Cerebral vasospasm
- Common phenomenon following brain bleeds (especially aneurysmal SAH), as blood is a CNS irritant.
- True incidence unknown, but estimated to occur in up to ~70% of TBI-related bleeds.
- Most often presents 3–7 days after aSAH, but may occur up to 21 days after the bleed.
- S/sx: New focal neuro deficits, altered consciousness, new or worsening headache, visual changes, etc.
- Varies by location and etiology.
- Focal neurologic deficits (FNDs) common, especially if stroke, malignancy, or trauma.
- Brainstem lesions may cause autonomic instability or altered consciousness.
- “Triple H therapy” = addresses hypertension, hemodilution, and hypervolemia
- Goal: Increase mean arterial pressure (MAP) while decreasing blood viscosity.
- Increasing MAP = pressors (phenylephrine, norepinephrine, dopamine).
- Prevention of vasospasm: Calcium channel blockers (incl. nimodipine) seem to improve neurologic outcomes; questionable evidence to support an overall reduction in mortality.
- Goal: Increase mean arterial pressure (MAP) while decreasing blood viscosity.
- If not averted/managed, vasospasm can lead to poorer functional outcomes and, potentially, demise in an otherwise-survivable injury.
Within the cerebra, cerebellum, or brainstem.
May result from a number of different insults, ranging from hemorrhagic stroke to infection, malignancy, vascular compromise (e.g. amyloid angiopathy), and trauma (incl. Coup/contrecoup injury). HTN usually involved.
Gross (autopsy) findings
- Blood within brain parenchyma (cerebra, cerebellum, brainstem).
- +/– visible trauma (e.g. skull fx, penetrating injury)
Coup-contrecoup brain injury
Basic definitions:
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- Coup: Ipsilateral brain injury; tends to occur when a moving object strikes a stationary head.
- Contrecoup: Contralateral brain injury; tends to occur when moving head strikes a stationary object.
- Coup-contrecoup: Bilateral brain injury, generally involving cerebral contusion or hemorrhage at the site of impact as well as opposite this location (> 90 degrees). Severe injury, often associated with DAI.
Ddx: DAI
In DAI, look for petechial hemorrhages at the gray-white matter junction as well as in the brainstem and corpus callosum.
- Depends on severity of injury.
- May require surgical decompression.
- If GCS <8, intracranial pressure monitoring indicated.
- If surgery not required, monitoring with repeat head CT at 12 and 24 hours is common.
Diffuse axonal injury (DAI)
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Mechanism of injury = shearing of axons due to overwhelming angular acceleration/acceleration-deceleration forces; often referred to as a “rotational injury.”
- A force overcomes the skull/brain’s moment of inertia → base of the neck forms axis of rotation → resulting torque generated by rapid rotation around this axis leads to axonal disruption.
- Axonal distortion and disruption is followed by increased focal permeability and dysregulation of Ca2+ and Na+ → unmitigated activation of toxic excitatory neurotransmitters and production of ROS.
- Often a cause of persistent vegetative state (PVS) in patients.
CT
- Generally not sensitive enough to demonstrate extent of injury; clinical presentation may be significantly worse than imaging findings.
MRI
- MRI (diffusion weighted/DWI): Study of choice for DAI.
- May see irregularities (including hyperintensity) at gray-white matter junction.
- Edema often present.
Gross (autopsy) findings
- May see petechial hemorrhages at gray-white matter junction.
- Cerebral edema may be pronounced.
- Some debate surrounding the necessity of observing an associated coup-contrecoup injury.
- Increasing severity of injury is associated with depth of white matter damage.
- Corpus callosum involvement common.
- As generated torque increases, injury to deeper brain structures occurs (thalamus, midbrain, pons, and medulla