Do you want to buy antibiotics online without prescription? http://buyantibiotics24h.com/ - This is pharmacy online for you!

Harvest center's post-polio library

FROM
Dr. Richard L. Bruno
Chairperson, International Post-Polio Task Force
Director
The Post-Polio Institute
and
International Centre for Post-Polio Education and Research
PostPolioInfo@AOL.COM

JOURNAL OF CHRONIC FATIGUE SYNDROME, 1998;
4: 61-76.

Elevated plasma prolactin and EEG slow wave power in
post-polio fatigue: Implications for a dopamine deficiency
underlying post-viral fatigue syndromes.

Richard L. Bruno Susan Creange, Jerald R. Zimmerman, and Nancy M.
Frick.

This research was supported by grants from the George A. Ohl, Jr., Infantile
Paralysis Foundation

ABSTRACT
To test the hypothesis that plasma prolactin and electroencephalographic
(EEG) slow wave activity are correlated with fatigue, 33 polio survivors
without medical or psychologic comorbidities were studied. Subjects were
administered the Post-Polio Fatigue Questionnaire (PFQ) and had resting

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] measurement of both plasma prolactin and bilateral temporal-occipital
power across the EEG frequency spectrum. Typical daily fatigue severity on
the PFQ was significantly correlated with daily difficulty with attention,
staying awake and motivation, but not with measures of acute polio severity
or the number of limbs affected by late-onset Post-Polio Sequelae symptoms.
Prolactin was significantly correlated with daily fatigue severity on the PFQ
(r=.39; p<.05). EEG power was equal between the two hemispheres across
all frequency bands. However, EEG slow wave power in the right
hemisphere was significantly correlated with daily fatigue severity and
prolactin level (r=.37; p<.05). Using multiple linear regression, age at acute
polio, frequency of difficulty with attention on the PFQ, prolactin and right
hemisphere slow wave power predicted 72% of the variance of the daily
fatigue severity rating (r=.85; p<.0001). These data suggest that increased
prolactin secretion and EEG slowing are related to the severity of post-polio
fatigue, findings similar to those in patients with acute paralytic and non-
paralytic poliomyelitis and with chronic fatigue syndrome. A primary role is
suggested for a dopamine deficiency (versus serotonergic receptor
supersensitivity) underlying impaired cortical activation and the symptoms
associated with putative post-viral fatigue syndromes.

INTRODUCTION
Fatigue is the most commonly reported and most debilitating of Post-Polio
Sequelae (PPS), the unexpected, late-onset symptoms affecting the more than
1.8 million North American polio survivors (1). In the 1985 National Survey
of polio survivors, 91% reported new or increased fatigue, 41% reported
fatigue significantly interfering with performing or completing their work
and 25% reported fatigue interfering with self-care activities (2).

Importantly, polio survivors differentiate between physical tiredness and
what they describe as "brain fatigue" that is associated with cognitive
difficulties. In the 1990 National Survey, between 70% and 96% of polio
survivors with fatigue reported concomitant problems with concentration,

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] memory, attention, word-finding, maintaining wakefulness and thinking
clearly, with 77% percent reporting moderate to severe difficulty with these
problems (3). Despite their multiple cognitive complaints, the only clinically
significant deficits on formal neuropsychologic testing in severely fatigued
polio survivors were in attention and information processing speed (4).

Postmortem studies performed during the polio epidemics of 50 years ago
demonstrated the consistent presence of poliovirus lesions in the midbrain
reticular formation, hypothalamus, thalamus, putamen and globus pallidus,
i.e. the reticular activating system (RAS) (3,5). RAS lesions have been
hypothesized to cause late-onset fatigue and attention impairments in polio
survivors (6). This hypothesis is supported by studies in which magnetic
resonance imaging of the brain has revealed small discrete or multiple
punctate areas of hyperintense signal in the reticular formation, thalamus,
putamen, and white matter tracts only in those polio survivors reporting
fatigue (3,7).

