Factors associated with decreasing diffusion-weighted imaging-positive area volume after mechanical thrombectomy in patients with large early ischemic changes.

OBJECTIVES: This study aimed to evaluate the factors associated with decreasing diffusion-weighted imaging (DWI) positive areas in patients with large early ischemic changes after mechanical thrombectomy (MT). MATERIALS AND METHODS: This retrospective single-center clinical study was conducted between January 2013 and December 2022. We included consecutive patients who underwent MT for acute large-vessel occlusion of the anterior circulation with low pretreatment DWI-Alberta Stroke Program Early Computed Tomography Scores (ASPECTS) (0-5), effective recanalization [thrombolysis in cerebral infarction (TICI) 2b or TICI3], and magnetic resonance imaging (MRI) acquired before and after MT. We measured the DWI-positive area volume before and after MT. The primary endpoint was the after/before-MT DWI-positive area-volume ratio. RESULTS: In total, 28 patients were included in this study. Eight patients (29%) had an after/before-MT DWI-positive area-volume ratio of <1. The median mean apparent diffusion coefficient (ADC) levels of the DWI-positive areas in the groups with a ratio of <1 or >1 were 717 × 106 mm2/s and 637 × 106 mm2/s, respectively (p = 0.011). Multivariate logistic regression analysis showed that ADC level (OR, 1.020 [95% confidence intervals (CIs), 1.001-1.040]; p = 0.040) was an independent predictor of a decreased DWI-positive area after MT. There was a negative correlation between the mean ADC level and the after/before-MT DWI-positive area-volume ratio (p < 0.001, |ρ| = 0.650), and the mean pretreatment ADC cutoff level was 649 × 106 mm2/s (area under the curve (AUC) = 0.806) for predicting a volume ratio of <1. CONCLUSIONS: The mean ADC level before-MT correlated with the after/before-MT DWI-positive area-volume ratio. A mean pretreatment ADC cutoff level of 649 × 106 mm2/s predicted a decreased DWI-positive area after MT.

Postoperative Serum C-Reactive Protein and Cerebrospinal Fluid Leakage after Endoscopic Transsphenoidal Surgery.

Objective Postoperative cerebrospinal fluid (CSF) leakage in endoscopic transsphenoidal surgery is a potential risk that requires immediate repair. We investigated the potential of common postoperative hematological examinations for diagnosing postoperative CSF leakage. Methods We retrospectively studied 214 consecutive cases who underwent endoscopic transsphenoidal approach (ETSA; transsellar approach) or extended ETSA (E-ETSA). Patients with postoperative CSF leakage were defined the leak group (group L), and patients without were defined as the nonleak group (group N). Postoperative C-reactive protein (CRP) was compared between the ETSA and E-ETSA groups, and between the N and L groups. Results The values of white blood cell count and CRP 1 to 7 days after surgery were significantly higher in the L group. Especially, CRP was clearly elevated in the L group ( p < 0.001). The CRP value was higher in patients in the N group after E-ETSA than after ETSA ( p < 0.001). CRP increased on the day after surgery but decreased gradually thereafter in patients after ETSA and in the N group. In contrast, CRP value tended to increase gradually after surgery in the L group. In particular, the CRP on the day before the CSF leak was confirmed was clearly higher than on the fifth to seventh days in the N group. Conclusion Elevated CRP after endoscopic endonasal transsphenoidal surgery is a potential marker of CSF leakage.

Glossopharyngeal neuralgia with repeated cardiac syncope: A case report.

Background: Glossopharyngeal neuralgia (GPN) is an uncommon craniofacial pain syndrome. Although rare, it is occasionally associated with cardiac syncope, as vago-glossopharyngeal neuralgia (VGPN). Case Description: We present the case of a 73-year-old man with VGPN misdiagnosed as trigeminal neuralgia. The patient was diagnosed with sick sinus syndrome, and a pacemaker was introduced. However, syncope still recurred. Magnetic resonance imaging revealed a branch of the right posterior inferior cerebellar artery contacting the root exit zone of the right glossopharyngeal and vagus nerves. We diagnosed VGPN due to neurovascular compression and performed microvascular decompression (MVD). The symptoms disappeared postoperatively. Conclusion: Diagnosis of VGPN needs appropriate medical interviews and physical examination. MVD is the only curative treatment for VGPN occurring as a neurovascular compression syndrome.

