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The hypothesis was tested that alexia associated with Broca's aphasia may often be a residual receptive disorder of a broader picture of global aphasia. It was found that alexia does tend to be associated, as expected, to the long-standing Broca's aphasias more often than to the recent ones. However, the CT scan failed to disclose larger and more posterior lesions in Broca's alexic than in Broca's non-alexic patients.
A case of probable herpetic viral encephalitis is presented. The clinical picture following the acute phase of disease was dominated by severe fluent aphasia, prominent oral tendencies, visual agnosia, and a decrease in fear reactions. Most of these symptoms, with the obvious exception of aphasia, are similar to those observed by Kluver and Bucy in rhesus monkeys that underwent bitemporal lobectomy. These manifestations may be explained by the tendency of the herpes simplex virus to invade the temporal lobes. "Agnosia" in the auditory field and changes in vocal behavior were observed by H. Kluver and P. C. Bucy (1939, Archives of Neurology and Psychiatry, 42, 949-1000) in some of their bitemporal monkeys. The association of sensory aphasia, as observed in this case, with the auditory "agnosia" observed in some bitemporal monkeys, is discussed.
We here report one case of hemichorea and Broca aphasia occurred with diabetic ketoacidosis. A 20-year-old woman with type 1 diabetes mellitus had experienced diabetic ketoacidosis fourth time after the onset of diabetes. At the third ketoacidotic episode, the patient was admitted to our hospital for the first time to show hemichorea of the left extremities. Brain computed tomography (CT) demonstrated a high-density area in the right caudate head and low-density area in the right putamen. Magnetic resonance angiography (MRA) demonstrated a stenosis at the root of the bilateral middle and anterior cerebral arteries. The hemichorea disappeared within 3 days. At the fourth ketoacidotic episode, not hemichorea but unconsciousness was there for 2 days even after ketoacidosis disappeared. After the unconscious state, Broca aphasia was demonstrated for 15 days. The cerebral angiography showed a finding compatible to Moyamoya disease. These findings support that chorea and Broca aphasia induced by diabetic ketoacidosis was developed in addition to blood vessel abnormalities such as Moyamoya disease. We suggest that poorly controlled diabetic patients with hemichorea should undergo cerebral angiography.
The effect of two linguistic factors in Broca's and Wernicke's aphasia was examined using Dutch and English subjects. Three tasks were used to test (1). the comprehension and (2). the construction of sentences, where verbs (in Dutch) and verb arguments (in Dutch and English) are in canonical versus non-canonical position; (3). the production of finite versus infinitive verbs. Proportions of errors as well as types of errors made by each aphasic group are similar on the sentence comprehension and sentence anagram tasks. On the verb production task the performance pattern is, again, the same, but the error types are different. The discussion focuses on how the similarities and differences across languages and across aphasia types may be interpreted with respect to the underlying deficit in Broca's and Wernicke's aphasia.
A productive, intelligent, 60-year-old practicing attorney slowly begins to notice that the language that he has commanded throughout his life is beginning to become more difficult to produce, exacting its toll on his mental energy and emotional stability. His search for answers to his diminished "memory for words" leads him through the fetid ranks of traditional medicine and into the search for a differential diagnosis involving clinical neurology, neuropsychology, and speech-language pathology. Consistencies and conflicts in the signs and symptoms between the competing diagnoses raise theoretical and clinical classification issues. A course of treatment for aphasia provides evidence to support the diagnosis of primary progressive aphasia, but the development of concommitant spastic dysarthria and dysphagia challenge current wisdom about the underlying neuropathology of aphasia and support a diagnosis of early dementia. A selective but steady and rapid decline of abilities over the course of 2 years leads to the patient's death and autopsy, from which a neuropathologic analysis was to provide the "final" and "ultimate" diagnosis. But it doesn't!
We present a patient (PW) with non-fluent progressive aphasia, characterized by severe word finding difficulties and frequent phonemic paraphasias in spontaneous speech. It has been suggested that such patients have insufficient access to phonological information for output and cannot construct the appropriate sequence of selected phonemes for articulation. Consistent with such a proposal, we found that PW was impaired on a variety of verbal tasks that demand access to phonological representations (reading, repetition, confrontational naming and rhyme judgement); she also demonstrated poor performance on syntactic and grammatical processing tasks. However, examination of PW's repetition performance also revealed that she made semantic paraphasias and that her performance was influenced by imageability and lexical status. Her auditory-verbal short-term memory was also severely compromised. These features are consistent with 'deep dysphasia', a disorder reported in patients suffering from stroke or cerebrovascular accident, and rarely reported in the context of non-fluent progressive aphasia. PW's pattern of performance is evaluated in terms of current models of both non-fluent progressive aphasia and deep dysphasia.
