ABSTRACT
OBJECTIVE: Myasthenia gravis (MG) is commonly viewed as a muscle disorder. Less is known about neurosensory function and dysfunction in MG. We aim to evaluate olfactory and gustatory behavior in Turkish patients with MG, and compare these results with age and sex-matched healthy controls. MATERIAL/METHODS: 30 individuals with MG, and 30 healthy volunteers were studied. Olfactory function was studied with the Sniffin' sticks test. Taste strip test was used for studying taste function. The t-test was used for analyzing continuous variables, and the chi-square test for categorical data. Clinical staging and medication status were included in a model analyzed using analysis of variances. RESULTS: MG patients showed significantly lower olfactory (p<0.001) and gustatory scores (p<0.001) than the healthy controls. In addition, olfactory loss correlated with the severity of the disease. Medications for MG did not influence these results. CONCLUSION: This study replicates the olfactory dysfunction found elsewhere in MG. Further, gustatory dysfunction, an activity unrelated to muscle strength, was also unveiled. Medications used for treating MG must not be blamed for the chemosensory dysfunction found in this neurological disorder.
Subject(s)
Gastrointestinal Diseases/etiology , Myasthenia Gravis/complications , Olfaction Disorders/etiology , Adult , Analysis of Variance , Case-Control Studies , Female , Humans , Male , Mental Status Schedule , Middle Aged , Myasthenia Gravis/epidemiology , Sensory Thresholds/physiology , Smell/physiology , Taste/physiology , Turkey/epidemiologyABSTRACT
OBJECTIVE: We present a patient who developed visual loss after carbon monoxide (CO) poisoning and was treated with hyperbaric oxygen. CLINICAL PRESENTATION AND INTERVENTION: A 21-year-old woman poisoned with CO (with coma lasting 4 h and carboxyhemoglobin level 46%) developed seizures and cortical blindness 3 days after poisoning. Four years later, her visual acuity was 0.2 in both eyes. An (18)F-fluorodeoxyglucose positron emission tomography (PET) scan showed reduced metabolism in the bilateral posterior temporal and occipital lobes. The patient received a total of 50 hyperbaric oxygen sessions over 3 months for visual loss and the visual acuity improved to 0.5 in both eyes. In addition, increased metabolism was detected in the brain in post-treatment PET scans. CONCLUSION: PET documented brain hypoperfusion 4 years after CO poisoning and hyperbaric oxygen therapy improved visual acuity. However, we cannot endorse routine use of hyperbaric oxygen for such patients, until results of further clinical trials demonstrate efficacy of hyperbaric oxygen in CO-induced chronic brain injury.
