NBB 1 Part 2 Flashcards
Describe the ventricular spaces associated with each of the subdivisions of the brainstem
- Cerebral aqueduct of Sylvius between 3rd and 4th ventricles is in the midbrain
- 3rd ventricle is in the diencephalon
- 4th ventricle dorsal to pons, shared between pons and rostral medulla (which has choroid plexus on dorsal side at caudal end of 4th ventricle)
What are the exit points for CSF circulation in the brainstem?
Where does CSF go afterwards? What are the cisterns
- Foramen of Magendie (medial)
2 + 3. Foramina of Luschka (lateral)
Drains into cisterna magna (second place you can obtain CSF fluid, after spinal tap) –> subarachnoid space –> drained via arachnoid granulations –> venous sinus
Cisterns: magna, prepontine, interpeduncular, and quadrigeminal
Differentiate between the levels of the brainstem (medulla, pons, midbrain) and explain the basis for their gross anatomical differences:
1. Medulla
- Medulla:
A. Ventral side of rostral medulla: anteromedial fissure for anterior spinal artery
-Most medial - pyramid
- then olive - covers the inferior olivary nucleus (winding snake like appearance)
- then inferior cerebellar peduncle
B. Dorsal side of rostral medulla:
-4th ventricle, plus choroid plexus
C. Ventral side of caudal medulla:
-pyramidal decussation of corticospinal tract (motor tract for body from primary somatosensory cortex)
D. Dorsal side of caudal medulla:
-gracile tubercle (2nd order synapse of axons from lower limbs from sensory DCMLS)
-cuneate tubercle (2nd order synapse of axons from upper limb from sensory DCMLS)
Review DCMLS and STT pathways and where they pass through the medulla
DCMLS: vibration, proprioception, soft touch
1st order in DRG, 2nd is gracile and cuneate nuclei of caudal medulla, decussation as internal arcuate fibers of lower medulla, ascends via medial lemniscus, 3rd order is VPL of thalamus
-travels through medial medulla
STT: pain, temperature, crude touch
1st order in DRG, 2nd order is Lissauer’s tract in dorsal horn, decussates at anterior white commissure and ascends for 2 spinal cord levels, ascends via anterolateral system, 3rd order is VPL of thalamus
-travels through lateral medulla
- Name the motor and sensory pathway that synapse in the medulla
- Name the motor and sensory pathway that travel through the medulla
1A.Corticobulbar (synapse with CN LMNs)
B. DCMLS (ipsilateral cuneate/gracilis nucleus then decussates as internal arcuate fibers)
2A. Corticospinal (pyramidal decussation then synapse in anterior horn of spinal cord)
B. Spinothalamic (synapse in Lissauer’s tract and decussate at anterior white commissure of spinal cord)
- What is the difference between a nerve and a tract?
- Define functions of the types of motor nuclei:
A. Somatic efferent nuclei
B. Visceral efferent nuclei - general
C. Visceral efferent nuclei - special
3. Define functions of the types of sensory nuclei: A. Somatic afferent nuclei - general B. Somatic afferent nuclei - special C. Visceral afferent nuclei - general D. Visceral afferent nuclei - special
- Both are bundles of axons
Nerve is in touch with periphery, tract with CNS - A. Somatic efferent nuclei GSA: framework of body e.g. skeletal muscles that originate from embryonic somites
B. Visceral efferent nuclei- general GVE: parasympathetic fibers for smooth muscles (viscera)
C. Visceral efferent nuclei - special SVE: activates striated muscle (from embryonic branchial arches i.e. jaw, face, larynx, pharynx, trap, sternocleidomastoid) - Somatic afferent- info about changes in environment from framework of body (receptors)
A. General GSA- impulses that begin near the body surface e.g. pain, temp, touch pressure
B. Special SSA- highly specialized sensory systems e.g. vision (light) and hearing (sound)
Visceral - impulses arising in/around the viscera or organs
C. General GVA- receptors from mucous membrane or in organ walls - physical (distension) or chemical composition
D. Special SVA- specialized chemical stimuli i.e. smell, taste
Describe distribution of cranial nerves throughout the brainstem and medially/laterally
Rule = 2:2:4:4 (out:Md:Po:Me)
I and II - outside the brainstem
II and IV - in midbrain
V, VI, VII, VIII - in pons
IX, X, XI, XII - in medulla.
