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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 68-year-old right-handed woman was admitted to Tokyo Metropolitan Geriatric Hospital because of slowly progressive dysarthria and writing disability over 2-year period. On admission, severe dysarthria was observed, but no dysphagia. The dysarthria mostly resembled a type of pseudobulbar palsy, although it was associated with effortful speech production. An oro-facial apraxia was also found. She could name objects, and could understand spoken words correctly. Examination using the Western Aphasia Battery showed diminution of word fluency, impaired repetition and perseveration and writing errors. On the Wechsler Adult Intelligence Scale-R verbal IQ was 100 and performance IQ was 87. These scores did not suggest any significant degree of general intellectual deterioration. Wisconsin card sorting test disclosed mild frontal dysfunction. Magnetic resonance imaging showed cortical atrophy in the bilateral frontal and temporal lobes. Measurements of regional cerebral metabolic rate by 18F-FDG-PET demonstrated decreased uptake in the latero-dorso-inferior area of the bilateral frontal lobes, especially on the left side. The present case showed slowly progressive dysarthria and progressive aphasia without generalized dementia, and without typical aphasia. These symptoms are speculated to be related to the atrophy in the bilateral frontal and temporal lobes shown by MRI and the decreased metabolic rate in the left dominant bilateral frontal lobes on PET study. The pathologic process responsible for these lesions remains obscure.
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PMID:[Slowly progressive dysarthria and impaired language function--a case report]. 128 97

Atypical dementias confront the adequacy of current diagnostic concepts. The two patients with atypical dementia syndromes described here shared common postmortem features of numerous neocortical neuritic (senile) plaques and microvascular amyloid, sparing of hippocampus and substantia nigra, and the virtual absence of neurofibrillary tangles. Microscopically, the two differed only by the presence of a few subcortical Lewy bodies in case 1. These similar morphologic features were associated with dramatically different clinical presentations. In the first patient, visual hallucinations, Capgras' syndrome, cognitive slowing, myoclonus, parkinsonism, and primitive reflexes evolved over 3 years. Memory and language were relatively spared. In the second, dysphagia, nonfluent aphasia, hypophonia, motor perseveration, and a severe disorder of attention developed during this 18-month illness. At autopsy, an unrecognized colon malignancy was found. Despite high neuritic plaque counts in cortex, neither the clinical nor the pathologic criteria for Alzheimer's disease adequately describe either case. The cases will be examined first as clinical, then as neuropathologic, entities. From this approach, we conclude that a specific clinical dementia syndrome may be expressed by several neuropathologic "diseases" and that a variety of clinical syndromes may represent a single neuropathologic diagnosis. This strategy identifies a conceptual dichotomy between Alzheimer's syndrome and postmortem Alzheimer's disease. Meticulous clinical and neuropathologic observation is essential in advancing an understanding of the relationship between the two.
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PMID:Alzheimer's disease or plaque disease? Two cases at the frontier of a definition. 141 64

Various modalities of six neuropsychological functions (graphia, calculia, finger gnosis, right-left orientation, praxia and constructive praxia) referred to as parietal or nonverbal have been investigated in the light of speech disorders. We examined 20 patients with brain lesion of vascular origin, who met the diagnostic criteria of mild and moderate dysphagia, 13 patients with Wernicke's and 7 with Broca's dysphasia. Verbal and nonverbal functions in patients with ischemic focuses of the speech area of the left hemisphere were investigated the Boston Diagnostic Aphasia Examination (BDAE). The investigation revealed that the presence and the type of mild and moderate dysphasia had a noteworthy role in pathoplasticity of correlated signs, thus implying in clinical practice a parietal lesion. Generally, poorer and at the same time more heterogeneous results were obtained in patients with Wernicke's dysphasia, mostly on calculia and right-left orientation. Finger agnosia was not considered as an authentic parietal sign, while each modality of graphia was impaired to a varying extent in speech disorders caused by presylvian and retrosylvian lesions. The paper also deals with the significance of lobulus parietalis inferior in speech.
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PMID:The disturbance of nonverbal functions in dysphasia. 170 13

The experience of 500 transcranial Doppler (TCD) sonographies at Siriraj Hospital between April 1988- June 1989 were reported. The indications for TCD study were hemiplegia 156 (31.20%), vertigo 119 (23.80%), transient ischemic attack (TIA) 26 (5.20%), hemihypalgesia 14 (2.80%), dysarthria-dysphagia syndrome 13(2.60%), visual problem 13(2.60%), syncope 10(2.00%), memory loss 8(1.60%), aphasia 6(1.20%), carotid bruit 6(1.20%), miscellaneous (artereovenous malformation, aneurysm, arteritis, carotico-cavernous fistula, tinnitus, etc) 25(5.00%), and healthy subjects 92(18.4%). Abnormal TCD studies were found in various conditions of different percentages, i.e. 91.03 per cent in hemiplegia, 76.47 per cent in vertigo, 65.38 per cent in TIA, 71.43 per cent in hemihypalgesia, 61.54 per cent in dysarthria - dysphagia syndrome, 38.46 per cent in visual problem and 30.43 per cent in normal subject. TCD is noninvasive, safe and painless. It is a useful screening test for prophylaxis of cerebrovascular disease in the elderly.
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PMID:Transcranial Doppler ultrasonography: experience of 500 patients. 228 86

