American Retrospect

1897 ◽  
Vol 43 (182) ◽  
pp. 592-603
Author(s):  
C. Hubert Bond

Epilepsy and other Convulsive Diseases: A Study in Neuro-dynamics and Pathogenesis.—Under this title Dr. Langdon, of Cincinnati, reviews (Journ. Nerv. and Mental Disease, September, 1896) the present state of our knowledge upon certain facts in the anatomy and physiology of the central nervous system; and puts forward some propositions to serve as a working hypothesis to explain epilepsy and other convulsive disorders in the light of modern histological research. He lays particular stress upon Cajal's demonstration of the individuality of the neuron as opposed to the older views. Though anatomically distinct units, neurons are in physiological relation with each other, by means of delicate projections termed gemmules or “contact granules.” The neuron-body (or nerve-cell) is to be considered, in his opinion, as mainly trophic in function; while the nervous activities themselves are to be looked for in the neuron processes, and accounted for upon the theory of inter-molecular and inter-atomic motion—this motion being the result of external stimuli acting upon the peripheral arborisations of neurons. In opposition to the many theories that have been advanced in the explanation and location of the epileptic convulsion, it is now almost universally conceded that: (1) the actual origin of the epileptic convulsion is in the cortex cerebri, and (2) that its nature is an “explosive discharge” in “unstable nerve tissue.” While the nerve-cell was considered the sole seat of all nervous activity, naturally the cause of convulsive phenomena was principally sought for within this nerve-cell. But Langdon quotes researches which show that the ultimate fibrillæ of the axis-cylinder may be traced through the neuron-body to finally ramify in “neuro-plexuses” composed of multitudinous interlacing “end-tufts,” with their contactbuds, and it is in this jungle that, in his opinion, any demonstrable lesions of the various convulsive disorders (including chorea, hysteria, and even uræmia) are to be sought. He is further of opinion that the cerebral cortex, instead of being a “centre of action,” has for its main function that of inhibition, in other words, that it is a centre for preventing, checking, directing and combining various activities which might otherwise occur in different order or intensity. The phenomena observed in the case of Goltz’ dog, which lived for eighteen months after having been deprived of its cerebral hemispheres, are cited in confirmation of this view. His propositions are summarised as follows:—(1) That epilepsy, the choreas, and probably most convulsive disorders, are the dynamical expression of an inhibitory insufficiency; not indications of an over production of nerve-energy, nor “explosions” due to a “molecular instability,” per se. (2) That the cause of this inhibitory insufficiency is to be sought for in the end-brushes of collateral processes of various cortical neurons, the situation varying with the type of the disease, whether sensory, psychic, or motor. (3) That the defect consists most probably in a structural incompleteness (small capacity, defective insulation, imperfect contact) or a numerical deficiency, or both, in the collateral processes of the neurons. (4) Defective collaterals may favour occurrence of convulsions in two ways: (a) by impairing connection with other neurons (inhibitory, storage?); (b) by increased “resistance” to overflow currents, causing temporary over-charging of motor axis-cylinders.

Author(s):  
А.В. Дробленков ◽  
Л.Г. Прошина ◽  
Ю.Н. Юхлина ◽  
А.А. Байрамов ◽  
П.Д. Шабанов ◽  
...  

