Hyperacute Vasospasm After Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Cerebral vasospasm after aneurysmal subarachnoid hemorrhage typically occurs 3-14 days after aneurysm rupture. We describe a series of patients who developed vasospasm within minutes of aneurysm rupture. This phenomenon, which we term, "hyperacute vasospasm," has been reported in animal models of SAH, but hitherto has been poorly described in humans. METHODS: Eleven patients were identified from an institutional registry who had aneurysmal rupture during catheter cerebral angiography between 1997 and 2009. We quantified the degree of vasoconstriction using vascular diameter index (VDI). The change in VDI (delta VDI or DVDI) was calculated by determining the difference in VDI before and after the procedure. We also examined the relationship between hyperacute vasospasm and delayed cerebral ischemia. RESULTS: Ten of eleven (91%) patients with intraoperative aneurysm rupture had cerebral vasoconstriction within minutes of intra-procedural aneurysmal rupture. Six of eleven patients (55%) with hyperacute vasospasm developed delayed cerebral infarction. CONCLUSIONS: Hyperacute vasospasm is likely common in patients with intraoperative aneurysm rupture and may be an unrecognized element of the natural history of aneurysmal subarachnoid hemorrhage. In this limited series, there was an association between hyperacute vasospasm and delayed cerebral infarction.

Cumulative radiation dose in patients admitted with subarachnoid hemorrhage: a prospective study using a self-developing film badge.

BACKGROUND AND PURPOSE: While considerable attention has been directed to reducing the x-ray dose of individual imaging studies, there is little information available on the cumulative dose during imaging-intensive hospitalizations. We used a radiation-sensitive badge on 12 patients admitted with SAH to determine if this approach was feasible and to measure the extent of their x-ray exposure. MATERIALS AND METHODS: After obtaining informed consent, we assigned a badge to each of 12 patients and used it for all brain imaging studies during their ICU stay. Cumulative dose was determined by quantifying exposure on the badge and correlating it with the number and type of examinations. RESULTS: The average skin dose for the 3 patients who had only diagnostic DSA without endovascular intervention was 0.4 Gy (0.2-0.6 Gy). The average skin dose of the 8 patients who had both diagnostic DSA and interventions (eg, intra-arterial treatment of vasospasm and coiling of aneurysms) was 0.9 Gy (1.8-0.4 Gy). One patient had only CT examinations. There was no effort made to include or exclude the badge in the working view during interventions. CONCLUSIONS: It is feasible to incorporate a film badge that uses a visual scale to monitor the x-ray dose into the care of hospitalized patients. Cumulative skin doses in excess of 1 Gy were not uncommon (3/12) in this group of patients with acute SAH. This approach could provide a measure of the cumulative dose and is a convenient tool to quantify the effect of dose-reduction strategies.

Endovascular treatment of unruptured intracranial aneurysms in the elderly: analysis of procedure related complications.

INTRODUCTION: The management of unruptured intracranial aneurysms in the elderly remains controversial. Treatment risks are thought to be higher in this group. Large series assessing endovascular treatment of unruptured intracranial aneurysms in the elderly are lacking. Our single center endovascular experience in treating unruptured intracranial aneurysms in the elderly is presented. METHODS: 77 patients, 70 years or older, were referred to the endovascular neurosurgery service for treatment of an unruptured intracranial aneurysm between February 2000 and May 2008. Hospital records, operative reports, angiograms and radiology reports were reviewed and analyzed retrospectively. RESULTS: 99 aneurysms were treated in 77 patients in 102 procedures. Mean patient age was 75±4 years, and the average aneurysm size was 11±7 mm. Adjuvant techniques were used in 66% of cases. Endovascular procedures included coiling alone (32%), balloon assisted coiling (19%), stent assisted coiling (37%), balloon assisted stent and coiling (8%), stent only (1%) and glue (2%). The permanent morbidity and mortality rates were 1% and 3%, respectively. Four adverse events were attributed to the patient's age. Posterior circulation aneurysms were associated with more adverse events (41%) than anterior circulation aneurysms (14%). Endovascular treatments using adjuvant techniques were associated with a higher complication rate than coiling alone. CONCLUSIONS: With only a 4% permanent rate of neurological morbidity and mortality, endovascular treatment of unruptured aneurysms can be performed safely in the elderly. Age should not be the limiting factor when considering endovascular therapy.

