Malignant Middle Cerebral Artery Infarction Due to Hyponatremia Following Traumatic Brain Injury: A Case Report.

BACKGROUND Development of syndrome of inappropriate antidiuretic hormone secretion or cerebral salt wasting has been commonly noted in post-traumatic brain injury, and this condition may lead to hyponatremia resulting in cerebral edema and possible cerebral herniation. However, the predominant topographic pattern of edema from hyponatremia has not been well documented. Unlike numerous reports on hyponatremia and vasospasm following aneurysmal subarachnoid hemorrhage, the data for traumatic brain injury patient are still limited. We report on a rare patient with malignant middle cerebral artery infarction as a result of hyponatremia following traumatic brain injury. CASE REPORT A 60-year-old Native American male with significant past medical history of alcoholism, hypertension, and hemorrhagic stroke presented to the emergency department by emergency medical service after he was struck by a vehicle in a hit-and-run incident. The patient sustained multiple abrasions, and he had elevated alcohol levels. His initial Glasgow Coma Score (GCS) was 14 with a confused conversation (V4). Computer tomography (CT) of the head showed 5 mm thickness acute subdural and subarachnoid hemorrhage of right frontal, temporal, and parietal areas, with 3 mm midline shift at the level of foramen of Monro. Traumatic brain injury conservative treatment was initiated as well as alcoholic withdrawal protocols in the intensive care unit. Patient initially improved neurologically despite low sodium levels. He recouped to fully conscious, with a GCS score of 15, at 24 hours after admission. On day 9, he was found unresponsive with a head CT showed malignant right middle cerebral artery infarction, resulted in 15 mm subfalcine herniation. The patient passed away 48 hours later, as patient's family declined further intervention. CONCLUSIONS The management and prevention of post-traumatic vasospasm may be complicated even in asymptomatic and neurologically intact patients. Close neurological monitoring and prevention protocols are important in activating appropriate management.

Artery of Percheron infarction results in severe bradycardia: A case report.

BACKGROUND: The thalamus is normally supplied by each posterior cerebral artery (PCA). The artery of percheron is a variant of this anatomy as it arises as a single trunk unilaterally from the PCA to supply the thalamus bilaterally. Occlusion of this artery is rare, and the diagnosis is usually missed without obtaining an MRI. CASE DESCRIPTION: We illustrate the case of a 68-year-old male who presented with coma, ocular gaze palsy, and severe bradycardia from bilateral thalamic nuclei and midbrain infarction, as described as an artery of Percheron infarction. The patient recovered neurologically under conservative treatment with a residual vertical diplopia from downward gaze palsy. He underwent cardiac pacer implantation for severe bradycardia at the end of his admission. The thalamic pathway associated with cardiac rhythm, especially the zona inserta, is discussed. Publications related to the artery of Percheron are reviewed. CONCLUSION: Coma and ocular gaze palsy are the most common presentations following thalamic and midbrain ischemia from artery of Percheron infarction. To our knowledge, only a single case of artery of Percheron infarction with severe bradycardia has been reported in the past. Our case attested the role of thalamic nuclei controlling cardiac rhythm.

Indications, technique, and safety profile of insular stereoelectroencephalography electrode implantation in medically intractable epilepsy.

OBJECTIVE Insular epilepsy is relatively rare; however, exploring the insular cortex when preoperative workup raises the suspicion of insular epilepsy is of paramount importance for accurate localization of the epileptogenic zone and achievement of seizure freedom. The authors review their clinical experience with stereoelectroencephalography (SEEG) electrode implantation in patients with medically intractable epilepsy and suspected insular involvement. METHODS A total of 198 consecutive cases in which patients underwent SEEG implantation with a total of 1556 electrodes between June 2009 and April 2013 were reviewed. The authors identified patients with suspected insular involvement based on seizure semiology, scalp EEG data, and preoperative imaging (MRI, PET, and SPECT or magnetoencephalography [MEG]). Patients with at least 1 insular electrode based on the postoperative 3D reconstruction of CT fused with the preoperative MRI were included. RESULTS One hundred thirty-five patients with suspected insular epilepsy underwent insular implantation of a total of 303 electrodes (1-6 insular electrodes per patient) with a total of 562 contacts. Two hundred sixty-eight electrodes (88.5%) were implanted orthogonally through the frontoparietal or temporal operculum (420 contacts). Thirty-five electrodes (11.5%) were implanted by means of an oblique trajectory either through a frontal or a parietal entry point (142 contacts). Nineteen patients (14.07%) had insular electrodes placed bilaterally. Twenty-three patients (17.04% of the insular implantation group and 11.6% of the whole SEEG cohort) were confirmed by SEEG to have ictal onset zones in the insula. None of the patients experienced any intracerebral hemorrhage related to the insular electrodes. After insular resection, 5 patients (33.3%) had Engel Class I outcomes, 6 patients (40%) had Engel Class II, 3 patients (20%) had Engel Class III, and 1 patient (6.66%) had Engel Class IV. CONCLUSIONS Insula exploration with stereotactically placed depth electrodes is a safe technique. Orthogonal electrodes are implanted when the hypothesis suggests opercular involvement; however, oblique electrodes allow a higher insular sampling rate.

