Download Internal Carotid Arteries (80%)

CNS Blood Supply
Monday, January 18, 2016
Blood to brain is 15-20% total Cardiac output and uses 25% of O2 in body
- 10 seconds of ischemia => loss of conciousness
- 20 seconds => loss of electrical activity
- Minutes => irreversible damage
General Blood Flow
- 20% from Vertebral and 80% from Internal Carotid Arteries -> Capillaries -> Veins following
arteries -> Dural Venous Sinuses -> Internal Jugular Vein
- Blood supply to DURA MATER is Middle meningeal a. (inside layers of dura) via EXTERNAL carotid
o If trauma to skull, you can get subdural hematoma from it
- Blood supply to Subarachnoid spaces + Brain from INTERNAL Carotid/Vertebral
Internal Carotid Arteries (80%)
- 4 segments
1) Cervical = bifurcates off Common Carotid Artery and enters carotid canal of temporal bone
2) Petrous = portion that is within carotid canal
3) Cavernous = Portion that travels within cavernous sinus, exits skull
- Unique because only place in body where artery runs through a venous sinus
4) Cerebral = leaves sinus and goes to brain; terminal portion that bifurcates in circle of willis
- Branches of ICA
- Middle Cerebral Artery
 Lenticulostriates branch from MCA (“end artery”)
 Supply Basal Ganglia and Internal Capsule
 Occlusion of these vessels  stereotypical stroke signs
- Anterior Cerebral Artery
 Gives off Anterior Communicating Artery
- Hypophyseal
 From ICA supply Pituitary Gland
- Ophthalmic
 First branch of ICA distal to cavernous sinus and supplies Globe/Orbit
 Occlusion  Blindness
- Choroidal
Vertebral Arteries (20%)
- 4 Parts
1) Subclavian Artery  Vertebral a.  Enters transverse foramen of C6 and ascends.
2) Ascends Transverse Foramina of Cervical spine up to C2 and exits
3) Continues through C1 TF and curves posteriorly then medially in groove for vertebral artery
(superior surface of posterior arch of atlas  SUBOX TRIANGLE) where it pierces Atlantooccipital
membrane/meninges of spinal cord into Subarachnoid Space
- Vertebral artery gives off Cervical branches before going through Foramen Magnum
4) Now ascends Foramen Magnum and becomes INTRACRANIAL then the two arteries unite to
become Basilar Artery
Neuroanatomy Page 1
- Intracranial branches (from vertebral a.) include
 Posterior Inferior Cerebellar Artery (PICA)
 Anterior Spinal (Travels down spinal cord in the Anterior Median Fissure of SC
 Posterior Spinal (2) (may come off PICA; travels down posterolateral sulcus of SC)
- Other branches of Vertebral Artery
 Labyrinthine (also called Internal Auditory Artery)
 Arise from AICA, but maybe basilar a.
 Supplies Inner Ear
 Pontine (branches of basilar a. over surface of pons)
 Stroke compromises function of neural pathways traveling through pons
 Anterior Inferior Cerebellar Artery
 Posterior Cerebral
 Posterior Communicating
Cerebral Arterial Circle (Circle of Willis)
- Arterial anastomosis formed by 4 arteries (2 ICA and 2 Vertebral)
- Formed by
 Anterior Cerebral Artery (A1)
 Anterior Communicating Artery (ACo)
 Internal Carotid Artery (ICA)
 Posterior Communicating Artery (PCoA)
 Posterior Cerebral Artery (P1)
- Impt if part of circle becomes blocked, blood flow continues from other portion to avoid ischemia
- Fewer than half exhibit normal pattern as some segments may be too small to be functional
(hypoplastic) or may be missing entirely
- Variants do not significantly affect blood flow but may cause asymmetrical blood flow
Cerebral Arteries (3 Pairs)
- Anterior Cerebral (from ICA) has 3 parts
 Part A1 = from origin from ICA to Anterior communicating Artery
 Part A2 = from Anterior Communicating Artery onwards
 Supplies medial aspects of frontal/parietal lobes, most of corpus callosum, basal ganglia and
internal capsule and CN 1
