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In internal carotid artery occlusion (ICAO), a spontaneous increase of cerebral vasoreactivity (CVR) may occur over time. Statins are known to increase CVR. We analyzed the influence of statin treatment and other cofactors on CVR improvement in patients with ICAO. Sixty-six patients with ICAO were reexamined after 15 ± 6 months. CVR in both middle cerebral arteries was assessed by transcranial Doppler and inhalation of 7% CO(2). Pre-defined cut-off values were used to define exhausted CVR. Cofactors analyzed were: age, sex, hypertension, diabetes, statin treatment, degree of contralateral stenosis, quality of intracranial collateral flow, duration of ICAO. Mean CVR did not differ between the two studies. Twenty patients had exhausted CVR at baseline, 11 of them improved above the cut-off at follow-up (55%). Factors significantly associated with this improvement were good collateral pattern at baseline (p = 0.0065) and statin treatment (p = 0.0179). Odds ratios for improving CVR were 36.0 [95% CI 2.7-476.3] for good collateral flow and 20.0 [95% CI 1.7-238.6] for statin treatment. In conclusion, exhausted CVR frequently improves during the course of ICAO. Good collateral function and statin treatment are significantly associated with improving CVR.

Sirs: Spinal subarachnoid hemorrhage (SAH) acounts for less than 1% of SAHs. Cerebral complications are uncommon and moderate in severity. We report on a 30year old woman suffering from severe cerebral vasospasms, without subarachnoid blood in successive cranial CT scans, due to spinal SAH caused by a ruptured solitary spinal aneurysm of unknown etiology. The patient suffered from a graft-versus-host reaction of her transplanted kidney. Under immunosuppression, she developed recurrent pneumonias and a septicemia with unknown germ that were treated by intravenous antibiotics. In the further course, she suddenly presented with headache, back pain and progressive behavioural disturbances. Cranial CT at this time was normal. Three lumbar punctures revealed a hemorrhagic CSF that was considered to be artificially bloody. Because of increasing paraparesis and rectal incontinence, the patient was referred to our clinic one week later. On admission, she was in poor clinical condition with reduced consciousness, no speech production, nuchal rigidity and paraplegia lasting for more than 24 hours. Cranial CT was normal, whereas cranial MRI showed bilateral MCA-infarction on diffusionweighted MRI (Fig. 1A). Spinal MRI revealed a ventrally located intraspinal circular tumour at the level of the twelfth thoracic vertebra with an intradural T1-hyperintensive signal in the thoracolumbar canal (Fig. 1B). Suboccipital puncture yielded a hemorrhagic CSF (2540 cells per ll). Conventional panangiography revealed a solitary aneurysm (8 · 15 mm) originating from the descending branch of the anterior spinal artery at the level of the twelfth thoracic vertebra (Fig. 1C) as well as generalised, severe cerebral vasospasms. Despite immediate triple-Hand nimodipine-therapy, CT 12h later demonstrated large bilateral MCAinfarction, but was still without any cerebral SAH (Fig. 1D). Because of the infavorable prognosis, palliative treatment was carried out until death due to a pneumogenic sepsis 23 days later. To date, 20 cases of spinal SAH due to a rupture of isolated spinal aneurysms have been reported [1–2, 4–16]. Of the eight reported patients with thoracolumbar aneurysms, all had an acute onset of pain in the thoracolumbar region [1, 8, 11, 13, 15]. Three also had paraparesis [1, 8]. Six of the eight patients were treated surgically [8, 11, 13, 15] whilst the other two had a conservative treatment [1]. All patients recovered either without or with minor neurological deficits. The authors found two dissecting aneurysms [8], an inflammation within the vessel wall in two cases [1, 11] and no evident etiology in the other four reports [1, 8, 13, 15]. In our patient, general autopsy did not reveal any underlying systemic (e.g. polyarteriitis nodosa, connective tissue disorder, syphilis), cerebral or further spinal vascular pathology. Since the SAH was related in timing to systemic infection in the context of immunosuppression, the aneurysm may result from a local inflammation. Morphologically, inflammatory aneurysms are characterised by proliferation of the tunica intima and media as well as inflammatory infiltrates. Infectious agents may be detected within the vessel wall [4, 11]. However, the aneurysm in our patient only yielded a prominent fibroblastic proliferation without inflammatory infiltrates (Fig. 2). Additional analysis of blood and CSF samples did not contain any germs and all serological tests were negative. Thus the inflammatory etiology remains speculative. In summary, we present the case of a young woman who suffered from symptomatic cerebral vasospasms due to spinal SAH caused by a ruptured solitary spinal aneurysm. Pathogenesis of cerebral vasospasm is unclear, but is most probably due to a distant inflammatory response caused by the subarachnoid blood [3]. Although there have been a few R. Surges AE M. Schubert AE C. Weiller A. Hetzel AE W.-D. Niesen (&) Dept. of Neurology University Clinics of Freiburg Breisacherstr. 64 79106 Freiburg, Germany Tel.: +49-761/270-5157 Fax: +49-761/270-5328 E-Mail: wolf-dirk.niesen@uniklinikfreiburg.de

Dynamic cerebral autoregulation assessed from blood pressure transients can be considerably impaired in severe internal carotid artery (ICA) obstruction. It is unknown whether impaired autoregulation indicates an increased risk of subsequent ischemic events in this situation. 165 patients with ICA stenosis (> 70 %) or occlusion were prospectively followed until anterior circulation stroke, transient ischemic attack, carotid recanalization without prior event, death or study end. Transcranial Doppler sonography was used to determine autoregulation in both middle cerebral arteries from spontaneous blood pressure fluctuations (correlation coefficient indices Dx and Mx) and respiratory- induced 0.1 Hz oscillations (phase). Standard CO(2) reactivity (CO(2)R) was additionally assessed. All indices were classified as impaired vs. preserved according to reference values from 79 agematched controls. During median follow-up of 24.5 months, there were 16 ischemic events over ipsilateral sides. Competing risk analysis revealed a significant predictive effect on ipsilateral ischemic events for impaired Dx (rate ratio 8.2 [95 % confidence interval 1.7-39], p = 0.0079), phase (5.0 [2-13], p = 0.0007) and CO(2)R (9.4 [2.2-40], p = 0.0025). Restricting analysis to severe stenosis alone (n = 103), only impaired phase (rate ratio 8.6 [1.6-45], p = 0.01) remained as a significant predictor. In a continuous statistical model, only Dx and Mx were significant predictors of ischemic events (p = 0.012 and p = 0.016). In conclusion, impaired dynamic cerebral autoregulation indicates an increased risk of subsequent ischemic events in severe obstructive ICA disease. Its clinical application might thus be of help in identifying higher risk patients.

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

Vertebral artery dissection may cause upper limb peripheral motor deficit. We report three young patients presenting with nuchal pain followed by a nearly painless proximal paresis of the arm several days later. The cause, as detected by colour-coded Duplex sonography and MRI, was an extracranial dissection of the vertebral artery. The proximity of the intervertebral segment to the vertebral artery and the nerve roots indicated that compression by an intramural haematoma was the likely cause of the disorder. Subsequent examinations during anticoagulation treatment showed almost complete disappearance of the intramural haematoma and of the neurological deficits within a few weeks. We believe that the occurrence of an upper limb peripheral motor deficit should be added to the spectrum of potentially misleading signs of vertebral artery dissection.