The neurobehavioural rating scale: assessment of the behavioural sequelae of head injury by the clinician.

Levin, Harvey S.; High, Walter M.; Goethe, Katherine E.; Sisson, Rebecca; Overall, John E.; Rhoades, Howard M.; Eisenberg, Howard M.; Kalisky, Zvi; Gary, Howard E.

doi:10.1136/jnnp.50.2.183

Cited by 450 publications

(212 citation statements)

References 30 publications

(3 reference statements)

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“…Patients with brain damage to more than one region were classified based on the region with the greatest percentage of brain damage (Gozzi et al, 2009). We used this procedure to guarantee that patients in a lesion group not only had brain damage to that region, but also had greater brain damage to that region than to the other regions under investigation (Mah et al, 2004). In addition, patients with brain damage Ͼ15% in more than one region or whose damage was Ͻ15% were excluded from this confirmatory analysis.…”

Section: Methodsmentioning

confidence: 99%

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Brain Regions Influencing Implicit Violent Attitudes: A Lesion-Mapping Study

et al. 2016

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Increased aggression is common after traumatic brain injuries and may persist after cognitive recovery. Maladaptive aggression and violence are associated with dysfunction in the prefrontal and temporal cortex, but such dysfunctional behaviors are typically measured by explicit scales and history. However, it is well known that answers on explicit scales on sensitive topics-such as aggressive thoughts and behaviors-may not reveal true tendencies. Here, we investigated the neural basis of implicit attitudes toward aggression in humans using a modified version of the Implicit Association Task (IAT) with a unique sample of 112 Vietnam War veterans who suffered penetrating brain injury and 33 healthy controls who also served in combat in Vietnam but had no history of brain injury. We hypothesized that dorsolateral prefrontal cortex (dlPFC) lesions, due to the crucial role of the dlPFC in response inhibition, could influence performance on the IAT. In addition, we investigated the causal contribution of specific brain areas to implicit attitudes toward violence. We found a more positive implicit attitude toward aggression among individuals with lesions to the dlPFC and inferior posterior temporal cortex (ipTC). Furthermore, executive functions were critically involved in regulating implicit attitudes toward violence and aggression. Our findings complement existing evidence on the neural basis of explicit aggression centered on the ventromedial prefrontal cortex. These findings highlight that dlPFC and ipTC play a causal role in modulating implicit attitudes about violence and are crucially involved in the pathogenesis of aggressive behavior.

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Section: Methodsmentioning

confidence: 99%

“…Using the Analysis of Brain Lesion (ABLe) software version 2.8b (Makale et al, 2002;Solomon et al, 2007) implemented in MEDx (Medical Numerics) version 3.44, we calculated lesion location and volume loss. To identify the location of each lesion, a neuropsychiatrist (V.R.)…”

Section: Methodsmentioning

confidence: 99%

Brain Regions Influencing Implicit Violent Attitudes: A Lesion-Mapping Study

et al. 2016

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“…A variety of rating scales have been developed for the identification of psychotic symptoms in AD, and scoring of their severity. 9,[14][15][16] When interrater reliability for measuring the severity of individual psychotic symptoms on these scales has been assessed, it has generally been high. 9,16,17 In contrast, little data are available to inform whether a classification of an individual as having AD þ P can be achieved reliably.…”

Section: Evidence For a Distinct Phenotypementioning

confidence: 99%

Psychotic symptoms in Alzheimer disease: evidence for a distinct phenotype

et al. 2003

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Though efforts to identify the genetic etiology of Alzheimer disease (AD) have made substantial progress, to date only some of the genes contributing to AD risk have been identified. Utilization of more etiologically homogeneous subphenotypes represents one strategy to facilitate the identification of novel risk genes in complex disorders. In this review, we evaluate the hypothesis that psychotic symptoms, such as delusions and hallucinations, define a suitable subphenotype in AD patients for gene-mapping efforts. Psychotic symptoms occur in 40-60% of patients with AD and are associated with more severe cognitive deficits and a more rapidly deteriorating course. The presence of psychotic symptoms in AD confers increased risk of similar symptoms to affected siblings. Candidate gene association analyses and initial linkage analysis have yielded significant results. We discuss possible genetic models of psychotic symptoms in AD, and suggest strategies for further investigation. Identification of such genetic factors may facilitate gene-mapping studies for both AD and idiopathic psychoses. OverviewThe genetic basis of Alzheimer disease (AD) is unknown, although considerable strides have been made using gene-mapping efforts. Success has been most notable for the highly heritable early onset form, which comprises a minority of the entire population of AD cases. 1 While the impact of apolipoprotein E e4 alleles (APOE4) is well established, the genetic architecture of the more common late-onset AD (LOAD) is unclear. Like other genetically complex disorders, such as diabetes mellitus, progressively greater attention has been paid to utilizing defined subgroups of AD (eg late age-of-onset, APOE4 presence, autopsy confirmation) for mapping liability genes. 2,3 We have previously proposed that the presence of psychotic symptoms, delusions and hallucinations, define a subgroup of AD 4 that may be suitable for genetic investigation. 5,6 To our knowledge, however, the available evidence pertaining to whether AD with psychosis (AD þ psychosis (AD þ P)) identifies a phenotype suitable for genetic study has not been the subject of critical review.Stedman's Medical Dictionary defines phenotype as 'the observable characteristics, at the physical, morphologic, or biochemical level, of an individual, as determined by the genotype and environment '. 7 The genes associated with a behavioral phenotype, however, are unknown. The task for the psychiatric geneticist, therefore, is to identify a behavioral phenotype that varies according to alleles at a restricted set of genes. As in all psychiatric nosology, a behavioral phenotype must be readily and reliably identifiable in all patients of interest. If this behavioral phenotype has clinical relevance (eg bipolar illness) it provides a measure of face validity, and adds significance to its use in the search for causative genes. Tsuang et al. 8 enumerated additional criteria for determining that a behavioral phenotype has a substantial genetic basis, including state independence, biolog...

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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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The neurobehavioural rating scale: assessment of the behavioural sequelae of head injury by the clinician.

Cited by 450 publications

References 30 publications

Brain Regions Influencing Implicit Violent Attitudes: A Lesion-Mapping Study

Brain Regions Influencing Implicit Violent Attitudes: A Lesion-Mapping Study

Psychotic symptoms in Alzheimer disease: evidence for a distinct phenotype

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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