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Bradyphrenia

Summary

Bradyphrenia is the slowness of thought common to many disorders of the brain.[1] Disorders characterized by bradyphrenia include Parkinson's disease and forms of schizophrenia consequently causing a delayed response and fatigue.[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.[3] The word 'bradyphrenia' originates from the ancient Greek meaning 'slow mind.'[4]

Bradyphrenia
Image depicting how an individual with bradyphrenia experiences fatigue and stress as they struggle with slow thinking.
SpecialtyNeurology, psychiatry
SymptomsSlowing of thoughts, delayed responses and lack of motivation

Evaluation edit

Parkinsonism edit

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.[2] Neurologists often saw the condition as an additional trait of Parkinson's disease as they found that patients with Parkinson's disease had often impaired traits that would be defined by bradyphrenia.[2] In the study conducted in 1966, Wilson et al. had found that bradyphrenia found in the patients with Parkinson's disease had increased their reaction time of retaining information.[5][6][7] Other studies exploring this theory confirmed that bradyphrenia was commonly seen in their studies of patients with Parkinson's disease[8] In addition, some researchers found that the condition does not impact all patients with Parkinson's disease.

Some neurologists had also suggested that bradyphrenia could exist without the presence of parkinsonism.[8] In some cases, it has been found that bradyphrenia has been mistaken for an inability to strategically complete tasks and therefore may often be categorised as the condition incorrectly.[6] Collectively, it was concluded that bradyphrenia does not commonly appear in parkinsonism but rather as a single entity that occurs in other conditions and not only in the single presence of Parkinson's disease.[6]

Despite the collective agreement of bradyphrenia being classified as a nosological entity. The neurological condition is still more often described in case studies where the subjects are analysed for having Parkinson's disease.[citation needed]

Effects in Parkinson's edit

There are several symptoms in Parkinson's disease which are influenced by the presence of bradyphrenia. Researcher Norberg discovered that a gradual cognitive slowing impacted the eating behaviour of these patients.[9] It was found that patients with Parkinson's disease would often experience extended periods of time attempting to process the food that they are eating, causing an increase in the time it took for them to consume their food.[9]

In another study examining the presence of bradyphrenia in Parkinson's disease, researchers had discovered that bradyphrenia was one of the reasons for slow auditory feedback as measured by the DAF (Delayed Auditory Feedback).[8] Dobbs et al., completed an experiment whereby the experimenter would communicate to the patient via a microphone and would ask the participant to complete a series of tasks. The participant, with or without Parkinson's disease, would receive this information through their headphones and respond via a microphone. 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] The researchers concluded that bradyphrenia was present in Parkinson's disease however also in older patients as they also had delayed feedback when completing the task.[8]

Depression and Parkinson's disease edit

Researchers Rogers et al. found bradyphrenia in light of Parkinson's disease was considerably similar to what is referred to as 'Psychomotor retardation.[10] Psychomotor retardation was proposed by the researchers as a condition particularly seen in major depressive disorders. Researchers had conducted a study to examine in ways in which the two conditions share similarities in analysing diagnosed Parkinson Disease patients and patients who had been diagnosed with depression. The participants were given two tasks to complete, one of the tasks is known as the digit symbol substitution test which consisted of the participants filling in a row of numbers which had a specific connection to a symbol. Another task which been referred to as the 'simpler task' which was to match the number on the screen that they had seen by pressing the same number on the keyboard.[10] Both of these measurements required a fast reaction time as their response was based on how quickly (in seconds) they would respond to each of the tasks. Researchers found that there had been no significant decrease in the response time for this test in participants with Parkinson's disease as their reaction time had been longer.[10] However, for participants having major depressive disorder, there had been an overall improvement in reaction time. 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. They had found that there had been notable impairments in their dopaminergic areas seen in both groups of disorders that could call for some similarities between the two conditions.[10]

Alzheimer's disease edit

Alzheimer's disease, another neurological condition involving cognition impairment.[11] Researchers found that there was a presence of cognitive slowing in patients with Alzheimer's.[11] Pate and Margolin, found that this was caused by damage to the cortical central.[12] The cortical central is the outer region of the cerebellum, a major component of the brain that controls motor functions.[13] Particularly in the older population, evidence of bradyphrenia had been seen in patients with Alzheimer's.

