LETTERS

Searching for Novelty: Challenges with Open Access

Data
Joseph C. Masdeu, MD, PhD
The issue raised in the July 2012 editorial
1
on the potential for
2 independent groups reporting on the same Alzheimers Dis-
ease Neuroimaging Initiative data set may be less critical than
suggested in that editorial. Furthermore, were its recommenda-
tions to be implemented, science would be delayed for no suffi-
cient reason. Is an article less important because it reports on
the same data and with the same findings as another simultane-
ously appearing paper? As scientists, we know how helpful it is
to have concordant findings from different laboratories. If the
findings are important, they do not become less important by
being independently duplicatedquite the opposite. As an
assiduous reader of Annals of Neurology, I would not be the least
bit concerned about wasting my subscription money by reading
important science that also appears in another journal. Nor
would I think that the journal in which the similar article was
published was cheated of an original contribution. Reading the
duplicate report will take less time and make me experience
the good feeling that the results published in the Annals of
Neurology were reliable. Furthermore, if I write a paper, I am
likely to cite both publications, unless a restriction on the number
of references prevents me from doing so. I want my readers to
feel as comfortable as I do about the reliability of the findings.
Acknowledgment
Although this work was supported by the Intramural
Research Program of the NIH, it reflects the authors
opinion and not an official position of the NIH.
Potential Conflicts of Interest
The author serves as Editor-in-Chief of the Journal of
Neuroimaging.
Section on Integrative Neuroimaging, Clinical Brain Disorders
Branch, National Institutes of Health, Bethesda, MD
Reference
1. Josephson SA, Johnston SC, Hauser SL. Searching for novelty:
challenges with open access data. Ann Neurol 2012;72:A5A6.
DOI: 10.1002/ana.23755
Goodbye Neurological Examination, Hello History?
Peter Soros, MD,
1,2
Shahram Abootalebi, MD,
1
and
Vladimir Hachinski, MD, FRCPC, DSc
1
Now that Johnston and Hauser have closed the discussion
on the neurological examination with a declaration of dual love
for the examination and data, we encourage a discussion on
neurological history taking.
1,2
Our vantage point is from an urgent transient ischemic
attack clinic, where we see a variety of patients with fleeting
neurological symptoms referred largely by family doctors and
emergency physicians. Many of our patients have had cerebro-
vascular events, but others present with focal seizures, migraine
aura, benign positional vertigo, and occasionally anxiety attacks
and hyperventilation syndromes.
In many patients, even a careful neurological examination
and additional diagnostic tests such as magnetic resonance
imaging or magnetic resonance angiography are often unhelpful
and at times misleading because of irrelevant imaging findings.
At such times, the only thing standing between appropriate
diagnosis and management and unnecessary tests, treatments, or
interventions is an accurate history.
Let the debate begin.
Potential Conflicts of Interest
Nothing to report.
1
Clinical Neurological Sciences and
2
School of Communication
Sciences and Disorders, University of Western Ontario, London,
Ontario, Canada
References
1. Johnston SC, Hauser SL. The beautiful and ethereal neurological
exam: an appeal for research. Ann Neurol 2011;70:A9A10.
2. Johnston SC, Hauser SL. The neurological exam: striking a nerve.
Ann Neurol 2012;71:A5.
DOI: 10.1002/ana.23742
Is Living Downwind of a Golf Course a Risk
Factor for Parkinsonism?
Margaret L. Parrish, MD, and Robert E. Gardner, MD
The article Solvent Exposure and Parkinson Disease
Risk in Twins in the June, 2012 issue of the Annals of
Neurology indicates the possibility of a public health risk
from solvent exposure.
1
We support the authors view and
suggest that golf courses, and pesticides broadly, may
present another public health risk, raising a question of
chemical hygiene.
We collected 26 cases of parkinsonism of all types, and
found that 19 of 26 in our cohort of mostly metropolitan
dwellers lived on or within 2.0 miles of a golf course. Such an
association could easily be dismissed as a function of the ubiq-
uity of golf courses in urban settings, but specifics may suggest
otherwise. Sixteen of the 19 patients resided downwind of a
golf course within a radius of about 160 degrees. Of the 3
VC
2012 American Neurological Association 983
patients who resided upwind of a golf course, 2 had additional
golf course exposure. Four others had occupational exposures to
various chemicals: 3 to solvents and 1, a synthetic chemist, to
organophosphate pesticides. A fifth patient was a chemist, but
his exposure is unknown.
