Psychiatric care of traumatic
brain injury
謝光煬
台灣大學醫學士暨理學博士
奇美醫學中心精神科主治醫師
南台科技大學生科所助理教授
Epidemiology of traumatic
brain injury (TBI)
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Leading causes: motor vehicle crashes, falls,
struck by/against events, violence.
High risk groups: adolescents and young adults,
people older than 75 years of age.
Male-to-female ratio = 2:1
Mortality rate: 5-6 %
Prevalence of TBI-related long-term disability in
general population: 1-2 %
Pathology of TBI
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Penetrating or closed injury
Epidural hemorrhage
Subdural hemorrhage
Subarachnoid hemorrhage
Intracerebral hemorrhage
Contusion
Diffuse axonal injury
Sequelae of TBI
Individual and variable
 Neurological symptoms:
Seizure
Blurred or double vision (diplopia)
Motor disorders:
weakness in limbs or facial muscles, muscle spasm,
incoordination of movements, unsteady gait.
Sensory disorders: tingling, numbness, pain.
Aphasia, slurred speech, dysphagia.
Dizziness, headache, vertigo.
 Psychiatric symptoms
Psychiatric symptoms of TBI
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Cognitive symptoms: decreased attention,
decreased speed in information processing,
impaired executive function, problems with
memory and learning new information.
Mood symptoms: depression, anxiety,
irritability, impulsivity, disinhibition,
emotional lability, inappropriate affect.
Psychotic symptoms: delusion, hallucination,
catatonia.
Personality change, behavior problem
(agitation, aggression, disturbing).
Pathogenesis of posttraumatic
psychiatric disturbance
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Preinjury factors: age, gender, neurogenetics,
baseline cognitive function, psychiatric
conditions, substance abuse, socioeconomic
environment, and risk-taking behaviors.
Injury characteristics: location, type, and
severity of neural damage.
Postinjury factors: social support, timely
medical and rehabilitative treatments,
socioeconomic status, and medicolegal issues.
(Am J Psychiatry. 2009; 166:653–661)
Natural course of TBI (1)
Stages of recovery:
 Acute stage: to stabilize the patient
immediately after the injury.
 Subacute stage: to rehabilitate and return
the patient to the community.
 Chronic stage: to continue rehabilitation
and treat the long-term impairments.
Natural course of TBI (2)
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There is a period of posttraumatic amnesia or
confusion, defined as occurring between the
time of injury and the return of continuous
memory.
A 6- to 12-month period of spontaneous
recovery follows. After this period, remaining
symptoms are likely to be permanent.
Long-term outcome: 22.2% improved, 15.2%
declined, and 62.6% unchanged from 1 year
after injury to 5 years.
(J Head Trauma Rehabil. 2001; 16:343-55.)
Indicators of prognosis
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Duration of coma: the shorter the coma,
the better the prognosis.
Posttraumatic amnesia/confusion: the
shorter this period, the better the prognosis.
Age: patients over 60 or under 2 years old
have the worst prognosis.
Pharmacological strategies
for neuroprotection in TBI
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Strategies targeting inflammation,
oxidative damage, glutamate
excitotoxicity, cell death and
regeneration have been proposed and
under investigation.
Psychiatric pharmacotherapy
at acute/subacute stage of TBI
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Posttraumatic amnesia/confusion or delirium is the
major psychiatric problem at acute/subacute stage of
TBI. However, using antipsychotics at this period has
a negative impact on cognitive recovery. It results in 7
more days required to clear posttraumatic amnesia.
(Brain Inj. 2006; 20:905-11.)
Avoid giving antipsychotics at this stage unless there
is confusion or delirium with significant behavior
problem.
Use 2nd-generation antipsychotics since they have less
negative effects on cognitive recovery.
Psychiatric pharmacotherapy at
subacute/chronic stages of TBI
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Psychiatric symptoms at subacute/chronic stage of
TBI need appropriate intervention since they
impede the recovery process and rehabilitation.
Patients with moderate to severe TBI who
developed mood disorders had significantly
smaller hippocampal volumes and worse
vocational outcomes at 1-year follow-up than
patients with equivalent severe TBI who did not
develop mood disturbance.
(Biol Psychiatry. 2007; 62:332-8. )
Current practice is a symptom-based approach.
Points for attention about
psychiatric pharmacotherapy of TBI
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Be aware that patients with TBI are especially
sensitive to extrapyramidal symptoms.
Sedative and anticholinergic effects of
medications may impede cognitive functions.
Start low and go slow.
Be careful of the motor and cognitive effects
of medications.
Assess risk and benefit.
Treating cognitive symptoms
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Stimulants: methylphenidate 20-40 mg/d
recommended for increasing attention and
speeding up information processing. Also
effective for depression.
Cholinergic agents: donepezil 5-10 mg/d
recommended for improving attention and
memory.
Dopaminergic agents: amantadine,
bromocriptine.
Treating behavioral symptoms
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Beta-blockers: propranolol 20-160 mg/d
recommended for aggression or agitation.
Underlying mood or psychotic symptoms
should be treated.
Treating mood symptoms
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Antidepressants: sertraline and other
selective serotonin reuptake inhibitors
(SSRIs) for depression and anxiety.
Anticonvulsants: valproate for irritability,
impulsivity and posttraumatic epilepsy.
Be careful of sedative and muscle-relaxing
effects of benzodiazepines. Avoid using
them in patients with TBI.
Treating psychotic symptoms
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It has been proposed that 2nd-generation
antipsychotics should be the primary agents for
psychosis and significant agitation after TBI.
There are some case reports and case series
using risperidone, ziprasidone, quetiapine,
olanzapine, or clozapine in TBI, mostly for the
management of agitation.
There is a lack of literature about zotepine,
aripiprazole and amisulpride in TBI.
Neuropsychological and
occupational assessment
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To evaluate the degree of damage and
recovery
To help application for disability
certificate and welfare
To provide evidence for lawsuit or
litigation
Holistic care of TBI
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Neuropsychiatric pharmacotherapy
Neuropsychological rehabilitation
Psychotherapy, cognitive behavioral
therapy
Social welfare and support
Thanks for attention