Ruwan M Jayatunge M.D.
A significant number of Sri Lankan soldiers
sustained head injuries during the Eelam War that lasted from 1983 to 2009.
These head injuries mainly occurred due to gunshot wounds, mortar blast injuries,
grenade explosions and artillery blasts. Traumatic Brain Injuries increased
High morbidity and mortality rates among the Sri Lankan combatants. Traumatic
Brain Injury (TBI) had been one of the signature injuries of the Eelam
War.
Traumatic brain injury has short and long term
consequences. It affects the physical, social, psychological and occupational
aspects of a combatant’s life. The combatants with severe TBI have
permanent neurobiological damage with profound psychosocial problems. TBI has been
identified as one of the disabling conditions among the combatants.
Traumatic brain injury (TBI) refers to a
physiologically significant disruption of brain function resulting from the
application of external physical force, including acceleration/deceleration
forces (Silver et al, 2009). The victims experience emotional lability, sensory
impairments, neuro- cognitive deficits and spasticity following traumatic brain
injuries.
Traumatic brain injury is a
common cause of neurological damage and disability among civilians and
servicemen (Auxéméry, 2012). Schneider and colleagues (2009) elucidate that
behaviorally the military population in general is considered to be a high
risk group for TBI. According to Scherer et al., (2013) within the
last decade, more than 220,000 service members have sustained traumatic brain
injury (TBI) in support of military operations in Iraq and Afghanistan.
In Sri Lanka from 1983 to 2009 over
200,000 military personnel were deployed in the operational areas and
considerable numbers sustained mild to severe head injuries following enemy
attacks. In a convenience sample of 824 Sri Lankan Army servicemen who were
referred to the Psychiatric ward Military Hospital Colombo during August 2002
to March 2006 time period 29 combatants (3.51%) were diagnosed with
TBI. These diagnoses were based on International Classification of
Diseases- Tenth Revision (ICD-10) criteria and done by the Consultant
Psychiatrist of the Sri Lanka Army.
The Immediate Impact of TBI
Traumatic brain injury has
immediate impacts. TBI combines mechanical stress to brain tissue with an
imbalance between cerebral blood flow and metabolism, excitotoxicity, oedema
formation, and inflammatory and apoptotic processes (Werner & Engelhard,
2007). The immediate effect of head trauma could be loss of consciousness
followed by headaches and dizziness. Sometimes confusion and
disorientation could occur from mild to moderate form of head injuries. In
a severe form of TBI prolonged periods of loss of consciousness, seizures and
paralysis could occur.
Traumatic Brain Injury in the War Zone
During the Eelam War some of the
combatants who sustained head injuries were not immediately evacuated due to
technical difficulties. Intensify heavy fighting and weather conditions
affected evacuation of the battle casualties. However the wounded received
first aid and then brought back to the rear zone medical aid point where they
were examined by a qualified medical officer. The head injuries were
assessed and then transferred to the Palali Military Hospital or to a nearby
hospital. Some battle casualties who sustained severe head trauma were
airlifted and transferred to major hospitals in Anuradhapura or in Colombo. In
these hospitals the war casualties received specialized treatment by the
Neurosurgeons.
TBI and Cognitive Impairments
The combatants who sustained serious
head trauma later found with cognitive impairments. Neurocognitive impairments
are prevalent in TBI. Among the debilitating conditions, memory impairments,
difficulty with attention and concentration, difficulty with new learning, and
impaired problem solving skills are frequently identified. As indicated by
Arciniegas (2003) cognitive impairments are among the most common
neuropsychiatric sequelae of traumatic brain injury at all levels of severity.
Traumatic brain injury (TBI) can produce persistent attention and memory
impairment that may in part be produced by impaired auditory sensory gating
(Arciniegas et al., 2000).
Cognitive dysfunctions associated with
TBI were known to military psychologists since World War One. The British
Physician Frederic Mott (WW1) and Dr Alexander Luria of the Soviet Army (in the
WW2) extensively studied the impact of combat related head injuries. Caveness ,
Walker, & Ascroft (1962) believed that World War I, World War II, and the
Korean war produced a large number of combatants with TBI and other associated
complications. In the Vietnam War 12 to 14 percent of all combat casualties had
a brain injury (Okie , 2005).
