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121 Cards in this Set

  • Front
  • Back
Two components of nervous system
Central nervous system (CNS) and peripheral nervous system (PNS)
What is the CNS composed of?
Brain, spinal cord, second cranial nerves
What is the PNS composed of?
Peripheral nerves (cranial nerves III-XII & 30 pairs of spinal nerves), sensory ganglia (collections of nerve cell bodies located outside of the CNS), sensory receptors outside CNS, and motor/ effector terminals located outside of the CNS
Nucleus
Collection of nerve cell bodies in the CNS
Ganglion
Collection of nerve cell bodies in the PNS
Autonomic Nervous System
Efferent or motor component of visceral nervous system. Includes elements of both CNS and PNS. Divided into sympathetic and parasympathetic nervous system.
Gray matter of CNS
Nerve cell bodies. Occurs on outer aspect of cerebral hemispheres, cerebellum, inside spinal cord, collections of nerve cell bodies (nuclei) within the CNS.
White matter of CNS
Axons (bundles of nerve fibers), predominately myelinated, often organized into tracts (no cell bodies)
How many regions in CNS?
7.
Region one of CNS
The two cerebral hemispheres are separated by the interhemispheric fissure (aka longitudinal fissure). These consist of the cerebral cortex (lobes, sylvian fissure, central sulcus), basal ganlia, deep white matter, corpus callosum
Region 1 in detail: Cerebral cortex
Gray matter that covers the surface of the hemispheres. Important for sensory and motor function and higher cortical functions. Located in frontal, parietal, temporal, and occipital lobes. Surface is convoluted (folds = gyri, grooves = sulci).
Separates the frontal and parietal lobes from the temporal lobe
Lateral or Sylvian fissure
Separates frontal lobe from the parietal lobe
Central or Rolandic sulcus
Region 1 in detail: Basal ganglia
Large mass of gray matter located at the "base" of each hemisphere. Includes the caudate, putamen, globus pallidus (important in cognitive/motor systems), and the amygdala (emotion)
Region 1 in detail: Deep white matter
Myelinated nerve axons that connect various parts of nervous system. Corpus callosum connects left,right hemispheres. Anterior commisure connects left/right temporal lobes.
Types of fibers in the deep white matter
Corpus callosum/anterior commissure connect two cerebral hemispheres, projection fibers connect cerebral cortex with lower brain and spinal cord, association fibers connect cortical areas in the same hemispheres
Region 2: Diencephalon ("between-brain")
Thalamus: consists mainly of nuclei, some relay sensory information from PNS to cortex, almost all are connected with areas of the brain responsible for sensory, motor, and cognitive functions.
Hypothalamus: below the thalamus, includes nuclei that control the ANS and endocrine system.
Epithalamus: contains pineal gland
Subthalamus: contains the subthalamic nucleus, a part of motor system
Region 3: Midbrain
Divided into the tectum (roof) and the cerebral peduncles
What structures are located in the cerebral peduncles?
Within each peduncle are located two important motor structures, the red nucleus and the substantia nigra
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Region 5: Cerebellum
Has cortical gray matter, deep white matter, and deep nuclei. Important part of motor system. Connects to midbrain, pons, and medulla by means of three paired cerebellar peduncles.
Region 6: Medulla
Contains ascending and descending tracts and nuclei. Important visceral control centers located here. Sometimes the word "bulb" is used to refer to medulla or whole brain stem.
Region 7: Spinal cord
Contains centrally located gray matter in shape of letter H surrounded by white matter.
What makes up brainstem?
Midbrain, Pons, Medulla
What is meant by the term "forebrain"?
cerebral hemispheres and diencephalon
What houses the brain?
Skull. Brain lies within the cranial vault of the skull
What houses the spinal cord?
Vertebral canal (the bony canal outside of SC)
How do the peripheral nerves pass to and from the CNS?
Through openings, termed foramina in the bony covering (Foramen magnum is where the spinal cord leaves the brain)
What are the three meninges between the CNS and bones that house it?
Pia, arachnoid, and dura
Pia
Thin, delicate layer of cells that lies on the surface of the brain and spinal cord
Arachnoid
Thin membrane of cells separated from the pia by the subarachnoid space (filled with CSF). The pia and arachnoid membranes are called the leptomeninges.
