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Evidence of Brainstem Dysfunction in Fibromyalgia Patients

  [ 8 votes ]   [ 1 Comment ] • September 27, 2013

Alterations in excitatory and inhibitory brainstem interneuronal circuits in fibromyalgia: Evidence of brainstem dysfunction.

By M. Kofler and W. Halder


OBJECTIVE: Patients with fibromyalgia syndrome (FMS) perceive stimuli differently and show altered cortical sensory representation maps following peripheral stimulation. Altered sensory gating may play a causal role.

METHODS: Blink reflex, blink reflex excitability recovery, and prepulse inhibition of the blink reflex - representing brainstem excitability - were assessed in 10 female patients with FMS and 26 female healthy controls.


  • Unconditioned blink reflex characteristics (R1 latency and amplitude, R2 and R2c latency and area-under-the-curve) did not differ significantly between patients and controls.

  • Blink reflex excitability recovery was enhanced in patients versus controls at all intervals tested.

  • Prepulses significantly suppressed R2 area and increased R2 latency in patients and controls.

  • However, R2 area suppression was significantly less in patients than in controls (patients: to 80.0±28.9%, controls: to 47.8±21.7%).

  • The general pattern of corresponding changes in R2c was similar.

CONCLUSIONS: Blink reflex is normal, whereas blink reflex excitability recovery is enhanced and blink reflex prepulse inhibition is reduced in patients with FMS, suggesting functional changes at the brainstem level in FMS.

SIGNIFICANCE: Reduced blink reflex prepulse inhibition concurs with altered sensory gating in patients with FMS.

Copyright © 2013 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Source: Clinical Neurophysiology, September 12, 2013. By M. Kofler and W. Halder. Department of Neurology, Hochzirl Hospital, Zirl, Austria.

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Article Comments Post a Comment

Posted by: IanH
Sep 27, 2013
I studied reflex and other prepulse inhibition under the influence of cannabinoids. This same phenomenon occurs under the influence of many neurological drugs.
It also occurs in some forms of schizophrenia.

It implies to me that the immune system cyokines, probably Il-6 and TNF-alpha as well as chronically elevated IFN-gamma are behind this lack of excitation inhibition maybe via impaired neuron-mitochondrial function.
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