TBI-related cognitive impairment
is common in veterans who have served in recent conflicts in the
Middle East and is often related to blasts from improvised explosive devices
(Halbauer et al., 2009). The Sri Lankan combat veterans who sustained severe
form of head injuries reported drastic impairments in memory and concentration.
Some were found with post-traumatic amnesia. A large percentage of
combatants were found with intellectual disabilities and impaired language
skills.
Personality Changes Following Head Injury
Personality change has been reported in
49% to 80% of patients with traumatic brain injury (Brooks et
al., 1986). A significant number of Sri Lankan combatants with TBI were
found with subsequent Personality changes. Some of the personality changes such
as agitation, paranoia, mood swings, aggression, lack of inhibition,
inappropriate sexual activity and impaired self control have caused major
barriers to their military and personal lives.
Prominent behavioral characteristics in
TBI patients have included altered emotion (including restricted emotions with
occasional inappropriate or uncontrolled emotional outbursts); impaired
judgment and decision–making (including difficulty arriving at decisions as
well as poor decisions); impaired initiation, planning, and organization of
behavior; and defective social comportment (including egocentricity and
impaired empathy). These impairments tend to be accompanied by a marked lack of
insight. (Fowler, 2011: Barrash et al.,2000). According to Oddy et al. (1985)
two thirds of individuals with TBI experience personality changes for long
periods and sometimes over 15 years.
TBI and Depression
Mood disturbances are common sequelae
of traumatic brain injury (Hurley & Taber, 2002). Bay and
colleagues (2004) are of the view that Pre-injury factors (such as mood
and anxiety disorders, psychosocial dysfunction, and alcohol abuse), injury
factors (such as left ventrolateral and dorsolateral injury and serotonergic
dysfunction), and post-injury factors (such as postconcussive symptoms,
psychosocial dysfunction, and lack of social supports) contribute to the
development of depression after TBI, although the relevance of each factor
varies among patients.
Combatants with TBI have a large array
of psychosocial problems that affect their professional and family lives. Jorge
et al. (2004) observed strong association between posttraumatic depression and
psychological and psychosocial factors.
Sometimes post TBI depression could
increases anger, aggression and suicide risk (Fann , Katon ,
Uomoto & Esselman, 1995). An increased suicide risk has been identified
among the combatants who fought in the Eelam War. According to the
Military Spokesperson of the Sri Lanka Army from 2009 to 2012 postwar period
nearly 400 soldiers had committed suicide (Sriyananda, 2012).
TBI and Posttraumatic Stress Disorder
Post-traumatic stress disorder (PTSD)
and traumatic brain injury (TBI) often coexist because brain injuries are often
sustained in traumatic experiences. In addition evidence suggests that mild TBI
can increase risk for PTSD (Bryant, R 2011).
Some investigators have argued that
individuals who had been rendered unconscious or suffered amnesia due to a TBI
are unable to develop PTSD because they would be unable to consciously
experience the symptoms of fear, helplessness, and horror associated with the
development of PTSD. Other investigators have reported that individuals, who
sustain TBI, regardless of its severity, can develop PTSD even in the context
of prolonged unconsciousness. (Sbordone & Ruff, 2010).
Despite the discrepancies, a strong
connection between Post-traumatic stress disorder and traumatic brain injury
has been reported from battlefields around the world. Hoge et al. (2008) point
out that mild traumatic brain injury (i.e., concussion) occurring among
soldiers deployed in Iraq is strongly associated with PTSD and physical health
problems 3 to 4 months after the soldiers return home. Elder & Cristian
(2009) too report high association of mild traumatic brain injury with
posttraumatic stress disorder among the veterans of the wars in Iraq and
Afghanistan. A notable number of Sri Lankan combatants have been diagnosed with
TBI and PTSD during the Eelam War.
Posttraumatic Epilepsy
Posttraumatic epilepsy is a major source
of disability following traumatic brain injury (TBI) and a common cause of
medically-intractable epilepsy (Guo et al., 2013). As indicated by
Diaz-Arrastia and colleagues (2009) posttraumatic epilepsy is a common
complication of traumatic brain injury (TBI), occurring in up to 15-20% of
patients with severe brain trauma. There are a number of risks associated
with Posttraumatic epilepsy. Yeh et al. (2012) hypnotize that the risk of
epilepsy after TBI varied by patient gender, age, latent interval and
complexity of TBI.