Postmortem histopathology also documented that neurons secreting
neurotransmitters known to activate the brain, especially dopaminergic
neurons in the substantia nigra and arcuate nucleus, were also damaged or
destroyed by the poliovirus (5-7). The inability of polio survivors' damaged
RAS to adequately activate the cortex, thereby impairing attention and
concentration and generating the subjective symptoms of fatigue, has been
hypothesized to result in part from reduced secretion of dopamine (3,6,8).
This hypothesis is supported by a double-blind, placebo-controlled pilot
study of bromocriptine mesylate, a direct-acting, post-synaptic dopamine 2
(D2) receptor agonist (9). An increasing daily dose of bromocriptine was
significantly negatively correlated with subjective reports of fatigue on
awakening as well as difficulty with staying awake during the day, attention,
cognition, word finding and memory. It is notable that bromocriptine was
effective only in the most neurophysiologically impaired subjects, i.e., those
with more than twice as many lesions on brain MRI, a blunted ACTH
response to an overnight fast and a baseline plasma prolactin level nearly
double that of the drug non-responders.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] If there is a dopamine deficiency in polio survivors it should be
physiologically evident. Resting plasma levels of prolactin should be elevated
since dopaminergic neurons in the arcuate nucleus were damaged by the
poliovirus and arcuate dopamine secretion inhibits prolactin release via D2
receptor stimulation (10). If a dopamine deficiency is preventing brain
activation and causing fatigue, elevated prolactin should be associated with
impaired cortical activation as evidenced by slowing of the
electroencephalogram (EEG). This study was undertaken to test the
hypothesis that fatigue, plasma prolactin and EEG slowing are significantly
correlated in polio survivors with fatigue.

Subjects. Subjects were recruited from patients treated by the Post-Polio
Service and from post-polio support groups. Potential subjects completed
and mailed to the laboratory a polio and medical history form and the Post-
Polio Fatigue Questionnaire (PFQ) which rates typical daily fatigue severity
on a six-point scale from "none" through "severe" (3). The PFQ also rates
the severity and the frequency (on a four-point scale from "never" through
"always") of difficulty with motivation, attention, mind wandering, thinking
clearly, concentration, word finding, memory, muscle weakness and staying
awake during the day. A phone interview was conducted and individuals
were excluded if they were over 59 years of age, had any medical or
psychological condition that could cause fatigue or cognitive impairment
(e.g., major depressive episode, thyroid, cerebrovascular or cardiac disease,
anemia, respiratory insufficiency, sleep apnea or hypopneas, lupus or
diabetes) or if they were taking medications that could cause fatigue or
cognitive impairment (e.g., anti-depressants, benzodiazepines). Subjects were
interviewed when they reported for testing and their medical and psychiatric
symptoms and history were confirmed. Thirty-three subjects were selected,
giving a power of .80 at a two-tailed alpha level of p<0.05.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] Power analysis of the EEG frequency spectrum using fast Fourier
transformations was performed using the Dantec NEUROSCOPE (Dantec,
Inc.). Electrodes were placed at T5-Oz (left hemisphere) and T6-Oz (right
hemisphere) with reference placed at FPZ of the International 10/20 System.
These placements have been found to be the most sensitive for identifying
EEG activity associated with decreased attention and the least affected by
eye movement and eye blink artifact (11,12). Scalp skin was wiped with
isopropyl alcohol and scrubbed with an abrasive pad; 1.0 cm. diameter
silver/silver chloride EEG electrodes were then attached with Ten20 EEG
electrode paste to achieve an impedance of <5K ohms. EEG was sampled at
128 Hz during 4 consecutive 4 second epochs with filters (having a 6dB roll-
off) set at 1.0 Hz and 32.0 Hz. Power in the delta (1-4 Hz), theta (4-8 Hz),
alpha (8-13 Hz) and beta (13-30 Hz) frequency bands was quantified in real
time and printed every 30 seconds. The percentage of power for each band
was calculated and power in delta and theta bands summed to calculate
EEG slow wave power.

