Recovery of function after brain damage: the chronic consequence of large neocortical injuries.

In the present experiment we addressed the common clinical finding that subsequent to recovery of function, there is often a lingering chronic dysfunction associated with extensive neocortical injury. We have confirmed this observation in the laboratory setting, and the data is compatible with the theoretical position that brain injury induces a shift in dominance of functional neural systems that normally control behavior. Although the present data do not suggest how this shift in dominance may be reversed, it does, nonetheless, demonstrate that the persistent chronic dysfunctions associated with neocortical injury may be effectively moderated within certain environmental situations.

Peripheral nerve implantation into a penetrating lesion of the eye: stimulation of the damaged retina.

A small penetrating incision made through the sclera, choroid and retina of the adult rat eye creates a unique lesion paradigm. More specifically, by one to two weeks after the incision the wound area stabilizes, leaving a clean inflammation-free degeneration gap or 'die-back zone' (200-300 microns wide) between the cut edges of the intact retina. The dependable formation of a small focal retinal lesion makes this an ideal model for the determination of conditions that may stimulate retinal regeneration, wound repair and/or cell survival. In other words, material may be injected or placed into the lesion site and the retina analyzed for responses to such treatments. Accordingly, the placement of a desheathed peripheral nerve implant (PNI) into the lesioned adult rat eye initiated the rescue of retinal tissue that would normally die due to trauma. In addition, the cut edges of the retina just lateral to the PNI actually touched and fused together, thus demonstrating a wound closure or healing phenomenon which was not observed in control situations. Also the thickness and organization of most retinal layers at the site of lesion were maintained at intact control levels in the presence of the PNI. However, controls not containing the PNI exhibited dramatic reductions in total and individual retinal layer thickness for up to approximately 500 microns lateral to the lesion site. Through the use of a double lesion paradigm, it was also determined that the wound repair phenomena could be influenced over a distance by (a) putative diffusable factor(s) elaborated or initiated by the PNI.

The role of stereotactic biopsy in the management of HIV-related focal brain lesions.

The criteria for brain biopsy in patients with acquired immunodeficiency syndrome (AIDS) remain unclear and without universal acceptance. In order to shed more light on this issue, the authors reviewed the records of 25 AIDS patients with focal cerebral lesions who consecutively underwent stereotactic biopsy between November 1988 and October 1990. The most frequently occurring diagnoses were lymphoma (36%), progressive multifocal leukoencephalopathy (24%), and toxoplasmosis (8%). Patients whose central nervous system disease resulted in their initial presentation (approximately 40%) survived a median of 37 weeks, as opposed to 6 weeks for those who had previous AIDS-related infections. The proportion of biopsies of contrast-enhancing lesions that were diagnostic and thereby contributed to the patients' therapeutic management was 87.5%. On the other hand, only 67% of the biopsies of nonenhancing lesions were diagnostic, and none of these lesions were treatable. All of the lymphoma patients had had AIDS for some time and, despite a reasonable preoperative Karnofsky score and postoperative radiation therapy, their median survival was only 6 weeks; however, biopsy was critical to their therapeutic management. Early brain biopsy, rather than empiric antitoxoplasmosis therapy, appears indicated for aggressive therapy of contrast-enhancing lesions in patients who have had previous manifestations of AIDS. The role for biopsy of nonenhancing lesions is less clear, but it may provide prognostic information.

Clinical presentation, radiological findings, and treatment results of coccidioidomycosis involving the spine: report on 23 cases.

OBJECT: This study was conducted to review the presentation and management of patients with coccidioidomycosis involving the spine. METHODS: The authors reviewed 23 cases of spinal coccidioidomycosis treated at their institutions. There were 20 males and three females who ranged in age from 9 to 62 years. Non-Caucasian individuals were disproportionately represented. Spinal disease was the first manifestation of disseminated coccidioidomycosis in 10 cases. Thirteen patients with meningitis, soft-tissue involvement, or pulmonary involvement developed new spinal lesions despite undergoing continued systemic therapy with amphotericin and/or fluconazole. In all patients computerized tomography and magnetic resonance imaging studies demonstrated preferential involvement of the disc spaces, vertebral bodies, and pedicles with extensive paravertebral phlegmons and retropharyngeal, mediastinal, or psoas abscesses. Despite the significant imaging findings, only four patients presented with a significant neurological deficit. Local pain or radiculopathy was the most common complaint. Twenty patients underwent invasive therapy. In five patients with prominent psoas abscesses and disc space disease, drainage was performed after inserting a percutaneous catheter. Progressive bone destruction necessitated debridement and fusion in one of these patients, and two others had poor outcomes after receiving antifungal therapy alone. Initially 15 patients underwent debridement and fusion in which instrumentation (10 cases) or bone graft alone was used (five cases). One patient worsened neurologically after surgery, and another patient required reoperation for a failed fusion and to correct progressive kyphosis. Four of the 23 patients died of complications related to fungemia. Most of the 15 surviving patients have required long-term antifungal therapy for spinal and extraspinal foci. CONCLUSIONS: Spinal coccidioidomycosis can be an aggressive disease process. Systemic antifungal therapy fails to prevent de novo spinal involvement and is usually insufficient treatment for established spinal disease.

Propofol in the treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial.

