Traumatic brain injury

• Two mechanisms :

1. Acceleration – deceleration injury

2. Rotational movement

 

• Acceleration – deceleration injury:

Because the brain floats freely in the CSF, blunt force to the head can cause the brain to accelerate in the head and abruptly decelerate upon hitting the skull. This result in coup and countercoup injury

 

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Effect of traumatic head injury

1. Primary (direct) injury:

Damage is caused by impact

2. Secondary injury:

damage results from subsequent swelling, intracranial hematoma, infection and ischemia. Ischemia is the most common

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• Diffuse injuries can be CONCUSION or DIFFUSE AXONAL INJURY

CONCUSION

• Momentary interruption of brain function with or without loss of consciousness.

• MILD: momentary loss of consciousness without demonstrable neurologic symptoms or residual damage. Microscopic changes can be detected in the neurons and supporting tissue within hours of injury. Recovery within 24 hours

• Post concussion syndrome: persistence of symptoms such as headache, irritability, insomnia and poor concentration and memory for months after injury

 

DIFFUSE AXONAL INJURY

• It a primary injury with diffuse microscopic damage to axons in in the cerebral hemisphere, corpus callosum and brain stem.

• Responsible for posttraumatic dementia

• Responsible for persistent vegetative state together with hypoxic-ischemic injury

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Focal brain injury

• Contusion: bruise to the cortical surface of the brain caused by blunt head trauma.

• They occur any place the brain comes in contact with the skull

• Result generally from anteroposterior displacement when the moving head strikes a fixed object

• They cause permanent damage to the brain. necrotic tissue is phagocytized by macrophages and scar tissue formed by astrocytes proliferation

 

Hematomas

• Result from vascular injury and bleeding. Named according to anatomic position of the ruptured blood vessel

• Epidural hematoma:

• Usually result from tear in an artery, most often the middle meningeal.

• Arterial bleeding results in rapid compression of the brain from the expanding hematoma

• Common in young persons as dura is not firmly attached to the skull as in older persons.

• Usually person present with history of head injury and brief period of unconsciousness followed by a lucid period followed by rapid progression to unconsciousness.

• Ipsilateral pupil dilatation and contralateral hemiparesis

• If hematoma is not removed the condition rapidly progress with increased ICP tentorial herniation and death

• Subdural hematoma: results from tear in small veins that connect veins on the surface of the cortex to the dural sinuses.

• Develops more slowly than epidural H.

• Can be acute, subacute and chronic

• Acute: rapid, within 24 hrs. of injury, death because of uncontrolled rise in ICP an edema

• Subacute: produce symptoms 2-20 days after injury

• Chronic hematoma: arise several weeks after injury. Seen in older persons where the brain is shrunken and seepage of blood is slow. Fibroblastic activity leads to encapsulation of the hematoma

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