Procedure. Subjects were asked to eat their usual morning meal and limit
themselves to only two 8 oz. cups of a caffeine-containing beverage on the
day of testing. On arriving at the Institute, the experimental procedure was
described to the subjects who gave written informed consent. Subjects were
then taken to the hospital's hematology laboratory where venous blood was
drawn. Plasma prolactin was assayed by a commercial laboratory using
CIBA-Corning ACS immunochemiluminometric kits. Pre-menopausal
women were studied during their luteal phase to control for the effects of
ovulation on prolactin. Blood was also drawn by finger-stick for a
simultaneous study of blood glucose and post-polio fatigue (data to be
presented elsewhere). Subjects were then escorted to the psychophysiology
laboratory where EEG electrodes were attached over the course of
approximately 20 minutes. The subjects were then requested to sit facing a
white wall that was one meter away, with their eyes open and their muscles
relaxed, and to refrain from talking or moving. Muscle (EMG) activity was
monitored both visually and via the NEUROSCOPE's EMG artifact
rejection software. After one minute of sitting, the subjects' first 16 seconds

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] of artifact-free EEG was recorded. Subjects then began taking
neuropsychologic tests of attention and word finding during which EEG was
also recorded (data to be presented elsewhere).

Data analysis. Statview 4.5 was used to perform statistical analyses.
Descriptive statistics were calculated for all variables as were product-
moment intercorrelations. The p value for correlations of daily fatigue
severity with subjective symptoms on the PFQ was corrected for multiple
comparisons using the Bonferroni inequality. Multiple linear regression was
performed to determine if the daily fatigue severity rating could be
predicted on the basis of the prolactin value and the demographic item, PFQ
subjective symptom of fatigue and EEG frequency band power most
significantly correlated with daily fatigue severity.

Eighteen females and 15 males participated, ages 38 to 59 years, having a
mean educational level of 16 years (Table 1). On average, the patients
contracted polio in 1951 when they were 5 years old, were hospitalized at
polio onset and had one limb permanently affected. This sample is typical of
the population of American polio survivors (2). Subjects were tested between
8:15 and 14:45 (x = 11:00).

Subjects had resting plasma prolactin values ranging from 2.7 to 16.3 ng/ml
(x = 6.9 ± 3.7), typical of the resting prolactin levels measured in both
healthy controls and CFS patients and within the normal range (13-17). As
opposed to other studies, there were no significant correlations between
prolactin and time of blood drawing, age or gender (17). Prolactin was
significantly correlated with daily fatigue severity on the PFQ (r=.39; p<.05).
Daily fatigue severity was also significantly correlated with age at acute polio
(r=.39; p<.05), the severity of difficulty with attention, mind wandering,

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] muscle weakness, concentration, staying awake and motivation, and the
frequency of difficulty with attention and mind wandering (Table 2). Fatigue
severity was not correlated with measures of acute polio severity or the
number of limbs affected by current PPS symptoms (e.g., muscle weakness
and pain). These relationships are consistent with the symptom profile of
polio survivors with fatigue seen in the 1990 National Post-Polio Survey (3).

EEG power was equal between the two hemispheres across all frequency
bands. However, EEG power in the right hemisphere was significantly
correlated with daily fatigue severity (slow wave and delta power) and
prolactin (slow wave and theta power) (Table 3).

Using multiple linear regression, the age when polio was contracted,
frequency of difficulty with attention on the PFQ, plasma prolactin and
right hemisphere slow wave power predicted 72% of the variance of the
daily fatigue severity rating (p<.0001) (Table 4).

DISCUSSION
These findings suggest the hypothesis should be accepted: there are
significant correlations between fatigue, plasma prolactin and slowing of the
EEG in polio survivors. The correlation of fatigue and prolactin with EEG
slow wave power only in the right hemisphere may be related to the
important role ascribed to the right hemisphere in cortical activation (18).
Since polio survivors have impaired visual memory, a function also ascribed
to the right hemisphere, they may have an as yet unexplained tendency
toward right hemisphere damage and therefore a predisposition to impaired
cortical activation and fatigue (4,19). The correlation of age at polio onset
with fatigue severity may be indicative of the brain's decreased ability to
compensate for poliovirus-induced damage inflicted at an older age because
of decreased neural plasticity as the brain develops.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] EEG slowing and fatigue. Slowing of the EEG has already been documented
following the acute episode of polio. Holmgren reported that 34% of 258
patients with acute spinal, spinal/bulbar and even non-paralytic polio
demonstrated "mental changes" such as "disorientation, apathy, (and)
irritability" (20). These changes were significantly correlated with abnormal
slowing of the EEG (i.e., the emergence of theta and delta activity) in 42% of
those with spinal or bulbar symptoms as well as in 33% of those with non-
paralytic polio.

