Traumatic Brain Injury- Epidemiology And Pathology

Because TBI is classified into two categories by the American Academy of Neurology: Moderate TBI and severe TBI. Different neurologists have different definitions of the condition. Mild, moderate, and severe. TBIs are the three categories based on the Glasgow Coma Scale (GCS).

Mild Traumatic Brain Injury 

Changes in mental status brought on by trauma may or may not include unconsciousness lasting less than 30 minutes and a GCS score of at least 13. There are typically no focal neurological symptoms, such as hemiparesis, cranial nerve abnormalities, or any kind of incoordination. Mild TBI is also known as concussion. If amnesia is present, it usually lasts for less than 24 hours.

Severe Traumatic Brain Injury

Radiological evidence of brain or skull damage • Prolonged loss of consciousness following a traumatic event lasting longer than 12 hours. Blood vessels inside the brain are affected.

History of Traumatic Brain Injury

The earliest physical evidence of a traumatic brain injury (TBI) caused by an assault was discovered in South Africa one million years ago. The earliest written record of a brain injury was discovered 500 years ago on the Edwin Smith papyrus. The treatise on head injuries is included in the hippocratic corpus.

Phineas Gage

Phineas Gage, a well-known example of a frontal lobe injury, sustained damage to his brain from an iron bar piercing his skull during an explosion. Despite his recovery, Gage doesn't seem to be the same person as before the incident. Family members noted that Gage has become more immature, careless, and poorly judgmental. Several other personality changes were also noted. Phineas Gage is brought up whenever head injuries are discussed.

Neuropsychiatric Consequences Of Traumatic Brain Injury

 There are two groups Conditions include sadness, delirium, and personality changes that are not associated with traumatic brain injury
Brain injury specific disorders such as anosognosia, pseudobulbar affect (PBA), and neglect; in comparative nosology, the effects of traumatic brain injury (TBI) are classified according to the time of symptom onset as acute syndromes and delayed (often irreversible). Acute syndromes include confusion, restlessness, irritability, agitation, and post-traumatic amnesia; delayed (often irreversible) is marked by cognitive disorders, traumatic dementia, and organic personality change. 

Epidemiology

 The majority of traumatic brain injuries (TBIs) have closed head injuries, whereas penetrating head injuries are less common; 80% of patients have mild head injuries, 10% have moderate head injuries, and 10% have severe head injuries; the most common age group with brain injuries is adolescent and young adults (entrance exam question); etc. These statistics are based on Kaplan and Sadock's book (9th edition).

The elderly are the second most affected age group. Men are 40% more likely than women to have a traumatic brain injury. Falling is the most prevalent cause of traumatic brain injury (TBI) in the United States (Kaplan and Sadock, book, 9th edition). Car crashes and assaults are the most frequent causes of traumatic brain injury among younger individuals. Injuries sustained during sports and leisure.

There is evidence that African Americans have higher TBI rates. Higher incidences of traumatic brain injury are likewise linked to lower socioeconomic level. 10% of individuals experience recurrent traumatic brain injury (TBI) within a year of the first incident. TBI history in the past is another significant risk factor. The biggest risk factor for traumatic brain injury is alcohol and drug addiction. TBI is referred to as a "signature wound" in US military operations in Afghanistan and Iran.
Blast exposure causes the majority of hallmark wounds; Blast injuries are more common than penetrating wounds in modern conflict because of high-tech weapons.

Pathology

There are two types for TBI pathology. Depending on the meningeal coverings' integrity; Depending on the type of lesion—focal or diffuse; Depending on how the injury happened—primary and secondary brain damage.

Depending On Integrity Of Meningeal Coverings

Two categories of injuries: piercing and closed.
• Closed Wounds: Meningeal covering integrity is unharmed
Increased frequency: The most prevalent cause is falls. Automobile accidents, assaults, and injuries sustained in sports are additional factors.
• Penetrating Injuries: Missile wounds are the most frequent cause; meningeal covering integrity is compromised. The majority of blast injuries are caused by contemporary combat; they typically affect the lungs, tympanic membrane, and eyes; and they typically result in concussions or contusions.

Depending On The Time At Which Changes Occurred

Primary and secondary brain injury are the two types.  

Primary Brain Damage

Initial brain injury Caused by contact and inertial forces at the scene of the injury. Contact forces result in contusions, scalp lacerations, fractures of the skull, intracranial hemorrhages, and intracerebral hemorrhages. Primary brain injury is the result of a direct force impact. 

Direct mechanical force (coup injury) causes the parenchyma of the brain to rupture. For example, when someone strikes their head directly, the brain tissue in that area is damaged. Additionally, the brain pushes against the opposing inner surface of the skull, resulting in countercoup injury. 

A coup injury is when someone is struck in the occipital region, directly affecting the brain beneath. On the other hand, a countercoup injury is caused by the impact of a coup injury when the opposite side of the brain collides with the inside of the skull. Since the anterior surface and middle cranial fossa encircle the frontal and temporal lobes, they are most vulnerable to countercoup injury.

Because the occipital lobe's skull is smooth and flat, it is less prone to sustain a countercoup damage. Primary brain injury can also result from inertial forces. Diffuse axonal forces are produced by inertial forces including rotation and acceleration/deceleration, and these forces ultimately result in acute subdural hematomas. The primary cause of this is the rupture of subdural bridging veins.

Secondary Brain Damage

Causes brain damage as a result of ischemia. These pathological processes are started at the time of injury and can last for a few days, weeks, or months after the trauma. For instance, hypotension and/or hypoxia at the moment of injury; potential swollen brain following brain damage; elevated intracranial tension due to a drop in cerebral perfusion pressure; and secondary brain damage from infection following injury.

