No abstract

The authors report 2 patients with subacute subdural hematoma (sASDH). An inflammatory process is known to be involved in the development of traumatic subdural effusion (TSE) evolving into chronic subdural hemorrhage (CSDH), but a similar event has not been previously described in acute subdural hematoma (ASDH) evolving into sASDH. In our cases, dexamethasone (DXM) and other conservative treatments were administered to our first patient with dramatic clinical outcome, and a postoperative pathologic examination of the neomembrane of the sASDH in the second patient was done, which showed marked inflammatory process with T-lymphocytes and neutrophils infiltration. The good response to DXM in the first patient and the definite laboratory result of the second patient and their radiologic presentations, as well as a review of relevant literature, suggest that a T-lymphocyte-mediated, delayed hypersensitive reaction triggered by undissolved blood clot may be the driving force of ASDH developing into sASDH, which starts after the seventh day, and peaked by the end of the second week of the clinical course.

Traditionally, lacerations of bridging vessels were surmised to cause chronic subdural hematoma (CSDH), although neither observation studies nor medical research was able to testify this. Nowadays, an inflammatory process is known to take place in the development of CSDH. Of note, post-traumatic angiogenesis at its early stage also features inflammation with immune cell infiltration. The authors found a patient suffering from CSDH with unusual angiogenesis between dura and pia matters. The observation of dura-and-pia angiogenesis may be a piece of evidence to underline compensatory reaction of central nervous system to offset the negative effects produced by CSDH, and points out to a possible approach of bolstering angiogenesis to manage ischemic diseases in cerebral hemispheres.