The Normal Histology and Pathology of the Neuroglia (in relation specially to Mental Diseases)

1897 ◽  
Vol 43 (183) ◽  
pp. 733-752 ◽  
Author(s):  
W. F. Robertson

It has long been recognised that the neuroglia presents difficulties of a very special kind in the way of its histological study. These difficulties are due mainly to the remarkable lack of affinity shown by its extra-nuclear part for the usual staining reagents. No histological method that has yet been described serves in a satisfactory manner for the complete investigation of this tissue in its normal and pathological states. The most generally serviceable at present in use is, I think, beyond all question the fresh method of Bevan Lewis. It at least furnishes us with a reliable test for the presence or absence of hypertrophy and sclerosis; but it does not give a complete or clear view of the normal tissue, the fibres remaining for the most part invisible (except in tissues from some of the lower animals), and the nuclear structure being quite obscured. Golgi's method gives us only a silhouette of a small proportion of the neuroglia-cells and fibres. It does not aid us in the solution of questions regarding nuclear and protoplasmic structure. Weigert's new method gives us a very clear view of the fibres and nuclei, but it leaves the protoplasm invisible in the normal state. Its chief deficiency, however, consists in the fact that its use is restricted to the fresh human brain. It is of little value for ordinary postmortem-room tissues, or for those of the lower animals. Other methods that might be mentioned are likewise imperfect in their results, or extremely limited in their utility. In these circumstances it is scarcely surprising that there is still the widest difference of opinion among the recognised authorities regarding the normal structure of the neuroglia. Yet until this question is carried beyond the stage of controversy it is obvious that all our views of the pathological changes occurring in the supporting tissue of the central nervous system must remain vague and unscientific.

Psychiatry ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 125-134
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.


1925 ◽  
Vol 71 (293) ◽  
pp. 192-218
Author(s):  
P. K. McCowan

For some time past there has been an increasing use of laboratory methods in the diagnosis of mental disorders. The following aims at offering further proof of the undoubted value of this method of approach in such cases. There seems, however, to be a growing tendency, not devoid of danger, to ascribe diagnostic specificity to one or other of the many tests in use for such examinations. Although it is undoubtedly true that an exhaustive analysis of a spinal fluid may in many cases lead to a correct diagnosis of the clinical condition of the patient from whom the specimen has been taken, it only requires a study of the literature to show that none of the reactions or group of reactions obtained from the spinal fluid can be regarded as pathognomonic of any disease of the central nervous system.


2019 ◽  
Vol 4 (4) ◽  
pp. 30-35
Author(s):  
A. V. Tereshchenko ◽  
I. G. Trifanenkova ◽  
A. M. Kodunov ◽  
A. A. Temnov ◽  
A. N. Sklifas

Background. In case of a corneal burn injury, cell transplantation into the damaged area must be performed within the first 12 hours, which makes it impossible to use autologous stem cells. One solution to this problem may be the use of peptides, derived from cultured stem cells in the treatment and prevention of complications in a burn eye disease. Aims: To study the dynamics of corneal tissue repair under the influence of a peptide solution on a corneal thermal burn model.Materials and methods. The study included 20 rabbits (20 eyes) of the gray Chinchilla breed weighing from 2.5 to 3.2 kg with a corneal thermal burn model. Depending on the method of treatment used, the animals were divided in two groups of 10 rabbits (10 eyes). In the experimental group, instillations of a peptide solution were used to treat corneal thermal burns; in the control treatment was carried out with a solution of moxifloxacin and gel “Solcoseryl”. On the 1st, 3rd, 7th, 14th, 30th days in each group, two animals were sacrificed to conduct a morphological study of the cornea. Results. In the experimental group, by the 30th day, according to a histological study, the inflammatory process was completed both on the surface and inside the cornea, with a tendency to restore its normal structure. In the control group of animals, significantly longer periods of corneal recovery and preservation of inflammation, despite the received therapy, were observed.Conclusions. The use of the peptide preparation is promising in the treatment of corneal thermal burn. Further research is needed in this area.


