Neuropsychiatry aspects of traumatic brain injury

1. Traumatic Brain Injury
Dr. Nor Afiza Azmee
BMed (Aus), MRCPsych(UK)
Department of Psychiatry
Hospital Sultanah Bahiyah, Alor Setar

2. What is Traumatic Brain Injury?
 “An insult to the brain, not of degenerative or congenital nature caused
by an external physical force that may produce a diminished or altered
state of consciousness, which results in an impairment of cognitive
abilities or physical functioning. It can also result in the disturbance of
behavioral or emotional functioning.
Brain Injury Association of America. Definition: Traumatic Brain Injury, 2011

3. Epidemiology
 Incidence of head injury in USA : 150/100,000 yearly
 Two age peaks:
 15-24 (MVA as the common cause)
 64 years (falls as the common cause)
 Males are more commonly affected than females at all age
 Alcohol intoxication is a very common factor - being found in from one-
third to one- half of all cases (Corrigan 1995).
Puri, Basant K.,Moore, David P (2012). Textbook of Clinical Neuropsychiatry
and Behavioral Neuroscience

4. Epidemiology in Malaysia
 5th (7.86%) commonest cause of hospitalisation in MOH hospital Malaysia
in 2014.
 The younger age group between 15-34 years (56.6%) was at the highest
risk of major trauma
 Road traffic accident - the commonest cause
 Commonest diagnosis leading to intensive care unit (ICU) admission in
2008. (National Audit on Adult Intensive Care Units (NAICU) report)
 Malaysian National Trauma Database 2009 Report:
 blunt trauma made up 96% of injury.
 Road trauma accounted for 75% of cases with motorcyclists being most
commonly injured
CPG Malaysia – Early Management of Head Injury in Adults

5. TBI Mechanism
 4 primary mechanisms of TBI
 Direct impact
 The head has struck something or an object has struck the head
 Sudden or rapid acceleration and deceleration
 Sudden or rapid acceleration and deceleration happens when nothing has come in direct contact
with the head, but the brain inside the skull still experiences violent motion. This is what happens in
the case of a whiplash injury, when the head moves rapidly forward and backward. Whiplash that
causes a rapid turning motion of the head results in a rotational injury.
 Penetrating injury
 high-velocity projectiles, such as bullets or shrapnel, or objects of lower velocity, such as knives or
bone fragments from a skull fracture, being driven into the brain.
 Blast Injury
 caused by the impact from a pressure wave generated by an explosion or direct trauma to the head
resulting from a blast.

7. TBI Mechanism
 Open TBI
 Results from bullet wounds, etc.
 Largely focal damage
 Penetration of the skull
 Effects can be serious
 Closed TBI
 Resulting from falls, motor vehicle crashes, etc.
 Focal damage and diffuse damage to axons
 Effects tend to be broad (diffuse)
 No penetration to the skull

8. Types of Injury
 There are three primary types of damage that can result from these external forces,
including:
 Diffuse axonal injury
 Widespread damage to the brain’s white matter.
 Due to shearing force – stretching, twisting, or tearing of the axon bundles.
 Associated with mild TBI but can occur with more severe TBIs
 Usually undetected in standard neuroimaging techniques. If severe, may be seen in MRI
 Focal contusions
 Brusies/ swellings in small specific areas of the brains.
 Usually due to coup and contrecoup injuries.
 Hematomas, or bleeding, in or around the brain
 EDH
 SDH
 SAH
 ICH
Puri, Basant K.,Moore, David P (2012). Textbook of Clinical Neuropsychiatry and Behavioral Neuroscience

9. Biomechanics of Concussion and TBI
 LOC more common in acceleration/deceleration injuries where there is a rotational
component.
 Rotations round a coronal axis, (the head moving from side to side) are probably more
likely to produce loss of consciousness than rotation around the sagittal axis (as in a
nodding movement of the head) (Smith & Meaney 2000).
 This may explain why impacts to the temporoparietal area are most likely to produce
concussion (McIntosh et al. 2000). Presumably rotational forces are particularly likely to
produce the swirling movement of the brain that has been observed in monkeys after
acceleration injury (Pudenz & Shelden 1946).
 Side impacts in car accidents are possibly more likely to be associated with severe head
injury, perhaps because of the side-to-side forces as the head hits the pillar between the
front and rear doors (Nirula et al. 2003).
 It was suggested that if the force is applied to the face, causing facial fractures, this acts
as a buffer reducing the brain injury (Löken 1959). However, a more recent study suggests
this is not the case and that, in those presenting to accident and emergency departments,
a facial fracture increases the likelihood of brain injury (Keenan et al. 1999).
Lishman’s Organic Psychiatry: A textbook of Neuropsychiatry 4th edition