Intracranial Cystic Myofibroblastoma: a Case Report with Literature Review.

BACKGROUND: Myofibroblastoma is a rare benign soft tissue tumor comprised of contractile myiod cells mostly in mammary gland. Only 4 prior cases arising in the central nervous system have been reported in the literature. We present a case of myofibroblastoma with a cystic component. CASE DESCRIPTION: The patient is a 76-year-old man with a history of Parkinson disease. The tumor was found incidentally after a minor fall. Magnetic resonance imaging revealed a 6.7-cm well-circumscribed, partly cystic mass with a 2.4-cm calcified central nodule located at the left sylvian fissure. The frontal dural base showed avid enhancing after gadolinium injection. Gross total resection was achieved. The tumor was marked by dense collagenous tissue and bland spindled cells in pathology review. The spindled cells demonstrated positive staining with antibodies to CD34, estrogen receptor, and smooth muscle actin. A blush of immunoreactivity is observed in scattered cells with antibody to progesterone receptor. Patient recovered well postoperatively. CONCLUSIONS: This is a rare condition of a benign soft tissue tumor of mammary gland presented primarily in the brain. The literature on myofibroblastomas arising in the central nervous system is reviewed.

Stereo-Electro-Encephalo-Graphy (SEEG) With Robotic Assistance in the Presurgical Evaluation of Medical Refractory Epilepsy: A Technical Note.

SEEG is a method and technique which is used for accurate, invasive recording of seizure activity via three dimensional recordings. In epilepsy patients who are deemed appropriate candidates for invasive recordings, the decision to monitor is made between the subdural grids versus SEEG. Invasive neuromonitoring for epilepsy is pursued in patients with complex, medically refractory epilepsy. The goal of invasive monitoring is to offer resective surgery with the hope of allowing seizure freedom. SEEG's advantages include access to deep cortical structures, an ability to localize the epileptogenic zone (EZ) when subdural grids have failed to do so, and in patients with non-lesional extra-temporal epilepsies. In this manuscript, we present a succinct historical overview of the SEEG and report on our experience with frameless stereotaxy under robotic. An imperative step of SEEG insertion is planning the electrode trajectories. In order to most effectively record ictal activity via SEEG trajectories should be planned based upon a hypothesis of where the seizure activity originates the presumed epileptogenic zone (EZ). The EZ hypothesis is based on a standardized preoperative workup including video-EEG monitoring, MRI (magnetic resonance imaging), PET (positron emission tomography), ictal SPECT (Single-photon emission computed tomography), and neuropsychological assessment. Using a suspected EZ, SEEG electrodes can be placed minimally invasively yet maintain accuracy and precision. Clinical results showed the ability to localize the EZ in 78% of difficult to localize epileptic patients.(1).

Technique, Results, and Complications Related to Robot-Assisted Stereoelectroencephalography.

