C. Nordborg et Bb. Johansson, SECONDARY THALAMIC LESIONS AFTER LIGATION OF THE MIDDLE CEREBRAL-ARTERY - AN ULTRASTRUCTURAL-STUDY, Acta Neuropathologica, 91(1), 1996, pp. 61-66
Earlier light microscopic, immunocytochemical and morphometric investi
gations indicate that noxious substances transported with the vasogeni
c edema from hemispheric infarcts influence the character, timing and
extent of the secondary thalamic lesions. The object of the present st
udy was to analyze the ultrastructure of the secondary damage and the
cytolytic nerve cell change which ensues in the thalamus within a week
after the infarction. Adult spontaneously hypertensive rats (SHR) wer
e stud; led either 7 days after permanent ligation of the right middle
cerebral artery (MCA) (n = 4) or 7 days after a 2-h temporary occlusi
on of the MCA (n = 4). Light microscopy revealed damage in the ipsilat
eral thalamic nuclei and the electron microscopic analysis showed that
the cytolytic nerve cell degeneration was somatodendritic. Central ch
romatolysis was not observed. Somatodendritic nerve cell degeneration,
as found in the secondary thalamic lesions in the present study, has
been described in excitotoxic brain damage as well as in chronic, edem
atous lesions in stroke-prone spontaneously hypertensive rats. The pos
sibility that the cytolytic thalamic nerve cell lesion is influenced b
y excitatory, noxious substances spreading with the edema fluid from t
he infarct has, thus, to be considered.