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

Communication impairments, with or without a swallowing disorder, are common among older adults. Aphasia, which is usually caused by a focal lesion, can affect spoken and written language, auditory comprehension, and reading ability but by itself does not affect intellectual and cognitive abilities. A cognitive-communicative impairment is related to underlying cognitive deficits in memory, attention, or visual perception and is seen with traumatic brain injury and nontreatable dementia. Voice and speech impairments such as dysarthria and apraxia of speech may lead to self-imposed social isolation and depression. Dysphagia may accompany a communication disorder or exist independently. As a primary care physician, your in-office workup can help diagnose a communication disorder and identify candidates for referral to an otolaryngologist and/or speech-language pathologist.
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PMID:Communication disorders: what to look for, and when to refer. 800 59

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

The purpose of the present study was to survey and compare the knowledge and attitudes of final year occupational therapy, physiotherapy and speech-language therapy students, concerning the role of the speech-language therapist as a member of the stroke rehabilitation team in the hospital setting. In order to achieve this aim, a questionnaire was administered to final year students in these three disciplines, and included questions on most areas of stroke rehabilitation with which the speech-language therapist might be involved, as well as the concepts of rehabilitation and teamwork in relation to stroke rehabilitation. Results suggested a fairly good understanding of the concepts of rehabilitation and teamwork. Students appeared to have a greater understanding of those disorders following a stroke, with which the speech-language therapist is commonly involved, such as Aphasia, Dysarthria, Verbal Apraxia and Dysphagia. However, students appeared to show less understanding of those disorders post-stroke, for which the speech-language therapist's role is less well defined, such as Agraphia, Alexia and Amnesia. In addition, a high percentage of role duplication/overlapping in several aspects of stroke rehabilitation, such as family and social support, was found. Several implications for facilitating communication, collaboration and understanding between paramedical professions, as well as for further research are also provided.
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PMID:The knowledge and attitudes of occupational therapy, physiotherapy and speech-language therapy students, regarding the speech-language therapist's role in the hospital stroke rehabilitation team. 860 43

OBJECTIVE--To analyse the natural history of progressive supranuclear palsy (PSP or Steele-Richardson-Olszewski syndrome) and clinical predictors of survival in 24 patients with PSP confirmed by necropsy, who fulfilled the NINDS criteria for a neuropathological diagnosis of typical PSP. METHODS--Patients were selected from the research and clinical files of seven medical centres involving tertiary centres of Austria, England, France, and the United States. Clinical features were analysed in detail. The patients' mean age at onset of PSP was 63 (range 45-73) years. RESULTS--The most frequent clinical features (occurring in at least 75% of the patients) were early postural instability and falls, vertical supranuclear palsy, akinetic-rigid predominant parkinsonian disorder characterised by symmetric bradykinesia and axial rigidity unrelieved by levodopa, pseudobulbar palsy, and frontal release signs. Occasionally, segmental dystonia or myoclonus were described, but neither aphasia nor alien limb syndrome was reported. Fractures occurred in 25% of the patients but were unrelated to the severity of the gait or to the presence of falls. Median survival time was 5.6 (range 2-16.6) years. Onset of falls during the first year, early dysphagia, and incontinence predicted a shorter survival time. Age at onset, sex, early onset of dementia, vertical supranuclear palsy, or axial rigidity had no effect on prognosis of survival. Pneumonia was the most common immediate cause of death. PSP was most often clinically misdiagnosed as Parkinson's disease. Errors in diagnosis suggest that PSP is underdiagnosed. CONCLUSION--Progressive onset of early postural instability with falls or supranuclear vertical palsy in the fifth decade, should suggest the diagnosis of PSP. Onset of falls during the first year are emphasised, as they could lead to an early diagnosis and influence the prognosis of patients with PSP. Whether appropriate treatment of the dysphagia could prolong the survival of PSP patients needs to be explored.
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PMID:Natural history of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) and clinical predictors of survival: a clinicopathological study. 864 26

This is a prospective study of 100 consecutive stroke patients. Within 24 h after stroke onset they were asked specifically about swallowing complaints and subjected to a clinical examination including neurologic examination, Mini-Mental test, and Barthel score. Dysphagic patients were examined with the repetitive oral suction swallow test (the ROSS test) for quantitative evaluation of oral and pharyngeal function at 24 h, after 1 week, and after 1 month. At 6 months, the patients were interviewed about persistent dysphagia. Seventy-two patients could respond reliably at 24 h after the stroke onset and 14 of these complained of dysphagia. Non-evaluable patients were either unconscious, aphasic, or demented. The presence of dysphagia was not influenced by age or other risk factors for stroke. Facial paresis, but no other clinical findings, were associated with dysphagia. Dysphagia 24 h after stroke increased the risk of pneumonia but did not influence the length of hospital stay, the manner of discharge from hospital, or the mortality. The initial ROSS test, during which the seated patient ingests water through a straw, was abnormal in all dysphagic stroke patients. One-third of the patients were unable to perform the test completely. Above all, dysfunction was disclosed during forced, repetitive swallow. All phases of the ingestion cycle were prolonged whereas the suction pressures, bolus volumes, and swallowing capacities were low. Abnormalities of quantitative swallowing variables decreased with time whereas the prevalences of swallowing incoordination and abnormal feeding-respiratory pattern became more frequent. After 6 months, 7 patients had persistent dysphagia. Five of these were initially non-evaluable because of unconsciousness, aphasia, or dementia.
Dysphagia 1998
PMID:Dysphagia in stroke: a prospective study of quantitative aspects of swallowing in dysphagic patients. 939 Dec 28


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