Ictal aphasia in adults is a rare phenomenon, with the majority of reported cases showing a nonfluent Broca's or mixed aphasic speech pattern associated with disturbances of level of consciousness. There is usually only one prolonged episode of aphasia with evidence of lateralized neurological findings and structural pathology on CAT scan. We describe a patient with intermittent episodes over a 10-year period of a fluent Wernicke's aphasia associated with paroxysmal posterior temporoparietal spike-wave activity on the EEG. Interictally, the patient was clear of neurologic signs and symptoms. These episodes were repeatedly misdiagnosed as psychotic breaks and treated with antipsychotic medication and psychiatric hospitalization. Unless language performance is assessed, these cases of focal epilepsy may be diagnosed as schizophrenic "word-salad," leading to delay of appropriate treatment.
Three patients are presented who developed conduction aphasia after a small infarction almost exclusively confined to the arcuate fasciculus. All of them were diagnosed as conduction aphasia within a week after the stroke and showed a rapid amelioration. On the basis of the 3 patients and conduction aphasics in the literature, the relation between conduction aphasia and the arcuate fasciculus is discussed.
We present a review of the literature on Primary Progressive Aphasia (PPA) together with the analysis of neuropschychological and neuroradiologic profiles of 42 PPA patients. Mesulam originally defined PPA as a progressive degenerative disorder characterized by isolated language impairment for at least two years. The most common variants of PPA are: 1) Progressive nonfluent aphasia (PNFA), 2) semantic dementia (SD), 3) logopenic progressive aphasia (LPA). PNFA is characterized by labored speech, agrammatism in production, and/or comprehension. In some cases the syndrome begins with isolated deficits in speech. SD patients typically present with loss of word and object meaning and surface dyslexia. LPA patients have word-finding difficulties, syntactically simple but accurate language output and impaired sentence comprehension. The neuropsychological data demonstrated that SD patients show the most characteristic pattern of impairment, while PNFA and LPA overlap within many cognitive domains. The neuroimaging analysis showed left perisylvian region involvement. A comprehensive cognitive, neuroimaging and pathological approach is necessary to identify the clinical and pathogenetic features of different PPA variants.
We compared the course of a preschool child we followed for 4 years with published reports of 24 children with fluent aphasia. Our patient spoke fluently within 3 weeks of the injury. She was severely anomic and made many semantic paraphasic errors. Unlike other children with fluent aphasia, her prosody of speech was impaired initially, and her spontaneous language was dominated by stock phrases. Residual deficits include chronic impairment of auditory comprehension, repetition, and word retrieval. She has more disfluencies in spontaneous speech 4 years after her head injury than acutely. School achievement in reading and mathematics remains below age level. Attention to the timing of recovery of fluent speech and to the characteristics of receptive and expressive language over time will permit more accurate description of fluent aphasia in childhood.
Electrical status epilepticus during slow sleep (ESES) is characterized by an EEG picture that justifies its name. It can be accompanied by epileptic seizures, speech and behavior disturbances and in rare cases by an acquired sensory aphasia. We describe the case of a six-year-old girl, whose EEG presented the typical ESES picture, and who in the span of one year developed a complete sensory aphasia, followed by motor aphasia. After 6 months of treatment with clobazam recovery of speech was nearly complete, but after 8 months clobazam lost its effectiveness and the girl presented a speech regression. Treatment with nitrazepam led to a complete recovery of speech for a second time, while at the same time ESES in the EEG again disappeared. This case, in addition to others described in the literature, suggests the possibility of a direct correlation between electrical abnormalities of the brain and cognitive and speech disturbances.
Analysis of language profiles and CT anatomy in transcortical motor aphasia (TCMA) suggests that the essential lesion is disruption of connections at sites between the supplementary motor area and the frontal perisylvian speech zone. If the lesion is extended, there may also be poor articulation (lesion deep to motor strip for face), impaired auditory comprehension (lesion in anterior head of caudate, anterior limb internal capsule, anterior putamen, and anterior portion of external capsule, claustrum, extreme capsule, and insula), or stuttering (lesion in pars opercularis and lower third of premotor region). This concept unifies disparate anatomic and psychophysiologic observations about three syndromes: classical TCMA, aphasia after left medial frontal infarction, and TCMA during recovery from Broca's aphasia.
We studied a patient with transcortical motor aphasia resulting from a traumatic interhemispheric left frontal hematoma. The aphasia was caused by compression exerted by the hematoma on the left supplementary motor area, which is known to have a function in speech. This cause of a transcortical motor aphasia has not been described earlier.
