This document summarizes a presentation on neuropsychiatric aspects of head injury. It begins with an introduction discussing the prevalence of head injuries. It then covers the history of understanding head injuries, comparative diagnostic classifications, epidemiology, types and pathophysiology of head injuries including acute and chronic behavioral consequences. The presentation also discusses clinical features such as cognitive impairment, personality changes, mood disorders, anxiety, aggression and psychosis. It concludes with discussing prognosis and predictors of outcome following head injury.
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Neuropsychiatric aspects of traumatic brain injury
1. Neuropsychiatric aspects of HEAD INJURY Speaker: Dr. Santanu Ghosh, Post Graduate student, Psychiatry. Moderator: Dr. J.N. Das, Asstt. Professor, Psychiatry. Assam Medical College, Dibrugarh. 1
2. Outline of presentation: Introduction History Comparative Nosology Epidemiology Types of head injury Pathophysiology Clinical features Prognosis Outcome Management Take home message Bibliography 2
3. Introduction: Head injuries are unfortunately common in today's world due to mass use of motor vehicles and widely misused alcohol. The peak incidence is between the ages of 15-24 & improved medical care has resulted in large numbers of individuals surviving with neuropsychiatric consequences. Most head injury survivors who present to psychiatric services have emotional symptoms & personality changes. A smaller number manifest serious and lasting cognitive sequelae such as apathy, disinhibition & amnesia. There are also important acute psychiatric effects of head injury. 3
4. History: Earliest written evidence of TBI found on Edwin Smith Papyrus 5000 years ago. The Hippocratic Corpus included treatise on head injury with thoughtful comments on skull #, delirium, seizure, coma. Adolf Mayer introduced the term ‘ traumatic insanity’ 4
5. Comparative Nosology: DSM-IV : Mental & behavioral problems due to traumatic brain injury. ICD-10: Other conditions associated with mental & behavioral disorders— -Chapter: XIX: S06- Intracranial injury 5
6. Epidemiology: 500,000 new cases of TBIs occur in the US each year.* 50,000 Deaths 235,000 Hospitalizations 80%-mild, 10%-moderate, 10%- severe TBI M:F=2-3:1 6 INCIDENCE: Closed TBI- 200/100,000 population Penetrating TBI- 12/100,ooo population
18. (Pathology- contd….) Clinical evidences: CSF finding of glutamate concentrations are significantly elevated for several days after TBI. Glutamate antagonists have shown beneficial effects in experimental models of TBI. 16
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20. (Pathology- contd….) Clinical evidences: A reduction in cholinergic transmission in hippocampal & neocortical areas observed after TBI . Dysfunction of the septohippocampal cholinergic pathway is observed in experimental models which has significant role in posttraumatic cognitive & behavioral deficits. 18
21. (Pathology- contd….) Ascending biogenic amine: 19 Synaptic conc. Of biogenic amine neurotransmitter Downregulation of biogenic amines Depressive symptoms
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23. Serotonegic & noradrenergic metabolites in CSF.
24. Dysregulation of mesolimbic & mesocortical dopaminergic pathway give rise to manic & hypomanic syndromes.20
25. Lobe Functions(Cerebral): 21 Parietal lobe Dominant side: Non-dominant side: - Calculation - spatial orientation - Language - constructional skills - Planned movement - Appreciation of size, shape, weight, texture Frontal lobe: - Personality - Emotional response - Social behavior
26. Contd… 22 Occipital lobe: - Analysis of vision Temporal lobe Dominant side Non-dominant side -Auditory perception -Auditory perception -Speech, language -Music, tone sequence -Verbal memory -Non-verbal memory -Olfaction
36. Retrograde amnesia (RA): Period between the last clearly recalled memory prior to the injury & the injury itself. Dense amnesia lasting seconds & minutes.27
40. Can lead to - self injurious behavior, decreased self management, caregiver management problemsSynonyms of PTD: acute confusional state, intensive care unit (ICU) psychosis, post-traumatic psychosis, metabolic encephalopathy, organic brain syndrome, sundowning, toxic encephalopathy 28
41. Clinical feature contd… Posttraumatic headache Walker and co-authors found that nearly 38% of patients with moderate or severe TBI had acute posttraumatic headache, usually daily and most commonly in the frontal region.Almost all of the patients who reported posttraumatic headache at 6 months also reported symptoms at 12 months 29
53. TBI is associated with expression of amyloid precursor protein, oxidative stress & deposition of amyloid beta peptide that lead to the onset of dementia.
54. Chronic subdural hematoma in elderly can lead to progressive dementia.31
59. Pseudo -psychopathic personality syndrome: disinhibition, egocentricity & sexual inappropriateness.32
60.
