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traumatic_brain_injury

Traumatic brain injury (TBI)

Traumatic brain injury (TBI) is defined as a result of a bump, blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain. This trauma can lead to temporary or permanent impairments of cognitive, physical and psychosocial functions, and an associated diminished or altered state of consciousness 1).

Although there are still contradictions regarding the clinical significance of the term “head injury”, it can not be considered synonymous with traumatic brain injury.

Brain injury from trauma results from two distinct processes:

1. primary brain injury: occurs at time of trauma (cortical contusions, lacerations, bone fragmenta- tion, diffuse axonal injury, and brainstem contusion)

2. secondary brain injury: develops subsequent to the initial injury. Includes injuries from intracranial hematomas, edema, hypoxemia, ischemia (primarily due to elevated intracranial pressure (ICP) and/or shock), vasospasm

Epidemiology

Classification

Risk Factors

When a detailed history is unavailable: the loss of consciousness may have preceded (and possibly have caused) the trauma. Therefore, maintain an index of suspicion for e.g. aneurysmal subarachnoid hemorrhage, hypoglycemia, etc. in the differential diagnosis of the causes of trauma and associated coma.

Head impact direction has been identified as an influential risk factor in the risk of traumatic brain injury (TBI) from animal and anatomic research.

Increased risk of incurring a subdural hematoma exists from impacts to the frontal or occipital regions, and parenchymal contusions from impacts to the side of the head. There was no definitive link between impact direction and subarachnoid hemorrhage. In addition, the results indicate that there is a continuum of stresses and strain magnitudes between lesion types when impact location is isolated, with subdural hematoma occurring at lower magnitudes for frontal and occipital region impacts, and contusions lower for impacts to the side.

This hospital data set suggests that there is an effect that impact direction has on TBI depending on the anatomy involved for each particular lesion 2).

Pathophysiology

Neuropathology

The neuropathology of traumatic brain injury (TBI) from various causes in humans is not as yet fully understood.

Penetrating head injury and closed head injury (CHI) that are moderate to severe are more likely than mild TBI (mTBI) to cause gross disruption of the cerebral vasculature. Axonal injury is classically exhibited as diffuse axonal injury (DAI) in severe to moderate CHI. Diffuse axonal injury is also prevalent in penetrating head injury (PHI). It is less so in mTBI. There may be a unique pattern of periventricular axonal injury in explosive blast mTBI. Neuronal injury is more prevalent in PHI and moderate to severe CHI than mTBI. Astrocyte and microglial activation and proliferation are found in all forms of animal TBI models and in severe to moderate TBI in humans. Their activation in mTBI in the human brain has not yet been studied 3).

Clinical features

Loss of consciousness.

When a detailed history is unavailable, remember: the loss of consciousness may have preceded (and possibly have caused) the trauma. Therefore, maintain an index of suspicion for e.g. aneurysmal SAH, hypoglycemia, etc. in the differential diagnosis of the causes of trauma and associated coma.

Delayed deterioration

≈ 15% of patients who do not initially exhibit signs of significant brain injury may deteriorate in a delayed fashion, sometimes referred to as patients who “talk and deteriorate” or when more lethal, patient who “talk and die”.

Physical examination

It is not possible to outline a physical exam that is universally applicable. Major trauma must be assessed rapidly, often under chaotic circumstances, and must be individualized based on patient’s medical stability, type of injury, degree of combativeness, use of pharmacologic paralytics, the needs of other caregivers attending to other organ injuries, the need to triage in the event of multiple patients requiring simultaneous attention…

The following describes some features that should be assessed under certain circumstances with the understanding that this must be individualized. This addresses only craniospinal injuries, and assumes that general systemic injuries (internal bleeding, myocardial and/or pulmonary

General physical condition (oriented towards neuro assessment)

1. visual inspection of cranium:

a) evidence of basal skull fracture:

● raccoon’s eyes: periorbital ecchymoses

● Battle’s sign: postauricular ecchymoses (around mastoid air sinuses)

● CSF rhinorrhea/otorrhea

● hemotympanum or laceration of external auditory canal

b) check for facial fractures

● LeFort fractures: palpate for instability of facial bones, including zygomatic arch

● orbital rim fracture: palpable step-o

c) periorbital edema, proptosis

2. cranio-cervical auscultation

a) auscultate over carotid arteries: bruit may be associated with indicate carotid dissection

b) auscultate over globe of eye: bruit may indicate traumatic carotid-cavernous fistula (Carotid-cavernous fistula)

