Neurohospitalist最新文献

The Neurohospitalist Core Competencies comprise a set of competency-based learning objectives that encapsulate the knowledge, skills, and attitudes of neurohospitalitists who specialize in the care of hospitalized patients with neurologic conditions. These competencies serve to characterize the rapidly expanding field of neurohospitalist medicine. The 27 chapters are divided into 3 sections entitled: neurological conditions, clinical interventions and interpretation of ancillary studies, and neurohospitalist role in the healthcare system. Each individual learning objective in the chapters describes a specific concept with an action verb to illustrate the behavior that the neurohospitalist exhibits. The individual neurohospitalist may not exhibit mastery in each of the topics included as individual practices vary in scope and practice pattern. A few examples of how the complete set of competencies may be used include in the creation of curricula for neurohospitalist fellowships, to assist in defining the scope of practice of neurohospitalists for administrative leaders of hospitals and departments, and in influencing the direction of further research and quality improvement in the field.

Brain metastases in prostate cancer are rare (<2% of cases). In magnetic resonance imaging, nearly all brain metastases exhibit contrast-enhancement, which may be affected by the time elapsed since the administration of the contrast agent. We discuss a case where the brain metastases in a patient with prostate cancer do not show a clear contrast-enhancement on magnetic resonance imaging using a standard brain metastases protocol. It also emphasizes the usefulness of delayed imaging in identifying blood-brain barrier damage. We present the case of a 69-year-old man diagnosed with prostate adenocarcinoma, currently in castration-resistant phase (last value of serum prostate-specific antigen: 45.1 ng/mL) with bone, mediastinal and inguinal lymph nodes, pulmonary, and hepatic metastases. In a contrast-enhanced whole-body computed tomography examination, the appearance of intra-axial brain lesions suspicious for metastases was documented. The subsequent contrast-enhanced brain magnetic resonance imaging showed the presence of 5 intra-axial lesions consistent with brain metastases. These lesions exhibited hyperintense signals in T2-fluid-attenuated inversion recovery images; after contrast agent administration, a ring-like contrast-enhancement was more clearly visible in T1-weighted images acquired later (about 15 minutes after contrast agent administration) than in those acquired earlier (about 5-7 minutes after contrast agent administration). In conclusion, for oncological subjects with multiple brain lesions lacking obvious contrast-enhancement using a standard magnetic resonance imaging protocol, we suggest acquiring late images. These might allow for the detection of even minimal post-contrast impregnation, improving confidence in the diagnosis of brain metastases.

Background: Moyamoya disease (MMD) is a rare pathological state characterized by progressive stenosis of the terminal portion of the internal carotid arteries (ICA). Complications include both ischemic and hemorrhagic strokes, for which there is no curative treatment for MMD. Early diagnosis with surgical intervention is vital for there is no definitive treatment. Due to the bimodal age distribution, moyamoya should be considered for patients presenting with stroke and supraclinoid ICA vasculopathy.

Case: We present a case of a 23-year-old female who presented with left arm weakness and sudden onset thunderclap headache. Upon further questioning, it was revealed that the patient had started an estrogen-containing birth control two weeks prior to presentation. Neuroimaging at our tertiary care center demonstrated simultaneous ischemic and hemorrhagic strokes in the bilateral hemispheres associated with vasculopathy seen in both invasive and noninvasive cerebrovascular imaging. She was diagnosed with idiopathic moyamoya disease since her serum and cerebrospinal fluid studies did not reveal any obvious precipitators to suggest moyamoya syndrome (MMS).

Conclusion: There were no obvious precipitating factors identified in the extensive workup for this patient. Therefore, further secondary prevention is difficult for this otherwise young and healthy individual. While there is data to support the use of antiplatelet medications for the prevention of ischemic stroke secondary to intracranial atherosclerotic disease, there are no clear guidelines for the treatment of MMD that simultaneously causes ischemic and hemorrhagic stroke. Further research on the pathophysiology and treatment modalities for MMD are needed to guide clinicians in treating this complex disease.

