Considering the major mental disorders as clinical expressions of periodic pathological oscillations of the overall operating mode of brain function

Pediaditakis, Nicholas

doi:10.1016/j.mehy.2005.09.015

Cited by 4 publications

(3 citation statements)

References 25 publications

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“…In agreement with LFP studies (Cassim et al, 2002;Magill et al, 2004;Van der Stelt et al, 2004;Boraud et al, 2005;Lee et al, 2006;Pediaditakis, 2006;Light et al, 2006), the electrophysiological network exhibits an oscillatory dynamical behaviour. Oscillations in neurotransmitter concentrations are expected due to the feedback-loops in the network, the non-linearities of the equations as well as the time delays.…”

Section: Discussionsupporting

confidence: 86%

Neurochemical Oscillations in the Basal Ganglia

Noori

Jäger

2009

Bull. Math. Biol.

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This work represents an attempt to elucidate the neurochemical processes in the basal ganglia by mathematical modelling. The correlation between neurochemistry and electrophysiology has been used to construct a dynamical system based on the basal ganglia's network structure. Mathematical models were constructed for different physical scales to reformulate the neurochemical and electrophysiological behaviour from synapses up to multi-compartment systems. Transformation functions have been developed to transit between the different scales. We show through numerical simulations that this network produces oscillations in the electrical potentials as well as in neurotransmitter concentrations. In agreement with pharmacological experiments, a parameter sensitivity analysis reveals temporary changes in the neurochemical and electrophysiological systems after single exposure to antipsychotic drugs. This behaviour states the structural stability of the system. The correlation between the neurochemical dynamics and drug-induced behaviour provides the perspective for novel neurobiological hypotheses.

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Section: Discussionsupporting

confidence: 86%

Neurochemical Oscillations in the Basal Ganglia

Noori

Jäger

2009

Bull. Math. Biol.

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“…The answer may very well be hiding in plain sight, as we are forced to consider that there exists an evolutionary advantage associated with the events and prior developments - to be considered later - which may also end up leading to the unfortunate occurrence of the disorders as an unavoidable evolutionary, down, trade-off. Promising answers as to how this happens may be gleaned from recent findings from molecular genetics [ 3 - 9 ], evolutionary biology [ 9 - 12 ] and clinical observations [ 13 - 15 ]. Significantly, these findings when considered together, point to mechanisms for their development [ 16 ]:…”

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confidence: 99%

“…The particularly underlying, synaptic, layout expressing the mentioned temperament, may trigger a vigorous response of pruning by the regulatory c4 gene, by either of the two, possible mechanisms mentioned above. This event by creating a criticality, for some of these individuals, results in altering the overall, coordinating and synchronizing property of brain function [ 14 , 15 ]. This crucial property - while not being previously taken into account in the modeling of the disorders - normally insures synchrony and the smooth, subtle expression of all higher, mental faculties, such as orderly thinking, coordinating of thinking with feelings, and appropriateness of social responses, all characteristics of normally functioning humans.…”

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confidence: 99%

An Emerging Natural History in the Development, Mechanisms and Worldwide Prevalence of Major Mental Disorders

Pediaditakis

2016

TONEUJ

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Conciliating recent findings from molecular genetics, evolutionary biology, and clinical observations together point to new understandings regarding the mechanism, development and the persistent worldwide prevalence of major mental disorders (MMDs), which should be considered the result of an evolutionary downside trade off. Temperamental/trait variability, by facilitating choices for individual and group responses, confers robustness flexibility and resilience crucial to success of our species. Extreme temperamental variants, originating evolutionarily from the asocial aspect of human nature, also constitute the premorbid personality of the disorders. The latter create vulnerable individuals out of whom some will develop MMDs but at much higher rate to that of the general population. Significantly, similar temperamental “lopsidedness” enables many of these vulnerable individuals, if intelligent, tenacious, and curious, to be creative and contribute to our survival while some may also develop MMDs. All have a common neural-developmental origin and share characteristics in their clinical expression and pharmacological responses also expressed as mixed syndromes or alternating ones over time. Over-pruning of synaptic neurons may be considered the trigger of such occurrences or conversely, the failure to prevent them in spite of it. The symptoms of the major mental disorders are made up of antithetical substitutes as an expression of a disturbed over-all synchronizing property of brain function for all higher faculties previously unconsidered in their modeling. The concomitant presence of psychosis is a generic common occurrence.

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