 |
|
Body Mass Index in Essential Tremor
Elan D. Louis, MD, MS;
Karen Marder, MD, MPH;
Eva C. Jurewicz, BA;
Dryden Watner, MA;
Gilberto Levy, MD;
Helen Mejia-Santana, MA
Arch Neurol. 2002;59:1273-1277.
ABSTRACT
| |
Background The pathogenesis of essential tremor (ET) is unknown, but it could be
neurodegenerative. Weight loss has been observed in patients with neurodegenerative
diseases.
Objectives To compare body mass index (BMI) (calculated as weight in kilograms
divided by the square of height in meters) in ET cases and controls and to
determine whether BMI is correlated with tremor severity and duration.
Methods Patients with ET were ascertained from the Neurological Institute of
New York, New York, NY. Control subjects were recruited from 2 studies at
the same institution. Height and weight were measured and BMI was calculated.
Dietary data were collected using a Willett Semi-Quantitative Food-Frequency
Questionnaire. Tremor severity was assessed using a clinical scale and the
Klove Matthews Motor Steadiness Battery.
Results The 78 cases and 242 controls were of similar age. Mean (SD) BMI in
cases vs controls was 26.5 (5.0) vs 28.2 (4.8) (P
= .008). This difference remained significant in an unconditional linear regression
analysis that adjusted for age, sex, ethnicity, and years of education (P = .02). Mean daily caloric intake was similar in cases
and controls. In cases, BMI was negatively correlated with both measures of
tremor severity (r = -0.22; P = .05 and r = -0.24; P = .03) and with tremor duration (r = -0.22; P = .05).
Conclusions The BMI was lower in ET cases than in controls, and lower BMI was associated
with disease of greater severity and longer duration. Caloric intake did not
differ between groups, suggesting that lower BMI is not due to a reduction
in calories. Lower BMI may be due to increased energy expenditure in ET.
INTRODUCTION
SEVERAL NEURODEGENERATIVE diseases are accompanied by progressive weight
loss,1-5
with hypothesized causes including decreased caloric intake and increased
caloric expenditures. Weight loss can be problematic, particularly in elderly
populations, where it has been linked with an increased risk of adverse outcomes
such as hip fractures and mortality.6-7
The pathogenesis of essential tremor (ET) is not known, but it could be neurodegenerative.
First, it is clinically progressive; there is an increase in tremor severity
with age and disease duration.8-9
Second, some patients eventually develop signs of more widespread cerebellar
involvement,10-12
basal ganglia involvement,13 and deficits in
several cognitive domains,14-15
suggesting that there may be progressive spread of the underlying pathologic
condition.
Patients with ET also experience tremor-related functional disability.16-19 Eating
and drinking can be difficult,16 and severely
affected end-stage patients may be unable to feed themselves independently.20 This could result in weight loss as well.
We hypothesized that patients with ET might exhibit weight loss unrelated
to caloric intake. In this cross-sectional study, we compared body mass index
(BMI) (calculated as weight in kilograms divided by the square of height in
meters) and daily caloric intake in ET cases and similarly aged control subjects
and studied the association between BMI and the severity and duration of tremor.
PARTICIPANTS AND METHODS
ET CASES
All ET cases were patients cared for at the Neurological Institute of
New York, Columbia-Presbyterian Medical Center. They were identified from
a computerized database that listed the names and diagnoses of patients billed
in the past 3 years. This database was supplemented by a computerized database
at the Center for Parkinson's Disease and Other Movement Disorders, Columbia-Presbyterian
Medical Center, New York, which listed the names and diagnoses of patients
cared for in the past 10 years. All patients had received a diagnosis of ET
from their treating neurologist.
Patients with ET were selected, alphabetically, from these databases
for enrollment in an ongoing study of environmental risk factors for ET. Office
medical records were reviewed, and patients with diagnoses or any physical
signs of dystonia, Parkinson disease (PD), or spinocerebellar ataxia were
excluded. Before enrollment, patients also underwent a brief 10-minute cognitive
assessment (the Telephone Interview for Cognitive Status),21
and those with evidence of cognitive impairment (score <30 of 41) were
not enrolled. Seventy-eight of 300 patients have been enrolled to date. Thirty-eight
patients declined enrollment. Declinees were similar to enrollees in terms
of age, ethnicity, and years of education; however, a larger proportion of
declinees were women (76.3% vs 52.6%,  2 = 6.02; P = .01).
