Disease relevance of Aphasia

• The authors describe a 45-year-old woman with adult-onset progressive aphasia, right hemiparesis, severe drug refractory epilepsy, and left cerebral hemisphere atrophy [1].
• A 6-year old girl developed acquired aphasia with epilepsy and a paroxysmal EEG (Landau-Kleffner syndrome) [2].
• An 18-year-old woman with a 4-year history of Rasmussen's encephalitis (RE) manifested by progressive aphasia, right hemiparesis, and nearly continuous intractable simple partial seizures that frequently secondarily generalized was treated with zidovudine (AZT) [3].
• This depression does not represent a misidentification of the negative symptoms affective flattening and alogia, as measured by the SANS, or parkinsonism or akathisia [4].
• One of these died, 1 had a protracted illness with gait ataxia and hydrocephalus and 1 other patient was disabled by hemiplegia, dysphasia and epilepsy but the remaining 8 recovered fully [5].

Psychiatry related information on Aphasia

• Detailed speech and language evaluation was used to identify three different clinical variants: nonfluent progressive aphasia (NFPA; n = 11), semantic dementia (SD; n = 10), and a third variant termed logopenic progressive aphasia (LPA; n = 10) [6].
• We studied three-dimensional regional cerebral blood flow (rCBF) in 13 children with dysphasia and/or attention deficit disorder (ADD), using xenon 133 inhalation and emission computed tomography [7].
• A dichotic monitoring test for the lateralisation of speech dominance was compared with testing for dysphasia after unilateral electroconvulsive therapy to each side of the head in 31 patients, and the intracarotid amylobarbitone test in four epileptic patients [8].
• Also, our patient differed from the progressive non-fluent aphasia patients reported as having Pick's disease, who were all Pick variants, revealing that classic Pick's disease can be included in the spectrum of progressive aphasia syndrome [9].
• Since endogenous digoxin can regulate neurotransmitter transport and dolichols can modulate glycoconjugate synthesis important in synaptic connectivity, the pathway was assessed in patients with dyslexia, delayed recovery from global aphasia consequent to a dominant hemispheric thrombotic infarct, and developmental delay of speech milestone [10].

High impact information on Aphasia

• Low activity in striatal and posterior periventricular areas was also seen in the 8 children with ADHD in combination with phonologic-syntactic dysphasia [11].
• Six patients had surgery; 1 with right-sided IAP language dominance but left-sided PET activation had dysphasia for 6 months after left temporal lobectomy [12].
• A factor analysis indicated three factors corresponding to the Affective Flattening or Blunting subscale, the Avolition-Apathy and Anhedonia-Asociality subscales, and the Alogia and Inattention subscales [13].
• Tau and alpha-synuclein inclusions in a case of familial frontotemporal dementia and progressive aphasia [14].
• A 55-year-old woman with an aortic arch syndrome of acute onset and dysphasia, resulting from the excessive administration of ergotamine tartrate suppositories, is described [15].

Chemical compound and disease context of Aphasia

• After 3 weeks of treatment with clobazam 20 mg a day, the patient developed, in association with his seizures, a neologistic jargon dysphasia but with loss of inflection, volume, and rhythm of speech, presumably as a result of the effect of the clobazam [16].
• Therefore, this behavioural dimension accounts for the variance of the SD2R, suggesting that the striatal dopamine system modulates symptoms such as flattened affect and alogia [17].
• Regional brain blood flow in congenital dysphasia: studies with technetium-99m HM-PAO SPECT [18].
• Sulfasalazine induced seizures and dysphasia [19].
• It is likely that the transient expressive dysphasia experienced by the four patients reported here was a neurotoxic reaction, rather than a seizure phenomenon [20].

Biological context of Aphasia

• The 2 patients of this pedigree shared an early clinical phenotype consisting of later-onset, progressive aphasia, but preserved visuospatial ability, which was indistinguishable from those of other PS1-associated Alzheimer disease cases [21].

Gene context of Aphasia

• Alzheimer disease and nonfluent progressive aphasia [22].
• Of all symptom measures derived from SANS and Manchester Scales, only alogia was related to verbal fluency in that superior improvement correlated inversely with the degree of alogia [23].
• These data, although not incompatible with the hypothesis of a direct route for action, are better accommodated by the idea of a distributed semantic memory, where different types of knowledge are represented, as proposed by Allport (Allport, D. A. Current perspectives in dysphasia, pp. 32-60. Churchill Livingstone, Edinburgh, 1985) [24].
• A 33-year-old right-handed woman had intractable simple and complex partial seizures (SPS, CPS) that began with global aphasia [25].
• RESULTS: Poor Wisconsin Card Sorting Test performance inversely correlated with insight in schizophrenic patients, as did the symptoms alogia, anhedonia, avolition/apathy, affective flattening, inappropriate affect, thought disorder and delusions [26].

Analytical, diagnostic and therapeutic context of Aphasia

• Transient expressive (nonfluent) dysphasia after metrizamide myelography [20].
• Current evidence from open clinical trials suggests that dopamine autoreceptor agonists may produce a minor to moderate improvement of symptoms like affective flattening, depressed mood, alogia and avolition [27].

References