scholarly journals O. Maas. On the question of Recklingausen'a disease. Beitrag zur Kentniss der Recklinghausenschen Krankheit. Monatschr. für Psychiatrie u. Neurol., Bd. XXVIII (1910 г.)

2021 ◽  
Vol XVIII (2) ◽  
pp. 500-500
Author(s):  
V. N. Leshchinsky

The author gives a medical history and the results of a detailed microscopic examination of a case in which he was diagnosed with multiple tumors of the nervous system during his lifetime. Based on post mortem research, which revealed the existence of numerous tumors of the membranes of the spinal cord and brain, peripheral nerves and roots, the author views this case as a rare form of Recklingausens disease, in which there are no skin tumors that occur in almost all cases of this disease.

Author(s):  
Preston Robb

ABSTRACT:Little attention has been paid to an early Canadian experiment in neuronal regeneration and what may have been the world's first attempt to replace a damaged spinal cord with a transplant. In 1905, a paper entitled “Regeneration of the Axones of Spinal Neurones in Man” was published in the Montreal Medical Journal. It had been read at the Panamerican Congress in Panama. The author was David Alexander Shirres, a Scot who had trained in Aberdeen in neurology and neuropathology. He came to Canada in 1902 to assume the position of neurologist at the Montreal General Hospital, with the responsibility of establishing clinics and teaching undergraduates about the mysteries of the nervous system. To my knowledge, he was the first man in Canada to be appointed as a neurologist. (There were others, notably James Stewart, who devoted most of their time and writing to diseases of the nervous system but considered themselves to be internists. Stewart, for example, left the MGH to become the first chief of medicine at the Royal Victoria Hospital in Montreal.)


Author(s):  
M Dlamini

Neuromonitoring is used during surgery to assess the functional integrity of the brain, brain stem, spinal cord, or peripheral nerves. The aim of monitoring is to prevent permanent damage by early intervention when changes are detected in the monitor. Neuromonitoring is also used to map areas of the nervous system in order to guide management in some cases. The best neuromonitor remains the awake patient. In the conscious state, the function of individual parts of the nervous system and the complex interactions of its different parts can be assessed more accurately. However, most surgical procedures involving the nervous system require general anaesthesia. Procedures that require neuromonitoring can have changes in their monitored parameters corrected by modifying the surgical approach or by having the anaesthesiologist manipulate the parameters under their control. An ideal neuromonitor would be one that is specific for the parameter of interest, and gives reliable, reproducible, or continuous results.


Author(s):  
Giuseppe Scalabrino ◽  
Daniela Veber

Cobalamin (Cbl) deficiency causes an imbalance in some cytokines and growth factors in the central nervous system and peripheral nervous system of the rat, and in the serum and cerebrospinal fluid (CSF) of adult Cbl-deficient (Cbl-D) patients. We hypothesized that an imbalance in normal prion (PrPC) levels and/or synthesis might be involved in the pathogenesis of Cbl-D neuropathy. Using different appropriate enzyme-linked immunosorbent assays (ELISAs), we determined the levels of Cbl, tumour necrosis factor-a, epidermal growth factor, and PrPC in spinal cord (SC) and CSF of Cbl-D rats treated or not with different molecules; in serum, CSF from Cbl-D or multiple sclerosis (MS) patients; and in post-mortem SC samples taken from MS patients and control patients. We have demonstrated that: (i) Cbl deficiency induces excess PrPC regions (particularly octapeptide repeated (OR) region) in rat SC; (ii) the SC increase is mediated by a local Cbl deficiency-induced excess of tumour necrosis factor- a; and (iii) CSF and serum PrPC concentrations in Cbl-D patients are significantly higher than in controls. CSF PrPC concentrations are significantly lower in MS patients than neurological controls. The Cbl, EGF, and PrPC levels were significantly decreased in post-mortem MS SCs in comparison with controls


2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Zijian Zhou ◽  
Dake Qi ◽  
Quan Gan ◽  
Fang Wang ◽  
Bengang Qin ◽  
...  