Depression edit

Evidence of bradyphrenia in patients with depression had been present if they had previous neurological damage.[13] In a study of elderly patients, it was found that patients with depression had not shown a significant delay in thought processing as did patients with depression and additional neurological damage to a part of their brain.[14]

Yet, Rogers et al., examined bradyphrenia and whether or not it was indicated by 'mental rotation' in melancholic and non-melancholic depressed patients. Researchers would ask the participants to participate in numerous tasks whereby their performance would be measured by their reaction time and accuracy of response.[15] The tasks that participants were asked to perform included being able to determine which direction a stimulus on the screen was pointing towards and were also told to determine if a stimulus shown was the normal positioning or whether it had been reversed.[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. Researchers had drawn the conclusion that the lesser slowness of the non-melancholic depressed groups in these tasks had not been intense enough to draw it to bradyphrenia.[15]

Huntington's disease and schizophrenia edit

Bradyphrenia had also been observed in Huntington's disease and schizophrenia.[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.[16] This study had shown that there had been a significant increase in time that it took for patients with Huntington's to solve the problem.[16] Participants with schizophrenia, however, performed the tasks in a smaller amount of time, faster than those in the control group within the experiment.[16] Hanes had suggested that bradyphrenia in schizophrenia was not as common as it was seen in Huntington's disease.[16]

Addiction edit

Experts including Martin et al. discovered that bradyphrenia is seen as one of the first stages of the ramifications of overdosing on an opioid like heroin. Bradyphrenia, however, had been considered the presence of bradyphrenia to be the most 'minor' of the ramifications.[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.[17] A case report had been done on a 63-year-old man who had been hospitalised for ten days and has been released with no notable impairments. The patient was hospitalised again several days later after showing abnormal behaviours in which specialists could only describe it as being bradyphrenia.[18] The patient's abnormal behaviour included having a diminished attention span as well as being unable to remember minor details. Researchers had justified this worsening of behaviour by abnormal neurological activity within the pre-frontal cortex.[18] The patient's cognitive abilities had improved with the use of an antioxidant therapy yet with some acts of abnormal behaviours still showing.[18][19]

Management edit

Currently, there are no pharmaceutical medications that will directly increase the rate of thoughts in patients with bradyphrenia experience.[20] The treatments for Parkinson's disease have been imposed as a model for treatment of bradyphrenia as in some cases the researchers have been able to treat the condition in patients with Parkinson's.[2]

Steroid therapy edit

During the time of the encephalitis lethargica period, the rise of bradyphrenia was seen in many of the cases. In one case in Russia it was believed that this condition could be treated with steroid therapy after the patient's condition had improved after three months using steroid.[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.[22] The effectiveness of steroid therapy had been observed within an MRI improvement as the number of lesions had decreased as well as the shift in behaviours of participants.[22][23]

L-DOPA and carbidopa regimen edit

In one trial it was found that bradyphrenia as well as bradykinesia, could be treated using the combination of a L-DOPA and carbidopa regimen. This combination was believed to alter these effects of Parkinson's disease.[24] In the short term, this combination had brought positive results as behaviours of these patients had improved.[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).[24]

H2 antagonists edit

H2 antagonists is a class of drugs that was found to provide positive outcomes throughout the treatment of Parkinson's disease.[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] Psychiatrist Kaminski found an improvement of this condition in Parkinson's disease with a positive correlation between the decrease of time in cognitive thought processing and the decrease in reaction time for tasks to be completed.[25]

History edit

Encephalitis lethargica era edit

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.[27] Naville was dealing with patients experiencing several symptoms which he could only describe as a gradual brain impairment. Several symptoms listed included decreased attention span, memory and lack of motivation to perform any tasks.[2] Naville had also observed the facial expressions of his patients with these symptoms' had become stagnant and disinterested over time.[2] Since Naville's publications in 1922, researchers often referred to this condition as 'psychic torpor' being translated as 'mental inactivity.'[28]

