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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

Dysphagia, or difficulty swallowing, can interfere with independent feeding in the physically disabled adult. The physiology of normal swallowing and neuromuscular pathology of dysphagia applicable to the occupational therapist are reviewed in this paper. Pertinent nursing care of the respiratory and gastrointestinal tracts are described. Normal and pathological reflexes involved in swallowing include gag, bite, and suck-swallow. Head, neck, and jaw stability are necessary for swallowing. Methods for evaluating the appropriate reflexes, sensation, and orofacial movement of the adult neurologically impaired patient are presented. Proper positioning is described and treatment suggestions are offered and applied to four case studies.
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PMID:Dysphagia: an evaluation and treatment program for the adult. 46 18

The findings on 13 patients with bulimia nervosa referred for evaluation of salivary glands and swallowing patterns are presented. Each patient completed a medical, oral, and social history questionnaire. A complete oral examination supported by appropriate dental radiographs and photographs was conducted. Unstimulated and stimulated parotid and submandibular saliva was collected. The presence or absence of pharyngeal and velar gag reflexes was ascertained. Real-time ultrasound scanning and barium swallow studies were used to evaluate the oral-motor functions while swallowing on 6 of the subjects. Activity of the pharynx, larynx, and esophagus was recorded during the videofluorographic studies. Saliva concentrations of amylase were determined in the referred subjects as well as 13 age-matched healthy controls. No significant difference was detected between the salivary gland flow rates and amylase concentrations of the two groups, whether stimulated or unstimulated. The pharyngeal gag reflex was absent in 9 of the 13 bulimic patients and a velar gag reflex could be elicited in only 1. All of the normal controls had both gag reflexes. All of the patients with bulimia were found to have abnormal oropharyngeal swallow patterns and an increased duration of dry swallow.
Dysphagia 1989
PMID:Dysphagia in bulimia nervosa. 248 80

Victor and his associates coined the term oculopharyngeal muscular dystrophy to describe a clinical syndrome characterised by dysphagia and ptosis. Subsequent authors have traced a large series in French Canadians to a single Quebec isolate and have emphasized that the condition is usually inherited as a dominant trait. In 1974 Fried reported two isolated cases in an Ashkenazi Jewish family of Hungarian extract in whom the condition was recessively inherited. In this paper we report an Irish family from North Cork with typical features of oculopharyngeal muscular dystrophy in whom the inheritance pattern is dominant with incomplete expression. In reporting such cases the ethnic and genetic heterogeneity of oculopharyngeal muscular dystrophy is highlighted. Case Report 1. A 68 year old farmer was admitted for investigation of recurrent chest infections. He complained of a 20 year history of progressive difficulty swallowing, productive cough and impaired vision. On examination he had a gaunt expressionless appearance with bilateral ptosis to mid pupillary level. Both right and left gag reflexes were noted to be reduced and sluggish, and on swallowing fluids were noted to regurgitate through his nostrils. Chest examination revealed the presence of bibasal coarse crepitations suggestive of aspiration. No further physical abnormalities were noted. On investigation, full blood count, urea, and electrolytes, liver function tests, sedimentation rate, thyroid function tests, muscle enzymes (PK, LDH) and electrocardiogram were normal. Chest radiograph confirmed aspiration. Tensilon test was negative. Oesophagoscopy outruled organic obstruction, and confirmed sluggish pharyngeal muscular activity. A clinical diagnosis of oculopharyngeal dystrophy was made on the basis of associated ptosis and dysphagia occurring in the presence of a supportive family history.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oculopharyngeal muscular dystrophy in an Irish family. 275 12

Hemifacial spasm is usually an isolated symptom resulting from facial nerve root compression. Three patients had, in addition, tinnitus, hearing loss, facial sensory loss, diminished gag reflex, dysphagia, and dysarthria. Acoustic reflexes were abnormal, and facial nerve conduction studies showed evidence of ephaptic transmission and ectopic excitation. Brain CT and metrizamide cisternography were normal. Surgical exploration showed compression of cranial nerve roots by posterior inferior cerebellar artery branches. After decompression, symptoms abated, and electrical signs of hemifacial spasm disappeared. Vascular compression of nerve roots in the cerebellopontine recess may cause multiple cranial neuropathy.
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PMID:Vascular compression, hemifacial spasm, and multiple cranial neuropathy. 399 Sep 69

