No abstract

The use of a benzodiazepine followed by an AED, such as phenytoin or levetiracetam, is common as first and second-line therapy for SE and appears to be associated with a shorter time to SE resolution. AED selection thereafter is highly variable. Patients without a history of seizure who develop SE had a higher mortality rate.

Prior to the approval of andexanet, there were no FDA-approved reversal agents indicated for the treatment of factor Xa inhibitor (FXaI) associated major bleed. Four-factor prothrombin complex concentrate (4F-PCC) has been widely used off-label for FXaI-associated bleeding. The purpose of this study was to compare the effectiveness and safety of andexanet and 4F-PCC for the reversal of FXaI-associated intracranial haemorrhage. The primary end point is in-hospital mortality; secondary endpoints include haemostatic efficacy and safety. This study is a singlecentre, retrospective chart review, including patients admitted between 1 January 2016 and 15 August 2019, who received 4F-PCC or andexanet for the management of FXaI-associated intracranial haemorrhage. Of the 45 patients included in this study, 23 patients were in the andexanet group and 22 were in the 4F-PCC group. At index admission, mean age was 76 years and the majority of patients (64%) were on apixaban with 33% presented with Glasgow Coma Scale 24 (GCS) score less than 12. At hospital discharge, 47% of patients in the andexanet group had died or discharged to hospice compared with 45% in the 4F-PCC group. No thromboembolic events were observed in either group within 5 days after administration of the reversal agent. The results of this study suggest that haemostasis and mortality at discharge during the index hospitalization appears to be similar between groups. Prospective randomized control trials comparing safety and efficacy of andexanet and 4F-PCC are needed.

Traumatic brain injury (TBI) is a leading cause of disability in the United States. With decreasing mortality rates, a higher number of patients are impacted by long-term neuropsychiatric sequelae, such as cognitive deficits, depression, anxiety, and sleep-wake disorders. These sequelae are primarily driven by the disruption of key neurotransmitter homeostasis including dopamine, norepinephrine, serotonin, and acetylcholine. Neurostimulants are centrally acting medications used to assist in restoring these neurotransmitter abnormalities and are pharmacologic options to ameliorate symptoms in post-TBI patients. Examples of neurostimulants include amantadine, selective serotonin reuptake inhibitors, tricyclic antidepressants, central stimulants (ie, methylphenidate), modafinil, and donepezil. Large, well-powered studies have not been performed to validate their use in patients with TBI, leaving uncertainty for these agents' place in therapy. Current practice is driven by consideration of patient-specific factors to select the most appropriate agent. This review provides clinicians with a summary of the available literature on neurostimulants following TBI to guide appropriate usage to help improve patients' symptoms and optimize safety.