CONTROL SUBJECTS
Sixty-seven control subjects were enrolled in the study of environmental
risk factors for ET. They were recruited from the tristate region (New York,
New Jersey, and Connecticut) by Audits and Surveys Worldwide, New York, using
random-digit dialing. These controls were frequency matched to cases by 5-year
age strata, sex, and ethnicity. Before enrollment, these subjects underwent
the Telephone Interview for Cognitive Status,21
and those with evidence of cognitive impairment were not enrolled. To increase
power, data were available on an additional 175 control subjects who had been
enrolled in a genetic epidemiologic study of PD at the Neurological Institute
of New York. For that study as well, most control subjects (n = 125) were
selected from the tristate region by Audits and Surveys Worldwide using random-digit
dialing. These controls were frequency matched to cases by 5-year age strata,
sex, and ethnicity. For that study, 50 additional controls were identified
from the community in northern Manhattan, NY. They were individually matched
to cases by age, sex, and ethnicity. The 175 controls from the PD genetic
epidemiology study underwent a standardized neuropsychological battery22 and were excluded from these analyses if they met
established criteria for dementia.23 All 242
control subjects were screened for neurological diseases via telephone using
a brief questionnaire.
EVALUATION OF ALL ET CASES AND ALL CONTROLS
Interview
Demographic information, including age, sex, ethnicity, and disease
duration, if applicable, was collected via interview. Ethnicity was self-reported
as non-Hispanic white, non-Hispanic black, Hispanic, or other.
Assessment of Weight and Height
Weight and height were assessed using a standard protocol. With the
individual standing, measurements were taken of body weight to the nearest
0.045 kg using a balance scale designed for field surveys (model 5600; Scale-Tronix,
White Plains, NY). Height was measured to the nearest 0.5 cm using a movable
anthropometer (GPM Martin Type; Pfister Inc, Carlstadt, NJ).
Videotaped Tremor Examination
A trained examiner videotaped a tremor examination that included 1 test
to elicit postural tremor and 5 tests to elicit kinetic tremor in each arm.24-26 Each videotaped tremor
examination was reviewed by 1 of 2 neurologists (E.D.L. and K.M.) with experience
in movement disorders who had reviewed a training videotape for the rating
of ET.27 Each neurologist rated the tremor
using a scale from 0 to 3 and assigned a total tremor score (range, 0-36).24-27 Based
on the videotaped tremor examination, the diagnosis of ET or not was confirmed
using published diagnostic criteria24-27
that require each case to have at least a moderate-amplitude tremor during
3 activities or a head tremor.
ADDITIONAL EVALUATION OF ET CASES AND CONTROLS ENROLLED IN THE STUDY
OF ENVIRONMENTAL RISK FACTORS FOR ET
Willett Semi-Quantitative Food Frequency Questionnaire
This 20-minute food frequency questionnaire28
includes questions about the frequency of current consumption of 61 foods
and on the use of vitamins and mineral supplements. Food-frequency data may
be used to compute mean daily caloric intake. The questionnaire has shown
good reliability and validity related to recent nutrient intake.28-29
Klove Matthews Motor Steadiness Battery
This battery includes a groove-type steadiness tester (model 32010;
Lafayette Instrument, Lafayette, Ind), which consists of 2 adjustable steel
plates that form the sides of a progressively narrowing groove, and a 9-hole
steadiness tester (model 32011; Lafayette Instrument), which consists of a
vertical metal plate with 9 holes of gradually diminishing size.30
Any contact between a handheld metal-tipped stylus and the steel wall of the
groove or hole completed a circuit and was recorded by a battery-operated
silent impulse counter (model 58023; Lafayette Instrument). The impulse counter
recorded the number of contacts between the stylus and the wall. After a practice
trial, the subject moved the stylus through the groove once and held the stylus
for 15 seconds in 3 of 9 holes. The total number of contacts was summed, yielding
a Klove Matthews test score.
Cumulative Illness Rating Scale
This scale was used to document and rate the severity of coexisting
illnesses. The severity of illness in each of 14 body systems (eg, cardiac,
renal, and pulmonary) was rated from 0 to 3. The Cumulative Illness Rating
Scale score can range from 0 (no illness) to 42 (severe comorbidity in all
14 systems).31 The scale has been validated
in geriatric populations.32
STATISTICAL ANALYSIS
Ethnicity was recoded as white (non-Hispanic white) and nonwhite (including
non-Hispanic black, Hispanic, and other). All statistical analyses were performed
using a statistical software package (SPSS version 9.0; SPSS Inc, Chicago,
Ill). To test whether the BMI was normally distributed, a 1-sample Kolmogorov-Smirnov
test was performed. In this test, failure to reject the null hypothesis (P>.05) was consistent with a normal distribution. 2 and 2-tailed t tests were used. Pearson correlation
coefficients were used to assess correlations between continuous variables.
