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Hypofrontality is a symptom of numerous neurological diseases defined as reduced utilization of glucose and blood flow in the prefrontal cortex. Hypofrontality can be difficult to detect under resting conditions, but under cognitive challenges, it has been seen to correlate with memory deficits along with executive function deficits.
Dysexecutive syndrome (DES) consists of a group of symptoms, [1] usually resulting from brain damage, that fall into cognitive, behavioural and emotional categories and tend to occur together.
Frontal lobe disorder, also frontal lobe syndrome, is an impairment of the frontal lobe of the brain due to disease or frontal lobe injury. [5] The frontal lobe plays a key role in executive functions such as motivation, planning, social behaviour, and speech production.
The orbitofrontal cortex (OFC) is a prefrontal cortex region in the frontal lobes of the brain which is involved in the cognitive process of decision-making.In non-human primates it consists of the association cortex areas Brodmann area 11, 12 and 13; in humans it consists of Brodmann area 10, 11 and 47.
Buchsbaum is a pioneer in the use of neuroimaging technology to study psychiatric disorders. In the early 1980s he, along with David Ingvar, performed the first positron emission tomography (PET) studies of patients with schizophrenia at the National Institutes of Health (NIH) and the patients had reduced glucose metabolism in the frontal lobe, a pattern known as hypofrontality. [3]
It is indicated that the common hypofrontality (underactivation of frontal brain regions) and cortical activation pattern induced by serotonergic and glutamatergic hallucinogens is due to a common disruption of thalamic gating of sensory and cognitive information. The CSTC feedback loop plays a major role in gating or filtering out external and ...
The Wisconsin Card Sorting Test (WCST) is a neuropsychological test of set-shifting, which is the capability to show flexibility when exposed to changes in reinforcement. [1] [2] The WCST was written by David A. Grant and Esta A. Berg.
The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms of schizophrenia linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors.