Comparison of subjective cognitive complaints with neuropsychological tests in individuals with mild vs more severe traumatic brain injuries

Jamora, Christina Weyer; Young, Ashley D.; Ruff, Ronald M.

doi:10.3109/02699052.2011.635352

Cited by 79 publications

(53 citation statements)

References 42 publications

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“…The outcome of the study is compatible with findings from other studies. However, in contrast to previous studies [1,13,16,17,19,[20][21][22][23], the MTBI patients showed no significantly reduced speed of information processing as was evaluated with the PASAT. An overview of the results of this study can be seen in Table 1.…”

Section: Cognitive Problems After Mild Traumatic Brain Injurycontrasting

confidence: 99%

“…In MTBI patients, mild impairments in speed of information processing, (sustained, divided, focused and/or alternating) attention and (auditory-verbal and/or visuospatial) memory have been found [1,13,16,17,19,[20][21][22][23]. With regard to memory, most patients displayed deficits concerning the storage of new information into memory and/ or the reproduction of recently learned information from memory.…”

Section: Cognitive Problems After Mild Traumatic Brain Injurymentioning

confidence: 99%

“…With regard to cognitive functioning, WI and MTBI patients often complain of poor attention and memory [7]. Several studies have looked for objective findings concerning cognitive dysfunctions after WI [1,2,[8][9][10][11][12][13][14][15] and MTBI [16][17][18][19][20][21][22][23] and have found the presence of only mild cognitive deficits, if any, in both patient groups, mainly in the domain of attention, information processing and memory.…”

Section: Introductionmentioning

confidence: 99%

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Whiplash Injury and Mild Traumatic Brain Injury: Differential Effects on Cognitive Functioning?

Beeckmans¹,

Michiels²

2017

Int J Neurorehabilitation Eng

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With regard to whiplash injury (WI) patients, some studies documented mild attention problems and a reduced speed of information processing. Most patients showed problems with sustained and/or divided attention. However, some patients had also problems with focused and alternating attention. Regarding memory, some studies detected mild (auditory-verbal and/or visuospatial) memory difficulties. Visuospatial and executive functions appeared mostly preserved. In mild traumatic brain injury (MTBI) patients, mild impairments in speed of information processing, (sustained, divided, focused and/or alternating) attention and (auditory-verbal and/or visuospatial) memory have been found. Furthermore, mild deficits could also be seen on tests measuring executive functions whereas visuospatial functioning seemed to be preserved. Until today, only two studies were devoted to evaluate possible differences in cognitive functioning between WI and MTBI patients. In these studies, both patient groups did not differ significantly with regard to measurements of attention, memory, and visuospatial and executive functions. Therefore, these authors conclude that MTBI patients do not perform more poorly on cognitive tests than WI patients, as might be expected from severity of trauma.

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Section: Cognitive Problems After Mild Traumatic Brain Injurycontrasting

confidence: 99%

Section: Cognitive Problems After Mild Traumatic Brain Injurymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Whiplash Injury and Mild Traumatic Brain Injury: Differential Effects on Cognitive Functioning?

Beeckmans¹,

Michiels²

2017

Int J Neurorehabilitation Eng

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“…PTSD is an anxiety disorder that develops following exposure to a potentially life-threatening event. Because PTSD and TBI are known to coexist, and because studies show an association between PTSD and chronic pain among individuals after TBI 10,37 especially among individuals with mild TBI, 38 we measured the severity of PTSD symptomatology among the participants. The PTSD Inventory was used.…”

Section: Sensory Testingmentioning

confidence: 99%

Deficient Pain Modulatory Systems in Patients with Mild Traumatic Brain and Chronic Post-Traumatic Headache: Implications for its Mechanism

