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)

The mute or nearly mute patient who is alert and has good understanding of speech and a right hemiparesis could have Broca's aphasia, akinesia of speech (transcortical motor aphasia), or aphemia. The patient who has Broca's aphasia does not write well, and his speech does not improve greatly with repetition. The speech of a patient with akinesia of speech improves with repetition. The aphemic patient writes normally, but his speech does not improve with repetition. The mute patient whose eyes are open but who is poorly responsive and moves little or not at all could be an akinetic mute (with either a cingulate or a thalamomesencephalic lesion) or have a locked-in syndrome. The latter is diagnosed by asking the patient to look up and down or to open and close his eyes. If he obeys these commands, the physician questions him using a code of eye movement responses. If the patient fails to respond at all, he is an akinetic mute; intense stimulation may result in speech or movement. If the patient is drowsy and has third nerve involvement, the lesion is in the thalamomesencephalic reticular formation. If the patient appears alert and has episodes of agitation, he probably has bilateral lesions in the gyri cinguli. Patients with weakness of the bulbar musculature (facial, palatal, and tongue weakness and dysphonia) may have either upper motor neuron or lower motor neuron lesions. Only bilateral upper motor neuron lesions produce permanent dysarthria. As a typical example, a patient has a transient left hemiparesis with dysarthria and almost completely recovers. Later, however, a right hemiparesis develops and the patient experiences severe bilateral facial weakness, drooling, dysphagia, and severe dysarthria. The absence of atrophy of the bulbar musculature, a hyperactive jaw jerk and gag reflex and, sometimes, inappropriate laughing or crying episodes indicate that the lesion is located above the medulla in the corticobulbar tracts. Flaccid paralysis, absence of the jaw jerk or gag reflex, and absence of other upper motor neuron signs, such as upgoing toes, indicate a lower motor neuron or neuromuscular junction problem. Appropriate tests to rule out myasthenia gravis should be done. The other conditions discussed here are often obvious from their clinical presentation. Although the specific disorder of speech sometimes is helpful in localizing the cause, in most patients, the associated deficits on neurologic examination are of greatest value.
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PMID:Nonlanguage disorders of speech reflect complex neurologic apparatus. 16 83

Continuous intravenous infusion of levodopa was used for eight days to manage a parkinsonian patient with "on-off" fluctuations who underwent abdominoperineal resection for carcinoma of the rectum. Reasonable control of parkinsonism was obtained initially with small doses of levodopa, but more than 4 g daily were eventually required. No adverse effects on cardiac rhythm, blood pressure, or gastrointestinal function occurred. Frequent adjustment of levodopa dosage was necessary in view of continuing "on-off" fluctuations. Severe akinesia, which can cause dysphagia, respiratory complications, and venous stasis in the legs, can benefit from this method of management after major abdominal surgery in a patient with advanced parkinsonism.
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PMID:Parkinsonism with 'on-off' phenomena. Intravenous treatment with levodopa after major abdominal surgery. 42 Jun 1

A 66-year-old man (case 1) and a 71-year-old woman (case 2) showed systemic degeneration of the globus pallidus, substancia nigra, subthalamic nucleus, centrum medianum thalami and at times, superior colliculus in the midbrain. In the pallido-nigral system, neuronal loss was severe in both cases and an increase of pigment and granular spheroids was marked in case 2, less in case 1. Electron-microscopically, the spheroids consisted of aggregates of highly dense material, often membrane-bound, and varying amounts of groups of loosely packed filaments. Clinical symptoms were stereotyped and unique, showing severe akinesia, no rigidity in the limbs, no tremor but retropulsions, upward gaze palsy, dysarthria, dysphagia and later, nuchal stiffness. Nosological identification is discussed.
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PMID:Pallido-nigro-luysial atrophy associated with degeneration of the centrum medianum. A clinicopathologic and electron microscopic study. 84 97

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

Experience with liver transplantation for patients with Wilson's disease who have major neurological impairment is limited, and this report describes the results obtained in two such patients. The first was a 30-year-old man with a 14-month history of hepatic and neurological impairment. In spite of treatment with d-penicillamine, he developed increasing dysarthria, dysphagia, akinesia and rigidity of all four limbs, and required continuous nursing care. Following transplantation, liver function was almost normal from four weeks onwards, but recovery of neurological function was much slower and was not seen until two to three months after surgery. By four months he was sufficiently mobile to be discharged, and when he returned for assessment at eight months, no abnormal neurological signs were detectable. The second patient was a 27-year-old woman with worsening liver dysfunction for eight years; one year previously she had developed dysarthria, akinesia, a fine tremor and moderate rigidity of all limbs as well as marked psychological impairment. There was no improvement on treatment with d-penicillamine or trientine, but as liver function returned to normal two months after liver grafting, her neurological and psychological function began to improve so that by three months she could be discharged.
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PMID:Reversal of severe neurological manifestations of Wilson's disease following orthotopic liver transplantation. 332 13

We describe a new, water-soluble formulation of levodopa plus benserazide (Madopar LIQ) for the treatment of Parkinson's disease. Two dosage strengths are available: 100 mg levodopa plus 25 mg benserazide and 50 mg levodopa plus 12.5 mg benserazide. Pharmacokinetic data show that levodopa absorption is more rapid than with standard Madopar, resulting in a shorter time to peak plasma concentration. Other pharmacokinetic values are comparable to those obtained with the standard formulation. We discuss the clinical advantages of this new water-soluble formulation, particularly when the patient requires rapid onset of action for morning or circadian akinesia. The indications of this formulation in patients with dysphagia and in other clinical situations, e.g. during the postoperative period and for levodopa dosage adjustment in ambulatory care, are discussed.
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PMID:[Benefits of a new galenic form of levodopa and benserazide in the treatment of patients with Parkinson disease]. 748 41

