and childhood diseases, influenza, and
possible environmental exposures:
 
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07594964 91113964
  Similarities of guamanian ALS/PD to post-encephalitic
parkinsonism/ALS:
possible viral cause.
  Hudson AJ; Rice GP
  Department of Clinical Neurological Sciences, University
Hospital,
London, Ontario.
  Can J Neurol Sci (CANADA) Nov 1990, 17 (4) p427-33, ISSN 0317-1671
Journal Code: CJ9
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
  JOURNAL ANNOUNCEMENT: 9105
  Subfile: INDEX MEDICUS
  Guamanian amyotrophic lateral sclerosis with
parkinsonism-dementia
(ALS/PD) has been the subject of intensive study since its discovery
in
1947 because of its extraordinarily high incidence in a small ethnic
group
(Chamorros) whose dietary lack and customs have suggested possible
causes.
As yet, these and other suspected causes have eluded proof. Because
of
marked similarities between Guamanian ALS/PD and late
onset
post-encephalitic (encephalitis lethargica) parkinsonism and ALS it
is
suggested that they have a common cause. The parkinsonism and ALS in
the
two disorders are clinically very similar and neuropathological
studies
have shown a very similar distribution of neurofibrillary tangles
in
neurons. Some clinical differences, such as ocular features in
the
post-encephalitic cases and dementia in Guamanian ALS/PD, can be
explained
by differences in the severity of infection and the interval between
the
encephalitis and onset of sequelae. Although unproven, influenza A
(HswilN1
strain) has long been suspected as the cause of encephalitis
lethargica
because of simultaneous pandemics of the two diseases in the 1920s.
Because
influenza A can persistently infect cells and has a marked propensity
to
mutate it is an optimal candidate among other RNA viruses for
delayed
nervous system infection as a possible cause of ALS/PD. (55 Refs.)
  Tags: Human
  Descriptors: *Amyotrophic Lateral Sclerosis--Microbiology--MI;
*Parkinson
Disease, Postencephalitic--Microbiology--MI;
Dementia--Complications--CO;
Guam
 
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07059495 89361495
  Could Parkinson's disease follow intra-uterine influenza? A
speculative
hypothesis [letter; comment]
  Singer C; Weiner WJ
  J Neurol Neurosurg Psychiatry (ENGLAND) Jul 1989, 52 (7) p931,
ISSN
0022-3050 Journal Code: JBB
  Comment on J Neurol Neurosurg Psychiatry 1988 Jun;51(6):753-6
  Languages: ENGLISH
  Document type: COMMENT; LETTER
  JOURNAL ANNOUNCEMENT: 8912
  Subfile: INDEX MEDICUS
  Tags: Female; Human
  Descriptors: *Parkinson Disease,
Postencephalitic--Etiology--ET;
*Prenatal Exposure Delayed Effects; Diseases in Twins; Pregnancy;
Risk
Factors
 
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07059484 89361484
  Does idiopathic parkinsonism in Aberdeen follow intrauterine
influenza?
  Ebmeier KP; Mutch WJ; Calder SA; Crawford JR; Stewart L; Besson JO
  Department of Mental Health, University of Aberdeen, UK.
  J Neurol Neurosurg Psychiatry (ENGLAND) Jul 1989, 52 (7) p911-3,
ISSN 0022-3050 Journal Code: JBB
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 8912
  Subfile: INDEX MEDICUS
  A study is presented which fails to replicate a recent report that
peak
years of birth of patients later developing Parkinson's disease are
related
to the influenza pandemics of the period 1890-1930. The years of birth
of a
whole population cohort of 243 patients suffering from Parkinson's
disease
examined in Aberdeen in 1983 and reexamined in 1986/7 were compared
with
deaths due to influenza in the City of Aberdeen in the years
1900-1930.
Although a significant peak of Parkinson births (compared with the
age
profile of the Aberdeen population in 1983) occurred in 1902,
there
appeared to be no systematic relationship between Parkinson births
and
influenza deaths. In addition, no season of birth effect could be
detected
in a comparison with 232 matched controls. The presence of peaks of
birth
years, for whatever aetiological reason, is of significance
 to
epidemiological studies in that prevalence estimates may be influenced
by
the year of study relative to these mini-cohorts.
  Tags: Female; Human; Support, Non-U.S. Gov't
  Descriptors: *Parkinson Disease,
Postencephalitic--Etiology--ET;
*Prenatal Exposure Delayed Effects; Aged; Aged, 80 and over; Cohort
Studies
; Follow-Up Studies; Middle Age; Pregnancy; Risk Factors; Scotland
 