3. physical signs of trauma to spine: bruising, deformity

4. evidence of seizure: single, multiple, or continuing (status epilepticus)

Neurologic examination

Scales

Despite many (valid) criticisms, the initial post-resuscitation Glasgow Coma Scale (GCS) score remains the most widely used and perhaps best replicated scale employed in for the assessment of head trauma. Problems with this type of scale is that it is an ordinal scale that is non parametric (i.e. does not represent precise measurements of discrete quantities), it is non-linear, and it is not an interval scale, so that for example, a decrease of 2 points in one parameter is not necessarily equal to a decrease in 2 points of another. Thus, performing mathematical manipulations (e.g. adding components, or calculating mean values), while often done, is not statistically sound.

Diagnosis

Complications

Outcome

Treatment

Models

Due to the marked heterogeneity of human traumatic brain injury (TBI), none of the available animal model can reproduce the entire spectrum of TBI, especially mild focal TBI.

A stereotaxic coupled weight drop device was designed. Principle arm of device carries up to 500g weights which their force was conveyed to animal skull through a thin nail like metal tip. To determine the optimal configuration of the device to induce mild TBI, six different trials were designed. The optimal configuration of the instrument was used for evaluation of behavioral, histopathological and molecular changes of mild TBI.

Neurologic and motor coordination deficits observed sharply within 24h post injury period. Histological studies revealed a remarkable increase in the number of dark neurons in trauma site. TBI increased the expression of apoptotic proteins, Bax, BCl2 and cleaved caspase-3 in the hippocampus.

This device is capable to produce variable severity of TBI from mild to severe. The main advantage of the new TBI model is induction of mild local unilateral brain injury instead of traumatization of the whole brain. This model does not require craniotomy for induction of brain injury.

This novel animal TBI model mimics human mild focal brain injury. This model is suitable for evaluation of pathophysiology as well as screening of new therapies for mild TBI 4).

Mechanical TBI models

Societies

Brain Injury Association of Tasmania http://www.biat.org.au

Brain Injury Network of South Australia http://www.binsa.org

Brain Injury Association of NSW http://www.biansw.org.au

Scores

The QOLIBRI-OS assesses a similar construct to the QOLIBRI total score and can be used as a brief index of HRQoL for traumatic brain injury TBI 5).

Case series

Books

References

1)
Traumatic Brain Injury Center. (n.d.). Centers for Disease Control and Prevention. Retrieved May 1, 2012, from http://www.cdc.gov/traumaticbraininjury/
2)
Post A, Hoshizaki TB, Gilchrist MD, Brien S, Cusimano M, Marshall S. Traumatic Brain Injuries: The Influence of the Direction of Impact. Neurosurgery. 2015 Jan;76(1):81-91. PubMed PMID: 25525694.
3)
de Lanerolle NC, Kim JH, Bandak FA. Neuropathology of Traumatic Brain Injury: Comparison of Penetrating, Nonpenetrating Direct Impact and Explosive Blast Etiologies. Semin Neurol. 2015 Feb;35(1):12-19. Epub 2015 Feb 25. PubMed PMID: 25714863.
4)
Garjan TG, Sharifzadeh M, Khodagholi F, Musavi SM, Hasanzadeh G, Zarindast M, Gorji A. A novel traumatic brain injury model for induction of mild brain injury in rats. J Neurosci Methods. 2014 Jun 3. pii: S0165-0270(14)00203-9. doi: 10.1016/j.jneumeth.2014.05.035. [Epub ahead of print] PubMed PMID: 24906055.
5)
von Steinbuechel N, Wilson L, Gibbons H, Muehlan H, Schmidt H, Schmidt S, Sasse N, Koskinen S, Sarajuuri J, Höfer S, Bullinger M, Maas A, Neugebauer E, Powell J, von Wild K, Zitnay G, Bakx W, Christensen AL, Formisano R, Hawthorne G, Truelle JL. QOLIBRI overall scale: a brief index of health-related quality of life after traumatic brain injury. J Neurol Neurosurg Psychiatry. 2012 Nov;83(11):1041-7. doi: 10.1136/jnnp-2012-302361. Epub 2012 Jul 31. PubMed PMID: 22851609.
traumatic_brain_injury.txt · Last modified: 2019/07/18 19:31 by administrador