Since then, research teams around the world have identified many more of the molecules and mechanisms of brain development.
However, the mechanisms of brain dysfunction that lead to these primary headache disorders, and more specifically to activation of the trigeminovascular pain pathway, remain largely unknown.
However, mechanisms of brain damage are different [17, 18], so that clinical prognostic tools used for decades in hypoxic encephalopathy have yet to be validated in hypoglycemic encephalopathy.
The normal physiological mechanisms of brain cooling are heat loss from the upper airways and through the skull, and these can produce selective brain cooling.
Because of complex non-linear mechanisms of brain integrative phenomena, a key tool for their understanding is represented by neurocomputational models.
Moreover, TMS represents a useful non-invasive approach for studying cortical physiology, and may be helpful in elucidating the pathophysiological mechanisms of brain reorganization after SCI.
Specifically, a major goal in the study of neuropsychiatric disorders has been to identify underlying mechanisms of brain dysfunction with the expectation that these insights may allow a better diagnosis, prevention and effective treatments for these disorders.
Here we address this question by drawing on recent advances in network control theory to model the underlying mechanisms of brain state transitions as elicited by the collective control of region sets.
These include: 1) diffusion tractography to study the anatomy of consciousness and the mechanisms of brain recovery following traumatic coma; 2) q-space measurements of axon diameter distributions in the in vivo human brain and 3) postmortem diffusion tractography as an adjunct to standard histopathological analysis.
In addition, changed neurotransmitter metabolism hints at specific mechanisms of brain dysfunction due to Mecp2 deletion.
We speculate below on mechanisms of brain network function, and TMS disruption thereof, on the basis of our combined studies.
