Curtis E. Doberstein

The temporal profile and morphologic features of neuronal death in human stroke resemble those observed in experimental forebrain ischemia: The potential role of apoptosis

Although neuronal death has been studied in experimental models of ischemia, the precise mechanisms regulating cell death remain unclear. Furthermore, the timing and pattern of neuronal death in human stroke has not been extensively studied. To further our understanding of ischemia-induced neuronal death, we examined the temporal profile of histochemical and morphologic characteristics of hippocampal neuronal death following experimental forebrain ischemia and compared these findings to human brain specimens obtained from subjects suffering cerebral infarction. Transient forebrain ischemia (TFI) was induced in normothermic adult rats by bilateral carotid artery occlusion combined with hypotension. Animals were sacrificed at 6, 12, 18, 24, 48, and 72 h and 7, 14, and 28 days following ischemia (n = 4 at each time point). Experimental tissue was analyzed using light and electron microscopy as well as TUNEL histochemistry. A total of 27 human brain specimens with neuropathological confirmation of ischemic damage and appropriate controls were also examined using light microscopy and TUNEL histochemistry. Dense TUNEL staining in hippocampal CA-1 neurons was present at 48 and 72 h following experimental ischemia. Prior to these times, little or no nuclear staining was noted and after 72 h nuclear staining diminished rapidly. Ultrastructural findings at these time points demonstrated many features similar to those seen in cells undergoing apoptosis, such as cell shrinkage with increased electron density, chromatin condensation with formation of heterochromatin, intact plasma membranes, and intact intracellular organelles. In a similar fashion, human stroke specimens during the subacute period showed dense nuclear TUNEL staining in penumbral neurons, whereas in the acute or chronic stages little or no staining was noted. Our results demonstrate that the timing of morphologic changes and TUNEL histochemistry following human stroke resembles that observed in experimental TFI. Furthermore, neuronal death in both experimental ischemia and human stroke share several features characteristic of apoptotic cell death.

Penetrating Brain Injury after Suicide Attempt with Speargun: Case Study and Review of Literature

Penetrating cranial injury by mechanisms other than gunshots are exceedingly rare, and so strategies and guidelines for the management of PBI are largely informed by data from higher-velocity penetrating injuries. Here, we present a case of penetrating brain injury by the low-velocity mechanism of a harpoon from an underwater fishing speargun in an attempted suicide by a 56-year-old Caucasian male. The case raised a number of interesting points in management of low-velocity penetrating brain injury (LVPBI), including benefit in delaying foreign body removal to allow for tamponade; the importance of history-taking in establishing the social/legal significance of the events surrounding the injury; the use of cerebral angiogram in all cases of PBI; advantages of using dual-energy CT to reduce artifact when available; and antibiotic prophylaxis in the context of idiosyncratic histories of usage of penetrating objects before coming in contact with the intracranial environment. We present here the management of the case in full along with an extended discussion and review of existing literature regarding key points in management of LVPBI vs. higher-velocity forms of intracranial injury.

Safety of intravenous heparin administration after endovascular treatment for ruptured intracranial aneurysms

Introduction Thromboembolic events are the primary complications encountered during endovascular treatment (EVT) of intracranial aneurysms. Intraprocedural heparinization is common during EVT but is less common post-procedure. The safety of heparinization following EVT is unknown, especially for ruptured aneurysms. Materials and methods The records of 138 consecutive patients at our institution from 1 January 2000 to 30 June 2007 who were treated with EVT for 140 ruptured intracranial aneurysms were reviewed. All patients were treated with low dose intravenous heparin post-procedure for 24 h as per the departmental protocol. Cases of worsening hemorrhage requiring surgical evacuation were considered significant hemorrhages. Prior surgical exploration and external ventricular drain (EVD) placement were also noted. Results There were two cases (1.4%) of significant worsening hemorrhage during post-procedure heparin administration. Among 13 patients who underwent craniotomy (for hematoma evacuation or attempted surgical clipping) prior to EVT, there was one (7.7%) case of significant hemorrhage. Among the 60 patients who underwent EVD placement prior to EVT, there was one (1.7%) case of significant hemorrhage. Conclusion Administration of systemic heparinization may be safe during the first 24 h post-EVT of a ruptured intracranial aneurysm in patients without recent craniotomy. Further study in determining the benefit of this protocol in reducing post-embolization thromboembolic complications may be warranted.

The safety and feasibility of outpatient carotid endarterectomy

BACKGROUND Carotid endarterectomy (CEA) is one of the most commonly performed and studied surgical procedures for extracranial ischemic disease. OBJECTIVE The authors reviewed the outcome of 39 consecutive carotid endarterectomy procedures performed by a single surgeon with emphasis on the safety of discharging patients the same day of the procedure. METHODS Retrospective analysis was performed over a two-year period on patients who were admitted as outpatients and underwent CEA. Following CEA, patients were observed for 4-6h in the recovery room and Duplex ultrasonography was completed to assess the endarterectomy repair. Determination was then made whether patients could be safely discharged home. RESULTS Over a two year period, CEA was performed 39 times in 37 outpatients. Twenty-five patients (64%) were discharged within 6h of surgery completion. The remaining 14 patients (36%) were admitted to the hospital for varying reasons. Six patients (43%) stayed either due to personal preference or the lack of supervision at home and six other patients (43%) stayed because of mild hemodynamic instability. Of the two remaining patients, one was admitted for chest pain and the other for a small wound hematoma. No patients developed postoperative neurologic deficits. Two-tailed Fisher test analysis of collected variables revealed that patients who had general anesthesia were more likely to be admitted (p<0.02). CONCLUSION Patients undergoing CEA can be safely discharged the same day after a brief period of postoperative observation. One factor that may predict the need for postoperative admission is the use of general anesthesia.

