Parinaud's syndrome: electro-oculographic and anatomical analyses of six vascular cases with deductions about vertical gaze organization in the premotor structures.

Six cases of Parinaud's syndrome, with downward (Cases 1, 2), upward (Cases 3, 4) and both downward and upward gaze paralysis (cases 5, 6) are reported. Four cases (Cases 1, 2, 3, 5) were studied anatomically using serial sections of the brain and 3 cases (Cases, 1, 4, 6) analysed electro-oculographically. In all the cases there were rather small vascular lesions in the mesodiencephalic region, sparing the oculomotor nuclei. Since the rostral interstitial nuclei of the medial longitudinal fasciculus (riMLF), located above the oculomotor nuclei, contain the final relays producing all vertical saccades, it is suggested that the different aspects of Parinaud's syndrome may result from damage to their cells or to their excitatory efferent tracts, or even to their afferent pathways. Downgaze paralysis results from bilateral lesions involving the regions located just caudal, medial and dorsal to the upper poles of the red nuclei. The critical area is probably related to the mediocaudal part of the riMLF, the lateral portion of which appears to be spared. These anatomical data, combined with the clinical observation that most downward eye movements (except slow reflex movements) are affected in the case with such paralysis, lead us to propose that it is the riMLF efferent tracts mediating downgaze and projecting on to the oculomotor nuclei that are principally damaged by the lesions. Upgaze paralysis results from unilateral lesions in or near the posterior commissure. The clinical data allow us to propose that it is also the riMLF efferent tracts, mediating upgaze, that are damaged in such cases. consequently these tracts, probably originating from the dorsolateral part of the riMLF, would decussate through the posterior commissure before they reach the oculomotor nuclei. Combined downgaze and upgaze paralysis results from bilateral lesions involving the region related to the whole riMLF on both sides. The principal conclusion is that the riMLF efferent tracts mediating upward and downward gaze have clearly separate courses in the immediate premotor structures.

[Parinaud's syndrome and tonic vertical gaze deviation. 3 anatomo-clinical observations]. / Syndrome de Parinaud et déviation tonique verticale du regard. Trois observations anatomo-cliniques.

Two anatomo-clinical cases of downward gaze palsy and one case of upward gaze palsy are reported. A tonic and intermittent downward gaze deviation is described. The supranuclear palsies of the downward gaze were related to paramedian lesions of the rostral mesencephalon; the lesions involved the rostral interstitial nucleus of the medial longitudinal fasciculus, the nucleus interstitial of Cajal, and/or their afferent and/or efferent pathways. The supranuclear palsy of the upward gaze was related to lesions of the posterior commissure. Tonic and intermittent downward deviation of gaze and ocular bobbing have opposed features. The former could be related to disinhibited reticular mesencephalic neurones activated by vestibular inputs. Tonic upward deviation of gaze is also related to a vestibulo-ocular reflex. In this case, partial or total damage of the nucleus of Cajal, and/or its input and/or its output fibers appears to have a critical role.

[Motor neglect of thalamic origin: report on two cases (author's transl)]. / La négligence motrice d'origine thalamique. A propos de deux cas.

Two cases of thalamic lesions with motor neglect are presented. The syndrome of motor neglect was complete in those cases with a) underutilization of left limbs, but good utilization upon verbal orders, b) loss of placement reaction, c) weakness of movement when hand was approaching the target, d) weakness of motor reaction to nociceptive stimuli. Those cases confirm that motor neglect exists after thalamic lesions and bring pathologic clues for topographic discussion. Motor neglect seems to be a particular case of partial unilateral neglect throwing some doubt on the hypothesis of a global trouble of hemispheric activation. Prevalence of left motor neglects suggests some linkage between propositional motility and language. One may suppose that in the right hemisphere language is able to have a vicarious action when spontaneous activation is lost; at the opposite, in the left hemisphere language and motility would be too linked to let this dissociation be generally possible.

Paramedian thalamic and midbrain infarct: clinical and neuropathological study.

