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Differences in Nocturnal and Daytime Sleep Between Primary and Psychiatric Hypersomnia: Diagnostic and Treatment Implications

From the Sleep Research and Treatment Center and Department of Psychiatry (A.N.V., E.O.B., A.K., C.C.), Pennsylvania State University College of Medicine, Hershey, PA; and Sleep Disorders Center and Autonomous University (A.V.-B.), Madrid, Spain.

Address reprint requests to: Alexandros N. Vgontzas, MD, Pennsylvania State University, College of Medicine, Department of Psychiatry, 500 University Dr., Hershey, PA 17033. Email: axv3{at}psu.edu

	ABSTRACT

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
OBJECTIVE: The differential diagnosis of primary (idiopathic) vs. psychiatric hypersomnia is challenging because of the lack of specific clinical or laboratory criteria differentiating these two disorders and the frequent comorbidity of mental disorders in patients with primary hypersomnia. The aim of this study was to assess whether polysomnography aids in the differential diagnosis of these two disorders.

METHODS: After excluding patients taking medication and those with an additional diagnosis of sleep-disordered breathing, we compared the nocturnal and daytime sleep of 82 consecutive patients with a diagnosis of either primary hypersomnia (N = 59) or psychiatric hypersomnia (N = 23) and normal control subjects (N = 50).

RESULTS: During nocturnal sleep, patients with psychiatric hypersomnia showed significantly higher sleep latency, wake time after sleep onset, and total wake time and a significantly lower percentage of sleep time than patients with primary hypersomnia and control subjects (p < .05). In addition, the daytime sleep of patients with psychiatric hypersomnia was significantly higher in terms of sleep latency, total wake time, and percentage of light (stage 1) sleep and lower in terms of percentage of sleep time and stage 2 sleep than in patients with primary hypersomnia and control subjects (p < .05). The daytime sleep of patients with primary hypersomnia as compared with that of control subjects was characterized by lower sleep latency and total wake time and a higher percentage of sleep time (p < .05). Finally, a sleep latency of less than 10 minutes or a sleep time percentage greater than 70% in either of the two daytime naps was associated with a sensitivity of 78.0% and a specificity of 95.7%.

CONCLUSIONS: Our findings indicate that psychiatric hypersomnia is a disorder of hyperarousal, whereas primary hypersomnia is a disorder of hypoarousal. Polysomnographic measures may provide useful information in the differential diagnosis and treatment of these two disorders.

Key Words: primaryhypersomnia • psychiatric hypersomnia • polysomnography

Abbreviations: ANCOVA = analysis of covariance; ANOVA = analysis ofvariance; BMI = body mass index; DSM-IV = Diagnosticand Statistical Manual of Mental Disorders, fourth edition; EDS = excessive daytime sleepiness; REM = rapid eye movement; SL = sleep latency; ST = sleep time; TWT = total waketime; WTASO = wake time after sleep onset.

	INTRODUCTION

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EDS occurs in about 5% of the population (1) and is the chief complaint of the majority of patients evaluated in sleep disorders clinics (2, 3). Approximately 10% to 15% of individuals who present to sleep disorders clinics with a chief complaint of daytime sleepiness are diagnosed as having either primary (idiopathic) hypersomnia or hypersomnia related to a mental disorder (2). However, these figures may vary considerably depending on the specific characteristics of the population of each sleep clinic and the criteria used to make a diagnosis.

The differential diagnosis of these two disorders is a challenging task. In DSM-IV, four of the five listed diagnostic criteria are identical for the two disorders (4). The only differential diagnostic criterion between the two disorders is that in psychiatric hypersomnia, excessive sleepiness is judged to be related to a mental disorder. However, the frequent comorbidity of psychiatric disorders in patients with primary hypersomnia (5) makes the differential diagnosis of these two disorders solely on a clinical basis particularly difficult. The diagnostic criteria of idiopathic hypersomnia in the revised edition of the International Classification of Sleep Disorders (3), in addition to the clinical criteria, which are similar to DSM-IV criteria, include one or more of the following polysomnographic features: 1) a sleep period that is normal or prolonged in duration, 2) a SL less than 10 minutes, 3) normal REM sleep latency, 4) a SL less than 10 minutes on the Multiple Sleep Latency Test, and 5) fewer than two sleep-onset REM periods. However, polysomnographic criteria are not included in the minimal criteria for the diagnosis of idiopathic hypersomnia, and their diagnostic utility in differentiating between idiopathic and psychiatric hypersomnia has not been systematically assessed.