Combat veterans with head trauma are at
high risk of developing posttraumatic epilepsy. As indicated by Chen and
colleagues (2009) both Korean and Vietnam War veterans with
penetrating TBI had a 53% risk of developing PTE.
Neurologist Ranjani Gamage (2003)
reported that in Sri Lanka there were 300,000 persons with epilepsy.
This number would have included combatants with epilepsy due to TBI
Psychiatric Symptoms Followed by TBI
The intersection between traumatic
brain injury and Psychosis has become one of the major concerns. Some of the
Sri Lankan combatants with TBI were later found with psychosis and these
individuals had disorganized thought and speech, paranoid delusions with loss
of contact with reality.
Koponen et al. (2002) suggest
that traumatic brain injury may cause decades-lasting vulnerability to
psychiatric illness in some individuals. In addition they hypnotize that
traumatic brain injury seems to make patients particularly susceptible to
depressive episodes, delusional disorder, and personality disturbances. In one
of the studies that was conducted by Deb and colleagues (1999) found that in
comparison with the general population, a higher proportion of adult patients
had developed psychiatric illnesses one year after a traumatic brain injury.
Fann et al. (1995) point out that psychiatric disorders are a major cause of
disability after traumatic brain injury.
Chronic Traumatic Encephalopathy in
Combatants
Chronic Traumatic Encephalopathy (CTE)
is thought to be a neurodegenerative disease associated with repeated
concussive and subconcussive blows to the head (Mez ,Stern & McKee ,
2013). During military training soldiers repetitively sustain mild head
trauma that has a negative impact on their mental health. According
to Zhang et al. (2013) subconcussive blows can result in cognitive
function changes that are consistent with mild traumatic brain injury of the
frontal lobes.
The soldiers who served in the artillery
batteries during the Eelam War were frequently exposed to blast impacts.
Furthermore they faced artillery attacks, mortar fire, grenade and claymore
blasts initiated by the enemy. Although a large number of combatants did not
sustain any head trauma a considerable percentage experienced the blast
shockwaves. The shock waves may have had a negative
cumulative effect on them. A considerable fraction of combatants who were
exposed to blast shockwaves complain of chronic headaches, tremors
and generalized body pain. This factor was evident in the numerous
battles that were fought in different countries.
Military physicians of World War One
believed that artillery blasts could cause miniature hemorrhages in the brain
causing tremors and long lasting headaches in soldiers. Teland,& Huseby
(2102) of the Norwegian Defence Research Establishment (FFI)
hypothesize that military personnel who are exposed to blast waves
during training and combat are at a significant health risk.
The combat-related traumatic brain
injuries (TBI) resulting from exposure to explosions is highly prevalent among
military personnel who have served in current wars. Blast trauma can
be understood as experiencing a shockwave on the brain and as a
psycho-traumatic event (Auxéméry, 2012). Chronic pain is a common complication
of TBI. It is independent of psychologic disorders such as PTSD and depression
and is common even among patients with apparently minor injuries to the brain.
(Nampiaparampil, 2008).
Head trauma could cause degenerative
changes in the brain tissue. Byrnes et al. (2012) point out that traumatic
brain injury initiates biochemical processes that lead to secondary
neurodegeneration. Traumatic brain injury causes
progressive neurodegeneration associated with chronic microglial
activation (Xue et al, 2013). Atrophic changes of the brain that are resulted
by TBI can have a lasting impact on soldiers. Symptoms can range to prolong
headaches to severe neurological and psychological consequences.
Treatment Options
TBI has drastic impacts on independent
living skills of the combatant. The survivors need effective psychosocial
rehabilitation. The outcome and impact evaluation following combat related TBI
is highly essential in the rehabilitation process. The concept of the
outcome of brain injury” needs to be viewed in the context of a dynamic and
changing series of events which occur throughout a person’s life Gainer, 2010).
