PROLONGED MUSCULAR FLACCIDITY AFTER STROKE - MORPHOLOGICAL AND FUNCTIONAL BRAIN ALTERATIONS

Patients with a motor deficit due to ischaemic stroke usually develop muscular spasticity but in some cases they may remain with a prolonged muscular flaccidity which impairs their recovery. Little is known abo ut the causes of these two different functional outcomes. We correlate d CT/MRI and Tc-99m HM-PAO SPECT with clinical findings in 42 patients at a mean time interval of 3 months after stroke. The patients were d ivided into two cohorts with either flaccid (prolonged muscular flacci dity) or spastic (muscular spasticity) hemiparesis. Although patients with prolonged muscular flaccidity had a greater motor deficit, the me an structural volume of the ischaemic lesion was similar to that of th e muscular spasticity cohort. There was a significantly higher prevale nce of structural involvement of the lentiform nucleus in prolonged mu scular flaccidity cases. Relative perfusion in the lentiform nucleus, thalamus and contralateral cerebellar hemisphere was significantly low er in prolonged muscular flaccidity than in muscular spasticity patien ts. A subgroup with only subcortical structural lesions also showed si gnificantly lower relative perfusion in the ipsilateral frontal associ ation areas. A primary involvement of the lentiform nucleus by the str uctural lesion seems to be crucial for the persistence of flaccidity a fter stroke. However cerebral blood flow (CBF) changes in other struct urally intact regions indicate their additional role. It is likely tha t both subcortical-cortical loops involved in motor control, i.e. cort ex-basal ganglia-thalamus-cortex and cortex-pons-cerebellum-thalamus-c ortex, are more widely and mo re severely affected in patients with pr olonged muscular flaccidity.