Traumatic Brain Injury (TBI)

Etiology: Usually follows trauma such as a fall, but can be caused by cerebral atrophy, alcoholism, or poor or absent blood flow. Symptoms can slowly emerge as long as 2 weeks after injury.

Symptoms at Onset: Weakness, Fluctuating levels of loss of consciousness, Lethargy, Vision changes, Nausea, Vomiting, Loss of appetite, Memory deficits, Dizziness, Seizures, Mood changes, & Irritability

Etiology: Mild head trauma or shaking of the brain. May cause mild brain injury.

Symptoms at Onset: short loss of consciousness, the patient appears dazed.

• Symptoms are based on the severity of the injury but can include: Dizziness, cognitive deficits, nausea/vomiting, headache, diplopia, & irritability

Etiology: Bruising of the brain resulting from the brain moving back and forth within the skull.

Can result in one or both of the following:

• Coup-contrecoup: brain hits opposite sides of the skull (coup—initial contusion; contrecoup—the location where the brain bounced off the other side). The base of the skull is rough, so regardless of the point of impact a contusion can occur.

• Diffuse axonal injury (shearing) caused with contrecoup. There is damage to the neurons and their connections.

Symptoms at Onset: Symptoms vary according to the severity of the injury. Often associated with a skull fracture

Most common type of TBI. Patients will have a loss of consciousness at the time of injury with prolonged post-traumatic coma. Involves significant white matter shearing usually due to high-speed impact. Coup–contrecoup shearing causes widespread damage to the neurons and their connections. The damage occurs primarily in the corpus callosum, white matter tracts, brainstem, and at junctions of grey and white matter.

Injury is considered mild if the coma lasts 6-24 hours, moderate if >24 hours, or severe (may not regain consciousness)

Classification

Grade 1

• Pathology: Diffuse axonal damage within the white matter of the cerebral hemispheres and grey-white matter interfaces

• Effect on Consciousness: Brief loss of consciousness

Grade 2

• Pathology: Tissue tear hemorrhages present; axonal damage of the white matter including grade 1 regions and the territory of the corpus callosum

• Effect on Consciousness: Variable recovery process, coma of unclear duration

Grade 3

• Pathology: Grade 2 findings in addition to tissue tear hemorrhages within the brainstem

• Effect on Consciousness: Instant coma with posturing and incomplete recovery

Symptoms at Onset

• vary based on severity of injury. WIll see posturing if severe. Increased intracranial pressure and increased mass effect.

Treatment Options & Management

Goal is to prevent secondary effects such as cerebral edema or hemorrhage. Close monitoring is required.

Prognosis

Dependent on the severity. Predictive correlation between the extent of brainstem DAI and the likelihood of persistent vegetative state. Outcomes and likelihood of coming out of the coma are worse when the brainstem is the primary area injured.

Etiology: Absence of oxygen to the brain for more than several minutes.

• Usually seen in patients with cardiac or respiratory arrest or near-drowning.

Symptoms at Onset:

• Disorders of consciousness ranging from coma to minimally conscious state

• Cognitive deficits: memory loss, apraxia, executive function deficits, attention deficits, decreased processing speed, personality/behavior changes, and affect/mood poorly regulated

• Visual processing deficits & field losses are common

• Diffuse cognitive and physical symptoms: movement disorders, bilateral proximal UE weakness with preserved LE strength, spasticity, contractures

• Deficits are not overtly focal, although one side may be slightly weaker than the other.

• Seizures can develop (in ~1/3 of patients), usually after the 1st 24 hours post-injury and can last indefinitely