Transcript
Traumatic brain injuryDr. Syed Faheem Shams
MD (Part III) studentDept. of Psychiatry
BSMMU
Objectives Traumatic brain injury- What? Epidemiology? Cause and
effect? Types? When to give attention?
Why we need to know?
Brain InjuriesBrain Injuries
Congenital brain injury
Pre-birth During birth
Acquired Brain Injury
After birth process
Traumatic Brain Injury(external physical force)
Non-traumatic Brain Injury
Closed Head Injury
Open Head
Injury
What is a TBI?What is a TBI?
Sudden damage to the brain due to an Sudden damage to the brain due to an external forceexternal force
Two types of TBITwo types of TBI OPEN-HEAD INJURY
(penetrating)
Example:• Skull fracture that
penetrates the brain• Gunshot wound
CLOSED-HEAD INJURY (non penetrating) when the head forcefully when the head forcefully
collides with another collides with another objectobject
Example:• Coup-Contra Coup• Diffuse axonal injury
ICD-10 S 06- Intracranial injuryS06.0 Concussion
Commotio cerebriS06.1 Traumatic cerebral oedema
S06.2 Diffuse brain injury Cerebral
contusion NOS laceration NOS
Traumatic compression of brain NOSS06.3 Focal brain injury
Focal: cerebral:
contusionlaceration
traumatic intracerebral haemorrhageS06.4 Epidural haemorrhageExtradural haemorrhage (traumatic)
S06.5 Traumatic subdural haemorrhageS06.6 Traumatic subarachnoid haemorrhage
S06.7 Intracranial injury with prolonged comaS06.8 Other intracranial injuries
Traumatic haemorrhage:cerebellar
intracranial NOSS06.9 Intracranial injury, unspecified
Brain injury NOS
Brain Injury Facts
Worldwide • Brain injury is the leading cause of death
and disability• Traumatic brain injury is the leading cause
of seizure disorders• The global incidence rate of TBI is
estimated at 200/100 000 people per year
http://www.internationalbrain.org/?q=brain-injury-facts http://injuryprevention.bmj.com/content/16/Suppl_1/A17.2.abstract
Brain Injury Facts(contd.)
United States
Europe
01 million hospital admissions per year
In the south of Europe, the main cause --traffic accidents
In the north of Europe, the major causes- falls, mainly related to alcohol use (Tagliaferri et al 2006)
http://injuryprevention.bmj.com/content/16/Suppl_1/A17.2.abstract
01 million Treated and released from hospital
80,000 Some TBI-related disability
50,000 die Males> females
15-24 years
EpidemiologyEpidemiologyPercentage of Average Annual TBI-related emergency department visits, Percentage of Average Annual TBI-related emergency department visits, hospitalizations, and deaths, by External Cause, United States, 1995-2001hospitalizations, and deaths, by External Cause, United States, 1995-2001
Falls, 28%
Motor Vehicle-Traffic, 20%
Struck By/Against, 19%
Assault, 11%
Unknown, 9%
Other, 7%
Pedal Cycle (non MV), 3%
Suicide, 1%
Other Transport, 2%
The greatest number of TBIs occur in people aged 15–24
TBI rates are higher in males
Occupational Therapy and Physical Dysfunction: Principles, Skills and Practice. Edinburgh: Churchill Livingstone. pp. 395–96
TBI in children can be TBI in children can be especially devastatingespecially devastating
Brain Rates of DevelopmentBrain Rates of Development
P-OCT
F-T
P-OCF-T P-O
T C
F-T
5 Distinct Periods of Maturation
P - O parietal/ occipital
C central (limbic & brainstem)
T temporal
F - T frontal/ temporal
Severity of traumatic brain injury
GCS PTA LOC
Mild 13-15 <1 day 0-30 min
Moderate 9-12 >1- 14 days >30 min– 6 hrs
Severe 3-8 >14 days >6 hrs
Lishman’s Organic psychiatry, 4th edition
In severe diffuse traumatic injury: PTA (weeks) = 0.4 × LOC (days) + 3.6
Katz and Alexander (1994)
Brain ConcussionBrain Concussion• Impaired function • No structural damage • Extreme variance in severity
– LOC• Diffuse
CONCUSSION vs CONTUSIONCONCUSSION
• Temporary loss of neurologic function with no structural damage lasting for a few seconds to few minutes
CONTUSION• More severe injury in