Актуальность. Значение недостаточности тестостерона для структурного гомеостазиса нейронов, регулирующих выработку гонадотропин-рилизинг гормона (ГнРГ) и синтезирующих данный гормон, мало изучены. Цель. Установить реактивные изменения, количество рецепторов к андрогенам (АР) и особенности их распределения в нейронах медиального аркуатного ядра гипоталамуса (МАЯ) при экспериментальном гипогонадизме, а также обратимость этих изменений после восстановительной терапии тестостероном. Методы. У самцов крыс Вистар (16 особей) моделировали гипогонадизм путем удаления одной гонады на 2-3 день постнатальной жизни и исследовали гистологические срезы каудальной части МАЯ у молодых животных (4 мес.) при отсутствии и осуществлении заместительной терапии. Контрольную группу составляли интактные самцы аналогичного возраста (8 особей). В середине левосторонней части МАЯ на площади 0,01 мм определяли реактивные изменения клеток и площадь тел малоизмененных нейронов (после окрашивания срезов методом Ниссля), а также число и долю тел нервных клеток, различавшихся по степени экспрессии АР. Результаты. Установлено, что нейроны МАЯ содержат большое количество АР, распределенных в различных частях их тела. При гипогонадизме происходит перераспределение АР и снижение степени их экспрессии (количества). Сгущение АР в области оболочки ядра и плазмолеммы, образование конгломератов в ядре и цитоплазме было характерно для нейронов с умеренной экспрессией. В цитоплазме и в области плазматической мембраны рецепторы отсутствовали у клеток со слабой и очень низкой экспрессией. Снижение степени экспрессии АР при гипогонадизме сопряжено с уменьшением площади тела и гибелью части нейронов. Заключение. Выявленные дегенеративные тестостерон-зависимые изменения нейронов МАЯ, которые синтезируют ГнРГ или пептиды, влияющие на его выработку, могут обусловить уменьшение высвобождения гонадолиберина, вторичное снижение синтеза андрогенов и реализацию морфофункциональных проявлений его вторичного дефицита. Заместительная терапия частично компенсирует дегенеративные изменения нейронов, восстанавливает интенсивность экспрессии АР, однако не влияет на процесс гибели нервных клеток. Background. Importance of testosterone deficiency for structural homeostasis of the neurons regulating production of gonadotropin-releasing hormone (GnRH) and synthesizing this hormone is insufficiently understood. Aim. To determine reactive changes, quantity of androgens receptors (AR), and features of their distribution in neurons of hypothalamic medial arcuate nucleus (MAN) in experimental hypogonadism and reversibility of these changes by restorative therapy with testosterone. Methods. Hypogonadism was modeled in 16 Wistar rats by removing one gonad on postnatal days 2-3, and histological sections of caudal MAN were examined in young, 4-month old animals with and without a replacement therapy. The control group consisted of 8 age-matched intact males. Cell reactive changes, areas of slightly changed neuron bodies (Nissl staining of sections), and the number and proportion of nerve cell bodies differing in the degree of AR expression were determined in the middle left-sided part of MAN, on an area of 0.01 mm. Results. MAN neurons contained a large quantity of AR distributed in different parts of the neuron body. In hypogonadism, AR redistributed and their expression (quantity) decreased. Condensation of AR in the region of nucleo- and plasmolemma and formation of conglomerates in the nucleus and cytoplasm were characteristic of neurons with moderate expression. In the regions of cytoplasm and plasma membrane, the receptors were absent in cells with low and very low expression. The reduced AR expression in hypogonadism was associated with a decreased neuron body area and death of a part of neurons. Conclusions. The identified degenerative changes in the testosterone-dependent neuronal MAN that synthesize GnRH or peptides affecting the GnRH production may decrease the release of GnRH, cause a secondary decrease in the androgen synthesis, and mediate morphological and functional manifestations of GnRH secondary deficit. The replacement therapy partially compensated for degenerative changes in neurons and restored the intensity of AR expression, however, it did not influence the process of nerve cell death.