 Lesions  Paralysis/Paresis/Anesthesia of CONTRALATERAL LOWER extremity
and Smell? in addition to other potential deficits
- Middle Cerebral (from ICA)
▪ Passes laterally through lateral Sylvian fissure before splitting into superior/inferior
▪ Supplies lateral frontal/parietal lobes (not superior 2-3 cm), Lateral temporal lobe, basal
ganglia and part of internal capsule
▪ Lesions  Paralysis/Paresis/Anesthesia of CONTRALATERAL FACE/ARM and aphasia
(language issue)
- Posterior Cerebral (off Basilar from Vertebral A) Has 4 parts (only need to know 2)
 Part P1 = From origin off Basilar Artery to posterior communicating artery
 Part P2 = from communicating artery onwards
o Supplies inferior temporal lobe, occipital lobe, posterior corpus callosum, part of thalamus
o Lesions => Visual deficits, some CN deficits, and memory deficits
Neuroanatomy Page 2
- WATERSHED areas  regions receives duel blood supply from MOST DISTAL BRANCHES of 2 arteries
WITHOUT overlap => hypoperfusion may occur b/c areas are vulnerable to reduced blood flow
- 2 exist
 Between Anterior and Middle Cerebral Arteries
 Between Posterior and Middle Cerebral Arteries
- Watershed Strokes occur due to ischemia/block at watershed
 Produce unique focal neuro symptoms that can be used to diagnose stroke
 Can be Cortical or internal strokes
Cerebellar Arteries
- PICA  Posterior and inferior portion of Cerebellum
- AICA  Supplies anterior and lateral portion of cerebellum
- SCA
o Last branch of Basilar Artery
o Supplies Superior Portion of Cerebellum
Veins
-
Superficial Cerebral Veins drain Superficial portions of cerebrum
Internal Cerebral and Great Cerebral veins drain deep portions of cerebrum
Cerebellar veins drain cerebellum
All veins drain into Dural Venous Sinuses which are NOT true blood vessels but are Dura
Superior Sagittal Sinus joins Inferior Sagittal Sinus (via Straight Sinus) at Confluence of Sinuses ->
Transverse Sinus -> Sigmoid sinus -> Internal Jugular Vein
- Cavernous sinuses near pituitary drain into sigmoid or internal jugular via Superior and
Inferior Petrosal Sinuses
Cavernous Sinus contains ICA, CN 3, CN 4, CN 5 (parts 1 and 2), CN 6
Vasculature of Spinal Cord
- SC is supplied by 2 sets of arteries
- Longitudinal Arteries (starts at cranium and descends)
 Anterior Spinal Artery (1) formed by vertebral arteries
 Supplies Anterior 2/3 of SC
 Posterior Spinal Artery (2) branches off vertebral arteries
 Supplies posterior 1/3 of SC
- Branches of Spinal arteries minimally overlap centrally => creates Watershed supply
- Segmental Arteries enter vertebral canal via IV Foramen
- Radicular Arteries Given off at every level
 Supplies dorsal and Ventral Roots
Neuroanatomy Page 3
- Segmental Medullary Arteries Given off at variable levels
Supply the Spinal Canal
- Arteria Radicularis Magna (Artery of Adamkiewicz) is the largest anterior segmental
medullary artery At Lower Thoracic/Upper Lumbar Level (usually on left)
Supply lower 2/3 of spinal cord via anterior spinal artery
Clinical Connections Strokes
- Caused by an obstruction or rupture of artery supplying the brain
- Signs include trouble speaking, memory loss, unilateral paralysis
- Ischemic Strokes
- Most common type
- Caused when artery is blocked
- Embolic Strokes occurs embolism occurs outside brain and moves into artery
- Thrombotic Strokes occur when blockage forms INSIDE brain artery
- Hemorrhagic Strokes
- Occurs when blood vessel bursts due to high pressure/aneurysms
- Intracerebral Hemorrhage
Occurs when blood vessel bleeds inside brain tissue => cells die and affected region
functions imporperly
- Subarachnoid Hemorrhage
 Blood vessels burst near surface of brain and into subarachnoid space => reduces
blood flow causing strokes
 Usually caused by Aneurysm
Aneurysms