which the brain is bruised, with possible surface hemorrhage
• Unconscious for more than a few seconds or minutes
• Picture is somewhat similar to that of shock
Coup Contra-Coup InjuryCoup Contra-Coup Injury
Epidural haemorrhage
Subdural haemorrhage
Subarachnoid haemorrhage
ManagementManagement The acute management of severe traumatic The acute management of severe traumatic
brain injury:brain injury:– 1. Protect the airway & oxygenation– 2. Ventilate to normocapnia– 3. Correct hypovolaemia & hypotension – 4. CT Scan when appropriate– 5. Neurosurgery if indicated– 6. Intensive Care for further monitoring and
management
Significant Head InjuriesSignificant Head Injuries Signs of increased ICP---Signs of increased ICP---
–Visual difficultiesVisual difficulties–VomitingVomiting–DyspneaDyspnea– BradycardiaBradycardia
How Brain Injuries How Brain Injuries treated?treated?
Interesting findings The most common areas to have focal
lesions in non-penetrating traumatic brain injury are the orbitofrontal cortex and the anterior temporal lobes
"Frontal lobe dysfunction following closed head injury. A review of the literature". Journal of Nervous & Mental Disorders 178 (5): 282–291. "Deformation of the human brain induced by mild acceleration". Journal of
Neurotrauma 22 (8): 845–856. "Frontal-subcortical circuits and human behavior".Archives of Neurology 50 (8): 873–880.
"TASIT: A new clinical tool for assessing social perception after traumatic brain injury". Journal of Head Trauma Rehabilitation 18 (3): 219–238.
Interesting findings (contd.)
• Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in 60.9% of individuals with TBI
Alexithymia and emotional empathy following traumatic brain injury". J Clin Exp Neuropsychol 32 (3): 259–67.
Is head injury a risk for dementia??
β-amyloid protein have been found to accumulate in about 30% of patients after TBI and may form plaques
(Roberts et al. 1994; Ikonomovic et al. 2004)
However, some groups have failed to find elevated Aβ after head injury
(Adle-Biassette et al. 1996; Macfarlane et al. 1999)
PSYCHIATRIC
PROBLEMS IN TBI?
Adolf Meyer published comprehensive case
reports about patients who presented behavior disturbances after head injuries and proposed a set of disorders called “traumatic insanities”, which included consciousness alterations, psychosis, and neurological symptoms (
Neylan 2000)
Post-traumatic delirium (post-traumatic
confusional state) and post-traumatic amnesia
Post-traumatic delirium (confusional state) shows much variation, depending on the severity of the injury and its complications
Post-traumatic delirium Apathetic Restless, Irritability Florid delirious statesWithdrawal
Fear, persecutory beliefs, and perplexity are common
Disorientation for time and place is marked at first
Post-traumatic delirium (contd.)
As the confusional state improves, confabulations come to dominate, almost always accompanied by lack of insight and disorientation
Associated with misinterpretation of surroundings and misidentification of people. It is not unusual for patients to believe that staff or other patients on the ward are familiar to them
Hallucinatory experiences may be troublesome;
visual hallucinations are most evident
Post-traumatic agitation
Patient may be abusive, aggressive, sexually disinhibited
Occurs in about 10% of patients with severe brain injury (Brooke et al. 1992)
Last a few days Agitated behavior is associated with
frontotemporal injury and doubles the risk of later emotional sequelae (van der Naalt et al. 2000).
Post-traumatic amnesia It ends at the time from which the patient
can later give a clear and consecutive account of what was happening around him
Period of unconsciousness + Post-traumatic delirium
Post-traumatic amnesia (contd.)
A study of orientation during PTA showed that the usual sequence of recovery was for person place time (Levin 1990).