10. Classification of Traumatic Brain Injury
 Mild
 Moderate
 Severe
 In considering the clinical features (and their treatment) of TBI, it is
convenient to divide them into two groups,
 acute phase – often dominated by delirium.
 chronic phase – as delirium/confusion clears, patients gradually enter into the
chronic phase, characterized by numerous sequelae including cognitive deficits,
that may at times be severe enough to constitute a dementia.
GCS PTA LOC
Mild 13-15 <1 day 0-30mins
Moderate 9-12 >1 to <7 day >30 mins to <
24 hours
Severe 3-8 >7 days >24 hours

11. TBI in DSM-5
 DSM-5 addresses Traumatic Brain Injury in the chapter entitled “Neurocognitive Disorders.”
 According to the DSM-5, the degree of the particular Neurocognitive Disorder Due to TBI can
either be Major or Mild.
Criteria:
 A. The criteria for Major or Mild Neurocognitive Disorder must be met.
 B. Evidence of a Traumatic Brain Injury – an impact to the head or other mechanisms of rapid
movement or displacement of the brain within the skull, with ONE or more of the following:
 Loss of Consciousness (LOC)
 Posttraumatic Amnesia (PTA)
 Disorientation and Confusion
 Neurological Signs (e.g., neuroimaging demonstrating injury; a new onset of seizures; a marked
worsening of a preexisting seizure disorder; visual field cuts; anosmia; hemiparesis)
 C. Major or Mild Neurocognitive Disorder presents immediately after the Traumatic Brain
Injury or after recovery of consciousness and lasts beyond the acute post-injury period.

12. Mild and Major Neurocognitive
Disorder
 Evidence of modest cognitive decline from a previous
level of performance in one or more cognitive domains
(complex attention, executive function, learning and
memory, language, perceptual-motor, or social
cognition) based on:
 Concern of the individual, a knowledgeable informant,
or the clinician that there has been a significant decline
in cognitive function; and
 A substantial impairment in cognitive performance,
preferably documented by standardized
neuropsychological testing or, in its absence, another
quantified clinical assessment.
 The cognitive deficits do not interfere with
independence in everyday activities (but greater effort,
compensatory strategies, or accommodation may be
required).
 The cognitive deficits do not occur exclusively in the
context of a delirium.
 The cognitive deficits are not better explained by another
mental disorder (e.g., major depressive disorder,
schizophrenia)
 Evidence of significant cognitive decline from a previous level of
performance in one or more cognitive domains (complex
attention, executive function, learning and memory, language,
perceptual-motor, or social cognition) based on:
 Concern of the individual, a knowledgeable informant, or the
clinician that there has been a significant decline in cognitive
function; and
 A substantial impairment in cognitive performance, preferably
documented by standardized neuropsychological testing or, in
its absence, another quantified clinical assessment.
 The cognitive deficits interfere with independence in everyday
activities (i.e., at a minimum, requiring assistance with complex
instrumental activities of daily living).
 The cognitive deficits do not occur exclusively in the context of a
delirium.
 The cognitive deficits are not better explained by another mental
disorder (e.g., major depressive disorder, schizophrenia)
Mild Major

13. Acute Phase of TBI
 Essentially all patients with significant TBI will initially be comatose.
 Among those who do survive, some will emerge from coma into a persistent vegetative
or minimally conscious state
 While the remainder emerge into a delirium.
 confusion, disorientation, and decreased short-term memory,
 often marked by hallucinations, delusions, and, especially, agitation, which is seen in the
majority of cases.
 Other factors contribute to delirium:
 Medications like opioids
 Metabolic factors: hyponatremia, hypoglycemia, hypomagnesemia
 systemic effects of infections, such as pneumonia
 Global hypoxic ischaemic injury : very common and occurs secondary to arrhythmias,
hypotension and pulmonary lesions
 In those with fractures of long bones, consideration must also be given to the fat embolism
syndrome.
Puri, Basant K.,Moore, David P (2012). Textbook of Clinical Neuropsychiatry and Behavioral Neuroscience