The author studies three patients with Broca aphasia characterized by the Boston Diagnostic Aphasia Examination, and following A.R. Luria's criterion on the use and comprehension of pragmatic elements of speech--deixis of time, person, place, discourse and social, implicatures of Grice, conventional, generalized and particularized and presupposition. For this, the author works on the development of three hours speech resulted from interviews and also uses specific tests. One of the patients lost the propositional content of speech and internal language, typical of severe dynamic aphasia. The other two showed instability in comprehension and use of time and place deixis only during the tests, not revealing this anomaly at non-artificial conditions. These findings suggest that metalanguage is upset with its specific temporo-spatial elements affected, and it is possible that there is a graduation in the loss of discourse linkage with verbal and nonverbal context in which mediation is made by pragmatic relation in frontal lesions.
This paper reports two cases of crossed dextral aphasia. The first patient was a 60-year-old right-handed male with no family history of sinistrality. He experienced sudden onset of left hemiplegia and loss of consciousness. A CT scan showed high-density area in the right fronto-parietal region. An angiography revealed an arteriovenous malformation (AVM) in the right parietal lobe. It was fed by a branch of the middle cerebral artery and drained through a cortical vein. Neuropsychological examination one week after the surgery showed severe defects of all language moderalities. He was alert and cooperative, but completely mute. He recognized common words by auditory and visual stimuli, but could not perform simple command. He wrote some meaningless letters when asked to write his own name. Auditory and reading comprehension gradually improved thereafter, but Broca's type of aphasia with non-fluent hesitant and effortful output was still present four months after the surgery. The second patient was a 38-year-old right-handed male. All members of this family are right-handed except for one sister who is left-handed. He suddenly suffered left hemiparesis and loss of consciousness. A CT scan disclosed a right parietal intracerebral hematoma. And an AVM which was fed by the angular artery and drained through a cortical vein was angiographically demonstrated in the same area. Postoperatively the left hemiparesis rapidly disappeared, but left homonymous hemianopsia and anomic type of aphasia still persisted. His speech was fluent and daily communication was possible in spite of circumlocutory paraphasic output.(ABSTRACT TRUNCATED AT 250 WORDS)
More than 70 cases of crossed dextral aphasia have been reported in the literature since the end of the XIXth century. If a genetic, environmental or even pathological factor--or lack of information about it--could be suspected to be responsible of a majority of these cases, 10 of them in which all these factors were eliminated still remain. A summary of the neurological, neuropsychological and neurolinguistic features of these 10 cases shows, among other things: 1. that nearly all of them present a (left) motor deficit associated with a quite large and deep right-hemispheric lesion; 2. that most of them also report the presence of one or the other of the neuropsychological signs usually seen in right hemisphere lesions in dextrals; 3. that if reduction and agrammatism are frequent aphasic signs, fluent jargon is also reported, more so in written than in oral expression. Some of the hypotheses put forward to explain crossed aphasia in dextrals are discussed in the light of these facts. It appears that none of these hypotheses can satisfactorily account for the occurrence of a right hemisphere aphasia in some dextrals.
So called transcortical motor aphasia (TCMA) is frequently subdivided, because the clinical features and the localization of the lesions are variable. The authors have been attempting to classify TCMA into three types according to the distribution of the lesions, such as Type F 1, Type F 2 and Type F 3. Case 1 N.S. belongs to Type F 1 showing the clinical features of TCMA with bleeding in the territory of the left anterior cerebral artery. Case 2 M.E. belongs to Type F 2 (published case). This case is similar to Luria's dynamic aphasia in its clinical features and results from the lesions including the posterior parts of left middle frontal gyrus. Case 3 N.T. belongs to Type F 3 who recovered from typical Broca aphasia after language training for four years. The case is similar to Goldstein's Type 1 of TCMA in its clinical features. These three cases are compared with regard to the fundamental bases of spontaneous speech disturbance. The items of comparison are as follows; the volume of speech production and the the time taken to start speech, word fluency test, cue effects necessary for the success of sentence constructions grammatical ability. The results are summerized in Table 2. Type F1 shows the most conspicuous defect of spontaneous speech, but no disturbance in grammatical ability. And when the top word of a sentence (a subject word) is given by the examiner, the patient can construct a structurally correct sentence. These findings imply that the spontaneous speech disturbance of Type F 1 is due to a defect of the starting mechanism of speech.(ABSTRACT TRUNCATED AT 250 WORDS)
A right-handed patient with no family history of either neurological disorders or of left-handedness was affected by crossed aphasia due to a focal hemorrhagic lesion in the right hemisphere at the level of the basal ganglia. The CAT-scan revealed the site of the brain change. Our case is uncommon in that the aphasia. Assessed by neuropsychological tests, was associated with impairment of right functions such as visual and spatial cognition. Thus he does not fit the classic description of crossed aphasia, exhibiting instead language disorders similar to those following deep brain lesions. Various hypotheses were considered in attempting to explain the pathogenesis of our neurological data, none of which proved adequate to account for all the reported findings.