DISCUSSION

The clinical presentation of basilar artery thrombosis is variable, but its evolution is commonly bad. Out patient had an atypical prolonged presentation of approximately 48 hours, with symptoms of transient and recurrent vertebro-basilar ischemia, including disarthria, hemiplagia, headache and vertigo and finally loss of consciousness. He arrived in a state of coma of about 1-2 hours in duration prior to the procedure.

The medical management of the patient upon arrival to our institution included stabilizing his cardiorespiratory function. The etiology of the clinical presentation of our patient was immediately evident. In fact, the clinical presentation of vertebro-basilar isquemia can be sometimes nonspecific. In this patient, the initial symptoms were not specific, and considering that the patient had 48 hours of symptomatology, it was possible to consider other etiologies in addition to isquemia, including an inflammatory process. Nevertheless, we opted to investigate the most urgently treatable etiology first, like a cerebro-vascular occlusion, possibly related to an arterial dissection considering the history of trauma. The cerebral angiogram showed a basilar occlusion embolic in origin, related to a traumatic vertebral dissection at the skull base level. Considering the poor prognosis of this lesion and also that the patient had been in coma for only 1-2 hours with no or minimal brain CT changes, we elected to perform intra-arterial thrombolysis. In the posterior circulation, there does not exist a limit as to the amount of time elapse from the beginning of the symptoms to perform thrombolysis, like exists in the anterior circulation of 3-6 hours. This is because thrombosis of the basilar artery has extremely high mortality and therefore thrombolysis is the only viable therapeutic alternative. Also, as an anecdotal observation, it may be that neuronal tissue in the pons, which is predominantly axonal, may be less vulnerable to isquemia. It is therefore, the clinical presentation and not the time elapse that directs the therapeutic conduct. If the patient is still not in coma, or if in coma, only for a short duration, the patient is a candidate for thrombolysis. We decided to perform thrombolysis intra-arterially and not intravenously, since the intra-arterial route of administration is associated with a higher recanalization rate (60-90% intra-arterial versus 30-50% intravenous) (12-13).

After having achieved an excellent result of recanalization, we decided to occlude the right vertebral artery proximal to the region of the dissection, in order to eliminate the possibility of another thrombus dislodging from the dissection site and the antegrade flow causing another thromboembolic occlusion of the basilar artery. It was possible to occlude the right vertebral artery since the right posterior inferior cerebellar artery (PICA) filled from retrograde flow from the left vertebral artery (Figure 2). A case report similar to ours was recently published which instead of occluding the damaged vessel with the dissection, it was possible to stabilize the segment with the dissection with angioplasty and stenting (7).

The first clinical series of intra-arterial thrombolysis for acute vertebro-basilar isquemia was published by Zeumer et al in 1983 (11). The results of clinical series of intra-arterial thrombolysis in the posterior circulation show a mortality of approximately of 25-50% (1,6). Patients that present in coma, like our case, have a higher mortality (1,6). In the series of Bercker et al. (6) there was a 100% mortality (3/3) for patients who presented in coma, even when a successful recanalization was obtained with intra-arterial thrombolysis. Other factors which are associated to a higher mortality rate include inability to obtain recanalization with thrombolysis, rethrombosis and hemorrhage post thrombolysis. The incidence of hemorrhage post vertebro-basilar thrombolysis is 0 - 15% (1,5). In the series of Bercke (6) 8 of 9 patients with imaging signs of infarct before thrombolysis did not have a hemorrhagic event post-thrombolysis. Our patient developed a small hemorrhage in the region of the infarct in the pons, without clinical manifestations.

Angiografic factors which are associated with a better outcome are the localization of the occlusion in the basilar in its distal segment, and the presence of bilateral posterior communicating arteries since from these can arise small perforating vessels that also supply the territory of thalamoperforators, in addition to the both posterior cerebral arteries. Also important is the location and severity of the brainstem infarct. Our patient had an excellent recovery even in the presence of a large pontine infarct.

The medical management of our patient after the thrombolysis included hypervolemic and hypertensive therapy. This type of treatment was maintained for about a week, keeping MAP between 100-120mm/Hg. Even several weeks after the pontine infarct event, the patient remained dependent on normal arterial pressures and was sensitive to any orthostatic hypotension event. After an abrupt neurological decline in relation to a hemodynamic event during a rehabilitation session, the patient responded rapidly to hypervolemic therapy.