Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Videofluoroscopy was used to examine movement patterns during swallowing and speech production in 6 parkinsonian subjects and 6 age-matched controls. Motility patterns for liquid and semisolid swallows were documented. We performed temporospatial analyses of oropharyngeal structures, particularly the velum, which is prominently involved in both motor speech production and swallowing. Differences were found between groups and conditions. All of the parkinsonian subjects exhibited abnormal oropharyngeal movement patterns and timing during the volitional oral as well as the pharyngeal stage of swallowing; only 50% of these subjects admitted to any swallowing difficulty upon questioning. Two of the subjects with Parkinson's disease aspirated liquids. Duration of velar movement during speech production significantly differentiated the groups (p less than 0.01), reflecting reduced range of velar motion. Our findings suggest that rigidity and bradykinesia underlie the volitional speech abnormality as well as the disordered oral and pharyngeal stages of swallowing. Findings indicate that parkinsonian patients may be "silent aspirators" with decreased cough reflexes and lack of awareness of aspiration. The clinical value of videofluoroscopic monitoring of swallowing is that aspiration may be detected and managed early.
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PMID:Swallowing and speech production in Parkinson's disease. 396 73

Several pharmacologic agents provide antihistamine effects by acting at the H1 histamine receptor site. The classic agents are relatively nonselective, resulting in a wide range of effects, both therapeutic and undesirable. The newer agents preferentially block peripheral H1 receptor sites and, consequently, have fewer side effects, including sedation. Antihistamines are useful in the treatment of allergic conditions, Parkinson's disease, insomnia and some forms of nausea, and provide symptomatic relief of cough and other conditions associated with respiratory tract infections. Certain agents may play a role in the treatment of asthma and anorexia. Selection of a specific agent should be based on cost and the minimization of side effects. The classic antihistamines provide an inexpensive and highly effective means of treating histamine-mediated symptoms. The bothersome central nervous system side effects can be alleviated by taking the drugs at bedtime; their prolonged tissue half-life allows dosing once or twice a day for 24-hour clinical relief. The newer, more expensive nonsedating antihistamines are acceptable alternatives for patients who are incapable of tolerating the effects of classic agents.
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PMID:Antihistamines: the old and the new. 762 32

Neurogenic dysphagia results from sensorimotor impairment of the oral and pharyngeal phases of swallowing due to a neurologic disorder. The symptoms of neurogenic dysphagia include drooling, difficulty initiating swallowing, nasal regurgitation, difficulty managing secretions, choke/cough episodes while feeding, and food sticking in the throat. If unrecognized and untreated, neurogenic dysphagia can lead to dehydration, malnutrition, and respiratory complications. The symptoms of neurogenic dysphagia may be relatively inapparent on account of both compensation for swallowing impairment and diminution of the laryngeal cough reflex due to a variety of factors. Patients with symptoms of oropharyngeal dysphagia should undergo videofluoroscopy of swallowing, which in the case of neurogenic dysphagia typically reveals impairment of oropharyngeal motor performance and/or laryngeal protection. The many causes of neurogenic dysphagia include stroke, head trauma, Parkinson's disease, motor neuron disease and myopathy. Evaluation of the cause of unexplained neurogenic dysphagia should include consultation by a neurologist, magnetic resonance imaging of the brain, blood tests (routine studies plus muscle enzymes, thyroid screening, vitamin B12 and anti-acetylcholine receptor antibodies), electromyography/nerve conduction studies, and, in certain cases, muscle biopsy or cerebrospinal fluid examination. Treatment of neurogenic dysphagia involves treatment of the underlying neurologic disorder (if possible), swallowing therapy (if oral feeding is reasonably safe to attempt) and gastrostomy (if oral feeding is unsafe or inadequate).
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PMID:Dysphagia associated with neurological disorders. 820 77

