The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury

Arciniegas, David B.

doi:10.1007/s11920-003-0074-5

Cited by 91 publications

(54 citation statements)

References 78 publications

(89 reference statements)

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“…For example, there is significant dysfunction of catecholaminergic systems associated with TBI (16)(17)(18). There is also evidence of altered central cholinergic tone (19)(20)(21)(22)(23) following trauma. The cholinergic system plays an important role in many cognitive domains, particularly memory and attention (24) and may play a role in the genesis of mood disorders, particularly depression (25).…”

Section: Relationship Of Profile Of Injury To Neurobehavioral Sequelaementioning

confidence: 99%

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

2008

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Traumatic brain injury (TBI) is a universal public health problem. A recent review of epidemiological studies in Europe suggests an incidence of 235 hospitalized cases (including fatalities) per 100,000 population (1). In the US, the incidence is estimated at 150 per 100,000 population (2). Less data is available from other regions of the world, but TBI is acknowledged as a significant problem worldwide. Of note is that the incidence rates are calculated from hospitalized cases only, and do not include injured individuals who do not seek or have access to care. Thus, the actual incidence of injury is probably 3 to 4 fold larger than the quoted numbers. Most studies suggest that the incidence rates for TBI are greatest in the second and third decades of life, with a secondary increase in the elderly stemming from falls (2,3). Males are more likely to suffer a TBI than females (2,3).In developed countries, there has been a reduction in the mortality rates associated with TBI over the last several decades, generally attributed to improved systems of trauma care and improved motor vehicle safety design. Many individuals with mild traumatic brain injury and virtually all individuals who survive moderate and severe TBI are left with significant long-term neurobehavioral sequelae (4-6). Thus, the reduction in TBI-associated mortality rates (7) has led to a significant increase in the number of individuals with long-term neurobehavioral disorders related to TBI (8,9).Brain trauma can be caused in a number of ways, including mechanisms which penetrate the substance of the brain (e.g., projectiles) and those that do not. This paper focuses on non-penetrating injuries. Despite different contexts and instruments, the physics and biomechanics underlying damage to the brain from non-penetrating injuries have some common features. This results in certain brain regions being at greater risk for damage than others and allows for some general statements to be made about typical profiles of brain injury associated with trauma. The assessment and treatment of the neurobehavioral sequelae of TBI follow logically from an understanding of this injury profile. RELATIONSHIP OF PROFILE OF INJURY TO NEUROBEHAVIORAL SEQUELAEThere are two broad categories of forces that result in brain injury: contact (or impact) and inertial (acceleration or deceleration). Contact injuries result from the brain coming into contact with an object (which might include the skull, or some external object). Contact mechanisms often result in damage to scalp, skull, and brain surface (e.g., contusions, lacerations, hematomas) (10). Frequent sites of such injury are the anterior temporal poles, lateral and inferior temporal cortices, frontal poles, and orbital frontal cortices.Inertial injury results from rapid acceleration or deceleration of the brain that produces shear, tensile, and compression forces. These forces have maximum impact on axons and blood vessels, resulting in axonal injury, tissue tears, and intracerebral hematomas. These mechanisms also produc...

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Section: Relationship Of Profile Of Injury To Neurobehavioral Sequelaementioning

confidence: 99%

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

2008

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“…The result is a decrease of synthesis, as well as acetylcholine neurons [141]. The decease in acetylcholine is thought to be the neurochemical basis for the cognitive deficits exhibited following TBI [142]. Further support of the cholinergic contribution to cognitive aspects of TBI is provided by studies of sensory gating, a parameter of attention that uses acetylcholine [143].…”

Section: Traumatic Brain Injurymentioning

confidence: 99%

Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury

Kennedy

Jaffee

Leskin³

et al. 2007

JRRD

235

156

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Abstract-In this article, we review the literature on posttraumatic stress disorder (PTSD) and PTSD-like symptoms that can occur along with mild traumatic brain injury (TBI) and concussion, with specific reference to concussive injuries in the military. We address four major areas: (1) clinical aspects of TBI and PTSD, including diagnostic criteria, incidence, predictive factors, and course; (2) biological interface between PTSD and TBI; (3) comorbidity between PTSD and other mental disorders that can occur after mild TBI; and (4) current treatments for PTSD, with specific considerations related to treatment for patients with mild TBI or concussive injuries.

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“…Amantadine, a drug with complex pharmacologic effects on dopaminergic, cholinergic and NMDA receptors, could also have some efficacy to treat motivational deficits (Kraus & Maki 1997;Meythaler et al 2002). Finally, there is some empirical evidence that cholinesterase inhibitors such as donepezil may improve cognitive functioning, motivation and general well being of patients with traumatic brain injury (Arciniegas et al 1999, Freo et al 2002, Arciniegas 2003.…”

Section: Treatment Of Apathymentioning

confidence: 99%

The prevalence, clinical correlates and treatment of apathy in Alzheimer's disease

2006

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-The aim for this article is to review the frequency, clinical correlates and treatment of apathy in Alzheimer's disease. Apathy is currently defined as diminished motivation as expressed in poor goal-oriented behaviours and cognitions. A structured clinical interview and a specific set of diagnostic criteria to diagnose apathy in dementia have been recently validated. There are several valid and reliable scales to measure the severity of apathy in adults with neuropsychiatric disorders. Apathy is present in about 20% of patients with mild dementia and in 60% of those with severe dementia. Among patients with Alzheimer's disease, apathy is significantly associated with older age, the presence of depression, and more severe cognitive and functional deficits, and also predicts a faster cognitive and functional decline. The mechanism of apathy in neuropsychiatric disorders is still unknown, but several studies suggest an important role for frontal lobe and basal ganglia dysfunction. There are no specific randomized controlled trials of psychoactive compounds to treat apathy in neuropsychiatric disorders. Evidence from case reports and small case series suggest the usefulness of psychostimulants to treat apathy in traumatic brain injury, whereas pharmacological trials for behavioural and psychological problems in dementia suggest that anticholinesterases may have some efficacy.

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The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury

Cited by 91 publications

References 78 publications

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury

The prevalence, clinical correlates and treatment of apathy in Alzheimer's disease

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