Decreased number and function of endothelial progenitor cells in patients with migraine.

OBJECTIVE: Migraine carries an increased risk for cardiovascular and cerebrovascular diseases that cannot be explained by traditional cardiovascular risk factors. The circulating endothelial progenitor cell (EPC) number is a surrogate biologic marker of vascular function, and diminished EPC counts are associated with higher cardiovascular risk. We investigated whether abnormalities in EPC levels and functions are present in migraine patients. METHODS: Consecutive headache patients (n =166) were enrolled, including those with tension type headache (TTH; n = 74), migraine without aura (MO; n = 67), and migraine with aura (MA; n = 25). EPC colony-forming units in peripheral blood samples and migratory capacity to chemoattractants (stromal cell-derived factor 1 and vascular endothelial growth factor) and cellular senescence levels were assayed in risk factor-matched subjects (n = 6 per group). RESULTS: The TTH group had more cardiovascular risk factors, more headache days, and higher Framingham risk scores than the other two groups. Mean numbers of EPC colony-forming units were 47.8 +/- 24.3 in TTH, 20.4 +/-22.2 in MO, and 8.6 +/- 10.1 in MA patients (p < 0.001 in TTH vs MO; p = 0.001 in MO vs MA). EPC colony counts of normal subjects (n = 37) were not significantly different from those with TTH. Multiple linear regression models identified only MO, MA, and the presence of migraine (MO + MA) as significant predictors of EPC levels. In addition, EPCs from migraine patients (MO and MA) showed reduced migratory capacity and increased cellular senescence compared with EPCs from TTH or normal subjects. CONCLUSION: Circulating endothelial progenitor cell (EPC) numbers and functions are reduced in migraine patients, suggesting that EPCs can be an underlying link between migraine and cardiovascular risk.

Sensory dermatomal representation in the medial lemniscus.

BACKGROUND: Restricted sensory deficits along the somatotopic topography of the medial lemniscus rarely develop in medial medullary infarction. We describe a patient with medial medullary infarction who presented with dermatomal sensory deficits caused by a medial lemniscal lesion. CASE DESCRIPTION: A 58-year-old man presented with sudden right-sided hemiparesis and paresthesia. He had noticed the paresthesia below the level of the right L5 dermatome, where his vibration and position senses were mildly diminished. His paresthesia was more severe over the right calf and foot. Magnetic resonance images of the brain showed an acute small infarct in the medial-ventral portion of the left rostral medulla oblongata. A nerve conduction study and electromyography showed no abnormalities. At follow-up, the patient's motor and sensory deficits had improved considerably. CONCLUSIONS: The patient showed lemniscal sensory deficits below the right L5 dermatome that were caused by the partial involvement of the medial lemniscus. These findings suggest that lemniscal sensory dermatomal representation is preserved at least up to the level of the medulla oblongata.