Volume Transmission-Mediated Protective Impact of Choroid Plexus-Cerebrospinal Fluid Growth Factors on Forebrain Ischemic Injury

Following brain or spinal cord ischemia, there is compensatory upregulation and distribution of many growth factors that contribute significantly to neuronal repair. Working homeostatically in concert with glial and cerebral endothelial cells, the epithelium of the choroid plexus secretes numerous peptides and proteins into the cerebrospinal fluid (CSF), which conveys these trophic factors, by volume transmission, to neurons at damage sites. Forebrain injury by transient global or focal ischemia results in considerable morbidity to choroid epithelial cells at the blood-CSF barrier; however, despite marked ischemic damage to the choroidal parenchyma, restorative processes ensure that the structural and functional integrity of this key transport interface is regained within several hours of interrupted blood flow. There is also an injury-induced elevation of growth factors in CSF and tissues bordering the cerebroventricular system. Our working hypothesis for the forebrain injury model is that the lateral choroid plexus-ventricular CSF system has an integral role in minimizing damage to adjacent regions, such as the hippocampus, by acting as a source in supplying trophic factors and as a sink in removing potentially deleterious metabolites. We marshal evidence that CSF-administered growth factors, delivered pre- as well as postischemia, attenuate neuronal damage or promote repair of injured brain and cord. Thus the choroid plexus, an expression source of numerous growth factors, is a useful protein- and CSF-generating organ for boosting growth factor availability to stressed neuropil regions.

Central fever as an early predictor of vasospasm in a child with isolated intraventricular hemorrhage

Cerebral vasospasm is a well-known complication of aneurysal subarachnoid hemorrhage (SAH) and can result in delayed schemic neurologic deficits. There are a few reports of intraentricular hemorrhage (IVH) leading to symptomatic vasospasm. owever, the majority of these cases are described in the setting f ruptured arteriovenous malformations (AVM) that are associted with subarachnoid blood [1,2,10,15]. Although several cases f vasospasm in patients with IVH and AVM without SAH have een reported in adults, only two cases in children have been pubished [13,17]. We describe the case of a young child who developed evere vasospasm associated with IVH (without SAH) and central evers and propose that vasospasm in this case was hypothalamially mediated. We would like to highlight that is it possible that fever of central origin could be an early sign of hypothalamic ysfunction and an early predictor of vasospasm in children with solated IVH.

Cerebellar pial arteriovenous malformations presenting with medullary venous hypertension: imaging and endovascular treatment

A patient in their 60s presented with headache and progressive lower extremity weakness over 1 week. Initial MRI was thought to represent venous hypertension secondary to a dural arteriovenous fistula. However, angiography revealed a cerebellar pial arteriovenous malformation with medullary venous hypertension. The imaging and endovascular treatment of this unusual case of a pial cerebellar arteriovenous malformation presenting in that manner is presented.

Atypical meningioma mimicking high-grade glioma.

A 52-year-old man presented following a motor vehicle collision. Examination revealed a Glasgow Coma Scale score of 15, with right lower extremity paresis. Noncontrast CT demonstrated a left frontal lesion. MRI further characterized the mass within the left superior frontal gyrus, suspicious for high-grade glioma (figure 1). Intraoperatively, the mass exhibited invasive margins, gross hypervascularity, and hemorrhage, without apparent dural attachment. Preliminary diagnosis was glial neoplasm. Final pathology was consistent with meningioma with focal brain invasion and rhabdoid differentiation, without anaplastic features, World Health Organization (WHO) grade II (figure 2). Outcome is correlated with WHO grade.1 Brain invasion is a new WHO diagnostic criterion of atypical meningioma.2

Cerebral Epidural Abscess Secondary to Blastomyces Masquerading as an Epidermoid Tumor

Abstract There have been infrequent reports of isolated central nervous system blastomycosis. We report a case of intracranial epidural abscess secondary to Blastomyces dermatitidis in a patient residing in Rhode Island with a history of remote travel to an endemic area. The clinical, radiographic, and pathologic features of this unique case are reviewed.

Trigeminal Neuralgia in the Rehabilitation Patient

Trigeminal neuralgia is a condition characterized by paroxysmal and lancinating pain of the face, within the distribution of the trigeminal nerve. The pain is often severe and debilitating to patients. Trigeminal neuralgia is most often caused by microvascular compression of the nerve root near the brainstem, resulting in demyelination and aberrant axonal firing. Here, we describe the clinical features, pathophysiology, diagnosis, and therapeutic modalities for the disease. While antiepileptic drugs are effective means of pain control in many patients, microsurgical exploration and decompression of the nerve in the posterior fossa is the treatment modality of choice for medically refractory cases due to its excellent long-term pain relief, low morbidity, and its nondestructive nature. Stereotactic radiosurgery is an effective and noninvasive treatment modality. Other treatment options include percutaneous rhizotomy.