Neuropsychiatric manifestations of head injury


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Neuropsychiatric manifestations of head injury

  1. 1. Neuropsychiatric aspects of HEAD INJURY<br />Speaker: Dr. Santanu Ghosh,<br /> Post Graduate student, Psychiatry.<br />Moderator: Dr. J.N. Das,<br />Asstt. Professor, Psychiatry.<br /> Assam Medical College, Dibrugarh.<br />1<br />
  2. 2. Outline of presentation:<br /> Introduction<br /> History<br /> Comparative Nosology<br />Epidemiology<br />Types of head injury<br />Pathophysiology<br /> Clinical features<br /> Prognosis<br />Outcome<br />Management<br /> Take home message<br /> Bibliography<br />2<br />
  3. 3. Introduction:<br />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.<br />3<br />
  4. 4. History:<br />Earliest written evidence of TBI found on Edwin Smith Papyrus 5000 years ago.<br /> The Hippocratic Corpus included treatise on head injury with thoughtful comments on skull #, delirium, seizure, coma.<br /> Adolf Mayer introduced the term ‘ traumatic insanity’<br />4<br />
  5. 5. Comparative Nosology:<br /> DSM-IV : Mental & behavioral problems due to traumatic brain injury.<br />ICD-10: Other conditions associated with mental & behavioral disorders—<br /> -Chapter: XIX: S06- Intracranial injury<br />5<br />
  6. 6. Epidemiology:<br />500,000 new cases of<br />TBIs occur in the US<br />each year.*<br />50,000 <br />Deaths<br />235,000<br />Hospitalizations<br /> 80%-mild, 10%-moderate,<br /> 10%- severe TBI<br />M:F=2-3:1<br />6<br />INCIDENCE: Closed TBI- 200/100,000 population<br /> Penetrating TBI- 12/100,ooo population<br />
  7. 7. Types of traumatic brain injury:<br /> The main categorization (Depending on the integrity of meninges)<br /><ul><li> Closed head injury: Motor vehicle injury is the most common cause.</li></ul>7<br />
  8. 8. Contd…<br /><ul><li> Penetrating head injury. Missile wounds are most common cause.</li></ul>8<br />
  9. 9. PATHOPHYSIOLOGY<br />9<br />
  10. 10. Neuropathological classification of TBI:<br />Focal lesions:<br /> Extracerebral hemorrhage: epidural,subdural,subarachnoid<br />Intracerbral hemorrhage<br /> Focal ischemic lesion<br />Diffuse lesions:<br />Diffuse axonal injury.<br />Diffuse ischemic damage. <br />10<br />
  11. 11. (Pathology- contd….)<br />Intracranial hematoma:<br />It is the most common cause of death & clinical deterioration. TBI hematomas are categorized as:<br /><ul><li> Epidural hematoma:</li></ul> - # of temporal bone.<br /> - Rupture of middle meningeal artery.<br /><ul><li> Subdural hematoma:</li></ul> - Rupture of bridging veins in subdural space.<br /><ul><li> Subarachnoid hematoma:</li></ul> - Rupture of blood vessels in posterior fossa stalk .<br />11<br />
  12. 12. (Pathology- contd….)Pathological consequences of TBI: <br /><ul><li> Primary brain injury: It is produced by contact & inertial forces that occur at the time of injury. It results in:</li></ul> Laceration to the sculp.<br /> Skull fracture.<br /> Intracranial hemorrhage.<br /> Contusions.<br /> Intracerebral hemorrhage.<br />Inertial loading consists of acceleration, deceleration, rotation.<br />12<br />
  13. 13. (Pathology- contd….)<br /><ul><li> 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:</li></ul> Brain damage secondary to ischemia.<br /> Brain swelling.<br /> Intracranial pressure.<br /> Infection.<br />13<br />
  14. 14. (Pathology- contd….)Neurobiological changes:<br /><ul><li> Abnormality in glutamate pathway.