Depending On The Kind Of Lesion

• Two types – Focal and diffuse lesions
• Focal Lesions

There is a predisposition for contusions and lacerations to form at the frontal and temporal poles. Hemorrhages, cuts, and contusions are common on the surface of the brain and are particularly noticeable at the crust of cerebral gyri. Burst lobe extracerebral hemorrhages can occur with lacerations. Knowledge of the different brain coverings is required in order to comprehend the various forms of hemorrhages in depth. 

The dura mater, arachnoid mater, and pia mater are the three layers that cover the brain. (To help remember, it might be shortened to "PAD"). The innermost layer that follows the sulci and adheres to the gyri is called the paramatter. The CSF-containing arachnoid mater, which surrounds the brain and spinal cord, is the middle layer. It also caps the sulci and places atop the gyri. 

The outermost dura mater is a thick layer of fibrous tissue that forms the falx and tentorium and is firmly adhered to the skull. It provides a great deal of venous system support. Epidural space: the area above the epidura Blood clots in these regions cause hemorrhages. Subdural space is the space beneath the dura mater. Subarachnoid space is the space below the arachnoid mater.

Hemorrhage

The first type of hemorrhage is called an epidural hemorrhage (epidural hematoma),

Which occurs in temporal bone fractures and concurrently has meningeal artery lacerations. Intracranial-extracerebral hemorrhage occurs in the subdural space between the dura mater and arachnoid mater, or in the subarachnoid space. Since it's arterial blood, more trauma is needed to generate the force.

Due to the arterial bleed, there are fast-growing, high-pressure blood clots in epidural hematomas. Transtentorial herniation is the result of the brain being compressed and forced through the tentorial notch. Epidural hematomas are typically deadly and require emergency care. Surgery can stop the bleeding right away.

Etiological Observation

Elliptical (biconvex) form. Given that dura mater is attached to the innermost surface of the skull, blood accumulation in this region causes the brain's underlying structure to become compressed and shifted
The CT scan frequently reveals a fracture in the underlying skull. Swirl signs, which are a few hyper-dense spots in the epidural hemorrhage, can occasionally be observed. The swirl indicator suggests that there is an ongoing bleeding in the areas that are extremely dense.

The second type of hemorrhage is the subdural hematoma 

Subdural hematomas are typically caused by slow bleeding bridging veins into the subdural space at relatively low pressure. If the brain dampens the bleeding, it suppresses further subdural space expansion. If the hematoma expands due to continuous blood flow, it causes cerebral or cerebellar herniation through the foramen magnum. Elderly people taking anticoagulants experience brain atrophy, which may increase the tension of bridging veins and cause subdural hematomas.
There are two types of subdural hematomas: acute and chronic. Acute subdural hematoma patients have headaches, disorientation, and a temporary loss of consciousness lasting between one and two days.

Patients with chronic subdural hematoma exhibit slowly developing headaches, personality changes (which may be inherited), and cognitive impairment.  The bleeding in chronic subdural hematoma lasts for weeks and spreads widely across the subdural area. When combined, they cause "rapidly developing dementia" in the elderly, which sets chronic subdural hematoma apart from other kinds of. When treating "reversible cause of dementia," there may be times when a spontaneous resolution occurs and other times when surgical evacuation is necessary.

Acute subdural hematomas are hyperdense, appearing brighter, while chronic subdural hematomas are hypodense, appearing darker.  An isodense condition occurs during the transition from acute to chronic, making it difficult to distinguish between the blood and the brain. When the blood follows the surface of the brain, the shape of the hematoma is concave or convex, known as the crescent or sickle shape. In an isodense condition, there may be shifting or compression of the gyri. 

The third type of hemorrhage is the subarachnoid hemorrhage 

The bleeding that takes place in the subarachnoid area between the pia mater and the arachnoid mater  The most severe headaches that patients experience are thunderclap headaches, which are a significant clinical manifestation.  The sulcal space contains blood in a subarachnoid hemorrhage.
Trauma is the most frequent cause of subarachnoid hemorrhage, while aneurysmal rupture is the nontraumatic cause.  Focal neurological signs, headache, dizziness, nausea, and vomiting are symptoms of elevated intracranial pressure.  To put it briefly, there are three different kinds of intracranial-extracerebral hemorrhages: subdural, subarachnoid, and epidural.

The most common causes of intra-cerebral hemorrhages are hypertension, contusions, and arteriovenous malformations. They can occur hours or days after the trauma and are frequently numerous, including the frontal, temporal, and basal ganglia. 

Lobar hemorrhage may occur in older patients with Alzheimer's disease as a result of cerebral amyloid angiopathy. Ischemic damage can result in focal lesions from arterial vasospasm or traumatic vascular lesions, such as arterial dissection, vascular distortion, compression, or venous thrombosis.

Diffuse Lesions

Diffuse Ischemic Damage (DID) and Traumatic Axonal Injury (TAI) are the two categories. 

Traumatic axonal injury (TAI) mostly affects the thalamus, dorsolateral quadrants of the upper brain stem, and the corpus callosum.
Acute and protracted coma is linked to TAI. Pathological mechanisms include axolemma fragmentation, interruption of axonal transport, axonal bulb development, astrogliosis, and microglial activation. Axonal disruption of a lesser degree may be observed in individuals with moderate brain traumas or lucid interval syndrome.  A significant number of serious head injuries result in diffuse ischemia damage (DID).

Hope you found this blog helpful for your Psychiatry residency Neurology and General Medicine preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.