Neuropsychiatric

aspects of Traumatic
Brain Injury

Presentor: Dr Abhishek Kumar Sharma and Dr Nandhini

Mentor Dr Pavithra
 Overview

Symptoms of TBI
General assessment of TBI
PTSD related with TBI
Personality changes associated with TBI
Neurocognitive changes associated with TBI
ASSESSMENT OF
TBI

Scoring of TBI is done on the

basis of GCS, loss of
consciousness and post traumatic
amnesia.
◦ PTA ends when GOAT scores
are greater than 75
◦ for two consecutive trials
◦ 24 hours apart
◦ Beginning at the end of coma
 Lab Tests:

Serum markers Neuroendocrine dysfunction Neuroimaging Electrophysiological studies

• Neuronal proteins • Particularly with • CT is study of choice • For status epilepticus:

localises post-traumatic
• Glial proteins pituitary hormone for evaluating patient epileptic focus
deficiencies with rapid changes • To evaluate slow wave
• Diabetes insipidus in • MRI is sensitive for abnormalities and in
acute stage, but other post-traumatic non diagnosis of TLE
may present haemorrhagic changes • Polysomnography for
evaluating atypical sleep
insidiously and small subdural disturbances
collections • Visual, auditory and
somatosensory evoked
potentials are useful to
localize the level of injury to
the CNS.
• Auditory evoked potentials
are particularly effective in
detecting brainstem
pathology.
Neuropsychiatric assessment

Bedside evaluation of frontal lobe

Neuropsychological screening
function
• Clock drawing test • MMSE
• Verbal fluency • Repeatable battery for assessment
• Set shifts and sequencing of neuropsychological status
• Fist-palm-side • Shipley institute of living scale
• Go-No go test • Barrow neurological institute
screen for higher cerebral functions
Post Traumatic Stress Disorder and TBI
Mechanism:

Mild TBI with little or no amnesia

Islands of memory during post

traumatic amnesia

No memory but trauma re-

experienced by unconscious,
implicit fear response

No memory but generation of

pseudomemories of what could
have happened
 Incidence with mild TBI
◦ Early incidence studies reported zero or close to zero rates of PTSD amongst populations with TBI.

◦ But those studies have now been superseded by recent large-scale studies where mild TBI had 11-24% prevalence of PTSD

◦ Recent studies also propose that mild TBI may increase the likelihood of developing PTSD.

◦ They hypothesized that it might be due to the combines effects of mild TBI causing

◦ Sufficient neural impairment to leas to disrupted information processing capabilities

◦ Insufficient neural impairment to lead to complete amnesia for the event

◦ Resulting in difficulties in emotionally processing the trauma

Incidence with severe TBI
◦ Studies with severe TBI are even fewer than mild TBI with PTSD

◦ Some studies have also suggested zero rates for the dual diagnosis in this group
◦ More recent studies however have reported much higher levels

◦ One study, which used unrepresentative sample showed 27% rate of dual diagnosis, while some studies with more
representative sample showed 11-18% rate
◦ One recent study might have explained for this higher range of findings
◦ Self reporting measures can dramatically over-diagnose PTSD association with severe TBI
◦ 44-59% rate with self reported measures, while only 3% rate with structured nterview
◦ These evidences point towards conclusion that severe TBI might provide significant but not total protection against
PTSD.
 Overlap of symptoms
◦ Many symptoms after mild (post concussion) or severe (cognitive impairments) TBI overlap with PTSD
alone.

◦ These are
◦ Sleep disturbances
◦ Irritability
◦ Memory and concentration difficulties
◦ Fatigue
◦ Nausea
◦ Depression
◦ Reduced speed of information processing and headaches
◦ Avoidance of tasks due to cognitive incapacity or for emotional reasons
◦ Intrusive thoughts due to gaps in their memory which they wish to fill or because of PTSD

◦ If symptoms are judged to be predominantly due to a severe TBI then there may be a strong likelihood that
they will be of a permanent nature

◦ If they are judged to be predominately due to PTSD they may be less permanent and some optimism about
their amelioration through treatment may be appropriate
 Treatment approach

◦ The current literature suggests that there are no PTSD treatments specifically designed for patients with the dual
diagnosis with a robust evidence base

◦ Intervention like CBT dominate the treatment literature

◦ Early education about this cycle alongside other concurrent interventions might be helpful.

