Diagnosis of Infectious or Inflammatory Psychosyndromes

Bechter, Karl

doi:10.2174/1874205x01206010113

Cited by 10 publications

(3 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our previous research investigated low level neuroinflammation (LLNI) subgroups in severe psychiatric disorders ( 4 ). Affective and schizophrenia spectrum disorders may be accompanied by pain and other sensory symptoms ( 5 ), which could be explained at least in part by LLNI pathomechanisms that arise from an interaction between CSF and peripheral nerves along the PCOP. It is also suggested that PCOP-associated symptoms prevail in classic neuroinflammation and possibly even in systemic inflammation ( 6 ).…”

Section: Introduction: the Peripheral Csf Outflow Pathways (Pcop)mentioning

confidence: 99%

Cerebrospinal fluid outflow along lumbar nerves and possible relevance for pain research: case report and review

Bechter¹,

Schmitz²

2014

Croat Med J

Self Cite

View full text Add to dashboard Cite

CSF outflow through the cribriform plate near the olfactory nerves and the outflow along brain and spinal nerves are together known as peripheral CSF outflow pathway (PCOP). It is still not clear whether the PCOP has pathogenetic relevance. Our previous clinical observations have indicated that CSF may interact with nerves along the PCOP and in this article we present our finding of CSF outflow demonstrated by myelography in a single patient. We also discuss unexplained experimental pain pathomechanisms against the background of the PCOP hypothesis. We observed that CSF flowed along lumbar nerves in distal direction at a speed of about 10 cm per hour on its way through the tissues, mainly muscles. Total CSF outflow volume at the lumbar site was remarkable. CSF outflow at lumbar nerves was also documented by neuroradiology. It is plausible that CSF signaling serves for interaction with nerves along the PCOP, which could explain previously unknown pathomechanisms in pain generation. Experimental findings of tactile pain hypersensitivity within lumbosacral pain pathways could be explained by releasing of molecules, microparticles, or exosomes into the CSF by mast cells, which then move with CSF outflow along the PCOP and interact with nerves, initiating even retrograde synaptic stripping.

show abstract

Section: Introduction: the Peripheral Csf Outflow Pathways (Pcop)mentioning

confidence: 99%

Cerebrospinal fluid outflow along lumbar nerves and possible relevance for pain research: case report and review

Bechter¹,

Schmitz²

2014

Croat Med J

Self Cite

View full text Add to dashboard Cite

show abstract

“…40,41 The relative success of using CSF filtration in treatment of psychiatric disease, neuroinflammatory disorders and chronic pain syndromes is based on the concept that CSF carries and transport antigens, not only centrally, but also along cranial and peripheral nerves; and the antigens triggers an immune response clinically expressed as mild `encephalitis' or pain and/or may be involved in pathophysiology by peripheral nerve-CSF signaling interactions. 42,43 The outflow pathways of CSF that are implicated in mediating the immunological CSN disease process are perfectly described in Quincke's study. 1 Quinke characterizes in detail the CSF outflow (via cinnabar deposits) along cranial nerves, intercostal nerves, lumbar and sacral nerves.…”

mentioning

confidence: 87%

Quinckes’ pioneering 19th centuries CSF studies may inform 21th centuries research

Bechter¹,

Benveniste

2015

Neurology, Psychiatry and Brain Research

Self Cite

View full text Add to dashboard Cite

“…Chronic encephalitis presents—with regard to the clinical picture—similarly to acute encephalitis, with the course just being protracted a priori , possibly with dominating or exclusive psychiatric symptoms in extended early stages of the disease. Respective psychiatric syndromes are typically unspecific, i.e., various and variant, though some symptom characteristics may be found, especially when including systemic signs and findings (14, 15).…”

Section: Critical Outline Of Terms In Clinical Use Around Neuroinflammentioning

confidence: 99%

Encephalitis, Mild Encephalitis, Neuroprogression, or Encephalopathy—Not Merely a Question of Terminology

Bechter

2019

Front. Psychiatry

Self Cite

View full text Add to dashboard Cite

Background: Psychoneuroimmunology research has presented emerging evidence of the involvement of inflammatory and immune mechanisms in the pathogenesis of severe mental disorders. In this context, new terms with increasing clinical relevance have been proposed, challenging the existing terms, and requiring consensus definitions of the new ones.Method: From a perspective of longstanding personal involvement in clinical settings and research in psychoneuroimmunology, the new and the existing terms are critically reconsidered.Results: Meningoencephalitis and encephalitis are comparably well defined clinical terms in neuropsychiatry, although in the individual case approach diagnosis can be difficult, for example in some cases of encephalitis that are described with normal cerebrospinal fluid findings, or often in chronic encephalitis. Encephalopathy is also a widely accepted term, however, with a surprisingly broad meaning with regard to the assigned underlying pathophysiology, ranging from one-hit traumatic encephalopathy to inflammatory encephalopathy, the latter term addressing a type of brain dysfunction secondary to acute systemic inflammation without proven brain autochthonus inflammation (neuroinflammation). However, this latter assumption and term may be wrong as neuroinflammation is difficult to prove in vivo. With emerging insights into prevailing inflammatory and neuroinflammatory mechanisms that are involved in the pathogenesis of severe mental disorders, the interdependent aspects of sensitive assessment and potential clinical relevance of mild neuroinflammation are becoming more apparent and of increasing clinical interest. The new terms “mild encephalitis,” “parainflammation,” and “neuroprogression” show considerable overlap in addition to gaps and hardly defined borders. However, details are hard to discuss as available studies use many biomarkers, but most of these are done without an established categorical attribution to exclusive terms. Most important, the three new concepts (neruoprogression, parainflammation, and mild encephalitis) are not mutually exclusive, even at the individual case level, and therefore will require state-related individual assessment approaches beyond large confirmatory studies.Conclusion: The newly proposed terms of mild encephalitis, parainflammation, and neuroprogression have an emerging clinical relevance, but respective borders, gaps and overlap in between them remain unclear, and these concepts may even be seen as complementary. Categorical delineation of the new and reconsideration of the existing terms with respect to individualized psychiatric treatment is required for better clinical use, eventually requiring a consensus approach. Here, a critique based on available data and a focus on clinical perspective was outlined, which may help to enhance fruitful discussion. The idea followed here is in line with pillar number six as proposed for the Research Diagnostic Domains, i.e., to provide and follow new concepts in psychiatric research.

show abstract

Diagnosis of Infectious or Inflammatory Psychosyndromes

Cited by 10 publications

References 52 publications

Cerebrospinal fluid outflow along lumbar nerves and possible relevance for pain research: case report and review

Cerebrospinal fluid outflow along lumbar nerves and possible relevance for pain research: case report and review

Quinckes’ pioneering 19th centuries CSF studies may inform 21th centuries research

Encephalitis, Mild Encephalitis, Neuroprogression, or Encephalopathy—Not Merely a Question of Terminology

Contact Info

Product

Resources

About