Feb 8, 2017

Polio victims may suffer psychiatric ills later

(Reuters Health) - 
People who had polio in childhood seem to be at somewhat increased risk of being hospitalized for a psychiatric disorder later in life, according to a Danish study.
"Chronic and life-threatening diseases are known to be accompanied by increased risk of anxiety, depression, and suicide," Dr. Nete Munk Nielsen, of Statens Serum Institut, Copenhagen, and colleagues write in the American Journal of Epidemiology. "It has furthermore been suggested that certain medical conditions such as childhood infections of the central nervous system could subsequently increase the risk of psychosis and schizophrenia."
In their study, the researchers studied database information on 4660 people who had polio between 1922 and 1954, along with 19,017 age- and gender-matched "controls" who did not have polio. These subjects were then linked to national records for people who were hospitalized for a psychiatric disorder between 1977 and 1993.
"Overall, history of poliomyelitis was associated with a 40% increased risk of being hospitalized for a psychiatric disorder," Nielsen's group reports.
The likelihood of suffering a mental disorder seemed to be higher before age 45 years, and among those who had polio before the age of 7.
"The overall increased risk of psychiatric hospitalizations could not be confined to specific groups of psychiatric disorders," the investigators added. Rather, there seemed to be "slightly increased risks of several different disorders, especially milder psychiatric disorders." These included personality disorders, substance/alcohol abuse, and other non-psychotic mental disorders.
The team says the reason for the higher odds of having mental problems isn't really known, but they point out that it might relate to the "very painful and fearful" experience of contracting polio, the stringent isolation from family for several weeks, and the difficulties of then overcoming physical handicaps and social prejudice.

SOURCE: American Journal of Epidemiology, February 2007.

Post Polio Litaff, Association A.C _APPLAC Mexico

Feb 7, 2017

What are some interesting facts about polio?

What are some interesting facts about polio?



Polio is a virus that formerly ravaged populations the world over in widespread epidemics, but has in modern times, been nearly eradicated. The virus is transmitted via the fecal-oral route and primarily affects newborns and young children.
What are some interesting facts about polio?
Credit: AFP/Getty Images AFP Getty Images


A visual symptom of the way polio attacks the body is by way of partial or total appendage paralysis, typically in the legs. Regardless, over 90 percent of people who carry the poliovirus show no symptoms of the disease. Polio is named after the Greek word for "gray," as in the gray matter of the central nervous system.
Hundreds of thousands of polio cases were reported annually until the first polio vaccines were developed and perfected during the 1950s. Since the vaccine's widespread adoption, polio cases have plummeted down to only several hundred reported cases worldwide. Unfortunately, an anti-vaccine culture and poor hygiene led to worldwide breakouts of the disease reported in May of 2014 by the World Health Organization.
According to the Disabled-World.com, one of the most famous faces of polio was Franklin Delano Roosevelt, the 32nd president of the United States. He contracted the illness at the age of 39, but it was largely hidden from the public view throughout his political career. Other well-known sufferers of polio to different degrees are author and futurist Arthur C. Clarke, musician Neil Young, actress Mia Farrow and golfer Jack Nicklaus.

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6 things all parents should know about enterovirus D68

There are more than 100 known varieties of non-polio enteroviruses in the world, and they cause 10 to 15 million infections every year, ranging from the common cold (rhinovirus), to hand, foot, and mouth disease (coxsackie), to meningitis and gastrointestinal illness. Enteroviruses are harbored in the GI tract, but they can cause symptoms all over the body depending on strain.
But what’s so unique about this strain of enterovirus D68, which was first identified in California in the 1960s? And why is it re-emerging now? According to the Centers for Disease Control and Prevention (CDC), more than 500 cases have been identified in 42 U.S. states. But that’s likely an underestimation because many cases may go unreported.
While adults can get the virus, children are more likely to have severe symptoms.
Here are six questions many parents have about enterovirus D68:
1. What makes this strain unique?
It is a respiratory strain that is especially sickening to young children with asthma, leading to numerous hospitalizations and — though health officials say it's unclear what role the virus played— has even been linked to four deaths. Parents of young children with asthma in infected areas should take their children to the pediatrician if they show any symptoms such as sneezing, coughing, fever, body aches, runny nose, wheezing or difficulty breathing. Young children have little lung reserve, so early treatment is crucial.
2. When will it end?
Enteroviruses are most common in the fall and generally tend to peter out by November. We don’t know if this strain will follow the usual fall cycle or last into the winter months.
3. What about the neurological symptoms?
Polio is also an enterovirus, but this strain is a non-polio enterovirus. Past enteroviruses have had neurological manifestations. This strain appears to be able to travel to the brain but has rarely caused muscle weakness or paralysis, but health officials are looking into nine cases in Denver in which patients with the virus developed paralysis-like symptoms. The truth is, we just don’t know enough yet.
4. Why is this strain so widespread?
It is likely that it has changed or mutated to become more transmissible, but this hasn’t been proven. Enteroviruses change frequently over time. It is also possible that the virus has been around for longer than we know, or that it was just overlooked or misdiagnosed until recently.
5. Is there any relationship between this outbreak and the massive numbers of illegal immigrants crossing the borders?
We don’t know. A 2013 National Institutes of Health (NIH) study published in Virology Journal determined that a high percentage of patients in Latin America with influenza-like illness actually suffered from an enterovirus infection. A CDC official told me that they “didn’t know” whether this outbreak of enterovirus D68 was traceable to the border camps for illegal immigrants.
6. What can parents do?
The main thing is to keep sick children home. We can tell kids to wash their hands and cover their mouths when they cough at school, but getting them to comply is easier said than done.
Marc Siegel MD is a professor of medicine and medical director of Doctor Radio at NYU Langone Medical Center. He is a member of the Fox News Medical A Team.
Dr. Marc Siegel, a practicing internist, joined FOX News Channel (FNC) as a contributor in 2008.

