Abstract
To clarify the pathophysiology of recurrent cerebral thrombosis, 22 patients with cerebral thrombosis who suffered a second attack under stable conditions more than 22 days after the initial stroke were studied by neuroradiological techniques. Hypertension, diabetes, and hypercholesterolemia was seen in 20, 8, and 12 out of the 22 patients, respectively. Neither antiplatelet therapy nor antihypertensive therapy with good control was carried out before recurrence in aproximately half of them. The patients were divided into three groups according to their symptoms. The co-existent group had symptoms that differed between the first and second attacks, the progressive group showed abrupt deterioration of their original symptoms, and the combined group had mixed symptoms. The majority of the 12 patients in the co-existent group had an initial hemiparesis followed by either contralateral hemiparesis or suprabulbar palsy. The interval until recurrence varied from 4 months to 9 years. As causative lesions in this group, CT/MRI findings indicated not only lacunae in both hemispheres, but also deep white-matter ischemia of the centrum semi-ovale. In two cases, supratentorial lesions were combined with infratentorial infarcts. In the 6 patients of the progressive group, hemiparesis or visual field defects deteriorated during a short interval of a few months. The recurrent interval was usually so short as a few months. Neuroimaging revealed not lacunae, but cortical infarction (superficial type due to thrombotic obstruction of middle or posterior cerebral artery branches) in the left hemisphere or deep white-matter ischemia (watershed infarction due to main trunk obstruction) in the right hemisphere. Two patients with cortical infarction had polycythemia. The 4 patients in the mixed group had deterioration of hemiparesis associated with aphasia. CT/MRI, SPECT and angiography indicated mainly deep white-matter ischemia caused by main trunk lesions in the left hemisphere. Regarding the pathophysiological aspects, the mixed type seemed to be equivalent to the progressive type except for the laterality of the lesion. The mechanism of recurrence could be hemodynamic changes, because the patients had uncontroled hypertension with fluctuating blood pressures.
In conclusion, recurrent lacunar thrombosis tended to produce infarcts at another site (co-existent symptoms), while cortical infarcts and watershed infarcts tended to expand with progressive or mixed symptoms. It is suggested that neuroradiological assessment of the initial stroke may help to predict the mode of recurrence to some extent, although the pathopysiology of cerebral thrombosis is complicated and varies case by case.
