8/23 Ventricles and Meninges - Glendinning Flashcards
cerebrospinal fluid
properties/volume
functions
clear, colorless liquid (140mL)
replaced 2-3x/day
fx:
- buoyancy, protection against sudden movements
- maintenance of intracranial pressure
- controls ECF of brain
- some antibacterial props
choroid plexus
tissue within brain ventricles that produces CSF
also forms blood-CSF barrier
- ependymal cells with adherent jx line ventricles : allow free movement of CSF into brain
- at choroid plexus, ependymal cells form tight jx → create choroid epithelium : blood-CSF barrier
- choroid epithelium has active transport, ion exchange mechs to determine flow of molecules
- implication : need active transport in order to make it from blood into the CSF!
- choroidal caps (in subarachnoid space) are fenestrated with no tight jx
lateral ventricles in cerebral hemispheres → intervertebral foramen of Monroe → 3rd ventricle in diencephalon → cerebral aqueduct in midbrain/mesencephalon → 4th ventricle in pons/medulla

blood brain barrier
formed by capillary endothelium and astroyte foot processes
fx:
- control ionic environment : neurotrans
- protects brain from toxins
- prevents drugs from enetering brain
- contains transporters for critical molecules (glucose, proteins)
BBB may be disrupted by infections, tumors, trauma → “vasogenic edema”
circumventricular organs
regions where BBB is interrupted → enables brain to respond to changes in blood chemistry
2 barriers between blood and brain
- blood-CSF barrier
* formed by choroid epithelium - blood-brain barrier
* formed by capillary endothelium
CSF flow from ventricles to subarachnoid space
how does CSF get from ventricles to venous sinuses? (pathway)
how specifically does CSF get from subarachnoid space into sinuses?
4th ventricle → foramen of Magendie (median) and Luschka (lateral x2) → subarachnoid space around brain and spinal cord → arachnoid granulations → venous sinuses
arachnoid villae : smal evaginations of arachnoid into sinus
- large villi = arachnoid granulations
- giant vacuoles engulf CSF materials
meninges
- dura, 2 layers : periosteal, meningeal
- arachnoid
- pia
dural layers : pachymeninges
arachnoid/pia : leptomeninges
cisterns
what is a cistern?
what are the main cisterns of the brain?
pools of enlarged areas of subarachnoid space
- interpeduncular cistern
- cisterna magna
- prepontine cistern
- quadrigeminal cistern
also ambient cistern, lumbar cistern
lumbar puncture
where?
whats teh point?
when should you use
L3-L4 in adults, L4-L5 in children
contraindicated if there’s increased intracranial pressure!
- if there’s pressure on the brain and you pull fluid from below → tentorial/cerebellar herniation risk
CSF pressure should be measured, should be < 20cm water
use in order to…
1. look out for:
- subarachnoid hemmorhage : blood
- infections ex. meningitis : high protein, high WBC, low glucose
- Guillan Barre : high protein, NL cell count
- MS : 70% of patients with high IgG, oligoclonal bands
2. push drugs into system
dura
arachnoid
pia
brain vs spinal cord
DURA
in brain, dura has 2 layers
- periosteal and meningeal (split to form sinuses)
in spinal cord, dura has 1 layer
- periosteum is a separate thing from the dura mater
- in between…epidural space!
ARACHNOID
in brain : arachnoid trabeculae and many cisterns
in spinal cord : fewer trabeculae and 1 cistern
PIA
spinal cord - forms denticular ligaments, filum terminale
dural folds
folds of inner dural layer between brain regions → create compartments in cranial cavity
- falx cerebri : between cerebral hemispheres (longitudinal fissure)
- falx cerebelli : between two hemispheres of cerebellum
- tentorium cerebelli : between posterior cerebral hemispheres and cerebellum
- diaphragm sellae : circular fold beneath the brain that covers teh sella turcica
trauma to the head
what should you be on the lookout for?
