022615 CNS trauma Flashcards
cerebral edema
accumulation of excess fluid in intracellular or extracellular spaces of brain
major forms of edema
vasogenic edema
cytotoxic edema
vasogenic edema
extracellular edema
disruption of BBB, resulting in shift of fluid from intravascular to extravascular compartment
predominantly involves white matter
most common causes of vasogenic edema
primary or secondary brain tumors
abscesses
contusions
intracerebral hematomas
cytotoxic edema
intracellular edema
occurs secondary to cellular energy failure
results in shift of water from extracellular to intracellular compartment
more pronounced in gray matter
most common causes of cytotoxic edema
ischemia/infarct meningitis trauma seizures hepatic encephalopathy
increased intracranial pres leads to
decreased perfusion
herniation syndromes
transtentorial herniation
uncus/medial temporal lobe is displaced through tentorial opening
complications of transtentorial herniation
ipsilateral CNIII nerve compression with pupillary dilatation
compression of brainstem (opposite midbrain peduncle containing corticospinal tracts)–the indentation is called Kernohan’s notch
posterior cerebral artery compression
Duret hemorrhage (infarct to midbrain)
what does Kernohna’s notch cause
weakness and Babinski sign ipsilateral to cerebral hemispheric lesion
Duret hemorrhage
FATAL brainstem hemorrhage
cerebellar tonsillar hernation is caused by
caused by SYMMETRIC expansion of supratentorial contents into posterior fossa or expanding mass lesion in posterior fossa
medullary comrpession results in cardiorespiratory arest
hydrocephalus
enlargement of ventricles associated with increase in CSF volume
communicating (non obstructive) hydrocephalus
ventricular system is patent
increased size of ventricles may be due to arachnoid villi obstruction OR overproduction of CSF from choroid plexus papilloma
non-communicating hydrocephalus
OBSTRUCTION within ventricular system
causes include tumor in ventricle, congenital malformation, thick meninges at base of brain blocking flow
open vs closed trauma
open-broke skull
focal trauma usually causes
focal neurological deficits, epilepsy
diffuse trauma usually causes
coma or vegetative state
comminuted skull fracture
multiple linear fractures radiate from point of impact
contusion
superficial bruises of the brain (can actually see it on gross specimen and in scans)
usually at crests of gyri
sm blood vessels, neurons, and glia are damaged
occur in orbital, temporal regions (also occipital)
result from fall or from direct blow to head
acute contusions
wedge shaped
superficial hemorrhage in cortex and meninges
micro:
- perivascular accumulation of blood
- after hrs, brain edema
old contusions
gyri indented, cavitated, with brown or orange discoloration
macrophages w hemosiderin, fibrillary astrocytes
coup contusion vs contrecoup contusion
coup-at point of impact
diffuse axonal injury
deceleration/acceleration or angular acceleration
loss of consciouness at onset WITHOUT lucid interval
unconscious or disabled until death. lesser degress may be compatible w varying severity of neurologic deficits
widespread damage to axons