Motor CNs are more medial, sensory more lateral e.g. VIII is most lateral
Medulla - most medial is hypoglossal nucleus, then parasympathetic dorsal motor nucleus of X, then sulcus limitans line, then sensory nuclei (spinal trigeminal, nucleus solitarius, vestibular nuclei)
CN XII (Hypoglossal) I. Which part of the brainstem does it travel through? II. What are its functions? III. Lesion of UMN (corticobulbar tract) vs LMN (hypoglossal nerve) vs bilateral lesion
I. XII is between olive and pyramids in the medulla (ventral side)
hypoglossal trigone on the floor of the 4th ventricle (dorsal side) –> visual aspect of the hypoglossal nucleus, which is a cell column –> LMNs extend the full length of the medulla
II. Innervated by:
A. Voluntary movements/articulation
- UMNs form corticobulbar pathway from cerebral cortex –> crossed/contralateral innervation (e.g. R cortex to L hypoglossal nucleus)
-LMNs from hypoglossal nucleus innervate all extrinsic and all but one (palatoglossus - CN X) extrinsic tongue muscles
-GSE - ipsilateral tongue muscles –> controls movement of tongue, maintains muscle tone
B. Reticular neurons for automatic/reflex movements - control of movements while eating and swallowing
III. Corticobulbar tracts usually bilateral, BUT are contralateral for XII
UMN lesion –> tongue deviates to opposite side of damage (e.g. if you lesion L corticobulbar tract –> affects R hypoglossal nerve –> tongue deviates to R side)
LMN lesion –> tongue deviates to same side of damage (e.g. if you lesion L hypoglossal nerve –> tongue deviates to L side) + severe muscle atrophy
Bilateral lesion –> disability speaking, swallowing food; due to motor neuron disease, demyelination (ALS), bleeding, tumors of medulla / base of skull
CN XI (Spinal Accessory) I. Which part of the brainstem does it travel through? II. What are its functions? III. What happens with lesion?
I. Lateral to XII in the medulla, one part from medulla (Accessory nucleus), other part is ventral motor horn of cervical spinal cord
II. CN XI = motor
A. SVE Branchial motor part –> innervates ipsilateral sternocleidomastoid and trapezius muscles (neck and shoulder) Special visceral efferent
B. Visceral motor part –> control of larynx, joins CN X
III. Lesion:
- cannot rotate head towards healthy side (away from lesion) against pressure
- ipsilateral shoulder drop
- weakened voice or hoarseness
CN X (Vagus) I. Which part of the brainstem does it travel through? II. What are its functions? III. What happens with lesion?
I. Efferent fibers exit medulla between olive and inferior cerebellar peduncle on ventral side; vagal triangle is also on the floor of the fourth ventricle on dorsal side, overlies the dorsal motor vagal nucleus adjacent to hypoglossal nucleus
-Although LMNs from multiple nuclei inside brainstem – axons come together to form single bundle at CNX level of medulla
II. CN X is mixed
A. Motor components:
1. general visceral efferent (dorsal vagal nucleus)–> preganglionic parasympathetic –> ganglia for heart, lungs, GI to splenic fixture
2. special visceral efferent /branchial efferent (nucleus ambiguus) –> pharyngeal muscles (swallowing), laryngeal muscles (vocalization)
B. Sensory components:
- GSA (joins nucleus of CN V) - touch, pain, pressure from small parts of face –> pharynx, meninges, small region of external ear (conscious)
- SVA (rostral nucleus solitarius)- taste for small part of mouth –> epiglottis and posterior pharynx
- GVA (caudal nucleus solitarius)- from chemoreceptors and baroreceptors from aortic arch (subconscious)
III. bilateral lesion is fatal !
Unilateral lesion - motor affected first –> contralateral uvula deviation, ipsilateral vocal muscle paralysis
CN IX (Glossopharyngeal) I. Which part of the brainstem does it travel through? II. What are its functions? III. What happens with lesion?
