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Association of meningiomas with obesity.

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with available height and weight measurements. Using this
criterion, any patient more than one standard deviation over
the mean Quetelet index (as obtained in the Framingham
study of cardiovascular diseases [h])for his or her height
was considered obese. T h e Quetelet index was used to validate our definition of obesity by calculating Cohen’s Kappa
index. Detailed information on height and weight was available for 40 patients. Because of the retrospective design of
the study, quantitative data to assess obesity could not be
obtained for all patients. Fifteen of the 40 were obese by our
criterion. O f the same 40, 10 were defined as obese using the
Quetelet index. (Cohen’s Kappa index of agreement = 0.60,
standard error = 0.15; Z = 3.96, p < 0.0001.) Thus there
was a high degree of agreement between the two criteria,
establishing the validity of o u r definition of obesity.
T h e Table summarizes the results. I t shows a Statistically
significant association between meningiomas arid subjectively assessed obesity in women using a case-control study
design.
Increasing evidence suMests that overfeeding increases
cancer risk in humans. Wynder and Mabuchi IS} reviewed
epidemiological evidence suggesting that overnutrition increases the risk of cancers of the breast, ovary, and endometrium in wornen and of the prostate in men. Other srudies
have found specific associations between obesity and breast
cancer [ I ) as well as obesity and endometrial cancer [ 2 ] .
Wynder and Gori [‘l]expressed thc view that food factors
were implicated in the causes of 60°C of cancers in women
and more than 4OT of cancers in men.
Obesity may thus play a role in the etiology of nervous
system tumors. Whether tumors other than menink’
’lomas are
also associated with obesity deserves to be evaluated, and
these suggestive findings in meningiomas need to be prospectively confirmed.
drome, and should be assumed to b e due to a neoplasm until
proved otherwise.
Depurtnient of Pedzutrics
DKZ
rsion of Pedzutrrc ATeurdoD
U C U Center for the Health Sireniec
MDCC 22-464
Los Angeles C A 90024
References
1 Jaffe H, Cassady JR, Filler RM, Perersen R TragRis D Herero-
chromia and Horner syndrome associated with cervical and
mediastinal neuroblastoma J Pediarr 87 ’5-”.
1y75
2 Menkes JH Textbook of Child Neurology Second edition Philadelphia, Lea & Febiger, 1980, p 2-0
3 Sauer C, Levinsohn MW Homer’s syndrome in childhvod
Neurology (Minneap) 26 216-220, 19-6
4 Volpe JJ Neurolog) ot the Newborn Philadelphia, Saunders
1981, pp 587-588
5 Weinstein JM, Zweifel TJ, Thompson HS Congenital Homer’s
syndrome Arch Ophthalmol 08 1074-1078, 1980
Association of
Meningomas with Obesity
Srinath N. Bellur, MD,” Vijay Chandra, M D , PhD,”
and Robert J. Anderson, P h D i
Some data suggest that obesity may be an important cause of
certain female-preponderant, hormone-related tumors [ 1, 2,
51. Because meningiomas are said to b e female preponderant
and hormonally dependent [3], we conducted a case-control
study of 176 such tumors diagnosed at the LJniversity of
Illinois Hospital over a twenty-year period. T h e control subjects were also drawn from the patients cared for by the
combined neurologyineurosurgery services of the University
of Illinois. T h e next consecutive patient following each study
patient matched for age (plus or minus five years) and sex was
selected as a control, regardless of diagnosis.
For our purpose, a patient was defined as “obese” if so
described by at ieast rwo different examiners o n separate
occasions. T h e Quetelet index was calculated for patients
‘Department oj‘Neurologli and i.1~pidemioloitv-Biomet~
Progruni
School of Public Health
Ciniz’rrsitl of I11inuij at Chicago
Chicago. IL 60611’
Refrenres
1. DeWaard I , Baanders-Van Halewijn EA: A prospecrive srudy in
general practice o n breast cancer risk i n post-menopausal women.
I n t J Cancer 14.153-160. 19’4
Summap of ReJults
Cases
Controls
Subjects
Total No.
of Patients
Tordl No.
No. Obesed of Patients
No. Obese’
Study population
Men
Women
I76
55
121
5’
27
5
52
176
55
121
?
20
Concordant
Pairsb
XLC
P
Odds Ratio”
10
0
10
14 06
0.333
19.69
0.00018
NS
a0.0001
2?(1
”Those described as “obese” by two independent observers o n separate occasions.
bThe number of pairs in matched-pair analysis in which both the study and control paricnrs were obese.
‘Calculated using McNemar’s chi-square statistic for pairecl data.
‘Estimate of the excess risk from obesity among study parients as compared with controls.
NS
= not
significant
346 Annals of Neurology Vol 1 3 No 3 March 1983
...