The clinical and neuropathological findings in 28 cases of paramedian thalamic and midbrain infarcts are reported. The 4 instances of unilateral paramedian thalamic infarct were characterized by mood and behavioral changes, limitation of the infarct to the center of the anatomical paramedian territory, and symmetrical configuration of the paramedian thalamic arteries. Basilar artery occlusion was found in 1 patient. The 5 cases of bilateral paramedian thalamic infarcts were characterized by disturbances of consciousness and behavior, extension of the infarct (to the mammillothalamic tracts in 4 cases, the red nuclei in 3, and the hypothalamus in 2), and a variable paramedian thalamic arterial pattern. The arterial pattern was symmetrical in 2 cases, asymmetrical in 1, and unilateral in 1. The basilar artery was occluded in 1 case, the basilar communicating and posterior cerebral arteries in 1, and a third patient had occlusion involving an aneurysm of the basilar artery. The 19 patients with paramedian thalamopeduncular infarcts had marked disturbances of consciousness (hypersomnia, deep coma, akinetic mutism) associated with ocular motility changes. Later, abnormal movements--always delayed--and memory disturbances were observed in some. Thalamic changes were restricted to beh paramedian territory in only 3 cases. The arterial pattern was symmetrical in 5. The basilar and posterior cerebral arteries were occluded in 4 patients each. Paramedian infarcts were rarely found as isolated lesions and were always bilateral when there was only one arterial pedicle. The paramedian thalamic pedicle can supply the polar thalamic territory.

[Progressive dialytic encephalopathy. Role of the aluminium and neurological study. One case (author's transl)]. / Encéphalopathie progressive des dialysés: rôle de l'aluminium et étude neuropathologique. Une observation.

Report a typical case of dialytic dementia in a patient treated with aluminium gels. The course was fatal in fifteen months duration. Before interruption of aluminium gel intake, the aluminium blood level measured by atomic absorption spectrography was at 1300 microgram/l (normal less than 40 microgram/l). Cerebral aluminium was studied by the method of Le Gendre and Alfrey. On the three studied specimens of gray matter including, the parieto rolandic cortex, the thalamus, the cerebellar cortex, the mean aluminium concentration was seven times higher than the witness. The optic and electronic microscopy study showed important accumulation of lipofuscin. No neurofibrillary degeneration was observed. In contrast to the intensity of the clinical signs and the fatal course the cerebral lesions were slight.

[Neuropathologic and toxicologic study of 12 cases of bismuth encephalopathy]. / Etude neuropathologique et toxicologique de douze cas d'encéphalopathie bismuthique (EB).

Examination of twelve cases of bismuth encephalopathy showed a constantand marked elevation of the bismuth levels in autopsy cerebral tissue (ranging from 2-8 mg/kg to 25 mg/kg). These values were found to be much higher than the last-measured Bismuth venous blood values. In every case, periveinular lymphocytic infiltration and abundant intra-cytoplasmic lipofuscin were seen. The microanalysis with Castaing's electrode revealed the presence of focal areas of bismuth in the leptomeningeal spaces. The significance of the lesions is not fully established and it will undergo further investigations.

[Presence of aluminum and magnesium in the cerebral arteries and parenchyma of patients with striatonigral syndrome: study by Castaing's microprobe]. / Présence d'aluminium et de magnésium au niveau des artères et du parenchyme cérébral de malades atteints de syndrome striatonigré: étude à la microsonde de Castaing

Electron probe microanalysis demonstrates the presence of aluminium, magnesium, iron, calcium, phosphorus in and around blood vessels in the pallidum (vascular siderosis) and in the putaminal parenchyma in five out of six cases of striatonigral degeneration, associated with orthostatic hypotension in two of these cases. These results suggest that striatonigral degeneration could be the result of a vascular disease, the result of an elemental intoxication of unknown cause.

[Catecholaminergic axons in the human cerebral cortex. Observation by histofluorescence of cerebral biopsies in 2 cases of Alzheimer's disease]. / Axones catécholaminergiques du cortex cérébral humain. Observation, en histofluorescence, de biopsies cérébrales dont 2 cas de maladie d'Alzheimer

Catecholamine axons have been visualized in human cerebral cortex obtained during routine neurosurgical operations. The fluorescence histochemical method of Lindvall et al. was used, slightly modified (calcium-deprived buffer, glyoxylic acid fixation followed by formaldehyde vapours exposition). The frontal cortex was more richely provided with catecholamine terminals than the parietal cortex. Two general types of axon morphology are evident. The most frequent is thin and sinous, sometimes forming clews, or loose basket-like arrangement around presumed nerve cells. The other one is moniliform and demonstrates spherical evenly-spaced varicosities. They look like, respectively, the well characterized dopaminergic and noradrenergic axons of the rat cerebral cortex. In two cases of Alzheimer's disease, noradrenergic-like fibers were missing and voluminous green-fluorescent varicosities, sometimes in obvious connection with typical axons, were observed in the proximity of senile plaques.