Neuropsychiatric manifestations of head injury

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.
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Outline of presentation:
Introduction
History
Comparative Nosology
Epidemiology
Types of head injury
Pathophysiology
Clinical features
Prognosis
Outcome
Management
Take home message
Bibliography
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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.
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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’
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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
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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
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INCIDENCE: Closed TBI- 200/100,000 population
Penetrating TBI- 12/100,ooo population

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.
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Contd…
Penetrating head injury. Missile wounds are most common cause.
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PATHOPHYSIOLOGY
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Neuropathological classification of TBI:
Focal lesions:
Extracerebral hemorrhage: epidural,subdural,subarachnoid
Intracerbral hemorrhage
Focal ischemic lesion
Diffuse lesions:
Diffuse axonal injury.
Diffuse ischemic damage.
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(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 .
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(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.
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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.
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(Pathology- contd….)Neurobiological changes:
Abnormality in glutamate pathway.
Abnormality in cholinergic neuronal activity.
Abnormality in ascending biogenic amine pathway.
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Excitotoxic injury
Glutamate Pathway:
Na+ & cl- influx
Cellular Edema
Ca2+influx
Expression of early transcription factors, acute phase proteins, caspases, proteolytic enzymes
Neuronal apoptosis
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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.
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TBI
Cholinergic pathway:
Pathological activation of basal forebrain nuclei
Blockade of Massive Ach release

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.
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Ascending biogenic amine:
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Synaptic conc. Of biogenic amine neurotransmitter
Downregulation of biogenic amines
Depressive symptoms

Clinical evidences:
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.
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Lobe Functions(Cerebral):
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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

Contd…
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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

Neuropsychiatric Syndromes Associated With Neuroanatomical Lesions
Lateral orbital pre-frontal cortex
- Irritability - Impulsivity
- Mood lability - Mania
Anterior cingulate pre-frontal cortex
- Apathy - Akinetic mutism
Dorsolateral pre-frontal cortex
- Poor memory search - Poor set-shifting / maintenance
Temporal Lobe
- Memory impairment - Mood lability
- Psychosis - Aggression
Hypothalamus
- Sexual behavior - Aggression
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CLINICAL FEATURES:
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Behavioral syndrome after TBI(DSM-IV-TR)
Delirium
Amnestic disorder - Transient/ chronic.
Dementia.
Personality change –
-Labile
-Disinhibited
-aggressive
-apathetic
-Paranoid
-combined
-unspecified
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CLINICAL FEATURES contd..
Mood disorder:
- with depressive feature
- with major depressive like episode
- with manic feature
- with mixed feature
Anxiety disorder:
- with generalized anxiety
- with panic attack
- with obsessive-compulsive symptoms
Posttraumatic stress disorder.
Psychotic disorder:
- with delusion
- with hallucination
CTP,8TH ed,page-390
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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)
Retrograde amnesia (RA): Period between the last clearly recalled memory prior to the injury & the injury itself. Dense amnesia lasting seconds & minutes.
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Post –traumatic delirium(PTD):
Increased risk in patients with TBI
Associated with 10-65% mortality
Variable confusion behavioral symptoms, paranoia, delusional misinterpretation & hallucination.
Can lead to - self injurious behavior, decreased self management, caregiver management problems
Synonyms of PTD:
acute confusional state, intensive care unit (ICU) psychosis, post-traumatic psychosis, metabolic encephalopathy, organic brain syndrome, sundowning, toxic encephalopathy
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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
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Chronic behavioral consequences:
Cognitive impairment:
Associated with PTA lasting >24 hours.
Focal cognitive deficits- amnesia, slowing ,apathy, affective lability, executive difficulties.
Catastrophic reactions, emotional incontinence might occur.
If symptoms are severe it is particularly important to rule out NPH, SDH. Coexisting DAT.
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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:
Memory dysfunction.
Executive dysfunction.
Relatively preserved visuospatial, praxis & primary linguistic function.
May be severely apathetic & withdrawn , slow information processing.
TBI is associated with Alzheimer’s disease.
TBI is associated with expression of amyloid precursor protein, oxidative stress & deposition of amyloid beta peptide that lead to the onset of dementia.
Chronic subdural hematoma in elderly can lead to progressive dementia.
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Personality or behavioral changes:
Associated injury to orbitofrontal lobe or anterior temporal lobe.
Frontal lobe syndrome is characterized by disinhibition, impulsivity, irritability, aggressive outburst.
Pseudo- depressed personality syndrome: apathy, blunted affect.
Pseudo -psychopathic personality syndrome: disinhibition, egocentricity & sexual inappropriateness.
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Depression / Apathy :
Prevalence of major depression 44.3% *
Increased suicide risk
Clinical presentation may vary
May occur acutely or post-acutely
May be related to neuropsychological impairment and neuroanatomical lesions
Associated with increased functional impairment and post-concussive symptoms
Apathy alone - prevalence 10%
disinterest, disengagement, inertia, lack of motivation, lack of emotional responsivity
* van Reekum et al. J Neuropsychiatry ClinNeurosci 2000;12:316-327
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One Year Cumulative Incidence of Mood Disorders After TBI
Jorge et al., 2004
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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

