Reversible Cerebral Vasoconstriction Syndrome Associated With Fluoxetine.

BACKGROUND: Reversible cerebral vasoconstriction syndrome (RCVS) is an increasingly recognized neurological syndrome that typically presents with a severe headache. The proposed etiology is transient and segmental constriction of cerebral arteries, which in severe cases can lead to cerebral ischemia. Multiple case reports have been identified associating the use of serotonergic medications with this syndrome. OBJECTIVE: A review of the literature describing RCVS in patients taking selective serotonin reuptake inhibitors and other serotonergic medications is summarized. This report also describes the case of a 32-year-old woman with a complicated psychiatric history diagnosed with RCVS who presented with progressive cerebral ischemia despite intensive medical intervention. Ischemic progression did not relent until her home medication fluoxetine was recognized as the likely etiology and discontinued. The psychiatric management of this patient is described after fluoxetine was discontinued. Other potential psychiatric treatments for patients with a history of RCVS are discussed. METHODS: A literature search was performed using PubMed with the following keywords: antidepressant, selective serotonin reuptake inhibitor, serotonin, fluoxetine, reversible cerebral vasoconstriction syndrome, RCVS, and Call-Fleming syndrome. RESULTS: Fifteen patients were identified to have RCVS with associated use of serotonergic medications from 10 case reports published between 2002 and 2019. CONCLUSIONS: It is important for psychiatrists to recognize the syndrome of RCVS in patients presenting with headache and ischemia due to the possibility of this syndrome being a rare but iatrogenic complication of a common psychiatric medication class. Additionally, identification of safe alternative treatments for patients with psychiatric illness who would otherwise be candidates for serotonergic medications is an important consideration for individuals affected by this disorder.

A Novel Approach to the Treatment of Orolingual Angioedema After Tissue Plasminogen Activator Administration.

Orolingual angioedema is a rare adverse effect of tissue plasminogen activator (tPA), with an incidence of 1% to 5%. There are currently no published reports describing resolution of tPA-induced orolingual angioedema with complement inhibitor therapy. A 72-year-old man receiving home angiotensin-converting enzyme inhibitor therapy presented to the emergency department with newly developed orolingual angioedema after treatment with tPA for acute ischemic stroke. Therapy was initiated with intravenous methylprednisolone 125 mg, famotidine 20 mg, and diphenhydramine 50 mg, without significant improvement. Because of increased concern for airway protection, plasma-derived C1 esterase inhibitor was administered. Concerns about progressive and airway-threatening orolingual angioedema subsided 2 hours after administration, and invasive airway maneuvers were avoided. Orolingual angioedema is an infrequent, severe adverse effect of tPA for treatment of acute ischemic stroke. Complement inhibitors may be an additional therapeutic option for patients presenting with orolingual angioedema with potential airway compromise that is refractory to standard anaphylactic therapies.

Impaired thymopoiesis in interleukin-7 receptor transgenic mice is not corrected by Bcl-2.

Murine thymocytes down-regulate IL-7 responsiveness following beta-selection and reacquire sensitivity after positive selection. To assess the potential consequences of IL-7 signaling during this phase of development, transgenic IL-7 receptor alpha (IL-7Ralpha) mice were evaluated for IL-7 responsiveness as gauged by STAT-5 phosphorylation. Transgenic IL-7Ralpha expression increased the percentage of thymocytes responsive to IL-7 yet resulted in a decrease in total thymic cellularity. Aberrant thymocyte development in transgenic mice was first manifested by a reduction of DN3 thymocytes that correlated with lower Bcl-2 expression. Surprisingly, transgenic restoration of Bcl-2 expression did not correct thymic hypocellularity induced by IL-7Ralpha overexpression. These findings demonstrate that failure to appropriately downregulate IL-7Ralpha expression interferes with thymocyte development past the pro-T stage resulting in significantly lower levels of mature thymocytes.