scholarly journals A Contribution to the Morbid Anatomy and the Pathology of General Paralysis of the Insane

1900 ◽  
Vol 46 (195) ◽  
pp. 688-711
Author(s):  
David Orr ◽  
Thomas Philip Cowen

At the last February meeting of the Manchester Pathological Society we made a preliminary communication upon this subject, limited to a description of the changes found in the cortical nerve-cells and the descending degenerations in the spinal cord. Since then we have examined a much larger number of cases, and can therefore give a fuller description, with observations upon other points in the morbid anatomy of general paralysis of the insane.

2021 ◽  
Vol 11 ◽  
Author(s):  
Sipin Zhu ◽  
Yibo Ying ◽  
Lin Ye ◽  
Weiyang Ying ◽  
Jiahui Ye ◽  
...  

Protecting the death of nerve cells is an essential tactic for spinal cord injury (SCI) repair. Recent studies show that nerve growth factors can reduce the death of nerve cells and promote the healing of nerve injury. To investigate the conducive effect of fibroblast growth factor 21 (FGF21) on SCI repair. FGF21 proteins were systemically delivered into rat model of SCI via tail vein injection. We found that administration of FGF21 significantly promoted the functional recovery of SCI as assessed by BBB scale and inclined plane test, and attenuated cell death in the injured area by histopathological examination with Nissl staining. This was accompanied with increased expression of NeuN, GAP43 and NF200, and deceased expression of GFAP. Interestingly, FGF21 was found to attenuate the elevated expression level of the autophagy marker LC3-II (microtubules associated protein 1 light chain 3-II) induced by SCI in a dose-dependent manner. These data show that FGF21 promotes the functional recovery of SCI via restraining injury-induced cell autophagy, suggesting that systemic administration of FGF21 could have a therapeutic potential for SCI repair.


1976 ◽  
Vol 13 (6) ◽  
pp. 428-435 ◽  
Author(s):  
M. Vandevelde ◽  
C. E. Greene ◽  
E. J. Hoff

A young cat had signs of tetraparesis that progressed to tetraplegia within a few weeks. Clinically, there was lower motor neuron disease with areflexia and muscle atrophy in all limbs. Degeneration of the motor neurons in the spinal cord was seen on histological examination. Ultrastructurally, the degeneration of nerve cells was characterized by abnormal proliferation of neurofilaments. These findings were compared to other motor neuron diseases and neurofibrillary accumulations in man and animals.


1875 ◽  
Vol 21 (93) ◽  
pp. 67-74
Author(s):  
George Thompson

In the introductory remarks contained in the previous portion of this essay, I said that, as far as possible, I would refrain from referring to the condition of the nervous centres as seen after death, except to explain the nature of certain phenomena seen in these diseases during life. Having arrived at the second portion of my subject, I shall draw attention to the condition of the brain and spinal cord where death has been the result of an epileptic fit, or while the patient has been in what is now so well understood as the Status Epilepticus.


Author(s):  
Katharine E Lewis

Understanding how the vertebrate central nervous system develops and functions is a major goal of a large body of biological research. This research is driven both by intellectual curiosity about this amazing organ that coordinates our conscious and unconscious bodily processes, perceptions and actions and by the practical desire to develop effective treatments for people with spinal cord injuries or neurological diseases. In recent years, we have learnt an impressive amount about how the nerve cells that communicate with muscles, motoneurons, are made in a developing embryo and this knowledge has enabled researchers to grow motoneurons from stem cells. Building on the success of these studies, researchers have now started to unravel how most of the other nerve cells in the spinal cord are made and function. This review will describe what we currently know about spinal cord nerve cell development, concentrating on the largest category of nerve cells, which are called interneurons. I will then discuss how we can build and expand upon this knowledge base to elucidate the complete genetic programme that determines how different spinal cord nerve cells are made and connected up into neural circuits with particular functions.


1866 ◽  
Vol 12 (59) ◽  
pp. 348-367
Author(s):  
Franz Meschede ◽  
G. F. Blandford

The disorder commonly called “general paralysis of the insane” presents so many points of interest to the pathologist and the physician, that as a necessary consequence it forms the commonest topic among the writings of those who specially study insanity. But after so much observation and so many treatises, it is disheartening to find that even now scarcely more than one fact with regard to it is laid down as settled and established beyond the possibility of doubt. One there is, the saddest that can be. It is, that for this malady we hitherto have found no cure; that to diagnose it is to pronounce the sentence, not only of incurable insanity, but also of speedy death. The marvel of the whole is, that although death occurs in every case at no very distant period, though postmortem examinations of general paralytics are made by hundreds every year in this and other countries, yet even at this day no two observers are agreed as to the pathology and morbid anatomy, as to the part in which it has its origin, or which constitutes its peculiar and proper seat. No wonder that the whole of the morbid anatomy of insane brain is vague and ill-defined, when this, the specially fatal form of mental disease, still hides itself from usâ still wraps itself in the mystery which envelopes all that relates to mind. I make no apology for drawing the attention of the readers of this Journal to a paper on the subject, published in the October and November numbers of ‘ Virchow's Archives/ 1865, and for giving a short and necessarily imperfect summary of its contents, it being too long for reproduction. But as every outline must needs be unsatisfactory, I trust my readers will go themselves to the original. In default of opportunity of examining many brains of paralytic patients, I present as a contribution to the English treatises on the subject these observations of another.


Sign in / Sign up

Export Citation Format

Share Document