Even in healthy subjects, EEG slowing is indicative of impaired cortical
activation and has been associated with decreased arousal, "drowsiness" and
impaired performance on neuropsychologic tests of attention (11, 21-23).
Since EEG slowing similar to that documented in polio survivors and
controls has also been noted in patients with putative post-viral fatigue
syndromes (PVFS), and since 85% of CFS patients demonstrated "an excess
of irregular slow wave activity" on EEG, decreased cortical activation may
be a common substrate of impaired attention and fatigue (24-27).

Dopamine and fatigue. The correlations of prolactin with daily fatigue
severity and EEG slow wave power suggest that a reduction in central
dopaminergic activity may underlie reduced cortical activation and the
symptoms of post-polio fatigue. This suggestion is supported by the finding
that D2 receptor antagonists increase EEG slow wave power, cause
subjective fatigue and difficulty concentrating, and produce dose-related
increases in subjective "drowsiness" and impairments on neuropsychologic
tests of attention (28,29).

Buspirone, a D2 receptor antagonist that is an even more potent serotonin
(5-HT) 1A receptor agonist, was also found to increase EEG slow wave
power, decrease subjective alertness, impair performance on

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] neuropsychologic tests of attention and cause a nearly two-fold increase in
prolactin release in healthy subjects (30). Identifying whether these
psychophysiological effects are caused by D2 receptor blockade or 5-HT1A
receptor stimulation is important since buspirone and other 5-HT mimetic
agents have been employed to study the pathophysiology of CFS. Buspirone
has been found to produce at least a twofold greater release of prolactin in
CFS patients as compared to healthy controls and to generate "excessive
fatigue" in CFS patients (13,16,31). Bakheit et al. concluded that the
prolactin elevation resulted from "increased sensitivity" of hypothalamic 5-
HT1A receptors in CFS patients (13).

A 5-HT releasing and reuptake blocking agent, d-Fenfluramine, was found
in one study to produce a 130% increase in prolactin in CFS patients as
compared to controls (14). Although the same researchers did not find a d-
fenfluramine-induced increase in prolactin in a second study of CFS
patients, they did find a significantly attenuated prolactin response to
hypoglycemia (15). The authors concluded that while impaired prolactin
release during hypoglycemia could have resulted from "subsensitivity" of
hypothalamic 5-HT1A receptors, the patients' intact ACTH/cortisol response
to hypoglycemia failed "to support a role for altered 5-HT
neurotransmission" in CFS. Further, when the authors compared their
failure to elicit a prolactin increase with d-fenfluramine to buspirone's
ability to release prolactin, they concluded that buspirone's D2 antagonist
properties may be "confounding the serotonergic effects on prolactin
secretion."

A neurotransmitter of fatigue? Buspirone's combined 5-HT1A agonist and
D2 antagonist properties confound any conclusions about altered central 5-
HT1A receptor sensitivity in CFS, since buspirone's blockade of D2 receptor
is the more likely cause of prolactin increases (32). But an additional
confound exists when using prolactin as an indicator of central 5-HT
receptor sensitivity following administration of 5-HT mimetics. In animals,
5-HT itself can directly inhibit dopaminergic neurons, reducing tyrosine
hydroxylase activity and dopamine release, suppressing nearly 70% of the

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] dopaminergic prolactin-inhibiting neurons in the arcuate nucleus and
lowering dopamine concentrations in portal blood (10,33,34).

In humans, a 5-HT mimetic drug (fluoxetine) has been seen to produce
Parkinsonian rigidity, akathisia and dystonia, while buspirone itself has been
shown to exacerbate Parkinsonian symptoms (34-39). These findings suggest
that the ability of 5-HT mimetics to trigger prolactin secretion, increase EEG
slow wave power, impair attention and alertness, and trigger symptoms of
fatigue is more likely due to 5-HT's "inhibitory influence on central
dopamine mechanism and functions" within an already dopamine-depleted
RAS, rather than an unspecified effect of unexplained increases in 5-HT1A
receptor sensitivity (34; cf 3,6,7). This conclusion would explain the failure
of one 5-HT mimetic agent (fluoxetine) to ameliorate symptoms of CFS in a
randomized, double-blind, placebo-controlled controlled study, and suggests
that serotonin reuptake blocking agents could actually reduce cortical
arousal, decrease alertness and induce fatigue via serotoninÕs inhibition of
central dopamine mechanism and functions (13,34,40,41).