Various risk factors for poor outcome
after TBI have been identified. Most of these are fixed at the time of injury
such as age, gender, mechanism of injury, and presenting signs (Glasgow Coma
Scale and pupillary signs), but some such as hypotension and hypoxia are
potential areas for medical intervention (Moppett, 2007).
Cerebral metabolic derangement and
excitotoxicity play critical roles in the evolution of traumatic brain injury
(Hwabejire et al., 2013). Expert opinion suggests that combination therapies
will be necessary to treat any stage of TBI recovery (Shear & Tortella,
2013). Drug management is important in seizure control. Chen and colleagues
(2009) are of the view that optimal seizure control is essential to the
physical and emotional health of veterans with TBI and to their
ability to lead productive lives.
Psychotherapy is an important component
of the treatment of neuropsychiatric problems following TBI (Arciniegas et al.,
2000). Cognitive rehabilitation may also be useful for the treatment
of impaired attention, interpersonal communication skills, and executive
function following TBI (Arciniegas et al., 2002). Bédard et al. (2003)
suggest mindfulness-based intervention to improve quality of life among
individuals who sustained traumatic brain injuries. In addition occupational
therapy, speech language therapy and physiotherapy play a key role in the
rehabilitation process.
Case Discussion
1) Private SNX764
joined the Army in 1991 and served in the operational areas. He took part in
several major military operations against the LTTE. In 1995 he was posted to
Mallakam -Jaffna. There he had to face fierce enemy attacks. Once the enemy
attacked them with mortars. Following nonstop mortar attacks, Private SNX764
was stunned and disoriented. His bunker was damaged severely and he wanted to
crawl to a safe area. When he tried to reach the next bunker an incoming
mortar blasted a few meters away from him. Suddenly he could feel bleeding from
his ears and he lost consciousness. After a few hours of fighting the enemy
retreated. Then he was evacuated and taken to the Palali military hospital.
He was treated for a head injury. Although he survived the mortar blast his
speech was impaired. He experienced severe intermittent headaches and insomnia.
By 1996 he had intrusions, flashbacks and marked avoidance for combat related
settings. His mental health started deteriorating further. Several
times Private SNX764 had tried to commit suicide while serving in the
operational areas. Finally he was referred for a psychological evaluation and
found with chronic PTSD.
2) Capt. KXXC385 was
an experienced field officer who participated in numerous commando operations.
He sustained a head injury as a result of a parachuting accident. He was
unconscious for over two weeks and treated at the Neurological unit.
After the acute phase he was referred for rehabilitation therapy. After years
of treatment he returned to his unit as a completely changed person. He had
difficulty in concentration, Emotional lability and cognitive impairments. His
personality changed tremendously after the head trauma. Once a skillful
professional soldier turned into a dependent unsteady person with marked
psychosocial dysfunctions. His professional and private life fell apart.
His decision–making and initiation were significantly deteriorated and
sometimes he engaged in socially inappropriate behavior failing to detect
social cues. Capt. KXXC385 was diagnosed with Personality changes following
head injury.
3) Major WXX856
sustained a head injury due to a grenade blast in a training mission. He was
unconscious and treated at the Neurosurgical unit of the National Hospital
Colombo. Major WXX856‘s injury was reordered as a moderate type of head injury
based on the Glasgow Coma Scale (GCS). After the injury he experienced frequent
headaches and irritability. He had low frustration tolerance and often became
very impulsive. His family members observed drastic changes in his behavior.
Frequently he engaged in family violence. His personality started to change
with head trauma. The senior officers found that Major WXX856 was neglecting
his duties. A number of times he was reprimanded. To displace his psychosocial
difficulties Major WXX856 started to drink alcohol in large quintiles in daily
basis. His treatment schedule was interrupted and eventually in the final two
years he did not receive any treatment at all. Major WXX856 became more and
more isolated and had homicidal urges. In 2004 Major WXX856 committed several
murders secretly and enjoyed the brutal acts. He took his final victim – a cab
driver to his remote camp and intoxicated him and then killed him by cutting
the victim’s throat. He had no remorse or any regrets after committing these
murders. Major WXX856 was looking for more victims to fulfill his homicidal
urge. In his final attempt he tried to abduct a victim near a remote tea
estate but the attempt was unsuccessful. Some estate workers alerted the
Police. Hence he was arrested and sent to the remand prison. The investigators
found several other murders that were committed by Major WXX856. While his
trial was pending Major WXX856 committed suicide by hanging.