middle meningeal artery bleeding!
epidural hematoma: between skull and dura
subdural hematoma: between dural and arachnoid
epidural hematoma
causes:
- trauma to skull → usually middle meningeal artery
- also sinuses (15%)
lens shaped structure on MRI
often period of lucidity before severe symptoms (from brain herniation)
subdural hematoma
often due to tears in bridging veins
- sometimes during rapid accelerations
symptoms may progress over longer periods
crescent shaped
subarachnoid hemorrhage
usually secondary to trauma
can also be “non traumatic” from bleeding from an AV malformation or ruptured aneurysm
classic presentation: sudden-onset, severe headache (due to blood irritating meninges)
- why? meninges are full of pain receptors! (in contrast, brain does not have sensory receptors!)
non-traumatic subarachnoid hemorrhage
burst aneurysm is cause of 80%
- aneurysm forms when vessel wall is weakened and burst under conditions of increased pressure
- most aneurysms occur in anterior circulation (internal carotid artery -supplied)
- most common MEN: anterior commmunicating a
- most common WOMEN: posterio communicating a
increased intracranial pressure
causes
- tumor
- hemorrhage
- abscess
- edema
- hydrocephalus
- infections
sx of incr intracranial pressure
- headache
- alt mental status
- nausea/vomiting
- eyes appearing to look downwards
- papilledema (swelling of optic papilla)
- visual loss
- diplopia (double vision)
- Cushing’s triad: HTN, bradycardia, irreg resp (brainstem)
- kids - skull can expand
types of brain herniation
1. subfalcine : under falx cerebri
- subdural hematoma → cingulate gyrus herniates below falx cerebri
2. transtentorial and central herniation : through tentorial notch
- tumor in temporal lobe → temp lobe herniates through tentorial notch
- aka uncal herniation
3. tonsillar herniation : through foramen magnum
- cerebellar tumor → cerebellum herniates through foramen magnum
hydrocephalus
what it is
causes
“water in the head”
condition of excess CSF
- excess production : choroid plexus tumors
- obstructed flow (in ventricles or subarachnoid space - tumors, malformations, hemorrhage)
- decreased reabsorption via arachnoid granulations
communicating vs noncommunicating hydrocephalus
communicating : lateral ventricles communicate with subarachnoid space
ex. prob within choroid plexus
non-communicating : flow obstructed WITHIN ventricular system
sx of hydrocephalus
decreased cognitive fx
neck pain
vomiting (esp in morning)
blurred vision (papilledema)
drowsines
failure of upward gaze
hydrocephalus : small children and infants
sx
signs: rapid head growth, bulding fontanelle, dilated scalp veins
symptoms : poor feeding, irritability, vomiting, lethargy, downward eyes
chiari malformations I-IV
congenital hindbrain anatomic anomalies (cerebellum, brainstem, or craniocervical jx)
- result in downward displacement of cerebellum
- tonsils can herniate through foramen magnum
sx usually in adults caused by…
- compression of medulla and upper spinal cord
- compression of cerebellum
- disruption of CSF flow through foramen magnum
→→→ produce hydrocephalus
Chiari I
most common
- oftentimes due to cyst in middle of spinal cord
1. cerebellar tonsils below foramen magnum
2. syringomyelia
3. compression of brainstem
most common symptoms:
- headache (due to incr ICP)
- ataxia (cerebellar dysfx)
- impaired movement (brainstem compression)
Chiari II
less common
can cause significant herniation through foramen magnum → aqueductal stenosis and hydrocephalus, usually with meningomyocele
Normal Pressure Hydrocephalus
elderly patients
- cause not entirely understood…maybe impaired reabs from meningitis/subarachnoid hem?
CLASSIC TRIAD
- gait disturbance
- dementia
- urinary incontinence (urgency, freq, diminished awareness of need to urinate)
NO HEADACHE bc no incr ICP! normal pressure