NEURO PSYCHIATRIC ASPECTS OF

TRAUMATIC BRAIN INJURY

Presenter: Dr Saaripalli Thapaswini,

PG
Moderator: Dr Ravi Kumar sir, Asst.
Professor

Institute of Mental Health,

Osmania Medical College, Hyderabad
Contents:
• Definition, prevalence
• History
• Pathophysiology, biomarkers
• Severity of head injury
• Investigations
• Aetiology of psychological sequelae
• Neuropsychiatric sequelae
• Head injury in children
• Sport-related head injury
• Management
Definition:
• Traumatic Brain Injury (TBI) is brain damage caused by an external force, such as a
blow or jolt to the head, leading to cognitive, physical or emotional impairments.
• Jolt = abrupt rough or violent movement

Prevalence in India:
• TBI affects around 1.7 million people annually
• RTAs leading cause, followed by falls
• Higher in urban areas and younger age groups.
History:
• The earliest written evidence of brain injuries appeared 5,000 years ago on the
Edwin Smith Papyrus, which contained the first 27 head injury records
• The Hippocratic Corpus included a treatise on head injury with thoughtful
comments on skull fractures, delirium, seizures, coma
• Medical literature has reported associations between TBI and neuropsychiatric
disorders for many years
• Adolf Meyer, identified a number of disorders…he referred them as “traumatic
insanities”
• The most famous case of frontal lobe injury, Phineas Gage, who suffered a
penetrating frontal brain injury…after an explosion shot an iron bar through his
skull
• After the injury he was described as childish, capricious, inconsiderate, profane,
having poor judgement
Phineas Gage
Pathophysiology:
• Types of head injury:
• Depending upon the integrity of meningeal coverings
• Closed injuries – Falls ( overall majority of TBIs)
RTAs
Assault
Sport-related injuries
• Penetrating injuries – Missile wounds
• Primary brain damage: contact & inertial forces, at the time of injury
Laceration to scalp
Skull fractures
• Contact forces Intracranial haemorrhages
Contusions
Intracerebral haemorrahges

• Inertial forces
Diffuse axonal injury
(acceleration, deceleration, rotational forces) Acute subdural haematoma
(tearing of subdural bridging
veins)
• Secondary brain damage: Pathological processes that are initiated at the moment
of injury but span a variable period following the traumatic episode.
• These include…
• Brain damage secondary to ischemia,
• Brain swelling,
• Raised intracranial pressure,
• Infection.
• Focal lesions:
• Contusions & lacerations…frontal and temporal poles
• Intracranial-extracerebral haemorrhages…epidural space, subdural space,
subarachnoid space
• Intracerebral haemorrhages…frontal lobes, temporal lobes, basal ganglia
• Diffuse lesions:
• Traumatic Axonal Injury (TAI)…corpus callosum, thalamus, brain stem
• Diffuse Ischaemic Damage (DID)

• Both focal & diffuse lesions may coexist

• Blast injurie due to IEDs
• Signature wound of military operations
• Complex in nature…preferentially involve lungs, tympanic membrane,
eyes, concussion/contusion of CNS
• Biphasic high pressure wave produced by the explosion…mechanical
tissue damage as well as injury due to release of heat, acoustic and
electromagnetic energy
• Injury by reflection of the wave when it hits the skull.
• Cerebral infarction from air embolism due to blast lung injury
Blood brain barrier (BBB) integrity is compromised, increased permeability, leakage of
blood constituents into brain tissue

Entry of inflammatory cells, cytokines, toxins into brain

Neuroinflammation, edema, elevated intracranial pressure, neuronal damage

Neurological dysfunction, complications, neuropsychiatric sequelae

Post traumatic changes in brain
neurotransmitters:
• Glutaminergic system:
• Excitotoxic neuronal injury
• Glutamate concentrations are Na+, Cl- influx
significantly elevated in CSF for several
Cytotoxic oedema
days
Ca+2 influx
• Glutamate antagonist – Ketamine
Expression of transcription
• Inhibitor of glutamate release – factors, acute phase proteins,
caspases, proteolytic enzymes
Riluzole…severe psychiatric side
effects