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)
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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)
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Mania:
Prevalence of Bipolar Disorder 4.2% *
High rate of irritability, “emotional incontinence”
May be associated with epileptiform activity
Potential interaction of genetic loading, right hemisphere lesions, and anterior subcortical atrophy
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Anxiety:
Often comorbid with and prolongs course of depression
Posttraumatic Stress Disorder: Prevalence 14.1% *
Reexperience, Avoidance, Hyperarousal
> 1 month, causes significant distress or impairment
Possibly more prevalent in mild TBI
Panic Disorder: Prevalence 9.2% *
Generalized Anxiety Disorder: Prevalence 9.1% *
Obsessive-Compulsive Disorder: Prevalence 6.4% *
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Aggression, Irritability, Impulsivity:
Up to 70% within 1 year of TBI
May last over 10-15 years
Characteristic features:
Emotional lability
Pathologic laughing and crying
Rage and aggression
Altered sexual behavior
Lack of concern over consequences of actions
Social indifference
Inappropriate joking and punning
Superficiality of emotions
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Psychosis:
Immediate or latent onset
Symptoms may resemble schizophrenia: prevalence 0.7% *
Schizophrenics have increased risk of TBI.
Patients developing schizophrenic-like psychosis over 15-20 years is 0.7-9.8%
May have epileptiform activity and temporal lobe lesions
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Post Traumatic Stress Disorder(PTSD):
PTSD Prevalence:11-27% *
Possibly more prevalent in mild TBI
Mediated 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 2000
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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.
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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.
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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.
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TBI-associated Disability
“Postconcussive Symptoms”
Cognitive
Physical: sensory and motor
Emotional
Vocational
Social
Family
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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
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Number of Postconcussive Syndrome:
* p=.05
All symptoms *
Depressive symptoms excluded
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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.
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PROGNOSIS
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Predictors:
GCS score-
- Mild: 13-15
- Moderate: 9-12
- Severe: 3-8
Loss of consciousness(LOC)-
-Mild: LOC <30 min.
- Moderate: LOC 30 min- 6 hrs
- Severe: LOC >6 hrs.
Galveston Orientation & Amnesia Test(GOAT)
Duration of PTA
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Prognosis contd….
Factors associated with increased psychiatric morbidity following TBI:
Increased duration of LOC.
Increased duration of PTA
Increased duration of PTD
Increased age, arteriosclerosis
Increased area of damage
Increased neurological sequelae
Dominant or bilateral involvement.
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Prognosis contd….
Factors influencing psychiatric disability:
Mental constitution- genetic vulnerability, temperament( risk in histrionic, hypochondriacal & dependent personality)
Emotional impact of injury
Iatrogenic factors
Home & social environment
Compensation & litigation issues
Post traumatic epilepsy- 5% in closed & 30% in open TBI
Size & location of brain damage: frontal, temporal, dominant side worse.
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Outcome:
Death
Persistent vegetative state
Severe disability(conscious but dependent for daily activities)
Moderate disability(disabled but living independently)
Good recovery.
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MANAGEMENT:
ASSESMENT
TREATEMENT
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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
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Laboratory investigations:
Serum biochemistry
Neuroimaging
Electrophysiological studies
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Lab. Investigations contd….