We report a 56-year-old woman with parkinsonism and dementia who died of respiratory failure. The patient was well until the age of 41 when she noted insidious onset of difficulty in moving around. Soon after, she noted tremor in both her hands and gait disturbance. She received stereotaxic right thalamotomy when she was 46-year-old; after thalamotomy, improvement was noted in her tremor, rigidity, and in gait. However, a few months later, she started to experience motor fluctuations with worsening of her symptoms in the afternoon. This worsening was temporarily relieved by increasing her levodopa/benserazide dose. She started to show visual hallucination and agitation when she was 54-year-old. Her symptoms had progressively become worse with marked motor fluctuations and she was admitted to our hospital when she was 56-year-old. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed that she was disoriented to time and place; memory was markedly disturbed and calculation was poor. Hasegawa dementia scale was 7/30. Higher cerebral functions appeared intact. She showed masked face, small voice, and some dysphagia. Other cranial nerves were intact including ocular movements. She was unable to walk by herself; when supported she walked in small steps with marked disturbance in the righting reflex. Mixed rigidity and Gegenhalten was noted in her four limbs and in the neck. Tremor was absent. She showed marked akinesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 56-year-old woman with parkinsonism and dementia with the age of onset at 41 years]. 754 42

We report one case of parkinsonism induced by cisapride and one case of Parkinson's disease whose symptoms were worsened by cisapride. Case 1. A 75-year-old female who had suffered from constipation and loss of appetite, was treated with cisapride for her gastro-intestinal symptoms. One year later, she developed progressive parkinsonian gait, cogwheel rigidity She showed parkinsonian gait, cogwheel rigidity and slowness in motion. Two months after cisapride was discontinued, her parkinsonism and depression disappeared. Case 2. A 66-year-old female with Parkinson's disease was given cisapride for constipation. Two months after starting cisapride, her akinesia and rigidity deteriorated gradually, and she became bed-ridden with dysphagia and dyspnea. After cisapride was discontinued, her parkinsonian symptoms improved gradually, and she became ambulant three months later. Cisapride is a benzamide derivative with a prokinetic action. Experimental studies have revealed that it has indirect cholinomimetic effects and potentially stimulates the gastrointestinal motor activity without blocking dopamine receptors or activating muscarinic cholinergic receptors. However, the present cases showed that cisapride could be a dopamine receptor blocker, and either induce or worsen parkinsonism. Therefore, cisapride should be avoided or very carefully used in parkinsonian patients and old people.
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PMID:[Parkinsonism induced or worsened by cisapride]. 772 93

We report a 78-year-old man with progressive gait disturbance, dementia, and dysphagia. He was apparently well until 75 years of age in 1989 when he had an insidious onset of gait disturbance. In October of 1991, he was treated with levodopa and amantadine HCl in another hospital, but he developed visual hallucination right after these medications, and the drugs were discontinued. He also developed difficulty in swallowing with frequent aspiration pneumonia. He was admitted to our hospital on January 13, 1992. On admission, the patient was chronically ill Japanese man; his blood pressure was 118/70 mmHg, body temperature 35.4 degrees C, and heart rate 72 and regular. No anemia or jaundice was noted; lungs were clear and no heart murmur was audible. The abdomen was flat but rigid to palpation without tenderness; no organomegaly was noted. On neurologic examination, he was alert but disoriented to all spheres; he was apparently demented and the score of the mini-mental test was 11. He did not appear to have aphasia or apraxia. Cranial nerves appeared intact, but he had a mask-like face and a slight limitation in the upward gaze; his voice was small. He was unable to stand or walk; he showed marked akinesia and moderate rigidity in his neck and the trunk. Deep reflexes were generally elicited normally or slightly weakly. Plantar response was extensor on the left and flexor on the right. No grasp reflex was present. Sensory examination showed questionable loss of touch in the glove- and -stocking distribution.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 78-year-old man with progressive gait disturbance, dysphagia, and dementia]. 819 46

Dysphagia in patients with Parkinson's disease (PD) is most often attributed to pharyngeoesophageal motor abnormalities. In our study of patients with idiopathic PD, attention was focused on prepharyngeal symptoms and motor functions. Using the Hoehn and Yahr disease severity scale, patients were grouped into those with mild/moderate disease [subgroup I (n = 38)] and those with advanced disease [subgroup II (n = 34)]. Dysphagia symptoms were present in 82% of all patients, but subgroup I patients voiced significantly more complaints. Conversely, many prepharyngeal abnormalities of ingestion, including jaw rigidity, impaired head and neck posture during meals, upper extremity dysmotility, impulsive feeding behavior, impaired amount regulation, and lingual transfer movements were statistically more frequent in subgroup II patients. Impaired mastication and oral preparatory lingual movements were the most common aberrations observed during dynamic videofluoroscopy (48/71), with most patients being concordant for both. The motor disturbances of ingestion reported herein reflect the disintegration of volitional and automatic movements caused by PD-related akinesia, bradykinesia, and rigidity.
Dysphagia 1996
PMID:Prepharyngeal dysphagia in Parkinson's disease. 855 74


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