1902 ◽  
Vol 48 (202) ◽  
pp. 434-450 ◽  
Author(s):  
T. S. Clouston

Dr. Clouston said that when he suggested toxæmia to the secretary as a suitable subject for a discussion at this meeting he had not intended to be the first speaker, because his object was to bring out more fully the views of the younger members who had recently committed themselves so strongly to the toxæmic and bacterial etiology of insanity, and so to get light thrown on some of the difficulties which he and others had felt in applying this theory to many of their cases in practice. It was not that he did not believe in the toxic theory as explaining the onset of many cases, or that he under-rated its importance, but that he could not see how it applied so universally or generally as some of the modern pathological school were now inclined to insist on. He knew that it was difficult for those of the older psychological and clinical school to approach the subject with that full knowledge of recent bacteriological and pathological doctrine which the younger men possessed, or to breathe that all-pervading pathological atmosphere which they seemed to inhale. He desired to conduct this discussion in an absolutely non-controversial and purely scientific spirit. To do so he thought it best to put his facts, objections, and difficulties in a series of propositions which could be answered and explained by the other side. He thought it important to define toxæmia, but should be willing to accept Dr. Ford Robertson's definition of toxines, viz., “Substances which are taken up by the (cortical nerve) cell and then disorder its metabolism.” He took the following extracts from his address at the Cheltenham meeting of the British Association (1) as representing Dr. Ford Robertson's views and the general trend of much investigation and hypothesis on the Continent.


1949 ◽  
Vol 95 (398) ◽  
pp. 180-181 ◽  
Author(s):  
A. Meyer ◽  
M. Meyer

Hydén and Hartelius in a recent monograph (1) described nerve cell abnormalities which they consider to be characteristic of mental disease. Their investigations were based on biopsies obtained during prefrontal leucotomy carried out in 11 psychotic patients, 10 of whom belonged to the schizophrenic group. The biopsies were investigated by means of the ultraviolet microscope and the results compared with brain material from normal patients fixed a few hours after death. Two types of abnormal nerve cells were found in the psychotic patients: one type is narrow and shrunken with corkscrew-shaped apical process and appears dark in the photographs in contrast to the other type which is swollen and appears light in the photographs. Both these cells lacked polynucleotides in their cell bodies and contained only a small amount of other protein substances, as shown by the ultraviolet absorption spectra.


Soft Matter ◽  
2020 ◽  
Vol 16 (28) ◽  
pp. 6591-6598 ◽  
Author(s):  
Fangwen Zha ◽  
Wei Chen ◽  
Lu Hao ◽  
Chunsheng Wu ◽  
Meng Lu ◽  
...  

Electrospun cellulose-based poly N-vinylpyrrole (PNVPY) and poly (3-hexylthiophene) (P3HT) nanofibrous mats and their influence on nerve cell behavior with electrical stimulation.


2001 ◽  
Vol 86 (2) ◽  
pp. 771-781 ◽  
Author(s):  
Yoshihiro Nishimura ◽  
Masaru Asahi ◽  
Koichi Saitoh ◽  
Hirofumi Kitagawa ◽  
Yuichi Kumazawa ◽  
...  

We examined the ionic mechanisms underlying burst firing in layer III neurons from cat sensorimotor cortex by intracellular recording in a brain slice. Regular spiking was observed in 77.4% of 137 neurons in response to constant intracellular current pulses of 0.5- to 1-s duration. The rest of the neurons showed burst firing. An initial burst followed by regular-spike firing was seen in 71.0% of 31 bursting neurons. The rest of the bursting neurons ( n = 9) exhibited repetitive bursting. In the bursting neurons, spikes comprising the burst were triggered from the afterdepolarization (ADP) of the first spike of the burst. We examined the ionic mechanisms underlying the ADP by applying channel-blocking agents. The ADP was enhanced (rather than blocked) by Ca2+ channel blockade. This enhancement of the ADP by Ca2+channel blockade was apparent even after blockade of the afterhyperpolarization by apamin or intracellular Ca2+ chelation by EGTA. The firing rate of the regular-spiking cells was increased by apamin, intracellular EGTA or Ca2+ channel blockers. In 17.9% of the neurons examined ( n = 56), these agents switched the regular-spiking pattern into a bursting one. Burst firing could not be changed to regular spiking by these agents. Four neurons that responded with a single initial burst in control solution responded with repetitive bursting after application of these agents. We conclude that the main function of Ca2+ influx in layer III neurons is to activate Ca2+-dependent K+ conductance, which prevents or limits burst firing. At a time when spike amplitude was unchanged, the ADP was blocked and the burst firing changed to regular spiking by extracellularly applied tetrodotoxin (TTX) or intracellularly applied N-(2,6-dimethylphenylcarbamoylmethyl) triethyl ammonium bromide (QX314). We concluded that a TTX- and QX314-sensitive Na+ current underlies the ADP and therefore contributes to the burst firing of layer III neurons from the cat cortex.