The Significance of the Intercarotid Distances for Transsphenoidal Pituitary Surgery: A Magnetic Resonance Imaging Study.

OBJECTIVE: We performed magnetic resonance imaging (MRI) to analyze the distance between the left and right internal carotid arteries (ICD) around pituitary tumors for transsphenoidal surgery (TSS). METHODS: Measurements were performed using thin slice T2-weighted MRI, and/or time-of-flight (TOI) MR angiography imaging for 64 nonfunctioning pituitary neuroendocrine tumors (NF-pitNETs), 22 growth hormone-producing pitNETs (GH producing pitNETs), and 46 normal controls. We measured the ICD at 3 anatomic levels: at the distal dural ring (ICD-A); at the most concave point of the C4-C5 bend (ICD-B); and at the most convex point of the C4 bend (ICD-C). Additionally, we measured the sagittal distance between the tuberculum selle and the junction of the sellar floor and clivus on the midsagittal MRI (TS-C). RESULTS: We found that ICD-B was the longest and that ICD-A was the shortest among the 3 distance parameters in all groups (P < 0.001). The comparison of the groups revealed that the NF-pitNET group had longer distances than the normal control group at all ICDs (P < 0.001). The GH producing pitNET group had longer distance than the normal control group at ICD-B (P < 0.001). Tumor volume was correlated with ICD-A and ICD-B in the NF-pitNET, and was correlated with ICD-C in the GH producing pitNET group. CONCLUSIONS: Among the distance parameters, ICD-B is the longest, and was approximately twice the width of the TS-C. The shape of the sella is an ellipse that is widest in the lateral dimension in TSS. A horizontal based dural incision may be more rational than a conventional X-shaped dural incision.

Emergent surgical evacuation of traumatic intracranial hematoma in patients with preoperative thrombocytopenia: surgical risk and early outcome.

BACKGROUND: Surgical evacuation of intracranial hematoma, including epidural, subdural, intracerebral, and intraventricular hematoma, is recommended in patients with traumatic brain injury (TBI) for prevention of cerebral herniation and possible saving of life. However, preoperative coagulopathy is a major concern for emergent surgery on patients with severe TBI. METHODS: We reviewed 65 consecutive patients with severe TBI who underwent emergency craniotomy for intracranial hematomas. RESULTS: Univariate analysis showed preoperative pupil abnormality, absence of pupil light reflex, respiratory failure, preoperative thrombocytopenia (< 100 × 109/L), increased activated partial thromboplastin time (> 36 s), low fibrinogen (< 150 mg/dL), platelet transfusion, red cell concentrate transfusion, and presence of brain contusion and traumatic subarachnoid hemorrhage (SAH) on computed tomography were correlated with poor outcome (death or vegetative state). Multivariate analysis revealed that pupil abnormality (p = 0.001; odds ratio [OR] 0.064, 95% confidence interval [CI] 0.012-0.344), preoperative thrombocytopenia (p = 0.016; OR 0.101, 95% CI 0.016-0.656), and traumatic SAH (p = 0.021; OR 0.211, 95% CI 0.057-0.791) were significant factors. Investigation of the 14 patients with preoperative thrombocytopenia found the emergency surgery was successful, with no postoperative bleeding during hospitalization. However, half of the patients died, and almost a quarter remained in the vegetative state mainly associated with severe cerebral edema. CONCLUSIONS: Emergent craniotomy for patients with severe TBI who have preoperative thrombocytopenia is often successful, but the prognosis is often poor. Emergency medical care teams and neurosurgeons should be aware of this discrepancy between successful surgery and poor prognosis in these patients. Further study may be needed on the cerebral edema regulator function of platelets.

Effect of vasopressin V2-receptor antagonist tolvaptan on syndrome of inappropriate antidiuresis (SIAD) after transsphenoidal pituitary surgery: recovery of measured osmolality.