In this context it is noteworthy that Parkinson's patients, with their
profound dopamine depletion, demonstrate impaired attention and marked
fatigue (42,43). "Excessive fatigue" was reported by 48% of Parkinson's
patients while nearly one-third reported that fatigue was their "most
disabling symptom" (43,44). Indeed, one of the first descriptions of cognitive
dysfunction in Parkinson's disease (PD) could serve as a description of post-
polio fatigue or chronic fatigue syndrome, i.e., a syndrome "characterized by
a diminution of voluntary attention, spontaneous interest, initiative and the
capacity for effort and work, with significant and objective fatiguability, and
a slight diminution of memory" (45).

However, if low central dopaminergic tone underlies the symptoms of
chronic fatigue, why was baseline prolactin found not to be related to
chronic fatigue in any of the buspirone and fenfluramine stimulation
studies? One possibility is that dopaminergic neurons are more severely

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] damaged by the poliovirus than by other putative PVFS-inducing agents,
thus allowing a prolactin/fatigue relationship to be more readily detected in
polio survivors. While PD symptoms were seen acutely during poliovirus
infection, the extent and severity of brain stem damage in these patients
proved fatal in nearly all of the reported cases (46-50). In contrast,
survivable parkinsonism was noted during PVFS outbreaks earlier in this
century and has even been documented recently in PVFS patients, suggesting
that dopaminergic neurons are damaged - albeit less severely - in PVFS
(Behan, Lapp, and Richardson, personal communications) (50,51).

A more readily testable explanation for the lack of elevated baseline
prolactin values in CFS patients is that the assayed blood was drawn
following an overnight fast. Although hypoglycemia is known to increase
prolactin secretion, this effect is significantly attenuated in CFS patients
(15,17). Fasting may increase only the control subjects' baseline prolactin
values and thereby obscure an elevated baseline prolactin in CFS patients.
This explanation is supported by a study of circadian hormonal variations,
in which non-fasting prolactin levels were significantly higher in CFS
patients, and a report that 25% of one group of PVFS patients had "high
basal prolactin levels" (51, 52).

Future research. These findings provide a rationale for further study of the
role played by the brain stem's reticular activating system and dopaminergic
neurons, especially within D2 receptor-mediated systems, in the genesis of
fatigue and other fatigue-related cognitive symptoms (cf 53,54). For example,
the word finding difficulty reported by 82% of polio survivors with fatigue,
which appears similar both to the "tip-of-the-tongue" phenomenon in PD
patients and word finding problems reported by CFS patients, may be
related to impaired dopaminergic neurotransmission (3,55,56, cf 57). For
example, the number of animals polio survivors could name in 60 seconds
was significantly positively correlated with their score on a neuropsychologic
test of vigilance but significantly negatively correlated with plasma prolactin
(-.36; p<.05) (58).

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] Further, recent research suggests that the emerging relationship between
chronic fatigue and fainting in CFS patients, polio survivors and even in
healthy subjects may have a dopaminergic component that is related to RAS
damage (cf 9, 59-62). However, the interactions of many brain
neurotransmitter systems - peptidergic, cholinergic, glutaminergic, as well as
monoaminergic - need to be considered and studied simultaneously to
determine whether neurotransmitter abnormalities underlie any of the
symptoms of fatigue in polio survivors, in those with CFS or with other
putative PVFS (3,6,8,62).

ACKNOWLEDGEMENTS
The authors gratefully acknowledge the participation of the subjects, the
continuing support of the George Ohl, Jr., Infantile Paralysis Foundation,
and the efforts and expertise of Carol Diveny and Mary Ann Solimine, R.N.,
M.L.S., without whom this work would not have been possible. We also
thank Drs. Charles Lapp, Peter Behan, John Richardson and Jesse Kaysen
for their comments and criticism, and Virginia Tegue for her expeditious
intervention and editorial expertise.

REFERENCES
1) Parsons PE. National Health Interview Survey. Washington, D.C.:
National Center for Health Statistics; 1989.

