Use of single versus multiple vasodilator agents in the treatment of cerebral vasospasm: is more better than less?

BACKGROUND: Patients with cerebral vasospasm caused by aneurysmal subarachnoid hemorrhage (aSAH) are often treated with intra-arterial (IA) vasodilator infusion. However, the optimal drug regimen is yet to be elucidated. METHODS: A retrospective review of patients with aSAH and cerebral vasospasm treated with IA vasodilator infusion was performed. Patients in group 1 (2008-2011) were treated with a single agent, either nicardipine or verapamil, and patients in group 2 (2010-2016) were treated with a regimen of nitroglycerin, verapamil, and nicardipine. The post-infusion improvement ratio (PIIR) was compared between groups. Adjusted multivariate logistic regression models were utilized to determine whether patients treated with multiple vasodilators had an improved functional outcome, defined by the modified Rankin Scale, at discharge and 90-day follow-up. RESULTS: Among 116 patients from group 1 (N = 47) and group 2 (N = 69), the median age was 54.5 years [IQR, 46-53 years] and 78% were female. Use of multiple-agent therapy resulted in a 24.36% improvement in vessel diameter over single-agent therapy (median PIIR: group 1, 10.5% [IQR, 5.3-21.1%] vs group 2, 34.9% [IQR, 21.4-66.0%]; p < 0.0001). In the adjusted multivariate logistic regression, the use of multiple-agent therapy was associated with a better functional outcome at discharge (OR 0.15, 95% CI [0.04-0.55]; p < 0.01) and at 90-day follow-up (OR 0.20, 95% CI [0.05-0.77]; p < 0.05) when compared to single-agent therapy. CONCLUSION: In this study, we found that patients treated for cerebral vasospasm with IA infusion of multiple vasodilators had an increased vessel response and better functional outcomes compared to those treated with a single agent.

Large-Scale Network Analysis of Whole-Brain Resting-State Functional Connectivity in Spinal Cord Injury: A Comparative Study.

Network analysis based on graph theory depicts the brain as a complex network that allows inspection of overall brain connectivity pattern and calculation of quantifiable network metrics. To date, large-scale network analysis has not been applied to resting-state functional networks in complete spinal cord injury (SCI) patients. To characterize modular reorganization of whole brain into constituent nodes and compare network metrics between SCI and control subjects, fifteen subjects with chronic complete cervical SCI and 15 neurologically intact controls were scanned. The data were preprocessed followed by parcellation of the brain into 116 regions of interest (ROI). Correlation analysis was performed between every ROI pair to construct connectivity matrices and ROIs were categorized into distinct modules. Subsequently, local efficiency (LE) and global efficiency (GE) network metrics were calculated at incremental cost thresholds. The application of a modularity algorithm organized the whole-brain resting-state functional network of the SCI and the control subjects into nine and seven modules, respectively. The individual modules differed across groups in terms of the number and the composition of constituent nodes. LE demonstrated statistically significant decrease at multiple cost levels in SCI subjects. GE did not differ significantly between the two groups. The demonstration of modular architecture in both groups highlights the applicability of large-scale network analysis in studying complex brain networks. Comparing modules across groups revealed differences in number and membership of constituent nodes, indicating modular reorganization due to neural plasticity.

Persistent Hypotension and Cerebral Swelling Resulting From Mesenteric Traction Syndrome After Omental-to-Pial Pedicle Flap Transfer in a Young Woman With Refractory Moyamoya Disease: A Case Report.

Superficial temporal arterial to middle cerebral arterial anastomosis is often the initial surgical treatment of Moyamoya disease. In refractory cases, placing a pedicle flap of omentum over the ischemic brain has resulted in clinical improvement or stabilization of symptoms. We present a case of persistent mesenteric traction syndrome manifested by hypotension unresponsive to conventional doses of vasopressors during and after pulling the omentum to the brain. As prostacyclin is a major mediator of hypotension from mesenteric traction syndrome and also a cerebral vasodilator, we discuss the possibility that brain swelling may be a manifestation of mesenteric traction syndrome.

Evaluation of Whole-Brain Resting-State Functional Connectivity in Spinal Cord Injury: A Large-Scale Network Analysis Using Network-Based Statistic.

Large-scale network analysis characterizes the brain as a complex network of nodes and edges to evaluate functional connectivity patterns. The utility of graph-based techniques has been demonstrated in an increasing number of resting-state functional MRI (rs-fMRI) studies in the normal and diseased brain. However, to our knowledge, graph theory has not been used to study the reorganization pattern of resting-state brain networks in patients with traumatic complete spinal cord injury (SCI). In the present analysis, we applied a graph-theoretical approach to explore changes to global brain network architecture as a result of SCI. Fifteen subjects with chronic (> 2 years) complete (American Spinal Injury Association [ASIA] A) cervical SCI and 15 neurologically intact controls were scanned using rs-fMRI. The data were preprocessed followed by parcellation of the brain into 116 regions of interest (ROI) or nodes. The average time series was extracted at each node, and correlation analysis was performed between every pair of nodes. A functional connectivity matrix for each subject was then generated. Subsequently, the matrices were averaged across groups, and network changes were evaluated between groups using the network-based statistic (NBS) method. Our results showed decreased connectivity in a subnetwork of the whole brain in SCI compared with control subjects. Upon further examination, increased connectivity was observed in a subnetwork of the sensorimotor cortex and cerebellum network in SCI. In conclusion, our findings emphasize the applicability of NBS to study functional connectivity architecture in diseased brain states. Further, we show reorganization of large-scale resting-state brain networks in traumatic SCI, with potential prognostic and therapeutic implications.