1991 ◽  
Vol 12 (Supplement) ◽  
pp. 211-214
Author(s):  
Rentaro Abumi ◽  
Takahiro Kuwasako ◽  
Tomomi Tamura ◽  
Minoru Inouye ◽  
Katsuya Nagai ◽  
...  

Neurosurgery ◽  
2018 ◽  
Vol 84 (5) ◽  
pp. 1000-1010 ◽  
Author(s):  
Jennifer Vogel ◽  
Ruben Carmona ◽  
Christopher G Ainsley ◽  
Robert A Lustig

Abstract Radiation therapy plays a significant role in management of benign and malignant diseases of the central nervous system. Patients may be at risk of acute and late toxicity from radiation therapy due to dose deposition in critical normal structures. In contrast to conventional photon delivery techniques, proton therapy is characterized by Bragg peak dose deposition which results in decreased exit dose beyond the target and greater sparing of normal structure which may reduce the rate of late toxicities from treatment. Dosimetric studies have demonstrated reduced dose to normal structures using proton therapy as compared to photon therapy. In addition, clinical studies are being reported demonstrating safety, feasibility, and low rates of acute toxicity. Technical challenges in proton therapy remain, including full understanding of depth of proton penetration and the biological activity in the distal Bragg peak. In addition, longer clinical follow-up is required to demonstrate reduction in late toxicities as compared to conventional photon-based radiation techniques. In this review, we summarize the current clinical literature and areas of active investigation in proton therapy for adult central nervous system malignancies.


1936 ◽  
Vol 63 (2) ◽  
pp. 227-240 ◽  
Author(s):  
G. J. Buddingh

1. Chick embryos infected by the chorio-allantoic route with a bacteria-free strain of vaccinia virus develop a general dissemination of the virus throughout the entire organism with the exception of the central nervous system. 2. Quantitative estimation of the distribution of the virus in the various organs of the infected chick by cutaneous inoculation on the rabbit skin offers no evidence for a heightened affinity of the virus for special tissues. 3. Histological study of the lesions in the various organs demonstrates the focal character of the lesions which apparently originate as perivascular infiltrations around the smaller blood vessels. No lesions could be demonstrated in the central nervous system proper. 4. In the earlier stages of the disease Guarnieri bodies are clearly demonstrable in the cells of the epidermis and the squamous epithelium of the buccal mucosa. Inclusion bodies closely resembling Guarnieri bodies are demonstrated in all the lesions occurring in the various other organs. 5. It was not possible to demonstrate conclusively the presence of Paschen bodies in the lesions of the internal organs by the Morosow method usually used for the demonstration of these bodies in the membranal lesion.


1964 ◽  
Vol 1 (4) ◽  
pp. 289-322 ◽  
Author(s):  
Roy C. Anderson

An experiment was undertaken to test the hypothesis that moose neurologic disease is cerebrospinal nematodiasis. Two moose calves ( Alces a. americana) were infected with Pneumostrongylus tenuis derived from white-tailed deer ( Odocoileus virginianus borealis). Two to three weeks later both calves became lethargic and seemed unwilling to rise. This weakness and ataxia became progressively more pronounced and terminated in paraplegia. One calf was autopsied on the 40th day, the other on the 60th day. Fifth-stage P. tenuis were found in saline in which the central nervous system of the first calf had been placed. Numerous subadult worms were found in subdural spaces of the cranium and vertebral column of the second moose. Histological study revealed additional worms and traumatic damage in the central canal and dorsal horns of the cord of both calves. Focal malacia with micro-cavitation was found in all regions of the cord. Infiltrations of round cells and eosinophils in the leptomeninges, the ventral fissure and the dorsal sulcus, perivascular cuffing with round cells, petechial haemorrhages, neuron degeneration and loss, as well as swelling and disappearance of axis cylinders and myelin sheaths were observed. The known distribution and characteristics of neurologic disease in wild moose supports the hypothesis that P. tenuis is the ætiological agent.


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