Romanian journal of neurology and psychiatry = Revue roumaine de neurologie et psychiatrie最新文献

The effect of large glucocorticosteroid hormones administered to two groups of adult rabbits with an experimental acute injury of the spinal cord was studied. In the former (10 rabbits), each animal received intravenous 30 mg/kg body weight of prednisolone-21-sodium-hemisuccinate after 30 minutes and further 15 mg/kg b.w. at intervals of 2, 24 and 48 hours since injury. In the latter (40 rabbits), each animal received 15 mg/kg b.w. methyl-prednisolone-21-hydrogen-sodium-hemisuccinate at 30 min, 2, 24 and 48 h postinjury. A group of 20 injured rabbits with the same experimental conditions was used as controls without glucocorticoid treatment. Clinically, both treated groups of rabbits showed a significant improvement of posterior limb movements and in the general state of health compared with the controls. The mean motor score (according to a 5-score scale) indicated a significant difference between the two treated groups (2.3 and 2.6, respectively and 1.7 for the controls). Histologically, the modifications correlated with the clinical posttraumatic symptomatology and severity in all the three groups: histopathological modifications consisted in oedema, ischaemic cells, diffuse microglial hyperplasia, microhaemorrhages, all of them located in the central gray matter. In all cases with a severe clinical evolution (score of 1-3), aggravated histopathological modifications both in the gray and white matter are evidenced: necrosis; vacuolization; cavitation; myelinic and axonal fragmentation, demyelination, mesenchymo-glial scar reaction. In all groups, regenerated nervous fibres were noticed in the dense scar of the injured cord.

The catecholamine (CA) response to upright posture was studied in 30 brainstem infarct patients with orthostatic arterial hypotension; the investigation was made before and after 10 days propranolol therapy (in 15 cases) and before and after 10 days metoclopramide therapy (in other 15 cases). Before treatment almost all patients responded to posture by a rise in adrenaline (A) excretion and by a depression in noradrenaline (NA) excretion. Propranolol therapy prevented the excessive A release produced by standing and normalized their NA response to posture. Metoclopramide administration also prevented the post-orthostatic A discharge but had no significant influence on NA response to posture. Both drugs exerted a favourable influence on postural hypotension of investigated patients. As post-orthostatic A discharge observed in patients with postural hypotension is involved in the pathogeny of this syndrome and both metoclopramide and propranolol are able to correct this disorder one may maintain that the clinical favourable results obtained with these drugs are ascribable at least partly to their blocking effect on A release.

The effect of forearm or calf ischemia on computerized EEG was studied in five patients with peripheral nervous system affections and five patients with cerebral infarction. Spatial analysis of power spectra in various frequency bands was performed in two 8-sec epochs, the former before ischemia and the latter after 5-min from the cessation of circulatory arrest which lasted 15 min. Transient peripheral ischemia resulted in consistent augmentation of alpha activity involving both the anterior and the posterior hemispheric areas, bilaterally. On the other hand, the slower frequency bands (theta, delta) underwent minor, nonsignificant alterations after ischemic stress. The rise of alpha amplitude induced by ischemic stress was ascribed to the activation of nonspecific thalamic system. The activation of this system might also be involved in the favourable effects exerted by ischemic stress on motor recovery of paretic limbs.

The problem of the late EP components generator localization has not yet been solved. This study aims to find out if a focal cortical epilepsy of the frontal (FLE) or of the temporal lobe (TLE) can modify the P300 component of the evoked response (either visual or auditory). Our data rely mainly on the selective differentiation test of an 80 dB click alternatively applied on the right or left ear, the patient having to give a motor response to those stimuli which have been chosen as target stimuli (probability of administration, 1:4). Under these circumstances, in normal subjects, evoked potentials showed deep P300 and an attenuated N2b in case of target stimulation and high, delayed N2b and an attenuated P300 for the nontarget stimulation, FLE did not abolish the late components of the EP; on the contrary, these were significantly augmented by the task. TLE, in exchange, severely attenuated differences between N2b-P300 components recorded from the scalp in case of target and nontarget stimulation. P300 was even higher at rest (possibly an effect of defective habituation). Rare or rapid stimuli application which was separately investigated gave another type of EPs modification compared to that specific for the auditory discrimination task. These facts are corroborated with the complete abolition of late EP components after lateral brain stem lesions. The conclusion is that N2a component has a reticular brain stem generator while N2b and P3 have initial generators in the temporal lobe (hippocampus).

