Neurohospitalist最新文献

Objective: To describe a case of delayed onset multiple cranial neuropathies as a manifestation of neurotoxicity after chimeric antigen receptor T-cell (CAR-T) therapy for multiple myeloma. While ICANS following CAR-T is a well-reported complication, it classically presents with encephalopathy, seizures, dysphasia, tremors, headache, and cerebral edema. Isolated unilateral facial neuropathies secondary to CAR-T neurotoxicity have been described, but progressive multiple cranial neuropathies have not. Herein, a 75-year-old male presented with left facial nerve palsy 19 days after initiating CAR-T therapy for multiple myeloma. Contrasted brain MRI showed contralateral right facial nerve enhancement, and his left facial palsy was treated with steroids and valacyclovir for 7 days. The facial palsy persisted and progressed to involve bilateral facial nerves and left cranial nerve VI by 31 days post-CAR-T. Specifically, his exam showed impaired abduction of left eye and nearly absent facial movement. Repeat contrasted MRI brain showed mild enhancement of bilateral facial nerves. Extensive serum and CSF testing was unremarkable. Initial treatment with oral steroids for 7 days was ineffective. Concern regarding the impact of steroids on CAR-T efficacy influenced treatment dose and duration. Anakinra was considered but not given. Subsequent treatment with intravenous high dose steroids, followed by a prolonged prednisone taper, led to resolution of CN VI palsy at 2.5 months from onset (2 weeks after completed therapy), and moderate improvement of bilateral facial palsy 5.5 months from onset (3.5 months after completed therapy). CAR-T neurotoxicity can present with progressive multiple cranial neuropathies. The best treatment of these cases is unknown; however, this patient improved in the context of corticosteroids and facial rehabilitation over a prolonged period of follow-up.

Objectives: Anemia has been associated with cerebral venous thrombosis (CVT) and poor outcomes. There have been no Indian studies in this regard. We studied the frequency and type of anemia, and CVT outcomes at 6 months.

Methods: In this ambispective, observational study imaging confirmed CVT patients were enrolled. Anemia was defined by WHO criteria: in men hemoglobin <13 g/dL, non-pregnant women hemoglobin <12 g/dL and pregnant women hemoglobin <11 g/dL. Mortality and poor outcome ie, modified Rankin scale (mRS) score of 3-6 at 6-month were the outcomes. Association between admission anemia and outcome was examined using binary logistic regression after adjusting for potential confounders-namely, age, sex, poor GCS, alcohol, smoking, and involvement of multiple sinuses.

Results: Data of 203 CVT patients (94 retrospective and 109 prospective) were analysed. Anemia was present in 96/203 (47%) patients, microcytic anemia being most frequent type (47/96, 49%) based on erythrocyte morphology. Severe anemia comprised 24% (23/96) of the patients with anemia. As per iron studies, 61/96 (64%) anemia patients had iron-deficiency anemia. At 6-month poor outcome was present in 38% vs 23% (P = 0.02), mortality was 34% vs 20% (P = 0.03) in anemic and non-anemic group respectively. After adjustment for confounders anemia was independently associated with increased risk of poor outcome (aOR 4.3; 95% CI 1.3-13.9) and mortality (aOR 5.2; 95% CI 1.4-19.3).

Conclusion: At admission, anemia is present in almost half CVT patients and is associated with increased risk of poor outcome and higher mortality.

Isolated bilateral vertical gaze palsy is an unusual presentation in acute settings. It is usually accompanied by subtle signs that can lead to precise anatomic localization. This case is notable for the rare co-occurrence of bilateral vertical gaze palsy, Collier's sign, and contralesional pseudo-abducens paresis with a unilateral dorsomedial thalamic infarct, highlighting the complexity of vertical gaze and convergence pathways.

Background: Ischemic stroke due to hypereosinophilic syndromes (HES) is a rare but severe neurological emergency. HES may be secondary to infections, autoimmune conditions, severe allergic reactions, or hematologic disorders. Among these, clonal forms associated with myeloproliferation are particularly aggressive and can lead to recurrent cerebral infarctions with high mortality. Purpose: We report the case of an elderly patient with newly diagnosed extreme eosinophilia who developed multiple progressive strokes and ultimately died despite early and aggressive treatment. Conclusions: This case emphasizes the importance of rapid recognition, highlights the unique radiological signature of border-zone infarctions in this context, and raises concern about the critical role of granulocytes in cerebral microcirculation. It also underscores that partial reduction of eosinophils may be insufficient for stroke prevention and that full normalization may be necessary.