  15. 15. Abnormality in cholinergic neuronal activity.
  16. 16. Abnormality in ascending biogenic amine pathway.</li></ul>14<br />
  17. 17. (Pathology- contd….)<br />Excitotoxic injury<br />Glutamate Pathway:<br />Na+ & cl- influx<br />Cellular Edema<br />Ca2+influx<br />Expression of early transcription factors, acute phase proteins, caspases, proteolytic enzymes<br />Neuronal apoptosis<br />15<br />
  18. 18. (Pathology- contd….)<br /> Clinical evidences:<br /> CSF finding of glutamate concentrations are significantly elevated for several days after TBI.<br /> Glutamate antagonists have shown beneficial effects in experimental models of TBI.<br />16<br />
  19. 19. (Pathology- contd….)<br />17<br />TBI<br /><ul><li> Cholinergic pathway:</li></ul>Pathological activation of basal forebrain nuclei<br />Blockade of Massive Ach release<br />
  20. 20. (Pathology- contd….)<br /> Clinical evidences:<br /> A reduction in cholinergic transmission in hippocampal & neocortical areas observed after TBI .<br /> Dysfunction of the septohippocampal cholinergic pathway is observed in experimental models which has significant role in posttraumatic cognitive & behavioral deficits.<br />18<br />
  21. 21. (Pathology- contd….)<br />Ascending biogenic amine:<br />19<br />Synaptic conc. Of biogenic amine neurotransmitter<br />Downregulation of biogenic amines<br />Depressive symptoms<br />
  22. 22. (Pathology- contd….)<br />Clinical evidences:<br /><ul><li>Circulating levels of catecholamine has significant correlation of TBI severity.
  23. 23. Serotonegic & noradrenergic metabolites in CSF.
  24. 24. Dysregulation of mesolimbic & mesocortical dopaminergic pathway give rise to manic & hypomanic syndromes.</li></ul>20<br />
  25. 25. Lobe Functions(Cerebral):<br />21<br />Parietal lobe<br />Dominant side: Non-dominant side:<br /> - Calculation - spatial orientation<br /> - Language - constructional skills<br /> - Planned movement<br /> - Appreciation of size, shape, weight, texture<br /> Frontal lobe:<br /> - Personality<br /> - Emotional response<br /> - Social behavior<br />
  26. 26. Contd…<br />22<br />Occipital lobe:<br /> - Analysis of vision<br />Temporal lobe<br /> Dominant side Non-dominant side<br /> -Auditory perception -Auditory perception<br /> -Speech, language -Music, tone sequence<br /> -Verbal memory -Non-verbal memory <br /> -Olfaction <br />
  27. 27. Neuropsychiatric Syndromes Associated With Neuroanatomical Lesions<br />Lateral orbital pre-frontal cortex<br />- Irritability - Impulsivity<br />- Mood lability - Mania<br />Anterior cingulate pre-frontal cortex<br />- Apathy - Akinetic mutism<br />Dorsolateral pre-frontal cortex<br />- Poor memory search - Poor set-shifting / maintenance<br />Temporal Lobe<br />- Memory impairment - Mood lability<br />- Psychosis - Aggression<br />Hypothalamus<br />- Sexual behavior - Aggression<br />23<br />
  28. 28. CLINICAL FEATURES:<br />24<br />
  29. 29. Behavioral syndrome after TBI(DSM-IV-TR) <br /><ul><li>Delirium
  30. 30. Amnestic disorder - Transient/ chronic.
  31. 31. Dementia.
  32. 32. Personality change – </li></ul> -Labile<br /> -Disinhibited<br /> -aggressive<br /> -apathetic<br /> -Paranoid<br /> -combined<br /> -unspecified<br />25<br />
  33. 33. CLINICAL FEATURES contd..<br /><ul><li>Mood disorder:</li></ul> - with depressive feature<br /> - with major depressive like episode<br /> - with manic feature<br /> - with mixed feature<br /><ul><li>Anxiety disorder:</li></ul> - with generalized anxiety<br /> - with panic attack<br /> - with obsessive-compulsive symptoms<br /><ul><li> Posttraumatic stress disorder.