The objectives of our study were 1) to contrast the daytime and nighttime sleep of patients with primary or psychiatric hypersomnia and normal control subjects and 2) to evaluate the utility of sleep measures in the differential diagnosis and treatment of these disorders.

	METHODS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
Subjects
Included in the study were 133 consecutive patients with a chief complaint of EDS who were diagnosed with either primary (idiopathic) hypersomnia (N = 98) or hypersomnia due to a mental disorder (N = 35) and 50 control subjects.

The complaint of EDS was initially validated by a structured intake interview that systematically reviewed general sleep habits, including quality and duration of sleep, snoring, breath cessation, daytime sleepiness, nap history, and cataplexy. The complaint was further verified by completion of a questionnaire developed and standardized by our sleep disorders clinic that provides detailed information about sleep history, medical and psychiatric factors, and medication history (6). This questionnaire evaluates various issues associated with EDS, including age of onset; frequency, severity, and variability of EDS; history and effectiveness of past treatments for EDS; and family history. The answers to these two instruments were thoroughly reviewed during the sleep history part of the clinical evaluation, which was conducted by two psychiatrists (one of them a sleep disorders specialist) and included a physical examination (including history) and a comprehensive psychiatric interview. The psychiatric interview was semistructured, required 45 to 60 minutes to complete, and included a history of the present illness, past history (including developmental and family histories), and a complete mental status examination. The mental status examination included a general description, mood and affect, speech characteristics, perception, thought content and process, sensorium and other cognitive function, and insight and reliability of the patient. In addition, both patients and control subjects completed the Minnesota Multiphasic Personality Inventory, the results of which will be reported in a subsequent publication. Essential laboratory tests (ie, complete blood count; urinalysis; measurement of serum glucose; liver, renal, and thyroid panels; and electrocardiography) were conducted for all patients and control subjects. The final diagnosis was based on a consensus between the two physicians, who were familiar with and applied DSM-IV criteria. When the two clinicians were uncertain of the diagnosis or could not reach a consensus, additional visits to the sleep disorders clinic were scheduled and included additional interviews, more extensive psychiatric and psychological evaluation, and, if indicated, repeated polysomnographic studies. All patients had a chief complaint of EDS of at least 6 months’ duration associated with significant distress or impairment in social, occupational, or other important areas of functioning. Daytime sleepiness was considered of clinical importance if it was 1) affecting work performance (eg, falling asleep frequently on the job, concern expressed by coworkers or supervisor, or change of job position or being dismissed) and/or 2) interfering with potentially dangerous situations (eg, falling asleep while driving even a short distance). Finally, the interviewers used DSM-IV criteria to assign a primary or secondary psychiatric diagnosis to patients who met these criteria.

All patients except six (95.5%) were referred to us by their physicians; 48% had undergone previous comprehensive evaluation of their daytime sleepiness by a specialist (eg, a neurologist, psychiatrist, pulmonologist, or sleep specialist). Notably, 20% of the total sample had undergone sleep laboratory testing before their evaluation in our center.

Polysomnographic data were used to confirm or rule out sleep apnea, nocturnal myoclonus, significant sleep fragmentation due to obesity or snoring, and the presence of a sleep-onset REM period. Patients with EDS judged to be related primarily to sleep apnea, narcolepsy-cataplexy, hypersomnia due to a medical condition (eg, fibromyalgia), obesity, snoring-induced sleep fragmentation or upper airway resistance syndrome (7), sleep deprivation, or insomnia were excluded from the study. Also, patients with a sleep-onset REM period at night or during at least one of the two naps were excluded from the study. In addition, patients who reported difficulty in initiating or maintaining sleep for an average of more than one night per week in the last 6 months were excluded from the study.