Twenty-six cases can only raise a question, but given the
potential health risk should there be an association between
living within close proximity to a golf course and parkinsonism,
we hope that someone with a large enough patient base will
adequately address this question.
North Carolina Department of Health and Human Services,
Raleigh, NC
Reference
1. Goldman SM, Quinlan PJ, Ross GW, et al. Solvent exposures
and Parkinson disease risk in twins. Ann Neurol 2012;71:
776784.
DOI: 10.1002/ana.23782
Neonatal Encephalopathy Or HypoxicIschemic
Encephalopathy?
Diana Schendel, PhD,
1
Karin B. Nelson, MD,
2,3
*
and Eve Blair, PhD
4
We agree with Dr Volpe
1
that a diagnosis of hypoxicis-
chemic encephalopathy (HIE) is appropriate for neonates who
have experienced asphyxial birth events such as uterine rupture
or cord prolapse, followed by marked acidosis and neonatal
neurologic depression, if other known causes of neonatal ence-
phalopathy (NE) have been excluded. However, population-
based studies of human infants with NE/HIE, and the few
studies in clinical samples that have examined a range of antece-
dents, have observed that many infants with NE/HIE have not
had recognized asphyxial birth events. Unless clinical details are
carefully examined in NE, and criteria for HIE have been care-
fully applied, the probability of overidentifying etiology as
hypoxicischemic may be high.
Volpe acknowledges that in NE, in the typical clinical
situation, the underlying mechanisms are not entirely known,
and cautions that the clinician must exert great vigilance not to
miss the great mimickers of neonatal HIE. He considers a com-
bination of signs such as abnormal fetal heart rate patterns, me-
conium in the amniotic fluid, low Apgar scores, and acidosis to-
gether with neuroimaging abnormalities, such as basal ganglia
thalamic injuries, to warrant a diagnosis of HIE. However, none
of these signs is etiologically specific, even the neuroimaging
abnormalities having been identified in infants with placental
inflammation and no asphyxial birth events.
2,3
The pathobiology of NE in human neonates is complex
and often multifactorial. The few systematic studies of antece-
dents of NE/HIE in representative populations have found a
number of nonasphyxial risk factors for NE: inflammation, fetal
growth restriction, maternal thyroid disorders, family history of
neurologic disease, and low socioeconomic status.
4
Studies that
have examined placentas of infants with NE/HIE find patho-
logic lesions, commonly inflammatory or vasculopathic, which
may contribute to or account for the NE.
2,3
Therapeutic cooling in infants with NE has been a major
advance, but only 1 infant in 6 benefits.
5
Neonates with inflamma-
tory placental lesions may respond less favorably to hypothermia.
2
The possibility that underlying pathobiology of NE influences
responsiveness to therapy should be investigated in future studies.
Experimental studies that impose hypoxia or ischemia on
previously normal young animals have added substantially to
our knowledge, but may not provide good models for a large
proportion of neonates with NE.
Terminology is important. When, as is often the case, the
etiology of NE is uncertain, we think the appropriate diagnosis is
NE. Acknowledging what is not known is key to further progress.
Potential Conflicts of Interest
Nothing to report.
1
National Center on Birth Defects and Developmental
Disabilities, Centers for Disease Control and Prevention,
Atlanta, GA,
2
Childrens National Medical Center,
Washington, DC,
3
National Institute of Neurological Disorders
and Stroke, Bethesda, MD, and
4
Telethon Institute for Child
Health, University of Western Australia, Perth, Australia
References
1. Volpe JJ. Neonatal encephalopathy: an inadequate term for
hypoxic-ischemic encephalopathy. Ann Neurol 2012;72:156166.
2. Wintermark P, Boyd T, Gregas MC, et al. Placental pathology in
asphyxiated newborns meeting the criteria for therapeutic hypo-
thermia. Am J Obstet Gynecol 2010;203:579.e1579.e9.
3. Hayes BC, Cooley S, Donnelly J, et al. The placenta in infants >
36 weeks gestation with neonatal encephalopathy: a case control
study. Arch Dis Child Fetal Neonatal Ed (in press).
4. Badawi N, Kurinczuk JJ, Keogh JM, et al. Intrapartum risk factors
for newborn encephalopathy: the Western Australian case-control
study. BMJ 1999;319:10541059.
5. Wachtel EV, Hendricks-Munoz KD. Current management of the
infant who presents with neonatal encephalopathy. Curr Probl
Pediatr Adolesc Health Care 2011;41:132153.
DOI: 10.1002/ana.23753
984 Volume 72, No. 6
ANNALS of Neurology