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06655091 88300091
  Could Parkinson's disease follow intra-uterine influenza?: a
speculative
hypothesis [see comments]
  Mattock C; Marmot M; Stern G
  Department of Community Medicine, University College and Middlesex
School
of Medicine, London, UK.
  J Neurol Neurosurg Psychiatry (ENGLAND) Jun 1988, 51 (6) p753-6,
ISSN 0022-3050 Journal Code: JBB
  Comment in J Neurol Neurosurg Psychiatry 1989 Jul;52(7):931
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 8811
  Subfile: INDEX MEDICUS
  Patients with idiopathic Parkinson's disease do not appear to
 be
distributed smoothly with respect to year of birth. Individuals born
within
the years 1892, 1904, 1909, 1918, 1919 and 1929 appear to have had
an
increased risk of developing idiopathic Parkinson's disease in later
life.
These years are close to those of the influenza pandemics of the
period
1890-1930. The estimated risk of an individual developing
idiopathic
Parkinson's disease shows a significant correlation with the
crude
influenza mortality for the year of his birth, within the range 1900
to
1930. It is suggested that intra-uterine influenza may be cytotoxic to
the
developing foetal substantia nigra, and that an affected individual may
be
born without evident disability but with limited striatal
neurochemical
reserves and a reduced nigral cell count. In later life normal
cellular
involution with ageing or exposure to environmental neurotoxic factors
may
further erode these reserves to a level where the substantia nigra
fails
and idiopathic Parkinson's disease becomes clinically apparent.
  Tags: Female; Human; Male
  Descriptors: *Disease Outbreaks--Epidemiology--EP;
*Influenza--Mortality
--MO; *Parkinson Disease--Mortality--MO; *Pregnancy
Complications,
Infectious--Mortality--MO; *Prenatal Exposure Delayed Effects; Aged;
Aged,
80 and over; England; Middle Age; Pregnancy; Risk Factors; Wales
 
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06312535 87286535
  Was a neurovirulent influenza virus the cause of amyotrophic
lateral
sclerosis and parkinsonism-dementia on Guam?
  Maurizi CP
  Med Hypotheses (ENGLAND) Jul 1987, 23 (3) p325-6, ISSN 0306-9877
Journal Code: M0M
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 8711
  Subfile: INDEX MEDICUS
  Tags: Human
  Descriptors: *Amyotrophic Lateral Sclerosis--Microbiology--MI;
*Dementia
--Microbiology--MI; *Orthomyxoviridae--Pathogenicity--PY;
*Parkinson
Disease--Microbiology--MI; Adolescence; Adult; Amyotrophic
Lateral
Sclerosis--Epidemiology--EP; Child; Child, Preschool;
Dementia
--Epidemiology--EP; Dementia--Etiology--ET; Guam; Middle Age;
Parkinson
Disease--Complications--CO; Parkinson Disease--Epidemiology--EP
 