- Berry Aneurysms are outpouchings protruding from arteries of circle of willis and its
branches
(usually occur at branching points)
- account for 80-90% of all intracranial aneurysms
- Generally Asymptomatic Transient
Ischemic attack (TIA)
- Temporary Ichemia in brain due to lack of blood flow -> artery is unblocked or separate route
"opens up" after time and symptoms disappear again
- Symptoms include numbness, weakness, vision loss, speech impairment, loss of balance
Hematomas (Hemorrhages)
- Defined by location relative to meninges
- Epidural
- Bleeding between Dura and Skull => compresses brain
- Generally caused by Arterial blood filling space
- Subdural
- Bleeding between Dura and Arachnoid Mater => Compresses brain
- Generally caused by venous blood filling space
- Subarachnoid
- Bleeding below Arachnoid mater => blood disperses under layer
Neuroanatomy Page 4
Neuronal Microenvironment
Wednesday, January 20, 2016
Axon
 Projects from Soma at Axon hillock and carries impulses AWAY
 Can be myelinated or unmyelinated
□ Myelinated axons have Nodes of Ranvier which allow Saltatory Conductions due to high
concentration of Na+ at nodes to REGENERATE AP signal
 Axons receive myelin sheath from Glial cells
 Glial Cells provide SUPPORT AND PROTECTION, form myelin, and help maintain homeostasis
- Axons vary in diameter and Degree of Myelinations
○ Axons larger than 1 micrometer in diameter are all myelinated
○ Axon types
 A-Alpha
□ Highly myelinated and large diameter => fastest conduction velocity
□ Found in Proprioceptors of skeletal muscle
 A-Beta
□ Slower and smaller than A-Alpha
□ Found in Mechanoreceptors of skin
 A-Delta
□ Smallest and slowest of A axons
□ Found in Pain and Temperature nerves
 C
□ Unmeylinated and smallest of axon types
□ Found in Temperature pain and itch nerves
○ DEMYELINATED is NOT the same as Unmeylinated
Demyelination does not kill axons but diminishes their ability to conduct AP
Glial cells
- Glial cells are non-neuronal cells that maintain homeostasis, myelin, support, protect neurons in CNS/PNS
- 2 major types in PNS
○ Schwann cells
 Schwann cells myelinate SINGLE axons in the PNS
□ Vitamin E prevents damage to Schwann cells and dorsal root ganglia
 Schmidt – Lanterman/ myelin cleft  visible under light microscope and cross myelin
sheath at irregular intervals
 At the Nodes of Ranvier  adjacent Schwann cells interdigitate, thus permitting more
complete covering of the axolemma
一Satellite cells

Satellite cells  analogous to astrocytes, form an intimate, complete covering
layer over the large neuronal cell bodies in the ganglia of the PNS
- 3 major types in CNS
○ Astrocytes  largest, most numerous of the glial cells
 Modify/control immediate environment of neruons
 Fibrous Astrocytes
□ Long, Thin, well-defined processes -> White Matter
Neuroanatomy Page 5
 Protoplasmic Astrocytes
□ Short, frilly processes -> Gray matter
Radial Glia
□ Bipolar cells common in developing brain that help create organized scaffolding from
ventricle to pial surface
Muller cells
□ Specialized cells in RETINA that support neurons in retina
□ Spatial buffering of K+ via K+ Siphoning
 ALL ASTROCYTE CYTOSKELETONS HAVE UNIQUE PROTEIN GLIAL FIBRILLAR ACIDIC PROTEIN
(GFAP)
 Astrocytes contain all of the glycogen/glycogenolysis enzymes present in the brain = Glycogen
Fuel Reserve buffer
□ In the absence of glucose from blood, astrocytes can sustain the brain for about 5 minutes
via Substrate Buffering with LACTATE
 In direct route, glucose diffuses from blood into BECF, and then into neurons where
it is oxidized
 In indirect route, glucose enters astrocytes, where it may be stored as glycogen, or
metabolized to lactate, which then diffuses into the neuron and is oxidized
 Astrocytes help regulate K+