Nineteen of the 98 patients with primary hypersomnia and 3 of the 35 psychiatric hypersomniacs had sleep-disordered breathing (>30 apneic or hypopneic events in an 8-hour polysomnographic study). Five of these patients were treated for obstructive sleep apnea or upper airway resistance syndrome with continuous positive airway pressure. If they remained sleepy despite elimination of sleep-disordered breathing by continuous positive airway pressure, then it was judged that sleep-disordered breathing was not the primary underlying cause of their EDS. Twenty-five patients with primary hypersomnia and 10 with psychiatric hypersomnia were using stimulants or psychotropic medication at the time of their evaluation in the sleep laboratory. To control for potential effects of medication and sleep-disordered breathing on sleep profiles, we excluded from our analysis patients who were using medication or who demonstrated sleep-disordered breathing. Thus, our final analysis included 59 patients with primary hypersomnia, 23 with psychiatric hypersomnia, and 50 control subjects.

Control subjects, who volunteered to participate, were recruited from the community, from the medical center (medical and technical staff and students), and by medical center personnel (friends and acquaintances). Control subjects completed a structured intake interview, a standardized comprehensive sleep questionnaire, a history, and a physical examination and were screened for mental disorders. None reported a sleep complaint or severe medical illness, and none were currently using any medications. Control subjects were able to comply adequately with the study requirements.

Sleep Laboratory Procedures
All patients and control subjects were monitored with use of 16-channel polygraphs (model 78d, Grass Instrument Co., Quincey, MA) in the sleep laboratory for one 8-hour nocturnal polysomnogram and for two daytime naps the next day in sound-attenuated and light- and temperature-controlled rooms. The two nap sessions lasted 60 minutes each and began at approximately 9:00 AM and 12:30 PM (8). This test provides a quantitative assessment of pathological diurnal sleepiness and has been suggested as an alternative to the Multiple Sleep Latency Test for determining sleepiness in disorders of EDS (8, 9). Electroencephalographic, electrooculographic, and electromyographic recordings were obtained in accordance with standard methods (10). The sleep records were subsequently scored, by an individual without any knowledge of the experimental conditions, according to standardized criteria (10). The following sleep parameters were calculated for each subject: sleep induction (SL), sleep maintenance (WTASO), TWT (the combined measure of sleep induction and sleep maintenance), percentage of ST, percentage of sleep stages (REM, 1, 2, 3, and 4), number of REM periods, and REM latency.

Sleep onset and REM latency were determined for each recording in the following manner. Onset of sleep was established by the presence of any sleep stage for a duration of 1 minute or longer. However, if the initial stage of sleep was stage 1, it had to be followed, without any intervening wakefulness, by at least 60 seconds of stage 2, 3, 4, or REM. SL was defined as the time elapsed from lights out to sleep onset; a SL value of 60 minutes was assigned to those who failed to sleep during the naps. REM latency was then defined as the total amount of time from sleep onset to the first appearance of REM sleep. During naps, REM latency and the percentage of REM sleep were calculated only for those who demonstrated REM sleep.

The distribution of wakefulness and REM sleep through the night was examined by thirds of the night. A third of the night was established by subtracting SL from the total amount of laboratory time and then dividing the remaining time into equal thirds.

Respiration was monitored throughout the night by use of thermocouples placed on the nose and mouth (model TCT 1R, Grass Instrument Co.) and thoracic strain gauges based on Wheatstone bridge technology. All-night records of hemoglobin oxygen saturation were obtained using an oximeter (PulseOx, Nonin, Plymouth, MN) attached to the finger. Respiratory data were quantified for the total number of apneic and hypopneic events and minimum oxygen saturation during the recording period. An apnea was considered to be present if there was a cessation of breathing of 10 seconds or more. Hypopnea was defined as a decrease of at least 50% in amplitude of thermocouple output with an associated desaturation of at least 4%.

Statistical Analyses
For the comparisons between the three groups, an ANOVA followed by a Dunn-Bonferroni multiple-comparison t test was performed. The potential confounding effects of age and BMI on the sleep profiles were assessed with ANCOVA. For comparisons between two groups, Student’s t test was used. Finally, to assess the diagnostic utility of daytime nap recordings for detecting idiopathic hypersomnia, we calculated the sensitivity (percentage of correctly identified patients with primary hypersomnia) and specificity (percentage of correctly identified psychiatric hypersomniacs) of an empirically selected sleep criterion (11). All statistical comparisons were computed using SPSS for Windows, version 8.0. Results are expressed as the mean ± SE. The critical value for significance was p < .05.