Background: Electroencephalography (EEG) is increasingly used in intensive care units (ICUs), primarily for seizure detection. However, the complex clinical context of critically ill patients and the dynamic ICU environment can complicate interpretation. Purpose: To highlight common pitfalls in ICU EEG interpretation and strategies to distinguish epileptic seizures from mimics. Research Design: Retrospective case series. Study Sample: Five ICU patients undergoing continuous video EEG (cvEEG) for altered mental status, status epilepticus, or paroxysmal events, with underlying conditions including malignancy, autoimmune encephalitis, neuromodulation therapy, and drug-resistant epilepsy. Results: Physiological artifacts, such as non-epileptic rhythmic movements, and device-related artifacts (e.g., pacemakers, ventilators) can mimic epileptic seizures. Plateau waves from elevated intracranial pressure may produce deficits resembling epileptic seizures. Accurate differentiation requires attention to clinical context, EEG features, and video correlation. Maintaining a broad differential and avoiding diagnostic anchoring are also essential to prevent misdiagnosis and unnecessary antiseizure medication therapy. Conclusions: ICU EEG interpretation is challenged by artifacts and non-epileptic movements that mimic epileptic seizures. Awareness of these issues, along with a thoughtful, multidisciplinary approach, is critical for improving diagnostic accuracy and optimizing patient outcomes during cvEEG monitoring.

We read with great interest the case report by Murray et al describing transverse myelitis associated with helminthic infection. While intriguing, several aspects of the diagnostic workup and clinical interpretation warrant further clarification. Pain, treatment response, and cerebrospinal fluid (CSF) and radiological follow-up findings suggest that a demyelinating centrale nervous system (CNS) disorder, such as MOG antibody-associated disease, multiple sclerosis, or neuromyelitis optica spectrum disorders (NMOSD), could represent a plausible alternative explanation. Additional investigations, including antibody testing and serial magnetic resonance imaging (MRI), would have strengthened the diagnostic conclusions. We argue that a more comprehensive assessment is essential to avoid premature attribution of the clinical picture solely to helminthic infection.

Background: Horizontal conjugate eye deviation (HCED) is typically associated with supratentorial strokes affecting the frontal eye fields and associated pathways. However, a rare form of HCED, ocular ipsipulsion, is caused by a lateral medullary lesion. The presumed mechanism involves disruption of decussating olivocerebellar fibers, leading to an imbalance in vestibular nuclei activity. Purpose: To report a case of isolated ocular ipsipulsion as a diagnostic clue to central vertigo. Research Design: Case report. Study Sample: An 82-year-old man with a right lateral medullary infarction. Data Collection: Neurological examination and brain magnetic resonance imaging (MRI) were performed. Ocular findings were documented through bedside observation and video recording. Results: The patient presented with acute vertigo and HCED consistent with ocular ipsipulsion, without other neurological signs. On brain MRI a right lateral medullary infarction was observed. Conclusions: This oculomotor dysfunction can be the only clue in the neurological examination to suspect a central vertigo. Clinicians should be aware of this sign and include its assessment in the bedside evaluation of acute vertigo in the emergency setting if a central cause is suspected.

Background: Postpartum subarachnoid hemorrhage caused by aneurysm rupture is a rare but potentially life-threatening complication that can mimic a benign postpartum headache, especially after neuraxial anesthesia.

Case report: We describe a 40-year-old woman who developed a severe headache, predominantly located in the occipital and posterior neck region, following cesarean section under spinal anesthesia. Initially presumed to be post-dural puncture headache, her condition deteriorated by postoperative day 5, with coma and seizures. Cranial computed tomography revealed diffuse subarachnoid and intraventricular hemorrhage. Vascular imaging showed a dissecting aneurysm of the right vertebral artery (V4 segment), with the posterior inferior cerebellar artery arising from the aneurysm dome. She underwent endovascular coiling with parent vessel sacrifice. Her recovery was favorable, with only mild cerebellar ataxia at discharge. At the 3-year follow-up, she was neurologically intact.

Discussion: This case underscores the importance of considering aneurysmal subarachnoid hemorrhage in postpartum patients with atypical or worsening headache following neuraxial anesthesia. Early neuroimaging and timely intervention can lead to excellent outcomes.

Miller Fisher Syndrome (MFS) is a rare neurological disorder characterized by ataxia, areflexia, and ophthalmoplegia. It is considered a variant of Guillain-Barré syndrome (GBS). Infections frequently precede the onset of MFS. A 44-year-old patient was referred to our Neurology Department due to rapidly progressive bilateral limb ataxia, areflexia, and external ophthalmoplegia following acute tonsillitis with fever and oral mucosal lesions. Initial extensive diagnostic work-up, including immunoglobulin M (IgM) serum antibodies against cytomegalovirus (CMV), was negative. However, due to clinical suspicion, anti-CMV IgM was tested again and subsequently found to be positive. Interestingly, antibodies against Q1B ganglioside, which are specific for MFS, were also negative. Our patient gradually improved after intravenous immunoglobulin administration and symptomatic treatment. No underlying cause of immunocompromise was identified. This case underscores the importance of persistent testing for CMV antibodies in immunocompetent patients, even in rare cases of GBS like MFS, to ensure accurate diagnosis and optimize treatment plans.