□ High neuronal activity leads to increases in K+ -> Astrocytes remove this excess K+ before
it affects normal function
□ Remove K+ by Increases Na/K ATPase activity
□ Astrocytes can network together and form a syncytium to control K+ via SPATIAL
BUFFERING => K+ taken up by astrocyte can be moved via gap junctions to a region with
less K+
Astrocytes Synthesize Neurotransmitters
□ ~ 20 neurotransmitters including Glutamate and GABA
 Glutamine is only produced in astrocytes by unique enzyme glutamine synthetase
and released to brain ECF to be converted to glutamate
 Glutamate may be converted into GABA while other is taken up again by astrocytes
◊ Important because excessive glutamate can cause excitotoxicity (as seen with
ischemia, anoxia, hypoglycemia, or trauma)
○ Oligodendrocytes
 Myelinate multiple neurons in CNS
 Leading edge of oligodendrocyte process flattens out sheet-like, wraps around axon,
cytoplasm is then squeezed out of all the layers in a process called compaction
 Contain most of Carbonic Anhydrase in brain which is used for Bicarb buffering
□ pH imbalance in the brain reduces seizure threshold
 Present in all regions of the CNS, predominant in white matter
○ Microglia
 Derived from Monocyte/macrophage cells
 Endogenous brain defense and immune system, responsible for CNS protection against various
types of pathogenic factors -> are most effective APC in brain
□ Rapidly activated by injury to brain => proliferate and become phagocytic
Demyelinating Diseases of CNS
- Multiple Sclerosis (MS)
○ MOST COMMON DEMYELINATING DISEASE OF CNS
○ Thought to be AUTOIMMUNE attack against OLIGODENDROCYTES
Neuroanatomy Page 6
○ Diagnosis relies on presence of neurological issues that REMITS and then returns at UNRELATED site
Exacerbation due to active inflammation of WHITE MATTER tracts in CNS
○ Common signs/symptoms
 Monocular blindness (lesion of optic nerve)
 Double vision (lesions of longitudinal fasciculus)
 Motor weakness/paralysis (lesion of corticospinal tract)
 Abnormal somatic sensation
 Dizziness (lesion of vestibular pathway)
- Guillain-Barre Syndrome
○ Segmental Demyelination in PNS
○ Follows a respiratory/GI viral or mycoplasmal infection
○ Most patients recover over weeks but residual disabilities are common
○ Signs and symptoms
 Severe respiratory limitations
 ASCENDING NEUROLOGICAL SYNDROME (starts at legs)
Neuroanatomy Page 7
Action Potential Review and Clinical Correlation
Wednesday, January 20, 2016
Cerebrospinal Fluid (review from lecture 2/3 worded differently)
- CSF is colorless, watery liquid filling ventricles of brain which provides buoyancy and maintains environment
for neurons/glia in CNS
○ CSF and Plasma have very similar composition to the point where their solute ratios are almost 1 for
everything
 CSF has LOWER amounts of K+ and Ca+ and HIGHER amounts of Mg+
 CSF should have virtually NO PROTEINS (RBC in CSF is bad)
- Secreted by Choroid Plexus (and some from capillaries) at about 500 mL/day
○ Formation starts in lateral ventricles and flows down pathway through Spinal Cord
 CSF that escapes in 4th ventricle goes into subarachnoid space -> over cerebral hemispheres ->
through arachnoid villi -> into Superior Sagittal Sinus
○ Specialized epithelium in choroid plexus form effective barrier with tight junctions to rigidly maintain
composition of CSF
- CSF can be collected from subarachnoid space via Lumbar Puncture generally at L4
- Rate of CSF production is independent of blood pressure/intraventricular pressure so CSF is produced
regardless of blockage/flow abnormalities => Hydrocephalus
○ As CSF pressure rises, ventricles expand at the expense of brain
○ CSF Shunt to venous blood or peritoneal cavity helps reduce CSF Pressure
○ 2 types of hydrocephalus