4) Private
KXXT342 met with a landmine explosion in Chunnakam –Jaffna in 1996 while
travelling in a military vehicle. Some of his buddies got killed due to the
blast. He could only remember the black smoke and fatal outcry of his buddies.
The soldiers from the second vehicle took the wounded to the hospital
immediately. Private KXXT342 sustained a head injury and was treated at the
Palali military hospital and then referred to the National Hospital -Colombo.
He underwent treatment for several months. He had impaired hearing, slurred
speech and loss of coordination after the injury. In addition he suffered
epileptic fits. Private KXXT342 was diagnosed with Posttraumatic Epilepsy. After
becoming a battle casualty Private KXXT342 experienced a number of psychosocial
problems which affected his life. He was treated with antiepileptic drugs and
CBT. Following treatment he was able to overcome most of his psychosocial
problems.
5) Corporal BXVX486
served in an artillery battery for over 9 years. During this time period his
team had fired a large number of artillery rounds. Although he was physically
unharmed throughout the war his luck changed dramatically. Corporal BXVX486
complained of tremors in both hands, frequent headaches and myalgia after
serving lengthy years in the artillery battery. The physicians who examined him
found no organic factor associated with his condition. There were no
Electroencephalography (EEG) changes and his brain scan and other reports were
normal. He was suspected as a malingerer at one point but later found that his
symptoms were real. Corporal BXVX486 poorly responded to the painkillers. His
condition started to improve with relaxation therapy and EMDR.
6) L/ Cpl AXXCX831
sustained a TBI following a gun short injury. After he became a battle casualty
L/ Cpl AXXCX831 experienced a number of psychosocial problems. He could not
control his anger and became extremely hostile. He used to physically abuse his
wife and children. He had depression and several times he planned to end his
life. Once he took poison and immediate hospitalization saved his life. He was
treated with Selective serotonin reuptake inhibitors (SSRI ) and mood
stabilizers with CBT. Following drug therapy and psychotherapy L/ Cpl
AXXCX831’s condition improved notably.
Conclusion
Although Traumatic Brain Injury has
impacted a large number of Sri Lankan combatants who fought in the Eelam War,
the psychological sequelae of brain trauma were not adequately studied. The
combatants who sustained TBI have persistent headaches, memory impairments,
sleep difficulties, low frustration tolerance, impaired life skills, emotional
difficulties, impaired decision making and behavioral changes.TBI has caused
profound psychosocial problems among the veterans. These problems affect their
private and professional lives. The combatants with TBI need effective
psychosocial rehabilitation to overcome their current difficulties. Further
research is needed to estimate the overall impact of TBI among Sri Lankan
combat veterans.
Acknowledgements
1) Dr. Rolf B. Gainer
– Consultant Neurologist – Brookhaven Hospital Tusla Oklahoma
2) Professor Daya
Somasundaram – University of Adelaide Australia
3) Dr. (Mrs) N.K
Ariyarathne – Consultant Physician – Military Hospital Colombo.
References
Arciniegas, D.B., Olincy, A., Topkoff,
J., McRae ,K., Cawthra ,E., Filley, C.M., Reite, M., Adle,r
L.E.(2000). Impaired auditory gating and P50 nonsuppression following traumatic
brain injury. Journal of Neuropsychiatry & Clinical Neuroscience .77-85.
Arciniegas, D.B., Topkoff, J., Silver,
J.M.(2000). Neuropsychiatric Aspects of Traumatic Brain Injury. Curr Treat
Options Neurol.169-186.
Arciniegas DB, Held K, Wagner P.(2002). Cognitive
Impairment Following Traumatic Brain Injury. Curr Treat Options Neurol.
4(1):43-57.
Arciniegas, D.B.(2003). The cholinergic
hypothesis of cognitive impairment caused by traumatic brain injury. Curr.
Psychiatry Rep. 5:391–399.
Auxéméry Y.(2012). Mild
traumatic brain injury and postconcussive syndrome: a re-emergent questioning.
Encephale. 38(4):329-35.