Hemorrhagic Complications Associated with Ventriculostomy in Patients Undergoing Endovascular Treatment for Intracranial Aneurysms: A Single-Center Experience.

BACKGROUND: Currently, a complete understanding of post-ventriculostomy hemorrhagic complications in subarachnoid hemorrhage due to ruptured aneurysms remains unknown. The present study evaluates the impact of periprocedural risk factors on rates of external ventricular drain (EVD)-associated hemorrhage in the setting of endovascular treatment of intracranial aneurysms. METHODS: A retrospective chart review of 107 patients who underwent EVD placement within 24 h of endovascular coiling was performed. CT of head without contrast was obtained after drain placement and before endovascular treatment. Post-procedural CT was also obtained within 48 h of embolization and was reviewed for new/worsened track hemorrhages. Chi-squared test was used in evaluation. RESULTS: Ninety-three of the 107 patients reviewed met the inclusion criteria. Four (25%) of the 16 patients on antiplatelet medications at presentation experienced post-EVD hemorrhage compared to 11 (14.3%) of 77 that were not (p = 0.29). Of the 13 patients given intraprocedural antiplatelets, 3 (23.1%) demonstrated hemorrhage compared to 12 (15%) of 80 not administered these medications (p = 0.46). Further, of 36 patients with intraprocedural anticoagulation, 6 (16.7%) exhibited hemorrhage compared to 9 (15.8%) of 57 in those without (p = 0.91). In 17 patients who received DVT prophylaxis, 2 (11.8%) exhibited hemorrhage compared to 13 (17.1%) of 76 who did not (p = 0.59). No post-EVD hemorrhage had attributable neurologic morbidity. CONCLUSION: Our results, demonstrating no significant risk factor related to EVD-associated hemorrhage rates, support the safety of EVD placement in the peri-endovascular treatment period.

Transnasal Penetration of a Ballpoint Pen: Case Report and Review of Literature.

BACKGROUND: Transnasal penetration by a nonmissile foreign body is a rare injury. Consequently, appropriate management remains controversial. We report a case of transnasal penetration by a ballpoint pen and review the literature. To our knowledge, this is the first living patient who sustained carotid artery damage from a transnasal penetrating intracranial injury. CASE DESCRIPTION: A 56-year-old female presented with a ballpoint pen lodged through her left nostril. She exhibited right cranial nerve palsies (III, IV, VI, and V1). A computed tomography (CT) scan of the head revealed a foreign body in the left nasal cavity traversing the ethmoid/sphenoid and likely through the right superior orbital fissure and cavernous sinus, with the distal tip adjacent to the right atrium. CT angiography revealed nonopacification of the right internal carotid artery (ICA) from the mid-petrous segment to the ophthalmic segment. Subsequently, she underwent coil embolization of the proximal right ICA, followed by a right frontotemporal craniotomy with anterior temporal lobectomy to skeletonize the pen and right distal ICA, and finally clipping of the ICA distal to the pen and prompt transnasal endoscopic removal of the pen. There were no hemorrhagic complications. She awoke at her neurologic preoperative baseline. CONCLUSION: Injuries such as the one described here should be managed through a multidisciplinary approach. The trajectory of the foreign body should be delineated through CT imaging, along with vascular imaging if appropriate. If there are signs of vascular injury, then attempts to maintain proximal and distal control are prudent to avoid hemorrhagic complications. This combined endovascular-endoscopic-open craniotomy approach has not been reported previously in the literature.

Alterations in Cortical Sensorimotor Connectivity following Complete Cervical Spinal Cord Injury: A Prospective Resting-State fMRI Study.

Functional magnetic resonance imaging (fMRI) studies have demonstrated alterations during task-induced brain activation in spinal cord injury (SCI) patients. The interruption to structural integrity of the spinal cord and the resultant disrupted flow of bidirectional communication between the brain and the spinal cord might contribute to the observed dynamic reorganization (neural plasticity). However, the effect of SCI on brain resting-state connectivity patterns remains unclear. We undertook a prospective resting-state fMRI (rs-fMRI) study to explore changes to cortical activation patterns following SCI. With institutional review board approval, rs-fMRI data was obtained in eleven patients with complete cervical SCI (>2 years post injury) and nine age-matched controls. The data was processed using the Analysis of Functional Neuroimages software. Region of interest (ROI) based analysis was performed to study changes in the sensorimotor network using pre- and post-central gyri as seed regions. Two-sampled t-test was carried out to check for significant differences between the two groups. SCI patients showed decreased functional connectivity in motor and sensory cortical regions when compared to controls. The decrease was noted in ipsilateral, contralateral, and interhemispheric regions for left and right precentral ROIs. Additionally, the left postcentral ROI demonstrated increased connectivity with the thalamus bilaterally in SCI patients. Our results suggest that cortical activation patterns in the sensorimotor network undergo dynamic reorganization following SCI. The presence of these changes in chronic spinal cord injury patients is suggestive of the inherent neural plasticity within the central nervous system.

