Protein C deficiency is a rare cause of thromboembolic disease. Venous thrombosis is the most common clinical manifestation of protein C deficiency, but there are also a few reports in the literature addressing the relationship between protein C deficiency and the occurrence of arterial thrombosis. I report the case of a 32-year-old male who presented with vomiting, dysarthria and left limb ataxia. Cranial computed tomography and magnetic resonance imaging disclosed an infarction in the left cerebellar hemisphere. Two months and ten days after onset, protein C activity was 37% (normal:70-140%). The protein C activity of both parents and two of the patient's brothers was within normal limits. During follow-up, there was a complete recovery of neurological signs and symptoms. Ten months after onset, the patient's protein C activity normalized (104%). My findings suggest that a decrease in protein C activity may be temporary in some patients with cerebral infarction. Follow-up of protein C activity is necessary even if there is no decrease in protein C activity in the patient's family members.
|Number of pages||4|
|Journal||Acta Neurologica Taiwanica|
|Publication status||Published - 1997|
All Science Journal Classification (ASJC) codes
- Clinical Neurology