Summary of findings for depression after TBI
Incidence 15.3%–33% Kim et al 2007
Prevalence 18.5%–61%Kim et al 2007 Abnormalities on CTLevin et al 2005 Lower bilateral hippocampal volumeJorge et al 2007
Volume reduction of the left prefrontal grey matterJorge et al 2004
UnemploymentSeel et al 2003; Dikmen et al 2004; Jorge et al 2004
Lower economic status; aggression; anxietyDikmen et al 2004
Why depression? Rupture of neural circuits involving the
prefrontal cortex, amygdala, hippocampus, basal ganglia, and thalamus may be related to the development of depression due TBI. (Jorge and Starkstein 2005)
The hippocampus is an anatomic region vulnerable to TBI (Campbell and MacQueen 2004)
Treatment of depression in TBI
Citalopram and sertraline (Turnes-Stokes and MacWalter 2005).
Citalopram (Rapoport et al 2008).
The use of fluoxetine, paroxetine,
venlafaxin, minalcipran, amitryptiline, desipramine, bupropio presented generally positive results (Alderfer et al 2005; Warden et al 2006).
Caution with TCAs Anticholinergic effects of TCAs can
exacerbate cognitive impairment.
Summary of findings for Mania after TBI
Incidence 9% Jorge et al 1999
Prevalence 4.2%van Reekum et al 2000
Higher rates for menvan Reekum et al 1996
Lesions in the temporal basal polesJorge et al 1993b; Murai and Fujimoto 2003
Treatment of Mania in TBI Valproic acid and lithium, while case
reports pointed out the usefulness of quetiapine, carbamazepine, clonidine, and electroconvulsive therapy
(Warden et al 2006; Oster et al 2007)
Summary of findings for Psychosis after TBI
Incidence 0.1%–9.8%David and Prince 2007 Prevalence 0.7%van Reekum et al 2000 Damage in frontal and temporal lobesAchte 1969; Sachdev et al 2001; Fujii and Ahmed 2002a Predominance of positive symptomsSachdev et al 2001
Persecutory (56%), reference (22%), control (22%), and grandiosity (20%).Fujii and Ahmed (2001)
Treatment of Psychosis in TBI
Typical antipsychotics have anticholinergic, hypotensive, or sedative effects, or a strong dopaminergic antagonism are potentially able to worsen the already existent deficits for TBI survivors.
(Feeney et al 1982; Goldstein 1993)
Summary of findings for OCD after TBI
Prevalence 1.6%–15%Hibbard et al 1998; Deb et al 1999 Oribitofrontal cortex, cingulate cortex and caudate nucleus damageBerthier et al 2001; Bilgic et al 2004; Ogai et al 2005 Obsessive slowness; compulsive exercises practice; aggressionBerthier et al 2001
Summary of findings for PTSD after TBI
Incidence 11.3%–24%Bryant and Harvey 1998; Bombardier et al 1999 Prevalence 3%–27.1%Bryant et al 2000; Glaesser et al 2004 Impaired quality of life and social function; chronic painBryant et al 1999 Posttraumatic amnesia as a protective factorSbordone and Liter 1995; Glaesser et al 2004; Gil et al 2005
Summary of findings for Personality change after TBI
Apathy Prevalence 34.5% after severe TBIPelegrín-Valero et al 2001
Younger age; more severe TBI
Kant et al 1998 Affective lability Prevalence 5%–32.7%
Zeilig et al 1996; Pelegrín-Valero et al 2001 Frontal lobe damage; aggression; anxietyRobinson et al 1993
Aggression Prevalence 16.4%–33.7%Pelegrín-Valero et al 2001; Tateno et al 2003
Predictors of poor outcome
• “ Poor response to psychiatric medications• “ Failure in behavioral programs requiring
memory and problem-solving• “ Social network failure: divorce, separation• Failure at work• “Persistence of chronic pain and headache
symptoms• “Lack of support system
OUTCOME In Severe Brain injury
Good recovery 25-30% Moderate disability 15-20% Sever disability 15% Vegetative stat 5% Death 30-35%
Thank you all !!
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