Resection of a recurrent cervical internal carotid artery pseudoaneurysm after failed endovascular therapy.

BACKGROUND: Recurrence of a cervical internal carotid artery (ICA) pseudoaneurysm initially treated by endovascular means is rare. We report an instance where a patient returned with a recurrent, enlarging cervical ICA pseudoaneursym, 15 years after initial complete, endovascular occlusion of the ICA. CASE DESCRIPTION: Patient is a 64-year-old male with a history of a right cervical ICA pseudoaneurysm diagnosed 15 years ago after a car accident. At the time, he received endovascular occlusion of his right ICA. Recent serial imaging demonstrated progressive enlargement of his pseudoaneurysm, up to 6 cm × 5 cm × 5.5 cm, without evidence of internal flow or extravasation. Due to dysphagia and hoarseness, resection of the pseudoaneurysm was recommended. Dissection occurred down to the lesion, where its borders were skeletonized. Its stump at the proximal ICA was mobilized and clamped; the lesion was incised and the existing thrombus, as well as the coil mass, was removed. The distal ICA appeared completely scarred with no retrograde filling. There were branches from the external carotid artery that appeared to supply the pseudoaneurysm. The scarred remnant of the distal ICA was sutured and the stump at the proximal ICA was ligated. Once hemostasis was obtained, closure occurred via anatomical layers. Postoperatively, the patient woke up well; at discharge, he exhibited no respiratory distress or dysphagia. At 5 months follow-up, a computed tomography angiography of the neck revealed no evidence for a residual pseudoaneurysm. He continues on lifelong aspirin. CONCLUSION: Recurrence of a cervical ICA pseudoaneursym is rare. We caution that such a clinical scenario is possible, even 15 years after endovascular occlusion of the ICA. Branches from the external carotid artery may feed the pseudoaneursym and cause recurrence. This mechanism has not been reported. Perhaps longer clinical follow-up is necessary, especially if endovascular therapy is the initial treatment option.

Temporal neocortical origin of pilomotor seizures in association with an infiltrating glioma: a case confirmed by intracranial electroencephalography monitoring.

Patients with seizures occasionally present with autonomic symptoms. Pilomotor seizures are uncommon and usually accompanied by other manifestations of complex partial seizures of limbic origin. Activation of the central autonomic network appears to be necessary for the development of ictal goose bumps. Pilomotor seizures have been reported to originate in the temporal lobe and other medial limbic structures. Ictal piloerection can arise due to a variety of brain pathologies. Isolated pilomotor seizures are very rare. The authors present the first case in which intracranial electroencephalography monitoring was used to confirm pilomotor seizures of temporal neocortical origin in association with an infiltrating tumor.

Abnormal glutamate receptor expression in the medial temporal lobe in schizophrenia and mood disorders.

Pharmacological and anatomical evidence suggests that abnormal glutamate neurotransmission may be associated with the pathophysiology of schizophrenia and mood disorders. Medial temporal lobe structural alterations have been implicated in schizophrenia and to a lesser extent in mood disorders. To comprehensively examine the ionotropic glutamate receptors in these illnesses, we used in situ hybridization to determine transcript expression of N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and kainate receptor subunits in the medial temporal lobe of subjects with schizophrenia, bipolar disorder (BD), or major depression (MDD). We used receptor autoradiography to assess changes in glutamate receptor binding in the same subjects. Our results indicate that there are region- and disorder-specific abnormalities in the expression of ionotropic glutamate receptor subunits in schizophrenia and mood disorders. We did not find any changes in transcript expression in the hippocampus. In the entorhinal cortex, most changes in glutamate receptor expression were associated with BD, with decreased GluR2, GluR3, and GluR6 mRNA expression. In the perirhinal cortex we detected decreased expression of GluR5 in all three diagnoses, of GluR1, GluR3, NR2B in both BD and MDD, and decreased NR1 and NR2A in BD and MDD, respectively. Receptor binding showed NMDA receptor subsites particularly affected in the hippocampus, where MK801 binding was reduced in schizophrenia and BD, and MDL105,519 and CGP39653 binding were increased in BD and MDD, respectively. In the hippocampus AMPA and kainate binding were not changed. We found no changes in the entorhinal and perirhinal cortices. These data suggest that glutamate receptor expression is altered in the medial temporal lobe in schizophrenia and the mood disorders. We propose that disturbances in glutamate-mediated synaptic transmission in the medial temporal lobe are important factors in the pathophysiology of these severe psychiatric illnesses.