<unk>  is a condition that is symptomatic of many neurological disorders and psychiatric diseases. This suggests that the mechanisms that cause<unk>  and these neurological conditions are likely to be similar.<unk>  likely has pathophysiological mechanisms and neuronal mechanisms. This means that<unk>  is likely to have causes that stem from bodily changes or changes in neurons. These mechanism names can be combined to be called neurophysiological mechanisms. Currently, the exact neurophysiological mechanisms that cause<unk>  are unknown. However, there are some possible mechanisms that are plausible and would account for many of the effects of<unk> . A diagram of proper synaptic connectivity The working explanation of the neurophysiological mechanism behind<unk>  is that<unk>  is possibly caused by impaired synaptic connections, which results in diminished neurotransmission. This means that the connections between axons are functioning incorrectly, resulting in the spread of less efficient signals. This proposed explanation could arise from a variety of factors, but it would most likely occur as a result of problems during brain development or genetic factors. If<unk>  is, in fact, caused by these inefficient synaptic connections, then the associated irregular dopaminergic activity in certain parts of the brain (the limbic striatum and mediodorsal thalamus) can be, in part, explained. Dopaminergic activity is the release (or lack thereof) of the neurotransmitter dopamine and the resulting cellular responses. The limbic striatum and mediodorsal thalamus (parts of the brain) have connections with a part of the prefrontal cortex called the corticolimbothalamic circuit. The corticolimbothalamic circuit has a high concentration of GABAergic interneurons, which are neurons that predominantly work with the inhibitory neurotransmitter GABA. As a result of the impaired synaptic connections, the GABAergic interneurons of the corticolimbothalamic circuit would adapt to release increasingly high amounts of GABA to send a signal of the correct strength. This recurrent activation of the GABAergic cells produces a strong inhibitory signal back to the limbic striatum and mediodorsal thalamus, which inhibits the dopaminergic activity in those parts of the brain. This resulting inhibition of dopaminergic activity produces reduced activity at the mRNA and protein level in cells. These cellular changes could call for less blood flow and glucose use specifically, or the less blood flow and glucose metabolism could simply be a result of the lowered cellular activity.
Hypofrontality
Neurodiversity
Hysteresivity
Codependency
Asociality
Social degeneration
Genetic exceptionalism
Oncogene addiction