Meninges, CSF, Blood Flow, & Stroke Flashcards
Meninges
1) Dura mater
2) Arachnoid
3) Pia mater
Dura mater
Two fused layers (except at the sinuses)
-Outer layer: periosteal/endosteal layer that
adheres to bone
-Inner layer: meningeal layer along the CNS
Spinal cord dura
-Single layer - continuation of meningeal layer
Arachnoid
Middle layer between dura and pia
Does not adhere to pia
-gap is the [subarachnoid space]*
Pia mater
Innermost layer
-on surface of CNS
Dural Sinuses*
(aka dural venous sinuses, cerebral/cranial sinuses)
Areas where the two dural layers separate
[Venous drainage]* eventually flows to internal jugular vein
Dural sinuses Anatomy
Superior sagittal sinus
Inferior sagittal sinus
Straight sinus
Transverse sinus
Sigmoid sinus
▪ drain into internal jugular vein
Dural Processes
Formed by :double layer” of meningeal dural layer
Anatomy:
-Falx cerebri
-Tentorium cerebelli
-Falx cerebelli
-Diaphragm sellae
Epidural space (dura-skull interface)
Potential space of meningeal layers
[Epidural hemorrhage]* into space due to trauma, rupture of middle meningeal artery
Sub-dural space (dura-arachnoid interface)
Potential space of meningeal layers
Contain blood vessels supplying the brain
[Sub-dural hemorrhage]* into “space” due to trauma, rupture of cerebral veins as they pass from the brain to venous sinus
Sub-arachnoid space (arachnoid-pia interface)
Potential space of meningeal layers
Space [contains CSF]*
Subarachnoid space extends down to the 2nd sacral segment
-lumbar cistern (L1-S2…lumbar puncture)
[Sub-arachnoid hemorrhage]* into space often due to saccular (‘‘berry”) aneurysms…sub-arachnoid headache
Cerebrospinal fluid (CSF)
▪ CSF protects the brain ( “cushions the brain”)
➢ NOTE: brain does purely “float”…arachnoid trabeculae in subarachnoid space help anchor brain
▪ CSF circulates throughout brain and spinal cord
▪ CSF helps maintains constant intracranial pressure
Ventricles
Network of communicating cavities filled with CSF
Ventricular system
2 lateral ventricles and a third ventricle
R/L interventricular foramen (of Monro)
-connect the R/L lateral ventricles with the third
Cerebral aqueduct (aqueduct of Sylvius)
-connects third and fourth ventricles
Fourth ventricle
-CSF from fourth exists to the subarachnoid
space of the spinal cord through 3 foramen
-R/L lateral foramen (of Luschka)
-midline foramen (of Magendie)
Choroid plexus*
Located in each ventricle
Produces CSF
More on CSF*
Produced in the ventricles
Fills ventricles of brain & central canal of spinal cord
Surrounds the CNS (both brain and SC) in subarachnoid space
Contained by the meningeal layers
CSF Function
Cushions and insulates the brain
Some exchange of gases (O2, CO2), nutrients and metabolic waste
Provide stable EFC environment for the brain
CSF Formation
Produced in 2 locations
-choroid plexus (approx. 50-70% produced)
CSF Pathway
Lateral ventricle → interventricular foramen → 3rd ventricle → cerebral aqueduct → 4th
ventricle → foramens of Magendie & Luschka into the subarachnoid space of the brain and
spinal cord
How is CSF absorbed back into blood stream?
absorbed into the [arachnoid villi]* → dural sinus → jugular system
Hydrocephalus
Abnormal increase in CSF volume
May be caused by obstruction(s)
▪ often in foramen
Treatment:
▪ shunt to relieve pressure
➢ usually to peritoneal cavity
Blood Brain Barrier
Chemically separates the brain from the circulatory system
1 protects CNS from harmful chemicals/ substances
2 allows/regulates transport of essential molecules
3 formed by specialized endothelial cells that line brain capillaries
Clinical
1 dysfunction implicated in many degenerative/autoimmune neuro disorders
2 BBB may limit efficacy of drug treatments
Stroke
Interruption in blood flow to CNS
▪ medical emergency
3rd leading cause of death in US
▪ 700,000 cases per yr; 20% mortality
What is a stroke?
An abrupt incidence of vascular insufficiency
What is an infarct?
A region of necrotic tissue
-lacune = tiny lesion (lacunar stroke)
What is a Transient ischemic attack (TIA)?
