Long-term psychiatric disorders after traumatic brain injury

Kings College London, Institute of Psychiatry, London, UK.
European Journal of Anaesthesiology - Supplement 02/2008; 42(supplement 42):123-30. DOI: 10.1017/S0265021507003250
Source: PubMed


In the long term after traumatic brain injury, the most disabling problems are generally related to neuropsychiatric sequelae, including personality change and cognitive impairment, rather than neurophysical sequelae. Cognitive impairment after severe injury is likely to include impaired speed of information processing, poor memory and executive problems. Personality change may include poor motivation, and a tendency to be self-centred and less aware of the needs of others. Patients may be described as lazy and thoughtless. Some become disinhibited and rude. Agitation and aggression can be very difficult to manage. Anxiety and depression symptoms are quite frequent and play a role in the development of persistent post-concussion syndrome after milder injury. Depression may be associated with a deterioration in disability over time after injury. Psychosis is not unusual though it has been difficult to confirm that traumatic brain injury is a cause of schizophrenia. Head injury may, many years later, increase the risk of Alzheimer's disease. Good rehabilitation probably minimizes the risk of psychiatric sequelae, but specific psychological and pharmacological treatments may be needed.

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    • "On the other hand, it has also been noted that functional factors can shape emotional adjustment following brain injury. For example, the level of awareness of disability (Fleminger, 2008) has been found to influence adjustment outcomes. In addition, the experience of loss (Carroll & Coetzer, 2011; Kaplan- Solms & Solms, 2000; Niemeier & Karrol, 2010; Nochi, 1998; Prigatano, 1999) has also been shown to be a significant mediator of emotional adjustment. "
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    ABSTRACT: Deficits in awareness are a common problem after traumatic brain injury (TBI), often compromising the process of emotional adjustment, including mourning. Unfortunately, there is little understanding of how the specific profile of cognitive impairment and emotional change often presented by individuals with TBI influences awareness and mourning. Concrete behaviour has been often described as a feature of TBI, with a difficulty detaching from immediate experience (both internal and external) as its signature. From a self-psychology perspective, concrete behaviour can be understood as a change in the cohesion and structure of the Self, where temporal and representational domains are modified. This paper offers a novel approach to problems of awareness and mourning after TBI, by considering how temporal and representational changes in the phenomenology of the Self alter individuals' emotional landscape. More specifically, it describes how concreteness modifies several aspects of emotional life that are central to awareness and mourning, such as emotional reactivity, emotional regulation, emotional understanding and signal anxiety. The impact that concreteness has in awareness and mourning is also discussed in detail throughout the paper, as well as the technical challenges implied. Finally, some general guidelines to address changes in the phenomenology of the Self in a therapeutic context are briefly described.
    03/2015; 17(1). DOI:10.1080/15294145.2015.1025819
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    • "TBI elicits immediate neuroinflammatory events that cause acute cognitive, motor and behavioral disturbances (Lifshitz et al., 2007b; McCrea et al., 2003; Tang et al., 1997; Woodcock and Morganti-Kossmann, 2013). Despite resolution of these acute complications, depression can develop and persist years after TBI (Fleminger, 2008; Jorge et al., 1993; Kreutzer et al., 2001). Indeed, individuals who suffer a TBI are 5e10 times more likely to develop symptoms of depression compared to the general population (Gualtieri and Cox, 1991). "
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    ABSTRACT: Glia of the central nervous system (CNS) help to maintain homeostasis in the brain and support efficient neuronal function. Microglia are innate immune cells of the brain that mediate responses to pathogens and injury. They have key roles in phagocytic clearing, surveying the local microenvironment and propagating inflammatory signals. An interruption in homeostasis induces a cascade of conserved adaptive responses in glia. This response involves biochemical, physiological and morphological changes and is associated with the production of cytokines and secondary mediators that influence synaptic plasticity, cognition and behavior. This reorganization of host priorities represents a beneficial response that is normally adaptive but may become maladaptive when the profile of microglia is compromised. For instance, microglia can develop a primed or pro-inflammatory mRNA, protein and morphological profile with aging, traumatic brain injury and neurodegenerative disease. As a result, primed microglia exhibit an exaggerated inflammatory response to secondary and sub-threshold challenges. Consequences of exaggerated inflammatory responses by microglia include the development of cognitive deficits, impaired synaptic plasticity and accelerated neurodegeneration. Moreover, impairments in regulatory systems in these circumstances may make microglia more resistant to negative feedback and important functions of glia can become compromised and dysfunctional. Overall, the purpose of this review is to discuss key concepts of microglial priming and immune-reactivity in the context of aging, traumatic CNS injury and neurodegenerative disease. Copyright © 2014. Published by Elsevier Ltd.
    Neuropharmacology 11/2014; 96(Pt A). DOI:10.1016/j.neuropharm.2014.10.028 · 5.11 Impact Factor
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    • "Recruitment has often been confined to hospital inpatients or chart information taken from inpatient wards, and in one circumstance potential cases were sought from a list of TBI patients referred for further neuropsychological testing (Fujii & Ahmed, 2001). Such sources miss mild to moderately brain-injured patients who may be experiencing psychotic symptoms (Burg et al., 1996; Fujii & Ahmed, 2001; Malaspina et al., 2001), or other psychiatric symptoms that may be inadvertently concealing symptoms of psychosis (i.e., symptoms of depression may co-occur with affective flattening ; see Fleminger, 2008; Koponen et al., 2002; Mainio et al., 2007 for rates of post-injury depression ). On the other hand, long-term PTA may be misdiagnosed as psychosis following severe TBI. "
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    ABSTRACT: Psychosis following traumatic brain injury (PFTBI) has received modest empirical investigation, and is subsequently poorly understood, identified and treated. The current article reports on consistencies in PFTBI phenomenology according to the existing peer-reviewed literature. The potential for psychotic symptoms post TBI, aetiological propositions, prevalence, significance of onset latency and injury severity, clinical and cognitive neuropsychological presentation and injury localisation/neuroimaging data are reviewed. Substantial methodological limitations associated with the majority of publications informing this work are also discussed. Despite controversies in the literature, psychosis following TBI appears to be three times more prevalent than psychotic disorders in the general population, and comparable in presentation to other idiopathic psychotic spectrum disorders, including schizophrenia.
    05/2013; 14(01). DOI:10.1017/BrImp.2013.10
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