Traumatic brain injury

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 !!