Neuroprotective effect of hypothermia on neuronal injury in diffuse traumatic brain injury coupled with hypoxia and hypotension.

It is well established in mechanical head trauma that posttraumatic secondary insults, such as hypoxia and hypotension exacerbate neuronal injury and lead to worse outcome. In this study, the neuroprotective effect of hypothermia on the reduction of supraventricular subcortical neuronal damage was evaluated using an impact-acceleration model of diffuse traumatic brain injury coupled with both moderate and severe periods of hypoxia and hypotension. A total of 135 adult male Sprague-Dawley rats (340-375 g) were divided into three experimental studies: (I) physiological evaluation (n = 36); (II) quantitative analysis of the effect of trauma coupled with moderate and severe hypotension on neuronal damage assessed at 4 (n = 39) and 24 h (n = 24); and (III) the neuroprotective effect of hypothermia following moderate secondary insult (n = 36). Induction of hypothermia occurred at 15 min postinjury, to a level of 30 degrees C for 60 min. At the designated time points (4 and 24 h), the animals were sacrificed via standard transcardial perfusion techniques for histological processing. Quantitative assessment of neuronal damage using routine H&E staining at 4 hours showed neuronal damage which correlated with the severity of secondary insult. Animals exposed to trauma alone had a mean number of damaged neurons of 7.61 +/- 3.08/high powered field (hpf) compared with a mean of 1.21 +/- 0.30/hpf in the sham operated group (p = 0.015). Animals exposed to trauma with 10 min of hypoxia and hypotension (THH-10) showed a statistically significant number of damaged neurons compared to the sham-operated animals (7.50 +/- 2.15 damaged neurons/hpf, p = 0.013), whereas, neuronal damage in animals undergoing trauma with a 30-min secondary insult of hypoxia and hypotension (THH-30) was markedly increased (100 +/- 30.20/hpf, p = 0.002). Statistical analysis showed no significant difference in neuronal damage in animals subjected to secondary insult alone. At 24 h, the evolution of neuronal damage in the trauma alone group (5.08 +/- 1.63/hpf) was relatively static; however, there was a remarkable increase in the neuronal damage of the THH-10 group (29.88 50 +/- 8.20/hpf). However, hypothermia provided nearly complete protection against secondary insults, and neuronal damage was equal to that of the trauma alone group (p = 0.42). The results of this study confirm that hypothermia provides remarkable protection against the adverse effects of neuronal damage exacerbated by secondary injury. This study also presents a new model of secondary insult, which can be used experimentally to further define the mechanism of increased vulnerability of the injured brain.

Evaluation of homeostatic changes in CSF circulation: in vivo analysis of the effect of neurotransmitter accumulation in the extracellular space following transient global ischemia.

Accumulation of potassium and excitatory amino acids (EAA) in the extracellular space (ECS) following ischemia has been well documented. Careful monitoring of these transients is crucial to gain a better understanding of CNS pathophysiology. This study was initiated to determine if CSF concentrations of EAAs reflect those measured in the ECS. Transient global ischemia, 20 minutes in duration, was produced by clamping the left subclavian and innominate arteries combined with hemorrhagic hypotension. The accumulation of glutamate and electrolytes were measured in CSF and the extracellular fluid (ECF) of cerebral cortex. Microdialysis (MD) was utilized to measure the extracellular concentrations while direct sampling of CSF was provided via cannulation of the cisterna magna. Hydrogen clearance and laser doppler methods were used to monitor regional cortical CBF. Our results show that extracellular concentrations of potassium ([K+]ECF) and glutamate significantly increased following the initiation of ischemia (p < 0.05). The extracellular concentration of these substances decreased with the restoration of CBF. In CSF, a similar trend was observed following re-circulation (p < 0.05). However, CSF glutamate levels did not return to pre-ischemic values.