Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Nonlanguage disorders of speech reflect complex neurologic apparatus. 16 83

Two cases of progressive supranuclear palsy (PSP) are reported in two men (49 and 75years old) who for one and four years respectively had sudden falling while walking. Rigidity of the neck was an carly feature that prgressed to involve the upper trunk while "subcortical dementia", dysarthria and dysphagia appeared. They had a complete paralysis of vertical eye movements and slow horizontal voluntary eye movements. Oculocephalic reflexes were intact. On caloric stimulation vestibulo-ocular responses were present but only slow saccadic eye movements were observed. With surface electrodes eye movements were studied during the REM phase of sleep. Our patients had both vertical and horizontal eye movements during paradoxal sleep. This findings is in keeping with a supranuclear ophtalmoplegia, and may help in antemorten diagnosis of PSP.
 ...
PMID:Progressive supranuclear palsy: report of two cases (author's transl). 18 May 89

A patient is reported whose ailment meets the criteria of CPM. The illness was complicated by pneumonitis, most likely of the aspiration type. Of particular interest was the reversibility of a clinical picture of marked deterioration when attention was paid to fluid and electrolyte balance and maintenance of respiration. This patient's illness appears to meet the criteria of CPM, namely impairment of the facial muscles and tongue with dysphagia and dysarthria, flaccid quadriparesis or quadriplegia, and frequently, lack of response to painful stimuli followed by respiratory paralysis. The presence of peripheral neuropathy has been previously noted in a patient with CPM, but it is not an integral part of the disease.
 ...
PMID:Central pontine myelinolysis. 37 56

Myasthenia gravis is a neuromuscular disease of insidious onset, characterized by weakness and fatigability of voluntary muscles. Most patients present with symptoms relating to the head and neck and thus may be seen first by the otolaryngologist. Predominant symptoms may be ocular (ptosis or diplopia) or related to fatigue of the oropharyngeal or laryngeal musculature (dysarthria, dysphonia, or dysphagia). Alleviation of muscular weakness and fatigability after administration of anticholinesterase drugs is pathognomonic of myasthenia gravis.
 ...
PMID:The otolaryngologic presentation of myasthenia gravis. 44 37

Amyotrophic lateral sclerosis (ALS) is a degenerative neurologic disease having both upper and lower motor neuron signs and symptoms. When the speech musculature is involved, a mixed dysarthria and dysphagia usually result. In a 49-year-old man with ALS, dysarthria and dysphagia progressed from mild to severe forms over 17 months. Eleven months after the patient first experienced symptoms, neurologic examination showed fasciculations of the extremities and tongue, limb weakness, and hyperreflexia of the limbs and velopharyngeal mechanism. Tongue strength was one-fourth that of normal. Lingual alternate motions rates for consonant-vowel syllables were also reduced. To enhance lingual strength and swallowing, a tongue-strengthening program was developed for use with articulation training; to augment velopharyngeal function, a palatal lift was fitted; and to increase extremity strength, physical therapy was initiated. Six months after the initial neurologic examination, medical and speech reevaluation showed progressive weakness of the body parts affected initially; continued decline in tongue strength and lingual alternate motion rate; hypoactive reflex activity, indicative of progressive involvement of the lower motor neuron system; and continued deterioration of articulation and phonation owing to the progressive nature of the disease.
 ...
PMID:Progressive speech deterioration and dysphagia in amyotrophic lateral sclerosis: case report. 49 10

A 64-year-old hypertensive man presented with the dysarthria--clumsy hand syndrome, manifested by dysarthria, dysphagia, central facial weakness, deviation of the tongue on protrusion, incoordination of the affected hand, and mild imbalance on walking. A computed tomograpphic scan demonstrated a resolving acute infarction in the vicinity of the genu of the internal capsule.
 ...
PMID:Dysarthria--clumsy hand syndrome produced by capsular infarct. 53 26

A family is described in which five males have late-onset facial weakness, dysarthria, dysphagia, and slowly progressive proximal weakness. Electrodiagnostic studies and muscle biopsy were compatible with spinal muscular atrophy. This family appears quite similar to several previously reported families with late-onset X-linked recessive spinal and bulbar muscular atrophy. Because of the relative homogeneity of this particular phenotype of spinal muscular atrophy, a single metabolic derangement was sought. Three obligate carriers were studied, and no abnormality was detected. A further family with this condition is briefly discussed.
 ...
PMID:Late-onset X-linked recessive spinal and bulbar muscular atrophy. 57 30

A 38-year-old man developed pain and peripheral-type weakness on the right side of his face and was discovered to have decreased hearing bilaterally, as well as optic nerve swelling on the right. The pain and optic nerve swelling subsided over a period of six weeks, but hearing loss and facial weakness persisted. Thirty months later, he developed dysphagia, ataxia, dysarthria, nystagmus, and progressive spastic quadriparesis. He died approximately four years after the onset of the illness. Although no evidence of disease was found other than in the central nervous system during life, two nodules in the right lower lung were found on autopsy. The examination of these nodules, as well as the brain stem, showed an angiocentric and angionecrotic process with lymphoreticular and plasmacytoid invasion.
 ...
PMID:Lymphomatoid granulomatosis clinically confined to the CNS. A case report. 58 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.
 ...
PMID:Pallido-nigro-luysial atrophy associated with degeneration of the centrum medianum. A clinicopathologic and electron microscopic study. 84 97

A case of left atrial myxoma with repeated multiple cerebral emboli is reported. A-44-year-old man first developed a sudden right hemiparesis in October 1969. After intensive physical theraphy, strength improved and he was able to return to his work. In March 1970, he suddenly lost consciousness and remained comatose for a day. Upon waking, he had a profound right hemiparesis, motor aphasia and Gerstmann's syndrome. He was admitted to Hiroshima City Hospital on August 1, 1970. The cardiac examination, including an electrocardiogram, was entirely normal. Laboratory studies revealed a normal blood count and urinalysis; erythrocyte sedimentation rate was elevated (32mm/hour). On a left cerebral angiographic study, performed on September 6, 1971, multiple aneurysmal dilatations of the branches of the left middle cerebral artery were demonstrated. No specific diagnosis was made. In January 1973, he developed dysarthria, dysphagia and quadriplegia because of the recurrent cerebral attacks. He had a high temperature continuously for three days and died on May 30, 1974. At autopsy a myxoma with the peduncle was attached to the septal wall of left atrium, and there were old infarcts in the brain, the myocardium and the kidneys.
 ...
PMID:[Left atrial myxoma with repeated multiple cerebral emboli]. 103 60


1 2 3 4 5 6 7 8 9 10 Next >>