14. Treatment During Acute Phase of TBI
 In ICU or trauma unit
 May need neurosurgical intervention
 evacuation of epidural or subdural hematomas or large contusions or intracerebral hemorrhages,
 serial CT scans are obtained.
 In comatose patients, intracranial pressure monitoring is often indicated
 Treatment with intravenous sedation, mannitol, and other agents may be required to reduce elevated
intracranial pressure.
 Intubation is almost universally required, and pneumonia is a frequent occurrence.
 In some cases, continuous EEG monitoring may be required to detect non-convulsive status
epilepticus.
Puri, Basant K.,Moore, David P (2012). Textbook of Clinical Neuropsychiatry and Behavioral Neuroscience

17. Treatment of Delirium In Acute Phase of TBI :
Non-Pharmacological Measures
 Delirium nursing and simple environmental measures to reduce confusion.
 quiet room, with a window.
 Large calendars and digital clocks should be in full view
 Sleep is essential and consequently the room should be darkened and very quiet at night,
 All non- emergency procedures (e.g. vital signs, weights, baths, laboratory testing) should be
forbidden during the sleeping hours.
 Restraints may occasionally be required and can be life-saving. For patients prone to get out of
bed unsupervised, keeping the bedrails up may be sufficient; if not, or if these are impractical,
utilizing a ‘low-boy’ bed, surrounded by mats, may help prevent injury.
 In some cases, round-the- clock sitters may be required.
Puri, Basant K.,Moore, David P (2012). Textbook of Clinical Neuropsychiatry and Behavioral Neuroscience

18. Treatment of Delirium In Acute Phase of TBI :
Pharmacological Measures
 Pharmacologic treatment may be considered with an antipsychotic for symptoms of hallucinations or
delusions, and are also effective for agitation.
 0.5-1mg Risperidone
 12.5-25 mg Quetiapine
 2.5-5 mg Olanzapine
 1.5-5 mg Haloperidol
 Gradually increased dose and continue until patient is stable for a significant period of time.
 Lorazepam is very commonly used, and, given the rapidity of its effectiveness when given intravenously,
has a place in emergency situations;
 However lorazepam may also worsen confusion
 it is appropriate to substitute another agent as soon as this is practical.
 If lorazepam is used, may administer 0.5 to 2mg intravenously every hour as needed until the patient is calm,
limiting side-effects (such as sedation) occur, or a maximum of approximately 12 mg is reached.
Puri, Basant K.,Moore, David P (2012). Textbook of Clinical Neuropsychiatry and Behavioral Neuroscience

19. Chronic Phase of TBI
 Cognitive Deficits
 Post-Traumatic Amnesia
 Anosognosia
 Focal signs and symptoms
 Sympathetic storms
 Personality change
 Depression
 Emotionalism
 Emotional incontinence
 Apathy
 Agitation
 Fatigue
 Mania
 Sleep disturbances
 Psychosis
 Post-traumatic seizures
 Endocrinologic changes
 PTSD

20. Cognitive Deficits
 Slowed information processing, poor attention & concentration, poor short- term memory,
impaired ability to plan and organize the day, and decreased abstracting ability.
 Can be mild, but can also be severe and disabling
 Most patients show improvement over the first 6 months, however, after 12 months, little
further spontaneous recovery can be expected.
 Check for the presence of depression, which, in and of itself, may cause cognitive
impairment.