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05746779 86047779
  Measles infection and Parkinson's disease.
  Sasco AJ; Paffenbarger RS Jr
  Am J Epidemiol (UNITED STATES) Dec 1985, 122 (6) p1017-31,
ISSN
0002-9262 Journal Code: 3H3
  Contract/Grant No.: CA 25264
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 8602
  Subfile: INDEX MEDICUS
  A case-control analysis of Parkinson's disease and infections
 in
childhood was conducted in a cohort of 50,002 men who attended
Harvard
College (Cambridge, MA) or the University of Pennsylvania
(Philadelphia,
PA) between 1916 and 1950 and who were followed in adulthood for
morbidity
and mortality data. Cases of Parkinson's disease were identified
from
responses to mailed questionnaires and death certificates through
1978.
Four controls from the same population were selected for each
case. A
reduced risk of Parkinson's disease was associated with most
childhood
viral infections. The negative association was statistically
significant
for a history of measles prior to college entrance (exposure odds
ratio =
0.53; 95% confidence limits: 0.31, 0.93). The reduced risk of
Parkinson's
disease among subjects with a positive history of measles in childhood
may
reflect an adverse effect of measles in adulthood or of subclinical
or
atypical measles. Furthermore, a negative history of measles, especially
if
associated with a lack of other common diseases, could be a marker
for
negative influenza history before 1918 and thus a higher risk of
infection
during the 1918 influenza epidemic, because of the lack of
partial
influenza immunity. These data may also suggest a truly protective
effect
of measles, compatible with some complex interaction between measles
virus
and the virus of the 1918 influenza epidemic.
  Tags: Human; Male; Support, Non-U.S. Gov't; Support, U.S. Gov't,
P.H.S.
  Descriptors: *Measles--Complications--CO; *Parkinson
Disease--Etiology
--ET; Adolescence; Adult; Aged; Child; Child, Preschool; Death
Certificates
; Epidemiologic Methods; Infant; Influenza--Complications--CO;
Longitudinal
Studies; Massachusetts; Measles--Epidemiology--EP; Middle Age;
Parkinson
Disease--Epidemiology--EP; Parkinson Disease--Mortality--MO;
Pennsylvania;
Questionnaires; Regression Analysis; Risk
 
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05597157 85213157
  Why was the 1918 influenza pandemic so lethal? The possible role
of a
neurovirulent neuraminidase.
  Maurizi CP
  Med Hypotheses (ENGLAND) Jan 1985, 16 (1) p1-5, ISSN 0306-9877
Journal Code: M0M
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 8509
  Subfile: INDEX MEDICUS
  Epidemiological, viral, behavioral and neuropathological
evidence
suggests that some influenza epidemics were neurovirulent.
Re-examination
of the data from the lethal 1918 pandemic armed with recent
observations
about the influenza virus implicates a neurovirulent influenza virus
in
manic-depressive disease, schizophrenia and Parkinson's disease.
The
neurovirulence seems to have been related to the species of
neuraminidase.
  Tags: Human
  Descriptors: *Encephalitis--Etiology--ET;
*Neuraminidase--Toxicity--TO;
*Orthomyxoviridae--Enzymology--EN; Antigens, Viral--Analysis--AN;
Brain
--Pathology--PA; Disease Outbreaks;
Encephalitis--Immunology--IM;
 Encephalitis--Mortality--MO; Influenza--Mortality--MO;
Orthomyxoviridae
--Pathogenicity--PY; Time Factors; Virulence
  CAS Registry No.: 0 (Antigens, Viral)
  Enzyme No.: EC 3.2.1.18 (Neuraminidase)
 
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05526368 85142368
  Influenza and mania: a possible connection with the locus ceruleus.
  Maurizi CP
  South Med J (UNITED STATES) Feb 1985, 78 (2) p207-9, ISSN
0038-4348
Journal Code: UVH
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 8506
  Subfile: AIM; INDEX MEDICUS
  I have presented a possible case of mania induced by influenza B.
Some
epidemic influenza viruses may be neurovirulent. These epidemics seem to
be
associated with postencephalitic Parkinson's disease, mania,
and
depression. Viral, neuroanatomic, neurophysiologic,
neurochemical,
pharmacologic, clinical, and epidemiologic evidence can be found to
suggest
a connection between the locus ceruleus, the influenza virus, and
the
induction of a manic psychosis.
  Tags: Case Report; Human; Male
  Descriptors: *Influenza--Complications--CO; *Locus Coeruleus;
*Manic
Disorder--Etiology--ET; Adult; Locus
Coeruleus--Microbiology--MI;
Orthomyxoviruses Type B
 