With increased patient volumes and complexity, stroke occurrence in hospitalized patients has become relatively more common. The process of activating a code stroke in-hospital differs in many institutions. An emergency team-based response to inpatient acute code stroke is warranted, with many protocols modeled similarly to the cardiac arrest response. However, several studies have demonstrated delays in recognition and management of acute stroke in-hospital as compared to those arriving directly to the emergency department (ED). Furthermore, there are several shared challenges with code stroke resuscitation in the emergency department and the ward, which include the assembly of ad hoc teams and requirement of access to urgent imaging. Delays in activating in-hospital code stroke contributes to increased morbidity, mortality, prolonged hospitalization, and associated health care costs. In the following commentary, we discuss the current landscape of acute in-hospital code stroke protocols, review the differences in neurologic outcomes between inpatient vs ED/out-of-hospital code stroke patients, and propose future directions for in-hospital code stroke paradigms for improved patient outcomes and quality of care.

Background and purpose: Neurohospitalists specialize in the care of hospitalized patients with neurological conditions. As the neurohospitalist model of patient care has grown rapidly and in diverse ways, there has been increasing demand for a formal definition of the field, particularly to support curriculum development for learners at multiple levels.

Methods: The Neurohospitalist Society (NHS) formed a Core Competencies Committee in 2021. This committee defined the scope of the Neurohospitalist Core Competencies and organized the competency topics into chapters. This chapter list was approved by the members of the NHS. An open invitation was made to the general membership of the NHS to write chapters on a first-come, first-served basis, using a standardized chapter template developed by the Committee. A three-step editing process was completed, with members of the Committee serving as editors. A dissemination strategy was designed, including drafting of 2 manuscripts (the Core Competencies themselves, and this accompanying manuscript) and outreach to the general membership of the NHS.

Results: The Neurohospitalist Core Competencies include 27 chapters divided into 3 sections: neurological conditions; clinical interventions and interpretations of ancillary studies; and neurohospitalist role in the health care system. The complete version of the Neurohospitalist Core Competencies is published as a separate manuscript in this issue of The Neurohospitalist.

Conclusions: The creation of the Neurohospitalist Core Competencies was a multi-year initiative intended to support practicing neurohospitalists, trainees interested in pursuing careers in the field, medical education leaders, and administrative leaders of hospitals and departments.

We describe the case of a 36-year-old woman with a past medical history of low grade right frontal lobe glioma and focal epilepsy presenting with subacute, progressive, multifocal myoclonus and neck and back pain. Unlike her typical seizures, the myoclonus exhibited a distinct semiology, involving both positive and negative muscle jerks affecting multiple limb muscles while sparing the face. In addition, neurological examination revealed low-amplitude, arrhythmic movements of the hands and fingers, resembling minipolymyoclonus. There were no other neurological exam findings, including mental status changes, extrapyramidal signs or signs of myelopathy. Brain and spine MRI indicated leptomeningeal and spinal "drop" enhancing lesions, suggesting likely malignant evolution of the glioma. EEG ruled out a cortical origin of the myoclonus. Pharmacological trials with benzodiazepines and other antiepileptic medications were ineffective. The patient's myoclonus was most likely spinal segmental in origin from meningeal spread of glioma. The spinal roots or anterior horns of the spinal cord may have represented a focus of hyperexcitability responsible for generating minipolymyoclonus. Our case expands the etiological spectrum of non-epileptic myoclonus and minipolymyoclonus to encompass meningeal carcinomatosis and drop metastases from glioma. These cases may occur even without overt signs of myelopathy. Recognizing such presentations holds significance due to the poor prognosis associated with meningeal spread of glioma and the limited response of non-epileptic myoclonus to symptomatic treatments.

This case describes a 76-year-old male with initial clinical concern for a high-grade glioma, who was ultimately diagnosed with cerebral amyloid angiopathy-related inflammation The patient's presentation included a tonic-clonic seizure followed by aphasia and right-sided hemiparesis. Magnetic resonance brain imaging demonstrated a large left frontal lesion with parenchymal contrast enhancement. Magnetic resonance spectroscopy indicated elevated choline to creatine and choline to N-acetyl aspartate ratios, further suggestive of high-grade glioma. However, subsequent biopsy findings revealed perivascular amyloid deposits, confirming the diagnosis of CAA-ri. To our knowledge, this is the first case in literature to report elevated choline to creatine and choline to N-acetyl aspartate ratios in cerebral amyloid angiopathy-related inflammation.