Symptoms usually resolve within an hour (temporary)
Common symptoms of stroke
-Sudden numbness or weakness of the face, arm or leg (especially on one side of the body)
-Sudden confusion, trouble speaking or understanding speech
-Sudden trouble seeing in one or both eyes
-Sudden trouble walking, dizziness, loss of balance or coordination
e-Sudden severe headache with no known cause
FAST – Face, Arm, Speech, Time
Hemorrhagic stroke
Less common than ischemic
Reported to be 10-15% of all strokes (some research reports as high as 45%)
Hemorrhagic stroke - Pathology
▪ bleeding into brain parenchyma
▪ primary destruction of neurons from hemorrhage
▪ secondary destruction from potential rise in intracranial pressure
▪ hematoma expands creating pressure
Hemorrhagic stroke - Mechanism of injury
▪ small vessel bleeding from hypertension
▪ anticoagulation therapy
▪ cocaine use
Ischemic stroke
More common
Ischemic stroke - Pathology
Decrease in blood flow
Ischemic stroke - Mechanism of injury
▪ thrombus/emboli occlusion
➢ extracranial embolism
➢ intracranial thrombus
Ischemic stroke - Medical Priority
▪ thrombolytic intervention ASAP
▪ Initial research: < 3-4.5 hour “window of time” to administer thrombolytic
Risk factors of stroke
-Family history of stroke, heart attack or TIA
-age > 55
-hypertension > 140/90
- elevated cholesterol/hyperlipdemia
▪ total > 200
- cigarette smoking
- diabetes-g obesity
- BMI > 3
- co-existing cardiovascular disease, heart failure, - heart defect, heart infection, or
abnormal heart rhythm
- previous stroke or TIA
- high levels of homocysteine
- use of birth control pills or other hormone therapy
- heavy or binge drinking
- use of illicit drugs such as cocaine
TIA (Transient ischemic attacks)
Transient loss of blood flow
“neurological deficits resolve within 24 hours”
▪ neurological symptoms usually last < 1 hour
Numerous causes…atherosclerosis, emboli, arterial dissection, arteritis, cocaine and other
drug use, etc…
TIA = increased risk of stroke
Blood Supply to Brain
Circle of Willis
Circle of Willis - Inputs
internal carotid artery (ICA)
vertebral arteries/basilar artery
Circle of Willis - Function
Origin of major blood vessels of the brain
▪ anterior, middle, & posterior cerebral arteries
Anastomosis pathways
Small perforating arteries
▪ a group of that contribute to blood supply to:
➢ subcortical regions of brain
▪ diencephalon (thalamus, hypothalamus, subthalamus)
➢ internal capsule
▪ pathway of myelinated axons leaving and entering the cerebral cortex
▪ located between thalamus and basal ganglia
▪ limbic structures (amygdala, hippocampus, etc…)
▪ pons
Branches of Circle of Willis
Anterior cerebral artery (ACA)
Middle (MCA)
Posterior (PCA)
Anterior cerebral artery (ACA)
Supplies:
▪ medial (sagittal) regions of each hemisphere
➢ motor and sensory areas of lower body (see homunculus diagram)
➢ prefrontal lobe
➢ small perforating arteries supply:
▪ portions of sub-cortical structures (internal capsule and basal ganglia)
ACA supplies blood to:
medial parts of the frontal lobe and paracentral lobule, which are involved in motor, sensory, and behavioral functions.
Infarction (occlusion) of ACA - Motor
Contralateral leg weakness: The ACA supplies the motor cortex responsible for movement in the lower limbs, so occlusion can cause weakness or paralysis, particularly in the leg (contralateral to the lesion).
Mild arm weakness: The motor area for the arms may also be affected, but usually less severely than the legs.
Gait disturbance: The combination of leg weakness and potential sensory deficits may affect walking ability.
Infarction (occlusion) of ACA - Sensory
Contralateral sensory loss: Sensory areas in the postcentral gyrus (somatosensory cortex) corresponding to the lower limbs may be affected, leading to numbness or impaired sensation, particularly in the leg.
Proprioception problems: There may be difficulty with spatial awareness or balance due to sensory loss in the leg
Infarction (occlusion) of ACA - Behavioral/Personality changes
Apathy or lack of motivation: The prefrontal lobe is involved in executive functions, decision-making, and motivation. Damage can result in a lack of initiative or interest in activities.
Impaired judgment and reasoning: Difficulty in planning, organizing tasks, and making sound decisions.
Changes in personality: The occlusion of the ACA can cause personality shifts, with some individuals becoming more impulsive or socially inappropriate.