Neuronal apoptosis
• Cholinergic system: Chronic stress
• Increases immediately after TBI, hypofunctional
cholinergic state later
Cholinergic dysfunction
• Blockade of massive acetylcholine release from
pathological excitation of basal forebrain nuclei…
prevents neuronal cell loss and associated behavioural Hippocampal pathology
deficits Altered neurogenesis
PFC hypofunction
• Reduction in cholinergic transmission in hippocampus Amygdala dominance
and neocortex
• Cholinergic deficits are lack of motivation, anhedonia,
agitation, disinhibited behaviour Cognitive
• Cholinesterase inhibitors may improve cognition in TBI impairments
• Ascending biogenic amine pathways:
• Circulating levels of catecholamines correlate with TBI
severity Increased synaptic
• Increased serotonergic, noradrenergic metabolites in CSF concentration of
biogenic amine
• Prolonged increase in synaptic concentration of
neurotransmitters
neurotransmitters results in subacute or chronic
downregulation of aminergic transmission and eventually Downregulation of
depressive symptoms biogenic amine
• Prefrontal damage…dysregulation of mesolimbic and transmission
mesocortical dopaminergic pathways…manic and
hypomanic symptoms Depressive symptoms
• Affect on restorative processes in chronic phase of TBI via
neurotrophic factors
Biomarkers in TBI:
1. S100 Calcium-Binding Protein B (S100B)
2. Glial Fibrillary Acidic Protein (GFAP)
3. Tau Protein
4. Neuron-Specific Enolase (NSE)
5. Ubiquitin C-Terminal Hydrolase-L1 (UCH-L)
6. MicroRNAs (miRNAs)
Head injury severity:
Clinical indicators of head injury severity:
1. Duration of retrograde amnesia – the period leading up to the injury for which
memories have been lost. Tends to shrink as the pt. recovers. Least valuable
2. Depth of unconsciousness – Glasgow Coma Scale.
3. Duration of coma
4. Neurological evidence of cerebral injury – neuroimaging or EEG
5. Duration of post-traumatic amnesia – interval between injury and the return of
normal day-to-day memories. Best indicator
• Predictors of worse outcome:
Moderate: GCS 9-12
Loss of Consciousness
<6 hours
PTA <2 weeks

Previous head injury Mild: GCS 13-15

Old age Loss of Consciousness
APOE e4 positive status <30 min
Substance dependence PTA <24 hours
Severe: GCS 3-8
Loss of Consciousness
>6 hours
PTA >2 weeks
Investigations:
• Neuroimaging: CT scan, MRI, SPECT, PET
• EEG
• Biomarkers
• Neuropsychological assessment: Useful as a baseline for future assessments and
to guide rehabilitation Wisconsin Card Sorting test, Goldberg Executive Control
Battery, Tower of London Test, Trail Making Test
Etiology of psychological sequelae:
• Who has been injured, what brain injuries they sustained, the consequences
• Pre-traumatic factors: some personality traits, poor premorbid social adjustment,
young men, past h/o head injury, cognitive dysfunction
• Trauma: early psychiatric symptoms within weeks and months of the injury
correlate better with the extent and location of brain injury than late psychiatric
symptoms
• Left hemisphere damage seems to be associated with greater psychiatric
morbidity
• Head injury…psychological trauma…amnesia for that event…protection against
PTSD…may not prevent psychological stress reaction
• Lack explicit memory but retain implicit memory
• Observed in one of Claperede’s amnesic patients.
• Islets of intact memory – extremely frightening
• Post-traumatic factors: Amenable to intervention
• Psychiatrist needs to consider the pt’s reaction to any disability, consequences of
the disability on the role of pt in family and society
Neuropsychiatric sequelae:
• Cognitive impairment
• Personality change
• Early mental symptoms following brain injury
• Psychosis after brain injury
• Mood disorders
• Anxiety disorders
• Agitation and aggression
• Alcohol and head injury
• Post-concussion syndrome
• Post-traumatic epilepsy
Cognitive impairment
• Strong correlation…severity of head injury…PTA
• Attention and concentration:
• Slowness, reduced concentration, stimulus bound, perseveration
• Dysexecutive syndrome:
• More specific impairments in organizing, planning, scheduling, prioritizing,
monitoring cognitive activities,
• Difficulty in attending two tasks at once, distractibility
• Medial orbito-frontal lesions, dorso-lateral prefrontal lesions
• Everyday life impaired, catastrophic
• Memory impairment:
• Most common cognitive impairment, very disabling
• Anterograde amnesia – these enduring problems in laying down new
information…leading to memory distortions, poor recall, poor monitoring, poor
insight, confabulations
• Combined damage to several areas…frontal injury
• Explicit memory impaired, implicit memory intact
• Communication:
• Dysphasia, jargon aphasia, dysprosody (right hemisphere damage), word finding
difficulties
• Visuospatial impairments:
• Spatial disorientation, visual agnosia, hemi-neglect (troublesome)
Causes of late deterioration in cognitive function after brain injury
Personality change:
• More suffering
• Sometimes, a personality trait present before the injury becomes much more
troublesome
• Medial and lateral frontal lobe lesions – impairments of drive
• Orbito-frontal lesions – impairments in social behaviour
• Maladaptive coping, chronic mental illness, chronic psychosocial stressors,
substance dependence…influence personality change
• Apathy, amotivation, childish, impulsivity, low tolerance to frustration,
demanding, self-centred, no independent decision making, fatuous, facetious,
antisocial behaviours, disinhibition, sexual disinhibition, inappropriately flirtatious
to indiscriminate sexual assaults
• Head injury probably a risk factor for acquired BPD, acquired ASPD.
• Effects family and caretakers, children ignored, partner’s needs ignored,
relationships destroyed, divorce, deterioration of personality, depression,
substance abuse
• Some investigators classify personality changes into two distinct syndromes…
pseudodepressed personality syndrome (apathy, blunted affect) and
pseudopsychopathic personality syndrome (disinhibition, egocentricity, sexual
inappropriateness)
 Neuroanatomical lesions Associated features
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 behaviour, aggression

