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.

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.

Therapeutic embolization of arteriovenous malformations: the case for and against.

The field of endovascular therapy has demonstrated stunning technical achievements in AVM embolization. Embolization has the potential to enhance the safety and efficacy of AVM treatment when applied in carefully considered cases. The utility of embolization, at the present time, is limited by the fact that the procedure may be associated with disabling or fatal complications, and because complete or near-complete AVM nidus occlusion can be achieved only in a minority of cases. Because of these factors, embolization should not be considered a "standard-of-care" for the management of all cerebral AVMs, and careful case selection for embolization, with well-defined treatment goals in mind, is essential. Finally, not all AVMs that can be embolized should be embolized.

Assessment of the value of MR imaging for examining patients with angiographically negative subarachnoid hemorrhage.

OBJECTIVE: Our goal was to assess the value of MR imaging to patient care in the setting of angiographically negative subarachnoid hemorrhage and to evaluate the potential of MR imaging for revealing the mechanism for idiopathic perimesencephalic subarachnoid hemorrhage. MATERIALS AND METHODS: We retrospectively reviewed 71 patients who presented with subarachnoid hemorrhage and in whom the results of a four-vessel cerebral arteriogram were negative, a CT scan showed no evidence of intraaxial hemorrhage, and MR imaging had been performed within 72 hr of presentation. MR imaging of the brain included sagittal spin-echo T1-weighted, turbo spin-echo proton density-weighted, T2-weighted, and axial T2-weighted gradient-echo sequences. MR imaging of the cervical spine, which was performed in 41 of the 71 patients, included sagittal spin-echo T1-weighted, turbo spin-echo proton density-weighted, T2-weighted, and axial T2-weighted gradient-echo sequences. RESULTS: Perimesencephalic subarachnoid hemorrhage was seen on CT in 25 patients; in four of these patients (16%), MR imaging revealed acute perforator territory infarction involving the caudate, putamen, or thalamus. In 26 other patients, nonperimesencephalic subarachnoid hemorrhage was revealed on CT; in two of these patients (8%), MR imaging showed the cause of the subarachnoid hemorrhage. By contrast, 20 patients had negative findings on CT scans but xanthochromic CSF on lumbar puncture; in two of these patients (10%), MR findings were interpreted as responsible for subarachnoid hemorrhage. CONCLUSION: MR imaging showed diagnostic value in patients with angiographically negative subarachnoid hemorrhage, revealing abnormalities in 14% of the 71 patients, and resulted in a significant change in patient treatment in 6% of the patients. MR imaging also revealed an association between perimesencephalic subarachnoid hemorrhage and infarcts involving the territory of perforating arteries at the base of the brain. This finding may provide insight into the pathogenesis of perimesencephalic subarachnoid hemorrhage.

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.

Posttraumatic cerebral arterial spasm.

Posttraumatic cerebral arterial spasm (vasospasm) has been demonstrated in the past by angiography, and recently by transcranial Doppler ultrasonography. Posttraumatic vasospasm is a delayed complication that involves the large basal intracranial arteries (e.g., internal carotid, middle cerebral, basilar) and occurs in 25-40% of head trauma patient. The time course of posttraumatic vasospasm resembles that of vasospasm associated with aneurysmal subarachnoid hemorrhage with onset occurring 2 or more days after injury. A study of the relationship of admission CT scan findings to the incidence of vasospasm suggests that intradural bleeding, which extends into the CSF (subarachnoid, intraventricular, and subdural hemorrhage), plays a role in the pathogenesis of posttraumatic arterial spasm. The preliminary results of a large prospective study of head trauma patients suggest that vasospasm may be an important determinant of outcome from severe head injury.

Cerebral blood flow measurement in neurosurgical intensive care.

This article has addressed the rationale for the clinical measurement of CBF in the neuro-surgical ICU. The techniques that are currently available for measurement of CBF have been reviewed, and those that are particularly appropriate for ICU use have been highlighted. Several examples of the role of CBF monitoring in the management of ICU patients have been described, and these clinical situations are considered further in other articles in this issue regarding the management of patients with head injury and subarachnoid hemorrhage. These CBF monitoring techniques should be integrated with TCD and cerebral metabolism monitoring as described elsewhere in this issue. With further clinical experience and research and development in the area of neurosurgical critical care, CBF monitoring is almost certainly destined to become a routine and widely employed technique.

Metabolic alterations accompany ionic disturbances and cellular swelling during a hypoxic insult to the retina: an in vitro study.