	RESULTS

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The mean age of patients with primary hypersomnia was 37.6 ± 1.5 years (range, 19–74 years); of patients with hypersomnia due to a mental disorder, 39.9 ± 2.4 years (range, 16–58 years); and of control subjects, 43.2 ± 1.8 years (range, 17–74 years) (NS). The mean BMI of patients with primary hypersomnia was 27.4 ± 1.0; of patients with hypersomnia due to a mental disorder, 28.3 ± 1.8; and of control subjects, 24.1 ± 0.5 (the difference between patients with primary hypersomnia and control subjects was significant at p < .05). Of the 23 patients with psychiatric hypersomnia, 12 had a primary diagnosis of a mood disorder, 6 had a primary diagnosis of a somatoform disorder, 4 had an anxiety disorder, and 1 had a personality disorder. About 36% of patients with primary hypersomnia (21 of 59) met DSM-IV criteria for a secondary psychiatric diagnosis (15 had a mood disorder, 1 had a somatoform disorder, 1 had an anxiety disorder, 2 had a personality disorder, and 2 had a substance abuse disorder).

Nocturnal Sleep Patterns
Sleep efficiency.
In general, the nocturnal sleep of patients with psychiatric hypersomnia was characterized by significant disturbances compared with the sleep of patients with primary hypersomnia and control subjects (Table 1). Specifically, SL was considerably higher in patients with psychiatric hypersomnia (54.1 ± 12.5 minutes) than in patients with primary hypersomnia (15.5 ± 2.0 minutes, p < .01) and control subjects (28.0 ± 3.5 minutes, p < .01). Also, WTASO was greater in patients with psychiatric hypersomnia (79.4 ± 11.2 minutes) than in control subjects (50.7 ± 6.0 minutes, p < .05) and patients with primary hypersomnia (56.8 ± 5.2 minutes, NS). TWT was significantly higher in patients with psychiatric hypersomnia (133.6 ± 13.8 minutes) than in those with primary hypersomnia (72.2 ± 5.8 minutes, p < .01) and control subjects (78.7 ± 7.5 minutes, p < .01). Finally, the percentage of ST was also significantly less in patients with psychiatric hypersomnia (71.7 ± 2.9%) than in those with primary hypersomnia (85.0 ± 1.2%, p < .01) and control subjects (83.6 ± 1.6%, p < .01).

Sleep Stages
Percentages of stage 1, stage 2, and slow-wave sleep were no different between the three groups. Amount of REM sleep was significantly lower in patients with psychiatric hypersomnia (56.2 ± 5.4 minutes) than in patients with primary hypersomnia (78.8 ± 3.70 minutes, p < .01) and control subjects (79.9 ± 4.2 minutes, p < .01). The decrease was more pronounced during the first third of the night. Number of REM periods was also lower in patients with psychiatric hypersomnia (3.1 ± 0.2) than in patients with primary hypersomnia (3.9 ± 0.1, p < .01).

Daytime Sleep Patterns
During the morning nap, 56 of the 59 patients with primary hypersomnia, 22 of the 23 patients with psychiatric hypersomnia, and 45 of the 50 control subjects had at least some sleep. During the afternoon nap, 52 of the 59 patients with primary hypersomnia, 13 of the 23 patients with psychiatric hypersomnia, and 40 of the 50 control subjects also had some sleep. No significant differences were observed among the three groups in terms of percentage of subjects who did not sleep at all during the two naps.

