Kapronczay Károly szerk.: Orvostörténeti Közlemények 198-199. (Budapest, 2007)

TANULMÁNYOK — ARTICLES - SZIRMAI, Imre - GOSZTONYI, Georg: Conceps of Localization of Neurological Functions in István Környei 's Oeuvre. - (Az idegműködések helyhez-köthetöségének elméletei Környei István életművében)

sion of emotional accompanying phenomena of external and internal stimuli, etc., while operations related to cognition are connected with the following structures: caudal part of Brodmann 24, Brodmann 32, the motor cingular cortex and the nociceptive cortex (Devinsky et al., 1995). The latter is regarded as important in giving response and in the elaboration of informations connected with cognition. The anterior cingular cortex is part of the rostral limbic system, which incorporates, moreover, the ventral part of the striatum, and the orbito-frontal and anterior insular cortical areas. These relations explain that transcortical motor aphasia develops not only in case of a lesion involving the supplementary motor area (which is damaged, as a rule, together with the cingular region, due to their common blood supply), but it also evolves due to damages involving the ventrolateral thalamic nucleus, the dorsolateral frontal cortex, lying anteriorly to the Broca area (this is presumed to cause the perseverative form of transcortical motor aphasia) and due to damages affecting the subcortical white matter in the neighbourhood of the left frontal horn (Caplan, 1990). Characteristic of this condition are the start hesitation and slowness of the speech, in spite of that, the understanding and the repetition remain regularly intact. Transcortical motor aphasia was also observed following haemorrhage and infarct of the left thalamus. This speech disorder has also been accompanied by hypophoria and dysarthria. Környey has not studied the effect of subcortical lesions on speech production. In the recent neurological literature several forms of subcortical aphasias were described in cases of vascular lesions in the following four cerebral areas: the striato-capsular region, the thalamus, the "quadrilateral space" of Marie, and the periventricular white matter. Naeser et al. (1982) differentiated three types of striatocapsular aphasia syndromes: (a) In case of injury of the frontal anterior-superior periventricular white matter the speech is stuttering, slow, and dysarthric ("expressive inertia"), enduring hemiparesis is present, but speech comprehension and grammatical rules are relatively spared. The underlying cause most probably is the interruption of the connections between the supplementary motor area, which is so important in the speech initiative, and the Broca's field, (b) Lesions extending to the posterior white matter are associated with impaired comprehension, fluent, but Paraphasie speech and hemiparesis. (c) Infarcts or haemorrhages extending to both regions elicit global aphasia and enduring hemiparesis. Aphasias which develop after damage to subcortical structures are not equivalent with the cortical ones. It was observed, that aphasias elicited by lesions destroying also the deep white matter of the dominant hemisphere remain unchanged after 6 to 12 months, in some patients even after 10 years following the insult. Thus, the damage to the white matter cannot be "compensated" by the preserved brain structures. This observation seems to reinforce the very old disconnection theory of aphasias. The damage to the paramedial thalamus of the left side leads to disturbances of the attention and memory, besides speech disturbance, especiallly ifit extends to the dorsomedial nucleus, the centrum medianum or to the lamina intramedullaris (Gorelick, 1984). According to Crosson (1999) thalamus aphasias can also be explained with the disturbance of the memory activating processes. It is probable that the lexical and semantic disorder is elicited by the disturbance of the working memory. The analysis of cortical aphasias also indicates that speech comprehension is determined by the capacity of the working memory. Based on its connections the thalamus aphasia (anomia) can be regarded as the consequence of a memory activating disturbance, following the damage to nuclear groups having important roles in memory processing. In a similar way, also mood- and motivation disturbances can