OBJECT: Sedation regimens for head-injured patients are quite variable. The short-acting sedative-anesthetic agent propofol is being increasingly used in such patients, yet little is known regarding its safety and efficacy. In this multicenter double-blind trial, a titratable infusion of 2% propofol accompanied by low-dose morphine for analgesia was compared with a regimen of morphine sulfate in intubated head-injured patients. In both groups, other standard measures of controlling intracranial pressure (ICP) were also used. METHODS: Forty-two patients from 11 centers were evaluated to assess both the safety and efficacy of propofol: 23 patients in the propofol group (mean time of propofol usage 95+/-87 hours) and 19 patients in the morphine group (mean time of morphine usage 70+/-54 hours). There was a higher incidence of poor prognostic indicators in the propofol group than in the morphine group: patient age older than 55 years (30.4% compared with 10.5%, p < 0.05), initial Glasgow Coma Scale scores of 3 to 5 (39.1% compared with 15.8%, p < 0.05), compressed or absent cisterns on initial computerized tomography scanning (78.3% compared with 57.9%, p < 0.05), early hypotension and/or hypoxia (26.1% compared with 10.5%, p = 0.07). During treatment there was a trend toward greater use of vasopressors in the propofol group. However, the mean daily ICP and cerebral perfusion pressure were generally similar between groups and, on therapy Day 3, ICP was lower in the propofol group compared with the morphine group (p < 0.05). Additionally, there was less use of neuromuscular blocking agents, benzodiazepines, pentobarbital, and cerebrospinal fluid drainage in the propofol group (p < 0.05). At 6 months postinjury, a favorable outcome (good recovery or moderate disability) was observed in 52.1% of patients receiving propofol and in 47.4% receiving morphine; the mortality rates were 17.4% and 21.1%, respectively. Patients who received the highest doses of propofol for the longest duration tended to have the best outcomes. There were no significant differences between groups in terms of adverse events. CONCLUSIONS: Despite a higher incidence of poor prognostic indicators in the propofol group, ICP therapy was less intensive, ICP was lower on therapy Day 3, and long-term outcome was similar to that of the morphine group. These results suggest that a propofol-based sedation and an ICP control regimen is a safe, acceptable, and, possibly, desirable alternative to an opiate-based sedation regimen in intubated head-injured patients.

Spontaneous acute subdural hematoma precipitated by cocaine abuse: case report.

A novel complication of the illicit use of cocaine, a spontaneous acute subdural hematoma, is described. This case represents another addition to the growing literature on the negative effects of cocaine on the central nervous system. Photographic documentation of the lesion responsible for the hematoma is presented, along with a discussion of the possible pathophysiologic mechanism.

Spontaneous subdural hematoma in the setting of immune thrombocytopenia complicated by ischemic infarcts.

The occurrence of spontaneous subdural hematoma (SDH) in immune thrombocytopenia (ITP) is rare. We report a spontaneous subacute subdural hematoma in a patient with chronic ITP. The patient presented with headache and a noncontrast head CT scan showed an 11 mm subacute right frontoparietal SDH causing an 8 mm right to left midline shift. The patient underwent medical management with platelets, FFP and packed RBC transfusions, steroids, IVIG and mannitol, which failed to prevent deterioration of her clinical condition. The patient then underwent burr hole drainage of the SDH. Her postoperative course was complicated by ischemic infarcts in the right posterior cerebral artery territory leaving her with a residual left homonymous hemianopia. Our patient was unique in the concurrent development of ischemic infarcts postoperatively, following burr hole drainage of the SDH in the setting of ITP. This case highlights the diagnostic and therapeutic dilemmas involved in taking care of such patients.

Retinal transplants and optic nerve bridges: possible strategies for visual recovery as a result of trauma or disease.

From the review of the current literature it is quite evident that some exciting prospects are on the horizon which will help to better explain the development and functioning of the visual system. In addition, the new technology of CNS tissue grafting coupled to other newly emerging technologies (i.e., microsurgical, microinjection, and micromanipulative techniques coupled with our knowledge of immunosuppressive methods) will allow for a realistic approach in exploring possible strategies for visual recovery as a result of trauma or disease within the near future. One specific area of research that hopefully will emerge from this new body of knowledge comes from the realization that at the present time there is no effective therapy for practically all types of hereditary retinal degenerative disorders in man. It would seem most appropriate to take advantage of the new neuronal transplantation technology mentioned in this article and the availability of hereditary retinal degeneration models in the hope of developing new methods for a therapeutic approach to this problem. Such an approach could involve replacing the abnormal, absent, and/or lost host retinal cells with tissue from healthy donors by means of a grafting technique with the goal of arresting and/or reversing the disease process. Of course, this is but one example of the many challenges in this area of research which increasingly appear to be within our grasp.

Ibuprofen improves cerebral blood flow after global cerebral ischemia in dogs.

In a canine model of global cerebral ischemia, 6 dogs received a saline placebo prior to the event and 5 received 12.5 mg/kg ibuprofen. Cerebral venous outflow from the confluence of the sagittal and transverse sinuses, systolic and diastolic arterial pressure, cardiac output, pH, Paco2, Pao2, and arterial and sagittal sinus thromboxane B2 and 6-keto-PGF1 alpha were measured at intervals up to 120 minutes thereafter. Postischemic cerebral hypoperfusion was significantly improved in the ibuprofen pretreatment group. Control dogs showed significant increases in sagittal sinus postischemic thromboxane B2 concentrations, but pretreated dogs showed nearly complete inhibition of postischemic thromboxane B2 production. Pretreated dogs also had significantly lower levels of 6-keto-PGF1 alpha from the sagittal sinus. There were no significant differences in the other variables at any interval. We conclude that ibuprofen ameliorates postischemic cerebral hypoperfusion, and that this improvement is associated with decreased sagittal sinus levels of thromboxane B2 and 6-keto-PGF1 alpha.