We studied the nature and frequency of nonmotor "off" phenomena in 130 consecutive patients with Parkinson's disease (PD) with motor fluctuations. Twenty-two patients (17%) experienced nonmotor fluctuations as an end-of-dose phenomenon. Previously unreported, or little appreciated, nonmotor "off" states include sensory dyspnea, nausea, facial flushing, cough, hunger, unilateral limb edema, proximal limb pain, and trigeminal neuralgia-like pain. We attempted treatment modification in 12 of 22 patients; nonmotor "off" symptoms improved in nine of these 12 patients (75%). Recognizing these phenomena will prevent unnecessary tests and treatments.
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PMID:Nonmotor fluctuations in patients with Parkinson's disease. 937 51

Bromocriptine, which is used in the treatment of Parkinson's disease, can cause adverse pleuropulmonary reactions. Exposure to asbestos can result in similar lesions. Fifteen patients with former exposure to asbestos, who developed pleural fibrosis after treatment with bromocriptine, were observed independently in Sweden (11 patients) and Australia (four patients). The patients complained of malaise, often associated with weight loss, dyspnoea, and a disturbing cough. Laboratory values included increased erythrocyte sedimentation rate and a low haemoglobin level. Lung function tests showed a restrictive lung function defect. Chest radiographs showed bilateral pleural fibrosis, with small amounts of fluid in some cases. Soon after bromocriptine was withdrawn, the patients improved clinically, and the laboratory values returned to normal. However, in most cases, pleural fibrosis and a restrictive lung function defect persisted to some extent. In conclusion, in patients who develop pleuropulmonary fibrosis whilst being treated with bromocriptine, former exposure to asbestos should be investigated. Conversely, when pleural changes develop in a patient on bromocriptine and with prior exposure to asbestos, the possible causative role of the drug should be discussed. Special follow-up may be indicated when bromocriptine is planned in a patient with previous asbestos exposure, and if symptoms or signs of pleural fibrosis develop, bromocriptine withdrawal should be considered.
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PMID:Pleural disease during treatment with bromocriptine in patients previously exposed to asbestos. 965 90

The high incidence of serious chest infections in patients with Parkinson's disease is unexplained, but an impairment in cough reflex may have a role. Maximal voluntary cough (MVC) and reflex cough (RC) to inhalation of ultrasonically nebulized distilled water were analyzed in patients with Parkinson's disease and age-matched control subjects by monitoring the integrated electromyographic activity (IEMG) of abdominal muscles. The peak amplitude of IEMG activity (IEMGP) was expressed as a fraction of the highest IEMGP value observed during MVC corrected to account for possible losses in abdominal muscle force due to reduced central muscle activation. Cough intensity was indexed in terms of both the IEMGP and the ratio of IEMGP to the duration of the expiratory ramp (TEC), i.e., the rate of rise of IEMG activity. Cough threshold was slightly higher in patients than in control subjects, but the difference failed to reach statistical significance. Compared with control subjects, patients displayed a lower IEMGP during maximal expiratory pressure maneuvers (PEmax), MVC, and RC (p always < 0.01); TEC during RC was longer (p < 0.01) than in controls. Consequently, the rate of rise of IEMG activity during cough was always lower in patients (p < 0. 01), especially during RC. Finally, PEmax, and both the peak and rate of rise of IEMG activity during RC were inversely related to the level of clinical disability (Spearman rank correlation coefficient, rs = -0.88, -0.86, and -0.85, respectively, p always < 0.01). The results indicate that the central neural mechanisms subserving the recruitment of motor units and/or the increase in their frequency of discharge during voluntary and, even more markedly, RC are impaired in patients with Parkinson's disease.
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PMID:Defective motor control of coughing in Parkinson's disease. 970 Jan 21

