Sirs: There is a frequent observation of reduced regional cerebral blood flow during the aura phase of migraine. Several studies employing different cerebral imaging techniques [2] provided the same evidence of transient, spatially restricted changes in cerebral blood flow during the aura phase of migraine. These changes have not been consistently observed in migraine without aura [5]. Because of the unpredictable episodic onset of migraine attacks, a non-invasive bedside method like transcranial ultrasound is desirable in order to further understand the underlying hemodynamic changes. Transcranial Doppler (TCD) studies has not shown consistent results, probably because it measures cerebral blood flow velocity which is susceptible to changes in vessel diameter. Cerebral ultrasound perfusion imaging (CUPI) is a new technique that utilizes contrast-specific harmonic imaging to display cerebral perfusion through the analysis of bolus injection kinetics. We present a 31-year-old woman, with sudden onset of numbness and weakness of the right hand followed by aphasia, who was emergently admitted to our stroke unit for thrombolytic therapy. The initial TCD assessment showed normal flow velocities in extraand intracranial arteries. CUPI was then immediately performed, about 3 hours after symptom onset, using a GE Logiq 7 system, with harmonic Phase Inversion mode in bilateral approach from the contralateral side to the supposed pathology at the diencephalic plane. CUPI was performed by bolus-kinetics using 2.4 ml SonoVue (Bracco international BV, Germany) flushed by 5 ml saline. The pathologically perfused areas were detected according to the changes in contrast-enhancement on the gray-scale images in cine mode. The perfusion-parameters of these areas were drawn from the time-intensity curves (TIC) of manually selected region of interest (ROI). The reference perfusion-parameters were drawn from apparently normally perfused areas in both hemispheres. CUPI revealed an area of hypoperfusion in the left temporooccipital region with inhomogeneously prolonged time-to-peak (TTP) and diminished peak-intensity (PI) (Fig. 1a) corresponding to the topography of aura symptoms. Despite persisting symptoms, MRI (including diffusion weighted imaging) revealed normal findings. Within one hour, the patient developed left-sided throbbing headache with nausea and photophobia. The patient’s history revealed a similar episode with completely inconspicuous investigations. The episode was defined as migraine with prolonged aura. The neurological deficits gradually subsided with remaining minimal subjective numbness of the left hand and slowing of speech. The EEG depicted regional slowing of EEG activity temporooccipitally matching the hypoperfused area. The postictal ultrasound examination (about 24 hours after symptom onset) then showed a relative hyperperfusion of the previously hypoperfused area (Fig. 1b). These changes were accompanied by a relative flow velocity increase in the left posterior cerebral artery on TCD. A second MRI examination (including DWI and FLAIR) done 4 days after symptom onset and a lumbal puncture revealed normal findings. The clinical and MRI findings did not support ischemic origin [7, 8]. Understanding of migraine pathophysiology has always been impeded by its paroxysmal and unpredictable nature. However, it is widely considered – although not fully understood – that spreading cortical depression may explain the neurological deficits during aura. Spreading depression is either accompanied [10] or followed by [3] spreading oligemia which is not limited to neurovascular territories. However, the extent of CBF reduction is lower than that associated with ischemic injury [10]. Hyperemia following hypoperfusion was also reported in migraine with aura in a SPECT study [1]. Animal experiments have provided evidence of disturbance of the autoregulation of cerebral blood flow in response to hypotension during the initial phase of cortical spreading depression [6]. Data on cerebral autoregulation in migraneurs are scarce and are only available interictally with differing results mainly presenting normal dynamic autoregulation. Ictal autoregulation has not been assessed so far and has not been investigated in the presented patient. LETTER TO THE EDITORS