2) Bruno RL, Frick NM. Stress and "Type A" behavior as precipitants of
Post-Polio Sequelae. In: LS Halstead and DO Wiechers, eds. Research and
Clinical Aspects of the Late Effects of Poliomyelitis. White Plains: March of

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] Dimes Research Foundation; 1987:145-155.
3) Bruno RL, Frick NM, Cohen, J. Polioencephalitis, stress and the etiology
of Post-Polio Sequelae. Orthopedics. 1991; 14:1269-1276.

4) Bruno RL, Galski T, DeLuca J. The neuropsychology of post-polio
fatigue. Arch Phys Med Rehabil. 1993; 74:1061-1065.

5) Bodian D. Histopathological basis of clinical findings in poliomyelitis. Am
J Med. 1949; 6: 563-578.

6) Bruno RL, Sapolsky R, Zimmerman JR, Frick NM. The pathophysiology
of a central cause of post-polio fatigue. Ann NY Acad Sci. 1995;753:257-275.

7) Bruno RL, Cohen J, Galski T, Frick NM. The neuroanatomy of post-polio
fatigue. Arch Phys Med Rehabil. 1994; 75:498-504.

8) Bruno RL, Frick NM, Creange SJ, Molzen T, Lewis T, Zimmerman JR.
Polioencephalitis and the brain fatigue generator model of post-viral fatigue
syndromes. JCFS. 1996; 2: 5-27.

9) Bruno RL, Zimmerman JR, Creange SJ, Lewis T, Molzen T, Frick NM.
Bromocriptine in the treatment of post-polio fatigue: A pilot study with
implications for the pathophysiology of fatigue. Am J Phys Med Rehabil.
1996; 75:340-347.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] 10) Pan J-T. Neuroendocrine functions of dopamine. In: T W Stone, ed.
CNS neurotransmitters and neuromodulators: Dopamine. Boca Raton: CRC
Press; 1996: 213-232.

11) Streitberg B, Rohmel J, Herrmann WM, Kubicki S. COMSAT rule for
vigilance classification based on spontaneous EEG activity.
Neuropsychobiol. 1987; 17:105-117.

12) Anderer P, Semlitsch HV, Saletu B, Barbanoj ML. Artifact processing in
topographic mapping of electroencephalographic activity in
neuropsychopharmacology. Psychiatry Res: Neuroimaging. 1992; 45: 79-93.

13) Bakheit AMO, Behan PO, Dinan TG, et al. Possible upregulation of
hypothalamic 5-hydroxytryptamine receptors in patients with postviral
fatigue syndrome. BJM. 1992; 304:1010-1012.

14) Cleare AJ, Bearn J, Allain T, et al. Contrasting neuroendocrine
responses in depression and chronic fatigue syndrome. J Affect Disorders.
1995; 35:283-289.

15) Bearn J, Allain T, Coskeran P, et al. Neuroendocrine responses to d-
fenfluramine and insulin-induced hypoglycemia in chronic fatigue syndrome.
Biol Psychiatry. 1995; 37:245-252

16) Richardson J. Disturbance of hypothalamic function and evidence for
persistent enteroviral infection in patients with chronic fatigue syndrome.
JCFS. 1995; 1:59-66.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] 17) McBride PA, Tierney H, De Meo, et al. Effects of age and gender on
CNS serotonergic responsivity in normal adults. Biol Psychiatry. 1990;
27:1143-1155.

18) Heilman KM, Van Den Abell T. Right hemisphere dominance for
mediating cerebral activation. Neuropsychologia. 1979; 17:315-321.

19) Freidenberg DL, Freeman D, Huber SJ, et al. Postpoliomyelitis
syndrome: Assessment of behavioral features. Neuropsychiatry,
Neuropsychology and Behavioral Neurology. 1989; 2:272-81.

20) Holmgren BE. Electro-encephalography in poliomyelitis. In:
Poliomyelitis. Philadelphia: Lippincott; 1952: 448-450.

21) Belyavin A, Wright NA. changes in electrical activity of the brain with
vigilance. EEG Clin Neurophys. 1987; 66:137-144.

22) Valentino DA, Arruda JE, Gold SM. Comparison of QEEG and response
accuracy in good vs. poor performers during a vigilance task. Int J
Psychophysiol. 1993;15:123-134.

