Neurohospitalist最新文献

Background/objectives: There is currently no consensus regarding the optimal strategy for reversal of anticoagulation in life-threatening hemorrhage associated with factor XIa (FXIa) inhibitors.

Methods: For this clinical case report, informed consent was obtained from surrogate.

Results and discussion: Here, we present the case of an 82-year-old female who sustained a large subdural hematoma after a fall. Her aPTT on admission was elevated at 90.4 s and remained persistently prolonged at 90.9 s 12-hour after receiving an adequate dose of 4-factor prothrombin complex concentrate (PCC). She was found to have received a factor XIa inhibitor in a clinical trial, and subsequently received recombinant activated factor VII (rFVIIa) 2 mg (45 mcg/kg) as a one-time dose, and tranexamic acid (TXA) 1 g intravenously for reversal given her intracranial bleeding in the setting of trauma complicated by recent factor XIa inhibitor use. However, given her clinical decline and high surgical risk, the patient's family elected to withdraw care and she expired three days later. Reversal of FXIa inhibitors is challenging but may best be achieved using a combination of rFVIIa and TXA.

Practical implications: Clinicians should consider administration of low dose recombinant activated factor VII (rFVIIa) in conjunction with an anti-fibrinolytic inhibitor such as tranexamic acid (TXA) for reversal of life-threatening hemorrhage in bleeding patients with exposure to novel factor XIa inhibitors that are currently in clinical trials.

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.

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.

We report a case highlighting key clinical, CSF, and imaging findings of primary diffuse leptomeningeal gliomatosis of the spine.

Subacute, painful weakness is a common problem encountered by neurologists and can be associated with systemic symptoms. The patient presented with 6 weeks of progressive neuropathic pain followed by sensory changes and distal-predominant weakness. This case reviews the broad differential for such a presentation and a comprehensive, stepwise approach to diagnosis. Particular attention is paid to the potentially treatable polyradiculoneuropathies, including more recently recognized immune-mediated etiologies. Through this stepwise approach, we review how a definitive diagnosis was made.

Deterioration of a patient's state of consciousness is among the most concerning signs encountered in clinical practice. The evaluation of this finding carries a broad initial differential diagnosis and must account for any relevant medical history. We describe the case of a 41-year-old male with known retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S) who presented with progressive mental status decline and acute onset intractable headache. Head computed tomography (CT) revealed extensive vasogenic edema, resulting in right to left shift of 11 millimeters at the level of the lateral ventricles, with associated uncal and subfalcine herniation. He was treated with a 5-day course of methylprednisolone, leading to resolution of his lethargy and headache. Follow up neuroimaging with magnetic resonance (MRI) brain demonstrated interval improvement with the midline shift reduced to 3 millimeters after completion of high dose corticosteroids. Neurosurgical intervention was considered, but ultimately not required given his improvement. This case describes the management of life-threatening cerebral edema as a complication of RVCL-S disease progression. Due to the rarity of this disease, there are no standardized guidelines for treatment and the care for such patients relies on expert opinion, case studies, and extrapolation of principles learned from related conditions. Our intention is that the reporting of this case will contribute to the limited body of literature and aid those affected by this condition.

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.

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.

Introduction: Post-Traumatic Stress Disorder (PTSD) is associated with exposure to traumatic events, especially in the military setting. However, patients who experience stroke may develop anxiety about their stroke event and may re-experience transient neurological symptoms as a result. A significant portion develop the persistent and disabling symptoms of PTSD.

Methods: At the University of South Florida, we conducted a single-center, IRB-approved, observational pilot study of 20 adult patients who were diagnosed with stroke or transient ischemic attack (TIA) in the previous 31 days to 1 year. Patients completed the post-traumatic stress disorder checklist-5 (PCL-5), Patient Health Questionnaire-9 (PHQ-9), Stroke specific Quality of Life Scale (SS-QOL-12), Modified Rankin Scale of disability (mRS), and National Institutes of Health Stroke Scale (NIHSS) and provided blood and saliva samples.

Results: All 20 subjects completed the PCL-5 and 19 subjects completed the follow up scales. Seven patients (35%) were found to have Post-Stroke Post-Traumatic Stress Disorder (PS-PTSD). Higher PCL-5 scores were significantly correlated with lower SS-QOL scores indicating worse quality of life (r = -0.709, P = .001) and higher PHQ-9 scores representing symptoms of depression (r = 0.727, P < 0.001).

Conclusion: Post-Stroke Post-Traumatic Stress Disorder (PS-PTSD) is prevalent after stroke and TIA with patients experiencing concurrent depressive symptoms, correlating with a worsened quality of life.