Dura (aka pachymeninx)
Tough, thick membrane that forms the outer covering of the brain and spinal cord
Ventricular system
4 cavities or ventricles filled with CSF
Lateral ventricle: located within each cerebral hemisphere
Third ventricle: slit-like space located between the left and right parts of the diencephalon
Fourht ventricle: in the midline at level of pons and medulla
Vestigial central canal: extends length of spinal cord but does NOT contain CSF
How does CSF flow in the CNS?
From the ventricular system within the brain to the subarachnoid space around the brain and spinal cord.
Four general types of neurons based on shape
Multipolar neurons (most common): numerous dendrites for inputs, decide whether to fire down the axon; may have short axon (interneuron aka golgi type II) or long axon (projection neuron aka golgi type I).
Bipolar neurons (especially "first order" neurons in the sensory systems)Have one process projecting from either end of elongated cell body
Unipolar neurons: have only a single process (pseudounipolar = begins as a bipolar neuron and with development has the two processes join; primary somatosensory neurons are pseudounipolar)
Anaxonic neurons: have no axons, both receptor and effector region located on dendrites
Neuron cell body (Soma): Nucleus
Nucleus is usually large, rounded, and centrally positioned within the soma. There is a large, obvious nucleolus.
Neuron cell body (Soma): Perikaryon
Cytoplasm, region of the cell around the nucleus. Includes following organelles:
Nissl substance = ribosomal RNA forming stacks of rough endoplasmic reticulum
Golgi apparatus: prominant in many neurons, often surrounds nucleus
Lysosomes: membrane bound vesicles containing hydrolytic enzymes
Mitochondria: throughout nerve cell cytoplasm
Neuron cell body (Soma): Three types of fibrillar longitudinal structures in perikaryon and nerve cell processes
Microtubules: hollow cylinders of tubulin, which orient as plymers along the long axis of axons and dendrites, involved in fast anterograde and retrograde axonal transport, part of neuron cytoskeleton (helps maintain shape of neuron cell body, dendrites, and axons)
Neurofilaments: polymers of three subunits, contribute to cytoskeleton of nerve cell body and axon
Microfilaments: composed of actin and associated proteins, primary cytoskeletal elements and also facilitate movement and growth
Neuron cell body (Soma): Microtubule-associated proteins
Specify the distance between microtuble polymers, which is different in axons and dendrites, and support the interaction between microtubules and other organelles
Example: Tau, a group of low molecular weight microtubule-associated proteins involved in AD
Nerve cell processes (neurites): Dendrites
Extensions of the cell body (contain the same cytoplasmic organelles), serve to increase surface area of cell body and increase possible number of synapses
Dendritic spines: occur on secondary and tertiary dendritic branches and serve to further increase surface area for synapses.
Nerve cell processes (neurites): Axon (Axis cylinder)
The conductive element of the neuron. Composed of an inital segment (arises from axon hillock of the perikaryon), projecting segment (often with collateral branches), and terminal branches (telodendria), and point of ending is called the axon terminal. Axoplasm contains the usual organelles except for Nissl substance. Axon cell membrane is called the axolemma. Axons form presynaptic terminals on dendrites, neuronal somata, or on other axons.
Synapses
Found in various forms, occasionally electrical but mostly chemical, neurotransmitter and modulator substances are often packaged in synaptic vesicles
Axonal Transport: 3 types
Fast anterograde axonal transport, Slow axoplasmic flow, retrograde axonal transport
Fast anterograde axonal transport
400 mm/day. Newly synthesized membranous organelles and synaptic vesicles or their precursors travel by this mechanisms from the nerve cell body to axon and distal nerve terminals (probably down microtubules in a stepwise or sliding manner). Process depends on oxidative metabolism (ATP), is not affected by protein inhibitors, and is independent of the cell body.
Axonal transport: Slow axoplasmic flow
10 mm/day. Transports cytoskeletal elements and soluble proteins down the axon
Axonal transport: Retrograde axonal transport
200 mm/day. Returns materials from nerve terminal to nerve cell body for degradation or reuse. Trophic factors, herpes virus, tetanus toxin.
Neuropil
Bulk of the CNS gray matter, no cell bodies, just the processes of neurons and glia. This is where the majority of synaptic contacts occur.
