Background/Objective: Malnutrition and sarcopenia are common complications after ischemic stroke and have a negative impact on prognosis. The C-reactive protein/albumin ratio (CAR) reflects both inflammation and nutritional status, but its predictive role in this setting has not been widely studied. This study aimed to investigate the predictive value of CAR (C-reactive protein/albumin ratio) for malnutrition risk and probable sarcopenia in patients with ischemic stroke. Methods: In this prospective observational study, 197 patients with acute ischemic stroke were evaluated. Patients with chronic renal or hepatic failure, malignancy, active infection, and hand disability preventing grip strength measurement were excluded. Demographic data (age, sex), vascular risk factors, the NIHSS score, and laboratory parameters were recorded. The nutritional status of patients was assessed using the Nutritional Risk Screening-2002 (NRS-2002), and sarcopenia risk was evaluated with the SARC-F questionnaire. Handgrip strength was measured in patients with high SARC-F scores to define probable sarcopenia. CAR was calculated from serum CRP and albumin levels. Logistic regression was applied to identify independent predictors, and receiver operating characteristic (ROC) analyses were performed to determine the discriminatory ability and cut-off values of CAR. The nutritional status of patients admitted to the neurology clinic with acute ischemic stroke was assessed using the Nutritional Risk Screening-2002 (NRS-2002), and sarcopenia risk was evaluated with the SARC-F questionnaire. Handgrip strength was measured in patients with high SARC-F scores to define probable sarcopenia. CAR was calculated from serum CRP and albumin levels. Logistic regression and receiver operating characteristic (ROC) analyses were performed. Results: Malnutrition risk was identified in 32.5% of patients, and probable sarcopenia was identified in 19.3% of patients. ROC analysis showed that CAR had acceptable discriminatory power for both conditions. In multivariate analysis, CAR was consistently identified as an independent predictor of malnutrition risk and possible sarcopenia. ROC analysis for malnutrition risk showed an AUC of 0.750 (cut-off: 0.306; sensitivity 68.8%; specificity 75.2%). In regression analysis, CAR (OR = 2.13; 95% CI: 1.39–3.26; p < 0.001), age (OR = 1.05; 95% CI: 1.02–1.09; p = 0.003), and NIHSS (OR = 1.11; 95% CI: 1.01–1.23; p = 0.026) were independent predictors. For probable sarcopenia, ROC analysis revealed an AUC of 0.814 (cut-off: 0.320; sensitivity 81.6%; specificity 71.7%). Multivariate analysis identified CAR (OR = 1.73; 95% CI: 1.19–2.52; p = 0.004), age (OR = 1.11; 95% CI: 1.05–1.18; p < 0.001), and NIHSS (OR = 1.19; 95% CI: 1.05–1.35; p = 0.007) as independent predictors. Conclusions: CAR was identified as an independent predictor of both malnutrition risk and probable sarcopenia in ischemic stroke patients. CAR may serve as a reliable biomarker for early nutritional and functional risk stratification in clinical practice.

This study aimed to assess the reliability and construct validity of the Turkish version of the Atroshi-Lyrén 6-Item carpal tunnel syndrome (CTS) Symptoms Scale (A-L Scale-Tr) and to examine its associations with patient-reported outcome measures, including the Boston Carpal Tunnel Questionnaire (BCTQ) and Quick Disability of the Arm, Shoulder and Hand (QuickDASH). A forward-backward translation procedure was performed following international guidelines. Sixty-two patients with unilateral CTS were invited to complete the A-L Scale-Tr. The test-retest reliability, convergent, and discriminant validity were evaluated. The A-L Scale-Tr revealed high values of internal consistency (Cronbach's alpha = 0.854), and test-retest reliability (ICC = 0.96, 95% CI = 0.93-0.98). In the A-L Scale-Tr the factor structure was found optimal and explained 58.39% of the variance. The validity analysis showed strong correlation with night pain (r = 0.821), moderate correlation with BCTQ Symptoms Severity Scale (r = 0.564) and BCTQ Functional Status Scale (r = 0.453), QuickDASH (r = 0.474), pain at rest (r = 0.557), and pain at activity (r = 0.497) (P < .001). It was found that the A-L Scale-Tr has good reliability and construct validity for symptom severity assessment in CTS. The A-L scale will be useful to clinicians and researchers in Turkish patients.

