ABSTRACT
Involuntary movement is a rare clinical manifestation of transient ischemic attack (TIA). However, limb-shaking TIA is well described presentation of carotid occlusive disease. We present the case of a patient who developed limb-shaking TIA associated with high-grade stenosis of middle cerebral artery (M1), which was treated with percutaneous transluminal angioplasty (PTA). The procedure was performed successfully without complication and the symptom disappeared immediately after the procedure. The patient remained free of symptoms at the 38-month follow-up. There was no tendency of restenosis of M1. In this case, PTA was technically feasible and beneficial for limb-shaking TIA with M1 stenosis. Limb-shaking TIA can be a symptom of high-grade stenosis of M1.
Subject(s)
Ischemic Attack, Transient/pathology , Middle Cerebral Artery/pathology , Aged , Angiography , Constriction, Pathologic , Female , Humans , Ischemic Attack, Transient/etiology , Ischemic Attack, Transient/surgery , Magnetic Resonance Imaging , Middle Cerebral Artery/surgeryABSTRACT
A 57-year-old woman developed muscular stiffness and painful cramps, which were relieved by administration of dantrolene sodium. Her serum level of antibodies to glutamic acid decarboxylase (GAD) was markedly elevated and continuous muscular activities were observed on resting surface EMG. These features were compatible with those in stiff-person syndrome (SPS). She was found to have thymoma on CT scan. Immediately after thymomectomy, which was histologically diagnosed as a benign hyperplasia, she developed head retraction reflex-like movements evoked by sensory stimulation to the face, which were followed by severe bulbar symptoms with dysphagia and respiratory arrest. Postoperative myasthenia gravis was excluded clinically. While somatosensory evoked EMG on splenius muscle initially showed biphasic responses with latency of 15 msec and 55 msec, respectively after oral angle non-painful electric stimulation, the late potential phase disappeared after the patient recovered from bulbar symptoms. This suggests that head retraction reflex-like movements of this patient reflected the attenuation of inhibitory potentials from the brainstem.
Subject(s)
Dyspnea/etiology , Head Movements , Reflex , Stiff-Person Syndrome/complications , Stiff-Person Syndrome/physiopathology , Autoantibodies/blood , Biomarkers/blood , Brain Stem/physiopathology , Dantrolene/therapeutic use , Deglutition Disorders/etiology , Female , Glutamate Decarboxylase/immunology , Humans , Middle Aged , Stiff-Person Syndrome/diagnosis , Stiff-Person Syndrome/drug therapy , Thymus Hyperplasia/complicationsABSTRACT
We described a patient with ataxic Guillain-Barré syndrome who subsequently developed facial diplegia. A 38-year-old man developed ataxia, distal limb paresthesias, mild dysphagia, urinary retention and orthostatic hypotension a week after an episode of laryngitis. He had high titers of serum anti-GQ1b, anti-GD1b, anti-GM1b, anti-GT1a, and anti-GD1a IgG antibodies during the acute phase. Although the initial symptoms markedly improved by intravenous immunoglobulin therapy, asymmetric facial diplegia subsequently occurred and remained longer than ataxia. Similar course of facial nerve palsy has been reported in patients with Fisher syndrome. Common pathophysiological mechanism may function in the development of delayed facial diplegia in Fisher syndrome and ataxic Guillain-Barre syndrome.