I. Exits upper medulla rostral to vagus nerve (bw olive and cerebellar peduncle)
II. CN IX is mixed
A. Motor components:
1. GVE (inferior salivator nucleus in the pons) - pregang parasympathetics for parotid gland
2. SVE / branchial efferent (nucleus ambiguus) - stylopharyngeal muscle –> elevates pharynx during talking and swallowing
B. Sensory components:
- GSA- touch pain pressure from small parts of face –> pharynx, posterior 1/3 tongue, middle ear, small region of external ear (conscious)
- SVA (rostral nucleus solitarius)- taste from posterior 1/3 tongue
- GVA (caudal nucleus solitarius)- chemoreceptors and baroreceptors from carotid body (subconscious)
III. problems with coughing, saying “Aah”, blowing out cheeks; due to polio, ischemic lesions, motor neuron disease, etc.
Differentiate between the levels of the brainstem (medulla, pons, midbrain) and explain the basis for their gross anatomical differences:
2. Pons
- Pons
A. Ventral side - 2 corticospinal tracts on ventral side, one CN trying to reach cerebellum
B. Dorsal side - facial colliculus, 3 cerebellar peduncles - superior, middle (made of contralateral pontine nuclei fibers), inferior; 4th ventricle
CN V (Trigeminal) I. Which part of the brainstem does it travel through? II. What are its functions and motor/sensory nuclei? III. What happens with lesion?
CN V (Trigeminal) I. Small motor part exiting on dorsal side but large sensory part coming in through middle cerebellar peduncle
- innervations are ALL ipsilateral
- V3 includes anterior 2/3 tongue (taste for that region comes from VII
II. Mixed - 4 nuclei
A. Motor components:
1. SVE/branchial motor (trigeminal motor nucleus)- muscles of mastication + tensor tympani muscle + bilateral corticobulbar projections for voluntary chewing
*more medial to the principal sensory nucleus, fibers leave from dorsal side
B. Sensory components:
- GSA - crude touch, pain, and temp + noxious stimuli/ nociception from V1-V3 (spinal nucleus) –> trigeminothalamic tract
- GSA - fine touch and pressure from V1-V3 (chief/ principal sensory nucleus) –> trigeminal lemniscus tract e.g. afferent aspect of c
- GSA - unconscious proprioception and bite strength (mesencephalic nucleus) –> NO tract to thalamus; only primary sensory neurons already in CNS, in the mesencephalic nucleus –> goes from pons to the midbrain
III. Lesion
- atrophy and chin deviation on side of lesion
- trigeminal neuralgia - idiopathic, brief severe pain in V2-V3 but facial sensation normal
- loss of jaw jerk reflex
CN V.
Describe the trigeminothalamic pathway (i.e. Trigeminal Chemosensory pathway)
Trigeminothalamic pathway - conveys pain and temperature from the head and face to thalamus for CN V (general sensory afferent)
*conveys nociception / noxious stimuli detection (eg chili peppers, vinegar) - separate pathway from CN I
1st order neuron - trigeminal ganglion outside the pons
fibers go downwards from pons
2nd order neuron - ipsilateral spinal nucleus of V (medulla) or in the spinal cord
ascends and decussates at the pons and medulla (at 2 levels) –> create trigeminothalamic fibers
3rd order neuron - VPM nucleus of thalamus
*Spinal Nucleus V also receives afferents that enter brainstem with
IX - sensation for back of ear, posterior 1/3 tongue, upper pharynx
X - sensation for pharynx, larynx, external ear
CN V.
Describe the trigeminolemniscal pathway
Trigeminolemniscal pathway - conveys touch and pressure from head and face to thalamus for CN V (General sensory afferent)
1st order neuron - trigeminal ganglion outside the pons
fibers enter and synapse right away
2nd order neuron - principal sensory nucleus of V in the pons –> decussation only at pontine level
3rd order neuron - VPM of thalamus
CN VII ( Facial) I. Which part of the brainstem does it travel through? II. What are its functions and motor/sensory nuclei? III. What happens with lesion?