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08981498 94296498
  Clinical spectrum of secondary parkinsonism in childhood: a
reversible
disorder.
  Pranzatelli MR; Mott SH; Pavlakis SG; Conry JA; Tate ED
  Department of Neurology, George Washington University, Washington,
D.C.
20010.
  Pediatr Neurol (UNITED STATES) Mar 1994, 10 (2) p131-40,
ISSN
0887-8994 Journal Code: AA5
  Contract/Grant No.: FD-U-000746-01/2, FD, FDA; FD-U-000955-01, FD, FDA
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
  JOURNAL ANNOUNCEMENT: 9410
  Subfile: INDEX MEDICUS
  Parkinsonism is an uncommon movement disorder in childhood. Six
unusual
cases of acquired parkinsonism in hospitalized children are
described.
Clinical manifestations included an akinetic-rigid syndrome with
and
without tremor, the combination of parkinsonism and dystonia,
and a
parkinsonism-plus syndrome. Altered mental status, mutism, dysphagia,
and
sialorrhea were frequent associations. Etiologies included
hypoxic-ischemic
encephalopathy; haloperidol treatment with and without
neuroleptic
malignant syndrome; toxicity of cytosine arabinoside,
cyclophosphamide,
amphotericin B, and methotrexate; St. Louis encephalitis and
other
encephalitides; and a pineal tumor with hydrocephalus. Cranial
magnetic
resonance imaging results ranged from normal to profound cerebral
and
cerebellar atrophy with chemotherapeutic toxicity. The illnesses
usually
were severe enough to require pharmacotherapy. Incorrect diagnoses
of
depression or catatonia delayed treatment or aggravated the problem.
Acute
treatment included amantadine, levodopa/carbidopa with or
without
selegiline, diphenhydramine, or benztropine. The concentration of
CSF
homovanillic acid was normal in a neuroleptic-associated patient, but
the
level was low in an encephalitic patient. All patients
demonstrated
dramatic improvement, including two who were not treated; some had
complete
resolution of symptoms and none required continued antiparkinsonian
drugs
despite poor scores on the Unified Parkinson's Disease Rating Scale and
the
Modified Hoehn and Yahr Rating Scales. The causes of parkinsonism
described
are more common in a general pediatric hospital than the
parkinsonism
associated with the popularized Segawa syndrome. (52 Refs.)
  Tags: Case Report; Female; Human; Male; Support, Non-U.S. Gov't;
Support,
U.S. Gov't, P.H.S.
  Descriptors: *Parkinson Disease, Symptomatic--Etiology--ET;
Adolescence;
Antiparkinson Agents--Adverse Effects--AE; Antiparkinson
Agents
--Therapeutic Use--TU; Atrophy; Brain--Drug Effects--DE;
Brain--Pathology
--PA; Child; Diagnosis, Differential; Follow-Up Studies; Magnetic
Resonance
Imaging; Neurologic Examination--Drug Effects--DE; Parkinson
Disease,
Symptomatic--Chemically Induced--CI; Parkinson Disease,
Symptomatic
--Diagnosis--DI; Parkinson Disease, Symptomatic--Drug
Therapy--DT;
Psychoses, Substance-Induced--Diagnosis--DI; Psychoses,
Substance-Induced
--Etiology--ET; Tomography, X-Ray Computed
  CAS Registry No.: 0 (Antiparkinson Agents)
 