Unconditional linear regression analyses were performed in which the dependent
variable was BMI and the independent variables in different models included
participant type (case vs control), age, sex, ethnicity (white vs nonwhite),
years of education, and duration quintile. Analysis of covariance was used
to test whether there was interaction between sex and participant type in
determining BMI. With 78 cases and 242 controls and  = .05, the study
had 80% power to detect a 6% difference in BMI between cases and controls.
Data are given as mean (SD).
RESULTS
There were 78 cases and 242 controls (67 in the study of environmental
risk factors for ET and 175 in the study of the genetic epidemiology of PD)
of similar age (Table 1). None
lived in nursing homes. Slightly more than half of the cases were women compared
with 43.8% of the controls, and 89.7% of the cases were white compared with
81.0% of the controls, a difference that approached significance (P = .07). On average, cases had had 3 years of college education compared
with 2 years in controls. The mean Cumulative Illness Rating Scale score was
similar in cases and controls.
|
|
|
|
Demographic and Clinical Characteristics of ET Cases and Control Subjects*
|
|
|
The BMI was normally distributed (Kolmogorov-Smirnov test, z = 1.14; P = .15). The BMI in men vs women
was 28.1 (4.5) vs 27.5 (5.3) (t = 1.14; P = .36) and in whites vs nonwhites was 27.6 (4.8) vs 28.7 (5.5) (t = 1.51; P = .13). There was
no correlation between BMI and years of education (r
= -0.06; P = .28). There was no correlation
between BMI and age (r = 0.08; P = .17), but in individuals older than 65 years, there was a negative
correlation (r = -0.18; P = .01).
The BMI in cases vs controls was 26.5 (5.0) vs 28.2 (4.8) (t = 2.67; P = .008), representing on average
a 6.0% reduction in BMI in cases. In an unconditional linear regression analysis
that adjusted for age, sex, ethnicity (white vs nonwhite), and years of education,
there was an association between BMI (dependent variable) and participant
type (case vs control; P = .02). We also stratified
by sex. The BMI in male cases vs controls was 26.2 (3.4) vs 28.7 (4.6) (t = 3.60; P = .001), which on
average was an 8.7% reduction. The BMI in female cases vs controls was 26.9
(6.1) vs 27.7 (5.0) (t = 0.86; P = .39), which on average was a 2.9% reduction. Sex did not interact
with participant type in determining BMI (analysis of covariance, F = 1.62; P = .20). Two cases (2.6%) and 7 controls (2.9%) had a
BMI less than 20.0, suggesting that malnutrition was not a concern in most
participants.
To minimize differences between cases and controls in ethnicity, sex,
and education, we restricted the sample to whites. These 70 cases and 196
controls were similar in age (67.8 [16.2] vs 67.1 [11.5] years, t = 0.34; P = .74), sex (50.0% vs 41.3% women, 2 = 1.58; P = .21), and years of education
(15.3 [3.0] vs 15.1 [3.0] years, t = 0.32; P = .75). The BMI in cases vs controls was 26.1 (4.6) vs
28.2 (4.7) (t = 3.17; P
= .002), which on average was an 7.5% reduction. In an unconditional linear
regression analysis that adjusted for age, sex, and years of education, BMI
was associated with participant type (case vs control, P = .003). We also stratified by sex. The BMI in male cases vs controls
was 26.2 (3.5) vs 28.8 (4.7) (t = 3.60; P = .001), which on average was a 9.0% reduction. The BMI in female
cases vs controls was 26.1 (5.6) vs 27.3 (4.6) (t
= 1.25, P = .21), which on average was a 4.4% reduction.
Dietary data were available on the first 80 participants enrolled (40
cases and 40 controls) who were similar in age, sex, ethnicity, and education.
Total daily caloric intake was similar for cases vs controls (1462.7 [398.3]
vs 1389.0 [657.8] kcal, t = 0.61; P = .55).
