Neuropsychiatric manifestations of head injury
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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.
Neuropsychiatric manifestations of head injury
- 1. Neuropsychiatric aspects of HEAD INJURYSpeaker: 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 NosologyEpidemiologyTypes of head injuryPathophysiology Clinical features PrognosisOutcomeManagement Take home message Bibliography2
- 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 injury5
- 6. Epidemiology:500,000 new cases ofTBIs occur in the USeach year.*50,000 Deaths235,000Hospitalizations 80%-mild, 10%-moderate, 10%- severe TBIM:F=2-3:16INCIDENCE: Closed TBI- 200/100,000 population Penetrating TBI- 12/100,ooo population
- 7. Types of traumatic brain injury: The main categorization (Depending on the integrity of meninges) Closed head injury: Motor vehicle injury is the most common cause.7
- 8. Contd… Penetrating head injury. Missile wounds are most common cause.8
- 10. Neuropathological classification of TBI:Focal lesions: Extracerebral hemorrhage: epidural,subdural,subarachnoidIntracerbral hemorrhage Focal ischemic lesionDiffuse lesions:Diffuse axonal injury.Diffuse ischemic damage. 10
- 11. (Pathology- contd….)Intracranial hematoma:It is the most common cause of death & clinical deterioration. TBI hematomas are categorized as: Epidural hematoma: - # of temporal bone. - Rupture of middle meningeal artery. Subdural hematoma: - Rupture of bridging veins in subdural space. Subarachnoid hematoma: - Rupture of blood vessels in posterior fossa stalk .11
- 12. (Pathology- contd….)Pathological consequences of TBI: Primary brain injury: It is produced by contact & inertial forces that occur at the time of injury. It results in: Laceration to the sculp. Skull fracture. Intracranial hemorrhage. Contusions. Intracerebral hemorrhage.Inertial loading consists of acceleration, deceleration, rotation.12
- 13. (Pathology- contd….) Secondary Brain injury: Produced by pathological process that are initiated at the moment of injury but span a variable period after the traumatic episodes. These are: Brain damage secondary to ischemia. Brain swelling. Intracranial pressure. Infection.13
- 14. (Pathology- contd….)Neurobiological changes: Abnormality in glutamate pathway.
- 15. Abnormality in cholinergic neuronal activity.
- 16. Abnormality in ascending biogenic amine pathway.14
- 17. (Pathology- contd….)Excitotoxic injuryGlutamate Pathway:Na+ & cl- influxCellular EdemaCa2+influxExpression of early transcription factors, acute phase proteins, caspases, proteolytic enzymesNeuronal apoptosis15
- 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
- 19. (Pathology- contd….)17TBI Cholinergic pathway:Pathological activation of basal forebrain nucleiBlockade of Massive Ach release
- 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:19Synaptic conc. Of biogenic amine neurotransmitterDownregulation of biogenic aminesDepressive symptoms
- 22. (Pathology- contd….)Clinical evidences:Circulating levels of catecholamine has significant correlation of TBI severity.
- 24. Dysregulation of mesolimbic & mesocortical dopaminergic pathway give rise to manic & hypomanic syndromes.20
- 25. Lobe Functions(Cerebral):21Parietal lobeDominant 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…22Occipital lobe: - Analysis of visionTemporal lobe Dominant side Non-dominant side -Auditory perception -Auditory perception -Speech, language -Music, tone sequence -Verbal memory -Non-verbal memory -Olfaction
- 27. Neuropsychiatric Syndromes Associated With Neuroanatomical LesionsLateral orbital pre-frontal cortex- Irritability - Impulsivity- Mood lability - ManiaAnterior cingulate pre-frontal cortex- Apathy - Akinetic mutismDorsolateral pre-frontal cortex- Poor memory search - Poor set-shifting / maintenanceTemporal Lobe- Memory impairment - Mood lability- Psychosis - AggressionHypothalamus- Sexual behavior - Aggression23
- 29. Behavioral syndrome after TBI(DSM-IV-TR) Delirium
- 30. Amnestic disorder - Transient/ chronic.
- 31. Dementia.
- 32. Personality change – -Labile -Disinhibited -aggressive -apathetic -Paranoid -combined -unspecified25
- 33. CLINICAL FEATURES contd..Mood disorder: - with depressive feature - with major depressive like episode - with manic feature - with mixed featureAnxiety disorder: - with generalized anxiety - with panic attack - with obsessive-compulsive symptoms Posttraumatic stress disorder.
