L1- Trauma, Hydrocephalus Flashcards
briefly describe the make-up of the meninges
Dura mater: dense CT
Arachnoid mater: loose CT, BVs
CSF present in between
Pia mater: contiguous to brain
(T/F) CNS does NOT have a lymphatic system
T
what are the main causes of increased ICP
Brain: tumor
Blood: hemorrhage (various locations)
Water: hydrocephalus (inc CSF, subarachnoid space), cerebral edema
list the possible results of increased ICP
Equilibration: compensatory mechanism to disperse the inc in ICP in order to avoid Sxs (more likely in slow cases, less in rapid developments)
Herniation: with asymmetrical pressure
Diffuse raised ICP –> possible Sxs
- (1) the main Sxs seen with raised ICP
- (2) the main risk/progression seen with raised ICP (explain)
1- HA, nausea, projectile vomiting
2- inc ICP —> inc systemic BP (difficult for blood to be pumped to the brain) => reflex bradycardia —> hypoxia –> stroke
briefly describe the 2 types of cerebral edema
1) Vasogenic edema:
- inc in extracellular fluid
- disruption in BBB
- Sxs: HA, nausea, projectile vomiting
2) Cytotoxic edema:
- inc in intracellular fluid
- cell membrane injury (neurons, glial cells, endothelial cells)
- possible causes: ischemia, hypoxia, change in [Na+]
(1) is defined as the accumulation of CSF w/in the ventricular system as a result from (2)
1- hydrocephalus
2:
- impaired flow (obstruction, non-communicating)
- impaired CSF resorption (communicating)
- CSF overproduction (rare- choroid plexus tumor)
list the types of hydrocephalus
Note- can be congenital or acquired
- communicating
- non-communicating
- ex vacuo
describe the cause and result of communicating hydrocephalus
Cause:
- poor absorption of CSF in arachnoid Villi
- overproduction of CSF in choroid plexus (rare, via tumor)
Result: enlargement of all ventricles
describe the cause and result of non-communicating hydrocephalus
Cause- obstruction in part of a ventricle (mostly foramens)
Results: enlargement of only affected ventricle
define ex vacuo (include common causes)
- brain atrophy causes a compensatory increase in CSF / ventricular volume
- infarctions, neurodegenerative diseases (Alzheimer’s, alcoholism)
describe the timing of hydrocephalus and the differences in signs and symptoms
BEFORE cranial sutures close –> inc in head circumference
AFTER cranial sutures close –> ventricular expansion, inc ICP (no inc in head circumference)
NPH = (1)
- (2) definition
- a type of (non-/communicating) hydrocephalus
- (4) Sxs
- (5) Tx (briefly)
1- normal pressure hydrocephalus
2- enlarged ventricular size w/ normal opening pressures on lumbar puncture
3- communicating
4- (wet, wacky, wobbly) urinary incontinence, dementia, gait disturbances
5- lumbar puncture, shunt
Benign Intracranial Hypertension = (1):
-(2) definition
1- pseudotumor cerebri
2: (must meet certain clinical criteria)
- isolated Sxs and signs of inc ICP w/o other evident cause of of intracranial HTN
- name distinguishes it from secondary intracranial HTN via neoplastic malignancy
Pseudotumor Cerebri:
- (1) main affected population
- (2) signs and sxs
- (3) Tx
1- overweight women child-bearing age
2- severe HAs, papilledema, vision loss
3- lumbar puncture, shunt; diuretics, corticosteroids
brain herniations:
- (1) definition
- (2) main consequences
- (3) types (indicate the worst type)
1- displacement of brain tissue from one compartment to another
2- compromises blood supply, infarctions, edema
3- subfalcine/cingulate, tonsillar** (worst), transtentorial/uncinate
(1) herniation is the unilateral or asymmetrical expansion of cerebral hemisphere displacing cingulate gyrus under the (2). It results in compressing (3).