CN VII
I. Ventral pons - nerve exits laterally to VI at the ponto-medullary junction
Dorsal pons - facial colliculus on floor of 4th ventricle - consists of fasicles of facial nerve looping around abducens nucleus
II. CN VII - Mixed
A. Motor components:
1. SVE - muscles of facial expression - stapedius muscle and part of digastric muscle motor parts of corneal, sucking, and blinking reflexes
2. GVE - pregang parasympathetic for salivatory gland (lacrimal, sublingual, submandibular) EXCEPT parotid (IX)
B. Sensory components:
- GSA - sensation from small region near outer ear (also IX, X)
- SVA - taste from anterior 2/3 tongue (sensory is from CN V, posterior 1/3 is CN IX) –> joins other taste fibers (IX, X) at the nucleus solitarius
- GVA - mucous membrane of nasopharynx
III. Lesions
A. UMN (corticobulbar tract) lesions - bilateral for upper face and contralateral for lower face –> only lower face weakness
refers to voluntary facial paresis; emotional expression comes from anterior cingulate cortex and hypothalamus –> joins corticobulbar tract at facial nucleus LMNs
B. LMN (CN VII) lesion e.g. Bell’s Palsy - ipsilateral for upper and lower face –> unilateral facial weakness, dry eye, loss of taste
Differentiate between the levels of the brainstem (medulla, pons, midbrain) and explain the basis for their gross anatomical differences:
3. Midbrain
- Midbrain
A. Ventral side - cerebral peduncles (axons) with interpeduncular fossa in between (interpeduncular cistern) and CN III oculomotor nerve exiting *CN III between superior cerebellar artery (SCA) and posterior cerebral artery)
B. Dorsal side (back side) - trochlear CN IV exits; cerebral aqueduct; quadrigemina composed of paired superior (visual) and inferior (auditory) colliculi (collection of cell bodies) –> quadrigeminal cistern
Midbrain contributes one tract to medial motor system (superior colliculus –> tectospinal - head movement) and one to lateral (red nucleus –> rubrospinal - voluntary contralateral flexors)
Describe the vascular supply of the midbrain and conditions that arise if it is compromised
Posterior cerebral artery - covers the cerebral peduncles where all the motor pathways (corticobulbar, corticopontine), and sensory pathways (anterolateral, spinothalamic, trigeminal thalamic, trigeminal lemniscus) are together
-covers substantia nigra, red nucleus, descending sympathetic fibers
Describe the development of the eye.
What are clinical implications of eye development?
Eyes form as an outgrowth the CNS (other sensory systems formed peripherally)
- Optic vesicle induces overlying ectoderm to differentiate into lens epithelium
- Optic vesicle folds in on itself and pulls in the forming lens
- Lens separates from ectoderm
- Outer layer differentiates into retinal pigmented epithelium; inner layer becomes neural retina –> retinal layer
- Surrounded mesenchyme becomes sclera (tough outer layer) and uvea (vascular layer)
optic nerve –> optic sheath –> subarachnoid space where CSF flows through –> dura
so increased intracranial pressure –> compresses optic nerve –> impairs venous return –> papilledema (optic nerve swelling that can be visualized through the pupil)
*swelling of optic nerve due to other causes = intraocular optic neuritis
What are the 3 distinct layers of the eye and their functions?
What are the segments of the eye?
3 layers (ie spheres lying inside one another):
I. tough outer layer –> sclera and cornea
II. vascular layer –> uvea with choroid posterior and ciliary body/lens and iris anterior
III. third inner layer –> retina, incomplete sphere with only posterior aspect
Fluid-filled segments:
1. Posterior segment - from retina to back of lens, filled with vitreous humor –> slow turnover
2. Anterior segment - from lens to cornea, filled with aqueous humor –> constantly replenished
A. Anterior chamber - in front of iris
B. Posterior chamber - behind iris
- Describe process of closing/opening eye
- Describe process of lacrimation
A. Dry eyes stimulation
B. lacrimation stimulation
1A. Opening eye - levator palpebrae superioris (CN III) and superior tarsal (sympathetic from superior cervical ganglion)
B. closing eye - obicularis oculi (CN VII) - orbital and palpebral portions motor limb of corneal reflex
- Lacrimation - lacrimal gland is superior and lateral –> produces tears which flow across eyes –> drain into lacrimal ducts near caruncle –> drain into inferior nasal meatus
sympathetic and parasympathetic (via CN VII) innervation:
A. dry eye signaled via afferent limb CN V to chief/principal sensory nucleus of trigeminal nerve
B. lacrimation stimulated via efferent limb of CN VII (parasympathetic fibers from superior salivary nucleus travel through greater petrosal nerve –> synapse on pterygopalatine ganglion –> innervate lacrimal gland)