Among cases, longer disease duration was associated with lower BMI (r = -0.22; P = .05), although
disease duration explained only 4.8% of the variance in BMI. We stratified
disease duration into quintiles (1-6, 7-11, 12-20, 21-32, and >32 years),
and the BMI in each respective quintile was 27.6 (4.7), 28.3 (6.7), 26.8 (3.4),
26.1 (5.1), and 24.3 (3.9). In an unconditional linear regression analysis
that adjusted for age, sex, ethnicity, and education, the association between
BMI and duration quintile was significant (t = 1.98; P = .05). Among cases, more severe tremor was associated
with lower BMI (total tremor score, r = -0.22; P = .05 and Klove Matthews test score, r = -0.24; P = .03).
COMMENT
Weight loss is a common accompaniment of neurodegenerative diseases.1-4 We found
that BMI was 6.0% lower, on average, in ET cases than in control subjects
and that lower BMI was associated with disease of greater severity and longer
duration. A similar reduction in BMI of 7.2% has been reported in patients
with PD compared with controls1 and of approximately
3% to 9% in patients with Alzheimer disease.3
Weight loss has been linked to an increased risk of hip fractures and mortality,6-7,33 and it is important
for physicians to be aware of the potential for progressive weight loss in
their patients with ET so that nutrition can be addressed as part of the treatment
plan. Weight loss might be prevented by routinely monitoring indicators of
nutritional risk and, if necessary, providing the appropriate intervention.
There are several possible explanations for the observed reduction in
BMI in ET cases. First, lower BMI could have been due to decreased caloric
intake in ET cases. Diminished appetite, impaired olfaction, difficulty eating,
or cognitive impairment could, in theory, result in decreased caloric intake.1 We assessed total daily kilocalories in a subsample
of our participants and found that they did not differ between ET cases and
controls. Lower BMI also could have been caused by increased energy expenditure
due to either the underlying disease rather than the movements themselves
or excessive involuntary movements. Both of these possibilities need to be
explored further. One final explanation is that ET and lower BMI are associated
because they are related to a common underlying factor. Although we excluded
factors such as age, sex, ethnicity, and education, we recognize that other
confounding variables could exist.
Lower BMI was more apparent in men with ET, where the difference with
controls reached significance. We are unsure of the explanation for this finding.
Age, ethnicity, tremor severity, and tremor duration were similar in men and
women with ET. Daily caloric intake in men with ET (1532.2 [478.1] cal) did
not differ from that of women with ET (1411.3 [329.5] cal, t = 0.90; P = .38). As noted in the previous
paragraph, lower BMI could be a clinical manifestation of the underlying disease.
Differences in the expression of ET in men and women have been reported previously,34 with head and voice tremor more common in women than
in men.
This study has limitations. Although we excluded patients with several
comorbidities that could have contributed to lower BMI (eg, PD and dementia),
and although we assessed age, sex, ethnicity, and education in cases and control
subjects and adjusted or stratified for these in the analyses, other differences
between cases and controls that we did not measure could have accounted for
differences in BMI. These differences (eg, depression, impaired olfaction,
use of medications that result in loss of appetite, and intentional dieting),
however, would have manifested themselves as a reduction in caloric intake,
which we did not find in our cases. Although other medical comorbidities could
contribute to lower BMI, we did not find a difference in Cumulative Illness
Rating Scale score between cases and controls, and neither have differences
in comorbidities been demonstrated between ET cases and controls in the literature.35 Second, this was a cross-sectional study, and the
association between BMI and tremor severity and disease duration needs to
be examined in a longitudinal study to determine whether the reduction in
BMI in ET is progressive or linear with respect to time. Finally, the difference
in BMI between female cases and female controls did not reach significance.
The study was not powered to detect differences between cases and controls
that were less than 6%, and in analyses stratified by sex, the power was lower.
In summary, BMI was lower in ET cases than in control subjects, and
lower BMI was associated with disease of longer duration and greater severity.
Lower BMI was more apparent in men with ET. Current caloric intake did not
differ in cases and controls, suggesting that lower BMI could be due to increased
caloric expenditure. Whether this increased expenditure is a manifestation
of the underlying disease or of the movements themselves needs to be explored
further.
AUTHOR INFORMATION
Accepted for publication March 8, 2002.
