Psychiatric disorders and traumatic brain injury

Schwarzbold, Marcelo Libório; Diaz, Alexandre Paim; Martins, Evandro Tostes; Rufino, Armanda Carla Teixeira Brandão Fragata; Amante, Lúcia Nazareth; Thais, Maria Emília Rodrigues de Oliveira; Quevedo, João; Hohl, Alexandre; Linhares, Marcelo Neves; Walz, Roger

doi:10.2147/ndt.s2653

Cited by 91 publications

(37 citation statements)

References 164 publications

(128 reference statements)

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“…However, the reductionism of Combe's distinction clearly emerges from the clinical observation given that a wide range of nervous system's illnesses with different etiology shows both neurological and psychiatric symptoms. Emotional and behavioral disturbances with a polymorphic symptomatology are often connected to neurological disorders such as Multiple Sclerosis (MS) [1][2][3] , Parkinson' s Disease (PD) [4] , stroke [5] , dementia [6] , traumatic brain injury [7] , epilepsy [8,9] , Amyotrophic Lateral Sclerosis (ALS) and others Motor Neuron Diseases (MND) [10,11] , pain syndromes (like headaches) and can be observed even with or without "organic" neurological diseases, thus miming in some cases an idiopathic psychiatric disorder.…”

Section: Neurology and Psychiatrymentioning

confidence: 99%

Effects of music and music therapy on mood in neurological patients

Raglio

Attardo

Gontero

et al. 2015

WJP

140

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Mood disorder and depressive syndromes represent a common comorbid condition in neurological disorders with a prevalence rate that ranges between 20% and 50% of patients with stroke, epilepsy, multiple sclerosis, and Parkinson's disease. Notwithstanding, these conditions are often under-diagnosed and under-treated in the clinical practice and negatively affect the functional recovery, the adherence to treatment, the quality of life, and even the mortality risk. In addition, a bidirectional association between depression and neurological disorders may be possible being that depressive syndromes may be considered as a risk factor for certain neurological diseases. Despite the large amount of evidence regarding the effects of music therapy (MT) and other musical interventions on different aspects of neurological disorders, no updated article reviewing outcomes such as mood, emotions, depression, activity of daily living and so on is actually available; for this reason, little is known about the effectiveness of music and MT on these important outcomes in neurological patients. The aim of this article is to provide a narrative review of the current literature on musical interventions and their effects on mood and depression in patients with neurological disorders. Searching on PubMed and PsycInfo databases, 25 studies corresponding to the inclusion criteria have been selected; 11 of them assess the effects of music or MT in Dementia, 9 explore the efficacy on patients with Stroke, and 5 regard other neurological diseases like Multiple Sclerosis, Amyotrophic Lateral Sclerosis/motor neuron disease, Chronic quadriplegia, Parkinson's Disease, and Acquired Brain dysfunctions. Selected studies are based on relational and rehabilitative music therapy approaches or concern music listening interventions. Most of the studies support the efficacy of MT and other musical interventions on mood, depressive syndromes, and quality of life on neurological patients.

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Section: Neurology and Psychiatrymentioning

confidence: 99%

Effects of music and music therapy on mood in neurological patients

Raglio

Attardo

Gontero

et al. 2015

WJP

140

View full text Add to dashboard Cite

show abstract

“…Despite recent advances in the knowledge of the mechanisms involved in mTBI, no treatments, except for palliative care, are currently available ( Loane and Faden, 2010 ). It is currently believed that the secondary neuropsychiatric changes that occur as a consequence of TBI are linked to plastic rearrangements in several brain areas including the hippocampal and medial prefrontal cortex (mPFC) circuitry ( Schwarzbold et al, 2008 ). The mPFC is also thought to play a key role in chronic pain-related negative affective states (i.e., anxiety, depression, and cognitive impairments), which are often present as comorbidities accompanying damages to the central or peripheral nervous system (CNS or PNS, respectively), such as neuropathy or trauma.…”

Section: Introductionmentioning

confidence: 99%

Palmitoylethanolamide Reduces Neuropsychiatric Behaviors by Restoring Cortical Electrophysiological Activity in a Mouse Model of Mild Traumatic Brain Injury

et al. 2017

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Traumatic brain injury (TBI) represents a major public health problem, which is associated with neurological dysfunction. In severe or moderate cases of TBI, in addition to its high mortality rate, subjects may encounter diverse behavioral dysfunctions. Previous reports suggest that an association between TBI and chronic pain syndromes tends to be more common in patients with mild forms of brain injury. Despite causing minimal brain damage, mild TBI (mTBI) often leads to persistent psychologically debilitating symptoms, which can include anxiety, various forms of memory and learning deficits, and depression. At present, no effective treatment options are available for these symptoms, and little is known about the complex cellular activity affecting neuronal activity that occurs in response to TBI during its late phase. Here, we used a mouse model to investigate the effect of Palmitoylethanolamide (PEA) on both the sensorial and neuropsychiatric dysfunctions associated with mTBI through behavioral, electrophysiological, and biomolecular approaches. Fourteen-day mTBI mice developed anxious, aggressive, and reckless behavior, whilst depressive-like behavior and impaired social interactions were observed from the 60th day onward. Altered behavior was associated with changes in interleukin 1 beta (IL-1β) expression levels and neuronal firing activity in the medial prefrontal cortex. Compared with vehicle, PEA restored the behavioral phenotype and partially normalized the biochemical and functional changes occurring at the supraspinal level. In conclusion, our findings reveal some of the supraspinal modifications responsible for the behavioral alterations associated with mTBI and suggest PEA as a pharmacological tool to ameliorate neurological dysfunction induced by the trauma.

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“…Disruptions to neural circuits and injuries to the amygdala, frontal cortex, and hippocampus may cause mood changes due to biochemical changes. 42 For example, an increase in dopamine and a decrease in serotonin levels is known to be associated with agitation and aggression. 43 Although research in this area has yielded inconsistent results, 42 our complex networks of interactions suggest that a change in neural function, which in our results manifested by aggression, may play the key connector function between this factor in this complex network.…”

Section: Discussionmentioning

confidence: 99%