I. Describe how the eye regulates light intensity.
II. Describe normal light and consensual reflexes
III. Differentiate bw light reflex results with II vs III lesion
I. Iris has 2 opposing muscle groups that regulate pupil diameter:
- Sphincter pupillae (parasympathetic via CN III; Edinger-Westphal nucleus) –> lesion leads to mydriasis “blown pupil”
- Dilator pupillae (sympathetic) –> dilates by pulling on sphincter muscle –> lesion leads to miosis
II. Light stimulus leads to constriction of stimulated (“direct”) and contralateral (“consensual”) pupils
Pathway: light –> afferent is II (i.e. optic nerve)–> information goes to prectal nucleus –> bilaterally to Edinger-Westphal nucleus (outer part of CN III nucleus)–> efferent limb is III –> synapses in parasympathetic ciliary ganglion –> postganglionic parasympathetic innervation to sphincter pupillae
III. Complete CN II lesion –> no direct or consensual reflex
Partial II lesion/ relative afferent pupillary defect / Marcus Gunn pupil –> decreased constriction in affected eye appears as dilation, use “swinging flashlight” test
III lesion –> no direct reflex, but consensual reflex still exists
Describe how the eye focuses light.
Describe role of lens in this process
What happens with presbyopia?
Light entering the eye is refracted by the cornea (bending) and the lens (fine tuning) to focus rays on the retina –> image is rotated 180 degrees
- myopia = image focused anterior to retina
- hypermetropia (far-sighted) = image focused posterior to retina
Lens changes thickness depending on object distance
- Distant objects: Ciliary muscle relaxed, Zonules (Suspensory ligaments) pull on lens –> lens is elongated and flattened (overcomes lens capsule force)
- Near objects: Ciliary muscle (parasympathetic innervation via Edinger-Westphal nucleus, part of ciliary body) contracts, Zonules relaxed –> lens capsule takes over and squeezes on the muscle –> lens becomes round
- -> this muscle tension during accommodation is why eyes get tired after reading
Presbyopia - lens hardens with age –> capsule still works but no matter how hard it squeezes, cannot get lens in rounder shape –> far-sighted
I. Describe the retinal layers
II. Describe the interdependence of retinal pigmented epithelium and photoreceptor cells
I. Retina began as 2 layers separated by actual space –> mature retina has 3 neural sub-layers and one epithelial outer layer
Retinal layers in order of looking in through pupil:
1. retinal ganglion cells (RGCs) –> only axons that leave the eye, form optic nerve
synapses on inner plexiform layer
2. inner nuclear layer (interneurons)
synapses on outer plexiform layer
3. outer nuclear layer (photoreceptors i.e. rods for B/w and cones for color)
4. Retinal pigmented epithelium (RPE)
II. Apex of outer segment of all photoreceptor cells is buried in the RPE –> crucial for function and survival
A. Rod outer segments contains stacked discs studded with photopigments that absorb light and convert into neural signals, these discs are pushed towards the apex and phagocytized by RPEs
B. Cones have sinusoidal plasma membrane with embedded photopigments
Eye pathology:
- Alport syndrome
- Wilson’s disease
- Corneal edema
- Alport syndrome - mutation in Type IV collagen genes –> affects basement membrane formation –> kidney failure, hearing loss (hair cell death), misshapen cornea and lens (anterior lenticonus); adult onset
“can’t pee, can’t see, can’t hear a bee” - Wilson’s disease (hepatolenticular degeneration) - recessive mutation that affects copper transporting ATPase –> inadequate copper excretion into bile and blood (decreased ceruloplasmin) –> copper deposits in body tissues –> liver fibrosis, neurological symptoms, Kayser-Fleischer ring in cornea, renal disease
- Corneal edema (hydrops): Cornea gets cloudy when fluid accumulates in connective tissue (normally pumped out by endothelium) –> solution is `cadaveric transplant to replace corneal epithelium don’t have to HLA match bc cornea is avascular
- Describe pathologies of the anterior segment of the eye and their role in glaucoma
- What are the two types of glaucoma?