Neuroglial cells
structural support, guide neurons during development, release trophic factors, possess receptors for transmitters, peptides, and hormones, role in pathological processes
Neuroglial cells: Astrocytes
Stellate (star-shaped), distributed in both white and gray matter.
Functions: structural support, repair, maintain ionic environment, electrical insulation of synapses, chemical isolation of synapses. Recognized on stains by their oval, pale, vesicular nuclei. In brain and spinal cord.
Neuroglial cells: Oligodendrocytes
Small, round, dense staining nuclei, distributed in both gray and white matter.
Functions: Axon ensheathment and myelin formation in the CNS, nutrition of neurons. They are able to myelinate several axons.
Neuroglial cells: Ependymal cells
Columnar/cuboidal cells.
Functions: Formation of selective barrier between CNS tissue and CSF (line cavities, especially ventricles and spinal cord central canal during development), modification of CSF by both secretary and absorptive mechanisms
Three types of ependymal cells
1. Ependymocytes: constitute the majority of ependymal cells
2. Tanycytes: extend from ventricle to pia, respond to biochemical signals in CSF and modify activity in neurons, hypothalamus at base of third ventricle
3. Choroidal epithelial cells: line the choroid plexus and secrete CSF
Neuroglial cells: Microglia
Small, dense cells with dark staining cigar-shaped nuclei. Two types:
1. Reactive microglia = phagocytes (react to trauma), arise from white blood cells (monocytes) that gain entrance to CNS via injured blood vessels
2. Resting microglia come from neuroectoderm (function unknown)
Neuroglial cells: Radial glial cells
Present only during development, help neurons migrate from origin site to proper location
Sheath cells
All axons in PNS and CNS are ensheathed by living cells (sheath cells). Sheath cells may produce myelin (white fatty substance composed of lipid and protein). Myelin sheath comprises about 50% of total dry weight of white matter. Myelin facilitates axonal conduction while conserving space and energy.
PNS axon ensheathment
Axons in PNS ensheathed by Schwann cells. Schwann cells myelinate only one axon, but can "support" up to 10 unmyelinated axons. Each cell can invest up to 200 mm of the axon's length. Where one Schwann cell leaves off and another begins there is a myelin free space called a node of Ranvier.
How is the myelin sheath formed in the PNS?
An individual Schwann cell spirals around the axon. In the process, layers of the cell's membrane come into contact and become compacted. The myelin sheath is formed by compacting many layers of plasma membrane. The outer portion of the Schwann cell retains cytoplasm and forms part of the outer sheath (neurolemma) of the nerve axon
What is a peripheral nerve fiber?
A PNS axon together with its surrounding myelin (if present) and Schwann cells
What is each ensheathed PNS axon surrounded by?
A basal lamina which is an extracellular matrix structure produced by the Schwann cell. This is part of the neurolemma of the axon.
Are there axons that are not ensheathed?
No, all axons are ensheathed and most axons are myelinated. Even unmyelinated axons need to be supported by Schwann cells or Oligos. In other words, if the Schwann cell just wraps around the axon once, it is supporting the axon, but the axon is not myelinated (Myelinating means wrapped around several times, squeeze out cytoplasm)
CNS axon ensheathment
Oligodendrocytes are the sheath cells of the CNS. Unlike Schwann cells, single oligos can myelinate segments of multiple axons (one oligo supports and myelinates one segment of many axons). Oligos processes encircle several axons. The processes spiral around the axon segments, forming multiple layers of cell membrane. Nodes of Ranvier between successive oligos along axon.
Myelin structure
Dry mass of CNS and PNS myelin has high proportion of lipid (70-85%) and low proportion of protein (15-30%). CNS and PNS myelin have very different proteins (this is why disorder of CNS myelin may not involve PNS and vice versa; also certain disorders that attack Schwann or oligo cells only).
What does the neurologist get from the neurological history?
Symptoms (what the patient reports), time course of onset, and subsequent course of disorder
What does the neurologist get from the neurological examination?
Signs (often objective, but can be subjective). Components of exam:
1. MSE: tests higher cortical function
2. Exam 12 cranial nerves
3. Coordination testing
4. Motor exam
5. Somatosensory exam
6. Reflexes
7. Posture and gait
8. General physical exam
Lesion
The "lesion" is the patient's neurological problem. The history and exam allow neurologist to localize the lesion (e.g., where is the lesion?)
What are the types of lesion distributions?