Post-encephalitis lethargica era edit

Swiss neurologist Steck completed a study investigating the case of bradyphrenia post- an epidemic, in 27 mental institutions. Within his research, he found that more than half of the patients hospitalised had the condition[2] Following Steck's discovery, for some period there had been no active research into the causes of bradyphrenia.[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.[2] Gradually, more neurologists began exploring bradyphrenia in the presence of other disorders including Alzheimer's disease, loss of motor control and psychiatric disorders.[citation needed]

See also edit

References edit

  1. ^ Blueprints Neurology, 2nd ed.[page needed]
  2. ^ a b c d e f g h i j Rogers, Daniel (9 July 2009). "Bradyphrenia in parkinsonism: a historical review". Psychological Medicine. 16 (2): 257–265. doi:10.1017/s0033291700009077. PMID 3523569. S2CID 37646114.
  3. ^ Revonsuo, A.; Portin, R.; Koivikko, L.; Rinne, J.O.; Rinne, U.K. (January 1993). "Slowing of Information Processing in Parkinson′s Disease". Brain and Cognition. 21 (1): 87–110. doi:10.1006/brcg.1993.1007. PMID 8424865. S2CID 25231613.
  4. ^ William S. Haubrich,. Medical Meanings : a Glossary of Word Origins [Rev. & expanded ed.]. Philadelphia, Pa: American College of Physicians, 1997
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  6. ^ a b c Spicer, Kevin B.; Brown, Gregory G.; Gorell, Jay M. (June 1994). "Lexical decision in parkinson disease: Lack of evidence for generalized bradyphrenia". Journal of Clinical and Experimental Neuropsychology. 16 (3): 457–471. doi:10.1080/01688639408402656. PMID 7929713.
  7. ^ Shindo, Akihiro; Ueda, Yukito; Kuzuhara, Shigeki; Kokubo, Yasumasa (21 July 2014). "Neuropsychological study of amyotrophic lateral sclerosis and parkinsonism-dementia complex in Kii peninsula, Japan". BMC Neurology. 14 (1): 151. doi:10.1186/1471-2377-14-151. PMC 4107997. PMID 25041813.
  8. ^ a b c d e Dobbs, R. J.; Bowes, S. G.; Charlett, A.; Henley, M.; Frith, C.; Dickins, J.; Dobbs, S. M. (April 1993). "Hypothesis: the bradyphrenia of parkinsonism is a nosological entity". Acta Neurologica Scandinavica. 87 (4): 255–261. doi:10.1111/j.1600-0404.1993.tb05504.x. PMID 8503252. S2CID 2658000.
  9. ^ a b Norberg, Astrid; Athlin, Elsy; Winblad, Bengt (July 1987). "A model for the assessment of eating problems in patients with Parkinson's disease". Journal of Advanced Nursing. 12 (4): 473–481. doi:10.1111/j.1365-2648.1987.tb01356.x. PMID 2958527. ProQuest 57739436.
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  12. ^ Nebes, Robert D.; Halligan, Edythe M.; Rosen, Jules; Reynolds, Charles F. (1 September 1998). "Cognitive and motor slowing in Alzheimer's disease and geriatric depression". Journal of the International Neuropsychological Society. 4 (5): 426–434. doi:10.1017/s1355617798455024. PMID 9745232. S2CID 23108612.
  13. ^ a b Ivry, Richard B.; Keele, Steven W. (April 1989). "Timing Functions of The Cerebellum". Journal of Cognitive Neuroscience. 1 (2): 136–152. doi:10.1162/jocn.1989.1.2.136. PMID 23968462. S2CID 22820283.
  14. ^ Mayberg, H. S. (November 1994). "Frontal lobe dysfunction in secondary depression". The Journal of Neuropsychiatry and Clinical Neurosciences. 6 (4): 428–442. doi:10.1176/jnp.6.4.428. PMID 7841814.