  34. 34. Psychotic disorder:</li></ul> - with delusion<br /> - with hallucination<br />CTP,8TH ed,page-390<br />26<br />
  35. 35. CLINICAL FEATURES(contd..)<br /><ul><li>Acute behavioral consequences:</li></ul> It involves a period of loss of consciousness(brief concussion to coma). Following recovery amnesia develops which is classified as-<br /><ul><li> Post traumatic amnesia(PTA): Period of (injury+ following injury)
  36. 36. Retrograde amnesia (RA): Period between the last clearly recalled memory prior to the injury & the injury itself. Dense amnesia lasting seconds & minutes.</li></ul>27<br />
  37. 37. CLINICAL FEATURES(contd..)<br />Post –traumatic delirium(PTD):<br /><ul><li>Increased risk in patients with TBI
  38. 38. Associated with 10-65% mortality
  39. 39. Variable confusion behavioral symptoms, paranoia, delusional misinterpretation & hallucination.
  40. 40. Can lead to - self injurious behavior, decreased self management, caregiver management problems</li></ul>Synonyms of PTD: <br />acute confusional state, intensive care unit (ICU) psychosis, post-traumatic psychosis, metabolic encephalopathy, organic brain syndrome, sundowning, toxic encephalopathy<br />28<br />
  41. 41. Clinical feature contd…<br />Posttraumatic headache<br /> 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<br />29<br />
  42. 42. CLINICAL FEATURES(contd..)<br />Chronic behavioral consequences:<br /><ul><li>Cognitive impairment:
  43. 43. Associated with PTA lasting >24 hours.
  44. 44. Focal cognitive deficits- amnesia, slowing ,apathy, affective lability, executive difficulties.
  45. 45. Catastrophic reactions, emotional incontinence might occur.
  46. 46. If symptoms are severe it is particularly important to rule out NPH, SDH. Coexisting DAT.</li></ul>30<br />
  47. 47. CLINICAL FEATURES(contd..)<br /><ul><li>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:
  48. 48. Memory dysfunction.
  49. 49. Executive dysfunction.
  50. 50. Relatively preserved visuospatial, praxis & primary linguistic function.
  51. 51. May be severely apathetic & withdrawn , slow information processing.
  52. 52. TBI is associated with Alzheimer’s disease.
  53. 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. 54. Chronic subdural hematoma in elderly can lead to progressive dementia.</li></ul>31<br />
  55. 55. CLINICAL FEATURES(contd..)<br /><ul><li>Personality or behavioral changes:
  56. 56. Associated injury to orbitofrontal lobe or anterior temporal lobe.
  57. 57. Frontal lobe syndrome is characterized by disinhibition, impulsivity, irritability, aggressive outburst.
  58. 58. Pseudo- depressed personality syndrome: apathy, blunted affect.