Barrash, J., Tranel, D., & Anderson
S. (2000). Acquired personality disturbances associated with bilateral damage
to the ventromedial prefrontal region. Developmental Neuropsychology, 78(3),
355-381.
Bay, E., Kirsch, N., Gillespie, B.
(2004). Chronic stress conditions do explain posttraumatic brain injury
depression. Res Theory Nurs Pract .213–228
Bédard, M., Felteau, M., Mazmanian, D.,
Fedyk, K., Klein, R., Richardson, J., Parkinson, W., Minthorn-Biggs,
M.B.(2003). Disabil Rehabil.25(13):722-31.
Brooks, N., Campsie, L., Symington, C.,
Beattie, A., McKinlay, W.(1986).The five year outcome of severe blunt head
injury: a relative’s view. J Neurol Neurosurg Psychiatry.49:764-770.
Bryant, R (2011). ‘Post-Traumatic
Stress Disorder vs traumatic brain injury’ Dialogues in Clinical Neuroscience
13(3), p251-262.
Byrnes,
K.R., Loane,D.J., Stoica, B.A., Zhang,
J., Faden,A.I.(2012). Delayed mGluR5 activation limits
neuroinflammation and neurodegeneration after traumatic brain injury.Journal of Neuroinflammation 9:43.
Caveness, W.F, Walker, A.E, Ascroft,
P.B. (1962). Incidence of posttraumatic epilepsy in Korean veterans as compared
with those from World War I and World War II. J Neurosurg.19:122–2
Chen, J.W., Ruff, .RL., Eavey, R,.
Wasterlain, C.G. (2009). Posttraumatic epilepsy and treatment.J
Rehabil Res Dev.685-96.
Deb, S., Lyons, I., Koutzoukis, C.,
Ali, I., McCarthy, G.(1999). Rate of psychiatric illness 1 year after
traumatic brain injury.Am J Psychiatry. ;156(3):374-8.
Diaz-Arrastia, R., Agostini, M.A.,
Madden, C.J., Van Ness, P.C. (2009). Posttraumatic epilepsy: the endophenotypes
of a human model of epileptogenesis. Epilepsia (Suppl 2): 14–20.
Elder GA, Cristian A. (2009).
Blast-related mild traumatic brain injury: mechanisms of injury and impact on
clinical care. Mt Sinai J Med.76(2):111-8
Fann, J.R., Katon, W.J., Uomoto, J.M.,
Esselman, P.C.(1995).Psychiatric disorders and functional disability in
outpatients with traumatic brain injuries. Am J Psychiatry.152:1493-1499.
Fowler, M (2011). Traumatic Brain
Injury and Personality Change Rtrived from http://www.readperiodicals.com/201105/2352132631.html
Franulic, A., Horta, E., Maturana, R.,
Scherpenisse, J., Carbonell, C.(2000). Organic personality disorder after
traumatic brain injury: cognitive, anatomic and psychosocial factors: a 6 month
follow-up. Brain Inj.14:431-439.
Gainer, R. et al. (2010). NRIO
Outcome Validation Study: 1997-2010, Neurologic Rehabilitation Institute of
Ontario, Etobicoke, Ontario.
Guo, D., Zeng, L., Brody, D.L., Wong,
M. (2013). Rapamycin Attenuates the Development of Posttraumatic Epilepsy in a
Mouse Model of Traumatic Brain Injury. PLoS ONE 8(5): e64078.
doi:10.1371/journal.pone.0064078.
Halbauer, J.D., Ashford, J.W., Zeitzer,
J.M., Adamson, M.M., Lew, H.L., Yesavage, J.A. (2009).J Rehabil Res Dev.757-96.
Hoge, C.W., McGurk, D., Thomas, J.L.,
Cox, A.L., Engel, C.C., Castro, C.A. (2008).Mild traumatic brain injury in U.S.
Soldiers returning from Iraq.N Engl J Med. 358(5):453-63.
Hurley, R.A., Taber, K.H.
(2002).Emotional disturbances following traumatic brain injury. Curr Treat
Options Neurol.;4:59-75.