1. Focal: single, well-defined, anatomical lesion
2. Multifocal
3. Diffuse: affects a functional or anatomical part of the nervous system because this part has a selective vulnerability to the lesion (often symmetrical, but may be asymmetrical like in Parkinson's)
What is an intraparenchymal lesion?
A lesion located within the nervous system tissue
What is an extraparenchymal lesion?
A lesion located outside the nervous system (e.g., a blood clot pushing on brain) that causes nervous system dysfunction
What is a mass lesion?
A mass lesion exerts part or all of its effect by pushing on normal tissue (either from within or from without the tissue). May stretch pain sensitive structures and cause headache. Brain tumors often present as mass lesions.
False localizing sign
Occurs when a lesion, generally associated with brain swelling or mass effect, causes a remote effect on another part of the nervous system.
What kind of lesion should we assume first?
Focal. Next, assume diffuse. Only occasionally will be multifocal.
What are the possible time courses of symptom onset?
We get the time course information from the history.
1. Acute: developed instantaneously or over minutes to hours.
2. Subacute: developed over days to months.
3. Chronic: developed over months to years.
(There may also be further exacerbations (periods of worsening) or remissions (periods of improvement)).
What are the different categories of neurologic disease?
Use VITAMIN DEC to remember.
1. Vascular
2. Infectious
3. Traumatic
4. Autoimmune/Immunologic
5. Metabolic/Toxic/ Endocronologic/Nutritional
6. Iatrogenic
7. Neoplastic
8. Degenerative
9. Episodic/Paroxsymal
10. Congenital/developmental
Vascular disorder
Primarily strokes. Focal and acute.
Infectious disorders
Caused by viruses, bacteria, or other agents. Diffuse, focal, or multifocal. Often subacute, but can be chronic or acute. Fever and elevated white blood cell count.
Traumatic disorders
Often accompanied by history of trauma and signs of trauma. Can be focal (contusions), multifocal (contusions), or diffuse (hemorrhages). Any time course.
Autoimmune/immunologic disorders
MS (focal or multifocal and chronic), Guillain-Barre syndrome, systemic lupus erythematosus. Can be focal, multifocal, or diffuse. Chronic?
Metabolic/toxic/endocrinologic/nutritional disorders
Diffuse (selective vulnerability). Usually subacute, but can be acute or chronic. Examples- alcohol intoxication, vitamin B12 deficiency
Iatrogenic disorders
Often metabolic/toxic and due to adverse effects of meds
Neoplastic disorders
Focal. Subacute (malignant) or chronic (benign) course. Sometimes multifocal (lung canses with multiple metastases to brain)
Degenerative disorders
Diffuse. Chronic. Examples - AD, PD, amyotrophic lateral sclerosis, muscular dystrophies
Episodic/paroxysmal disorders
Each episode has acute course, but episodes recur over months or years. Examples- migraine, epilepsy, syncope, vertigo, narcolepsy
Congenital/developmental disorders
Present from birth (sometimes childhood or young adulthood). Usually diffuse and chronic. Occasionally focal with any time course.
Diagnostic or confirmatory neurological tests
EMG and nerve conduction studies: measure electrophysiological function of nerves/muscles
EEG: measure electrophysiological function of the cerebral cortex
Neuropsych tests: measures higher brain function
Neuroimaging: demonstrate anatomical or physiological status of parts of the nervous system
Spinal tap: spinal fluid examination to look for evidence of infection or inflammation in or near the meninges
Neurological treatment
Supportive therapy: education, psychological support for patient and caregivers
Symptomatic therapy: for symptoms associated with the disorder (often meds)
Specific therapy for the neurological disorder: meds, surgery, or other treatments
MS: Epidemiology
Common disorder, prevelance 0.1%. Can begin at any age but often starts between age 20-30.
Risk factors: living in cold and "temperate" latitudes during first 15 years of life, white race, female gender, having first degree relative with MS
What happens in Multiple Sclerosis?
