Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Miller-Fisher syndrome (MFS) typically presents with ophthalmoplegia, ataxia, and areflexia. Atypical MFS additionally includes bulbar impairment, affection of the limbs, or abortive presentations. Mostly, MFS follows an infection with Campylobacter jejunii. Aspergilloma has not been reported to trigger MFS. In a 48-year-old male tiredness, tinnitus, otalgia, parietal hyperaesthesia, coughing, plugged nose, hypoacusis, globus sensation, epipharyngeal pain, dysarthria, hypogeusia, arthralgia, lid cloni, facial hypaesthesia and tooth ache consecutively developed. There were occasional lid cloni, left-sided facial hypaesthesia, reduced gag reflex, divesting soft palate, and absent tendon reflexes. CSF investigations revealed normal cell-count but increased protein. Antibodies against GM1 and GQ1b were negative. Atypical MFS was diagnosed. Otolaryngological examinations revealed chronic sinusitis maxillaris from an aspergilloma. After immunoglobulins and resectioning of the aspergilloma, neurological abnormalities disappeared within 19d. MFS may manifest as unilateral lower cranial nerve lesions without affection of the upper cranial nerves or ataxia. Atypical MFS may be triggered by parasinusoidal aspergilloma.
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PMID:Anti-GQ1b-negative Miller-Fisher syndrome with lower cranial nerve involvement from parasinusoidal aspergilloma. 1608 Nov 59

The child who presents with acute coma runs a high risk of cardiopulmonary insufficiency, direct brain injury or even cerebral herniation. The case-management of such child requires a coma-specific emergent evaluation, immediate treatment of any hypoxicischemic insults and of the underlying cause. The coma-specific examination includes performance of child-adapted Glasgow Coma Score, the evaluation of brain stem functions such as pupillary response to light, cough- and gag reflex, and determination of all vital signs including body temperature. Treatment of hypoxicischemic insults includes control of airways and ventilation in patient with coma defined as GCS <8; liberal treatment of impaired cardiovascular states with isotonic fluids such as 0.9% sodium chloride; and treatment of cerebral herniation with head elevation, mannitol, hypertonic sodium chlorid fluids, steroids and hyperventilation. Immediately treatable causes are hypoglycemia, meningitis/encephalitis, opioid overdose and status epilepticus. Exclusion of rapidly progressive intracranial lesions almost always requires referral to the tertiary centre with head CT-scan facilities. Finally, an extensive etiology search of the stable coma is performed by looking for disease or trauma of the brain, for metabolic causes, for intoxications and for cardiopulmonary problems.
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PMID:[The comatose child]. 1613 15

A 27-year-old male intravenous drug user presented to the Emergency Department of St James's Hospital with a 1-week history of progressive dysphasia, dysphagia and difficulty 'holding his head up' and 'keeping his eyes open'. He also complained of increasing weakness in his upper limbs, as a result of which he kept dropping things. He was on a methadone program but was using both intravenous heroin and cocaine at the time of presentation. Examination of his motor function revealed generalized hypotonia, hyporeflexia and reduced power in both upper limbs. No sensory loss was observed. Co-ordination was intact. The clinical picture of a proximal symmetrical descending weakness and an absence of sensory loss was suggestive of botulism. Clostridium botulinum is a spore-forming, obligate anaerobe. The three forms of human botulism are food-borne, wound and intestinal. A fourth man-made form is produced from aerosolized botulinum toxin and results in inhalational botulism. A little as 1 g of aerosolized botulinum toxin has the potential to kill 1.5 million people. Toxin is detected in serum or stool specimens in only approximately 46% of clinically diagnosed cases. Treatment involves supportive care and early passive immunization with equine antitoxin. Patients should be regularly assessed for loss of gag and cough reflex, control of oropharyngeal secretions, oxygen saturation, vital capacity and inspiratory force. When respiratory function begins to deteriorate, anticipatory intubation is indicated. Early symptom recognition and early treatment with antitoxin are essential in order to prevent mortality, and to prevent additional cases, it is important to ascertain the presence of similar symptoms in contacts of the patient and local public health officials must be notified as one case may herald an outbreak. Given the continued threat of bioterrorism, the Centre for Disease Control Surveillance System in the United States must also be notified of any cases of botulism.
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PMID:Descending polyneuropathy in an intravenous drug user. 1617 64

