Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.

A group of 59 patients with stroke due to acute vertebrobasilar or carotid territory occlusion have been treated by local intra-arterial fibrinolysis (LIF). A high recanalisation rate was accomplished with either urokinase or recombinant tissue plasminogen activator (r-TPA). However, with either substance, even if a high dose was used, recanalisation was a time-consuming process which usually took 120 min. A reasonable explanation for the lack of effectiveness of these plasminogen-activating substances might be a deficit of substrate, e.g. plasminogen, in aged thrombus. LIF was capable of improving clinical outcome in acute vertebrobasilar artery occlusion, reducing mortality to 50% in patients fulfilling inclusion criteria. In the carotid territory multiple occlusions had a poor prognosis while good clinical results could be achieved in occlusions of the proximal middle cerebral artery or single branches.

To study vascular abnormalities in migraine, transcranial Doppler (TCD) was used for evaluation of 100 consecutive patients with either common or classic migraine during the headache-free period. We insonated the basal cerebral arteries and the internal carotid artery (ICA) in the neck. Particular ultrasonic features in migraineurs included intracranial elevations of mean flow velocity (MFV) above 3 standard deviations of normal values in 16%, probably reflecting increased vasotonus. Marked asymmetry of MFV in corresponding intracranial arteries was found in 12%, and could represent "asymmetrical" vascular tone. Characteristic vascular bruits of low frequency and sometimes harmonic quality were detected in 56%. When compared to TCD findings in 40 young controls, MFV were significantly higher in all intracranial arteries in migraineurs, but not in the cervical ICA. Marked differences were also found for incidence of MFV elevations and vascular bruits (p less than 0.0001). Vascular reactivity in response to eye closing as measured by flow changes in the posterior cerebral artery (visually evoked flow) was significantly greater in migraineurs than in controls (%MFV change, 14.1 +/- 5.4 vs 11.4 +/- 4.8; p = 0.004). TCD features did not discriminate common from classic migraine. Taken together, our results support the view of intracranial vascular abnormality in migraineurs reflecting, in particular, a narrower and more reactive arterial tree. The value of TCD in the differential diagnosis of "vascular headache" and in the study of migraine pathophysiology will have to be determined in the future.

Four cases of cervical vertebral artery (VA) dissection are reported. In three patients VA dissection was associated with neck trauma. All patients were young or middle-aged (range 27 to 49 years). In two there was a history of migraine. Pain preceded neurological symptoms from hours to six weeks. Three patients had neurological deficits including elements of the lateral medullary syndrome, and one experienced recurrent transient ischaemic attacks in the vertebrobasilar territory. Angiographic findings included irregular stenosis, occlusion and pseudoaneurysm; in two patients VA abnormalities were bilateral. All patients were treated with anticoagulants and improved.

Transcranial Doppler (TCD) examinations were performed in 13 patients with common and 5 patients with classic migraine during attacks and compared to TCD findings during the headache-free period. Two distinct patterns of flow changes were detected to distinguish common from classic migraine on the basis of TCD findings. During attacks, patients with common migraine exhibited reduction of flow velocities associated with an increase of pulse wave amplitudes. Vascular bruits that were heard during the headache-free interval often disappeared. Opposite changes were found in attacks of classic migraine during the headache phase with increase of flow velocities, decrease of pulsatility and more prominent or newly appearing bruits. These findings were often diffuse and did not appear to correlate with side of headache or side of neurological aura. Uniform changes occurred in the cervical internal carotid artery and the basal cerebral arteries in either form of migraine. We propose that these changes represent caliber fluctuations of the large arteries, suggesting vasodilatation during attacks of common migraine and vasoconstriction during attacks of classic migraine. We do not intend to imply a casual role of these preliminary findings in migraine pathogenesis, but we suggest that TCD be used in combination with other methods to study vascular changes in migrainous disorders.