Discharge characteristics of laryngeal single motor units during phonation in young and older adults, and in persons with Parkinson disease. The rate and variability of the firing of single motor units in the laryngeal muscles of young and older nondisordered humans and people with idiopathic Parkinson disease (IPD) were determined during steady phonation and other laryngeal behaviors. Typical firing rates during phonation were approximately 24 s/s. The highest rate observed, during a cough, was 50 s/s. Decreases in the rate and increases in the variability of motor unit firing were observed in the thyroarytenoid muscle of older and IPD male subjects but not female subjects. These gender-specific age-related changes may relate to differential effects of aging on the male and female voice characteristics. The range and typical firing rates of laryngeal motor units were similar to those reported for other human skeletal muscles, so we conclude that human laryngeal muscles are probably no faster, in terms of their contraction speed, than other human skeletal muscles. Interspike interval (ISI) variability during steady phonation was quite low, however, with average CV of approximately 10%, with a range of 5 to 30%. These values appear to be lower than typical values of the CV of firing reported in three studies of limb muscles of humans. We suggest therefore that low ISI variability is a special although not unique property of laryngeal muscles compared with other muscles of the body. This conceivably could be the result of less synaptic "noise" in the laryngeal motoneurons, perhaps as a result of suppression of local reflex inputs to these motoneurons during phonation.
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PMID:Discharge characteristics of laryngeal single motor units during phonation in young and older adults and in persons with parkinson disease. 1032 54

The purpose of this study was to investigate the relationship between weight loss and dysphagia in Parkinson's disease. We compared the height, body weight and the data of self-administered questionnaires concerning food intake and deglutition feelings in patients suffering from Parkinson's disease with normal controls. A structured interview was performed by nutritionists and nutrient intakes were calculated from the reported food intake over 5 days. Biochemical parameters were chosen from the chart. The subjects were 105 patients with Parkinson's disease, 34 males with a mean age of 67.7 +/- 8.6 years and 71 females with a mean age of 69.1 +/- 10.0 years (Hoehn-Yahr stage I6, II25, III51, IV20, V3). In addition, 47 family members were used as control subjects: 26 males, 70.6 +/- 7.6 years and 21 females, 64.9 +/- 7.7 years. Body mass index (BMI) in females with Parkinson's disease (20.2 +/- 3.5 kg/m2) was significantly lower (p < 0.005) than that in control females (23.0 +/- 3.0 kg/m2). There was no significant difference in BMI in males. The BMI was 21.9 +/- 3.0 kg/m2 in male patients with Parkinson's disease and 22.6 +/- 3.1 kg/m2 in controls. The occurrences of symptoms such as choking, cough, sputum, food in sputum, wet voice and pharyngeal discomfort following food intake in patients with Parkinson's disease vs. those in controls were 22% vs. 6%, 16% vs. 2%, 7% vs. 4%, 2% vs. 0%, 5% vs. 2% and 11% vs. 0%, respectively. Concerning symptoms such as choking, cough and pharyngeal discomfort, the occurrence was significantly more frequent in patients with Parkinson's disease than in controls (p < 0.05, p < 0.05, p < 0.05). We defined the dysphagic Parkinson patients as those who have at least one symptom of dysphagia such as choking, cough, sputum, food in sputum, wet voice and pharyngeal discomfort following food intake. The dysphagic subjects were present in 31% of Parkinson patients and in 7% of control subjects (p < 0.005), although half of the dysphagic Parkinson patients did not recognize it. No relationship between the occurrence of dysphagic symptoms and the Hoehn-Yahr stage was found. In patients with Parkinson's disease. BMI in the dysphagic group (19.1 +/- 3.6 kg/m2) was significantly lower than that in the non-dysphagic group (21.6 +/- 3.0 kg/m2) (p < 0.005). There was no relationship between BMI and the dose of levodopa. Patients in the dysphagic group showed significantly lower carbohydrate intake (186 +/- 49 g) than those in the non-dysphagic group (215 +/- 52 g) (p < 0.05). Biochemical nutritional parameters were lower in the dysphagic group than those in the non-dysphagic group; 6.6 +/- 0.7 g/dl vs. 6.9 +/- 0.4 g/dl (p < 0.005) in serum total protein, 3.8 +/- 0.5 g/dl vs. 4.1 +/- 0.4 g/dl (p < 0.01) in albumin and 173.4 +/- 33.0 mg/dl vs. 199.7 +/- 40.7 mg/dl (p < 0.05) in total cholesterol. These findings suggest that dysphagia, especially unrecognized dysphagia, plays a role in weight loss in Parkinson's disease.
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PMID:[Relationship between weight loss and dysphagia in patients with Parkinson's disease]. 1065 60