Cerebral venous sinus thrombosis is a rare cause of stroke, and the first-line treatment is anticoagulation. Endovascular treatment may be considered in cases that do not respond to treatment or in cases with venous hemorrhagic infarction. The use of intravascular thrombolysis in conjunction with endovascular (venous mechanical thrombectomy) treatment increases the rate of good clinical outcomes. Headache, epileptic seizures, and focal neurological findings are frequently encountered clinical findings. An 18-year-old male patient with no prior medical history presented to the hospital with complaints of headache, altered consciousness, and weakness in his left arm and leg, where he was diagnosed with cerebral venous thrombosis. Due to the regression of his clinical findings despite anticoagulant treatment, we admitted him to our hospital for endovascular treatment. The patient was taken to the angiography unit, intubated, and given general anesthesia. Digital subtraction angiography revealed venous thrombosis in the right transverse sinus and superior sagittal sinus. Venous system recanalization was achieved with aspiration technique. Following recanalization, 10 mg of alteplase was administered into the sinus over 5 minutes. The patient, who could not be extubated due to status epilepticus (despite 3000 mg/day levetiracetam and 200 mg/day lacosamide), was initially given propofol and midazolam infusions by the same physician, followed by thiopental infusion as seizures did not stop. Seizure control was achieved with thiopental. During follow-up, the patient was extubated and transferred to the neurology ward. The patient had a history of using weight-loss medication 3 days prior to the onset of clinical symptoms and a history of head trauma on the day of clinical symptoms. The etiology of the young patient showed only lupus anticoagulant positivity. The patient was discharged on the 20th day of hospital admission with mRS 1. In treatment-resistant cases, the decision for endovascular treatment should be made quickly, and anesthetic agents should be initiated without delay to prevent the development of complications in treatment-resistant status epilepticus.

Background: Bee stings usually cause local reactions, whereas ischemic stroke is a rare complication. We report a case of large vessel occlusion due to internal carotid artery instent thrombosis shortly after a bee sting in the absence of anaphylaxis. Case Presentation: A 77-year-old man who had undergone left internal carotid artery stenting 15 days earlier developed sudden right hemiplegia and aphasia 30 minutes after a bee sting. Neurological examination revealed an NIHSS score of 20. Imaging demonstrated occlusion of the left internal carotid artery stent and a large left hemispheric infarct. Mechanical thrombectomy was performed 300 minutes after symptom onset. Balloon angioplasty and repeat aspiration were required. The patient was discharged with a favorable functional outcome (mRS 2 at 3 months). Conclusion: Acute ischemic stroke should be considered in patients presenting with neurological deficits after a bee sting. In those with recently implanted vascular stents, early stent thrombosis may represent the underlying mechanism.

Background: Although numerous magnetic resonance imaging (MRI) findings have been described in idiopathic intracranial hypertension (IIH), the potential contribution of craniocervical junction morphology to disease pathophysiology and diagnosis remains largely unexplored. This study aimed to evaluate foramen magnum morphology and cerebrospinal fluid (CSF) spaces at the craniocervical junction in patients with IIH and to investigate their associations with disease severity and diagnostic performance. Methods: In this retrospective case–control study, 70 patients diagnosed with IIH according to the modified Dandy criteria and 70 age- and sex-matched controls were included. Brain MRI examinations were retrospectively reviewed. Optic nerve sheath diameter, optic nerve tortuosity angle, foramen magnum anteroposterior and transverse diameters, foramen magnum area, foramen magnum index, and anterior and posterior subarachnoid CSF spaces were measured. Correlation analyses with lumbar puncture opening pressure and papilledema grade were performed. Independent imaging predictors of IIH were identified using multivariable logistic regression analysis, and diagnostic performance was assessed using receiver operating characteristic (ROC) analysis. Results: Compared with controls, patients with IIH demonstrated significant alterations in craniocervical junction morphology, including smaller foramen magnum anteroposterior diameter, foramen magnum area, foramen magnum index, and anterior subarachnoid CSF space, together with increased optic nerve sheath diameter and reduced optic nerve tortuosity angle (all p < 0.001). Foramen magnum morphometric parameters and anterior subarachnoid CSF space were significantly associated with both lumbar puncture opening pressure and papilledema grade. Multivariable logistic regression identified optic nerve sheath diameter (OR = 2.143, p = 0.002), optic nerve tortuosity angle (OR = 0.925, p < 0.001), and foramen magnum index (OR = 0.526 per 0.1-unit increase, p = 0.001) as independent imaging predictors of IIH. The combined prediction model demonstrated excellent diagnostic performance (AUC = 0.901), with 81.4% sensitivity and 87.1% specificity. Conclusions: Craniocervical junction morphometric features and subarachnoid CSF spaces at the foramen magnum differed between patients with IIH and controls and may provide complementary imaging information. These cross-sectional associations do not establish whether the observed differences are pre-existing anatomical characteristics or secondary changes related to chronically elevated intracranial pressure. Prospective multicenter studies incorporating dynamic CSF-flow imaging are warranted to validate these findings and clarify the temporal relationship between these morphometric features and disease development.

Fibrocartilaginous embolism (FCE) is a rare and highly morbid cause of spinal cord infarction. Diagnosis can be difficult in the absence of predisposing factors. Treatment is controversial. The probable mechanism is retrograde embolism of nucleus pulposus material into the arterial system of the spinal cord. A previously healthy 70-year-old male patient presented to our emergency department with neck and back pain that started 24 hours after carrying firewood, followed by sudden quadriparesis. The patient’s clinical findings and neuroimaging results were consistent with spinal cord ischemia secondary to acute vertebral disc herniation at the C4-5 level (extending between C5-8). Laboratory investigations revealed no evidence of infectious, autoimmune, inflammatory, or neoplastic causes. After ruling out other possible diagnoses, he was diagnosed with spinal cord ischemia secondary to fibrocartilaginous embolism. We wanted to present this rare phenomenon, which often goes undiagnosed unless it’s considered.