[2] Patients with bradyphrenia may describe or may manifest slowed thought processes, evidenced by increased latency of response and also involve severe memory impairment and poor motor control.
'[4] In his research, Steck found that almost half the patients with Parkinson's disease in the psychiatric ward during the post-encephalitic period had Bradyphrenia.
The experimenters had asked the participants to complete the following tasks; counting to 20, repeat several simple sentences and read a series of words from a card.
[8] Researchers Rogers et al. found bradyphrenia in light of Parkinson's disease was considerably similar to what is referred to as 'Psychomotor retardation.
Rogers, Lees and Smith had then eventually concluded that bradyphrenia explored in the presence of Parkinson's disease was very similar to psychomotor retardation in a major depressive disorder with a few differences.
[15] From this study, researchers had concluded that in melancholic participants with major depression their slowing in reaction time was higher, in contrast to the control group, which indicated the presence of bradyphrenia.
[16] To examine the role of bradyphrenia within these conditions the researchers used the Tower of London Test which is a task that requires cognitive processing.
[17] Martin et al. found that stage three of symptoms of overdose entailed the high risk around 20% of those that reach what has been described as 'stage three' will die.
[21] In another more recent case, an 80-year-old woman had been diagnosed with Cerebral Amyloid Angiopathy (CAA) and was described to have symptoms of bradyphrenia after showing abnormalities within the pre-frontal cortex of the brain through a magnetic resonance imaging system (MRI) that had shown a significant increase in lesions.
[22] The patient had been put on steroid therapy which researchers McHugh et al. had found a significant improvement of cognitive abilities over time.
[24] Yet these researchers found that in the long-term this combination provided a reverse effect, accelerating the cognitive slowing of the brain (bradyphrenia) and motor movement (bradykinesia).
[25][26] Some studies have shown that through oral admission, the H-2 antagonist will target specific receptors in the brain by crossing the blood–brain barrier and will alter the rate of cognitive thought processing.
[25] The first sightings of bradyphrenia were documented by French neurologist Naville in the early 20th century, during the time of the epidemic of encephalitis lethargica, as it appears, he was investigating this disorder.
[2] This epidemic involved inflammation of the brain (encephalitis), and affected people tended to experience mental delays and remain motionless for extended periods of time due to an unknown cause.
'[28] Swiss neurologist Steck completed a study investigating the case of bradyphrenia post- an epidemic, in 27 mental institutions.
[2] Steck's work stimulated the interest of other neurologists including Aubrun, who investigated bradyphrenia creating a new direction by linking it to Parkinson's disease.