Oropharyngeal dysphagia is frequent during the acute phase of stroke, but most patients recover. Dysphagia is related to higher incidence of aspiration, pneumonia and death. Frequently neither clinical history nor neurological evaluation predicts the presence of aspiration. In 64 patients not recovered from severe stroke after the acute phase with clinically suspected oropharyngeal dysphagia we investigated: (i) the correlation between clinical manifestations and videofluoroscopic findings; (ii) predictive factors of aspiration and silent aspiration. Clinical examination showed that 44% had impaired gag reflex, 47% cough during oral feeding, and 13% changes in voice after swallowing. Videofluoroscopy revealed some abnormality in 87%: 53% in the oral phase and 84% in the pharyngeal phase (aspiration in 66%; half being silent). Impaired pharyngeal safety was more frequent in posterior territory lesions and patients with a history of pneumonia (P<0.01). No correlation was found between clinical evaluation findings and presence of aspiration. Silent aspirations were more frequent in patients with previous orotracheal intubation (P<0.05) and abnormalities in velopharyngeal reflexes (P<0.05). We concluded that in patients not recovered from severe stroke after the acute phase and with suspected oropharyngeal dysphagia, clinical evaluation is of scant use in predicting aspiration and silent aspiration. Videofluoroscopic examination is mandatory in these patients.
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PMID:Oropharyngeal dysphagia after the acute phase of stroke: predictors of aspiration. 1648 10

This retrospective study determined whether specific neurological features were associated with initial and final swallowing outcomes in acute stroke patients. A chart review of 65 acute stroke patients suggested that certain clinical and neurocognitive behaviors were associated with swallowing outcomes. Hemispatial neglect was significantly associated with initial nonoral dietary intake, whereas aphasia was not associated with swallowing outcome. Results from the initial clinical swallowing evaluations suggested that the presence of at least four of six clinical features (cough after swallow, voice change after swallow, abnormal volitional cough, abnormal gag reflex, dysphonia, and dysarthria) were associated with poor initial and final swallowing outcomes. Whether specific lesion location, size, or a combination of clinical neurological deficits are associated with poor initial and final swallowing outcomes is unclear. Prospective studies are warranted for further investigation of these relationships.
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PMID:Clinical and cognitive predictors of swallowing recovery in stroke. 1704 16

Aspiration in critically ill patients frequently causes severe co-morbidity. We evaluated a diagnostic protocol using routine FEES in critically ill patients at risk to develop aspiration following extubation. We instructed intensive care unit physicians on specific risk factors for and clinical signs of aspiration following extubation in critically ill patients and offered bedside FEES for such patients. Over a 45-month period, we were called to perform 913 endoscopic examinations in 553 patients. Silent aspiration or aspiration with acute symptoms (cough or gag reflex as the bolus passed into the trachea) was detected in 69.3% of all patients. Prolonged non-oral feeding via a naso-gastric tube was initiated in 49.7% of all patients. In 13.2% of patients, a percutaneous endoscopic gastrostomy was initiated as a result of FEES findings, and in 6.3% an additional tracheotomy to prevent aspiration had to be initiated. In 59 out of 258 patients (22.9%), tracheotomies were closed, and 30.7% of all 553 patients could be managed with the immediate onset of an oral diet and compensatory treatment procedures. Additional radiological examinations were not required. FEES in critically ill patients allows for a rapid evaluation of deglutition and for the immediate initiation of symptom-related rehabilitation or for an early resumption of oral feeding.
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PMID:Fiberoptic endoscopic evaluation of swallowing in intensive care unit patients. 1796 75

A two-year-old male entire border collie dog was evaluated for a short history of mixed bowel diarrhoea, coughing, vomiting and stranguria. Physical examination revealed dyspnoea with increased ventral lung sounds and a flaccidly distended bladder. Neurological examination revealed poor pupillary light reflexes, an absent gag reflex and a poor anal tone. Thoracic radiography was consistent with megaoesophagus and aspiration pneumonia. Clinicopathological testing revealed an elevated muscular nicotinic acetylcholine receptor antibody titre. The dog was euthanased because of clinical deterioration. Cerebrospinal fluid (CSF) collected immediately post-mortem revealed macrophagic pleocytosis. Post-mortem histopathological examination was consistent with dysautonomia. This is the first report of coexisting autoimmune myasthenia gravis and dysautonomia in a non-human species. The concomitant diseases may suggest a common immunopathological aetiology.
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PMID:Autoimmune myasthenia gravis and dysautonomia in a dog. 1868 49

