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Problems about therapy of the acute cerebral ischemia

Achieving the resolution of a clinical picture of acute cerebral insufficiency by a thrombolytic treatment is a topic of evident scientific value and of undeniable practical and therapeutic meaning. This topic, which for several years has been regarded under both a clinical and an experimental point of view, gives some hints, worth of careful reconsideration. The remark which is at the base of the use of the thrombolytic drug in the reminded conditions, is that over 80% of cerebral focal ischemic attacks comes from an athero thrombotic occlusive disease, on which an action of the thrombolytic drug can just be guessed.
In this context, the points to be underlined can be so summarised:

• there is a set of experimental results, which demonstrate that in rats embolised by homologous clots in the carotid district, a praecox infusion of the thrombolytic drug gets an important mean volume decrease of cerebral infarct (from 19% in the control group to 4.6% in the treated group). The "praecox" property refers to the time interval needed to pass from blood flow stop to the irreversible neuronal ischemic damage; this interval in rat ranges to a maximum of 120 m', while in man it is comprised within 4 and 6 hours.
• the possibility of haemorrhagic evolution is a natural problem for the assessment of the safety of thrombolytic therapy. However it must be underlined that the traditional idea by which the haemorrhagic evolution can be regarded as a not easily avoidable consequence of thrombolytic action, can be revisited as no essential differences have been observed with regard to patients treated with placebo. As to possible connections between haemorrhage and thrombolytic use, the possibility of the intervention of some etiologic factors is hypothesised, such as the long time interval between the start of the symptoms and the exposition to thrombolytic drug; arterial hypertension; enhanced drug doses, if compared to a light body mass.
• the evaluation of the obtained results must rely on well definable and measurable parameters, mainly on the residual neurological deficit.
• the recanalisation of occlusions of carotid and vertebro-basilar districts within 4 and 6 hours from the symptoms onset by means of the thrombolytic drug is technically possible, but within the actual state of knowledge it is difficult to say if the recanalisation must be constantly regarded as a pre-requisite to a favourable prognosis or if it is instead only an epiphenomenon.

The surgical treatment of recanalisation qualifies itself as a presidium of opposed applied sign, but with the same aims as the thrombolysis in the achievement of the same target, i.e. the remission of neurological symptoms after an episode of acute cerebral ischemia. It deals with a topic which has by now its own history - the first intervention of carotid recanalisation for an acute disease dates back to 1953 - by the need of the detection of elements and criteria of sure indication, to avoid uncertainties which repeatedly come to observation and to support an interest on the base of certain data.
The surgical recanalisation in emergency of the internal carotid artery can be considered in a series of clinical conditions, characterised by cerebrovascular insufficiency, but with not exactly superimposable symptomatic characteristics, i.e.:

• the Acute Carotid Occlusion;
• the Crescendo TIA;
• the Fluctuating Stroke;
• maybe the Pre-Occlusive Stenosis.

• a limited therapeutic window (within 6 and 12 hours from the acute event) is a favourable premise for a good anatomical and therapeutic result;
• the risk of cerebral haemorrhage following surgical recanalisation in emergency is suggested in some reports, in which the onset of haemorrhage after the reperfusion of an already damaged cerebral tissue has also been documented;
• in the cases characterised by Progressive Stroke and by Crescendo TIA, the therapeutic result is generally evident, sometimes in an impressive way.