  59. 59. Pseudo -psychopathic personality syndrome: disinhibition, egocentricity & sexual inappropriateness.</li></ul>32<br />
  60. 60. <ul><li>Depression / Apathy :</li></ul>Prevalence of major depression 44.3% *<br />Increased suicide risk<br />Clinical presentation may vary<br />May occur acutely or post-acutely<br />May be related to neuropsychological impairment and neuroanatomical lesions<br />Associated with increased functional impairment and post-concussive symptoms<br />Apathy alone - prevalence 10%<br />disinterest, disengagement, inertia, lack of motivation, lack of emotional responsivity<br />* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-327<br />33<br />
  61. 61. One Year Cumulative Incidence of Mood Disorders After TBI<br />Jorge et al., 2004<br />34<br />
  62. 62. Rates of Major Depression after TBI(N=559)<br />Bombardier, Fann et al, unpublished<br />Percent of cases (N=559)<br />Cumulative incidence (53%)<br />Prevalence<br />Incidence<br />Months after traumatic brain injury<br />
  63. 63. Impact of Depression on Outcomes<br />Depression after TBI contributes to: <br />increased aggressive behavior and anxiety (Tateno et al., 2003; Jorge et al., 2004; Fann et al., 1995) <br />significantly higher rates of suicidal plans (Kishi et al., 2001)<br />8 times more attempts (Silver et al., 2001)<br />3-4 times more completed suicide than in the general population and non-brain injured controls (Teasdale and Engberg, 2001) <br />36<br />
  64. 64. Impact of Depression on Outcomes<br />Depression after TBI contributes to: <br />Poorer cognitive functioning (Rappoport et al., 2005)<br />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)<br />Poorer recovery (Mooney et al., 2005)<br />More post-concussive symptoms (Fann et al., 1995; Rapoport et al., 2005)<br />37<br />
  65. 65. CLINICAL FEATURES(contd..)<br /><ul><li>Mania:</li></ul>Prevalence of Bipolar Disorder 4.2% *<br />High rate of irritability, “emotional incontinence”<br />May be associated with epileptiform activity<br />Potential interaction of genetic loading, right hemisphere lesions, and anterior subcortical atrophy<br />* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-327<br />38<br />
  66. 66. CLINICAL FEATURES(contd..) <br /><ul><li> Anxiety:</li></ul>Often comorbid with and prolongs course of depression<br />Posttraumatic Stress Disorder: Prevalence 14.1% *<br />Reexperience, Avoidance, Hyperarousal<br />> 1 month, causes significant distress or impairment<br />Possibly more prevalent in mild TBI<br />Panic Disorder: Prevalence 9.2% *<br />Generalized Anxiety Disorder: Prevalence 9.1% *<br />Obsessive-Compulsive Disorder: Prevalence 6.4% *<br />* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-327<br />39<br />
  67. 67. Clinical feature contd…<br /><ul><li>Aggression, Irritability, Impulsivity:</li></ul>Up to 70% within 1 year of TBI<br />May last over 10-15 years<br />Characteristic features:<br /><ul><li>Emotional lability
  68. 68. Pathologic laughing and crying
  69. 69. Rage and aggression
  70. 70. Altered sexual behavior
  71. 71. Lack of concern over consequences of actions
  72. 72. Social indifference
  73. 73. Inappropriate joking and punning
  74. 74. Superficiality of emotions</li></ul>40<br />
  75. 75. CLINICAL FEATURES(contd..)<br /><ul><li>Psychosis:
  76. 76. Immediate or latent onset
  77. 77. Symptoms may resemble schizophrenia: prevalence 0.7% *
  78. 78. Schizophrenics have increased risk of TBI.
  79. 79. Patients developing schizophrenic-like psychosis over 15-20 years is 0.7-9.8%
  80. 80. May have epileptiform activity and temporal lobe lesions</li></ul>* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-327<br />41<br />
  81. 81. <ul><li>Post Traumatic Stress Disorder(PTSD):</li></ul>Clinical feature contd…<br />PTSD Prevalence:11-27% *<br />Possibly more prevalent in mild TBI<br />Mediated by implicit memory or conditioned fear response in amnestic patients?<br />PTSD Phenomenology: **<br />Intrusive memories: 0-19%<br />Emotional reactivity: 96%<br />Nightmares, emotional reactivity .<br />* Warden 1997, Bryant 1995, Flesher 2001, Bombardier 2006<br />** Warden et al 1997, Bryant et al 2000<br />42<br />