1- subfalcine (cingulate)
2- falx cerebri
3- ACA
(1) herniation is where (2) are displaced through the foramen magnum. (3) is the main risk as a result from compression of (4).
1- tonsillar
2- cerebellar tonsils
3- death
4- respiratory and cardiac centers w/in brain stem
(1) herniation is the result of the medial temporal lobe compressing against (2). (3) is present in the midbrain.
1- transtentorial / uncinate
2- free margin of tentorium (see Sx card for specific structures)
3- duret hemorrhages: linear / flame shaped hemorrhages
list the symptoms of transtentorial / uncinate herniations
- Oculomotor (CN-III) compression –> mydriasis, impaired eye movements
- PCA compression
- pressure on midbrain and contralateral cerebral peduncle –> ipsilateral hemiparesis
list the types of CNS traumas (head/brain)
- skull fractures
- Parenchymal injuries: concussions, contusions, diffuse axonal injuries
- traumatic vascular injuries: subdural, epidural hemorrhages
Skull fractures are more likely to occur if the head is (moving/stationary). (2) are the common vascular complications as a result of a skull fracture.
1- stationary
2- epidural and subdural hemorrhages
list and briefly define the types of skull fractures
Linear: straight, sharply defined (80% of all cranial fractures)
Depressed: fractured edges overlap
Basilar: bones broken at base of skull – easily missed on imaging
define concussion
- response to blunt head trauma
- reversible altered brain function
- w/ or w/o LOC
-recovery is normal, although event amnesia may persist
Note- unknown pathogenesis, but repeated episodes may lead to later development of cognitive impairment and neurodegenerative processes
brain contusion:
- (1) definition
- (2) characteristics (signs / sxs)
- (3) are the types of contusions present based on location
1- bruise of brain surface following head injury
2- neuron damage, edema, pinpoint punctures / depressions, hemorrhaging
3- Coup (site of impact) + Contracoup (opposite pole where other side of brain hit the skull)
Diffuse axonal injuries:
- (1) definition
- (2) cause (specific)
- (3) main presentation
- (4) appearance on imaging
1- subtle widespread injury to axons
2- head trauma involving rotational acceleration –> shearing forces on axons –> stretched beyond elastic point (mainly car accidents)
3- LOC –> coma (no lucid intervals), if patients survives neurological deficit will be present
4- normal imaging
Epidural hemorrhage:
- (1) main cause (specific)
- (2) affected BV
- (3) clinical presentation
- (4) radiological presentation
1- skull fracture, mainly temporal bone
2- middle meningeal artery (rapid blood accumulation)
3- initial LOC –> followed by lucid interval (conscious recovery) –> continued hematoma expansion => death
4- convex lens shape (doesn’t cross suture lines)
Subdural hemorrhage:
- (1) affected BV
- (2) is a big risk factor
- (3) clinical presentation timing
- (4) radiological appearance
1- bridging veins (note w/in subarachnoid space, slow blood accumulation)
2- brain atrophy (or other diseases weakening BVs, i.e. alcoholism)
3- Sxs can appear w/in hrs or be delayed by days or wks (common in trivial falls of the elderly)
4- crescent shape (crosses suture lines)
connect the BV with the related hemorrhage:
- (1) middle meningeal artery
- (2) bridging veins
1- epidural hemorrhage (rapid blood accumulation)
2- subdural hemorrhage (slow blood accumulation)
connect the radiological presentation with the related hemorrhage (explain):
- (1) crescent shaped
- (2) convex lens shape
1- subdural (crosses cranial sutures)
2- epidural (doesn’t cross cranial sutures)
connect the following with the related hemorrhage:
- (1) skull fracture
- (2) brain atrophy and mild trauma
- (3) lucid interval
1- epidural
2- subdural
3- epidural
connect the following clinical presentation timing with the related hemorrhage:
- (1) acute presentation
- (2) delayed presentation
1- epidural and subdural hemorrhage
2- subdural hemorrhage only