BACKGROUND: Robot-assisted stereoelectroencephalography (SEEG) may represent a simplified, precise, and safe alternative to the more traditional SEEG techniques. OBJECTIVE: To report our clinical experience with robotic SEEG implantation and to define its utility in the management of patients with medically refractory epilepsy. METHODS: The prospective observational analyses included all patients with medically refractory focal epilepsy who underwent robot-assisted stereotactic placement of depth electrodes for extraoperative brain monitoring between November 2009 and May 2013. Technical nuances of the robotic implantation technique are presented, as well as an analysis of demographics, time of planning and procedure, seizure outcome, in vivo accuracy, and procedure-related complications. RESULTS: One hundred patients underwent 101 robot-assisted SEEG procedures. Their mean age was 33.2 years. In total, 1245 depth electrodes were implanted. On average, 12.5 electrodes were implanted per patient. The time of implantation planning was 30 minutes on average (range, 15-60 minutes). The average operative time was 130 minutes (range, 45-160 minutes). In vivo accuracy (calculated in 500 trajectories) demonstrated a median entry point error of 1.2 mm (interquartile range, 0.78-1.83 mm) and a median target point error of 1.7 mm (interquartile range, 1.20-2.30 mm). Of the group of patients who underwent resective surgery (68 patients), 45 (66.2%) gained seizure freedom status. Mean follow-up was 18 months. The total complication rate was 4%. CONCLUSION: The robotic SEEG technique and method were demonstrated to be safe, accurate, and efficient in anatomically defining the epileptogenic zone and subsequently promoting sustained seizure freedom status in patients with difficult-to-localize seizures.

Low-dose lipopolysaccharide injection prior to subarachnoid hemorrhage modulates Delayed Deterioration associated with vasospasm in subarachnoid hemorrhage.

There is increasing evidence that inflammation plays a role in the development of Delayed Deterioration associated with vasospasm (DDAV) after subarachnoid hemorrhage (SAH). Lipopolysaccharide (LPS) is an activator of the innate inflammatory system that causes DDAV in animal models. The effect of low-dose LPS has been shown to be protective in stroke models but has not been investigated in SAH. Two treatments were studied: (1) a single intraperitoneal dose of 0.6 mg/kg injected 24 h prior to SAH and (2) four daily doses administered prior to SAH. DDAV was determined by India ink angiography at day 6; behavioral testing was done in a different cohort of animals, and analysis of brain chemokine levels was accomplished by dot blot. Vessel caliber was improved compared to the SAH group in the single-injection group (ldLPS ×1) (p < 0.05). In the multiple-injection group (ldLPS ×4), the vessel caliber was similar to SAH (p < 0.05). ldLPS ×1 improved performance on the Barnes maze test, whereas the ldLPS ×4 was worse (p < 0.001). Brain levels of the inflammatory chemokine KC (keratinocyte-derived chemokine) were decreased in the ldLPS ×1 and increased in the ldLPS ×4 group. Single-injection low-dose LPS preconditioning was protective for delayed deterioration associated with vasospasm (DDAV), whereas the multiple-injection course exacerbated DDAV. This further supports that inflammation plays an important role in the development of DDAV, and that modulating the inflammatory system may be a potential target for future therapies in SAH.

Comparison of techniques for stent assisted coil embolization of aneurysms.

INTRODUCTION: Stent assisted coiling (SAC) of aneurysms has been adopted with potential mechanical, hemodynamic and biologic properties imparting an advantage over coil embolization alone. The purpose of this investigation is to compare the various techniques of SAC at a single institution with regards to clinical, technical and angiographic complications and success. METHODS: Patients who underwent SAC between 2003 and 2010 were identified. Clinical charts, procedures, angiographic and non-invasive radiological images were analyzed to determine the anatomical and procedural details and adverse events. Immediate post-procedural angiograms as well as follow-up imaging were studied to assess the degree of aneurysm occlusion. RESULTS: 260 aneurysms were identified. The 'coil through' technique was employed in 37.3%, 'balloon stent' in 36.2%, 'jailing' in 10.8% and the 'coil stent' technique in 7.7%. Overall rate of adverse events was higher with the 'coil stent' and 'jailing' techniques compared with the 'balloon stent' technique. The 'coil through' technique was associated with a significantly lower packing density (31.4±20%) than all other techniques ('coil stent' 45.4±22%, 'jailing' 42.2±20%, 'balloon stent' 44.3±22%). Among 'coil stent' patients, an initial Raymond class 1 was achieved in 40%, compared with 57% of 'jailing', 28% of 'coil through' and 63% of 'balloon stent' cases. CONCLUSION: Balloon assisted coil embolization followed by adjunctive stent deployment across the aneurysm neck appears to be the superior technique among stent assisted coiling methods at our institution. It combines a lower rate of thrombotic and coil related complications with a high rate of complete occlusion on initial and follow-up imaging.