Long noncoding RNAs (lncRNAs) have attracted extensive attention due to their regulatory role in various cellular processes. Emerging studies have indicated that lncRNAs are expressed to varying degrees after the growth and development of the nervous system as well as injury and degeneration, thus affecting various physiological processes of the nervous system. In this review, we have compiled various reported lncRNAs related to the growth and development of central and peripheral nerves and pathophysiology (including advanced nerve centers, spinal cord, and peripheral nervous system) and explained how these lncRNAs play regulatory roles through their interactions with target-coding genes. We believe that a full understanding of the regulatory function of lncRNAs in the nervous system will contribute to understand the molecular mechanism of changes after nerve injury and will contribute to discover new diagnostic markers and therapeutic targets for nerve injury diseases.


2003 ◽  
Vol 40 (1) ◽  
pp. 95-97 ◽  
Author(s):  
M. Sasaki ◽  
R. Pool ◽  
B. A. Summers

An 11-year-old dog succumbed to a seizure disorder of 18 days duration. At necropsy, an area of hemorrhage and discolored parenchyma was identified in the left pyriform lobe of the brain. Microscopic examination revealed a localized, necrotizing vasculitis with associated cerebral necrosis. Vasculitis was not present in other organs. This presentation is consistent with isolated central nervous system (CNS) angiitis, a rare form of vasculitis in humans.


2018 ◽  
Vol 30 (1) ◽  
pp. 185
Author(s):  
H. J. Oh ◽  
M. J. Kim ◽  
G. A. Kim ◽  
E. M. N. Setyawan ◽  
S. H. Lee ◽  
...  

Neurodegenerative disorders, such as Alzheimer’s disease, affect neurons in large areas within the central nervous system. The selective expression of disease-causing and therapeutic genes in susceptible regions and cell types is critical to the generation of animal models. In our previous studies, we reported production of a transgenic dog by nuclear transfer using donor cells that had been stably transfected by vector containing the red fluorescence protein (RFP) and human synapsin I (SynI) promoter, a neuron-specific promoter. Here, we evaluated whether RFP expression in transgenic dog with SynI (SynI dog) had high neuronal specificity and strong transcriptional activity. For confirmation of neuron-specific RFP expression, tissue samples were obtained from a killed 4-year-old SynI dog. Quantification of RFP in heart, kidney, liver, lung, spleen, cerebrum, cerebrum, cerebellum, midbrain, hippocampus, peripheral nerves, skin, and spinal cord of SynI dog was analysed using ELISA (Cell Biolabs, San Diego, CA, USA). Moreover, the distribution of RFP activity in neural system of the SynI dog was determined by immunohistochemistry. The first antibody, rabbit polyclonal RFP antibody (1:200, ab62341, Abcam, Cambridge, MA, USA) was applied, and antibody labelling was visualised by incubation with avidin-biotinylated horseradish peroxidase complex (1:1,000; ABC Elite, Vector Laboratories, Burlingame, CA, USA). In the 4-year-old SynI dog, RFP was observed only in neuronal tissues including brain, spinal cord, and peripheral nerves, but was not detected in non-neuronal tissue such as heart, kidney, and skin. In addition, robust RFP expression was observed in the neurons of the peripheral nerve, spinal cord, and prefrontal cortex. In the hippocampus and cerebellum, the RFP-expressing cells appeared heterogeneous in hippocampus neurons and purkinje cells. In conclusion, we report that human SynI promoter is functional in neural cells of dogs. A neural specific-transgene expressed dog could be applied as a research tool in the study of neurodegenerative disorders. This research was supported by RDA (#PJ010928032017), Korea IPET (#316002-05-2-SB010), NRF (#2016R1D1A1B03932198), and Research Institute for Veterinary Science, the BK21 plus program.