Hwabejire, J.O,
Jin, G., Imam, A.M., Duggan, M., Sillesen, M., Deperalta, D., Jepsen, C.H., Lu,
J., Li, Y., deMoya, M.A, Alam, H.B.(2013). Pharmacologic modulation of
cerebral metabolic derangement and excitotoxicity in a porcine model of
traumatic brain injury and hemorrhagic shock. Surgery. 154(2):234-43.
Jennett, B., Bond, M.(1975). Assessment
of outcome after severe brain damage. A practical scale. Lancet.480–4.
Jorge, R.E., Robinson, R.G., Moser, D.,
Tateno, A., Crespo-Facorro ,B., Arndt, S.(2004). Major depression following
traumatic brain injury. Arch Gen Psychiatry. 61:42–50.
Koponen, S., Taiminen, T., Portin, R.,
Himanen, L., Isoniemi, H., Heinonen, H., Hinkka, S., Tenovuo, O.(2002).
Am J Psychiatry. 159(8):1315-21.
Mez J, Stern RA, McKee AC.(2013).Curr
Neurol Neurosci Rep. (12):407.
Moppett, I.K. (2007).Traumatic brain
injury: assessment, resuscitation and early management.Br J Anaesth.18-31.
Nampiaparampil, D.E.(2008).Prevalence
of chronic pain after traumatic brain injury: a systematic review.JAMA.
711-9.
Oddy, M.,
Coughlan, T., Tyerman, A., & Jenkins, D. (1985). Social adjustment after
closed head injury: A further follow–up seven years after injury. Journal of Neurology, Neurosurgery and Psychiatry, 48,
564–568.
Okie S. (2005). Traumatic brain injury
in the war zone. N. Engl. J. Med. 352, 2043–2047.
Sbordone, R. J., & Ruff, R. M.
(2010). Re-examination of the controversial coexistence of traumatic brain
injury and posttraumatic stress disorder: Misdiagnosis and self-report
measures. Psychological Injury and Law, 3, 63-76.
Scherer, M.R., Weightman, M.M.,
Radomski, M.V., Davidson, L.F, McCulloch, K.L. (2013). Returning service
members to duty following mild traumatic brain injury: exploring the use of
dual-task and multitask assessment methods. Phys Ther. 93(9):1254-67.
Schneider,S. L., Haack,
L., Owens, J., Herrington,D. P., Zelek ,A (2009). An
Interdisciplinary Treatment Approach for Soldiers With TBI/PTSD: Issues and
Outcomes. Perspectives on Neurophysiology and Neurogenic Speech and Language
Disorders .vol. 19 no. 2 36-46.
Shear, D.A., Tortella, F.C.(2013). A
military-centered approach to neuroprotection for traumatic brain injury.Front
Neurol. 12;4:73.
Silver,J. M., McAllister, T. W.,
Arciniegas, D. B. (2009). Depression and cognitive complaints following mild
traumatic brain injury. American Journal of Psychiatry.166:653–661.
Sriyananda, S.
(2012 September 24). Nearly 400 soldiers commit suicide in peacetime. The
Island Newspaper. Retrieved on February 14, 2013, from http://www.island.lk/index.php?page_cat=article-details&page=article-details&code_title=62302
Teland, J.A., Huseby, M.
(2102). Blast wave propagation into the brain.Norwegian Defence Research
Establishment (FFI). Retrieved from http://www.ffi.no/no/Rapporter/12-02416.pdf
Werner C, Engelhard K.(2007).
Pathophysiology of traumatic brain injury. Br J Anaesth. 99: 4–9.
Xue, F., Stoica, B.A., Hanscom, M.,
Kabadi, S.V., Faden, A.I. (2013). Positive Allosteric Modulators (PAMs) of
Metabotropic Glutamate Receptor 5 (mGluR5) Attenuate Microglial Activation”.
Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/24168364
Yeh, C.C., Chen, T.L., Hu, C.J., Chiu,
W.T., Liao, C.C.(2012). Risk of epilepsy after traumatic brain injury: a
retrospective population-based cohort study. J Neurol Neurosurg
Psychiatry.84(4):441-5.
Zhang, M.R., Red, S.D., Lin, A.H.,
Patel, S.S., Sereno, A.B. (2013). PLoS One. e57364. doi: 10.1371.