Cases reported "Myasthenia Gravis"

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11/76. Ocular myasthenia mimicking a one-and-a-half syndrome.

    A 52-year-old patient developed an eye movement disorder first resembling a left internuclear ophthalmoplegia and subsequently a "one-and-a-half syndrome" as the presenting symptoms of ocular myasthenia gravis. No accompanying myasthenic features were present except for the fluctuation in the amplitude of dissociated nystagmus. This patient shows that an oculomotor disorder considered a typical pontine lesion may instead be caused by myasthenia gravis, even in the absence of other clinical and electrophysiologic features of neuromuscular deficit.
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keywords = motor
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12/76. Pseudomyasthenia resulting from a posterior carotid artery wall aneurysm: a novel presentation: case report.

    OBJECTIVE AND IMPORTANCE: Painful oculomotor palsy can result from enlargement or rupture of intracranial aneurysms. The IIIrd cranial nerve dysfunction in this setting, whether partial or complete, is usually fixed or progressive and is sometimes reversible with surgery. We report an unusual oculomotor manifestation of a posterior carotid artery wall aneurysm, which mimicked ocular myasthenia gravis. CLINICAL PRESENTATION: A 47-year-old woman developed painless, intermittent, partial IIIrd cranial nerve palsy. She presented with isolated episodic left-sided ptosis, which initially suggested a metabolic or neuromuscular disorder. However, digital subtraction angiography revealed a left posterior carotid artery wall aneurysm, just proximal to the origin of the posterior communicating artery. INTERVENTION: The aneurysm was successfully clipped via a pterional craniotomy. During surgery, the aneurysm was observed to be compressing the oculomotor nerve. The patient's symptoms resolved after the operation. CONCLUSION: The variability of incomplete IIIrd cranial nerve deficits can present a diagnostic challenge, and the approach for patients with isolated IIIrd cranial nerve palsies remains controversial. Although intracranial aneurysms compressing the oculomotor nerve classically produce fixed or progressive IIIrd cranial nerve palsies with pupillary involvement, anatomic variations may result in atypical presentations. With the exception of patients who present with pupil-sparing but otherwise complete IIIrd cranial nerve palsy, clinicians should always consider an intracranial aneurysm when confronted with even subtle dysfunction of the oculomotor nerve.
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keywords = motor
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13/76. myasthenia gravis: the otolaryngologist's perspective.

    myasthenia gravis is a motor neuron disease caused by the presence of antibodies against acetylcholine receptors that interfere with the proper function of the neuromuscular junction. Twenty percent of patients with myasthenia gravis present some type of bulbar deficits such as rhinolalia, dysphagia or dysphonia as the first symptom of disease. We report 5 patients with deficits that illustrate different aspects of the disease. Our role as otolaryngologists is to establish a diagnosis or to provide a solution for the respiratory failure caused by chronic aspiration.
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14/76. Respiratory failure due to vocal cord paresis in myasthenia gravis.

    This report describes a female patient with myasthenia gravis who developed respiratory failure due to vocal cord paresis. The diagnosis was delayed due to the absence of other myasthenic symptoms (e.g. ptosis, muscle weakness and dysphagia). On direct laryngoscopy, her vocal cords were seen to be in the paramedian position and to move apart after the intravenous injection of edrophonium. The patient initially presented with ocular myasthenia and later returned with isolated respiratory failure. A review of the pertinent literature revealed few reports on myasthenia gravis presenting in this manner.
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ranking = 339.65569103867
keywords = vocal
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15/76. Transient eyelid retraction in myasthenia gravis.

    Three patients with myasthenia gravis had transient retraction of the upper eyelids which usually followed prolonged upgaze and which persisted for many seconds. This could result from post-tetanic facilitation, myotonia, or a transient contracture. Retraction of this type is to be distinguished from both the long-standing unilateral retraction associated with ptosis of the contralateral eyelid and the fleeting lid twitch sign.
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ranking = 2.0123049588927
keywords = transient
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16/76. Clinical correlates with anti-MuSK antibodies in generalized seronegative myasthenia gravis.