Disinhibition: The loss of control over social behavior may occur, leading to impulsivity or socially inappropriate actions.
Middle Cerebral Artery (MCA)
Supplies:
▪ lateral aspect of each hemisphere (frontal, parietal and temporal lobes)
▪ motor and sensory areas of trunk and upper extremities
▪ association areas
▪ prefrontal lobe
▪ portion of optic tract
Infarction (occlusion) of MCA
➢ MCA infarcts will vary depending on location
➢ dominant and non-dominant hemisphere loss with MCA infarction
MCA - Dominant hemisphere
(usually the left hemisphere for most people) typically controls language and certain cognitive functions
Symptoms:
-aphasia
-apraxia
-CL sensory loss (arm, face)
-CL hemiparesis (arm, face)
MCA - Non-dominant hemisphere
(usually the right hemisphere) controls aspects like spatial awareness, attention, and emotional processing
Symptoms:
-CL neglect (L-sided)
-hemianopia
-visuospatial deficits
-denial of illness (anosognosia)
-emotional blunting/disinhibition
Motor Changes with MCA Infarction
Contralateral hemiparesis or hemiplegia: Weakness or paralysis of the contralateral side of the body, typically affecting the face, arm, and hand more than the leg, due to the area of the primary motor cortex that the MCA supplies.
Contralateral apraxia: Difficulty performing purposeful movements, especially in the arm and hand, despite normal strength.
Facial weakness: Often, the face will be more affected than the lower limbs due to the way the motor cortex is organized in the MCA territory
Sensory Changes with MCA Infarction
Contralateral sensory loss: Sensory impairment, especially affecting the face, arm, and hand (again, more than the lower limbs) because the MCA supplies the sensory cortex areas corresponding to these body parts.
Impaired proprioception: Difficulty in knowing where limbs are in space, particularly in the arm and face.
Contralateral visual field deficits: Often a homonymous hemianopia (loss of vision in the same half of the visual field in both eyes), which occurs due to the MCA’s involvement in the occipital lobe’s visual processing areas
Behavioral/Personality Changes with MCA Infarction
Contralateral neglect (more common in non-dominant hemisphere infarcts): Patients may fail to attend to or recognize stimuli on the opposite side of the body (e.g., ignoring one side of the body or visual field).
Apathy, depression, or impulsivity: Emotional regulation might be disrupted due to the damage to the frontal lobe, which is involved in decision-making and emotional responses.
Disinhibition or poor judgment: The frontal lobe’s role in self-control and executive functions may be impaired, leading to impulsive behaviors or poor decision-making.
Posterior cerebral artery (PCA)
Supplies:
▪ occipital lobe
▪ inferior regions of temporal lobe
Infarction (occlusion) of PCA
▪ small branches of PCA supply some of thalamus and midbrain
➢ potential for sensory or motor symptoms in addition to visual changes
Perforating arteries
▪ numerous small branches that originate from the circle of Willis and the ACA, MCA,
PCA and basilar arteries)
Perforating arteries Supply:
▪ subcortical regions
➢ diencephalon (thalamus, hypothalamus, subthalamus)
▪ internal capsule
➢ pathway of myelinated axons leaving and entering the cerebral cortex
➢ located between thalamus and basal ganglia
Infarction (occlusion) = “lacunar stroke/small vessel stroke”
▪ most common area: lenticulostriate arteries (branches of MCA)/perforating
arteries
▪ supply the internal capsule and thalamus
Lacunar strokes are categorized common patterns
Lacunar stroke Pathology
➢ micro-deposits of connective tissue or fatty tissue blocks artery
➢ obstruction results in small necrotic tissue
▪ necrotic tissue is removed by macrophages: leaves “hole” (period of few
months)
➢ small penetrating arteries are not usually directly affected by atherosclerosis
Risk factors for lacunar stroke:
hypertension, smoking and diabetes
Pure motor stroke
▪ contralateral hemiparesis/hemiplegia
* face/arms/hands/legs
Pure sensory stroke
▪ contralateral hemiparaesthesia along face/arm/leg/trunk
▪ usually affects limbs more than face/trunk
Mixed motor and sensory involvement
▪ contralateral hemiparesis and hemiparaesthesia
▪ face/arm/trunk/leg