Autoimmune attacks against CNS myelin resulting in "plaques" of demyelination
MS: Symptoms and signs
Related to distribution of symptomatic lesions within patient's CNS. Can be neuropsychiatric difficulties, visual impairment (including optic neuritis or inflammation of optic nerve), internuclear opthalmoplegia, vestibular dysfunction (vertigo), motor difficulties (fatigue, upper motor neuron syndrome, cerebellar syndrome), somatosensory dysfunction, difficulties with bladder, bowel, sexaul dysfunction
MS: Symptoms and signs
Related to distribution of symptomatic lesions within patient's CNS. Can be neuropsychiatric difficulties, visual impairment (including optic neuritis or inflammation of optic nerve), internuclear opthalmoplegia, vestibular dysfunction (vertigo), motor difficulties (fatigue, upper motor neuron syndrome, cerebellar syndrome), somatosensory dysfunction, difficulties with bladder, bowel, sexaul dysfunction
MS: Symptoms and signs
Related to distribution of symptomatic lesions within patient's CNS. Can be neuropsychiatric difficulties, visual impairment (including optic neuritis or inflammation of optic nerve), internuclear opthalmoplegia, vestibular dysfunction (vertigo), motor difficulties (fatigue, upper motor neuron syndrome, cerebellar syndrome), somatosensory dysfunction, difficulties with bladder, bowel, sexaul dysfunction
How does temperature influence MS symptoms?
Demyelinated fibers are highly sensitive to change in temperature (decreased current generation that causes impulse conduction to worsen).
Fever, heavy physical exertion, hot weather, or hot shower/bath each may cause a transient and generally reversible worsening of existing symptoms. This is due to slowed conduction on partially myelinated axons that is worsened and may turn into a conduction block.
Lowering temperature (e.g., cold pool, cold shower) may result in temporary improvement of function.
What are MS lesions?
Called plaques, they are small areas of partial or complete demyelination. They occur only in the CNS and exact cause in unknown (may be autoimmune process directed against CNS myelin that is triggered by exposure to some antigen, perhaps viral, during the patient's first 15 years).
Negative symptoms of MS
Ms plaques cause negative symptoms (loss of function) by disrupting axonal conduction. The demyelinated portion of a nerve fiber can't conduct nerve impulses because the density of sodium channels in the previuosly myelinated sections is probably too low to support impulse conduction and the excess potassium channels keep the axon membrane near its resting potential.
Conduction depends on ability to propagate nerve impulses across (rather than through) acutely demyelinated segments to successive nodes of Ranvier
Negative symptoms of MS: What happens to conduction in moderately and severely demyelinated fibers?
Moderately demyelinated fibers: decrased conduction velocity because it takes successive nodes of Ranvier longer to reach threshold (loss of speed) and temperal dispersion impulse conduction (loss of synchrony of impulses carried by fibers with different degrees of demyelination)
Severely demyelinated fibers: conduction block may occur because successive nodes of Ranvier are unable to reach threshold (can be related to frequency or can be blocked totally)
MS positive symptoms
Pain, other abnormal sensation (e.g., tingling, electric-shock in response to flexion of neck called Lhermitte's sign -- reflects increased mechanosensitivity of demyelinated axons in dorsal colums of cervical spinal cord), or spasms. Within plaque, some axons may have an abnormal excitability (focal accumulation of ion channels in densities that cause baseline resting potential to be much closer to action potential threshold).
Ms positive symptoms: Types of hyperexcitability
They are all ectopic, meaning the action potential starts in the wrong place.
Spontaneous or mechanosensitive ectopic excitation.
Autoexcitation: Ectopic excitation caused by previous activity within same nerve fiber
Ephaptic excitation (e.g., cross talk): ectopic excitation is caused by normal electrical activity in an adjacent fiber.
Remission of MS symptoms
Never 100% gone, symptoms can flare back up. Some factors:
1. Resolution of inflammation/edema (contribute to abnormal conduction in acute stage)
2. Remyelination in CNS plaques may occur to a small extent.
3. Conduction may occur through alternative pathways.
4. Reorganization of demyelinated axon membrane, with acquisition of sufficient numbers of sodium channels to support conduction.
Clinical course of MS
Occurs in well-defined attacks or exacerbations that are followed by improvement or complete recover and then by periods of "remission" without attacks. Exacerbations often last many weeks. Not every new lesion is associated with a clinical attack (in other words, if not seeing symptoms doesn't mean not getting more lesions). Baseline level shifts to a worse/lower level at every attack (over time accumulating disability).
What is the difference between secondary progressive and primary progressive in MS?
Secondary progressive: chronic progressive neurological deficits that follow an inital relapsing-remitting course.