- What are therapeutic options?
- Ciliary body epithelium produces aqueous humor and fills anterior/posterior chambers of the anterior segment –> flows toward junction between uvea and sclera (between middle and outer layer) –> collects in canal of schlemm and returns to venous system;
Imbalance leads to increased intraocular pressure in anterior chamber affects what is most vulnerable –> compresses the optic nerve (“cupping”) and compromises retinal ganglion cell (RGC) axons as they make a 90 degree turn leaving the eye –> RGCs generating the axons + downstream targets in LGN die –> glaucoma (vision loss)
2A. Open angle - fluid has unimpeded access to canal of schlemm but reabsorption is reduced –> slow onset
B. Closed angle –> lens moves anteriorly, displaces iris –> fluid cannot get resorbed –> rapid onset, acute loss of vision; use oral glycerol or IV mannitol
3A. Mechanical - insert stent in anterior chamber and reinforce connection to canal of schlemm; can only do this if having cataract surgery
B. Pharmacologic: first line is prostaglandin analog i.e. latanoprost - increases outflow
i. Beta blockers i.e. timolol reduce production of aqueous humor
ii. Muscarinic agonists i.e. pilocarpine, bethanechol- contract ciliary muscle to facilitate outflow of aqueous humor
more common in older age bc lens increases in size and can block pupil; other pathology common in old age is cataracts (clouding of lens)
Describe retinal pathologies:
- Macular degeneration
A. dry
B. wet - Stargardt disease
- Retinitis pigmentosa
- Diabetes
A. Nonproliferative
B. Proliferative - Retinoblastoma
- Macula - region of retina that encompasses fovea (Where we have best vision); degeneration of macula –> lose high quality vision in center of visual field, retain peripheral vision
A. Dry degeneration - drusen (debris) accumulation between choroid and RPEs - slow progression and no therapy
B. Wet degeneration - abnormal angiogenesis in choroid–> rapid progression and treatment with angiogenesis blockers (anti-VEGF i.e. bevacizumab) - Stargardt disease - genetic mutation –> buildup of Vitamin A on outer segment of photoreceptors –> passed to retinal pigment epithelial cells (RPEs) –> RPEs and photoreceptors killed –> fovea affected first so you lose central vision
- Retinitis pigmentosa - mutations in gene involved in signal transduction that affects rods first–> night blindness and loss of peripheral vision
- Diabetes - vision loss consequent to vascular changes leading cause of blindness
A. Nonproliferative - damaged vessels between retina and vitreous humor leak blood –> hemorrhages in retina and macular edema
B. Proliferative hypoxia –> new angiogenic factors and new vessels (which tend to burst)–> leaking leads to scar formation –> scar traction on neural retina –> separates photoreceptors from RPE; die if they are not reattached - Retinoblastoma - due to RB gene mutation (E2F no longer inhibited - keep going through cell cycle); tumor in eye glows; 1 eye is spontaneous mutation and 2 is inherited
What is the role of photoreceptors?