2020 ◽  
Vol 57 (5) ◽  
pp. 700-705 ◽  
Author(s):  
Ayumi Ono ◽  
Yumi Nakayama ◽  
Maki Inoue ◽  
Tokuma Yanai ◽  
Tomoaki Murakami

AA amyloidosis is characterized by amyloid deposition in systemic organs, but amyloid deposition in the central nervous system (CNS) or peripheral nervous system (PNS) is rare. In this study, AA amyloidosis was observed in 31 of 48 flamingos that died at a Japanese zoo. Almost all cases developed AA amyloidosis secondary to inflammatory diseases such as enteritis. Affected flamingos had AA amyloid deposition around blood vessels in periventricular white matter of the brain and in peripheral nerves. In addition, cerebral Aβ amyloidosis was observed in one of the 31 cases with AA amyloidosis. In conclusion, flamingos in the zoo commonly developed systemic amyloidosis with frequent amyloid deposition in the CNS and PNS, which seems to be a unique distribution in this avian species. Comparative pathological analyses in flamingos may help elucidate the pathogenesis of amyloid neuropathy.


2015 ◽  
Vol 4 (1) ◽  
pp. 25-27 ◽  
Author(s):  
Vikram Singh Tanwar ◽  
Harpreet Singh ◽  
Nikhil Govil ◽  
Sameer Arora ◽  
Ruchi Jagota

Central nervous system tuberculosis is a serious form of tuberculosis. Tuberculous CNS involvement can occur in the form of TB meningitis, tuberculous Vasculitis, tuberculoma and rarely brain abscess. Tubercular granulomas generally solitary and occurs in the brain but it may be multiple and involve other areas such as spinal cord, epidural space and subdural space also. Tuberculoma in the spinal cord is rare. Concurrent occurrence of brain tuberculomas along with intramedullary spinal tuberculoma is even rarer. Only few cases have been reported in world literature. We are reporting a 28 years old female who presented with headache and progressive paraparesis in which imaging revealed intracranial and intramedullary tuberculoma and recovered completely with antitubercular therapy without any surgical intervention.Journal of Advances in Internal Medicine 2015;04(01):25-27


1987 ◽  
Vol 35 (8) ◽  
pp. 865-870 ◽  
Author(s):  
W Cammer ◽  
F A Tansey

Rat sciatic nerve, spinal root, and cranial nerve were immunostained with an antibody against rat brain carbonic anhydrase II (ca), to determine the localization of ca in the rat peripheral nervous system (PNS). Similar methods were applied to mouse nerves to see if that antigen could be detected in the PNS of this species. In rat nerves, intense immunostaining was observed in the axoplasm of many of the myelinated fibers, whereas others were stained less intensely or were negative. A heterogeneous pattern of immunostaining was also found in neuronal perikarya within the ganglia, and in some regions of the ganglia ca immunostaining was found in putative satellite cells and their processes. Ca in rat PNS therefore appears to occur at both neuronal and glial sites, whereas it is exclusively glial in the CNS. In longitudinal sections of some fibers within rat nerves, ca immunostaining could be detected at the inner boundaries of the myelin sheaths. In mouse nerves, axoplasmic staining was observed but it was fainter than in rat nerves. Interspecies differences were most obvious in the dorsal columns of the spinal cord. In rat, intensely stained axons proceeded through the roots into the gracilis or cuneate and often into the gray matter. In mouse, there was much less immunostaining of axons but more intense ca immunostaining in CNS myelin than in the CNS myelin in the rat cord. The implications concerning putative functions of ca in the rodent nervous system are discussed.


1914 ◽  
Vol 60 (249) ◽  
pp. 184-191
Author(s):  
D. Orr ◽  
R. G. Rows

For some years, we have been engaged in an investigation into the mode of action of toxins upon the central nervous system, and up to the present time have devoted our attention exclusively to the question of the upward passage of bacterial poisons along the sheaths of peripheral nerves to the spinal cord and brain. Experiment has shown us that toxins readily travel upwards in the perineural lymphatics, in which they induce an inflammation whose phenomena vary with the intensity of the irritant; and that this is continued without interruption to the central nervous system, granted that the toxins gain that level. Continuity of extension is, therefore, an important feature of lymphogenous inflammation, and is as constant in the central as in the peripheral nervous system.


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