    The term seronegative myasthenia gravis (SNMG) refers to the generalized disease without detectable anti-acetylcholine receptor (anti-AChR) antibodies. In these patients, IgG antibodies against the muscle-specific kinase (MuSK) have been described, which reduced agrin-induced AChR clustering in vitro. We have assayed anti-MuSK antibodies in 78 patients with SNMG, who have been followed for many years in our Institution. Here we describe the clinical phenotype of the 37 patients whose results were positive on this assay. MG with anti-MuSK antibodies was characterized by a striking prevalence of female patients (eight men and 29 women). age of onset ranged from 6 to 68 years, with 56.8% of patients presenting under 40 years of age. All these patients shared a similar pattern of muscle weakness, with prevalent involvement of cranial and bulbar muscles and a high frequency of respiratory crises; the involvement of limb muscles was comparatively less severe and inconsistent. Single-fibre-EMG confirmed the most sensitive examination in the EMG diagnosis of MuSK-positive disease, while, owing to weakness topography, repetitive nerve stimulation in limb muscles was diagnostic in 56.8% of cases. The effect of edrophonium (or neostigmine) injection was equivocal or negative in 11 of 37 patients (29.7%), and the response to oral pyridostigmine was even more unsatisfactory, ranging from mild benefit to overt intolerance. In thymectomized patients, thymus was normal for age or atrophied, and no benefit from surgery was noticed. Thirty-five of 37 patients were given immunosuppressive therapy and 22 received plasma-exchange. The course of the disease was often characterized by periodic exacerbation phases requiring hospitalization and even assisted ventilation; plasma-exchange produced marked improvement in these cases. At the end of the observation period, most patients, although improved, were still symptomatic, having developed permanent facial and pharyngeal weakness together with some atrophy of facial muscles. MuSK-negative disease was comparatively more heterogeneous. Most patients were affected with mild to moderate symptoms and responded well to pharmacological treatment; however, a few subjects in this group had severe refractory disease, poorly responsive to both acetylcholinesterase inhibitors and immunosuppressants.
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ranking = 56.609281839779
keywords = vocal
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17/76. Acute stridor due to bilateral vocal fold paralysis as a presenting sign of myasthenia gravis.

    We describe a case of myasthenia gravis in a 46-year-old man presenting as acute stridor with bilateral abductor paralysis of the vocal folds. Prompt diagnosis and medical treatment with pyridostigmine avoided the need for tracheostomy. It is important to remember the possibility of myasthenia gravis in cases of stridor due to bilateral vocal fold paralysis, since effective medical treatment is available.
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ranking = 339.65569103867
keywords = vocal
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18/76. Unusual neurophysiological and immunological findings in myasthenia gravis: a case report.

    We describe the case of a male patient with ocular myasthenia gravis who developed a diabetic neuropathy similar to chronic inflammatory demyelinating polyradiculoneuropathy associated with transient generalized 'myokymic' discharges and distal weakness. He had antibodies against acetylcholine receptor and GQ1b ganglioside, but not anti-voltage-gated K( ) channel antibodies. Serial electrophysiological and immunological findings showed that diabetes was involved in the immune-mediated mechanism of peripheral neuropathy. We hypothesize that the concomitant appearance of distal motor weakness and decreased compound muscle action potentials upon repetitive nerve stimulation, together with increased distal motor latency and generalized peripheral nerve hyperexcitability, were all related to transient serum positivity to anti-GQ1b antibodies.
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ranking = 4.0123049588927
keywords = transient, motor
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19/76. Myasthenia in a patient with sarcoidosis and schizophrenia.

    A 44-year-old male patient was hospitalised with paranoid schizophrenia in 1985. Depot neuroleptic treatment was started which successfully prevented further psychotic relapses for the next ten years. His myasthenia gravis started with bulbar signs in 1997 and the symptoms soon became generalized. The diagnosis of myasthenia gravis was confirmed by electromyography, by positive anticholinesterase test and by the detection of anti-acetylcholine receptor antibodies in the serum. Mediastinal CT examination showed enlarged hilar lymph nodes on the left but no thymic pathology was observed. mediastinoscopy was performed and biopsies were obtained from the affected nodes. histology revealed sarcoidosis. The patient suffered respiratory crisis following the thoracic intervention (in September 1998). Combined oral corticosteroid (64 mg methylprednisolone/e.o.d.) and azathioprine (150 mg/day) treatment regimen was initiated and complete remission took place in both the myasthenic symptoms and the sarcoidosis. The follow-up CT scans showed no mediastinal pathology (January 2000). During steroid treatment a transient psychotic relapse occurred which was successfully managed by supplemental haloperidol medication added to his regular depot neuroleptics. The patient currently takes 150 mg/day azathioprine and receives 40 mg/month flupentixol depot i.m. His physical and mental status are stable and he has been completely symptom free in the last 24 months. The association of myasthenia gravis and sarcoidosis is very rare. To our best knowledge no case has been reported of a patient suffering from myasthenia gravis, sarcoidosis, and schizophrenia at the same time.
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ranking = 1.0061524794463
keywords = transient
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20/76. pupil-sparing, painless compression of the oculomotor nerve by expanding basilar artery aneurysm: a case of ocular pseudomyasthenia.

    BACKGROUND: oculomotor nerve paresis may have relatively benign but also life-threatening causes. Distinguishing between these is of great clinical importance. OBJECTIVE: To reveal a potential pitfall of the clinical evaluation of oculomotor nerve paresis. PATIENT: Single case observation. RESULTS: A 56-year-old man had fluctuating diplopia and fatigable ptosis, promptly relieved by intravenous edrophonium, leading to the diagnosis of ocular myasthenia gravis. His pupillary function was intact. A few days after the initial diagnosis, he suffered a subarachnoid hemorrhage secondary to the rupture of a basilar artery aneurysm. His ocular symptoms were related to aneurysmal oculomotor nerve compression. CONCLUSION: patients with oculomotor nerve dysfunction need more detailed evaluation because the underlying cause cannot be safely determined on a clinical basis.
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ranking = 8
keywords = motor
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