Blink reflex in migraine patients and healthy controls

Migraine head pain arises within the trigeminal system and the processing of
its nociceptive input plays an important role in the pathofysiology of acute
migraine attacks. The pathofysiology of migraine headache as well the
anti-nociceptive mechanisms of migraine drugs are still poorly understood. The
trigeminal system can be measured with the blink reflex, what is essentially
the electrical correlate of the clinically evoked corneal reflex. This is a
trigeminofacial brain stem reflex leading to activation of the orbicularis
oculi muscle after electrical or mechanical stimulation of the supraorbital
region.

The blink reflex has three components, an early R1 and a late R2 and R3. The R1
response is usually present ipsilaterally to the stimulation side, whereas the
R2 response is typically present bilaterally. The pathways of R1 and R2 are
anatomically different, whereas the former is located in the pons and the
latter in the medulla. The third component R3 is also located in the medulla.

In a small percentage of normal individuals the R1 response cannot be reliably
elicited on either side. ( Preston, 1998,Chapter 5).

MRI studies show that migraine patients are at increased risk for subclinical
brain lesions. Infratentorial hyperintensities were identified in 13 of 295
(4.4%) migraineurs and in 1 of 140 (0.7%) controls (P=0.04). Twelve cases had
hyperintensities, mostly bilaterally, in the dorsal basis pontis.

In patients with unilateral R1 pathology in 50% isolated acute brainstem
lesions are documented by diffusion-weighted MRI

1. To investigate the prevalence of an absent R1 component in migraine
patients compared with healthy controls.

2. Do headache characteristics differ between migraine patients with a R1
response and those without a R1 response ( Fast progressing vs slow progressing
headache, accompanying symptoms, allodynia, age of onset, predominant orbital
pain, yawning)

3. To compare the individual sensory thresholds and pain thresholds as well as
latencies of R1 and R2.

cross sectional
30 patients with migraine with aura ( IHS classification) and 30 age and gender
matched healthy subjects without personal or family history of migraine or
cluster headache will be included. Both patients and controls will be included
if they are 45-65 years old.
Patients will be excluded if they have a history of facial paralysis or other
cranial neuropaties or a demyeliating disorder in history.
Headache characteristics will be recorded in al patients.

Blink reflex will be elicited using a surface stimulating electrode on the
right and left forehead, 10 mm above the entry zone of the supra-orbital nerve.
A block of 6 monopolar square pulses, duration 0.3 ms, interstimulus interval
15-17 seconds, stimulation intensity 1.5 times the individual pain threshold.

Migraine patients will be investigated inter-ictally and controls on a
headache free moment.

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