Background: Delayed hyponatremia after pituitary surgery can be treated with the V2-receptor antagonist, oral tolvaptan. We investigated the pharmacological effect of oral tolvaptan against SIAD in patients with hyponatremia after pituitary surgery. Methods: Thirty-nine patients with pituitary adenoma treated by endoscopic transsphenoidal surgery developed SIAD according to the major guidelines, and 7 patients (17.9%) were treated with tolvaptan. Tolvaptan was administrated orally half a tablet (3.75 mg) once in the first two cases, and half a tablet twice in the other five cases. Serum osmolality, urinary osmolality, urinary sodium concentration, urinary volume, and serum sodium and potassium concentration were evaluated before administration, and after the last oral administration of tolvaptan. Serum osmolality and urine osmolality were physically measured. Results: Serum sodium concentration was significantly increased from 132.1 ± 4.0 to 143.0 ± 2.9 mmol/L (mean ± standard deviation, n = 7, P < 0.001). Serum osmolality was significantly increased from 266.3 ± 7.7 to 289.6 ± 6.7 mOsm/kg (n = 7, P < 0.001). Urine osmolality was significantly reduced from 607.1 ± 240.4 to 262.7 ± 115.6 mOsm/kg (n = 7, P = 0.01). Urinary sodium concentration was significantly decreased from 121.3 ± 48.4 to 36.9 ± 35.0 mOsm/kg (n = 7, P = 0.001). Urine output (24-hour including the first administration) was significantly increased from 1384.2 ± 550.7 to 3291.3 ± 1710.9 mL/day (n = 6, P = 0.026). Conclusions: Oral tolvaptan administration corrects SIAD after pituitary surgery. Hyponatremia after pituitary surgery was confirmed to be due to SIAD.

Disordered branched chain amino acid catabolism in pancreatic islets is associated with postprandial hypersecretion of glucagon in diabetic mice.

Dysregulation of glucagon is associated with the pathophysiology of type 2 diabetes. We previously reported that postprandial hyperglucagonemia is more obvious than fasting hyperglucagonemia in type 2 diabetes patients. However, which nutrient stimulates glucagon secretion in the diabetic state and the underlying mechanism after nutrient intake are unclear. To answer these questions, we measured plasma glucagon levels in diabetic mice after oral administration of various nutrients. The effects of nutrients on glucagon secretion were assessed using islets isolated from diabetic mice and palmitate-treated islets. In addition, we analyzed the expression levels of branched chain amino acid (BCAA) catabolism-related enzymes and their metabolites in diabetic islets. We found that protein, but not carbohydrate or lipid, increased plasma glucagon levels in diabetic mice. Among amino acids, BCAAs, but not the other essential or nonessential amino acids, increased plasma glucagon levels. BCAAs also directly increased the intracellular calcium concentration in α cells. When BCAAs transport was suppressed by an inhibitor of system L-amino acid transporters, glucagon secretion was reduced even in the presence of BCAAs. We also found that the expression levels of BCAA catabolism-related enzymes and their metabolite contents were altered in diabetic islets and palmitate-treated islets compared to control islets, indicating disordered BCAA catabolism in diabetic islets. Furthermore, BCKDK inhibitor BT2 suppressed BCAA-induced hypersecretion of glucagon in diabetic islets and palmitate-treated islets. Taken together, postprandial hypersecretion of glucagon in the diabetic state is attributable to disordered BCAA catabolism in pancreatic islet cells.

Basilar Artery Dissection Complicated with Infective Endocarditis.

A 14 year-old boy developed infective endocarditis of the mitral valve caused by Methicillin-sensitive Staphylococcus aureus and became comatose. Isolated basilar artery dissection was initially observed on the 3rd day by magnetic resonance imaging (MRI), ie, it did not exist on day 1. He underwent successful urgent mitral valve repair on the 5th day because of highly mobile vegetations and a newly emerged brain infarction under optimal antibiotic administration. Postoperatively, he recovered well and the basilar artery dissection was found to have recovered on an MRI on the 25th day without any specific intervention. This clinical course indicated that intracranial artery dissection may occur as a complication of infective endocarditis and supports the importance of the careful evaluation of brain MRI in patients with infective endocarditis.