Kinurenines in Central Nervous System under neuropathic pain – clinical implications from basic research

Ból ◽  
2020 ◽  
Vol 20 (3) ◽  
pp. 32-39
Author(s):  
Katarzyna Ciapała ◽  
Ewelina Rojewska

Central nervous system disorders are often accompanied by changes in tryptophan metabolism. Kynurenine pathway is known to be the main route by which this essential amino acid is catabolized to a plenty of metabolites. Intermediates of this cascade are responsible for a wide spectrum of effects, including endogenous regulation of neuronal excitability and immune cells response. Excessive or disrupted activation of the pathway can lead to the accumulation of neurotoxic compounds, and in consequence, contributes to the development of various type of pathologies. These aspects shed new light on the kynurenine pathway as a promising target for development of new therapeutic strategies. Following work briefly characterizes the kynurenine pathway and discusses the neurobiological functions of kynurenines, with particular focus on their role in the development and persistence of neuropathic pain. It is also presenting the potential clinical implications of modulation of the kynurenine pathway in pharmacological therapy of chronic pain.

CNS Spectrums ◽  
2005 ◽  
Vol 10 (4) ◽  
pp. 298-308 ◽  
Author(s):  
Walter Zieglgänsberger ◽  
Achim Berthele ◽  
Thomas R. Tölle

AbstractNeuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.


2012 ◽  
Vol 13 (2) ◽  
pp. 32-42 ◽  
Author(s):  
Yvette D. Hyter

Abstract Complex trauma resulting from chronic maltreatment and prenatal alcohol exposure can significantly affect child development and academic outcomes. Children with histories of maltreatment and those with prenatal alcohol exposure exhibit remarkably similar central nervous system impairments. In this article, I will review the effects of each on the brain and discuss clinical implications for these populations of children.


Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1831
Author(s):  
Camilla Russo ◽  
Carmela Russo ◽  
Daniele Cascone ◽  
Federica Mazio ◽  
Claudia Santoro ◽  
...  

Neurofibromatosis type 1 (NF1), the most frequent phakomatosis and one of the most common inherited tumor predisposition syndromes, is characterized by several manifestations that pervasively involve central and peripheral nervous system structures. The disorder is due to mutations in the NF1 gene, which encodes for the ubiquitous tumor suppressor protein neurofibromin; neurofibromin is highly expressed in neural crest derived tissues, where it plays a crucial role in regulating cell proliferation, differentiation, and structural organization. This review article aims to provide an overview on NF1 non-neoplastic manifestations of neuroradiological interest, involving both the central nervous system and spine. We also briefly review the most recent MRI functional findings in NF1.


2019 ◽  
Vol 21 (11) ◽  
pp. 1450-1463 ◽  
Author(s):  
P. D. Delgado-López ◽  
E. M. Corrales-García ◽  
E. Alonso-García ◽  
R. García-Leal ◽  
R. González-Rodrigálvarez ◽  
...  

2011 ◽  
Vol 64 (9-10) ◽  
pp. 443-447
Author(s):  
Milan Cvijanovic ◽  
Svetlana Simic ◽  
Sofija Banic-Horvat ◽  
Zita Jovin ◽  
Petar Slankamenac ◽  
...  

Introduction. Neuropathic pain, or pain associated with disease or injury to the peripheral or central nervous system, is a common symptom of a heterogeneous group of conditions, including diabetic neuropathy, trigeminal neuralgia, postherpetic neuralgia and spinal cord injury. Chronic neuropathic pain should not be thought of as a symptom. It should truly be thought of as a disease with a very complicated pathophysiology. Pathophysiology. The mechanisms involved in neuropathic pain are complex and involve both peripheral and central pathophysiologic phenomenon. The underlying dysfunction may involve deafferentation within the peripheral nervous system (e.g. neuropathy), deafferentation within the central nervous system (e.g. post-thalamic stroke) or an imbalance between the two (e.g. phantom limb pain). Clinical characteristics. Neuropathic pain is non-nociceptive, in contrast to acute nociceptive pain, and it can be described as ?burning?, ?electric?, ?tingling?, and ?shooting? in nature. Treatment. Rational polypharmacy is often necessary and actually it is almost always the rule. It would be an exception if a patient was completely satisfied with his treatment. Treatment goals should include understanding that our patients may need to be titrated and managed with more than one agent and one type of treatment. There should be the balance of safety, efficacy, and tolerability. Conclusion. There are many new agents and new applications of the existing agents being currently studied which will most certainly lead to even more improved ways of managing this very complicated set of disorders.


Cornea ◽  
2017 ◽  
Vol 36 (11) ◽  
pp. 1408-1414 ◽  
Author(s):  
Yan Xiang ◽  
Wenchang Zhou ◽  
Ping Wang ◽  
Hui Yang ◽  
Feng Gao ◽  
...  

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