PEDIATRICS ◽  
1949 ◽  
Vol 4 (6) ◽  
pp. 790-797
Author(s):  
M. G. PETERMAN ◽  
J. L. GARVEY

THIS case is presented because the circumstances provided an unusual opportunity to review and study a rare condition. The child concerned had been diagnosed as having a case of hypothyroidism and epilepsy and the parents had been advised to place her in an institution. The child was referred to the authors in a further effort to obtain relief or advice. CASE HISTORY A 12 yr. old girl was examined because of "incessant talking in a silly, immature fashion; excessive greed for food and salt; lethargy, fatigue, over-affection and clumsiness, awkwardness, inability to skate or ride a bicycle." A year before admission she began to scream in her sleep once or twice every night. Six months later she began to scream during the day. The attacks of screaming occurred suddenly without warning. She abruptly stopped what she was doing, stared ahead and screamed in a loud, hoarse voice for several seconds. Immediately afterward, she was embarrassed and tried to withdraw from the scene. Treatment elsewhere with adequate doses of phenobarbital, tridione, benzedrine, thyroid and pituitary extract had been ineffective. Report of a previous examination at a university clinic was "moderately plump girl with a round face and lethargic appearance. There was narrowing of the right palpebral fissure and mild ataxia of the lower extremities. The physical examination was otherwise unimportant. The IQ was 80." Examination later at a hospital-clinic was reported as "revealing obesity and cretinism in spite of a basal metabolic rate of minus 6 and minus 7." Mother and father are intelligent and the 4 siblings are normal and well-adjusted. There is no history of convulsive disorders or mental disease.


1997 ◽  
Vol 139 (5) ◽  
pp. 1317-1324 ◽  
Author(s):  
Yonghong Li ◽  
Pamela Maher ◽  
David Schubert

Glutathione depletion occurs in several forms of apoptosis and is associated with Parkinson's disease and HIV toxicity. The neurotransmitter glutamate kills immature cortical neurons and a hippocampal nerve cell line via an oxidative pathway associated with glutathione depletion. It is shown here that soluble guanylyl cyclase (sGC) activity is required for nerve cell death caused by glutathione depletion. Inhibitors of sGC block glutamate toxicity and a cGMP analogue potentiates cell death. Glutamate also induces an elevation of cGMP that occurs late in the cell death pathway. The resultant cGMP modulates the increase in intracellular calcium that precedes cell death because sGC inhibitors prevent calcium elevation and the cGMP analogue potentiates the increase in intracellular calcium. These results suggest that the final pathway of glutamate induced nerve cell death is through a cGMP-modulated calcium channel.