Describe actions of photoreceptors in dark vs light
Light comes down layers of retina to photoreceptors –> Photoreceptors convert light image into a neural signal –> electrical impulse then travels back up the layers of the retina to the thalamus –> visual cortex
- Dark: inflow of Na+ through cGMP gated channels > outflow of K+ –> photoreceptor cells depolarized “dark current” –> maximal neurotransmitter release
- Light: light acts as ligand and activates G-protein coupled receptors (opsin + Vit A) –> activate G-protein (tranducin) by removing repressors –> transducin activates phosphodiesterase PDE by removing repressors –> PDE cleaves and inactivates cGMP –> cGMP decreases –> Na+ channels close but still K+ efflux –> photoreceptors hyperpolarize –> neurotransmitter release diminished (graded in that more light lost –> larger decrease in glutamate)
* no action potentials - this cascade removes inhibition of ON bipolar cell and sends excitatory signal down neural pathway*
Describe the cell types of interneurons involved in signal compression in the inner nuclear layer of the retina
- Bipolar cells
- Horizontal cells
- Amacrine cells
- Bipolar cells - vertical transmission between photoreceptors and RGCs with graded response and glutamate neurotransmitter; minimal signal compression (1:50 rods, 1:4 cones)
- Horizontal cells - lateral inhibition of photoreceptor hyperpolarization and bipolar response –> involved in center-surround inhibition; primary point of signal compression – decide what to pass on and what to throw out
- Amacrine cells - also involved with lateral inhibition, double filter to reconsider information the horizontals let through
- Describe the center-surround receptor field concept of RGCs
- Differentiate 2 classes of RGCs
- Describe how the 2 RGC classes lead to 2 visual systems at the lateral geniculate nucleus LGN
- Visual system detects edges; Retinal Ganglion Cells (outermost layer of retina) have center-surround receptive fields
- stimulate just the center i.e. defined “Edge”–> retinal ganglion cell (RGC) is highly active (bc horizontal cells dont intervene)–> bipolar signals –> increased firing from RGCs
- stimulate center + surround –> not an edge so horizontal intervenes and bipolar blocked –> just above baseline firing
- stimulate surround but not center –> depresses firing, increased firing when stimulus is removed - P and M
P = precision; P cells have small receptive fields and small caliber axons; carry info on form and shape
M = motion; M cells have large receptive fields and large caliber axons; carry info on motion detectors (cannot detect the motion themselves but relay to cells in visual cortex that can) - LGN - relay center in thalamus for visual input from retina
Magnocellular - for movement (input from M cells); ancient system but gets to cortex faster bc larger axons –> important for reading
Parvocellular - for discrimination (input from P cells); newer system
Differentiate between histology of macula and optic disc
Both are areas of the retina
Central portion of macula is the fovea –> best vision bc overlying. intervening cells are pushed aside and light hits the cones directly
Macula is the larger region of high visual acuity –> central vision
Optic disc is where the axons from retinal ganglion cells RGCs coalesce and exit and w`here blood vessels enter –> no photoreceptors –> blind spot
- Describe segregation of sensory input from retina at LGN
- Describe effect of glaucoma on LGN
- Where do axons from LGN go?
- LGN - relay center in thalamus for visual pathway; signals leave retina as retinal ganglion cell RGC axons –> travel down optic nerve and tract –> 90% of axons from the eye go to LGN, where they segregate into 6 layers, each innervated by only one eye
Mnemonic: See I? I see, I see! for inner –> outer layers - LGN neurons die with glaucoma; can figure out which LGN is based on which layers atrophy
e. g. if layers 2, 3, and 5 die –> glaucoma on ipsilateral side - Axons from LGN travel through 2 divisions of optic radiations to V1 (i.e. primary visual cortex, striate cortex)
A. information from superior retina –> inferior visual field –> upper banks calcarine fissure
B. information from inferior retina –> superior visual fields –> lower banks calcarine through Meyer’s loop
- Describe the location and structure of the primary visual cortex (V1, striate cortex)
- Perfusion to V1 and clinical implication for cortex lesions
- Describe eye specific and orientation columns
- V1 (primary visual cortex; striate cortex) is in occipital lobe; encompasses calcarine fissure and contains retinotopic map; Cortex layers 4 & 6 prominent
A. Upper calcarine fissure –> information from superior retina –> inferior visual field
B. Lower calcarine fissure (Meyer’s loop) –> information from inferior retina –> superior visual field - Notched hemifield/ macular sparing with Posterior cerebral artery (PCA) infarct or V1 cortex lesion bc fovea can be supplied by middle cerebral artery; differentiates it from optic tract lesion
3.
A. Eye specific layer in LGN –> eye specific columns in V1
B. Orientation columns - simple V1 cells fire only if stimulus lines up at specific orientation column and in center of receptive field
Complex V1 cells fire with specific orientation but at multiple points in receptive field earliest cells that can detect and respond to motion
Describe visual cortex regions V1-V5 and effect of lesions
What is prosopagnosia?