Propensity to fall asleep (SL).
During the first nap, patients with primary hypersomnia fell asleep significantly earlier than control subjects (12.7 ± 1.7 vs. 21.3 ± 2.6 minutes, p < .01) and patients with psychiatric hypersomnia (28.0 ± 3.1 minutes, p < .01) (Table 2). Also, during the second nap, patients with psychiatric hypersomnia fell asleep significantly later than those with primary hypersomnia (39.9 ± 4.1 vs. 22.1 ± 2.4 minutes, p < .01) and control subjects (27.7 ± 2.8 minutes, p < .05) (Table 3). The average nap SL of patients with psychiatric hypersomnia was significantly longer than that of patients with primary hypersomnia (33.3 ± 2.9 vs. 17.4 ± 1.7 minutes, p < .01) and control subjects (24.5 ± 2.0 minutes, p < .05). Patients with primary hypersomnia fell asleep faster than control subjects (17.4 ± 1.7 vs. 24.5 ± 2.0 minutes, p < .05).

In terms of sleep stages, patients with psychiatric hypersomnia had a significantly higher percentage of stage 1 sleep during the first nap than patients with primary hypersomnia (28.4 ± 5.5% vs. 14.6 ± 1.7%, p < .01) and control subjects (17.3 ± 1.9%, p < .05). Similarly, during the second nap, patients with psychiatric hypersomnia had a significantly higher percentage of stage 1 sleep compared with patients with primary hypersomnia (41.9 ± 6.2% vs. 21.1 ± 2.4%, p < .01) and control subjects (17.7 ± 3.2%, p < .01). Furthermore, the average nap data indicated that patients with psychiatric hypersomnia had a significantly higher percentage of stage 1 sleep compared with patients with primary hypersomnia (31.3 ± 4.3% vs. 18.0 ± 1.6%, p < .01) and control subjects (17.0 ± 1.8%, p < .01) and a significantly lower percentage of stage 2 sleep than these two groups (63.4 ± 5.5% vs. 76.5 ± 1.8%, p < .01, and 76.8 ± 2.0%, p < .01, respectively).

Influence of Age, BMI, and Psychopathologic Condition on Nocturnal and Daytime Sleep Profiles
To evaluate the influence of age and BMI on nocturnal and daytime sleep variables, we repeated all of the previously described ANOVAs using ANCOVA with age and BMI as covariates. In all cases, inclusion of the two covariates in the analysis did not change any of the statistical findings generated by the original analysis. To assess whether any psychopathologic conditions in the group of patients with primary hypersomnia had an effect on daytime and nighttime sleep patterns, we divided this group of patients into those with an axis I or axis II diagnosis and those without a mental diagnosis. The comparison between patients with primary hypersomnia with a secondary psychiatric diagnosis (N = 21) and the 23 patients with psychiatric hypersomnia revealed differences in terms of nocturnal and daytime sleep similar to those described between the entire group of patients with primary hypersomnia and those with psychiatric hypersomnia. Also, there were no significant differences between patients with primary hypersomnia with a psychiatric diagnosis and those without one in any variables of nocturnal or daytime sleep.

Diagnostic Value of Daytime Nap Recordings
The criterion of a SL less than 10 minutes or a percentage of ST more than 70% in the first nap had a sensitivity of 72.7% and a specificity of 95.7%. The same criterion in the second nap had a sensitivity of 42.5% and a specificity of 95.2%. Finally, the sensitivity and specificity of this criterion during either nap were 78.0% and 95.7%, respectively.

	DISCUSSION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
The primary finding of our study is that both nighttime and daytime sleep of patients with psychiatric hypersomnia seem to be disturbed compared with that of both patients with primary hypersomnia and control subjects. This finding seems to have important implications in regard to the pathophysiology, diagnosis, and treatment of this disorder.

Patients with psychiatric hypersomnia have a significantly higher nighttime SL than patients with primary hypersomnia and control subjects. This is consistent with previously reported findings of the nighttime SL differences between patients with idiopathic hypersomnia and those with psychiatric hypersomnia (12).

In addition, our study showed that the nocturnal sleep of patients with psychiatric hypersomnia is different than the sleep of patients with primary hypersomnia and control subjects not only in terms of SL but also in terms of WTASO, TWT, percentage of ST, amount of REM sleep, and number of REM periods. Previously reported findings seem to be consistent with our findings. For example, Billiard et al. (13) reported a significantly decreased total sleep time and a nonsignificant increase of WTASO in patients with hypersomnia due to mood disorders compared with patients with idiopathic hypersomnia. Also, in two studies, REM latency was nonsignificantly increased in patients with psychiatric hypersomnia compared with patients with idiopathic hypersomnia (12, 13).

