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Biomedical subjects

G Assal

Publications and source records attributed to G Assal.

At least 55 records · Page 3Linked to original sources
PubMed1992

[Atypical verbal behavior in a 30 year follow-up of an acquired aphasia-epilepsy syndrome].

Detailed study of the communication of one of the patients followed-up by Deonna et al. (1989) who has been suffering since age seven of an atypical acquired aphasia-epilepsia syndrome. Seizures as well as peculiar verbal productions persist at adult age. After a thirty year follow-up, only a small lexicon has been acquired, mostly made of onomatopeia and idiosyncrasies. We describe this lexicon and discuss the quality of the communication in a real-life ecological situation. We then compare it to the jargon and the aphasic productions of the standard neuropsychological examination.

Adult↗
PubMed1991

[Should aphasias be classified?].

In the same sense as classical monuments are classified? The more so as the classification described here goes back to the end of the 19th century, for it is the one which was designed by Wernicke (Breslau, Germany) and Lichtheim (Bern, Switzerland) and was remarketed by the Boston school (Geschwind, Goodglass, Kaplan, etc.) which invaded even the Japanese market. In view of their diversity, disorders of language in patients with cortical and subcortical lesions must be reorganized into syndromes that do not express a nuclear linguistic deficit. Interindividual differences are still the rule, which is not surprising in view of the numerous variance factors.

Aphasia↗
PubMed1991

Loss of psychic self-activation with bithalamic infarction. Neurobehavioural, CT, MRI and SPECT correlates.

Two patients with bilateral thalamo-mesencephalic infarct in the paramedian territory developed vertical gaze dysfunction and marked behavioural changes, in the absence of significant motor inability and formal neuropsychological impairment. While they were physically and emotionally active before stroke, they became apathetic, aspontaneous, indifferent, and seemed to have lost motor and affectic drive, as well as the need itself for any psychic activity. However, this mental and motor inertia was reversible when the patients were repeatedly stimulated by another person. This need for constant external programming, together with a lack of emotional reactivity, made the patients resemble robots. CT and MRI suggested involvement of the dorsomedial and midline nuclei of the thalamus, and SPECT showed remote frontomesial hypoperfusion. A disturbance of the striatal-ventral pallidal-thalamic-frontomesial limbic loop is suggested by previous reports of a similar "loss of psychic self-activation", "pure psychic akinesia", or "athymhormia" with bipallidal, bistriatal, or subcortical bifrontal lesions.

Arousal↗
PubMed1990

[Systematized temporal delusion and hearing disorders of cortical origin].

We report a case of delusion characterized by a time disorientation with a constant three days advance. Five years previously, the patient had suffered a left hemisphere stroke with aphasia. The delusional belief appeared at the same time as a cortical deafness following a second right hemisphere infarction. There was severe behaviour disturbances which lasted seven months, then cleared without any other change in the clinical picture. The lesions involved the left parietal lobe as well as the temporal and insular regions of both hemispheres.

Aphasia↗
PubMed1988

Subcortical neglect: neuropsychological, SPECT, and neuropathological correlations with anterior choroidal artery territory infarction.

In 2 patients with infarction in the territory of the right anterior choroidal artery, hemiparesis, hemihypesthesia (in 1), and hemianopia or superior quadrantanopia were associated with severe multimodal hemineglect, without anosognosia, disorientation, or asomatognosia. Single-photon emission tomography showed that marked hypoperfusion was not limited to the right posterior capsular region, but also involved the overlying parietal cortex, and to a lesser extent the frontal cortex. At autopsy in 1 patient, the infarct was nearly limited to the deep white matter of the temporal isthmus and the retrolenticular part of the internal capsule; only minute lesions were present in the globus pallidus, body of caudate, and amygdala. These findings are consistent with a disconnection phenomenon as the basis for subcortical neglect with ipsilateral deactivation of the parietofrontal cortex.

Aged↗
PubMed1988

Acute transcortical mixed aphasia. A carotid occlusion syndrome with pial and watershed infarcts.

