ABSTRACT
ABSTRACT A 37-year-old female presented with severe apraxia of lid opening (ALO) affecting the right upper lid associated with Becker congenital myotonia (MC). The patient had a history of right upper lid ptosis for 25 years that was exacerbated over the previous month with severe incapacity to open her right eye. No other associated neurological or ophthalmic symptoms were observed. The patient was treated with botulinum toxin (BoNT-A) injection into the pretarsal and lateral canthus region of the orbicularis oculi of the affected eyelid. Treatment with BoNT-A is an effective method of managing ALO in Becker MC. This is the first case of unilateral ALO in the course of Becker MC that was successfully treated with injections of botulinum toxin.
RESUMO Trata-se de uma mulher de 37 anos apresentando grave apraxia de abertura da pálpebra (AAP) superior direita associada com miotomia congênita de Becker (MC). A paciente há 25 anos apresentava ptose palpebral a direita e há um mês desenvolveu incapacidade de abertura do olho direito. Não havia associação com outro sintoma neurológico ou oftalmológico. A paciente recebeu injeção de botulinum toxin (BoNT-A) no músculo orbicular a direita, na região pretarsal e no canto lateral. A BoNT-A foi efetiva para o tratamento da AAP associada com miotomia congênita de Becker.
Subject(s)
Humans , Female , Adult , Apraxias/drug therapy , Botulinum Toxins, Type A/therapeutic use , Eyelid Diseases/drug therapy , Myotonia Congenita/complications , Neurotoxins/therapeutic use , Apraxias/etiology , Time Factors , Reproducibility of Results , Treatment Outcome , Eyelid Diseases/etiology , Facial Muscles/drug effects , Facial Muscles/physiopathology , Oculomotor Muscles/drug effectsABSTRACT
Clinical evidence and the use of experimental models in laboratory animals indicate that the intestine is a reservoir of microorganisms that can cause systemic infection in the human. The purpose of this work was to study the possible effect of intestinal obstruction (IO) on the mechanical and chemical barriers that bring protection against microorganisms crossing from the intestinal lumen towards the systemic tissues. We demonstrated that 24 hours after IO, histological and ultrastructural alterations do occur, seriously compromising the structure of the intestinal barrier in 100 per cent of the studies animals. Likewise, it was observed that during the same period, microorganisms translocation from intestine to the peritoneal cavity and liver (100 and 80 per cent respectively) occurred. The lungs were spared. Changes observed in the intestinal epithelium are related to a process similar to that produced by intestinal ischemia: mitochondrial destruction, with subsequent decrease of its capacity to supply eb