Central nervous system bioaminergic responses to mechanical trauma

Eghwrudjakpor, Patrick O.; Miyake, Hirohisa; Kurisaka, Masahiro; Mori, Koreaki

doi:10.1016/0090-3019(91)90004-s

Cited by 39 publications

(14 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, few studies [20][21][22] offer support for the hypothesis that cerebral catecholamine levels are chronically altered by TBI; instead, most suggest only that acute elevations of striatal dopamine are predictive of poor recovery from TBI [23][24][25]. However, no human studies have demonstrated a clear relationship between in vivo markers of dopaminergic function and long-term cognitive deficits in traumatically brain-injured humans.…”

Section: Opinion Statementmentioning

confidence: 99%

Cognitive impairment following traumatic brain injury

Arciniegas¹,

Held²,

Pk³

2002

Curr Treat Options Neurol

216

140

View full text Add to dashboard Cite

Cognitive impairments due to traumatic brain injury (TBI) are substantial sources of morbidity for affected individuals, their family members, and society. Disturbances of attention, memory, and executive functioning are the most common neurocognitive consequences of TBI at all levels of severity. Disturbances of attention and memory are particularly problematic, as disruption of these relatively basic cognitive functions may cause or exacerbate additional disturbances in executive function, communication, and other relatively more complex cognitive functions. Because of the high rate of other physical, neurologic, and psychiatric syndromes following TBI, a thorough neuropsychiatric assessment of the patient is a prerequisite to the prescription of any treatment for impaired cognition. Psychostimulants and other dopaminergically active agents (eg, methylphenidate, dextroamphetamine, amantadine, levodopa/carbidopa, bromocriptine) may modestly improve arousal and speed of information processing, reduce distractibility, and improve some aspects of executive function. Cautious dosing (start-low and go-slow), frequent standardized assessment of effects and side effects, and monitoring for drug-drug interactions are recommended. Cognitive rehabilitation is useful for the treatment of memory impairments following TBI. Cognitive rehabilitation may also be useful for the treatment of impaired attention, interpersonal communication skills, and executive function following TBI. This form of treatment is most useful for patients with mild to moderate cognitive impairments, and may be particularly useful for those who are still relatively functionally independent and motivated to engage in and rehearse these strategies. Psychotherapy (eg, supportive, individual, cognitive-behavioral, group, and family) is an important component of treatment. For patients with medication- and rehabilitation-refractory cognitive impairments, psychotherapy may be needed to assist both patients and families with adjustment to permanent disability.

show abstract

Section: Opinion Statementmentioning

confidence: 99%

Cognitive impairment following traumatic brain injury

Arciniegas¹,

Held²,

Pk³

2002

Curr Treat Options Neurol

216

140

View full text Add to dashboard Cite

show abstract

“…Excess production or delivery of these neurotransmitters occurs acutely [7][8][9][10][11][12][13][14], and such alterations may contribute to arousal, attention, memory, and other cognitive impairments characteristic of the acute injury period. The evidence for long-term dysfunction of these systems among persons with persistent post-traumatic cognitive impairments is less consistent, with the exception of that regarding the cerebral cholinergic system.…”

Section: Introductionmentioning

confidence: 99%

The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury

Arciniegas

2003

Curr Psychiatry Rep

View full text Add to dashboard Cite

Cognitive impairments are among the most common neuropsychiatric sequelae of traumatic brain injury at all levels of severity. Cerebral cholinergic neurons and their ascending projections are particularly vulnerable to acute and chronic traumatically mediated dysfunction. In light of the important role of acetylcholine in arousal, attention, memory, and other aspects of cognition, cerebral cholinergic systems contribute to and may also be a target for pharmacologic remediation among individuals with post-traumatic cognitive impairments. This article will review the evidence in support of this hypothesis. Evidence of relatively selective damage to cholinergic injury, the development of persistent anticholinergic sensitivity, and the effects of cholinergic augmentation on memory performance are presented first. Thereafter, neuropathologic, electrophysiologic, and pharmacologic evidence of cholinergic dysfunction after traumatic brain injury in humans is reviewed. Finally, future directions for investigation of the cholinergic hypothesis and possible clinical applications of this information are discussed.

show abstract

“…The long-term effect of repetitive IPC needs further research. So far, mechanisms by which IPC can protect the spinal cord after ischemic injury are unknown, however, possible mechanisms included were synthesis of HSP (Sakurai et al, 1998), restraining the excessive release of catecholamine (Eghwrudjakpor et al, 1991) and accelerating the release of taurine (Miyamoto and Miyamoto, 2000) and adenosine (Zvara et al, 1999). One research had indicated that the changes of multi-ion channels, which were introduced by K ATP channel, were the key points in IPC produced ischemia tolerance (Kouchi et al, 1998).…”

Section: Discussionmentioning

confidence: 99%