Ataxic hemiparesis
▪ combination of cerebellar/motor symptoms
▪ site of lesion involves cerebellar tracts as well as motor pathways
▪ “homolateral ataxia and crural paresis”
Blood supply of brainstem
Vertebral arteries
Basilar artery
Vertebral arteries
Estimated that 10% of population have one underdeveloped VA
Branches of vertebral artery
- Anterior spinal artery
- PICA (posterior inferior cerebellar artery)
Anterior spinal artery
▪ branches directly off of vertebral artery
▪ descends to supply anterior regions of spinal cord
PICA (posterior inferior cerebellar artery)
▪ Supplies:
➢ lateral medulla and cerebellum
▪ occlusion: PICA syndrome – see notes below
▪ PICA depends solely on VA for blood supply
➢ therefore VA occlusion may “create” PICA syndrome
Basilar artery
▪ R/L vertebral arteries merge to form basilar artery
➢ ascends anterior to brainstem
▪ divides into R/L posterior cerebral arteries to form part of Circle of Willis
Branches of basilar artery
▪ R/L Posterior cerebral arteries
▪ Long circumflex branches
▪ Superior cerebellar artery
▪ Anterior inferior cerebellar artery
▪ Pontine branches
Superior cerebellar artery
➢ supplies superior cerebellum and portions of midbrain
➢ infarction: Perinaud Syndrome (Dorsal Midbrain Syndrome)
Anterior inferior cerebellar artery
➢ supplies anterior/inferior quarter of cerebellum
➢ infarction: AICA or lateral pontine syndrome
Pontine branches
➢ small vessels that emerge from basilar artery to supply pons
➢ motor tracts – corticospinal tract
Basilar artery occlusion
acute complete occlusion associated with poor prognosis
”Locked-In Syndrome”
▪ infract in the base of pons
poor prognosis
Vascular occlusion:
▪ lower paramedian branches of basilar artery
Functional deficits:
▪ reticular system spared
➢ the patient remains “awake” but unable to function
▪ Quadriplegia
▪ Sensory
Quadriplegia
➢ unable to move except:
▪ blinking & move eyes vertically
▪ communication accomplished only with eye movement
➢ all motor tracts and lower CN impaired
Sensory
➢ “can’t move but can feel pain”
▪ Spinothalmic tract intact – so pain/temp not affected
➢ bilateral loss of discriminatory touch, vibration and proprioception
▪ due to loss of medial lemniscus pathway in medulla
Dorsal midbrain (Parinaud) syndrome
Blood vessel:
▪ superior cerebellar arteries, small arteries of PCA/basilar artery
➢ NOTE: usually non-vascular cause – pineal or midbrain tumor compression
Lesion damages:
▪ superior colliculus, pre-tectal area and cerebral aqueduct
PICA syndrome, Lateral medullary syndrome (aka Wallenberg syndrome)
PICA originates directly from VA
Supplies: lateral medulla and cerebellum
“PICA syndrome” result of:
▪ PICA occlusion
▪ vertebral artery occlusion
Impairments associated with PICA syndrome
▪ Cerebellar tract signs:
➢ hypotonia, disequilibrium, dyssynergia
▪ Descending sympathetic tracts
▪ Horner’s syndrome (ipsilateral)*
➢ Ptosis: drooping of eyelid (superior tarsal muscles innervated by sympathetics)
➢ Anhidrosis: decreased sweating on face
➢ Miosis: constriction of pupil
➢ Enophthalmos: appearance of eye “sunken in”
➢ Loss of ciliospinal reflex: pupil dilation in response to pain stimulus
Blood Supply of spinal cord
Anterior spinal artery
Right/Left Posterior spinal arteries
Anterior spinal artery
- supplies ventral 2/3 of spinal cord
- originate from R/L vertebral arteries
- various segmental branches supply anterior spinal artery at each level of spinal cord
- descends along anterior midline of spinal cord
Right/Left Posterior spinal arteries
- originate from R/L PICA
- various segmental branches supply anterior spinal artery at each level of spinal cord
- R/L descend along R/L posterior region of spinal cord
Complete transection injuries to spinal cord
Poor prognosis for recovery
Complete loss of function below level of injury
Partial transection injuries to spinal cord
Anterior cord syndrome
Posterior cord syndrome
Anterior cord syndrome
➢ anterior spinal artery occlusion/infarction
* fig 9-6; 10-5,10-6, 10-7 Greenberg
➢ more common (than posterior stroke)
▪ but uncommon in cervical region
* i.e., most infarcts in thoracic or lumbar regions
Posterior cord syndrome
➢ less common
▪ due to
* paired posterior spinal arteries
* multiple feeder vessels
