The management of trigeminal neuralgia with triptans, a narrative review of the literature.

OBJECTIVE: The objective of this paper is to present a narrative review of the use of triptans in the treatment of trigeminal neuralgia (TN), as well as to outline possible therapeutic mechanisms of action. BACKGROUND: TN is a debilitating neuropathic disorder with a variety of surgical and pharmacological treatments currently available. Despite treatment being heavily individually tailored, some patients remain refractory to management. The use of triptans for the treatment of TN has been commented on in the literature, yet major trials showing their effectiveness are lacking. METHODS: A narrative review of current literature was conducted to identify published original research analyzing the usage of triptans in TN via PubMed and Google Scholar. RESULTS: Limited case reports and studies have been done to analyze the use of triptans for the treatment of TN. Despite the limited results, the studies that have been done show some promise for triptans as an alternative treatment, in particular to those with refractory TN. Given the incapacitating nature of TN, another alternative treatment may be of benefit to those patients and can help reduce its associated morbidity. CONCLUSION: Patients with refractory TN may find relief of symptoms from the use of triptans. Larger clinical trials are needed to help determine which patients would benefit from their use as well as specific dosing. Caution should be given regarding the long-term use of triptans, in particular for the typical patient population with TN.

Tofacitinib-Associated Cerebral Venous Sinus Thrombosis.

Tofacitinib is a Janus kinase inhibitor indicated to treat adult patients with moderately to severely active ulcerative colitis (UC). Although thrombosis is a known adverse event of tofacitinib, there are no reports specific to cerebral venous sinus thrombosis (CVST). We present a report of a patient presenting with a CVST several months after starting tofacitinib. Initially, this 60-year-old man with poorly controlled UC who previously had a nonthrombotic hemorrhage was found to have venous sinus thromboses of the right transverse and sigmoid sinuses. Hematological workup did not reveal any underlying hypercoagulable conditions, aside from UC. This is the first report of a patient with CVST likely resulting from the Janus kinase inhibitor tofacitinib. This case report should prompt compilation of all thrombotic events in patients receiving tofacitinib.

Pediatric middle meningeal artery embolization for chronic subdural hematoma: A case report.

BACKGROUND: The most common neuroradiological finding in pediatric nonaccidental trauma (NAT) is subdural hematoma (SDH). Management options for pediatric SDH range from conservative clinical surveillance to craniotomy or decompressive craniectomy. The middle meningeal artery (MMA) indirectly feeds the hematoma; thus, MMA embolization is an alternative or adjunct to current surgical treatments in adults. Herein, we present, to the best of our knowledge, the first reported case of successful MMA embolization in a pediatric patient as an adjunct to current standard treatment for chronic SDH (cSDH). CASE DESCRIPTION: An 18-month-old male with a history of NAT presented at 5 months of age with an acute right parietal skull fracture and bilateral SDH treated with burr hole drainage. He was lost to follow-up until 15 months of age with an increased head circumference and new dysconjugate gaze. Imaging revealed a right-sided cSDH and underwent craniotomy. Six-week follow-up revealed significant improvement in the SDH but cSDH remained at the periphery of the craniotomy's reach. The patient symptoms continued. The right-sided MMA embolization was offered as option to avoid repeat craniotomy. Follow-up CTs at 2 weeks, 3 months, and 6 months postprocedure revealed decrease of cSDH size and density. At 8-month follow-up, the patient continued to meet developmental milestones with near resolution of his dysconjugate gaze. CONCLUSION: This case report details the first successful use of MMA embolization in the treatment of pediatric cSDH as an adjunct to standard treatment. Further investigation of MMA embolization in pediatrics should be made to expand options available for cSDH in this patient population.

Successful treatment of ventriculitis caused by Pseudomonas aeruginosa and carbapenem-resistant Klebsiella pneumoniae with i.v. ceftazidime-avibactam and intrathecal amikacin.

PURPOSE: A patient with carbapenem-resistant Klebsiella pneumoniae infection is described, and treatment options are discussed. SUMMARY: Few antibiotics to treat carbapenem-resistant Enterobacteriaceae (CRE) infection are available, and treatment is further complicated by the limited ability of many antibiotics to penetrate into the cerebrospinal fluid (CSF). Currently, there is a lack of clinical data on the treatment of central nervous system CRE infections, and therapy is based on case reports, case series, and small retrospective studies. A patient was admitted to the emergency department with intracranial hemorrhage and ventriculitis due to traumatic injury. A ventriculostomy and, subsequently, a ventriculoperitoneal (VP) shunt were placed. After approximately a month of treatment with various antibiotic regimens, the patient's VP shunt was externalized, and a CSF culture speciated carbapenem-resistant K. pneumoniae and Pseudomonas aeruginosa. The patient was then switched to i.v. ceftazidime-avibactam and intrathecal amikacin therapy. His CSF cultures were sterile 3 days after initiation of those antibiotics, and subsequent CSF cultures resulted in no growth. After the patient was treated with intrathecal amikacin 30 mg daily for 4 weeks and i.v. ceftazidime-avibactam 2.5 g every 8 hours for 6 weeks, the ventriculitis resolved, the external ventricular drain was removed, and he was transferred to a long-term care facility for rehabilitation. CONCLUSION: A man with ventriculitis caused by P. aeruginosa and carbapenem-resistant K. pneumoniae was successfully treated with i.v. ceftazidime-avibactam and intrathecal amikacin.