Early mental symptoms following brain
injury
• On recovery of consciousness…period of delirium with clouding of consciousness
• After clouding of consciousness resolves, confusion, disorientation, muddled
thinking, rambling talk, perseveration, misperception, misrecollection, fear
• Distortions of memory:
• Confabulations, brief-lived false memories
• Occasionally after a severe head injury…islets of memory in the dense amnesic
period.
• Recollections, fabricated memories, delusional memory
• Alterations of mood and perception:
• Oneroid states, perplexed
• Derealisation/depersonalization experiences, agitation
• Hallucinations (particularly visual), illusions, déjà vu, distortions of sense of
familiarity
• Apathetic states:
• No positive features, withdrawn state
Pseudobulbar affect:
• Sudden and uncontrollable affective outbursts…crying or laughing
which may or may not be congruent with the patient’s mood, occur
spontaneously, may be triggered by minor stimuli
• Differentiation from depressive d/o is no pervasive alteration of
mood, no vegetative symptoms
• Pathological Laughter and Crying Scale
• Frontal lobe lesions involving lateral and ventral aspects of PFC
• Also aggressive outbursts, poor social functioning
• SSRIs, combination of Dextomethorphan and quinidine.
Psychosis after brain injury:
• Early psychotic symptoms:
• In vast majority of patients, delusions and hallucinations occurred in the early
recovery period remit spontaneously and not relapse.
Delusional misidentification:
• Place, persons, objects, events
• Reduplicative paramnesia – duplication of events or places
• Delusional misidentification of person = Capgras syndrome…schizophrenia, TBI
• Result of interaction between organic brain disease and psychological disorder
• Lesions of right hemisphere in combination with frontal injury
• More diffuse brain injury
• Late psychosis:
Schizophrenia-like psychosis:
• A psychotic illness may develop long after the acute confusional state has
resolved
• Davidson and Bagley – head injury…two to three fold increased risk of developing
schizophrenia-like psychosis.
• Late teens to early 20’s – risk factor for both schizophrenia and head injury
(apparent association)
• Reverse causality?!
Paranoid psychosis:
• Occurs relatively early
• Occurs in a patient with severe cognitive impairment and personality change
• Memory impairment…persecutory ideas, delusion of reference…aggression
Mood disorders:
• Depression:
• Belief that life is not worth living with disability
• Apathy, anhedonia, depressed mood, self deprecation, guilt
• Risk factors: past h/o depression, severe disability, lack of support systems
• Interferes with rehabilitation and associated with aggression, cognitive impairment,
pseudodementia
• Suicide:
• Rates of attempted suicide increased by 3 times
• Mania:
• Association with post-traumatic epilepsy, lesions of ventral & anterior aspects of
temporal lobe (temporal lobe epilepsy)
• Higher rates of secondary mania…due to abnormal electrical activation patterns in limbic
network, functional changes in aminergic inhibitory systems, presence of aberrant
regeneration patterns
Anxiety disorders:
• Common after head injury
• GAD in 10-15% of cases
• Derealisation, depersonalisation, perplexity
• Amnesia surrounding the incidence may cause great distress
• Catastrophic reaction (in moderate and severe cognitive impairment)…failing to
perform a task, inability to communicate…sudden distress
• Depression, post-concussion syndrome, PTSD (recurrent intrusive recollections,
distressing dreams and flashbacks of the traumatic event)
• Phobic avoidance like travel anxiety
• Apprehension…mc complaint…due to cognitive impairment
• OCD – recognized sequelae…due to inflexibility and rigidity of the brain injured
person, or a response to doubt resulting from memory impairment.
Agitation and aggression:
• Most common complaints for psychiatric consultation
• Agitation that occurs in the early recovery period may improve or may be
followed by more intractable aggressive behaviour
• Major predictor – premorbid personality maladjustments
• Aggressive behaviour early in the confusional state or shortly after it’s
resolution…largely due to organic
• A pattern of aggression…highly stereotyped, erupting over seconds, with no or
trivial triggers, bizarre, against a background of calm behaviour…possibility of
epilepsy
• Important to r/o medical and surgical complications eg. Subdural haematoma,
infection
• Pain, fear, worry, phobic anxiety disorder need to be considered
• Some drugs make agitation worse
• Drug dependence, mental illness, communication difficulties, persecutory
delusions, mania, depression, anxiety…other causes of agitation and aggression
Alcohol and head injury:
• ADS complicates the management
• Previous head injuries may be present, alcoholic brain damage, poor physical
health
• Alcohol cravings interfere with medical care and rehabilitation
• ADS often gets worse because of poor impulse control
• New onset dependence due to relief from anxiety symptoms with substance
Post-concussion syndrome:
• Poorly defined
• Constellation of symptoms that may result in surprisingly more disability after
mild head injury (may be observed in moderate and severe head injuries also)
• No consistent relationship between prevalence of pcs and the severity of head
injury
• Phenomenology:
• Headache, dizziness, diplopia, impairment of speed of processing information
and concentration, fatigue, noise sensitivity…immediate aftermath
• Anxiety, depression, irritability…latent period
• Occasional symptoms are tinnitus, unsteadiness, muscular pains
• Symptoms overlap with PTSD and chronic fatigue
• Recovers by 2-6 months
• Few patients have persisting symptoms lasting for years, psychological factors are
important in these patients
• Aetiology:
Brain injury:
• Microscopic lesions described at post-mortem following mild head injury
• Functional imaging…SPECT,PET – showed abnormalities, evidence of cerebral
dysfunction
Psychosocial factors:
• Important if symptoms last longer than 1 year
• Example: Accident at work and the person blames their employer, symptoms are
more likely, involving compensation claims increases symptoms by 25%
• Greatest role in very mild head injuries and very chronic symptoms
Model of interaction:
• Lishman proposed a model in which early disturbance of brain function after mild
head injury results in the early symptoms of pcs
• In most patients these symptoms resolve and good recovery is made
• Post-Concussion syndrome may develop if psychological effects interfere with
the normal process of recovery
• Anxiety is thought to play a large part in impeding recovery i.e., the patient
worries about the symptoms and focuses on them
• Symptoms are aggravated in patients who are vulnerable for somatisation,
compensation claims at stake
Post-Traumatic Epilepsy
• Early Seizures… within the first week, relatively benign, sensitive to prophylactic
anti-convulsants...weak predictors of later epilepsy
• 5% closed head injuries and 30% open head injuries develop PTE
• Depressed skull fracture, intracranial haematoma, early seizure, severity of head
injury…likelihood of developing seizures
• EEG not a good predictor of PTE
• PTE increases psychiatric morbidity, mood d/o, late dementia
• Prophylactic anti-convulsants…no effect on reducing the incidence of late PTE
• Carbamazepine doc rather than phenytoin (CBZ – less effect on cognition)
• PTE remission by 5 to 10 years
Head injury in children
• Better outcome than adults due to neuroplasticity
• More likely to suffer cerebral oedema and early PTE
• Personality change with emotional lability, overactivity, reduced attention span,
irritability, temper outbursts and rage