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08794985 94109985
  Birthplace as a risk factor in motor neurone disease and
Parkinson's
disease.
  Betemps EJ; Buncher CR
  University of Cincinnati College of Nursing and Health, OH 45221.
  Int J Epidemiol (ENGLAND) Oct 1993, 22 (5) p898-904, ISSN
0300-5771
Journal Code: GR6
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 9404
  Subfile: INDEX MEDICUS
  A proportional mortality study was conducted to determine if state
of
birth is a risk factor associated with motor neurone disease (MND)
and
Parkinson's disease (PD) using US death certificate information for
1981.
State of birth was used as a surrogate variable for location of
early
childhood environment. A gradient of risk by geographical area in the
US
was found for MND and PD. Cerebral vascular accident (CVA) deaths served
as
a comparison group. Multiple sclerosis (MS) deaths were analysed
to
validate the methods used. A geographical relationship between
latitude
proportional mortality ratios for MND, PD and MS by state of birth,
and a
geographical relationship between latitude and proportional
mortality
ratios for MND and MS by state of birth were found. Statistical
modelling
was used to compare the deaths from MND, PD, MS, CVA to all other deaths
in
the US by state of birth. The resulting models were evaluated to
determine
if any individual states were not well represented by the model for
each
disease. As predicted, no pattern was evident for CVA. The
geographical
gradient observed for MS was as predicted by other studies.
The
geographical pattern found for MND has a northwest to southeast
gradient
and the pattern found for PD has a west to east gradient.
  Tags: Comparative Study; Female; Human; Male; Support, Non-U.S. Gov't
  Descriptors: *Motor Neuron Disease--Epidemiology--EP; *Parkinson
Disease
--Epidemiology--EP; Cause of Death; Cerebrovascular
Disorders--Mortality
--MO; Death Certificates; Models, Statistical; Motor Neuron
Disease
--Mortality--MO; Multiple Sclerosis--Mortality--MO; Parkinson
Disease
--Mortality--MO; Risk Factors; United States--Epidemiology--EP
 
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08721869 94036869
  Parkinsonian syndrome in childhood after sodium valproate
administration.
  Alvarez-Gomez MJ; Vaamonde J; Narbona J; Barao M; Barona P; Brannan
T;
Gudin M; Ibanez R
  Pediatric Neurology Unit, University of Navarra, Pamplona, Spain.
  Clin Neuropharmacol (UNITED STATES) Oct 1993, 16 (5) p451-5,
ISSN
0362-5664 Journal Code: CNK
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 9402
  Subfile: INDEX MEDICUS
  Among the side effects attributed to sodium valproate administration,
the
production of a parkinsonian syndrome is very uncommon, particularly
in
children. We report a 12-year-old girl with secondary epilepsy; 7
days
after the initiation of valproate therapy she developed parkinsonism
that
disappeared completely when valproate was replaced by carbamazepine.
We
discuss the possible role of alterations in GABAergic neurotransmission
in
the extrapyramidal syndrome that developed.
  Tags: Case Report; Female; Human
  Descriptors: *Parkinson Disease, Symptomatic--Chemically
Induced--CI;
*Valproic Acid--Adverse Effects--AE; Child
  CAS Registry No.: 99-66-1 (Valproic Acid)
 
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08185442 92323442
  Life-style and dietary factors early and late in Parkinson's disease.
  Vieregge P; von Maravic C; Friedrich HJ
  Klinik fur Neurologie, Medizinische Universitat zu Lubeck,
Federal
Republic of Germany.
  Can J Neurol Sci (CANADA) May 1992, 19 (2) p170-3, ISSN 0317-1671
Journal Code: CJ9
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 9210
  Subfile: INDEX MEDICUS
  The study investigated features of life-style and dietary habits
early
and late in life of patients with idiopathic Parkinson's disease
(IPD).
Seventy-one patients and 103 controls were interviewed personally
with a
structured questionnaire. Living in villages during primary school time
was
significantly more frequent among patients, and in the urban
environment
patients had lived less frequently in larger-sized towns.
Mushroom
harvesting during childhood was more frequent among patients. No
difference
between patients and controls was found in childhood water supply,
habits
of fishing in the countryside or at the seaside, and eating such
fish.
Actual food preference in patients was greater for almonds and plums,
while
no difference was found in the actual intake of mushrooms,
peanuts,
oil-dressed salad, fish and animal offals. The study did not
indicate a
higher consumption of foods known to harbour heavy metals and pesticides
in
IPD patients either long before or during the disease. Reduced
consumption
of foodstuffs rich in vitamin E, as reported previously for
premorbid
patients, is no longer observed in patients with overt disease.
  Tags: Animal; Female; Human; Male
  Descriptors: *Food Habits; *Life Style; *Parkinson
Disease--Psychology
--PX; Adolescence; Adult; Aged; Basidiomycetes; Cookery; Fishes;
Meat;
Metals--Analysis--AN; Middle Age; Questionnaires; Rural Population;
Urban
Population; Water Supply--Analysis--AN
  CAS Registry No.: 0 (Metals)
 