61. One Year Cumulative Incidence of Mood Disorders After TBI Jorge et al., 2004 34
62. Rates of Major Depression after TBI(N=559) Bombardier, Fann et al, unpublished Percent of cases (N=559) Cumulative incidence (53%) Prevalence Incidence Months after traumatic brain injury
63. Impact of Depression on Outcomes Depression after TBI contributes to: increased aggressive behavior and anxiety (Tateno et al., 2003; Jorge et al., 2004; Fann et al., 1995) significantly higher rates of suicidal plans (Kishi et al., 2001) 8 times more attempts (Silver et al., 2001) 3-4 times more completed suicide than in the general population and non-brain injured controls (Teasdale and Engberg, 2001) 36
64. Impact of Depression on Outcomes Depression after TBI contributes to: Poorer cognitive functioning (Rappoport et al., 2005) Lower health status and greater functional disability (Christensen et al., 1994; Levin et al 2001; Fann et al., 1995; Hibbard et al., 2004; Rapoport et al., 2003) Poorer recovery (Mooney et al., 2005) More post-concussive symptoms (Fann et al., 1995; Rapoport et al., 2005) 37
80. May have epileptiform activity and temporal lobe lesions* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-327 41
81.
82. Posttraumatic seizures: It frequently occur after moderate or severe TBI. The incidence of late PTS is in the range of 5-18.9%. Seizures are usually general or partial, and absence seizures are uncommon Immediate seizures < 24 hours. Early seizures 2-7 days, and late seizures - after 7 days. 43
83. Punch-drunk syndrome: Boxers may develop diffuse injury to the cortex, basal ganglia. Extra pyramidal symptoms or a subcortical dementia. Pathology shows cerebral atrophy & neurofibrillary tangles. 44
84. Sequelae in children: Less psychopathology after TBI due to increased brain plasticity. Recovery may continue for up to 5 years after injury. Problems are generally behavioral in nature – aggression, delinquency, ADHD like syndrome. 45
88. Thursday, February 8, 2007 PRO FOOTBALL Expert Ties Ex-Player's Suicide To Brain Damage From Football Since the former National Football League player Andre Waters killed himself in November, an explanation for his suicide has remained a mystery. But after examining remains of Mr. Waters's brain, a neuropathologist in Pittsburgh is claiming that Mr. Waters had sustained brain damage from playing football and he says that led to his depression and ultimate death. 49
104. Size & location of brain damage: frontal, temporal, dominant side worse.53
105. Outcome: Death Persistent vegetative state Severe disability(conscious but dependent for daily activities) Moderate disability(disabled but living independently) Good recovery. 54
107. Neuropsychiatric History Psychiatric symptoms may not fit DSM-IV criteria Focus on functional impairment Document and rate symptoms Explore circumstances of trauma LOC, PTA, hospitalization, medical complications Subtle symptoms - may fail to associate with trauma How has life changed since TBI? Thorough review of medical and psychiatric records. Talk with family, friends, caregivers Assess level of care and supervision available Assess rehabilitation needs and progress 56
123. GOLDEN RULE: START LOW, GO SLOW May still need maximum doses Therapeutic onset may be latent Medications may lower seizure threshold Medications may slow cognitive recovery Monitor and document outcomes 61
124. Neuropsychiatric Treatment: Use Biopsychosocial Model Treat maximum signs and symptoms with fewest possible medications TBI patients more sensitive to side effects 62
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126. Treatment contd… Dementia: behavioural modification cognitive rehabilitation psychotropic medication for specific syndromes or symptoms Piracetam Donepezil family or network intervention social services medical support in legal proceedings. 64
127. Treatment contd… Depression / Apathy Selective serotonin re-uptake inhibitors (SSRIs) - sertraline - paroxetine - fluoxetine - citalopram - escitalopram venlafaxine, duloxetine (may help with pain) bupropion (may decrease seizure threshold) nefazedone (may be too sedating, liver toxicity) mirtazapine (may be too sedating) Tricyclics: nortriptyline, desipramine methylphenidate, dextroamphetamine Electroconvulsive Therapy – consider less frequent, nondominantunilateral Apathy: Dopaminergic agents - methylpyhenidate, pemoline, bupropion, amantadine, bromocriptine, modafinil 65
132. Behavioral & Psychotherapeutic treatment: Behavioral rehabilitation program- contingency contracts & token economy. CBT Group therapy Family therapy 70
133. Take home messages: Neuropsychiatric syndromes are common after TBI They can present in many different ways. They can significantly increase distress, disability, and health care utilization. Use biopsychosocial and multidisciplinary approach. Treat as many symptoms with as few medications as possible. Monitor systematically and longitudinally 71