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)

Pseudoephedrine and dextromethorphan are therapeutic constituents of numerous commonly used, over-the-counter cough and cold preparations. Although this drug combination is generally considered quite safe if utilized in recommended doses, overmedication or overdose can result in serious neurologic and cardiovascular abnormalities that occasionally can be life-threatening. We present a case of a 2-year-old child who developed hyperirritability, psychosis, and ataxia after being overmedicated with a pseudoephedrine/dextromethorphan combination cough preparation, and discuss probable mechanisms of toxicity and risk factors for adverse events.
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PMID:Dextromethorphan- and pseudoephedrine-induced agitated psychosis and ataxia: case report. 1019 88

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Cases involving ingestion of a dextromethorphan-containing product recorded at a poison control center were studied. A retrospective review of all consultations involving the ingestion of Coricidin HBP Cough & Cold tablets recorded by the California Poison Control System was conducted for the period from January 1 to October 1, 2000. Computerized charts on the consultations were reviewed to obtain data on patient age and sex, number of tablets taken, reason for tablet ingestion, symptoms, treatment, disposition, and outcome. A total of 92 charts (for 92 patients) documenting Coricidin HBP Cough & Cold tablet ingestion were reviewed. The reason for tablet ingestion was classified as abuse in 65 patients (71%), a suicide attempt in 8 (9%), misuse in 1 (1%), malicious administration in 1 (1%), and normal use (but with an adverse drug reaction) in 1 (1%); 16 patients (17%) consumed the tablets for an unknown reason. The 92 patients comprised 42 males and 50 females. Among all patients, 78 (85%) were 13-17 years old, and among those classified as having abusive intent, 58 (89%) were in the same age range. The most commonly reported signs and symptoms associated with ingestion were tachycardia (50 patients), hypertension (29), lethargy (40), mydriasis (20), agitation (15), ataxia or dizziness (20), and vomiting (9). Sixty-one patients (66%) had some alteration in mental status. Fifty-six (61%) were treated in the emergency department; 11 (12%) were admitted. All patients recovered completely. Information on the ingestion of Coricidin HBP Cough & Cold tablets recorded at a poison control center indicated a high rate of abuse of the product among teenagers.
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PMID:Abuse of Coricidin HBP cough & cold tablets: episodes recorded by a poison center. 1159 95

The relation between clinical outcome and single photon emission tomography (SPECT) results in cerebellitis has not been studied. A 63-year-old man developed cerebellar dysfunction with left emphasis one week after onset of cough. The only abnormality on analysis of cerebrospinal fluid was elevated protein (68 mg/dl). Magnetic resonance imaging was normal on the ninth day of ataxia. SPECT showed unilateral cerebellar hypoperfusion on the 13th day, but was normal on the 20th day. His gait improved a little by discharge on the 28th day and his tandem gait was only slightly unsteady six months later. This is the first evidence that normalization of cerebellar hypoperfusion in adult patients with cerebellitis is related to good outcome. Normalization of cerebellar hypoperfusion can occur in three weeks even when ataxia remains severe.
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PMID:Temporary cerebellar hypoperfusion with good outcome in cerebellitis. 1287 Feb 74

As increasing numbers of people choose to sojourn or retire to the mountains, high-altitude illness is becoming a pathological phenomenon about which healthcare providers should have greater awareness. Hypoxia is the primary cause of high-altitude illness, but other stressors on the sympathetic nervous system, such as cold and exertion, also contribute to disease development and progression. Although variable across persons, symptoms of high-altitude disorders usually occur at altitudes over 7000 feet, and typically in 1 of 3 forms: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), or high-altitude pulmonary edema (HAPE). Major symptoms include nausea, poor sleep, headache, lassitude, cough, dyspnea on exertion and at rest, ataxia, and mental status changes. As a rule, illness occurring at high altitude should be attributed to the altitude until proven otherwise. Treatment is best accomplished by descent and by oxygen or pharmacologic intervention if necessary. Under no circumstances should a person with worsening symptoms of high-altitude illness delay descent. As will be discussed in part II of this article, gradual ascent and subsequent acclimatization to altitude is the most effective prevention, though acetazolamide (Diamox) may be a useful prophylactic measure in some.
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PMID:High-altitude-related disorders--Part I: Pathophysiology, differential diagnosis, and treatment. 1513 83

