Transcript of "Neuropsychiatric manifestations of head injury"
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 />
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 />
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 />
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 />
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 />
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 />
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 />
Contd…<br /><ul><li> Penetrating head injury. Missile wounds are most common cause.</li></ul>8<br />
(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 />
(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 />
(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 />
(Pathology- contd….)Neurobiological changes:<br /><ul><li> Abnormality in glutamate pathway.
(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 />
(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 />
(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 />
(Pathology- contd….)<br />Ascending biogenic amine:<br />19<br />Synaptic conc. Of biogenic amine neurotransmitter<br />Downregulation of biogenic amines<br />Depressive symptoms<br />
(Pathology- contd….)<br />Clinical evidences:<br /><ul><li>Circulating levels of catecholamine has significant correlation of TBI severity.
Serotonegic & noradrenergic metabolites in CSF.
Dysregulation of mesolimbic & mesocortical dopaminergic pathway give rise to manic & hypomanic syndromes.</li></ul>20<br />
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.
Psychotic disorder:</li></ul> - with delusion<br /> - with hallucination<br />CTP,8TH ed,page-390<br />26<br />
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)
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 />
CLINICAL FEATURES(contd..)<br />Post –traumatic delirium(PTD):<br /><ul><li>Increased risk in patients with TBI
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 />
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 />
If symptoms are severe it is particularly important to rule out NPH, SDH. Coexisting DAT.</li></ul>30<br />
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:
<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 />
One Year Cumulative Incidence of Mood Disorders After TBI<br />Jorge et al., 2004<br />34<br />
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 />
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 />
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 />
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 />
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 />
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
Patients developing schizophrenic-like psychosis over 15-20 years is 0.7-9.8%
May have epileptiform activity and temporal lobe lesions</li></ul>* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-327<br />41<br />
<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 />
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 />
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 />
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 />
Number of Postconcussive Syndrome:<br />* p=.05<br />All symptoms *<br />Depressive symptoms excluded<br />48<br />
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 />
Post traumatic epilepsy- 5% in closed & 30% in open TBI
Size & location of brain damage: frontal, temporal, dominant side worse.</li></ul>53<br />
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 />
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 />
Lab. Investigations contd….<br />Neuroimaging:<br /><ul><li>CT scan: Investigation of choice for hematoma.
MRI scan : Investigation of choice for non-hemorrhagic lesions.
Delayed MRI scan: Indicated after 2 weeks with persistent neurological deficit after a neurosurgical procedure if the previous CT scan is normal.
PET & SPECT : gives additional information regarding metabolic rates of cortical & subcortical structures.
Proton magnetic resonance spectroscopy(MRS): More accurate than conventional MRI
Diffuse tensor MRI: For Degree of diffuse axonal injury & white matter pathology</li></ul>59<br />
Lab. Investigations contd….<br />Electrophysiological studies:<br /><ul><li>Conventional EEG: In ICU for monitoring procedures & brain death diagnosis, localizing epileptic focus.
Video EEG or 24 hr ambulatory EEG: for unclear paroxysmal behavioral disturbances.
Quantitative EEG(QEEG): for slow wave abnormalities following TBI & post traumatic temporal lobe epilepsy.
Polysomnography: for diagnosing atypical sleep disturbance occurring after TBI.
Auditory evoked potentials: In detecting brain stem pathology.</li></ul>60<br />
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 />
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 />
<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 />
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 />
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 />
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 />
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 ed.page:747-768<br />Indian journal of Psychiatry<br />The American journal of Psychiatry<br /> Internet:<br /><ul><li> www. emedicine.com