Serum biochemistry:
Neuronal proteins: neuron specific enolase, CPK-BB
Glial proteins: Myelin basic protein, Syneptophysin-100B
Neuroendocrine assessment:
- Growth hormone.
- Thyroid profile.
Serum electrolytes: Na+ , K+ , Mg2+ , Cl-
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Neuroimaging:
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
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Electrophysiological studies:
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.
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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
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Neuropsychiatric Treatment:
Use Biopsychosocial Model
Treat maximum signs and symptoms with fewest possible medications
TBI patients more sensitive to side effects
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Delirium
Identify and correct underlying cause
e.g., seizures, hydrocephalus, hemorrhage, drug side effect or interactions, endocrine (hypothalamic, pituitary dysfunction),electrolyte imbalance.
Pharmacologic management
Antipsychotics
haloperidol, droperidol, risperidone, olanzapine, quetiapine
Benzodiazepines (combined with antipsychotics)
Lorazepam
Avoid polypharmacy
Medical management
Frequent monitoring of safety, vital signs, mental status and physical exams
Maintain proper nutritional, electrolyte, and fluid balance
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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.
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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
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Treatment contd… Mania
Acute
Benzodiazepines
Antipsychotics
olanzapine, risperidone, clozapine, others
Anticonvulsants
valproate
Electroconvulsive Therapy
Chronic
valproate
carbamazepine
lamotrigine
lithium carbonate (neurotoxicity)
gabapentin, topiramate (adjunctive treatments)
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Anxiety
Benzodiazepines:
e.g., clonazepam, lorazepam, alprazolam
Watch for cognitive impairment, dependence
Buspirone (for Generalized Anxiety Disorder)
Antidepressants
SSRIs, venlafaxine, nefazedone, mirtazapine, TCAs
Beta-blockers, verapamil, clonidine
Anticonvulsants: valproate & gabapentin have some anxiolyticeffects
Psychosocial
Individual, couples, family, group
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Psychosis
Antipsychotics
Typical: e.g. haloperidol, chlorpromazine
Atypical: e.g., risperidone olanzapine, quetiapine, ziprasidone, aripiprazole, clozapine.
Start with low doses
TBI pts have high risk of anticholinergic and extrapyramidal side effects
May cause QTc prolongation
Use sparingly - may impede neuronal recovery acutely (from animal data)
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Aggression, Agitation, Impulsivity
Acute
Antipsychotics
Benzodiazepines
Chronic
*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 efficacy
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Behavioral & Psychotherapeutic treatment:
Behavioral rehabilitation program- contingency contracts & token economy.
CBT
Group therapy
Family therapy
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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
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Bibliography:
CTP- Sadock & Kaplan, 8th edition, Page: 390-403.
Oxford Handbook of Psychiatry page: 154-157.
Principles of Neurology-Adam & Victor 8th ed.page:747-768
Indian journal of Psychiatry
The American journal of Psychiatry
Internet:
www. emedicine.com
www.medspace.com
www.braininjury.com
www.traumaticbraininjury.net
www.northeastcentre.com
www.googleimage.com
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THANK YOU

Cognitive Impairment
May accelerate recovery May impede recovery
amphetamine haloperidol
Norepinephrine (TCAs) phenothiazines
gangliosides prazosin
methylphenidate, dextroamphetamine clonidine
amantadine phenoxybenzamine
L-dopa/ carbidopa GABA
bromocriptine benzodiazepines
pergolide phenytoin
physostigmine phenobarbital
donepezil idazoxan
selegiline
apomorphine
caffeine
phenylpropanolamine
Naltrexone
atomoxetine
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Neuropsychiatric manifestations of head injury

by Dr. Santanu Ghosh, MD (Psy)

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Neuropsychiatric manifestations of head injury Presentation Transcript