- 34. Psychotic disorder: - with delusion - with hallucinationCTP,8TH ed,page-39026
- 35. CLINICAL FEATURES(contd..)Acute behavioral consequences: It involves a period of loss of consciousness(brief concussion to coma). Following recovery amnesia develops which is classified as- Post traumatic amnesia(PTA): Period of (injury+ following injury)
- 36. Retrograde amnesia (RA): Period between the last clearly recalled memory prior to the injury & the injury itself. Dense amnesia lasting seconds & minutes.27
- 37. CLINICAL FEATURES(contd..)Post –traumatic delirium(PTD):Increased risk in patients with TBI
- 38. Associated with 10-65% mortality
- 39. Variable confusion behavioral symptoms, paranoia, delusional misinterpretation & hallucination.
- 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 encephalopathy28
- 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 months29
- 42. CLINICAL FEATURES(contd..)Chronic behavioral consequences:Cognitive impairment:
- 43. Associated with PTA lasting >24 hours.
- 44. Focal cognitive deficits- amnesia, slowing ,apathy, affective lability, executive difficulties.
- 45. Catastrophic reactions, emotional incontinence might occur.
- 46. If symptoms are severe it is particularly important to rule out NPH, SDH. Coexisting DAT.30
- 47. CLINICAL FEATURES(contd..)Dementia: It is a syndrome in which there is impairment of memory & at least one other cognitive domain in the absence of an alternation of consciousness. It is characterized by:
- 50. Relatively preserved visuospatial, praxis & primary linguistic function.
- 51. May be severely apathetic & withdrawn , slow information processing.
- 52. TBI is associated with Alzheimer’s disease.
- 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
- 55. CLINICAL FEATURES(contd..)Personality or behavioral changes:
- 56. Associated injury to orbitofrontal lobe or anterior temporal lobe.
- 57. Frontal lobe syndrome is characterized by disinhibition, impulsivity, irritability, aggressive outburst.
- 58. Pseudo- depressed personality syndrome: apathy, blunted affect.
- 59. Pseudo -psychopathic personality syndrome: disinhibition, egocentricity & sexual inappropriateness.32
- 60. Depression / Apathy :Prevalence of major depression 44.3% *Increased suicide riskClinical presentation may varyMay occur acutely or post-acutelyMay be related to neuropsychological impairment and neuroanatomical lesionsAssociated with increased functional impairment and post-concussive symptomsApathy alone - prevalence 10%disinterest, disengagement, inertia, lack of motivation, lack of emotional responsivity* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-32733
- 61. One Year Cumulative Incidence of Mood Disorders After TBIJorge et al., 200434
- 62. Rates of Major Depression after TBI(N=559)Bombardier, Fann et al, unpublishedPercent of cases (N=559)Cumulative incidence (53%)PrevalenceIncidenceMonths after traumatic brain injury
- 63. Impact of Depression on OutcomesDepression 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 OutcomesDepression 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
- 65. CLINICAL FEATURES(contd..)Mania:Prevalence of Bipolar Disorder 4.2% *High rate of irritability, “emotional incontinence”May be associated with epileptiform activityPotential interaction of genetic loading, right hemisphere lesions, and anterior subcortical atrophy* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-32738
- 66. CLINICAL FEATURES(contd..) Anxiety:Often comorbid with and prolongs course of depressionPosttraumatic Stress Disorder: Prevalence 14.1% *Reexperience, Avoidance, Hyperarousal> 1 month, causes significant distress or impairmentPossibly more prevalent in mild TBIPanic Disorder: Prevalence 9.2% *Generalized Anxiety Disorder: Prevalence 9.1% *Obsessive-Compulsive Disorder: Prevalence 6.4% ** van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-32739
- 67. Clinical feature contd…Aggression, Irritability, Impulsivity:Up to 70% within 1 year of TBIMay last over 10-15 yearsCharacteristic features:Emotional lability
- 68. Pathologic laughing and crying
- 71. Lack of concern over consequences of actions
- 73. Inappropriate joking and punning
- 76. Immediate or latent onset
- 77. Symptoms may resemble schizophrenia: prevalence 0.7% *
- 78. Schizophrenics have increased risk of TBI.