23) O'Hanlon JF, Beatty J. Concurrence of electroencephalographic and
performance changes during a simulated radar watch and some implications
for the arousal theory of vigilance. In: RR Mackie, ed. Vigilance. New York:
Plenum; 1977: 189-201.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] 24) Jamal GA. Evidence for organic disturbance in Post Viral Fatigue
Syndrome. In: Hyde BM, Goldstein J, Levine P, eds. The Clinical and
Scientific Basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.
Ottawa: The Nightingale Research Foundation; 1992:414-424.

25) Ramsay AM, O'Sullivan E. Encephalomyelitis simulating poliomyelitis.
Lancet. 1956; i: 762-767.

26) Galpine JF, Brady C. Benign myalgic encephalomyelitis. Lancet. 1957;
i:757-758.

27) Daikos GK, Garzonis S, Paleologue A, et al. Benign myalgic
encephalomyelitis. Lancet. 1959; i: 693-696.

28) McClelland GR, Cooper SM, Pilgrim A. comparison of the CNS effects
of haloperidol, chlorpromazine and sulpiride in normal volunteers. Br J Clin
Pharmacol. 1990; 30:795-803

29) Fagan D, Scott DD, Mitchell M, Tiplady B. Effects of remoxipride on
measures of psychological performance in healthy volunteers.
Psychopharmacology. 1991; 105:225-229.

30) Holland RL, Wesnes K, Dietrich B. Single dose human pharmacology of
umespirone. Eur J Clin Pharmacol. 1994; 46:461-468.

31) Barberio A, DeRemigis PL, Raccciatti D, et al. Buspirone challenge test
file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] in chronic fatigue syndrome. Proceedings of the American Association for
Chronic Fatigue Syndrome Clinical Conference. San Francisco: AACSF;
1996.

32) Meltzer H, Lee, HS, Nash JF. Effect of buspirone on prolactin in not
mediated by 5-HT1a receptor stimulation. Arch Gen Psychiatry. 1992;
49:163.

33) Dewey SL, Smith GS, Logan J, et al. Serotonergic modulation of striatal
dopamine measured with positron emission tomography (PET) and in vivo
microdialysis. J Neurosci. 1995; 15:821-829

34) Arya DK. Extrapyramidal symptoms with selective serotonin reuptake
inhibitors Br J Psychiatry. 1994; 165:728-733.

35) Lipinski JF Jr, Mallya G, Zimmerman P, Pope HG Jr. Fluoxetine-
induced akathisia: clinical and theoretical implications. J Clin Psychiatry.
1989; 50:339-342.

36) Steur EN. Increase of Parkinson disability after fluoxetine medication.
Neurology. 1993; 43:211-213

37) Coulter DM, Pillans PI. Fluoxetine and extrapyramidal side effects. Am
J Psychiatry. 1995; 152:122-125

38) Meltzer HY, Young M, Metz J. Extrapyramidal side effects and
increased serum prolactin following fluoxetine, a new antidepressant. J

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] Neural Trans. 1979; 45:167-175
39) Ludwig CL, Weinberger DR, Bruno G, et al. Buspirone, Parkinson's
disease and the locus ceruleus. Clinical Neuropharm. 1986; 9:373-378.

40) Vercoulen JHMM, Swanink CMA, Zitman FG, et al. A randomized,
double-blind, placebo-controlled controlled study of fluoxetine chronic
fatigue syndrome. Lancet. 1996; 347:858-61.

41) Rammsayer T. Dopaminergic and serotonergic influence on duration
discrimination and vigilance. Pharmacopsychiat. 1989; 22:39-43 (Supp).

42) Brown RG, Marsden CD. Cognitive function in Parkinson's disease.
TINS. 1990; 1:21-28.

43) Friedman J, Friedman H. Fatigue in Parkinson's disease. Neurology.
1993; 43:2016-2018.

44) Hilten JJ van, Hoogland EA , van der Velde, A et al. Diurnal effects of
motor activity and fatigue in Parkinson's disease. J Neurol Neurosurg
Psychiatry. 1993; 56:874-877.

45) Naville F. Encephale. 1922; 17:369-375.
46) Bickerstaff ER, Cloake PCP. Mesencephalitis and rhombencephalitis.
file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] Brit Med J. 1951; 2:77-81.
47) Barrett AM, Gardner D, McFarlan AM. An outbreak of encephalitis,
possibly due to poliomyelitis virus. Brit Med J. 1952; 1:1317-1322.

