Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen patients with severely handicapped children were divided into 3 groups; tube-fed patients (group 1, n = 8), oral-fed patients with dysphagia (group 2, n = 3) and oral-fed patients (group 3, n = 8). Clinical symptoms, past history, cranial CT, EEG, blink reflex and auditory brainstem response were evaluated in these patients. All patients of group 1 and 2 could not control head or sit by themselves. They needed naso-oral suction. However, nasal airway, intubation and tracheostomy were necessary only in group 1 patients. Five out of 8 patients of group 3 could control head and sit by themselves. No one needed naso-oral suction. CT revealed ventricular dilatation or prominent destructive lesions in group 1. However, patients of group 2 and 3 showed the lesions of mild to moderate degree. EEGs showed poorly developed background activities or electrical status epilepticus in group 1, while they showed relatively well-developed background activities with less prominent paroxysmal discharges in group 2 and 3. R2 component of blink reflex was absent bilaterally in 90% patients of group 1 and 2, while unilateral R2 at least was present in group 3. Feeding problems in severely handicapped children were affected by combination of cerebrum and brainstem involvements. Examination of cranial CT, EEG and blink reflex was useful to determine the method of feeding.
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PMID:[Feeding problems in severely handicapped children]. 138 24

This study reports on a girl with a permanent cerebral lesion and opercular syndrome after status epilepticus (SE). She had previously been healthy and had her first focal motor seizure at 5 years of age, which was controlled with intravenous phenytoin and rectal diazepam. Twenty-four hours later, she developed partial SE consisting of right facial twitching and right-hand clonic movements. These uncontrollable seizures lasted for 5 days, after which the partial SE changed to generalized SE, and the seizures continued for another 5 days. CT performed the day before onset of SE revealed no brain abnormality. Another CT performed a year later disclosed bilateral brain lesions, more severe in the left hemisphere. Follow up at 16 years of age revealed moderate motor sequelae of the right-hand side of the body, anarthria, difficulty chewing, dysphagia, bilateral facial weakness, and drooling, all of which clinically characterize opercular syndrome. An MRI study performed at 14 years of age showed a cerebral parenchymatous lesion which extended between the parietal cortices of both hemispheres, more severe on the left side, and which crossed the corpus callosum, destroying the posterior-middle zone. Evidence from the CT indicates that the lesion was not present before onset of SE. It seems likely that the focal SE caused the focal brain damage, but the possibility that the subsequent generalized SE played a role cannot be excluded.
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PMID:Status epilepticus-induced brain damage and opercular syndrome in childhood. 1087 32

A 64-year-old man developed progressive dementia and altered consciousness with myoclonus over 2 months. Neurological examination revealed mild dysphagia and negative myoclonus of both hands. Electroencephalography (EEG) showed continuous periodic synchronous discharge (PSD) of 1 Hz, although his EEG abnormality was not similar to that usually observed in Creutzfeldt-Jakob disease (CJD). Magnetic resonance imaging (MRI) of the brain revealed only few lacunes. Laboratory data were also normal. Since his consciousness level fluctuated and the PSD were spiky, we came to a diagnosis of nonconvulsive status epilepticus (NCSE). After administering the valproic acid, his symptoms and EEG finding improved. Nine months after the onset, despite his continued valproic acid, the patient had recurrent NCSE and PSD of 1 Hz. Diffusion-weighted MRI showed a T2-hyperintense lesion in the right parietal lobe, where SPECT scans showed hyperperfusion. After adding zonisamide, he improved slowly. The follow-up MRI and SPECT showed a disappearance of the previous lesion. Now CT scans of the abdomen showed enlarged periaortic lymph node and endoscopic ultrasonography disclosed a submucosal tumor of the stomach. Biopsy of the periaortic lymph node by laparotomy revealed undifferentiated adenocarcinoma with its origin being unclear. Chemotherapy didn't work well for the tumor and the patient underwent a downhill course, although his mental and neurological manifestation were mostly unremarkable. Two years and four months after the onset, he died in emaciation. Autopsy confirmed small cell carcinoma originating in the stomach and metastases in the liver and lungs. Neuropathological examination revealed only mild scattered gliosis. This case was unique in the prolonged CJD-like manifestations, which turned out to be due to NCSE. Despite anti-neuronal antibodies were not detected, we suspect yet another paraneoplastic brain syndrome in this patient.
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PMID:[An autopsy case of encephalopathy associated with small cell carcinoma of the stomach with nonconvulsive status epilepticus resembling Creutzfeldt-Jakob disease]. 1283 85

The vagus nerve stimulator has become a standard modality for intractable pediatric epilepsy. We reviewed our experience with major adverse events, after accidental puncture of a stimulator wire by an emergency room physician seeking intravenous access to treat status epilepticus. The Children's National Medical Center database was reviewed for patients undergoing vagus nerve stimulator placement between January 1988 and June 2006. Patient characteristics, duration of therapy, and treatment-limiting adverse events were noted. Of 62 patients implanted over 8 years, 22 (35%) had adverse events which led to a change in therapy. Adverse events included prominent drooling, coughing, throat discomfort, dysphagia, wound infection, difficulty breathing, vomiting, vocal-cord weakness, lead failure, and iatrogenic (piercing of wire; surgical clipping of wire during revision). Eight patients required nonroutine surgical intervention (13%). There were two unusual case presentations. In a 13-year-old boy with status epilepticus at an outlying emergency department, the stimulator line was pierced in search of intravenous access. In a 25-year-old housepainter, neck paresthesias upon right lateral neck turning were attributed to insufficient strain relief. Treatment-limiting adverse events occurred in approximately one-third of patients. Unanticipated adverse events included misidentification of the wire for intravenous access, clipping of the wire during surgical dissection, and cervical dysesthesias associated with head-turning.
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PMID:Misidentification of vagus nerve stimulator for intravenous access and other major adverse events. 1835 2

The literature data on using intravenous forms of AEDs that expand treatment possibilities for patients with epilepsy are presented. AEDs can be used in different situations, when patients are not able to take AEDs in per os. These situations can include seizure emergencies (recurrent seizures, clusters, status epilepticus), caused by disease decompensation; acute symptomatic seizures; perioperative preparation in the case of surgery; dysphagia; gastrointestinal problems; psychiatric disorders, and others. This article is based on a review of International and Russian expert consensus practice guidelines for management of clinical situations mentioned above. The authors present data on available Russian parenteral forms of drugs used today (valproats, levetiracetam, lacosamide, diazepam, midazolam, propofol, thiopental potassium). It has been concluded that an ideal intravenous AED should be highly effective, acts fast, has no severe adverse effects, has low drug-drug interactions, does not require frequent plasma concentration monitoring, and should be easily switched to a per os form without any additional titration. The importance of separate treatment approaches on different stages of medical help is emphasized. The choice of drug used can be influenced by a particular clinical situation, indications/contraindications, the recommended infusion speed, side effects, possible drug-drug interactions with other AEDs and other drugs used for the treatment of concomitant diseases, availability of a particular drug at the moment and the level of a physician's knowledge of usage of intravenous forms of AEDs.
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PMID:[Possibilities of using intravenous forms of antiepileptic drugs in epileptic seizures]. 2487 39

Maternal status epilepticus can cause fetal hypoxic ischemic encephalopathy that in turn results in acute polyhydramnios caused by fetal dysphagia; thus, acute polyhydramnios is a symptom that should lead to a suspicion of fetal dysphagia caused by hypoxic ischemic encephalopathy.
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PMID:Acute polyhydramnios after maternal status epilepticus. 2633 Oct 18