Nurses and other carers of people with learning disabilities must be able to manage choking events and perform basic life support effectively. UK guidelines for assessment of airway obstruction and for resuscitation do not take account of the specific needs of people with profound multiple learning disability. For example, they fail to account for inhibited gag and coughing reflexes, limited body movements or chest deformity. There are no national guidelines to assist in clinical decisions and training for nurses and carers. Basic life support training for students of learning disability nursing at Birmingham City University is supplemented to address these issues. The authors ask whether such training should be provided for all nurses including those caring for children and young people. They also invite comment and discussion on questions related to chest compression and training in basic life support for a person in a seated position.
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PMID:Basic life support and children with profound and multiple learning disabilities. 1898 40

Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with the demyelination of extrapontine areas of the central nervous system. It typically occurs 0.5-7 days after a rapid increment in serum Na level in hyponatremic patients and may lead to death. A 2.5-year-old child with a diagnosis of acute myeloblastic leukemia developed febril neutropenia, diarrhea, gastrointestinal hemorrhage followed by pulmonary aspergillosis. He could not tolerate enteral nutrition. He was given broad spectrum antibiotics and antifungal treatment. Laboratory tests showed electrolyte abnormalities including hyponatremia, hypokalemia and hypophosphatemia in a chronic course. Twenty three days after a rapid correction of hyponatremia (16 mEq/L/24 h) he revealed flask quadriparesis, disphagia, mutism, irregular respiratory pattern and loss of cough and gag reflex. Cranial magnetic resonance showed central pontine and extrapontine myelinolysis. He required mechanical ventilation and then he regained his neurologic functions. He completed chemotherapy protocol and underwent hematopoietic stem cell transplantation. After 2.5 years of the occurrence of CPM he is in completely normal physical and neurological status. CPM is a very severe but rare disorder in children with underlying disease. In the presence of multiple etiologic factors it may reveal a delayed onset and optimum outcome can be seen even in the severe clinical presentation with adequate intensive support.
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PMID:Complete clinical recovery of a central pontine and extrapontine myelinolysis delayed onset in a child with acute myeloblastic leukemia. 2131 30

Chimpanzee attacks can be vicious, mutilating, and disabling if not fatal. Stereotypically, the hands and face are targeted, and in male victims, genitalia are mutilated. The authors present a case highlighting the difficulties with early neurological assessment following such an attack. This 55-year-old woman was attacked by a 14-year-old chimpanzee. She suffered mutilation of both hands, severe midface bony, soft-tissue, and eye injuries, and scalp degloving. An emergency tracheotomy was performed at the scene, with an unclear duration of hypoxia. The patient was unresponsive without spontaneous movements, papillary or corneal reflexes, cough, or gag. Attempts to lighten sedation were not tolerated. Brain CTs were normal. Intracranial pressure monitoring was deemed infeasible. Brain MR imaging suggested diffuse axonal injury consistent with severe shaking trauma. Diffusion tensor imaging indicated intact corticospinal tracts, confirmed by somatosensory evoked potentials. Magnetic resonance imaging suggested left optic nerve transaction, and right retinal detachment was diagnosed. Electroencephalography showed severe diffuse encephalopathy. Auditory evoked potentials showed absent auditory pathway responses except for a right delayed wave V. Visual evoked potentials indicated absent visual function. At 1 month after the attack, sedation and analgesia weaning revealed lower-extremity movement to command, but no upper-limb response. Cervical spine and brachial plexus MR imaging showed brachial plexus edema. Two months after the attack, the patient regained strength in all her extremities and verbally communicated using a Passy-Muir tracheostomy valve. Chimpanzee attacks on humans can cause extensive, life-threatening injuries. The neurological assessment of such patients is challenging, complicated by limb and craniofacial disfigurement and the need for heavy sedation. Initial assessment of nervous system integrity may rely on costly imaging and electrophysiological studies.
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PMID:Difficulties with the neurological assessment of humans following a chimpanzee attack. 2196 65


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