Psychosis secondary to traumatic brain injury

Guerreiro, Diogo Frasquilho; Navarro, R; Silva, Manuela; Carvalho, M.; Góis, Carlos

doi:10.1080/02699050902800918

Cited by 33 publications

(19 citation statements)

References 13 publications

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“…Primary neurodegeneration caused by the acute initial impact inevitably triggers waves of secondary injury from inflammation [2–5] and initiates progressive neuronal demise in multiple regions of the brain [6–8]. These damaging sequelae can lead to behavioral deficits [8–11] and even psychosis [12–14]. The behavioral deficits from TBI involve dysfunction in sensorimotor abilities, memory, and cognition.…”

Section: Introductionmentioning

confidence: 99%

Neurorestorative Effect of Urinary Bladder Matrix-Mediated Neural Stem Cell Transplantation Following Traumatic Brain Injury in Rats

Wang

Liou

Ren

et al. 2013

CNSNDDT

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Traumatic brain injury (TBI) is a leading cause of cell death and disability among young adults and lacks a successful therapeutic strategy. The multiphasic injuries of TBI severely limit the success of conventional pharmacological approaches. Recent successes with transplantation of stem cells in bioactive scaffolds in other injury paradigms provide new hope for the treatment of TBI. In this study, we transplanted neural stem cells (0.5×105 cells/μl) cultured in a bioactive scaffold derived from porcine urinary bladder matrix (UBM; 4 injection sites, 2.5μl each) into the rat brain following controlled cortical impact (CCI, velocity, 4.0 m/sec; duration, 0.5 sec; depth, 3.2mm). We evaluated the effectiveness of this strategy to combat the loss of motor, memory and cognitive faculties. Before transplantation, compatibility experiments showed that UBM was able to support extended proliferation and differentiation of neural stem cells. Together with its reported anti-inflammatory properties and rapid degradation characteristics in vivo, UBM emerged to be an ideal scaffold. The transplants reduced neuron/tissue loss and white matter injury, and also significantly ameliorated motor, memory, and cognitive impairments. Furthermore, exposure to UBM alone was sufficient to decrease the loss of sensorimotor skills from TBI (examined 3–28 days post-CCI). However, only UBMs that contained proliferating neural stem cells helped attenuate memory and cognitive impairments (examined 26–28 days post-CCI). In summary, these results demonstrate the therapeutic efficacy of stem cells in bioactive scaffolds against TBI and show promise for translation into future clinical use.

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Section: Introductionmentioning

confidence: 99%

Neurorestorative Effect of Urinary Bladder Matrix-Mediated Neural Stem Cell Transplantation Following Traumatic Brain Injury in Rats

Wang

Liou

Ren

et al. 2013

CNSNDDT

View full text Add to dashboard Cite

show abstract

“…In addition to this, brain injuries that often involve BBB breakdown and astrocytic response increase the risk of significant neuropsychiatric conditions, including personality changes, depression, anxiety, dementia and perhaps psychosis [98,99]. Cytokine receptors are expressed in glia and neuronal cells throughout the human brain, albeit at low levels relative to the periphery [102].…”

Section: Such Disruptions In Homeostatic Mechanismsmentioning

confidence: 99%

Recent advances in psychoneuroimmunology: Inflammation in psychiatric disorders

Debnath

Doyle

Langan

et al. 2011

Translational Neuroscience

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Psychiatric disorders are common and complex and their precise biological underpinnings remain elusive. Multiple epidemiological, molecular, genetic and gene expression studies suggest that immune system dysfunction may contribute to the risk for developing psychiatric disorders including schizophrenia, bipolar disorder, and major depressive disorder. However, the precise mechanisms by which inflammationrelated events confer such risk are unclear. In this review, we examine the peripheral and central evidence for inflammation in psychiatric disorders and the potential molecular mechanisms implicated including inhibition of neurogenesis, apoptosis, the HPA-axis, the role of brain-derived neurotrophic factor and the interplay between the glutamatergic, dopaminergic and serotonergic neurotransmitter systems.

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“…In each of these cases, olanzapine was combined with another medication, and of note, valproate alone has been effective in treating mania secondary to TBI [15], making it challenging to know if the patient improved related to olanzapine or valproate. Furthermore, olanzapine monotherapy has been shown to be effective in treating psychotic symptoms following traumatic brain injury in two case reports [31, 32]. In the case presented here, the patient was not agreeable to other pharmacologic treatments despite being offered lithium and valproate augmentation.…”

Section: Discussionmentioning

confidence: 78%

A Case Report of Mania and Psychosis Five Months after Traumatic Brain Injury Successfully Treated Using Olanzapine

Cittolin-Santos

Fredeen

Cotes

2017

Case Reports in Psychiatry

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Background There are few published pharmacologic trials for the treatment of acute mania following traumatic brain injury (TBI). To our knowledge, we present the first case report of an individual being treated and stabilized with olanzapine monotherapy for this condition. Case Presentation We describe the case of a 53-year-old African American male admitted to an inpatient psychiatric hospital with one month of behavioral changes including irritability, decreased need for sleep, hyperverbal speech, hypergraphia, and paranoia five months after TBI. Using Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) criteria, he was diagnosed with bipolar disorder due to traumatic brain injury, with manic features. He was serially evaluated with clinical rating scales to measure symptom severity. The Young Mania Rating Scale (YMRS) score upon admission was 31, and the Clinician-Rated Dimensions of Psychosis Symptom Severity (CRDPSS) score was initially 9. After eight days of milieu treatment and gradual titration of olanzapine to 15 mg nightly, his symptoms completely abated, with YMRS and CRDPSS scores at zero on the day of discharge. Conclusion Olanzapine was effective and well tolerated for the treatment of mania following TBI.

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Psychosis secondary to traumatic brain injury

Cited by 33 publications

References 13 publications

Neurorestorative Effect of Urinary Bladder Matrix-Mediated Neural Stem Cell Transplantation Following Traumatic Brain Injury in Rats

Neurorestorative Effect of Urinary Bladder Matrix-Mediated Neural Stem Cell Transplantation Following Traumatic Brain Injury in Rats

Recent advances in psychoneuroimmunology: Inflammation in psychiatric disorders

A Case Report of Mania and Psychosis Five Months after Traumatic Brain Injury Successfully Treated Using Olanzapine

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