Chemokine detection in the cerebral tissue of patients with posttraumatic brain contusions.

OBJECT: The clinical outcome of patients with severe head injuries is still critically dependent on their secondary injuries. Although hypoxia and hypotension appear to mediate a substantial proportion of secondary injuries, many studies associate secondary brain injury with neuroinflammatory responses. Chemokines have been detected in the cerebrospinal fluid but not in the brain tissue of patients with head trauma. This study was performed to determine if chemokines were expressed in pericontusional brain tissue in patients with moderate or severe head trauma who underwent surgical evacuation of their brain contusions. METHODS: Twelve patients with posttraumatic cerebral contusion requiring a surgical evacuation were studied. A 20- to 40-mg sample of white matter was removed from the surgical cavity in the pericontusional area. Two patients undergoing elective surgery for clip ligation of an unruptured aneurysm were used as controls. The median interval from trauma to biopsy procedure was 44 hours (range 3-360 hours). Total RNA was isolated from these samples and a ribonuclease protection assay was performed to measure the mRNA levels of several chemokines: CCL2, CCL3, CCL4, CCL5, CXCL8, CXCL10, and XCL1. RESULTS: The CCL2, a monocyte chemoattractant produced by activated astrocytes, was the most strongly expressed chemokine, followed by CXCL8, CCL3, and CCL4. The chemokines CXCL10 and CCL5 were expressed at very low levels, and XCL1 was not detected. CONCLUSIONS: Chemokine activation occurs early after moderate or severe head trauma and is maintained for several days after trauma. This event may contribute to neuroinflammatory exacerbation of posttraumatic brain damage in the pericontusional brain tissue.

Uncommon presentation of ruptured intracranial aneurysm during surgical evacuation of chronic subdural hematoma: case report.

BACKGROUND: There are many factors that predispose an aneurysm to rupture, but there are few real, demonstrable causes that lead to rupture of the aneurysmal sac with a precise cause-effect mechanism. CASE DESCRIPTION: We report a 74-year-old male patient with chronic subdural hematoma after head trauma, who underwent surgery for evacuation of the hematoma. During surgery, there was sudden copious loss of blood from the drainage tubes that were positioned subdurally. Immediate cerebral computed tomography scan and angiography revealed a subarachnoid hemorrhage at the level of the basal cisterns from a ruptured basilar apex aneurysm. We discuss the cause-effect relationship between the surgery with its positioning of subdural drains and the rupture of a previously unrecognized cerebral aneurysm. CONCLUSIONS: The rupture of an unknown, previous "unruptured" aneurysm after craniotomy with subdural positioning of drainage, must be considered a possible complication.

Spinal Cord Stimulation for the Treatment of Upper and Lower Extremity Neuropathic Pain due to Lyme Disease.

Background. Lyme disease is caused by Borrelia, a bacterium transmitted by the bite of a deer tick. A slow developing encephalopathy or an axonal polyneuropathy with distal paresthesia and spinal or radicular pain rarely occurs and can be hard to treat. Materials and Methods. We report here the case of a 44-year-old woman with four-limb, intolerable, neuropathic pain as sequelae to Lyme disease, which was resistant to conservative measures and was treated successfully with concurrent, thoracic, and cervical percutaneous spinal cord stimulation (SCS). Results. After 18 months of therapy and follow-up, this patient's analgesia, as a result of SCS, continues to be excellent, with almost complete subjective pain relief and cessation of adjuvant analgesic medication. Conclusions. SCS may be efficacious for the treatment of neuropathic pain due to Lyme disease.