4.2
2. Dunn LJ, Bradbury JT: Endocrine factors in endometrial carcinoma: a preliminary report. Am J Obstet Gynecol 97:465-471,
1967
2a. Florey CV: The use and interpretation of ponderal index and
other weight-height ratios in epidemiological studies. J Chronic
Dis 2393-103, 1970
3. Schoenberg BS, Christine BW, Wishnant JW: Nervous system
neoplasms and primary malignancy of other sites. Neurology
251705-712, 1975
4. Wynder EL, Gori GB: Contribution of the environment to cancer
incidence: an epidemiologic exercise. J Natl Cancer Inst 582325832, 1977
5. Wynder EL, Mabuchi K: Etiologic and preventive aspects of human cancers. Prev Med 1:300-334, 1972
Sudden Deafness
in Chickenpox:
A Case Report
Rajan Bhandari, MD," and Gerald S. Steinman, M D
In a review of sudden deafness, Jaffe [4]reported 143 cases,
5 of which showed bilateral involvement and only 1 of which
was attributed to chickenpox. The case report was not described, and it is unclear whether the hearing loss was unilateral or bilateral, permanent or temporary. Standard textbooks of pediatric neurology [ 1,9] and neurology [51 do not
mention hearing loss as a complication of chickenpox.
A fourteen-month-old infant in previous good health developed the characteristic papulovesicular rash of chickenpox
accompanied by excessive upper respiratory symptoms, feeding difficulty, fever, vomiting, irritability, and lethargy. Five
days later he developed gait ataxia, which progressed to
marked swaying of the body, frequent falls, and a refusal to
walk. The next day his mother noted the onset of auditory
inattention, and the day after he was admitted to the hospital.
Developmental milestones and language were appropriate
for age. There was no family history of progressive neurological disease.
Physical examination upon admission revealed a playful
infant who was in no acute distress if left alone. His general
examination was normal except for healing crusted lesions
consistent with chickenpox.
The neurological examination revealed a normal fundoscopic appearance with good extraocular movements and
pupillary responses. The infant did not react to clapping,
calling his name, or loud bangs. Muscle strength and tone
were normal. Rapid alternating movements and rapid fast
movements were minimally slowed. While sitting, he demonstrated good posture without titubations. He was unable to
stand without two-handed support and was quite ataxic when
he walked. His muscle stretch reflexes were hyperactive but
symmetrical and his toes were down-going on plantar stimulation. Sensory examination yielded normal responses to pin*Present address: Department of Neurology, Stanford University
and Department of Neurology, Santa Clara Valley Medical Center,
San Jose, CA 95128.
prick, light touch, and vibration, and proprioception was normal.
Routine laboratory data revealed a mild microcytic hypochromic anemia. A head computed tomographic scan utilizing contrast was normal. An EEG showed bilateral diffuse
and excessive slowing without epileptiform activity. Spinal
fluid analysis and culture were normal. Pure-tone audiometry
revealed extensive bilateral hearing loss. Brainstem auditory
responses could not be evoked using maximal stimuli of
93 d B and averaging 1500 clicks.
Over the following three weeks, the infant's coordination
returned to ncrmal. Six months later he was still completely
deaf as judged by absence of response to loud noise.
The nervous system complications of chickenpox are relatively infrequent and include cerebellar ataxia, aseptic meningitis, acute transverse myelitis, chickenpox-Reye syndrome,
and, less commonly, aphasia, hemiplegia, and seventh cranial
nerve palsy [ 5 ] .
Congenital deafness has occurred with rubella, mumps,
rubeola, cytomegalovirus, and varicella-zoster virus 17,81. In
such cases deafness has been thought to occur secondary to
endolymphatic labyrinthitis secondary to viremia or, perhaps,
a perilymphatic infection C81. Alternate speculations are of a
postinfectious allergic demyelination [2], although in a review of varicella cases, clear-cut evidence was lacking 131.
Other causes of sudden, severe, at times complete (even permanent) deafness include common cold, upper respiratory
infection, meningitis, head trauma, hypertension, and, rarely,
carbon monoxide poisoning 141.
It appears that this patient suffered bilateral complete
deafness without vestibular involvement, as reflected by the
absence of nystagmus and lack of lateralized ataxia. Hearing
aids did not improve auditory evoked responses, although
improvements have previously been reported [GI.
Department of Neurology
Ohio State University
Columbus, OH 43210
References
1. Bell WE, and McCormick WF: Neurologic infections in childhood. Philadelphia, Saunders, 1975, pp 217-218
2. Dutta SR, Barat D: Post infective allergic demyelination following
varicella. J Assoc Physicians India 25:577-580, 1977
3. Griffith JF, Salam MV, Adams RD: The nervous system disease
associated with varicella. Acta Neurol Scand 46279-300, 1970
4. Jaffe BF: Sudden deafness: an otologic emergency. Arch
Otolaryngol 86:81-86, 1967
5. McKendall R, Klawans H: Nervous system complications of
varicella-zoster virus. In Vinken PJ, Bruyn G W (eds):Handbook
of Clinical Neurology, Vol 30. Amsterdam, North Holland,
1978, pp 161-183
6. Rapin I, Graziani LJ: Auditory-evoked responses in normal,
brain-damaged, and deaf infants. Neurology (Minneap) 17:881894, 1967
7. Siege1 M: Congenital malformations following chickenpox,
measles, mumps, and hepatitis: results of a cohort study. JAMA
226:1521-1527, 1973
8. Strauss M, Gustave DL: Viral disease of the labyrinth. I. Review
of the literature and discussion of the role of CMV in congenital
deafness. Ann Otol Rhino1 Laryngol 82:577-583, 1973
9. Swaiman KF, Wright FS: The practice of pediatric neurology.
St Louis, Mosby, 1975, pp 582-583
Notes and Letters
347
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