Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 69-year-old man who developed paralytic poliomyelitis in childhood and then decades later suffered from fatal respiratory failure. Six months before this event, he had progressive weight loss and shortness of breath. He had severe muscular atrophy of the entire right leg as a sequela of the paralytic poliomyelitis. He showed mild weakness of the facial muscle and tongue, dysarthria, and severe muscle atrophy from the neck to proximal upper extremities and trunk, but no obvious pyramidal signs. Electromyogram revealed neurogenic changes in the right leg, and in the paraspinal, sternocleidomastoid, and lingual muscles. There was a slight increase in central motor conduction time from the motor cortex to the lumbar anterior horn. Pulmonary function showed restrictive ventilation dysfunction, which was the eventual cause of death. Some neuropathological features were suggestive of amyotrophic lateral sclerosis (ALS), namely Bunina bodies. In patients with a history of paralytic poliomyelitis who present after a long stable period with advanced fatal respiratory failure, one may consider not only respiratory impairment from post-polio syndrome but also the onset of ALS.
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PMID:Respiratory failure in a patient with antecedent poliomyelitis: amyotrophic lateral sclerosis or post-polio syndrome? 1616 67

A 29-year-old man, with no significant past medical history, was in his usual state of health until the afternoon of admission. The patient was seated at work eating lunch when he suddenly noticed that his vision became blurry. He covered his right eye and had no visual difficulty but noted blurry vision upon covering his left eye. At this point, the patient tried to stand up, but had difficulty walking and noticed he was "falling toward his left." Facial asymmetry when smiling was also appreciated. The patient denied any alteration in mental status, confusion, antecedent or current headaches, aura, chest pains, or shortness of breath. He was not taking any prescribed medications and had no known allergies. The patient denied any prior hospitalization or surgery. He denied use of tobacco, alcohol, or illicit drugs, and worked as a maintenance worker in a hotel. His family history is remarkable for his father who died of pancreatic cancer in his 50s and his mother who died of an unknown heart condition in her late 40s. Vital signs on presentation to the emergency department included temperature of 97.6 degrees F; respiratory rate of 18 per minute; pulse of 68 per minute; blood pressure of 124/84 mmHg; pulse oximetry of 99% on ambient air. His body mass index was 24 and he was complaining of no pain. The patient had no carotid bruits and no significant jugular venous distention. Cardiovascular exam revealed a regular rate and rhythm with no murmurs. Neurological exam revealed left-sided facial weakness, dysarthria, and preserved visual fields. He was able to furrow his brow. Gait deviation to the left was present, and Romberg sign was negative. Deep tendon reflexes were 2+ throughout, and no other focal neurological deficit was present. The patient was admitted to the hospital with a diagnosis of stroke. Electrocardiogram, fasting lipid profile, computed tomography (CT) scan of head, magnetic resonance imaging (MRI) of head and neck, and transthoracic echo with bubble study were ordered. The initial head CT did not reveal bleeding. He was started on aspirin (ASA). On the second hospital day, the symptoms improved with resolution of dysarthria. His ataxia had also improved. Fasting lipid profile revealed mildly elevated low-density lipoprotein and total cholesterol. His head MRI revealed an acute right thalamic stroke. Echocardiography was significant only for a patent foramen ovale (PFO) with transit of agitated saline "bubbles" from right atrium to left heart within three cardiac cycles (Figure). Doppler ultrasound of extremities revealed no evidence of deep venous thrombosis. A complete resolution of symptoms occurred by the third hospital day. The patient was discharged on full dose aspirin and a statin and was referred for consideration of enrollment in a PFO closure versus medical management trial.
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PMID:Clinical case of the month. A 29-year-old man with acute onset blurry vision, weakness, and gait abnormality. Stroke. 2010 23

Legionnaires' disease is primarily a pneumonic process caused by Legionella pneumophilia, a gram-negative aerobic bacillus but also has multiple system involvement. The most common manifestation is encephalopathy suggesting a generalized brain dysfunction but focal neurological manifestations have been reported. We report a patient with Legionella pneumonia associated with cerebellar dysfunction and unilateral facial nerve weakness. 51-year-old previously healthy male presented with shortness of breath, cough, slurred speech, and unsteadiness on feet associated with malaise, fevers and myalgias. Patient's family reported facial asymmetry for 2 days. Patient had no significant medical history and was not on any medication. He denied smoking, alcohol or illicit drug use. Chest X-ray showed bilateral lower lobe infiltrates. Urinary antigen assay for Legionella pneumophilia serogroup 1 was positive. Patient was started on intravenous moxifloxacin. On day 5 the patient was discharged home and continued oral moxifloxacin for two weeks. After the two weeks, his respiratory symptoms, gait ataxia and dysarthria resolved. We report the first case of Legionnaires' disease with cerebellar dysfunction and seventh nerve palsy. Legionnaires' disease should be considered in patients with any neurological symptoms in the setting of pneumonia. Failure to recognize and treat the infection may lead to poor outcomes.
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PMID:Legionnaires' disease with facial nerve palsy. 2146 Oct 48

Inadvertent injection of nonepidural drugs into the epidural space is a rare situation, which is under-reported, and can lead to serious complications, such as cardiovascular and respiratory complications, paraplegia, or quadriplegia, and can worsen the patients' outcome from surgery. Succinylcholine administered epidurally leads to the appearance of fasciculation and shortness of breath and can prolong neuromuscular blockade. We report a case of accidental administration of 100 mg of succinylcholine via an epidural catheter as a test dose instead of 2 ml 0.5% bupivacaine in a patient planned for major abdominal surgery. After 2 min, the patient complained of shortness of breath; dysarthria; and fasciculation in the trunk, upper limbs, and face. This was managed with induction to general anesthesia (GA). In the postoperative period, no neurological or cardiovascular complications were observed. There is no adequate drug as an antidote of accidentally given nonepidural drugs via an epidural catheter. Succinylcholine given via epidural catheter has been shown to prolong neuromuscular blockade. Proper labeling and storage of syringes are of utmost importance for avoiding these unpleasant situations.
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PMID:Accidental injection of succinylcholine into epidural space as a test dose. 3231 84

This case describes a 60-year-old immunosuppressed man after renal transplant who presented to the emergency department with 1 week of generalized weakness, a 20-lb unintentional weight loss, sore throat, dysarthria, dysphagia, cough, and shortness of breath. Additionally, he developed tinnitus, headaches, photophobia, and neck stiffness. He underwent an extensive workup including a lumbar puncture with meningitis and encephalitis panel, which was positive for varicella zoster virus. He never developed a dermatomal vesicular rash but had persistent dysphagia and aspiration and was eventually diagnosed with Vernet syndrome. This case highlights theories for the increase in varicella zoster virus encephalitis cases causing neurologic symptoms and proposes that this trend is likely to continue.
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PMID:Cranial nerve involvement in varicella zoster virus after renal transplantation. 3310 May 43