PEDIATRICS ◽  
1949 ◽  
Vol 3 (6) ◽  
pp. 783-800
Author(s):  
HERBERT H. JASPER

The principal applications of electroencephalography to child neurology, neurosurgery and psychiatry are as follows: Abnormalities in the EEG of parents or siblings of patients with nervous or mental disease assists in evaluating possible hereditary factors. Nervous and mental disorders caused by abnormalities of intrauterine development, injuries or anoxia at birth, encephalopathies of toxic, metabolic or infectious origin, and severe head injuries, may be reflected in abnormal brain waves in many but not all cases. In some, the location and type of cerebral pathology may allow marked changes in behavior, such as spastic paraplegia, with no significant alteration in the EEG. The EEG gives little reliable information with regard to intelligence and the finer structure of personality. Cerebral damage due to tumor, abscess, trauma or local vascular lesion may be localized by the EEG but pathologic diagnosis must be made from a careful history and other methods of clinical examination in most cases.proved methods, deepseated lesions involving subcortical structures, as well as superficial lesions, may frequently be accurately localized by the EEG. Subdural hematomata are not accurately diagnosed by the EEG in most cases. The EEG is most useful in the epilepsies and convulsive disorders. Differential diagnosis between idiopathic epilepsy and symptomatic convulsive disorders can usually be made by the EEG except for certain postencephalitic conditions which may simulate the electroencephalographic patterns of the idiopathic or "genetic" epilepsies. The form of clinical seizure depends upon the brain area of onset of the epileptic discharge, and its path of spread. The form of electrical disturbance has no specific significance except as pointing to a certain localization of onset. A wide variety of seizures are caused by focal epileptic discharge arising primarily in various areas of the cortex. These may be localized by the EEG when on the convexity of the hemispheres, but may be missed when buried in fissures or on the ventral or mesial surfaces of the brain. They are frequently discovered only when electrodes are placed directly on the brain surface exposed at operation. Bifrontal rhythmic disturbances may be caused by foci on the mesial or orbital surface of one frontal lobe. Bitemporal rhythmic disturbances may be caused by a focal epileptogenic lesion deep in one temporal region. The wave and spike pattern of petit mal epilepsy can be reproduced by local stimulation in certain parts of the thalamus. The EEG may be of assistance in assessing the initial severity and progress of recovery from cerebral trauma due to head injury. Profound alterations in the EEG occur during the acute stage of any form of encephalitis. Residual changes are of value in prognosis, especially with regard to epileptiform disorders. In child psychiatry, the EEG may point to an unsuspected organic basis for particularly intractable behavior. However, it is of little value for specific diagnostic purposes except as related to epileptic equivalent states and disorders due to focal lesions or diffuse encephalopathy.


Author(s):  
Kazuya Matsumoto ◽  
Yusuke Morita ◽  
Eiji Nakamachi

Recently, the electromagnetic and mechanical stimulation have been recognized as the effective extracellular environmental factor to enhance the defected peripheral nerve tissue regeneration. We designed and fabricated a bioreactor device, which can load the uniform AC magnetic field (ACMF) and the uniform tensile strain to stimulate PC12 nerve cell. For ACMF stimulation system, we used the pole piece structure to enable the uniform ACMF and in-situ microscopic observation. We confirmed the uniformity of magnetic field in the experiments. Further, the uniform strain in the stretch stimulation device was confirmed, even a slightly deviation from the designed strain was observed. It was a negligible small error. Next, we validated the effectiveness of PC12 axonal extension enhancement by two stimulation methodologies, ACMF and the cyclic stretch, under individual and combined stimulation conditions. ACMF showed a best enhancement effect on axonal extension, such as 70 μm at 96 h culture period, which rate is larger than the case of control. On the other hand, the stretch stimulation caused the exfoliation of cells. Hybrid stimulation succeeded to inhibit the exfoliation. However, the extensional rate was less than the case of ACMF. These results can be used to fabricate a bioreactor of nerve cell regeneration.


2017 ◽  
Author(s):  
Olga N. Oztel ◽  
Adil Allahverdiyev ◽  
Aysegul Batioglu Karaaltin ◽  
Melahat Bağırova ◽  
Ercument Ovali

AbstractBackgroundExperimental studies performed with human olfactory nerve stem cells haveshown that these cells can ameliorate nerve cell regeneration. Developing a method of repairing nerve damage solely using stem cells without the need of any supporting material is important.MethodsA multilayer cell mass was obtained from olfactory tissue-derived mesenchymal stem cells with high viability and proliferation capability using a protocol devoid of scaffolds or any other artificial supporting material. First, human olfactory tissue-derived mesenchymal stem cells were isolated, cultured, and characterized. Next, consecutive passages were conducted to obtain multilayer cell growth. The resulting cell mass could be suitable for tissue engineering models as well as nerve cell or tissue regeneration studies in the future.ResultsViability and adhesive properties of the resulting cell mass were examined and found to be suitable for use in nerve tissue regeneration.ConclusionIt is suggested that an in vitro-produced olfactory stem cell mass can be applied to a very small damaged region and could have a high potential for microenvironment formation.


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