To study the ionic, metabolic, and morphologic derangements that occur following brain injury we utilized a retina in vitro model of hypoxia. Retinas were dissected into oxygenated (95% O2, 5% CO2) Ames medium, a physiologic solution resembling cerebrospinal fluid, and randomly assigned to either experimental hypoxic conditions (95% N2, 5% CO2) or control conditions. All retinas were incubated and maintained at 37 degrees C. Changes in extracellular K+ and lactate concentration, intracellular incorporation of 45Ca and 14C-leucine, uptake of glucose using [14C]-2-deoxy-D-glucose (2DG), and cell size were determined at 10, 20, 30, and 60 minute time intervals. The results show that compared to control retinas hypoxia produced: (1) an early increase in extracellular concentration of K+ and lactate, (2) a delayed increase in the intracellular incorporation of 45Ca, (3) an early onset of cellular swelling, and (4) a decrease in the intracellular incorporation of 14C-leucine, and (5) increased glucose utilization. All of the results were statistically significant (p < 0.05) and exhibited a dose response relationship with the exception of intracellular incorporation of 45Ca which did not become significantly different until 30 minutes post-hypoxia. A 16% increase in cell size was noted after 10 minutes of hypoxia. Increased hypoxic cell size persisted for 30 minutes but after 60 minutes the control retinas appeared enlarged as well. Our results suggest that ionic, metabolic, and morphologic derangements can be demonstrated utilizing an in vitro model of hypoxia which are similar to those seen following in vivo traumatic brain injury. With use of this model the mechanisms behind these ionic-metabolic relationships can be addressed at the molecular level.

Clinical considerations in the reduction of secondary brain injury.

Craniocerebral trauma renders the brain vulnerable to a variety of secondary insults that must be prevented or promptly corrected before irreversible neurologic damage occurs. These secondary insults can include hypoxia, ischemia, or both, which result in significant cell loss. The trauma-induced state of vulnerability appears to be due to cellular ionic and metabolic alterations that make up the basic physiologic sequelae after brain injury. We discuss clinical aspects regarding these potentially devastating injuries in an effort to enhance their recognition and aid in their management.

Posttraumatic cerebral arterial spasm: transcranial Doppler ultrasound, cerebral blood flow, and angiographic findings.

Thirty patients admitted after suffering closed head injuries, with Glasgow Coma Scale scores ranging from 3 to 15, were evaluated with transcranial Doppler ultrasound monitoring. Blood flow velocity was determined in the middle cerebral artery (MCA) and the intracranial portion of the internal carotid artery (ICA) in all patients. Because proximal flow in the extracranial ICA declines in velocity when arterial narrowing becomes hemodynamically significant, the extracranial ICA velocity was concurrently monitored in 19 patients. To assess cerebral perfusion, cerebral blood flow (CBF) measurements obtained with the intravenous 133Xe technique were completed in 16 patients. Vasospasm, designated as MCA velocity exceeding 120 cm/sec, was found in eight patients (26.7%). Severe vasospasm, defined as MCA velocity greater than 200 cm/sec, occurred in three patients, and was confirmed by angiography in all three. Subarachnoid hemorrhage (SAH) was documented by computerized tomography in five (62.5%) of the eight patients with vasospasm. All cases of severe vasospasm were associated with subarachnoid blood. The time course of vasospasm in patients with traumatic SAH was similar to that found in patients with aneurysmal SAH; in contrast, arterial spasm not associated with SAH demonstrated an uncharacteristically short duration (mean 1.25 days), suggesting that this may be a different type of spasm. A significant correlation (p less than 0.05) was identified between the lowest CBF and highest MCA velocity in patients during the period of vasospasm, indicating that arterial narrowing can lead to impaired CBF. Ischemic brain damage was found in one patient who had evidence of cerebral infarction in the territories supplied by the arteries affected by spasm. These findings demonstrate that delayed cerebral arterial spasm is a frequent complication of closed head injury and that the severity of spasm is, in some cases, comparable to that seen in aneurysmal SAH. This experience suggests that vasospasm is an important secondary posttraumatic insult that is potentially treatable.

Cystic neoplasms of the pancreas.

Cystic neoplasms of the pancreas can be easily misdiagnosed and mistreated by the surgeon unfamiliar with the pathology, natural history, and operative strategy specific to these uncommon tumors. The authors have treated nine patients over a seven-year period involving four cystadenocarcinomas, two mucinous cystadenomas, two serous cystadenomas, and one solid and papillary epithelial tumor. Our experience illustrates the inaccuracies in both clinical and pathologic diagnosis. Suspected cystic neoplasms are optimally managed by resection. Their slow growth and late metastasis permits curative surgery after a previous drainage or bypass procedure. An aggressive surgical approach is therefore warranted, and multimodal treatment with radiation and chemotherapy may be clinically applicable to large, invasive cystadenocarcinomas.

Group B beta-hemolytic streptococcal osteomyelitis of the heel. A case report.

Staphylococcus aureus is the most frequently reported, though not the only, causative organism in children who have osteomyelitis. In an 11-year-old child with osteomyelitis of the calcaneus, the etiologic agent was identified as a Group B beta-hemolytic streptococcal organism. This organism seems not to have been previously reported as the cause of osteomyelitis in the heel.