MRI studies reveal a characteristic well-circumscribed, isodense or hypodense mass on T1-weighted images, with hyperdensity on T2 imaging. Yet current radiological methods insufficiently distinguish tectal plate gliomas from brainstem tumors or gliomas in the neighboring structures, and a definitive diagnosis requires biopsy and histopathological analysis. Management is planned according to the degree of associated signs and symptoms, and may range from diligent observation and periodic screening for advancing tumor development, to cerebrospinal fluid shunting in an effort to resolve obstructive hydrocephalus, to radio- and chemotherapy. A wide range of minimally invasive approaches using endoscopy is available for the neurosurgeon, including endoscopic third ventriculostomy and endoscopic aqueductoplasty.

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The International League Against Epilepsy (ILAE) classification of focal seizures uses recall of experiences post‐ictally to assess for awareness and not ictal responsiveness to external stimuli, stating that responsiveness is often not tested. We investigated how clinicians assess for seizure awareness by administering an online survey. We found that most respondents use both responsiveness and recall to assess for awareness in the clinic (78%) and in the epilepsy monitoring unit (72%). Furthermore, 60% of respondents believe that the ILAE recommends using both measures. Given our results, we believe that using both responsiveness and recall would provide a more practical classification of impaired consciousness in focal seizures.

Thrombocytosis can be either primary or secondary, and it can cause venous pro-thrombotic states like cerebral venous thrombosis. Untreated iron deficiency anemia is postulated to cause reactive (secondary) thrombocytosis due to the proliferation of common progenitor cells. Here we present a case of a middleaged woman with polycystic ovary syndrome and episodes of menorrhagia. She presented with headache and focal sensory deficits, and her neuroimaging showed evidence of cerebral venous sinus thrombosis (CVST). Laboratory tests showed microcytic hypochromic anemia, low ferritin, high total iron-binding capacity (TIBC), and thrombocytosis with a platelet count of 1,523,000/mm³. A comprehensive workup for hypercoagulable states and primary causes of thrombocytosis was negative. It was concluded that the etiology of her CVST was a reactive thrombocytosis from chronic untreated iron deficiency anemia. Anticoagulation with apixaban and corrective treatment for iron deficiency anemia was initiated. A repeated neuroimaging after four months showed significantly less clot burden in the cerebral venous sinuses, and then apixaban was stopped after six months. Laboratory tests after one year of iron replacement therapy showed improvement in the hemoglobin and hematocrit as well as normalization of platelet count. This case highlights a rare yet potentially dangerous complication of a common untreated condition, i.e., iron deficiency anemia.