Clinical Neuroscience - 1951;4(04)

Clinical Neuroscience

DECEMBER 19, 1951

[Parietal syndromes (Gerstmann's syndrome, attitudinal diseases) in the light of conditioned reflexology]

JUBA Adolf

[Anomia, parietal agraphia and alexia, and finally ujjagnosia were found in three circumscribed skull lesions of the left parietal landscape (the fossa in case 1 affecting the junction of the gyr. angularis, gyr. supramarginalis and the peduncular segment of the 1st temporal gyrus, in observations 2 and 3 the gyr. angularis and partly the occipital cortex). The anomia can be interpreted, following the Pavlovian doctrines, in terms of increased iraddition of the stimulus, reduced concentration, and ultimately degradation of differential inhibition: patients vocalise a series of similar words but do not always reach the adaequate word trace. A similar mechanism is at work in the development of agraphia and alexia, exacerbated by the limitation of dynamic stereotypy to capture the word composed of letters. Parietal foci thus limit speech in its entirety and the pathology of the lesion cannot be seen as a negative of the normal functioning of the site. Finger agnosia in case 1 presented as a simple finger anomaly; in cases 2 and 3, where the occipital cortex was also damaged, the disorder corresponded to Gerstmann's true finger agnosia. Here, a multilayered inhibition of the conditional connections is expected, in which the relaxation of the kinaesthesia-optic junction plays a major role. In a fourth brain lesion in j.o., the foci were located in the more superior lip of the posterior segment of the right interparietal sulcus. In the aura of the epileptic seizures, there was a rotating dizziness, with an onset of contralateral adversion, all of which could be evaluated as focal symptoms. Macropsia developed during the aura and can be understood as a distortion of the optic and oculomotor connections (Pavlov), which indicate the size of objects, and developed in response to the pathological stimulus.]

HUN 1951;4(04)

Clinical Neuroscience

DECEMBER 19, 1951

[Data on cerebral histological changes and their origin after CO intoxication]

FAZEKAS I. Gyula, GERÉB Tibor

[The brain of a 33-year-old man who died 3 months after CO poisoning was examined histologically with the following results: 1. There was a high degree of fatty degeneration of the cortical and medullary nuclei and endothelial fatty degeneration of both the cortical and medullary vessels with perivascular granule cell accumulation. No calcification of blood vessels was observed. 2. In addition, a marked proliferation of microglia, hypertrophy and hyperplasia of macroglia, and the transformation of microglia and oliodendroglia into granule cells were observed, accompanied by generalized watery phenomena. 3. In addition to lens opacities on both sides, diffuse patchy demyelination was found in the white matter of the cerebrum, with ring-like sparing of the vascular surroundings. Both demyelination and rings of sparing, as well as a high degree of fat deposition (fat-filled granular cells) were observed in other intact-appearing brain areas. 4 Our case suggests that white matter disease can be diffuse and extensive even in the presence of negative or insignificant lesions in the medulla. 5. We consider the anoxaemic state to be a primary factor in the pathomechanism of CO poisoning. In addition, however, there is no doubt that CO itself plays a role in the development of brain tissue lesions through its direct tissue paralysis effect. 6. Based on the histological picture of our case and recent physiological observations, we do not exclude Hallervorden's view that oedema may also play a role in the development of white matter lesions, probably by obstructing cerebral blood flow and thus increasing anoxaemia by increasing intracranial and cerebral pressure, which leads to the development of pathological lesions. The perivascular sparing rings are explained by the fact that the blood vessels in the immediate vicinity still receive enough oxygen from the circulating blood to prevent severe destruction of their tissue elements, but that the more distant tissue elements no longer receive sufficient oxygen and that the anoxic condition leads to the destruction of these tissue elements.]

HUN 1951;4(04)

Clinical Neuroscience

DECEMBER 19, 1951

[Clinically observed retroolivarial softening]

SOÓS Imre

[Five clinically observed cases of retroolivar ankylosis with typhoidal history and symptomatic pathology were described. The pathology is characterized by an ictus-like onset, nodal cerebellar symptoms, crossed anaesthesia, and lacunar lesions of the bulbar nuclei on the same side as signs of damage to the posterior landscape of the olive. In our cases, by following the behaviour of sensory disturbances during the course of the disease, a certain regularity was observed, in that the initial sensory loss was replaced over time by hypersensitivity or central sensory disturbances (dysaesthesias, contraer heat sensations). Blood pressure was persistently subnormal in all our patients. Of our five patients, three had obstruction of the art. fossae. lat. bulbi described by Foix, and two had typus Wallenberg's syndrome. This fact speaks in favour of the high relative frequency of retroolivar tissue softening.]

HUN 1951;4(04)

Clinical Neuroscience

DECEMBER 19, 1951

[Foreign Language Summaries]

[A summary of the articles published in the issue in Russian and German]

HUN 1951;4(04)