RESUMO
Visual loss in the young adult can be caused by demyelinating diseases, inflammatory and autoimmune processes, infections, ischaemic events, and compressive lesions of the optic nerve. Diagnosis of the aetiologies of visual loss is reached by combining data from radiological studies, electrophysiological tests, and blood and cerebrospinal fluid analysis. Treatment is primarily aimed at decreasing the insult on the optic nerve and eventually controlling the primary disorder. The literature discusses separately the different aetiologies of visual loss. We present a review of the clinical characteristics of visual loss in the young adult, the different diagnostic measures, and the latest therapeutic strategies. The aim of this work is to summarise this entity in a practical way to guide clinicians in the diagnosis and management of this disorder.
Assuntos
Cegueira/etiologia , Doenças Desmielinizantes/complicações , Nervo Óptico/patologia , Neurite Óptica/complicações , Doença Aguda , Cegueira/diagnóstico , Cegueira/fisiopatologia , Cegueira/terapia , Doenças Desmielinizantes/diagnóstico , Doenças Desmielinizantes/fisiopatologia , Doenças Desmielinizantes/terapia , Técnicas de Diagnóstico Oftalmológico , Medicina de Emergência , Humanos , Neurite Óptica/diagnóstico , Neurite Óptica/fisiopatologia , Neurite Óptica/terapia , Guias de Prática Clínica como Assunto , Adulto JovemRESUMO
It is known that after exposure to (3 mM) tetraethylammonium (TEA), guinea-pig isolated trachealis generates tonic spasm followed by phasic tension changes. We found that 8-Br-cAMP or 8-Br-cGMP (10(-6)-5 x 10(-4) M) suppressed tonic spasm secondary to TEA and induced rapid mechanical oscillations. NaN3, forskolin, aminophylline, and isoprenaline had effects similar to those of the cyclic nucleotides. Tetrodotoxin, atropine, diphenhydramine, and cimetidine were without effect on the rapid oscillations. KCl (16 mM) stimulated the oscillations in tissue treated with TEA or TEA plus 8-Br-cGMP. Diltiazem abolished all rhythmic activity in TEA plus 8-Br-cGMP-treated tissues. We conclude: (A) The rapid oscillations are a result of increased cytoplasmic calcium flux with K+ affecting the contractile arm by increasing Ca2+ entry and cyclic nucleotides affecting the relaxant arm by reducing cytosolic free Ca2+. (B) The cyclic nucleotide effect is direct. (C) Cyclic nucleotides may enhance the rate of contraction and relaxation in the presence of some forms of phasic activity.