Communicating = impaired reabsorption or impaired flow in subarachnoid space
□ "Normal Pressure" Hydrocephalus shows normal spinal tap pressure even though MRI
shows ventricular enlargement
Caused by infections of meninges damaging arachnoid villi
Normally seen in elderly => see Dementia, Urinary Incontinence, Gait disturbance
Non-Communicating (Obstructive) = Blockages within Ventricular system
□ Papillomas (tumors of choroid Plexus) can potentially "bottleneck" CSF flow especially at
Interventricular Foramen (Lateral Ventricles affected) or
Squeezing the cerebral aqueduct (both lateral and 3rd ventricles)
Pineal Gland Tumors also can squeeze cerebral aqueduct
Neuronal Signals (ACTION POTENTIAL  EXTRA STUFF FROM THE LECTURE HE SKIPPED)
• Synapse
○ Area where Pre-synaptic and post-synaptic neuron communicate = Synaptic Cleft
○ Types of synapses are named by the contact site
 Axodendritic, Axosomatic, Axoaxonic
○ AP causes neurotransmitter-filled vesicles to release into the cleft at presynaptic nerve terminal
 Neurotransmitter then binds to receptors on postsynaptic nerve terminal
 Myasthenia Gravis is an AUTOIMMUNE DISEASE in which Ab bind to ACh receptors at NMSK
junction
□ Symptoms = fatigue and eye muscle weakness (ptosis) and rapid tiring
□ Tx = Acetylcholinesterase inhibitors so that concentration of ACh is increased/maintained
to increase chance of binding
Neuroanatomy Page 8
• Signals are generally known as Action Potentials which are measured in mV to gauge changes in neuronal
activity
• Resting Potential = -60 to -70 mV
○ Created by ion gradient due to Na/K ATPase pump (2 K in and 3 Na out)
 Also by lipid bilayer preventing diffusion
○ Na+, Ca+, and Cl- are higher OUTSIDE the neuron
○ K+ (and organic anions) are higher INSIDE the neuron
• As membrane potential increases, Na+ channels open first allowing Na+ to flood in and then K+ channels
open to let K+ out
○ This balance can be tipped by excitatory or inhibitory inputs
 Excitatory neurotransmitters produce DEPOLARIZING Excitatory PSP (EPSP) => more likely to
fire AP
□ Excitatory => increases Na+ permeability => Na+ floods in due to large electrochemical
gradient
 Can also increase Ca+ and depress Cl-/K+ conductance
 Either increases positive Charge of Cell => likely to AP
 Inhibitory neurotransmitter produces HYPERPOLARIZING Inhibitory PSP (IPSP) => less likely to
fire AP
□ Inhibitory increases efflux of K+ and Cl- influx => decreases positive charge of cell => less
likely to AP
○ Tetrodotoxin (TTX) is a Neurotoxin that binds to voltage gated Na+ channels From
pufferfish
○ EPSPs or IPSPs can be added together over SPACE = Spatial Summation
○ EPSPs or IPSPs can be added together over TIME = Temporal Summation
○ Graded potentials are created by permeability changes caused by ligand-gated channels at postsynaptic sites or by stimulus-gated channels in sensory receptor membranes
• AP are All or none => as long as threshold is reached, a neuron fires with same strength/magnitude each
time
○ FREQUENCY of firing can vary = conveys how intense the stimuli is
 I.e. more intense stimuli will have a rapid firing
• Phases of Action Potential
○ Key to know that each AP curve is different based on what cell is stimulated
a. From resting potential, an excitatory input reaches threshold (-55 mV) => AP
b. Cell depolarizes due to influx of Na+
c. Overshoot phase (anything OVER 0 mV) is at Peak of AP where Na+ CLOSE and become refractory; K+
continues to leave cell
d. Repolarizes as K+ continues to leave and decreases potential
e. K+ channels close and Na+ RESETS
f. Undershoot/Hyperpolarization phase occurs when some K+ channels remain open and creates
refractory period to prevent AP from traveling backwards
Neuroanatomy Page 9