Author contributions: Study concept and design (Drs Louis, Marder, and Levy); acquisition of data (Dr Louis, Mss Jurewicz, Watner, and Mejia-Santana); analysis
and interpretation of data (Drs Louis, Marder, and Levy); drafting of the manuscript (Drs Louis, Marder, and
Levy); critical revision of the manuscript for important intellectual
content (Drs Louis, Marder, and Levy; Mss Jurewicz, Watner,
and Mejia-Santana); statistical expertise (Drs Louis,
Marder, and Levy); obtained funding (Dr Louis);
administrative, technical, and material support (Dr Louis,
Mss Jurewicz, Watner, and Mejia-Santana); study supervision (Dr Louis).
This study was supported in part by grants R01 NS39422 (Dr Louis), P30
ES09089 (Dr Louis), and R01 NS36630 (Dr Marder) from the Parkinson's Disease
Foundation (New York, NY) the Taub Institute for Alzheimer's Disease and Aging
Brain (New York) (Dr Marder), and grant RR00645 from the National Institutes
of Health, Bethesda, Md. (Drs Louis and Marder).
Corresponding author and reprints: Elan D. Louis, MD, MS, Unit 198,
Neurological Institute, 710 W 168th St, New York, NY 10032 (e-mail: EDL2{at}columbia.edu).
From the Gertrude H. Sergievsky Center (Drs Louis, Marder, and Levy,
and Mss Jurewicz, Watner, and Mejia-Santana) and the Department of Neurology
(Drs Louis and Marder), College of Physicians and Surgeons, Columbia University,
New York, NY.
REFERENCES
| |
1. Beyer PL, Palarino MY, Michalek D, Busenbark K, Koller WC. Weight change and body composition in patients with Parkinson's disease. J Am Diet Assoc. 1995;95:979-983.
FULL TEXT
|
ISI
| PUBMED
2. Abbott RA, Cox M, Markus H, Tompkins A. Diet, body size and micronutrient status in Parkinson's disease. Eur J Clin Nutr. 1992;46:879-884.
ISI
| PUBMED
3. Cronin-Stubbs D, Beckett LA, et al. Weight loss in people with Alzheimer's disease: a prospective population
based analysis. BMJ. 1997;314:178-179.
FREE FULL TEXT
4. Wolf-Klein GP, Silverstone FA, Lansey SC, et al. Energy requirements in Alzheimer's disease patients. Nutrition. 1995;11:264-268.
ISI
| PUBMED
5. Shoulson I, Miller C, Welle S, et al. Huntington's disease: body weight and basal metabolic indices [abstract]. Ann Neurol. 1984;16:126.
FULL TEXT
6. Gilmore SA, Robinson G, Posthauer ME, Raymond J. Clinical indicators associated with unintentional weight loss and pressure
ulcers in elderly residents of nursing facilities. J Am Diet Assoc. 1995;95:984-992.
FULL TEXT
|
ISI
| PUBMED
7. Stevens J, Cai J, Pamuk ER, et al. The effect of age on the association between body-mass index and mortality. N Engl J Med. 1998;338:1-7.
FREE FULL TEXT
8. Critchley M. Observations on essential (heredofamilial tremor). Brain. 1949;72:113-139.
FREE FULL TEXT
9. Hubble JP, Busenbark KL, Koller WC. Essential tremor. Clin Neuropharmacol. 1989;12:453-482.
ISI
| PUBMED
10. Stolze H, Petersen G, Raethjen J, Wenzelburger R, Deuschl G. Gait analysis in essential tremor: further evidence for a cerebellar
dysfunction [abstract]. Mov Disord. 2000;15(suppl 3):87.
11. Deuschl G, Wenzelburger R, Loffler K, Raethjen J, Stolze H. Essential tremor and cerebellar dysfunction: clinical and kinematic
analysis of intention tremor. Brain. 2000;123:1568-1580.
FREE FULL TEXT
12. Singer C, Sanchez-Ramos J, Weiner WJ. Gait abnormality in essential tremor. Mov Disord. 1994;9:193-196.
FULL TEXT
|
ISI
| PUBMED
13. Rajput AH, Rozdilsky B, Ang L, Rajput A. Significance of Parkinsonian manifestations in essential tremor. Can J Neurol Sci. 1993;20:114-117.
ISI
| PUBMED
14. Gasparini M, Bonifati V, Fabrizio E, et al. Frontal lobe dysfunction in essential tremor: a preliminary study. J Neurol. 2001;248:399-402.
FULL TEXT
|
ISI
| PUBMED
15. Lombardi WJ, Woolston DJ, Roberts WJ, Gross RE. Cognitive deficits in patients with essential tremor. Neurology. 2001;57:785-790.