21. Medication Studies Outcome
Methylphenidate 0.6
mg/kg (divided into a
twice-a-day schedule)
-speed of information processing was
evaluated in four studies,
-attention was also evaluated in four
studies,
-Speed and information processing: 3 studies found
improvement, 1 didn’t.
-Attention : 2 studies found improvement, 1 study
shows a trend towards improvement, 1 study found
no improvement.
Donepezil 10 mg 1 double blind study (Zhang et al) Improved both attention and memory
Rivastigmine Evaluated in 2 studies (Silver et al,
Tenuvo et al)
-Dose 3-6 mg: improve both attention and memory
in those with moderate to severe memory
impairment (Silver et al)
-Average dose 8 mg: Improve both speed of
information processing and attention
Amantadine
100 mg BD
2 studies (Meythaler et al., Schneider
et al.)
Mythaler et al: there was overall cognitive
improvement as measured by the Folstein mini-
mental status exam;
Schneider et al. 1999), no overall improvement, nor
was there any improvement on specific measures of
attention or memory.

22. Post Traumatic Amnesia
 The period of post-traumatic amnesia spans, at a minimum, the period of time from the
injury itself up to that point where the patient is able to again ‘lay down’ new
memories, as evidenced by an ability to recall most events that transpired the day
before being tested, or by the ability to recall three out of three words after 5 minutes.
 Thus defined, post-traumatic amnesia represents primarily an anterograde amnestic
disturbance
 However, in most cases there is also an associated retrograde amnesia, of variable
extent: thus, patients typically are unable to recall events that occurred prior to the
accident, and this ‘blanket’ of retrograde amnesia may encompass anywhere from the
mere hours preceding the injury, up to days, weeks, or longer.
 Characteristically, this retrograde ‘blanket’, however, gradually ‘shrinks’ in size over time, such
that most patients, although still left with the anterograde component, are eventually able to
recall most events prior to the injury, even, in some cases, up to minutes before the injury
itself.

23. Post Traumatic Seizures
 May be defined as occurring early, during the first 7
days post-injury, or late, occurring at any time
thereafter.
 Early seizures reported in 15-20% of cases and
most likely to occur during the first 24 hours.
Metabolic causes, such as hyponatremia,
hypocalcemia, or hypomagnesemia are not
uncommon, although the vast majority of
seizures occurring post-traumatically are due to
the intracranial pathology itself.
 Late seizures are seen in from 5 -10% of cases,
and in those destined to have a late seizure, the
first one usually occurs within the first year post-
injury (Mazzini et al. 2003.) The range here,
however, is wide, from weeks to up to 15 years.
 Risk features for occurrence of late seizures:
 having an early seizure
 the presence of contusions or intracerebral
hemorrhages
 intracranial operations
 dural penetration with bone or metal fragments
 Treatment : two aspects exist: prophylaxis against an early seizure, and
treatment after a seizure
 Prophylaxis: double-blinded studies have demonstrated that both
phenytoin (Temkin et al. 1990) and valproate (Temkin et al. 1999) are
more effective than placebo, and, between the two, given that there was a
trend toward increased mortality with valproate, phenytoin appears
preferable
 More recent single-blinded study (Szaflarski et al. 2010), however,
compared intravenous fosphenytoin with intravenous levetiracetam and
found equal effectiveness in seizure prophylaxis but an overall better
tolerability for levetiracetam.
 No benefit after first week if patient is seizure-free. May discontinue.
 Treatment of Seizure:
 If a patient had an early seizure despite prophylactic treatment, some
clinicians would continue the drug, on the theory that without it
there might be a higher frequency of seizures, whereas others would
opt for a different agent.
 In cases where there were no seizures during the first week, but one
occurred later, there are no firm guidelines regarding treatment, and
consideration could be given not only to phenytoin or levetiracetam,
but also to other agents, such as carbamazepine, oxcarbazepine,
gabapentin, etc.

24. Personality Changes
 Found in up to two-thirds of all cases over long-term follow-up
 Reminiscent of a frontal lobe syndrome, with childish and socially inappropriate behavior and
disinhibition, which may lead to sexual improprieties
 There may be restlessness, emotional lability and impulsivity, and anger, and in disinhibited
patients argumentativeness and assaultive behavior may occur.
 Some patients, however, may become withdrawn, listless, and apathetic.
 Before making this diagnosis, due regard must be paid to the patient’s premorbid personality, with
special attention to the presence of either an antisocial or a borderline personality disorder.
 The pharmacological treatment of impulsivity, anger and assaultiveness is not well worked out.
 One single-blinded study (Mooney and Haas 1993) of young males found that methylphenidate in a
dose of 30mg/day was superior to placebo for anger.
 In practice, many such patients are treated with an antipsychotic, such as quetiapine, or an AED, such as
carbamazepine.