- 79. Patients developing schizophrenic-like psychosis over 15-20 years is 0.7-9.8%
- 80. May have epileptiform activity and temporal lobe lesions* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-32741
- 81. Post Traumatic Stress Disorder(PTSD):Clinical feature contd…PTSD Prevalence:11-27% *Possibly more prevalent in mild TBIMediated by implicit memory or conditioned fear response in amnestic patients?PTSD Phenomenology: **Intrusive memories: 0-19%Emotional reactivity: 96%Nightmares, emotional reactivity .* Warden 1997, Bryant 1995, Flesher 2001, Bombardier 2006** Warden et al 1997, Bryant et al 200042
- 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 uncommonImmediate 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
- 85. TBI-associated Disability“Postconcussive Symptoms”CognitivePhysical: sensory and motorEmotionalVocationalSocialFamily46
- 86. Postconcussive Syndrome:Headache Dizziness Blurred Vision Bothered by Noise Bothered by Light Loss of Temper Easily Memory Difficulties Fatigue Trouble Concentrating Irritability Anxiety Sleep Disturbance 47
- 87. Number of Postconcussive Syndrome:* p=.05All symptoms *Depressive symptoms excluded48
- 88. Thursday, February 8, 2007PRO FOOTBALLExpert Ties Ex-Player's Suicide To Brain Damage From FootballSince 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
- 89. PROGNOSIS50
- 90. Predictors: GCS score- - Mild: 13-15 - Moderate: 9-12 - Severe: 3-8Loss of consciousness(LOC)- -Mild: LOC <30 min. - Moderate: LOC 30 min- 6 hrs - Severe: LOC >6 hrs. Galveston Orientation & Amnesia Test(GOAT)Duration of PTA51
- 91. Prognosis contd….Factors associated with increased psychiatric morbidity following TBI:Increased duration of LOC.
- 92. Increased duration of PTA
- 93. Increased duration of PTD
- 94. Increased age, arteriosclerosis
- 95. Increased area of damage
- 96. Increased neurological sequelae
- 97. Dominant or bilateral involvement.52
- 98. Prognosis contd….Factors influencing psychiatric disability: Mental constitution- genetic vulnerability, temperament( risk in histrionic, hypochondriacal & dependent personality)
- 99. Emotional impact of injury
- 100. Iatrogenic factors
- 101. Home & social environment
- 102. Compensation & litigation issues
- 103. Post traumatic epilepsy- 5% in closed & 30% in open TBI
- 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 HistoryPsychiatric symptoms may not fit DSM-IV criteriaFocus on functional impairment Document and rate symptomsExplore circumstances of traumaLOC, PTA, hospitalization, medical complicationsSubtle symptoms - may fail to associate with traumaHow has life changed since TBI?Thorough review of medical and psychiatric records.Talk with family, friends, caregiversAssess level of care and supervision availableAssess rehabilitation needs and progress56
- 108. Laboratory investigations: Serum biochemistry NeuroimagingElectrophysiological studies57
- 109. Lab. Investigations contd….Serum biochemistry: Neuronal proteins: neuron specific enolase, CPK-BB
- 110. Glial proteins: Myelin basic protein, Syneptophysin-100B
- 111. Neuroendocrine assessment: - Growth hormone. - Thyroid profile.Serum electrolytes: Na+ , K+ , Mg2+ , Cl- 58
- 112. Lab. Investigations contd….Neuroimaging:CT scan: Investigation of choice for hematoma.
- 113. MRI scan : Investigation of choice for non-hemorrhagic lesions.
- 114. Delayed MRI scan: Indicated after 2 weeks with persistent neurological deficit after a neurosurgical procedure if the previous CT scan is normal.
- 115. PET & SPECT : gives additional information regarding metabolic rates of cortical & subcortical structures.
- 116. Proton magnetic resonance spectroscopy(MRS): More accurate than conventional MRI
- 117. Diffuse tensor MRI: For Degree of diffuse axonal injury & white matter pathology59
- 118. Lab. Investigations contd….Electrophysiological studies:Conventional EEG: In ICU for monitoring procedures & brain death diagnosis, localizing epileptic focus.
- 119. Video EEG or 24 hr ambulatory EEG: for unclear paroxysmal behavioral disturbances.
- 120. Quantitative EEG(QEEG): for slow wave abnormalities following TBI & post traumatic temporal lobe epilepsy.
- 121. Polysomnography: for diagnosing atypical sleep disturbance occurring after TBI.