  82. 82. Posttraumatic seizures:<br /> It frequently occur after moderate or severe TBI.<br />The incidence of late PTS is in the range of 5-18.9%. <br />Seizures are usually general or partial, and absence seizures are uncommon<br />Immediate seizures < 24 hours. <br /> Early seizures 2-7 days, and <br /> late seizures - after 7 days.<br />43<br />
  83. 83. Punch-drunk syndrome:<br />Boxers may develop diffuse injury to the cortex, basal ganglia.<br /> Extra pyramidal symptoms or a subcortical <br /> dementia.<br /> Pathology shows cerebral atrophy &<br /> neurofibrillary tangles.<br />44<br />
  84. 84. Sequelae in children:<br /> Less psychopathology after TBI <br /> due to increased brain plasticity.<br /> Recovery may continue for up to <br /> 5 years after injury.<br />Problems are generally behavioral<br /> in nature – aggression, delinquency,<br /> ADHD like syndrome.<br />45<br />
  85. 85. TBI-associated Disability<br />“Postconcussive Symptoms”<br />Cognitive<br />Physical: sensory and motor<br />Emotional<br />Vocational<br />Social<br />Family<br />46<br />
  86. 86. Postconcussive Syndrome:<br />Headache <br />Dizziness <br />Blurred Vision <br />Bothered by Noise <br />Bothered by Light <br />Loss of Temper Easily <br />Memory Difficulties <br />Fatigue <br />Trouble Concentrating <br />Irritability <br />Anxiety <br />Sleep Disturbance <br />47<br />
  87. 87. Number of Postconcussive Syndrome:<br />* p=.05<br />All symptoms *<br />Depressive symptoms excluded<br />48<br />
  88. 88.  Thursday, February 8, 2007<br />PRO FOOTBALL<br />Expert Ties Ex-Player's Suicide To Brain Damage From Football<br />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.<br />49<br />
  89. 89. PROGNOSIS<br />50<br />
  90. 90. Predictors:<br /> GCS score-<br /> - Mild: 13-15 <br /> - Moderate: 9-12 <br /> - Severe: 3-8<br />Loss of consciousness(LOC)- <br /> -Mild: LOC <30 min.<br /> - Moderate: LOC 30 min- 6 hrs<br /> - Severe: LOC >6 hrs.<br /> Galveston Orientation & Amnesia Test(GOAT)<br />Duration of PTA<br />51<br />
  91. 91. Prognosis contd….<br />Factors associated with increased psychiatric morbidity following TBI:<br /><ul><li>Increased duration of LOC.
  92. 92. Increased duration of PTA
  93. 93. Increased duration of PTD
  94. 94. Increased age, arteriosclerosis
  95. 95. Increased area of damage
  96. 96. Increased neurological sequelae
  97. 97. Dominant or bilateral involvement.</li></ul>52<br />
  98. 98. Prognosis contd….<br />Factors influencing psychiatric disability:<br /><ul><li> Mental constitution- genetic vulnerability, temperament( risk in histrionic, hypochondriacal & dependent personality)
  99. 99. Emotional impact of injury
  100. 100. Iatrogenic factors
  101. 101. Home & social environment
  102. 102. Compensation & litigation issues
  103. 103. Post traumatic epilepsy- 5% in closed & 30% in open TBI
  104. 104. Size & location of brain damage: frontal, temporal, dominant side worse.</li></ul>53<br />
  105. 105. Outcome:<br /> Death<br /> Persistent vegetative state<br /> Severe disability(conscious but dependent for daily activities)<br />Moderate disability(disabled but living independently)<br /> Good recovery.<br />54<br />
  106. 106. MANAGEMENT:<br />ASSESMENT<br />TREATEMENT<br />55<br />
  107. 107. Neuropsychiatric History<br />Psychiatric symptoms may not fit DSM-IV criteria<br />Focus on functional impairment <br />Document and rate symptoms<br />Explore circumstances of trauma<br />LOC, PTA, hospitalization, medical complications<br />Subtle symptoms - may fail to associate with trauma<br />How has life changed since TBI?<br />Thorough review of medical and psychiatric records.<br />Talk with family, friends, caregivers<br />Assess level of care and supervision available<br />Assess rehabilitation needs and progress<br />56<br />
  108. 108. Laboratory investigations:<br /> Serum biochemistry<br /> Neuroimaging<br />Electrophysiological studies<br />57<br />
  109. 109. Lab. Investigations contd….<br />Serum biochemistry:<br /><ul><li> Neuronal proteins: neuron specific enolase, CPK-BB
  110. 110. Glial proteins: Myelin basic protein, Syneptophysin-100B
  111. 111. Neuroendocrine assessment:</li></ul> - Growth hormone.<br /> - Thyroid profile.<br /><ul><li>Serum electrolytes: Na+ , K+ , Mg2+ , Cl- </li></ul>58<br />
  112. 112. Lab. Investigations contd….<br />Neuroimaging:<br /><ul><li>CT scan: Investigation of choice for hematoma.