◦ Treatment plans should be developed using a multidisciplinary approach that encompasses evaluation and
management of all potential symptoms from each TBI symptom cluster (physical, cognitive, and emotional) to
assure maximal chance of recovery of all symptoms.
Strategies for Post Traumatic Amnesia

◦ If the amnesia is chiefly organic, then treatment might focus on

◦ the impossibility of regaining memory for the event

◦ the acceptance of this fact

◦ the acceptance of the emotional consequences of this

◦ facilitating the ‘reconstruction’ of events to help emotional closure

◦ using generic stimuli in exposure work to facilitate habituation rather than using patchy and unreliable
measures (e.g., videos of traffic)

◦ If the amnesia is chiefly psychogenic the patient is likely to be encouraged in therapy to recall the amnesic
periods as part of the exposure elements of the intervention.
TBI and
Personality
change
◦ Traumatic brain injury
(TBI) is frequently
complicated by alterations
in temperament and
character that have adverse
consequences for day-to-
day living, manifesting as
poor decision-making,
interpersonal problems,
communication problems,
and often overall poor
quality of life.
Personality changes
◦ Muriel Lezak described alterations in personality after TBI as
◦ Impaired social perceptiveness,
◦ Impaired self-control and regulation
◦ Stimulus-bound behavior
◦ Emotional change
◦ Inability to learn from social experience
◦ Hibbard et al. (2000), using the Structured Clinical Interview for DSM-IV Axis II Personality Disorders
found that two-thirds of their cohort of individuals with brain injury met criteria for a DSM-IV-TR
(American Psychiatric Association 2000) personality disorder diagnosis after injury that was
independent of injury severity, age at injury, or time since injury occurred
Personality changes- Presentation
◦ Clinically disruptive personality change following traumatic brain injury may mimic Cluster B
personality traits, paranoia, or dependent/avoidant traits.
◦ Seventy percent of individuals with traumatic brain injury sustain injury to the frontal lobes.
◦ Impairment of auditory processing can mimic attention deficit disorder.
◦ Visual dependence to maintain balance can mimic avoidant, agoraphobic, or anxiety disorders.
Personality changes- assessment
◦ When interviewing a patient with a suspected traumatic brain injury, one should stay alert for evidence of
propositional language difficulties (e.g., hesitant or delayed responses, circumlocution, paraphasia,
reduced expressive or receptive lexicon), pragmatic deficits (e.g., interruptions, impaired closure,
impaired cohesion), and prosodic dysfunction (e.g., blunted inflection, inability to respond to
humor/irony).
◦ Using both an open-ended style of interview (“Tell me about...”) and a review of systems (yes-no format)
to obtain the history will minimize underreporting due to impaired self-awareness.
◦ An interview with a collateral informant for complementary information on current and preinjury
functioning is essential.
Personality changes- management
◦ Treatment of personality change requires a comprehensive neurorehabilitation effort to reduce the
anxiety generated by failure of preinjury sensory, cognitive, and executive capacities.
◦ Prior to pharmacological intervention, stabilization of hydration, nutrition, sleep, exercise, analgesia, and
hormonal status must be addressed.
◦ An oral history and a mental status exam are not sufficient for examination of a patient with traumatic
brain injury. A physical/neurological examination including testing of olfaction, auditory processing,
visual-spatial integrity, and higher-level balance must be performed by the psychiatric physician.
TBI and Seizures
◦ Seizures occurring 1 week or more after trauma (late seizures) carry a much higher risk of epilepsy than
those occurring the first week (early seizures).
◦ The risk of a first seizure remains elevated for as long as 20 years after a severe traumatic brain injury.
◦ Greater degrees of cortical damage and hemorrhage increase the risk of developing posttraumatic
epilepsy.
◦ Partial seizures from the temporal and frontal regions may not produce ictal electroencephalographic
changes and may be confused with psychiatric disorders.
TBI and Seizures
◦ A routine electroencephalogram may be normal in up to 59% of patients with definite epilepsy.
◦ Prophylactic antiepileptic medication, particularly phenytoin, is indicated only in the first week
following severe traumatic brain injury.
◦ Antiepileptic drug treatment should be individualized and should ideally attempt to treat multiple
problems.
◦ Depression is the most common psychiatric comorbidity in epilepsy.
◦ Fifty percent of those with posttraumatic epilepsy will be in remission after 15 years.
Cognitive changes