Four of 1,200 consecutive patients with their first stroke showed acute transcortical mixed aphasia (TMA) characterized by nonfluent speech with impaired naming, semantic paraphasias, echolalia, impaired comprehension, good repetition, reading, and writing on dictation. All 4 had left internal carotid artery (ICA) occlusion with ipsilateral anterior pial territory infarction (precentral-central sulcus artery territory) and watershed infarction between the middle and posterior cerebral artery territories, which spared and 'isolated' the perisylvian speech areas. Although rare, acute TMA is highly suggestive of infarction due to ICA occlusion, in that it is probably related to simultaneous embolism (anterior pial infarction) and haemodynamic insufficiency (posterior watershed infarction).

Acute Disease↗
PubMed1988

Manic delirium and frontal-like syndrome with paramedian infarction of the right thalamus.

A disinhibition syndrome affecting speech (with logorrhoea, delirium, jokes, laughs, inappropriate comments, extraordinary confabulations), was the main manifestation of a right-sided thalamic infarct involving the dorsomedian nucleus, intralaminar nuclei and medial part of the ventral lateral nucleus. Resolution of conflicting tasks was severely impaired, suggesting frontal lobe dysfunction. These abnormalities correlated with the finding on SPECT of a marked hypoperfusion in the overlying hemisphere predominating in the frontal region. We suggest that this behavioural syndrome was produced by disconnecting the dorsomedian nucleus from the frontal lobe and limbic system.

Afferent Pathways↗
PubMed1988

[Inability to voluntarily close the eyes. Discussion of supranuclear disorders in palpebral closure based on 2 cases, with a review of the literature].

We studied 2 cases of supranuclear palsy of eye closure in patients who were unable to close their lids under command, but still conserved the possibility of closing them by syncinetic or reflex stimulations as well as during the sleep. The first patient had bilateral infarcts in sylvian watershed zones of fronto-parietal lobe and the second patient had a right cortico-subcortical superficial sylvian infarct. None of the 2 cases had an evolution towards motor impersistence of lid closure. We made a review of the literature and exposed the most debated hypothesis about this phenomenon, i.e. apraxia of lid closure or liberation of "grasping" phenomenon on the face. We expose the possibility of a disconnexion syndrome between motor supplementary area of the right hemisphere, supposed to be dominant for lid closure, and the premotor cortex area, based on reconstructions from CT Scan.

Aged↗
PubMed1987

Lingual and fusiform gyri in visual processing: a clinico-pathologic study of superior altitudinal hemianopia.

A macular-sparing superior altitudinal hemianopia with no visuo-psychic disturbance, except impaired visual learning, was associated with bilateral ischaemic necrosis of the lingual gyrus and only partial involvement of the fusiform gyrus on the left side. It is suggested that bilateral destruction of the lingual gyrus alone is not sufficient to affect complex visual processing. The fusiform gyrus probably has a critical role in colour integration, visuo-spatial processing, facial recognition and corresponding visual imagery. Involvement of the occipitotemporal projection system deep to the lingual gyri probably explained visual memory dysfunction, by a visuo-limbic disconnection. Impaired verbal memory may have been due to posterior involvement of the parahippocampal gyrus and underlying white matter, which may have disconnected the intact speech areas from the left medial temporal structures.

Aged↗
PubMed1987

[Crossed aphasia in a child].

Aphasia due to a cortical--subcortical infarct occurred in a right-handed, five year-old boy. Twelve years later, language disturbances were still present.

Aphasia↗
PubMed1987

[Infarct in the area of the left anterior cerebral artery. II. Language disorders].

Language disturbances and other neuropsychological dysfunctions were evaluated in 10 right-handed patients with left anterior cerebral artery (ACA) infarcts with CT correlation. Transcortical motor aphasia was present in 4 cases, related to involvement of the supplementary motor area (SMA) or the underlying and immediately anterior white matter. In 4 patients with sparing of the SMA but with involvement of the cingulate region, only alterations of verbal memory were found. Sensory or mixed transcortical aphasia was not observed, in any of the patients, including those in whom the supplementary sensory area (SSA) or the underlying white matter were involved, casting doubt upon the presumed receptive role in language function attributed to the SSA by some authors. Buccolingual-facial apraxia was related to subcortical lesions. A callosal disconnection syndrome was uncommon (2 patients) and no hemi-neglect was encountered, even in those cases with cingulate involvement.

Aphasia↗