- 122. Auditory evoked potentials: In detecting brain stem pathology.60
- 123. GOLDEN RULE:START LOW, GO SLOWMay still need maximum dosesTherapeutic onset may be latentMedications may lower seizure thresholdMedications may slow cognitive recoveryMonitor and document outcomes61
- 124. Neuropsychiatric Treatment:Use Biopsychosocial ModelTreat maximum signs and symptoms with fewest possible medications TBI patients more sensitive to side effects62
- 125. DeliriumIdentify and correct underlying causee.g., seizures, hydrocephalus, hemorrhage, drug side effect or interactions, endocrine (hypothalamic, pituitary dysfunction),electrolyte imbalance.Pharmacologic managementAntipsychoticshaloperidol, droperidol, risperidone, olanzapine, quetiapineBenzodiazepines (combined with antipsychotics)LorazepamAvoid polypharmacyMedical managementFrequent monitoring of safety, vital signs, mental status and physical examsMaintain proper nutritional, electrolyte, and fluid balance63
- 126. Treatment contd… Dementia:behavioural modification cognitive rehabilitationpsychotropic medication for specific syndromes or symptomsPiracetamDonepezil family or network intervention social services medical support in legal proceedings. 64
- 127. Treatment contd… Depression / ApathySelective serotonin re-uptake inhibitors (SSRIs)- sertraline - paroxetine - fluoxetine - citalopram - escitalopramvenlafaxine, duloxetine (may help with pain)bupropion (may decrease seizure threshold)nefazedone (may be too sedating, liver toxicity)mirtazapine (may be too sedating)Tricyclics: nortriptyline, desipraminemethylphenidate, dextroamphetamine Electroconvulsive Therapy – consider less frequent, nondominantunilateralApathy: Dopaminergic agents - methylpyhenidate, pemoline, bupropion, amantadine, bromocriptine, modafinil65
- 128. Treatment contd… ManiaAcuteBenzodiazepinesAntipsychoticsolanzapine, risperidone, clozapine, othersAnticonvulsantsvalproate Electroconvulsive TherapyChronicvalproate carbamazepinelamotriginelithium carbonate (neurotoxicity)gabapentin, topiramate (adjunctive treatments)66
- 129. AnxietyBenzodiazepines: e.g., clonazepam, lorazepam, alprazolamWatch for cognitive impairment, dependenceBuspirone (for Generalized Anxiety Disorder)AntidepressantsSSRIs, venlafaxine, nefazedone, mirtazapine, TCAsBeta-blockers, verapamil, clonidineAnticonvulsants: valproate & gabapentin have some anxiolyticeffectsPsychosocialIndividual, couples, family, group67
- 130. PsychosisAntipsychoticsTypical: e.g. haloperidol, chlorpromazineAtypical: e.g., risperidone olanzapine, quetiapine, ziprasidone, aripiprazole, clozapine.Start with low dosesTBI pts have high risk of anticholinergic and extrapyramidal side effectsMay cause QTc prolongationUse sparingly - may impede neuronal recovery acutely (from animal data)68
- 131. Aggression, Agitation, ImpulsivityAcuteAntipsychoticsBenzodiazepinesChronic *Beta-blockers (e.g. propranolol, pindolol, nadolol) *valproate, Carbamazepine, gabapentin Lithium (narrow therapeutic window) buspirone Serotonergic antidepressants (e.g., SSRIs, trazodone) Antipsychotics (esp. second and third generation) amantadine, bromocriptine, bupropion clonidine, methylphenidate, naltrexone, estrogen* Has most evidence for efficacy69
- 132. Behavioral & Psychotherapeutic treatment: Behavioral rehabilitation program- contingency contracts & token economy. CBT Group therapy Family therapy70
- 133. Take home messages:Neuropsychiatric syndromes are common after TBIThey 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 longitudinally71
- 134. Bibliography:CTP- Sadock & Kaplan, 8th edition, Page: 390-403. Oxford Handbook of Psychiatry page: 154-157. Principles of Neurology-Adam & Victor 8th ed.page:747-768Indian journal of PsychiatryThe American journal of Psychiatry Internet: www. emedicine.com
- 135. www.medspace.com
- 136. www.braininjury.com
- 140. 73THANK YOU
- 141. Cognitive ImpairmentMay accelerate recovery May impede recoveryamphetamine haloperidolNorepinephrine (TCAs) phenothiazinesgangliosides prazosinmethylphenidate, dextroamphetamine clonidineamantadine phenoxybenzamineL-dopa/ carbidopa GABAbromocriptine benzodiazepinespergolide phenytoinphysostigmine phenobarbitaldonepezil idazoxanselegilineapomorphine caffeine phenylpropanolamineNaltrexoneatomoxetine 74