48) Magoun HW In: Poliomyelitis. Philadelphia: Lippincott; 1949: 250.
49) Duvoisin RC, Yahr MD. Encephalitis and parkinsonism. Arch Neurol.
1965; 12:227-239.

50) Acheson ED. The clinical syndrome variously called benign myalgic
encephalomyelitis, Iceland Disease and epidemic neuromyasthenia. Am J
Med. 1959; 26: 569-595.

51) Hyde BM. Post-viral fatigue syndrome research in Glascow: A review of
lectures given by Professor Peter Behan. In Hyde BM, Goldstein J, Levine P,
eds. The Clinical and Scientific Basis of Myalgic Encephalomyelitis/Chronic
Fatigue Syndrome. Ottawa: The Nightingale Research Foundation;
1992:235-243.

52) Racciatii D, Sensi S, De Remigis PL, et al. Neuroendocrine aspects of
chronic fatigue syndrome. Proceedings of the American Association for
Chronic Fatigue Syndrome Clinical Conference. San Francisco: AACFS;
1996.

53) Costa DC, Tannock C, Brostoff J. Brainstem perfusion is impaired in
chronic fatigue syndrome. Q J Med. 1995; 88:767-773.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] 54) Tavio M, Chierochetti F, Bianchini, et al. Brain positron emission
tomography (PET) in chronic fatigue syndrome: A useful tool for differential
diagnosis. Proceedings of the American Association for Chronic Fatigue
Syndrome Clinical Conference. San Francisco: AACFS; 1996.

55) Altay HT, Toner BB, Brooker H, et al. The neuropsychological
dimensions of postinfectious neuromyasthenia. Int'l J Psychiatry in Med.
1990; 20:141-149.

56) Matison R, Mayuex R, Rosen J, Fahn S. "Tip-of -the-tongue"
phenomenon in Parkinson disease. Neurology. 1982; 32:567-570.

57) Gupta SR, Mlcoch AG. Bromocriptine treatment of nonfluent aphasia.
Arch Phys Med Rehabil. 1992; 73: 373-376.

58) Bruno RL, Creange SJ, Frick NM. Parallels Between Post-Polio Fatigue
and Chronic Fatigue Syndrome: A Common Pathophysiology? Am J Med.
1997; (in press).

59) Rowe PC, Bou-Holaigah I, Kan JS, Calkins H. Is neurally mediated
hypotension an unrecognized cause of chronic fatigue syndrome? Lancet.
1995; 345:623-624.

60) Bou-Holaigah I, Rowe PC, Kan JS, Calkins H. The relationship between
neurally mediated hypotension and the chronic fatigue syndrome. JAMA.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM] 1995; 274:961-967.
61) Bruno RL, Frick NM: Parasympathetic abnormalities as post-polio
sequelae. Arch Phys Med Rehabil. 1995; 76:594.

62) Bruno RL. Chronic fatigue, fainting and autonomic dysfunction: Further
similarities between post-polio Fatigue and Chronic Fatigue Syndrome?
Journal of Chronic Fatigue Syndrome. 1997; 3: 107-117.

file:///C|/Users/Dean/Desktop/HarvestDOCS/library/eegpro.html[8/13/2010 2:15:34 AM]

Source: http://www.postpolioinfo.com/library/eegpro.pdf

mendocino.edu

Term Effective: Full Title: Advanced Cardiac Life Support (limit to 50 characters including spaces) If this is a variable unit course, then the relationship between units and any difference in expected SLO’s should be explained. Student Learning Outcomes: (Enter the SLO’s in an outline format. Use the Ctrl + Tab keys to indent for subtopics.) At the conclusion of this cour

bloomlifestyle.co

The Vestibular Autorotational Test (VAT), Vestibular Rehabilitation (VRT) and Balance Retraining (BRT) By Steven M. Kaye, MDExecutive Director, Lifeline Balance CenterThe following discussion was prepared to document the medical necessity and efficacy of using the VAT and VRT/BRT as part of a comprehensive individualistic program to diagnose and treat patients suffering from chronic episodic a

Copyright © 2010-2014 Medical Pdf Finder