Crossed Wernicke's aphasia (CWA) following a stroke is a rare clinical phenomenon, particularly when associated with seizures. This case report presents a unique instance of crossed CWA accompanied by focal clonic cluster seizures affecting the left arm and face, with secondary generalization, in a monolingual Bengali-speaking patient following a right middle cerebral artery ischemic stroke. The patient, a 70-year-old male from rural India, presented with acute behavioral abnormalities and language impairment. He experienced left-sided focal motor-onset clonic seizures with impaired awareness, followed by fluent yet unintelligible speech, characterized by phonemic and semantic paraphasias, as well as neologistic jargon. Neuroimaging revealed a right parieto-occipital infarct. Although initially misdiagnosed and treated for acute psychosis, thorough clinical evaluation ultimately led to the diagnosis of CWA-a rare form of aphasia in a right-handed individual after a right hemisphere stroke. This case underscores the diagnostic challenges associated with stroke-related language disorders and highlights the importance of recognizing variations in language lateralization. Furthermore, the occurrence of CWA in a Bengali-speaking individual emphasizes the potential impact of linguistic and cultural factors on brain organization and language processing. This case also adds to the limited body of literature regarding the co-occurrence of post-stroke seizures and aphasia, particularly in atypical presentations such as CWA.

Background: In this COVID-19 Critical Care Consortium (CCCC) sub-study, we qualified neurological complications associated with SARS-CoV2 infection.

Methods: The CCCC is an international, multicenter study. Eligible patients were COVID-19 patients admitted to intensive care units (ICU) across 23 centers between 1/7/2020 to 6/23/2022. Incidence of neurological complications was estimated as number of events per hospital days and per admission using Poisson regression. Associations between neurological complications and risk factors were assessed using multivariable Poisson regression.

Results: 713 patients were included. Median age = 56 years (interquartile range (IQR) = 45-65). Neurological complications reported in 61/480 patients (12.7%) with the majority being ischemic stroke (2.9%), intracranial hemorrhage (ICH) (2.8%), and seizures (2.6%). Multivariable analysis for neurological complications per admitted days showed comorbid neurological conditions (incidence rate ratio (IRR) = 6.35, 2.57-15.7) were an independent risk factor for ischemic stroke. Extracorporeal membrane oxygenation (IRR = 5.32, 1.52-18.6), low-middle income countries (LMIC) vs high income countries (HIC) (IRR = 4.70, 1.62-13.7), and age >55 (IRR = 3.66, 1.23-10.9) were independent risk factors for ICH. Co-morbid neurological conditions (IRR = 3.43, 1.11-10.6), LMIC vs HIC (IRR = 8.69, 2.15-35.2), July-December 2020 vs January-June 2020 (IRR = 0.17, 0.04-0.69) and age >55 (IRR = 4.05, 1.15-14.3) were independent risk factors for seizure.

Conclusions: Decision-making should incorporate salient risk factors to inform management of SARS-CoV2 infection and avoid neurological complications.

Background: Impingement of an elongated styloid process (ESP) or calcified stylohyoid ligament on surrounding neck structures defines Eagle syndrome. The vascular variant, also called stylocarotid syndrome, results from impingement of vascular structures and remains poorly known among physicians. Research Design: We report our own experience and review the literature in order to clarify the diagnostic and therapeutic management. Patients with vascular events in relation to an ESP and hospitalized at our institution were extracted from our databank and retrospectively reviewed. We also performed a comprehensive review of the literature on Eagle syndrome using PubMed® and Google Scholar, analysing the presentation, management, and follow-up. Results: We report five cases of the vascular variant of Eagle syndrome: one carotid perforation, one focal arteriopathy, one with both acute and chronic dissection and two acute internal carotid dissection. Vascular compression, whether permanent or transient, is also reported in the literature. Management varies, although styloidectomy is deemed appropriate for symptomatic compression, while stenting is preferred in cases of perforation. Conclusions: A common definition of Eagle syndrome is required for better diagnosis and management. The choice of styloidectomy is understandable for compression but remains to be investigated in other cases.