Crescendo transient ischemic attacks due to intracranial atrery stenosis. Two case reports and literature review
STOURAITIS G., SPENGOS K., TSIVGOULIS G., DIMITRAKOPOULOS A., VEMMOS K., SFAGOS K., ZIS V., VASILOPOULOS D.

Crescendo transient ischemic attacks (TIAs) are defined as disabling, recurrent transient cerebral ischemic episodes characterized by an increased frequency, duration, or severity of events. A hemodynamically relevant extracranial stenosis of the internal carotid artery is the most common cause of crescendo-TIAs. However, in extremely rare cases, this uncommon clinical syndrome has been attributed to intracranial stenosies of the internal carotid artery or the proximal portion of the middle cerebral artery.

We report the cases of two male patients with a known history of hypertension and smoking who, during the last 24 hours before hospital admission, presented repeated short lasting episodes of left side hemiparesis with aphasia and right side hemiparesis, respectively. These attacks showed an increasing duration and clinical severity. The first patient initially presented slight weakness of the arm and paraphasias. The following episodes were significantly more critical lasting almost 20 minutes. Complete hemiparesis and Brocas aphasia with a duration of almost 40 minutes was documentated while at his stay in the emergency department of our hospital. Fortunately, all symptoms resolved spontaneously, as it had happened in all previous events. Similarly, the second patient first presentated a slight left side hemiparesis (MRC 4/5) with concomitant hypesthesia, which became more severe after the third episode (MRC 3/5), which lasted more than 15 minutes. These typical cli-nical features allowed the diagnosis of crescendo TIAs. In both cases, atherosclerotic lesions of the extracranial supplying arteries or a dissection of the supplying internal carotid artery were definitely excluded. The normal electrocardiography recording showed no permanent atrial fibrillation, atrial flutter or sick sinus syndrome. Intermittent atrial fibrillation was excluded by means of Holter 24hour electrocardiography. Finally, tranthoracic echocardiography revealed no eardiac wall or valvular abnormalities as possible sources of cardioembolism. Intensive diagnostic workup with Transcranial Doppler and intracranial magnetic resonance angiography revealed in both cases an intracranial stenosis of the Middle Cerebral Artery as cause of transient ischemia due to distal hypoperfusion and probable local thrombosis at the sight of stenosis. According to given guidelines both patients were systematically treated with anticoagulants. Initially, intravenous heparin was applied (25.000 I.U. per day) followed by coumadin per os for further six months. Afterwards, both patients went on antiplatelet agents and still remain free of any focal ischemic symptoms after 10 and 12 months respectively.

In conclusion crescendo-TIAs can exceptionally be caused by intracranial artery stenosis. In our cases distal hypoperfusion and local thrombosis at the sight of the atherosclerotic intracranial stenosis seem to be the pathogenetic mechanisms of the focal transient ischemic events. Systemic anticoagulation, initially with heparin and later with coumadin seems to be the most effective and also safe therapeutic approach.

Key words: Crescendo transient ischemic attack, intracranial stenosis, middle cerebral artery, transcranial Doppler, MRA.