Defrin

Riabinin

Feingold

et al. 2015

Journal of Neurotrauma

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Although the prevalence rate of chronic post-traumatic headache (CPTHA) after mild traumatic brain injury (TBI) reaches up to 95%, its mechanism is unknown, and little is known about the characteristics of the pain system in this condition. Our aim was to investigate the capabilities of two pain modulatory systems among individuals with CPTHA and study their association with CPTHA, here for the first time. Forty-six subjects participated; 16 with TBI and CPTHA, 12 with TBI without CPTHA, and 18 healthy controls. Testing included the measurement of heat-pain (HPT) and pressure-pain (PPT) thresholds in the forehead and forearm, pain adaptation to tonic noxious heat, and conditioned pain modulation (CPM).The participants completed a post-traumatic stress disorder (PTSD) questionnaire. The two TBI groups did not differ in the TBI and background characteristics. However, TBI patients with CPTHA had significantly higher HPT and lower PPT in the cranium and higher PTSD symptomatology than TBI patients without CPTHA and healthy controls. Adaptation to pain and CPM were diminished in the CPTHA group compared with the two control groups. The intensity of CPTHA correlated negatively with cranial PPT, magnitude of pain adaptation, and CPM. CPTHA intensity correlated positively with PTSD symptomatology. CPTHA appears to be characterized by cranial hyperalgesia and dysfunctional pain modulation capabilities, which are associated with CPTHA magnitude. It is concluded that damage to pain modulatory systems along with chronic cranial sensitization underlies the development of CPTHA. PTSD may reinforce CPTHA and vice versa. Clinical implications are discussed.

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“…While deficits in cognitive ability increase as a function of injury severity, [1][2][3][4] episodes of depression and anxiety are as prevalent after mild TBI as they are after moderate/severe TBI. [1][2][3][4] Temporary amnesia, headaches, and sleep disorders are also common, even after a mild TBI. The etiology of such diverse symptomology is unknown; however, the loss of excitatory synapses may explain the appearance of some of these symptoms.…”

Section: Introductionmentioning

confidence: 99%

Controlled Cortical Impact Results in an Extensive Loss of Dendritic Spines that Is Not Mediated by Injury-Induced Amyloid-Beta Accumulation

Winston

Chellappa

Wilkins

et al. 2013

Journal of Neurotrauma

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The clinical manifestations that occur after traumatic brain injury (TBI) include a wide range of cognitive, emotional, and behavioral deficits. The loss of excitatory synapses could potentially explain why such diverse symptoms occur after TBI, and a recent preclinical study has demonstrated a loss of dendritic spines, the postsynaptic site of the excitatory synapse, after fluid percussion injury. The objective of this study was to determine if controlled cortical impact (CCI) also resulted in dendritic spine retraction and to probe the underlying mechanisms of this spine loss. We used a unilateral CCI and visualized neurons and dendtritic spines at 24 h post-injury using Golgi stain. We found that TBI caused a 32% reduction of dendritic spines in layer II/III of the ipsilateral cortex and a 20% reduction in the dendritic spines of the ipsilateral dentate gyrus. Spine loss was not restricted to the ipsilateral hemisphere, however, with similar reductions in spine numbers recorded in the contralateral cortex (25% reduction) and hippocampus (23% reduction). Amyloid-b (Ab), a neurotoxic peptide commonly associated with Alzheimer disease, accumulates rapidly after TBI and is also known to cause synaptic loss. To determine if Ab contributes to spine loss after brain injury, we administered a c-secretase inhibitor LY450139 after TBI. We found that while LY450139 administration could attenuate the TBI-induced increase in Ab, it had no effect on dendritic spine loss after TBI. We conclude that the acute, global loss of dendritic spines after TBI is independent of c-secretase activity or TBI-induced Ab accumulation.

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Comparison of subjective cognitive complaints with neuropsychological tests in individuals with mild vs more severe traumatic brain injuries

Cited by 79 publications

References 42 publications

Whiplash Injury and Mild Traumatic Brain Injury: Differential Effects on Cognitive Functioning?

Whiplash Injury and Mild Traumatic Brain Injury: Differential Effects on Cognitive Functioning?

Deficient Pain Modulatory Systems in Patients with Mild Traumatic Brain and Chronic Post-Traumatic Headache: Implications for its Mechanism

Controlled Cortical Impact Results in an Extensive Loss of Dendritic Spines that Is Not Mediated by Injury-Induced Amyloid-Beta Accumulation

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