25. Other Sequelae
Emotionalism
-Labile tearfulness
-Very common
-Must be differentiated from emotional
incontinence and depression
-Unlike depression, no vegetative
symptoms, such as fatigue, loss of interest
etc.
-Distinguishing emotionalism from
emotional incontinence is made by
attending to whether the tearfulness is
associated with an experienced sense of
sadness, which is present in emotionalism
but absent in emotional incontinence.
-May respond to fluoxetine.
Emotional Incontinence
-Involuntary appearance of a sad or happy
affect in the absence of any corresponding
sense of sadness or mirth.
‘empty’ displays of affect may be seen as a late
sequelae in from 5 to 10 percent of patients.
Both citalopram and paroxetine, each in doses
of from 10 to 40 mg/day, were effective in an
open study (Muller et al. 1999), sometimes in
as little as 2 or 3 days.
Depression
-appears during the first 2 years in up to one-
half of patients
-Typical symptoms of depression are present –
fatigue and poor concentration are especially
problematic.
-Rule out emotinalism and emotional
incontinence.
-Find out if patient has MDD before brain injury,
-Sertraline, citalopram, methylp[henidate and
desipramine have been studied.
(however, desipramine may lower the seizure
threshold)

26. Other Sequelae
Agitation
-common
-tends to fluctuate in severity,
- may occur in up to two-thirds of
all patients in the first few months
-associated aggression may be
seen in roughly one-fourth of
patients
-consideration must be given to
the possibility that the agitation in
question is not directly due to the
brain injury but is rather secondary
to other causes, such as pain,
delusions of persecution, or
akathisia.
Mania
-relatively uncommon
-may occur in the year following
head injury
-more likely when the polar
regions of the temporal lobes have
been involved, as for example by
contusions
-Important to differentiate manic
exuberance from the disinhibition
that is seen in the frontal lobe
syndrome: the main differential
point here is that, whereas mood is
heightened in mania, it is not in
the frontal lobe syndrome.
Psychosis
-rare, but has been reported as a
long-term sequelae to TBI
-In the reported cases, latencies of
1-5 or more years are reported
between the head injury and the
gradual onset of the psychosis,
and a family history of
schizophrenia was found to be a
significant risk factor.
Treatment involves use of an
antipsychotic, preferably one of
the better tolerated second-
generation agents, such as
risperidone or quetiapine.

27. Other Sequelae
Sympathetic Storms
-consist of episodes characterized by
profuse diaphoresis, tachycardia,
tachypnea, pupillary dilation, and, in
some, rigid extensor posturing.
-During the episode, patients may
grimace as if in pain, and family
members and other observers may
become quite alarmed.
-comes in discreet episodes
-The episodes themselves last from
minutes to hours, and terminate
slowly.
Treatment with propranolol or
bromocriptine usually prevents
further attacks; alternatives include
gabapentin and morphine.
Fatigue
-Fatigue may be present in up to
one-third of patients (Hillier et al.
1997),
its treatment is uncertain.
Modafinil, in doses up to 400
mg/day, in a double-blinded study
(Jha et al. 2008), was not superior
to placebo.
Whether methylphenidate would
be effective is not known.
Endocrinologic
Changes
-May occur secondary to pituitary or
hypothalamic damage.
-Appear in majority of patients with
TBI
-Diabetes insipidus, with
hypernatremia, may occur early on.
-other endocrinologic changes, such
as hypothyroidism or gonadal failure,
may not become evident for months
to years after the injury.
it is prudent to check a thyroid profile
in any patient who develops
depression, apathy or fatigue, and a
testosterone level in patients who
develop decreased libido.

28. Non-Pharmacological Management
 Multidiscioplinary team
 Includes –
 Pharmacotherapy appropriate for the respective TBI sequelae
 physiotherapy
 occupational therapy
 recreation therapy
 speech therapy
 vocational rehabilitation.

29. References
 Puri, Basant K.,Moore, David P (2012). Textbook of Clinical Neuropsychiatry and
Behavioral Neuroscience
 DSM-5
 CPG Malaysia – Early Management of Head Injury in Adults