  113. 113. MRI scan : Investigation of choice for non-hemorrhagic lesions.
  114. 114. Delayed MRI scan: Indicated after 2 weeks with persistent neurological deficit after a neurosurgical procedure if the previous CT scan is normal.
  115. 115. PET & SPECT : gives additional information regarding metabolic rates of cortical & subcortical structures.
  116. 116. Proton magnetic resonance spectroscopy(MRS): More accurate than conventional MRI
  117. 117. Diffuse tensor MRI: For Degree of diffuse axonal injury & white matter pathology</li></ul>59<br />
  118. 118. Lab. Investigations contd….<br />Electrophysiological studies:<br /><ul><li>Conventional EEG: In ICU for monitoring procedures & brain death diagnosis, localizing epileptic focus.
  119. 119. Video EEG or 24 hr ambulatory EEG: for unclear paroxysmal behavioral disturbances.
  120. 120. Quantitative EEG(QEEG): for slow wave abnormalities following TBI & post traumatic temporal lobe epilepsy.
  121. 121. Polysomnography: for diagnosing atypical sleep disturbance occurring after TBI.
  122. 122. Auditory evoked potentials: In detecting brain stem pathology.</li></ul>60<br />
  123. 123. GOLDEN RULE:<br />START LOW, GO SLOW<br />May still need maximum doses<br />Therapeutic onset may be latent<br />Medications may lower seizure threshold<br />Medications may slow cognitive recovery<br />Monitor and document outcomes<br />61<br />
  124. 124. Neuropsychiatric Treatment:<br />Use Biopsychosocial Model<br />Treat maximum signs and symptoms with fewest possible medications <br />TBI patients more sensitive to side effects<br />62<br />
  125. 125. <ul><li>Delirium</li></ul>Identify and correct underlying cause<br />e.g., seizures, hydrocephalus, hemorrhage, drug side effect or interactions, endocrine (hypothalamic, pituitary dysfunction),electrolyte imbalance.<br />Pharmacologic management<br />Antipsychotics<br />haloperidol, droperidol, risperidone, olanzapine, quetiapine<br />Benzodiazepines (combined with antipsychotics)<br />Lorazepam<br />Avoid polypharmacy<br />Medical management<br />Frequent monitoring of safety, vital signs, mental status and physical exams<br />Maintain proper nutritional, electrolyte, and fluid balance<br />63<br />
  126. 126. Treatment contd… Dementia:<br />behavioural modification<br /> cognitive rehabilitation<br />psychotropic medication for specific syndromes or symptoms<br />Piracetam<br />Donepezil<br /> family or network intervention<br /> social services<br /> medical support in legal proceedings. <br />64<br />
  127. 127. Treatment contd… Depression / Apathy<br />Selective serotonin re-uptake inhibitors (SSRIs)<br />- sertraline - paroxetine - fluoxetine <br />- citalopram - escitalopram<br />venlafaxine, duloxetine (may help with pain)<br />bupropion (may decrease seizure threshold)<br />nefazedone (may be too sedating, liver toxicity)<br />mirtazapine (may be too sedating)<br />Tricyclics: nortriptyline, desipramine<br />methylphenidate, dextroamphetamine <br />Electroconvulsive Therapy – consider less frequent, nondominantunilateral<br />Apathy: Dopaminergic agents - methylpyhenidate, pemoline, bupropion, amantadine, bromocriptine, modafinil<br />65<br />