Post Polio Litaff, Association A.C _APPLAC Mexico

Zika Virus

The Zika virus is spread by the yellow fever or dengue mosquito (aedes aegypti). Although the disease (Zika fever) is usually fairly mild, there are increasingly more indications that an infection during pregnancy can harm the unborn child.

In May 2015 the first patients with Zika were diagnosed in Brazil. This outbreak has spread across various countries in South and Central America. In November 2015 doctors saw the first indications that an infection with the Zika virus during pregnancy could possibly harm the unborn child. Research into this is currently being carried out and is being coordinated by the WHO
In The Netherlands infection with the Zika virus has been found only in people who have contracted the virus abroad. To date over seventy people have been diagnosed with the infection but there are probably a lot more people who have been infected, as only one in five people actually have symptoms after being infected. It is unlikely that the Zika virus will spread within The Netherlands as the mosquitoes responsible for transmission do not occur in The Netherlands.

Advice for pregnant people and their partners

  • Pregnant women and women who want to become pregnant during or immediately after their journey are advised to postpone non-essential journeys to a country where the Zika virus is prevalent. They should discuss the need for the journey and possible preventive measures with their GP. 
  • Pregnant women should report any recent visit to countries where the Zika virus is prevalent during their regular check-ups with their obstetrician or GP, especially if they have any symptoms within two weeks of their return that are in keeping with an infection by the Zika virus. 
  • Men who have been in countries where the Zika virus is prevalent and whose wife is pregnant are advised as a precaution to use a condom in the case of sexual contact for up to two month after their return. 
  • People who want to become pregnant are advised to postpone this until at least a month after their return from a country where the Zika virus is prevalent. During this time they should use a condom in the case of sexual contact.


Symptoms of Zika fever occur usually 3 - 12 days after a bite from an infected mosquito. People who are infected with the Zika virus do not always get any symptoms. Around one in five people have symptoms. Most people recover within a week without any serious problems. 

Possible symptoms of Zika fever are:

  • acute, but usually not high, fever
  • non-suppurative eye infection 
  • muscle and joint pain (in particular in hands and feet, sometimes with joint swelling)
  • skin rash (often starting on the face and spreading over the rest of the body)
  • and less often: headache, lack of appetite, vomiting, diarrhoea and abdominal pain.


Possible complications from Zika fever are rare. During outbreaks the following complications were described: 
  • Guillain-Barré syndrome. It is still unknown how often this occurs but it is probably relatively rare.
  • There are increasingly more indications of a link between infection with the Zika virus during pregnancy and a brain malformation in the unborn child. Research is currently being carried out to ascertain whether this brain malformation is actually caused by an infection with the Zika virus during pregnancy. 

Infection and prevention

The Zika virus is transmitted by certain mosquitoes that occur in and around the home in the Tropics. The yellow fever or dengue mosquito (Aedes aegypti) is the main transmitter of the virus. This mosquito feeds primarily on human blood and bites both during the day and in the early evening.
  • It is important to take measures to protect against mosquitoes during the day and in the early evening in areas where the Zika virus occurs.
  • Cover your skin with clothing (long sleeves, long trousers).
  • Use a mosquito repellent containing DEET on uncovered skin. Children under two and pregnant women should only use products with a maximum of 30% DEET
  • Always sleep under an (impregnated) mosquito net or in a mosquito-free room. 
Travellers with an immune disorder or a chronic illness are advised, as in the case of pregnant women, to seek advice from a GP or a travel clinic before setting off. 
If you have symptoms within two weeks of your return, contact your GP or specialist. There are no vaccines to prevent infection and there are no drugs that will kill the Zika virus. Treatment consists of treating the symptoms. 

Where does Zika fever occur?

The Zika virus was first found in Uganda and Tanzania in 1947. Then it was found in Asia. It then spread to Micronesia (a group of islands in the Pacific Ocean) (2007), to French Polynesia (2013) and towards South America (2015). In the earlier areas the virus probably still circulates regularly among the population. This means that the virus is in fact there but, as far as we know, a lot fewer people become ill than is the case now in South and Central America, as more people have built up a resistance to the virus. The risk of contracting the Zika virus in these countries is therefore probably very small.

Countries where the Zika virus currently occurs

You can find an up-to-date overview of the countries where the Zika virus occurs on the ECDCwebsite. 
It is likely that the disease will spread further in the near future across the (sub)tropical parts of the American c

Post Polio Litaff, Association A.C _APPLAC Mexico

Feb 5, 2017

Elevated Plasma Prolactin and EEG Slow Wave Power in Post-Polio Fatigue

(Numbers within the article refer to reference numbers at the bottom of page) Taken from: JOURNAL OF CHRONIC FATIGUE SYNDROME, 1998; 4: 61-76. Richard L. Bruno, Ph.D.,1 Susan Creange, Ph.D.,1 Jerald R. Zimmerman, M.D.,1 and Nancy M. Frick, M.Div, Lh.D.2
1 The Post-Polio Institute Englewood Hospital and Medical Center, Englewood, New Jersey 07631
2 Harvest Center Hackensack, New Jersey

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

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 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.
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, memory, attention, word-finding, maintaining wakefulness and thinking clearly, with 77% percent reporting moderateto 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.
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 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 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 

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 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 regressions 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, 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).

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.

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 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, and 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 dopaminergic prolactin-inhibiting neurons in the arcuate nucleus and lowering dopamine concentrations in portal blood (10, 33, and 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 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 poliosurvivors 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).
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).

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.

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