• ADHD, OCD
• Very young children with severe head injury suffer a double hazard i.e., loss of
acquired skills and interference with development
Sport-related head injuries:
• Professional boxers…a chronic traumatic encephalopathy (dementia pugilistica),
the punch-drunk syndrome
• Pts with CTE…damage to extrapyramidal system, cerebellar, Pyramidal pathways,
upper brainstem lesions, cerebral atrophy, white matter changes, damage to
diencephalic structures
• Characteristic finding – perforation of septum pellucidum…separates the two
lateral ventricles
• Slow, ataxic, cognitive impairment, dementia
• APOE e4 positive status…Punch drunk syndrome…Amyloid formation
• Professional Footballers… subtle impairments of thinking…repeated blows to
head by heading the ball and head-to-head contact
Management:
• In the immediate aftermath of the head injury, the mx rests with the acute
surgical and medical team
• Not infrequently head injury leads to a psychiatric consultation
• Need to consider interplay between brain and head injury and the
psychodynamic processes that follow the injury
• Management of early neurobehavioural problems:
• Interventions aimed at reducing the post-concussional symptoms after milder
head injuries – brief psychoeducation, supportive therapy
• Mx of behavioural and mental symptoms following severe head injury – difficult
• Review history, pay attention to the period leading up to injury, general physical
examination, thorough neurological examination, monitoring vitals, documenting
conscious levels, orientation
• Routine blood tests, chest x ray
• Medications needs to be scrutinized
• Neuroimaging, EEG
• Lumbar puncture…to see for meningitis…only with specialist advice
• Safe environment, general care, explanation to patient and family members is
required
• Management of late mental sequelae:
Psychological interventions:
• CBT – persistent post-concussion syndrome
• Cognitive rehabilitation
• Community therapy
• Timely access to rehabilitation – reduces mental sequelae
• Some need formal vocational rehabilitation
• Neuropsychological assessment – to determine injury severity and pattern of
impairments
• Support and guidance to family members, advice on managing challenging
behaviours
Pharmacological management:
• Psychotropics are given if absolutely necessary
• Avoid multiple drugs concurrently
Agitation and aggression:
• Lack of trials…trial and error…good monitoring and documentation of behaviour
• Valproate, Carbamazepine doc…anticonvulsant and mood-stabilizing effects
• Antipsychotics for delusions, but may perpetuate agitation by inducing akathisia
• Atypical antipsychotics better
• Anti depressants particularly SSRIs – anxiety, depression (TCAs not used because of
anticholinergic properties)
• Trazodone HS for sleep disturbance
• Prazosin for traumatic brain injury related nightmares
• Benzodiazepines – agitation and aggression during early recovery period
• Contraindicated for chronic aggressiveness…increases confusion, effect on cognition,
paradoxical violence due to disinhibition, potential for addiction
Mood disorders and psychosis:
• Depression after head injury more difficult to treat
• Confabulations and delusions early after brain injury are allowed to resolve
spontaneously wherever possible
• Established psychotic symptoms – atypical antipsychotics
Apathy:
• Bromocriptine
• Methylphenidate – risk of addiction, side effects, under consultant supervision
Cognitive enhancers – Nootropics:
• Methylphenidate – deficits in attention, speed of information processing
• Donepezil – attention, memory problems
• Bromocriptine – executive problems

• ECT is not contraindicated in head injury patients, can be administered when and
wherever necessary
• Other neurostimulation therapies are also not contraindicated
Prescribing psychotropics in brain injury:
Thank you