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07867018 92005018
  Parkinson's disease and exposure to rural environmental
factors: a
population based case-control study.
  Semchuk KM; Love EJ; Lee RG
  Department of Community Health Sciences, University of Calgary,
Canada.
  Can J Neurol Sci (CANADA) Aug 1991, 18 (3) p279-86, ISSN 0317-1671
Journal Code: CJ9
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 9201
  Subfile: INDEX MEDICUS
  To determine whether a history of exposure to rural environmental
factors
leads to an increased likelihood of developing idiopathic
Parkinson's
disease, we conducted a case-control study of 130 cases and 260
randomly
selected community controls (matched with the cases by sex and age +/-
2.5
years at a ratio of 2 controls: 1 case) in the city of Calgary. The
data
were collected by personal interviews and were analyzed using
conditional
logistic regression for matched sets. The ages of the cases ranged
from
36.5 to 90.7 years (mean = 68.5 +/- 11.3 years). The mean age at
diagnosis
was 61.1 +/- 12.4 years. The mean duration of disease was 7.8 +/-
0.6
years. Eleven (9.1%) cases were diagnosed before age 40. In this
sample
from the Province of Alberta, Canada, no significant increase in risk
for
Parkinson's disease was associated with a history of rural living,
farm
living, or well water drinking in early childhood or at any time during
the
first 45 years of life.
  Tags: Female; Human; Male; Support, Non-U.S. Gov't
  Descriptors: *Environmental Exposure; *Parkinson
Disease--Epidemiology
--EP; *Rural Health; Adult; Aged; Aged, 80 and over;
Alberta--Epidemiology
--EP; Case-Control Studies; Middle Age; Regression Analysis; Risk
Factors
 
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07681441 91200441
  Encephalitis lethargica-like illness in a five-year-old.
  Mellon AF; Appleton RE; Gardner-Medwin D; Aynsley-Green A
  Newcastle General Hospital.
  Dev Med Child Neurol (ENGLAND) Feb 1991, 33 (2) p158-61,
ISSN
0012-1622 Journal Code: E83
  Languages: ENGLISH
  Document type: JOURNAL ARTICLE
  JOURNAL ANNOUNCEMENT: 9107
  Subfile: INDEX MEDICUS
  A five-year-old boy presented with an encephalitis
lethargica-like
illness, characterised by somnolence, mutism and Parkinsonian rigidity
two
weeks after an acute exanthem. Investigation revealed increased
serum
measles antibody titre. He made a complete recovery.
Encephalitis
lethargica associated with Parkinsonism in childhood is rare and
usually
carries a poor prognosis.
  Tags: Case Report; Human; Male
  Descriptors: *Arousal--Physiology--PH;
*Encephalomyelitis--Diagnosis--DI;
*Neurologic Examination--Methods--MT; *Parkinson Disease,
Postencephalitic
--Diagnosis--DI; Akinetic Mutism--Diagnosis--DI; Akinetic
Mutism
--Physiopathology--PP; Brain--Physiopathology--PP; Child,
Preschool;
Encephalomyelitis--Physiopathology--PP; Follow-Up Studies;
Parkinson
Disease, Postencephalitic--Physiopathology--PP; Spinal
Cord--Physiopatholog
y--PP
 
==============================================================
 
Part Two to Follow
 
Best,
 
Bob
 
--
********************************************************
 
Robert A. Fink, M. D., F.A.C.S. Phone: 510-849-2555
Neurological Surgery FAX: 510-849-2557
2500 Milvia Street Suite 222
Berkeley, California 94704-2636
USA
 
E-Mail: [log in to unmask]
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