RESUMEN
Intracerebral hemorrhage occurs when a diseased blood vessel within the brain bursts. We present a case of 69-year-old patient with two sequential episodes of lobar intracerebral hemorrhage occurring during sexual intercourse. Both episodes were associated with the use of phosphodiesterase-5 inhibitors. This is the first case reported which is temporally associated with isolated bilateral lobar bleeds with appropriate use of phosphodiesterase-5 inhibitor on two different occasions associated with sexual intercourse.
Asunto(s)
Hemorragia Cerebral/etiología , Inhibidores de Fosfodiesterasa 5/efectos adversos , Citrato de Sildenafil/efectos adversos , Tadalafilo/efectos adversos , Anciano , Hemorragia Cerebral/diagnóstico por imagen , Coito , Disfunción Eréctil/tratamiento farmacológico , Humanos , Masculino , Inhibidores de Fosfodiesterasa 5/administración & dosificación , Citrato de Sildenafil/administración & dosificación , Tadalafilo/administración & dosificación , Tomografía Computarizada por Rayos XRESUMEN
BACKGROUND AND PURPOSE: Although femoral neuropathy is recognized as an adverse consequence following transfemoral neuroendovascular procedures, no reliable estimates are available. We analyzed data from a prospective registry to ascertain the frequency and characteristics of femoral neuropathy following transfemoral neuroendovascular procedures. METHODS: Consecutive patients who underwent neuroendovascular procedures through the transfemoral route were included. Detailed assessment was performed if any patient reported occurrence of sensory or motor symptoms in the femoral or lower extremity region including neurological examination (sensory/motor deficits) and femoral region ultrasound. RESULTS: Femoral neuropathy was diagnosed following 4 of 270 neurovascular procedures with an occurrence rate of 1.5% (95% confidence intervals = .4-3.7%). The symptoms were exclusively sensory without any motor involvement. The femoral neuropathy appeared to involve anterior femoral cutaneous nerves in all and medial cutaneous branches in 2 patients, and more than one nerve distribution in 1 patient in whom lateral cutaneous nerve appeared to be involved. All patients reported resolution of symptoms within a period ranging from 1 week to 2 months. No local hematoma or arterial pseudoaneurysm was identified at femoral region ultrasound. CONCLUSIONS: Femoral neuropathy is a rare occurrence following transfemoral neuroendovascular procedures and it usually occurs with pure sensory manifestations with complete resolution.
Asunto(s)
Procedimientos Endovasculares/efectos adversos , Nervio Femoral/diagnóstico por imagen , Neuropatía Femoral/diagnóstico por imagen , Adulto , Anciano , Femenino , Neuropatía Femoral/etiología , Humanos , Masculino , Persona de Mediana Edad , Sistema de Registros , UltrasonografíaRESUMEN
Brain aging is associated with diminished circadian clock output and decreased expression of the core clock proteins, which regulate many aspects of cellular biochemistry and metabolism. The genes encoding clock proteins are expressed throughout the brain, though it is unknown whether these proteins modulate brain homeostasis. We observed that deletion of circadian clock transcriptional activators aryl hydrocarbon receptor nuclear translocator-like (Bmal1) alone, or circadian locomotor output cycles kaput (Clock) in combination with neuronal PAS domain protein 2 (Npas2), induced severe age-dependent astrogliosis in the cortex and hippocampus. Mice lacking the clock gene repressors period circadian clock 1 (Per1) and period circadian clock 2 (Per2) had no observed astrogliosis. Bmal1 deletion caused the degeneration of synaptic terminals and impaired cortical functional connectivity, as well as neuronal oxidative damage and impaired expression of several redox defense genes. Targeted deletion of Bmal1 in neurons and glia caused similar neuropathology, despite the retention of intact circadian behavioral and sleep-wake rhythms. Reduction of Bmal1 expression promoted neuronal death in primary cultures and in mice treated with a chemical inducer of oxidative injury and striatal neurodegeneration. Our findings indicate that BMAL1 in a complex with CLOCK or NPAS2 regulates cerebral redox homeostasis and connects impaired clock gene function to neurodegeneration.