An important finding of our study was that the daytime sleep of patients with psychiatric hypersomnia is characterized not only by significantly prolonged SL but also by significantly increased TWT and percentage of stage 1 sleep and a significantly lower percentage of sleep time and stage 2 sleep compared with patients with primary hypersomnia and control subjects. Two previous studies showed that patients with psychiatric hypersomnia have increased daytime SL compared with patients with idiopathic hypersomnia (12, 13).

Our findings on the nighttime and daytime sleep of patients with psychiatric hypersomnia indicate that these patients, although they complain of EDS, show a sleep propensity that is in fact less than that of persons with idiopathic hypersomnia and even control subjects. Similar findings were reported in a study that assessed objectively the complaint of sleepiness in patients with bipolar depression and hypersomnia (14). Also, Roth and Broughton (5) reported no "genuine sleep" according to electroencephalographic criteria in three patients who were diagnosed with "neurotic hypersomnia." Furthermore, even when they are able to sleep, our patients with psychiatric hypersomnia demonstrate sleep that is lighter and disturbed (significantly higher percentage of stage 1 sleep). This may explain why these patients feel unrefreshed even after prolonged periods of sleep.

The nocturnal sleep of patients with primary hypersomnia was not significantly different than that of control subjects, consistent with findings of a previous study that reported no differences in nighttime sleep between patients with idiopathic hypersomnia and control subjects (15). However, patients with primary hypersomnia tended to sleep better than control subjects, and the lack of a significant difference may be due to the relatively small sample size and/or recording on only a single night.

From a pathophysiologic standpoint, the sleep disturbance in psychiatric patients with the chief complaint of hypersomnia seems to be associated with a centrally driven hyperarousal, whereas primary hypersomnia is associated with a centrally driven hypoarousal. This hypothesis is supported by the measured sleep parameters, which indicate that the two groups exhibit not only alterations of their nighttime sleep but also a change of their daytime alertness. Our postulation that these two disorders are disorders of altered regulation of arousal and not sleep per se is further supported by the fact that idiopathic hypersomnia is associated with dysfunction of the autonomic nervous system, eg, orthostatic hypotension (5) and hypoactivity of the corticotropin-releasing hormone neuron system (a system that is directly linked to arousal) (16), whereas psychiatric hypersomnia is secondary most frequently to depression and anxiety, conditions considered to be associated with hyperarousal. However, more research into other physiologic parameters (eg, metabolic rate and temperature) is necessary to test our thesis that these two disorders are disorders of arousal.

From a diagnostic standpoint, polysomnographic measurements may provide useful information to the clinician who is faced with the challenging task of differentiating these two sleep disorders. A SL of less than 10 minutes or a percentage of ST of more than 70% in either of the two daytime naps was associated with moderate sensitivity (78%) and high specificity (about 96%). These values suggest that when the clinician is faced with the difficult task of diagnosing a patient with both a hypersomnia complaint and a psychopathologic condition, sleep electroencephalographic criteria may be useful in ruling out psychiatric hypersomnia and should be added to the DSM-IV criteria. Furthermore, it seems that the assessment of sleep organization, including wakefulness after sleep onset and sleep stages, contributes additional diagnostic information in comparison to a mere assessment of SL in differentiating primary hypersomnia from psychiatric hypersomnia. This is consistent with previous findings and clinical observations of other investigators (17–19). However, daytime naps are of limited value in assessing the circadian and ultradian effects on sleepiness in healthy individuals and patients.

Finally, from a therapeutic standpoint, our conclusion that primary hypersomnia is a disorder of hypoarousal tends to support the clinical experience that stimulants, albeit sometimes ineffective, are indicated for primary hypersomnia. In contrast, in psychiatric hypersomnia, the use of stimulants is contraindicated, and medication reducing nocturnal disturbance (sedatives) may be more useful.

	ACKNOWLEDGMENTS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 
We thank Deborah Kantner for her technical assistance in this study and Barbara Green for her assistance in word processing and overall preparation of the manuscript.

Received for publication May 17, 1999.

Revision received August 25, 1999.

	REFERENCES

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION ACKNOWLEDGMENTS REFERENCES

 

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