  15. ^ a b c Rogers, M.A.; Bradshaw, J.L.; Phillips, J.G.; Chiu, E.; Mileshkin, C.; Vaddadi, K. (9 August 2010). "Mental Rotation in Unipolar Major Depression". Journal of Clinical and Experimental Neuropsychology. 24 (1): 101–106. CiteSeerX 10.1.1.211.3788. doi:10.1076/jcen.24.1.101.974. PMID 11935428. S2CID 13606621.
  16. ^ a b c d e Hanes, Karl R. (9 September 2010). "Brief Report: Bradyphrenia in Parkinson's disease, Huntington's Disease, and Schizophrenia". Cognitive Neuropsychiatry. 1 (2): 165–170. doi:10.1080/135468096396622. PMID 16571481.
  17. ^ a b Martin, Michele; Hurley, Robin A.; Taber, Katherine H. (July 2007). "Is Opiate Addiction Associated With Longstanding Neurobiological Changes?". The Journal of Neuropsychiatry and Clinical Neurosciences. 19 (3): 242–248. doi:10.1176/jnp.2007.19.3.242. PMID 17827409.
  18. ^ a b c King, Franklin; Morris, Nicholas A.; Schmahmann, Jeremy D. (24 December 2015). "Delayed Posthypoxic Leukoencephalopathy: Improvement with Antioxidant Therapy". Case Reports in Neurology. 7 (3): 242–246. doi:10.1159/000441892. PMC 4777931. PMID 26955335.
  19. ^ Pan, Jing; Zhang, Qi; Zhang, Yuntao; Ouyang, Zhuqing; Zheng, Qiusheng; Zheng, Rongliang (May 2005). "Oxidative stress in heroin administered mice and natural antioxidants protection". Life Sciences. 77 (2): 183–193. doi:10.1016/j.lfs.2004.12.025. PMID 15862603.
  20. ^ Eric J Ahlskog. The New Parkinson's disease Treatment Book : Partnering with Your Doctor to Get the Most from Your Medications 2nd ed. New York, New York: Oxford University Press, 2015.[page needed]
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  22. ^ a b c McHugh, John C.; Ryan, Aisling M.; Lynch, Timothy; Dempsey, Elizabeth; Stack, John; Farrell, Michael A.; Kelly, Peter J. (2007). "Steroid-Responsive Recurrent Encephalopathy in a Patient with Cerebral Amyloid Angiopathy". Cerebrovascular Diseases. 23 (1): 66–69. doi:10.1159/000097030. PMID 17108675. S2CID 32136122. ProQuest 68921253.
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  24. ^ a b c Rao, Jayaraman (September 1999). "Treatment of Parkinson's disease" A Brand New Approach". The American Journal of Geriatric Psychiatry. 7: 27. doi:10.1097/00019442-199911001-00091.
  25. ^ a b c Molinari, S. P.; Kaminski, R.; Rocco, A.; Yahr, M. D. (June 1995). "The use of famotidine in the treatment of Parkinson's disease: a pilot study". Journal of Neural Transmission. Parkinson's Disease and Dementia Section. 9 (2–3): 243–247. doi:10.1007/BF02259665. PMID 8527008. S2CID 34470332.
  26. ^ Rinne, J. O.; Anichtchik, O. V.; Eriksson, K. S.; Kaslin, J.; Tuomisto, L.; Kalimo, H.; Röyttä, M.; Panula, P. (21 May 2002). "Increased brain histamine levels in Parkinson's disease but not in multiple system atrophy". Journal of Neurochemistry. 81 (5): 954–960. doi:10.1046/j.1471-4159.2002.00871.x. PMID 12065607.
  27. ^ Ravenholt, R.T; Foege, WilliamH (October 1982). "1918 influenza, encephalitis lethargica, parkinsonism". The Lancet. 320 (8303): 860–864. doi:10.1016/s0140-6736(82)90820-0. PMID 6126720. S2CID 45138249.
  28. ^ McCowan, P. K. (19 February 2018). "Encephalitis Lethargica: Its Sequelæ and Treatment. By Constantine von Economo. Translated and adapted by K. O. Newman. Oxford University Press (Humphrey Milford), 1931. Pp. 216. With 21 illustrations. Price 18s. net". Journal of Mental Science. 78 (321): 395–396. doi:10.1192/bjp.78.321.395.

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