Encephalopathy associated with autoimmune thyroid disease in patients with Graves' disease: clinical manifestations, follow-up, and outcomes

<p>Abstract</p> <p>Background</p> <p>The encephalopathy associated with autoimmune thyroid disease (EAATD) is characterized by neurological/psychiatric symptoms, high levels of anti-thyroid antibodies, increased cerebrospinal fluid protein concentration, non-specific electroencephalogram abnormalities, and responsiveness to the corticosteroid treatment in patients with an autoimmune thyroid disease. Almost all EAATD patients are affected by Hashimoto's thyroiditis (HT), although fourteen EAATD patients with Graves' disease (GD) have been also reported.</p> <p>Methods</p> <p>We have recorded and analyzed the clinical, biological, radiological, and electrophysiological findings and the data on the therapeutic management of all GD patients with EAATD reported so far as well as the clinical outcomes in those followed-up in the long term.</p> <p>Results</p> <p>Twelve of the fourteen patients with EAATD and GD were women. The majority of GD patients with EAATD presented with mild hyperthyroidism at EAATD onset or shortly before it. Active anti-thyroid autoimmunity was detected in all cases. Most of the patients dramatically responded to corticosteroids. The long term clinical outcome was benign but EAATD can relapse, especially at the time of corticosteroid dose tapering or withdrawal. GD and HT patients with EAATD present with a similar clinical, biological, radiological, and electrophysiological picture and require an unaffected EAATD management.</p> <p>Conclusions</p> <p>GD and HT equally represent the possible background condition for the development of EAATD, which should be considered in the differential diagnosis of all patients with encephalopathy of unknown origin and an autoimmune thyroid disease, regardless of the nature of the underlying autoimmune thyroid disease.</p

Ocrelizumab versus Interferon Beta-1a in Relapsing Multiple Sclerosis

Supported by F. Hoffmann–La Roche

Vestibular evoked myogenic potentials in evaluating brainstem lesions in multiple sclerosis

32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS) -- SEP 14-17, 2016 -- London, ENGLANDWOS: 000383267201306European Comm Treatment & Res Multiple Sclerosi

Late onset multiple sclerosis: clinical features and misdiagnosis

29th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis / 18th Annual Conference of Rehabilitation in MS -- OCT 02-05, 2013 -- Copenhagen, DENMARKWOS: 000328751401009European Comm Treatment & Res Multiple Sclerosi

Clinical and electrophysiological evaluation of dysphagia in myasthenia gravis

OBJECTIVE—To evaluate dysphagia at the oropharyngeal stage of swallowing and to determine the pathophysiological mechanisms of dysphagia in patients with myasthenia gravis.
METHODS—Fifteen patients with myasthenia gravis with dysphagia and 10 patients without dysphagia were investigated by a combined electrophysiological and mechanical method described previously. Laryngeal movements were detected by a piezoelectric transducer and the related submental EMG (SM-EMG) and sometimes the EMG of cricopharyngeal muscle of the upper esophageal sphincter (CP-EMG) were recorded during dry or wet swallowing. The results of these electrophysiological variables were compared with those of normal age matched control subjects.
RESULTS—In patients with myasthenia gravis with dysphagia, it was found that the time necessary for the larynx to remain in its superior position during swallowing and swallowing variability in successive swallows increased significantly compared with normal subjects and with patients with myasthenia gravis without dysphagia. The total duration of SM-EMG activity was also prolonged in both groups but more severely in the dysphagic patients. Electromyographic activity of the CP sphincter was found to be normal in the dysphagic patients investigated. All the patients with myasthenia gravis with dysphagia had pathological dysphagia limits (<20 ml water) whereas other patients except two, were within normal limits.
CONCLUSIONS—Because the electrophysiological variables related to oropharyngeal swallowing were prolonged even in patients with myasthenia gravis without dysphagia, it is concluded that the submental and laryngeal elevators are involved subclinically in myasthenia gravis and, because of compensating mechanisms, the patient may not be dysphagic. As the CP-EMG behaviour was found to be normal, a coordination disorder between normal CP sphincter muscle and the affected striated muscles of the laryngeal elevators may be one of the reasons for dysphagia in myasthenia gravis. This method also made it possible to investigate the myasthenic involvement in the laryngeal elevators that cannot be evaluated by other electrophysiological methods in myasthenia gravis.