Systemic administration of LPS worsens delayed deterioration associated with vasospasm after subarachnoid hemorrhage through a myeloid cell-dependent mechanism.

BACKGROUND: Delayed deterioration associated with vasospasm (DDAV) after aneurismal subarachnoid hemorrhage (SAH) is a major cause of morbidity. We have previously shown that myeloid cell depletion before experimental SAH in a murine model ameliorates DDAV. In this study, we address whether systemic administration of lipopolysaccharide (LPS) worsens DDAV in a myeloid cell-dependent fashion. METHODS: We challenged mice in our experimental SAH model with LPS before hemorrhage and evaluated the degree of vasospasm on day 6 with India ink angiography; behavioral deficits by rotorod, Y-maze, and Barnes maze testing; microglial activation early after SAH by immunohistochemistry; and the brain levels of the chemokines CCL5 and KC at the time of vasospasm. Another group of animals were given the myeloid cell-depleting antibody against the neutrophil antigen Ly6G/C prior to LPS administration and SAH. RESULTS: LPS followed by SAH significantly worsens angiographic vasospasm as well as performance on the Barnes maze but not the Y-maze or rotorod tests. There was an increased activation of microglia in animals with LPS before SAH compared to SAH alone. Depletion of myeloid cells before LPS administration inhibited the development of vasospasm, improved the performance on behavioral tests, and reduced microglial activation. The chemokines CCL5 and KC were incrementally elevated in SAH and LPS SAH, but suppressed in animals with myeloid cell depletion. CONCLUSIONS: LPS administration before SAH worsens DDAV through a myeloid cell-dependent mechanism supporting studies in humans which show that systemic inflammation increases the likelihood of developing DDAV.

Depletion of Ly6G/C(+) cells ameliorates delayed cerebral vasospasm in subarachnoid hemorrhage.

BACKGROUND: The etiology of delayed cerebral vasospasm (DCV) after aneurysmal subarachnoid hemorrhage (SAH) has remained elusive. Growing evidence supports a role for inflammation in the pathogenesis of DCV. We showed that CSF neutrophils predict which patients will develop DCV. METHODS: We evaluated a murine model of SAH to test the hypothesis that myeloid cells are required for the cerebral damage associated with DCV. RESULTS: SAH was associated with decreased middle cerebral artery caliber on day 1 which normalized at day 3 and recurred at day 6. In addition, behavioral testing with a Barnes maze showed executive dysfunction that progressively worsened after the seventh day post hemorrhage. To test the role of innate immune responses, we administrated a myeloid cell-depleting monoclonal antibody against Ly6G/C prior to experimental SAH. Myeloid cell depletion ameliorated angiographic vasospasm measured by MCA vessel caliber and normalized behavioral testing. CONCLUSION: Our findings support the role of Ly6G/C(+) cells in the development of DCV after SAH and suggest that immune modulation of neutrophils or other Ly6G/C(+) cells may be a strategy for the prevention of DCV.

A novel method for subarachnoid hemorrhage to induce vasospasm in mice.

UNLABELLED: Mouse models take advantage of genetic manipulations that can be achieved in this species. There are currently two accepted mouse models of subarachnoid hemorrhage (SAH) and cerebral vasospasm (CVs). Both are technically demanding and labor intensive. In this study, we report a reproducible and technically feasible method to induce SAH, and subsequently CVs, in mice. We tested this model in multiple strains of mice that are commonly used for genetic manipulation. METHODS: SAH was induced in C57BL/6NCr, FVB, 129S1, BalbC and SJL mice, weighing 28-32 g, by an intracisternal vessel transection technique. Animals were perfused with India ink at 24h postprocedure and vessel diameters were quantified. Brain slices were obtained for hematoxylin-eosin staining (H&E) to look for vascular changes consistent with CVs. RESULTS: There was no mortality during or after the procedure. Four of the five mouse strains showed significant CVs at 24 h postprocedure characterized by decreased vessel diameter of the middle cerebral artery close to the Circle of Willis. Histologically, the vessel wall displayed significant corrugation and thickening, consistent with CVs. CONCLUSION: A novel mouse model to induce SAH is described and tested in several mouse strains. Four of the five strains used in this study developed CVs after the induction of SAH. The procedure is brief, straightforward, reproducible with low mortality, and applicable to commonly used background strains for genetically engineered mice.