Because of adverse reactions, early efforts to introduce high affinity competitive or use-dependent NMDA receptor antagonists into patients suffering from stroke, head trauma or epilepsy met with failure. Later it was discovered that both low affinity use-dependent NMDA receptor antagonists and compounds with selective affinity for the NR2B receptor subunit met the criteria for safe administration into patients. Furthermore, these low affinity antagonists exhibit significant mechanistic differences from their higher affinity counterparts. Success of the latter is attested to the ability of the following low affinity compounds to be marketed: 1) Cough suppressant-dextromethorphan (available for decades); 2) Parkinson's disease--amantadine, memantine and budipine; 3) Dementia--memantine; and 4) Epilepsy--felbamate. Moreover, Phase III clinical trials are ongoing with remacemide for epilepsy and Huntington's disease and head trauma for HU-211. A host of compounds are or were under evaluation for the possible treatment of stroke, head trauma, hyperalgesia and various neurodegenerative disorders. Despite the fact that other drugs with associated NMDA receptor mechanisms have reached clinical status, this review focuses only on those competitive and use-dependent NMDA receptor antagonists that reached clinical trails. The ensuing discussions link the in vivo pharmacological investigations that led to the success/mistakes/ failures for eventual testing of promising compounds in the clinic.
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PMID:Neuroprotection by NMDA receptor antagonists in a variety of neuropathologies. 1155 51

A 73-year-old African American female presented to our clinic with painful lower extremity lesions of 2 weeks duration. She was in her usual state of health until 3 months prior to presentation when she reported symptoms of fatigue and weakness. She also noticed an enlarging mass on the left side of her neck. She denied fevers, chills, night sweats or cough. Her symptoms were unresponsive to a course of oral dicloxacillin. The neck mass enlarged over 8 weeks and she was referred to our institution for evaluation. CT scan of the neck showed an enlarged lymph node. Ten days prior to her presentation in dermatology, a fine needle aspirate of the enlarging lymph node revealed necrotizing granulomas. Tissue was sent for routine mycobacterial and fungal cultures. Routine blood work, chest radiograph, and a tuberculin skin test were also performed. At the time of her dermatology visit she described the development of multiple new painful, non-pruritic lesions, bilaterally on the lower extremities. She also reported a red crusted area that appeared at the site of her tuberculin test that was placed subsequent to the development of her lower extremity lesions. Her past medical history was significant for Parkinson's disease, hypothyroidism and hypertension. Her current medications included l-thyroxine, estrogen and diltiazem. Her travel history was only remarkable for a trip to Jamaica the previous spring. She was born and raised in Haiti. She reported a history of a positive tuberculin skin test 20 years ago, but received no therapy. Physical examination revealed a 2 x 3 centimeter firm, nontender left lateral neck mass (Fig. 1). Her right forearm revealed an erythematous, ulcerated, indurated plaque 1.5 cm in diameter (Fig. 2.). Her lower extremities revealed tender 0.5 to 1 cm erythematous nodules below the knees bilaterally (Fig. 3). A punch biopsy of a lower extremity nodule revealed a mild pervisacular dermal infiltrate. Within the subcutaneous tissue there was septal widening. There was also a lymphohistiocytic infiltrate with a slight admixture of neutrophils within the septa of the fat lobules. There was no evidence of necrotizing vasculitis or collagen necrosis. An acid-fast stain was not performed. The histologic findings were consistent with a diagnosis of erythema nodosum. Her laboratory evaluation including CBC, electrolytes, thyroid studies, angiotensin converting enzyme level and chest radiograph were normal. Approximately 1 week after her dermatological evaluation, the fine-needle aspirate culture grew Mycobacterium tuberculosis. A diagnosis of tuberculous lymphadenitis associated with erythema nodosum was confirmed. The patient was started on quadruple therapy of isoniazid, rifampin, ethambutol and pyrazinamide. Her lower limb skins lesions rapidly resolved over the subsequent month and her neck mass also diminished in size. She completed 6 months of antituberculous therapy with complete resolution of her lymphadenopathy.
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PMID:Erythema nodosum associated with reactivation tuberculous lymphadenitis (scrofula). 1201 Mar 45


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