FREE FULL TEXT
16. Louis ED, Barnes LF, Albert SM, et al. Correlates of functional disability in essential tremor. Mov Disord. 2001;16:914-920.
FULL TEXT
|
ISI
| PUBMED
17. Bain PG, Findley LJ, Thompson PD, et al. A study of heredity of essential tremor. Brain. 1994;117:805-824.
FREE FULL TEXT
18. Rautakorpi I. Essential Tremor: An Epidemiological, Clinical and
Genetic Study. Turku, Finland: Department of Neurology, University of Turku; 1978.
Research Report No. 12.
19. Busenbark KL, Nash J, Nash S, Hubble JP, Koller WC. Is essential tremor benign? Neurology. 1991;41:1982-1983.
FREE FULL TEXT
20. Koller WC, Biary N, Cone S. Disability in essential tremor: effect of treatment. Neurology. 1986;36:1001-1004.
FREE FULL TEXT
21. Brandt J, Spencer M, Folstein M. The Telephone Interview for Cognitive Status. Neuropsychiatry Neuropsychol Behav Neurol. 1988;1:111-117.
22. Stern Y, Andrews H, Pittman J, et al. Diagnosis of dementia in a heterogeneous population: development of
a neuropsychological paradigm-based diagnosis of dementia and quantified correction
for the effects of education. Arch Neurol. 1992;49:453-460.
ABSTRACT
23. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders,
Revised Third Edition. Washington, DC: American Psychiatric Association; 1987.
24. Louis ED, Ottman RA, Ford B, et al. The Washington Heights Essential Tremor Study: methodologic issues
in essential-tremor research. Neuroepidemiology. 1997;16:124-133.
ISI
| PUBMED
25. Louis ED, Ford B, Lee H, Andrews H. Does a screening questionnaire for essential tremor agree with the
physician's examination? Neurology. 1998;50:1351-1357.
FREE FULL TEXT
26. Louis ED, Ford B, Frucht S, Barnes LF, Tang M-X, Ottman R. Risk of tremor and impairment from tremor in relatives of patients
with essential tremor: a community-based family study. Ann Neurol. 2001;49:761-769.
FULL TEXT
|
ISI
| PUBMED
27. Louis ED, Barnes L, Wendt KJ, et al. A teaching videotape for the assessment of essential tremor. Mov Disord. 2001;16:89-93.
FULL TEXT
|
ISI
| PUBMED
28. Willett WC, Sampson L, Stampfer MJ, et al. Reproducibility and validity of a semiquantitative food frequency questionnaire. Am J Epidemiol. 1985;122:51-65.
FREE FULL TEXT
29. Willet W. Nutritional Epidemiology. New York, NY: Oxford University Press; 1990.
30. Louis ED, Yousefzadeh E, Barnes LF, Yu Q, Pullman SL, Wendt KJ. Validation of a portable instrument for assessing tremor in epidemiological
field studies. Mov Disord. 2000;15:95-102.
FULL TEXT
|
ISI
| PUBMED
31. Linn BS, Linn MW, Gurel L. Cumulative illness rating scale. J Am Geriatr Soc. 1968;16:622-626.
ISI
| PUBMED
32. Parmelee PA, Thuras PD, Katz IR, Lawton MP. Validation of the cumulative illness rating scale in a geriatric residential
population. J Am Geriatr Soc. 1995;43:130-137.
ISI
| PUBMED
33. Senarth Yapa RS, Playfer JR, Lye M. Anthropometric and nutritional assessment of patients with Parkinson's
disease. J Clin Exp Gerontol. 1989;11:155-164.
34. Hubble JP, Busenbark KL, Pahwa R, Lyons K, Koller WC. Clinical expression of essential tremor: effects of gender and age. Mov Disord. 1997;12:969-972.
FULL TEXT
|
ISI
| PUBMED
35. Rajput AH, Offord KP, Beard CM, Kurkland LT. Essential tremor in Rochester, Minnesota: a 45-year study. J Neurol Neurosurg Psychiatry. 1984;47:466-470.
ABSTRACT
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Personality in essential tremor: further evidence of non-motor manifestations of the disease
Chatterjee et al.
J. Neurol. Neurosurg. Psychiatry 2004;75:958-961.
ABSTRACT
| FULL TEXT
Reduced Body Mass Index in Patients With Essential Tremor: A Population-Based Study in the Province of Mersin, Turkey
Dogu et al.
Arch Neurol 2004;61:386-389.
ABSTRACT
| FULL TEXT
|