Primary progressive: course that is gradually progressive from onset (Meds don't work for this course, 10-15% males).
Progression of MS in an individual patient is unpredictable.
How is MS diagnosed?
Multiple CNS lesions in space and time, characteristic brain MRI abnormalities (lesions of MS within the CNS white matter), and evidence of immunoglobulin production in the CNS (oligoclonal bands, elevated IgG synthesis rate). Evoked potentials occasionally used to demonstrate a "second lesion" (e.g., visual EP can confirm if someone ever had demyelination in the optic nerve)
Treatment of MS
Goal: Prevent relapses
1. Supportive treatment (education and psychological support)
2. Symptomatic therapy (Fatigue, spasticity, shooting pains, burning pains, urinary urgency, frequency, constipation, rare surgical procedure to treat movement disorder)
3. Specific therapy for MS --[short term use of corticosteroids; Use of immunomodulators (interferons beta, glatiramer acetate, mitoxantrone, natalizumab)].
What is the only common cause of acute demyelination of the peripheral nerves?
Guillain-Barre syndrome (GBS). GBS is an inflammatory polyneuropathy with a monophasic coursse.
Clinical picture of GBS
In 2/3 of patients a viral infection occurs 1-3 weeks before onset. Progressive ascending weakness with mild sensory loss (negative symptoms) over several days to weeks. Muscle stretch reflexes lost early. Weakness of respiratory muscles and autonomic dysfunction may occur.
Despite severe paralysis for weeks to months, most people have complete recoveries.
No temperature dependence or positive symptoms.
Pathophysiology of GBS
May be due to an autoimmune process directed against PNS myelin that is triggered by recent exposure to some antigen, perhaps viral
How can a patient with GBS lose reflexes before loss of somatosensory and motor functions?
Variable amounts of proximal demyelination mean that the afferent activity for stretch reflex on Ia fibers is temporally dispersed and does not arrive synchronously on the alpha motor neurons. There is no temporal summation so adequate stimulus can't excite the reflex arc.
What is chronic inflammatory demyelinating polyneuropathy?
The chronic form of GBS (happens repeatedly). Thought to also be autoimmune.
Where are the cerebral peduncles and what are the surface of these peduncles composed of?
They are located on the base of the midbrain. They are composed of large bundles of nerve fibers termed the crus cerebri.
Where is the tectum and what is it composed of?
The tectum is the roof or cover of the midbrain. It is composed of the inferior colliculus and the superior colliculus.
What is the fused potion of the right and left dural sheets called?
falx cerebri
What is the name of the venous channel at the base of the falx cerebri?
inferior sagittal sinus
What is the name of the double layer of dura that separates the cerebellum and the cerebrum?
Tentorium cerebelli
What is the name of the venous channel that is formed by the superior margin of the falx cerebri and the periosteum of the inner surface of the skull?
superior sagittal sinus. This drains the smaller veins of the hemispheres.
What is a venous sinus?
An endothelium-lined tubular passage that conducts blood
What are arachnoid granulations?
Nodules protruding into the superior sagittal sinus. They are hypertrophied remnants of arachnoid villi that accumulate with age.
Where do the blood vessels on the brain surface lie (membrane-wise)?
They lie below the arachnoid membrane in the subarachnoid space (this space contains CSF)
What is the potential space between the arachnoid membrane and the dura called?
Subdural space
Normal: this is a mere cleft containing a minute amount of extracellular fluid.
Abnormal: Blood may force a separation between these two membranes forming a space termed a subdural hematoma
What is the name for the delicate arachnoid-pia complex (e.g., the arachnopia)?
Leptomeninges (means small/thin meninges)
Which vessels supply the anterior cerebral circulation?
Internal carotid arteries (right and left). Enter the cranial cavity via the carotid canals in base of skull.
Which vessels supply the posterior cerebral circulation?
Vertebral arteries (right and left). Enter the cranial cavity via the foramen magnum.
What is the arterial circle of Willis?
The connections (anastomoses) between the internal carotid and vertebral circulations via the posterior communicating arteries form a circular pattern known as the arterial circle of Willis.
What vessels is the Circle of Willis composed of?
The circle of Willis is comprised of nine vessels (left/right internal posterior cerebral arteries, left/right posterior communicating arteries, left/right internal carotid arteries, left/right anterior cerebral arteries, anterior communicating artery