Parallels between post-polio fatigue and chronic fatigue syndrome: a common pathophysiology?

Abstract:

Fatigue is the most commonly reported and most debilitating of post-polio sequelae affecting the >1.8 million North American polio survivors. Post-polio fatigue is characterized by subjective reports of difficulty with attention, cognition, and maintaining wakefulness. These symptoms resemble those reported in nearly 2 dozen outbreaks of post-viral fatigue syndromes (PVFS) that have recurred during this century and that are related clinically, historically, anatomically, or physiologically to poliovirus infections.

This article reviews recent studies that relate the symptoms of post-polio fatigue and chronic fatigue syndrome (CFS) to clinically significant deficits on neuropsychologic tests of attention, histopathologic and neuroradiologic evidence of brain lesions, impaired activation of the hypothalamic-pituitary-adrenal axis, increased prolactin secretion, and electroencephalogram (EEG) slow-wave activity.

A possible common pathophysiology for post-polio fatigue and CFS, based on the Brain Fatigue Generator Model of PVFS, and a possible pharmacotherapy for PVFS based on replacement of depleted brain dopamine, will be described.

 

Source: Bruno RL, Creange SJ, Frick NM. Parallels between post-polio fatigue and chronic fatigue syndrome: a common pathophysiology? Am J Med. 1998 Sep 28;105(3A):66S-73S. http://www.ncbi.nlm.nih.gov/pubmed/9790485

 

Increased prolactin response to buspirone in chronic fatigue syndrome

Abstract:

We studied the endocrine and subjective responses that followed acute administration of the 5-HT1A receptor agonist buspirone (0.5 mg/kg orally) in 11 male patients with chronic fatigue syndrome (CFS) and a group of matched healthy controls.

Patients with CFS had significantly higher plasma prolactin concentrations and experienced more nausea in response to buspirone than did controls. However, the growth hormone response to buspirone did not distinguish CFS patients from controls.

Our data question whether the enhancement of buspirone-induced prolactin release in CFS is a consequence of increased sensitivity of post-synaptic 5-HT1A receptors. It is possible that the increased prolactin response to buspirone in CFS could reflect changes in dopamine function.

 

Source: Sharpe M, Clements A, Hawton K, Young AH, Sargent P, Cowen PJ. Increased prolactin response to buspirone in chronic fatigue syndrome. J Affect Disord. 1996 Nov 4;41(1):71-6. http://www.ncbi.nlm.nih.gov/pubmed/8938208

 

Postviral fatigue syndrome

Comment on: Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome. [BMJ. 1992]

 

EDITOR,-A M 0 Bakheit and colleagues report an enhanced prolactin response to buspirone in patients with postviral fatigue syndrome and suggest this may be due to upregulation of hypothalamic 5-hydroxytryptamine receptors. They fail to mention the considerable evidence indicating that the drug is a moderately potent dopamine antagonist, a pharmacological action which suggests an alternative explanation for their data.

They administered a single 60 mg dose of buspirone-in excess of the daily maximum of 45 mg recommended by the British National Formulary-so antidopaminergic effects may well have been significant in their studies. The fact that the prolactin releasing effect of buspirone can be blocked by the drug metergoline does not prove 5-hydroxytryptamine receptor specificity. Indeed, metergoline is used commonly as an alternative dopamine agonist to bromocriptine in managing hyperprolactinaemia. Thus enhanced prolactin release after buspirone in postviral fatigue syndrome may reflect, at least in part, inhibition of increased hypothalamic dopaminergic tone on the  It would be interesting to study the same groups of patients using a specific D2 dopamine antagonist (such as domperidone) to see whether this is the case.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882431/pdf/bmj00077-0052d.pdf

 

Source: Bevan JS. Postviral fatigue syndrome. BMJ. 1992 Jun 13;304(6841):1566; author reply 1567. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882431/