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

Arnold-Chiari I malformation (Chiari I) is a congenital disorder characterized by caudal herniation of cerebellar tonsils through the foramen magnum. The symptoms and signs include headaches precipitated by coughing or exertion, dizziness, visual or oculomotor symptoms, dysphagia, trunk or extremity dysesthesias, ataxia, and drop attacks indicating cerebellar or cervical cord lesion. The symptoms may be provoked by increased intracranial pressure. The mean age of onset of symptoms is 25 years; consequently, previously unidentified Chiari I malformations occur in military personnel. Chiari I is associated with deaths following minor trauma, with acute respiratory failure, and with transient quadriparesis occurring in contact sports. Furthermore, Chiari I symptoms may be aggravated by chiropractic manipulation. This report describes symptoms and signs of Chiari I in four military conscripts in the Finnish Defense Forces. It is important to detect Chiari I in military personnel to establish appropriate service fitness and safety for these patients.
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PMID:Arnold-Chiari malformation type I in military conscripts: symptoms and effects on service fitness. 1657 91

Headache is the cardinal symptom of acute mountain sickness (AMS). The headache normally worsens, with increased cerebral affection and the development of high-altitude cerebral edema (HACE). A Norwegian expedition aimed to climb Baruntse (7129 m) in Nepal in 2003. At 5400 m a 35-year-old man felt exhausted. The next day he aborted his attempt at further climbing as a result of extreme fatigue. Over the next 24 hours he developed cough, dyspnea, and severe hypoxia before progressing to ataxia and blurred vision. At no point did he experience headache or nausea. The patient was evacuated by helicopter. He improved immediately after descent and recovered completely within a week. The speed of progression from AMS to HACE varies. Abrupt onset of HACE is occasionally reported. High-altitude pulmonary edema (HAPE) may induce severe hypoxia that can lead to rapid development of HACE. High-altitude cerebral edema in the setting of HAPE was the most likely diagnosis despite the unusual lack of headache. Rapid onset of HAPE with subsequent severe desaturation should raise awareness of the development of HACE, even in the absence of headache.
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PMID:High-altitude cerebral edema with absence of headache. 1744 14

A 58-year-old male with migraine headaches, complex partial epilepsy, and secondary progressive multiple sclerosis treated with mitoxantrone was admitted to our facility in August 2005 with febrile neutropenia, worsening ataxia, aphasia, cough, and declining mental status. Bone marrow aspirate was consistent with acute nonlymphoblastic leukemia. Review of the literature reveals ten reported cases of nonlymphoblastic leukemias following treatment with mitoxantrone. Although de novo leukemia cannot be fully excluded, the likelihood of de novo disease is low given the patient's medical history. This case continues the important discussion of efficacy versus toxicity when selecting mitoxantrone as a therapeutic option for patients with multiple sclerosis. Although leukemia is rarely seen, the potential for this outcome warrants careful consideration before initiating this therapy.
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PMID:Therapy-related acute nonlymphoblastic leukemia following mitoxantrone therapy in a patient with multiple sclerosis. 1793 54

We present a case of a 4-year-old who presented to the emergency department with an unsteady gait for 2 days. Ataxia is a rare but known manifestation of cerebellar involvement in Lyme disease. A 4-year-old (17 kg) boy with no significant medical history presented to the emergency department (ED) with history of nonbloody emesis for 2 weeks and an unsteady gait for 2 days. Over the past 2 days, his gait had gotten progressively worse until he was unable to walk without assistance. The vomiting would usually occur 1 hour after eating meals. He had also complained of a single headache, which occurred approximately 10 days before admission. The headache did not occur in the early morning hours or wake him up from his sleep. His appetite for the weeks before admission had progressively decreased, and he had also become more irritable, especially when stimulated. He had increased fatigue for the week before presentation. His parents denied any fever, rhinorrhea, cough, diarrhea, rash, bruising, bleeding, or hematuria. The patient denied any abdominal pain or headache while in the ED.
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PMID:Acute ataxia in a 4-year-old boy: a case of Lyme disease neuroborreliosis. 1909 Dec 90


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