Hypofrontality
[1][2][3] This condition was initially described by Ingvar and Franzén in 1974, through the use of xenon blood flow technique with 32 detectors to image the brains of patients with schizophrenia.
[4][7][8][9] Hypofrontality is a symptom of numerous neurological diseases defined as reduced utilization of glucose and blood flow in the prefrontal cortex.
[11] The transient hypofrontality hypothesis proposes that there is a temporary decrease in the functioning of the prefrontal cortex during high-intensity exercise, specifically affecting tasks such as working memory.
The complex mechanisms involved include diverting resources away from cognitive tasks and resulting in a noticeable decrease in prefrontal cortex activity.
Mostly in the frontal cortex, these differences often stem from a smaller brain volume, and the decreased blood flow that results influences the hypofrontality.
Negative symptoms, referred to as "psychomotor poverty," are linked to decreased frontal activation during tasks, resulting in slowed mental processing and planning deficits.
The underlying cause of Bipolar Disorder is not fully understood, but it is believed that abnormalities in the prefrontal cortex may contribute to the lack of emotional control and regulation.
[10] Major depressive disorder, or MDD, is diagnosed by a persistent low mood that affects the way a person sees themselves and how they live their life.
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.
[15] Moreover, recent studies have shown that the alpha 2 receptor agonists such as clonidine and guanfacine can treat hypofrontality associated with ADHD, PTSD and depression.
[16][17][18] Hypofrontality is still not fully understood in its entirety, but there are a number of research projects that have been conducted, leading to progress in recognizing the signs of the symptom.
Sagvolden and company conducted a loss-of function mutation where mutant mice lacked the NK1R protein resulting in a low dopaminergic transmission supporting the hypothesis of hypofrontality in ADHD.
Possible causes are hypothesized to be impaired synaptic connectivity and neurotransmission resulting from neurodevelopmental and/or genetic factors but there is not a complete understanding hypofrontality as a whole.