  128. 128. Treatment contd… Mania<br />Acute<br />Benzodiazepines<br />Antipsychotics<br />olanzapine, risperidone, clozapine, others<br />Anticonvulsants<br />valproate <br />Electroconvulsive Therapy<br />Chronic<br />valproate <br />carbamazepine<br />lamotrigine<br />lithium carbonate (neurotoxicity)<br />gabapentin, topiramate (adjunctive treatments)<br />66<br />
  129. 129. <ul><li>Anxiety</li></ul>Benzodiazepines: <br />e.g., clonazepam, lorazepam, alprazolam<br />Watch for cognitive impairment, dependence<br />Buspirone (for Generalized Anxiety Disorder)<br />Antidepressants<br />SSRIs, venlafaxine, nefazedone, mirtazapine, TCAs<br />Beta-blockers, verapamil, clonidine<br />Anticonvulsants: valproate & gabapentin have some anxiolyticeffects<br />Psychosocial<br />Individual, couples, family, group<br />67<br />
  130. 130. <ul><li>Psychosis</li></ul>Antipsychotics<br />Typical: e.g. haloperidol, chlorpromazine<br />Atypical: e.g., risperidone olanzapine, quetiapine, ziprasidone, aripiprazole, clozapine.<br />Start with low doses<br />TBI pts have high risk of anticholinergic and extrapyramidal side effects<br />May cause QTc prolongation<br />Use sparingly - may impede neuronal recovery acutely (from animal data)<br />68<br />
  131. 131. <ul><li>Aggression, Agitation, Impulsivity</li></ul>Acute<br />Antipsychotics<br />Benzodiazepines<br />Chronic<br /> *Beta-blockers (e.g. propranolol, pindolol, nadolol)<br /> *valproate, Carbamazepine, gabapentin<br /> Lithium (narrow therapeutic window)<br /> buspirone<br /> Serotonergic antidepressants (e.g., SSRIs, trazodone)<br /> Antipsychotics (esp. second and third generation)<br /> amantadine, bromocriptine, bupropion<br /> clonidine, methylphenidate, naltrexone, estrogen<br />* Has most evidence for efficacy<br />69<br />
  132. 132. Behavioral & Psychotherapeutic treatment:<br /> Behavioral rehabilitation program- contingency contracts & token economy. <br /> CBT<br /> Group therapy<br /> Family therapy<br />70<br />
  133. 133. Take home messages:<br />Neuropsychiatric syndromes are common after TBI<br />They can present in many different ways.<br />They can significantly increase distress, disability, and health care utilization.<br />Use biopsychosocial and multidisciplinary approach.<br />Treat as many symptoms with as few medications as possible.<br />Monitor systematically and longitudinally<br />71<br />
  134. 134. Bibliography:<br />CTP- Sadock & Kaplan, 8th edition, Page: 390-403.<br /> Oxford Handbook of Psychiatry page: 154-157.<br /> Principles of Neurology-Adam & Victor 8th<br />Indian journal of Psychiatry<br />The American journal of Psychiatry<br /> Internet:<br /><ul><li> www.
  135. 135.
  136. 136.
  137. 137.
  138. 138.
  139. 139.</li></ul>72<br />
  140. 140. 73<br />THANK YOU<br />
  141. 141. Cognitive Impairment<br />May accelerate recovery May impede recovery<br />amphetamine haloperidol<br />Norepinephrine (TCAs) phenothiazines<br />gangliosides prazosin<br />methylphenidate, dextroamphetamine clonidine<br />amantadine phenoxybenzamine<br />L-dopa/ carbidopa GABA<br />bromocriptine benzodiazepines<br />pergolide phenytoin<br />physostigmine phenobarbital<br />donepezil idazoxan<br />selegiline<br />apomorphine <br />caffeine <br />phenylpropanolamine<br />Naltrexone<br />atomoxetine <br />74<br />