Executive Language
Attention
functioning

Social
Memory
cognition
Cognitive changes
◦ Cognitive and neurobehavioral changes are often the most salient features following TBI at any level of
severity.
◦ Mild and severe brain injuries represent different locations on a continuum of cerebral involvement.
◦ Discrete focal lesions may produce classic neurobehavioral syndromes such as aphasia, but these are
commonly superimposed on more global dysfunction arising from diffuse injury.
◦ Impairments of attention are among the most prevalent findings after TBI. The most robust finding is a
reduction in processing speed; abnormalities of divided attention are also consistently noted.
Cognitive changes
◦ Memory dysfunction is another cardinal finding after TBI, with impaired episodic memory a hallmark.
Executive contributions to memory dysfunction are often implicated, such as a failure to apply
organizing strategies when learning, as are impairments of working memory, prospective memory, and
metamemory.
◦ Frontal executive functions are higher-order capabilities that control other mental activities, such as
attention, memory, and motor behavior, and critically influence functional outcome after TBI.
◦ Four categories of executive function are proposed: executive cognitive, activation regulating, behavior-
regulating, and metacognitive functions.
Cognitive changes
◦ Social cognition is an important facet of cognition with strong links to executive processes.
◦ Studies in TBI patients have emphasized unique contributions from the ventromedial prefrontal cortex
region to social cognitive function.
◦ Impairments of language and communication after TBI may include classic aphasia syndromes; many
more individuals have impairments of basic linguistic functions, such as word retrieval, verbal fluency,
and auditory comprehension of complex information.
◦ Dysarthria is relatively common and may persist. The assessment of naturalistic language production or
discourse may reveal deficits such as less productive, less efficient speech. Deficits in pragmatics, or the
use of language, are also frequently evident and include reduced ability to meet the needs of a listener
and to perceive sarcasm.
Cognitive changes- Treatment

• During brain injury, disruption occurs within multiple neurotransmitter systems— namely, the systems known to
mediate attention, memory, and executive function.

• The clinical literature provides support for several pharmacological interventions that can potentially enhance
rehabilitative efforts, particularly in relation to cholinergic and catecholaminergic agents.

• Despite methodological shortcomings, the accumulated data indicate frequent benefit with respect to alertness and
mental processing speed. Memory improvement has at times been shown. However, the extent to which complex
executive functions may improve with drug therapy remains unclear.

• Additional research is needed to determine the extent to which improvements noted on laboratory measures
translate into real-world benefits that enhance the daily function of individuals with TBI.
Cognitive
changes-
Treatment
Dementia and TBI
Dementia due to head injury is characterized by prominent memory and executive dysfunction with relative preserved
visuospatial, praxis and primary linguistic functions.
In addition, these patients may be severely apathetic and withdrawn and may demonstrate markedly slow information
processing.
Physical examination may reveal extrapyramidal signs.
A chronic subdural hematoma in the elderly may present as a progressive dementia.
There is evidence that previous traumatic episodes is a risk factor for the development of Alzheimer’s disease. TBI is
associated with:
◦ Expression of amyloid precursor protein.
◦ Oxidative stress
◦ Increased deposition of ß – amyloid.
Dementia and TBI
DEMENTIA PUGILISTICA
Multiple TBI associated with boxing occur in approximately 20% of professional boxers.
The diagnosis is dependent on documenting progressive dementia that is associated with chronic and
repeated brain trauma and that is unexplainable by an alternative pathophysiological process
Pathologically dementia pugilistica shares many characteristics with Alzheimer’s disease:
◦ Neurofibrillary tangles
◦ Diffuse amyloid plaques
◦ Tau immunoreaction
Non-pharmacological treatments for psychological
and behavioural disorders following TBI

International recommendations – Wiart et al 2016

◦ Non- pharmacological treatment is recommended in first intention, whatever the stage in the condition
◦ The non-pharmacological treatment includes different approaches: holistic, cognitive behavioural,
systemic, familial and psychoanalytical
◦ Holistic approach = Planned care itineraries, occupational activities, social activity, professional activity
◦ Different approaches can be combined depending on the predominance of certain symptoms or
comorbidities and if necessary, backed up by specific treatments (e.g. PTSD, Addiction etc)
Interpersonal and adaptive approach
◦ As far as possible to adjust the behaviours of the patient’s close circle and adapt the environment so as to avoid
behavioural disturbances triggered by outside factors like noise, annoyance, excessive demands etc.
◦ It is recommended that stressful situations be avoided, avoid distractions or tasks that ake too long or allow for fatigue

◦ Remain structured, clear and precise in communication

◦ Maintain respect for the person and their need for autonomy

◦ Encourage them
◦ Avoid feeling targeted by any irritability or aggression

◦ For the patient, training exercises in controlling aggression, detecting the sensation of increased tension

◦ For the family, identifying the triggers and aggravating factors, recalling pleasant moments
BT and CBT for TBI
◦ Cognitive restructuring and identifying malfunctioning thoughts, testing the validity of thoughts and
developing rational alternatives
◦ Development of internal dialogue, the use of notes and diaries, role play and training in problem solving
◦ Training in relaxation techniques
Other therapeutic techniques
◦ Family therapy

◦ Yoga

◦ Tai chi

◦ Music therapy

◦ Hypnosis

◦ Mindfulness

◦ Positive psychology