Fifteen patients with pharyngeal stage dysphagia were studied clinically and by motion fluoroscopy. Eleven patients demonstrated laryngeal penetration during swallowing. There was high incidence of impaired pharyngeal gag and wet-hoarse voice quality among this group. Other observations were found to correlate poorly with penetration. Cough was an unreliable indicator of laryngeal penetration. Penetration was most likely when liquids were swallowed and least likely when semisolids were swallowed. Motion fluoroscopy of swallowing was necessary for detecting penetration reliably, identifying that dysphagia depends, in part, on bolus qualities, and planning a feeding approach consistent with remaining swallowing functions.
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PMID:Dysphagia: predicting laryngeal penetration. 686 Jan

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85

We report on a Samoan man with dysphagia, voice hoarseness, facial erythema, and edema. Neurologic examination revealed hypesthesia at the site of the facial rash, enlarged auricular nerves, a right facial palsy, decreased gag reflexes, and voice hoarseness. Laryngoscopic examination showed paralysis of the left vocal cord, and a barium swallow revealed a possible compressive lesion. A skin biopsy specimen was diagnostic of tuberculoid leprosy. This patient has an unusual case of leprosy with multiple cranial neuropathies.
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PMID:Multiple cranial neuropathies associated with leprosy. 809 Dec 62

We report a case of chronic progressive external ophthalmoplegia with pituitary hypothyroidism. This patient had complained of hearing-loss at the age of fourteen and loss of body weight at fifteen. She was examined by otorhinolaryngologists at large hospitals yearly over a period of 5-6 years, but hearing-loss remained unknown. As her ophthalmoplegia progressed (as is evident from family photographs from the age of sixteen onward), with hindsight it should have been recognized. When examined on October 11, 1991, she complained of ptosis, speech disturbance and dysphagia at the age of thirty-four. Neurological examination revealed limitation of ocular movement, bilateral ophthalmoplegia, facial muscle atrophy, and weak gag reflex. She showed muscle atrophy in her neck including both sternocleidomastoid, major and minor rhomboid, girdle and distal parts of upper and lower extremities. Muscle biopsy of her biceps demonstrated ragged-red fibers, cytochrome c oxidase (CCO) deficient fibers and deletion of mitochondrial DNA. A plain CT scan revealed bilateral periventricular lucency, and a brain MR image showed a normal sized pituitary gland but diffuse high-signal intensities in the both periventricular white matter with proton density weighted and T2-weighted axial MR image. And also her electroencephalogram showed diffuse 7 Hz slow waves in all areas and increased slow waves by hyperventilation, and all waves from I to V of the auditory brain stem response disappeared. The effect of TRH on serum TSH secretion was not evident in this patient. This case was ascertained to be chronic progressive external ophthalmoplegia with pituitary hypothyroid function.
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PMID:[A case of chronic progressive external ophthalmoplegia with pituitary hypothyroidism]. 821 98

A 59-year-old female was admitted with complaints of vertigo, dysarthria and dysphagia. On neurological examination, right-sided cranial nerve signs included ptosis, Bruns's nystagmus, decreased corneal sensation, diminished facial pain and temperature sensation, decreased palatal excursion and loss of gag reflex. There was no evident motor weakness, but deep tendon reflexes were slightly exaggerated on the left extremities. Coordination testing showed right cerebellar signs. Sensory examination of the remaining parts of the body was quite normal. X-ray CT scan showed multiple high density areas in the right medulla, right pons, right temporal and frontal lobes. T2 weighted MRI demonstrated these lesions as mixed signal intensity areas with marked low signal intensity rim. There were multiple black dots in the bilateral frontal and temporal lobes, cerebellar hemispheres on T2-weighted images. Carotid and vertebral angiograms showed no abnormality. This is the first report of the cavernous malformation presenting as lateral medullary syndrome.
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PMID:[Lateral medullary syndrome due to cavernous malformation in the brain stem]. 840 82


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