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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite 60 years of study, the brain mechanisms for stuttering are unknown. In an effort to shed light on these mechanisms, we studied two cases in which the fluency of speech changed after brain damage in adulthood. The first, an ambidextrous man, ceased to stutter after a head injury. The second, a converted left-handed man, experienced recurrence of childhood stuttering after a stroke.
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PMID:Stuttering: disappearance and reappearance with acquired brain lesions. 373 77

Following a right hemisphere stroke, a right-handed, 50-year-old male experienced a permanent dysfluency characterized by phoneme and syllable reiterations and, to a lesser extent, word and phrase reiterations. The reiterations occurred in initial, medial, and final positions and for all sentence elements (e.g., subject nouns, object nouns, verbs, modifiers). There was a notable loss of verbal automatisms (poems, songs, etc.). The patient's symptoms conform to the acquired stuttering syndrome described by A. Helm, R. Butler, and D.F. Benson (1978, Neurology, 28, 1159-1165).
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PMID:Severe stuttering associated with right hemisphere lesion. 395 41

A late onset progressive dysfluency following a right hemisphere stroke occurred in a 62-year-old male. Dysfluency was characterized by pronounced word and phrase reiterations, and sound and syllable reiterations to a lesser degree. Spontaneous speech was significantly more dysfluent than oral reading and repetition. Recitation and singing were minimally dysfluent. Reiterations were accompanied by reduced vocal loudness and increased rate of speech. Reiterations occurred in initial, medial, and final sentence position. Secondary symptoms such as facial grimacing were absent. In contrast to acquired cortical stuttering which is characterized by a preponderance of sound and syllable sentence initial repetitions, dysfluency was more closely characteristic of palilalia. The dysfluency occurred as a symptom of a diffuse nonspecific subcortical projection system defect related to massive infarction in the right middle cerebral artery distribution with associated atrophy.
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PMID:Progressive dysfluency associated with right hemisphere disease. 683 35

A patient is presented who had severe headache and then developed a stuttering course of clinical neurological deficits. Arteriography demonstrated an ipsilateral proximal middle cerebral embolus. With recurrence of symptoms, repeat arteriography showed another, more proximal embolus with areas of distal occlusion. The headache probably occurred when the embolus became lodged in a pain sensitive cerebral vessel at the base of the brain. The subsequent stuttering neurological deficits were due to fragmentation of the embolus as well as recurrence.
Stroke
PMID:Headache in cerebral embolic disease. 724 4

Sudden onset stroke occurred in a right-handed vietnamese woman speaking, reading and writing french fluently. When first seen in our department, the patient had mild right facial paresis and non fluent atypical aphasia. CT scan and MRI showed a left subcortical infarct in the superficial territory of the middle cerebral artery; only white matter of the semiovale centre was involved. Neurological examination revealed linguistic impairment resembling transcortical motor aphasia, with unusual stuttering, hypophonia, occasional semantic paraphasias and phonological reading and writing abnormalities. Non verbal cognitive function, gestural and buccofacial praxes were normal. Cerebral blood flow study by SPECT was consistent with left sylvian functional deactivation.
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PMID:[Aphasia caused by isolated lesion of the semi-ovale centre: contribution of the measurement of cerebral blood flow]. 753 25

A review of hospital admissions during 80 months revealed only 8 patients with episodes of priapism of approximately 400 pediatric male patients with sickle cell disease. The patients, who ranged in age from 5 to 19 years, underwent a 99mtechnetium penile scan, and 4 had a low and 4 had a high flow scan. Three cases resolved with hydration alone. Five patients received exchange transfusion of whom 3 subsequently underwent shunt procedures. One patient with a 5-year history of recurrent stuttering episodes was placed on transfusion therapy for 6 months and stuttering episodes have not recurred. One patient had a cerebrovascular accident 1 day after hospital discharge and another had priapism while on chronic transfusion therapy for a cerebrovascular accident. Each postpubertal patient had a severe clinical course; 1 had temporary impotence for 3 months and another had impotence at 2 weeks but was lost to followup. While 99mtechnetium penile scans may help clarify the severity of vascular stagnation, in our small group they were not helpful in predicting clinical course.
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PMID:Priapism in children with sickle cell disease. 760 95

An almost two-year-old left-handed girl with a history of a left-hemisphere stroke at the age of one year developed a transient stutter with newly acquired white matter infarctions. Her course suggests that developmental stuttering may reflect anomalous dominance and/or atypical interhemispheric connectivity.
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PMID:Acquired stuttering after a second stroke in a two-year-old. 813 18

The pathophysiology of developmental or acquired stuttering still remains an enigma. In a few cases, the developmental stuttering that had disappeared spontaneously or as a result of therapy reoccurred following a brain lesion. We report on a patient with return of developmental stuttering following a left hemispheric stroke. This case supports the theory that acquired brain lesions may cause a return of stuttering, possibly by interfering with the compensatory mechanism(s) that once had relieved the developmental stuttering.
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PMID:Return of stuttering after stroke. 1087 40

Stuttering is an uncommon presentation of acute stroke. Reported cases have often been associated with left sided cortical lesions, aphasia, and difficulties with other non-linguistic tests of rhythmic motor control. Three patients with subcortical lesions resulting in stuttering are discussed. In one patient the ability to perform time estimations with a computerised repetitive time estimation task was characterised. One patient had a pontine infarct with clinical evidence of cerebellar dysfunction. A second patient had a left basal ganglionic infarct and a disruption of timing estimation. A third patient had a left subcortical infarct and a mild aphasia. These findings expand the reported distribution of infarction that can result in acquired stuttering. Subcortical mechanisms of speech control and timing may contribute to the pathophysiology of acquired stuttering.
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PMID:Subcortical infarction resulting in acquired stuttering. 1099 May 23

A 53-year-old right-handed man acutely developed stuttering. On his examination there was blocks and repetitions exclusively on first syllables of words in conversational speech, improving in automatic tasks. There was neither aphasia, nor other neurological deficits. An MR imaging of the brain showed a circumscribed cortical infarct on the left precentral circunvolution. Cerebral angiography was consistent with atherosclerotic narrowing of the intracavernous segment of left internal carotid artery. Artery-to-artery embolism was the suggested mechanism for this stroke and the patient was treated with oral anticoagulants for six months. Stuttering improved progressively and the patient became asymptomatic a month after the stroke. Ictal acquired stuttering symptomatic of ischemic stroke without aphasia or other neurological deficit is exceptional. An small infarct on the left motor area as cause of isolated acquired stuttering adds new information about neural circuits involved in this phenomenon.
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PMID:[Stuttering as the only manifestation of a cerebral infarct]. 1119 52


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