Three cases with Wallenberg's syndrome were reported, in which CT-scan revealed silent old right temporal infarction, right recent cerebellar haematoma and left calcified parietal subdural haematoma evidenced after 10 years since trauma due to a traffic accident. Although Wallenberg's syndrome constitutes a fully clinical diagnosis, CT-scan does not seem to be justified by the management logical deductions of the medical act; however, it is better to perform it in order to identify a possible associated pathology.

Despite many efforts, the etiopathogenesis of ALS remains unknown. During the last decade evidence for an autoimmune involvement in motoneuron degeneration and death has remarkably increased. Multiple reports have documented significant expression of proteins associated with immune function in affected areas of ALS patients. Two animal models of immune-mediated motoneuron destruction have been developed that closely resemble clinical, electrophysiological and morphological features of human ALS. Inflammatory foci within the spinal cord, and IgG at the neuromuscular junction as well as within upper and lower motoneurons found in the animal models support the role of autoimmune mechanisms of motoneuron destruction in this model. IgG from ALS patients and from the animal models can passively transfer physiological changes at the neuromuscular junction in mice. That ALS IgG interact with calcium channels and induce an alteration of their function is now electrophysiologically and biochemically evident. Furthermore, it has been documented that motoneurons may be selectively vulnerable since they have a deficient calcium buffering capacity. Although further research efforts are necessary to elucidate the interaction of the ALS antibodies with the calcium channel function and how defective calcium handling by the motoneurons is important in their degeneration, the current data strongly suggest the involvement of autoimmune mechanisms in ALS etiopathogenesis.

Tomaculous neuropathy represents the morphological substrate of the recurrent familial neuropathy with liability to pressure palsies. Some ultrastructural changes characterizing the tomaculous neuropathy can occur as incidental aspects in other different neuropathies. Few tomaculous neuropathy cases with clinical aspect of chronic polyneuropathy without paretic episodes have been mentioned in the literature. In the present work, we report four cases who offered the morphological surprise of a true tomaculous neuropathy with 15-37% of the teased fibres bearing tomaculae sized: 55-106 microns/20-23 microns, on the background of a demyelinating neuropathy with 25-56% of the teased fibres showing segmental de- or remyelination. The clinical and electrophysiological diagnoses of these 4 patients were: HSMN type I (2 cases), HSMN type VIII (polyneuropathy associated with a cerebello-extrapyramidal syndrome -1 case), and a neurogenic scapuloperoneal syndrome (1 case). The specificity of the tomaculous neuropathy is discussed.

The influence of acetazolamide in patients with hemorrhagic stroke was assessed in 54 patients in comparison with the influence of other therapies in 68 patients included in a control group. Modified Rankin Scale and mortality rate were evaluated at three different moments: onset, 72 hours and control (3 weeks-one month from the onset). A better outcome was seen when acetazolamide was given. Mortality rate was significantly lower in the group of acetazolamide. This therapy may be safely used in haemorrhagic stroke, especially when hydrocephalus is associated.

Neoplasms are relatively rare in the lumbosacral region. The present study presents two cases with tumors in the lumbosacral region, a chordoma and a tumor with multinucleated giant cells which further showed a presacral development. Some common aspects of the clinical and radiologic symptomatology were evidenced as well as the specific characteristics of each separate tumor in our cases. The diagnosis was possible due to the modern radiologic equipment.

The initial objective of the present study was to investigate the role of excitatory and inhibitory amino acids in generalized as compared to focal epilepsy, both forms being induced by the same convulsant agent, i.e. penicillin. Our attempts to obtain in the rat the generalized epilepsy, constantly induced in cats by systemic administration of penicillin, were unsuccessful. This is probably due to the rudimentary development of the cerebral cortex in rodents as compared to the feline cortex. The tentative conclusion was drawn that the cortex is the brain structure mainly involved in the genesis of petit mal seizures. Penicillin was applied to the cortex of 40 white Wistar rats and the electrical cortical activity was registered. The concentrations of glutamate, aspartate, glycine, GABA and serine were determined in the cerebral cortex, the brain stem and the cerebellum. The same amino acids were determined in the brain of 20 controls. No significant changes in the amino acid contents were obtained in the cerebral cortex. In the brain stem the glutamate level was significantly increased while the glycine content was markedly decreased. These findings are consistent with the involvement of the brain stem structures in seizure activity.