V1 is primary visual cortex, V2-V5 are secondary visual cortex
V1 - raw data / all visual inputs –> cortical blindness (similar to severed optic nerve)
V2/V3 - form and shape –> aperceptive agnosia (acuity intact but cannot integrate visual input e.g. cannot draw a key by looking at the picture, but can draw from memory)
V4 - color –> achromatopsia (color loss)
V5 - motion –> akinetopsia (things disappear once the start moving)
Prosopagnosia - bilateral damage to fusiform gyrus (visual object recognition archives in the temporal lobes) –> inability to recognize faces; bilateral damage due to trauma/stroke
What is the significance of dorsal and ventral visual streams?
Dorsal and ventral are separate but interacting visual streams
Dorsal stream - vision for action “where” (subconscious)–> splits from ventral stream as early as V2 –> tap into stream by approaching object to interact
-lesions here: spatial disorders (e.g. akinetopsia, hemispatial neglect)
Ventral stream - vision for identification “what” (conscious)–> form a percept where all features (V1-V5) are integrated –> compare the percept to your archives
- lesions here: visual object agnosia –> see objects fully formed but cannot recognize them unless interacting with object
- unlike aperceptive agnosia (V2/V3 damage) - where objects are not fully formed*
- ID the site and function of autonomic receptors in the eye
- What are the effects of atropine and other antimuscarinic agents on the eye?
- Autonomic receptors lie on muscles that control the:
- dilator pupillae - alpha adrenergic receptors [sympathetic] –> increase pupil size
- sphincter pupillae - muscarinic cholinergic receptors [parasympathetic]–> decrease pupil size
- ciliary muscle - muscarinic receptors [parasympathetic]–> accommodation to near object, tension on trabeculae to facilitate aqueous humor outflow
- ciliary epithelium - beta adrenergic receptors [sympathetic]–> produces aqueous humor - Antimuscarinic agents block muscarinic receptors e.g. atropine (7-10 days), tropicamide (1/4 day)- induce mydriasis for optho exam, block accommodation
however, antimuscarinic excess –> dry as a bone, blind as a bat, mad as a hatter, hot as hell, red as a beet, and full as a flask
*alpha adrenergic agonist phenylephrine used to facilitate mydriases as well
CN III
I. Which part of the brainstem does it travel through?
II. What are its functions and motor/sensory nuclei?
III. What happens with lesion?
CN III - Oculomotor
I. exits through interpeduncular fossa ventrally at rostral midbrain; between PCA and SCA
II. Motor components:
A. GSE - motor to 4 extraocular muscles (MR, IO, SR, IR) and 1 eyelid muscle (levator palpebrae superioris)
B. GVE - preganglionic parasympathetic fibers to pupillary constrictor and lens ciliary muscle; come from Edinger-Westphal nucleus
III. Lesion - ipsilateral eye droops and moves down and out, “blown” or dilated pupil with loss of constriction and accommodation; diplopia
CN III susceptible to compression from aneurysms or ICP, GVE on outside so pupil changes are first symptoms
What is an uncal herniation?
What are the clinical signs of uncal herniation?
Uncus = on the parahippocampal gyrus of the medial temporal lobe, can herniate through tentorium cerebelli due to epidural hematoma, mass, hydrocephalus
Uncal herniation - type of transtentorial herniation:
- Ipsilateral CN III - Ipsilateral “blown” pupil (PNS fibers affected first), then down and out gaze
- Ipsilateral PCA (Posterior Cerebral artery) - Contralateral homonymous hemianopia with macular sparing
- Contralateral crus cerebri at the Kernohan notch (anterior portion of cerebral peduncles) - ipsilateral hemiparesis
If reticular formation in brainstem is compressed –> coma
Transtentorial herniation–> caudal displacement of brainstem –> rupture of paramedian branches of basilar arteries (midbrain) duret hemorrhages –> Death
CN IV
I. Which part of the brainstem does it travel through?
II. What are its functions and motor/sensory nuclei?
III. What happens with lesion?
CN IV - Trochlear
I. in caudal midbrain, decussates to contralateral side and exits on dorsal side
II. GSE - innervates superior oblique eye muscle –> depression in adducted position, abduction, intorsion (inward rotation)
III. CN IV palsy - due to lesion of right trochlear nerve or, less likely, nucleus –> extorsion (outward rotation) with hypertropia (one eye is on higher visual axis) –> patient tilts head to prevent diplopia
CN VI
I. Which part of the brainstem does it travel through?
II. What are its functions and motor/sensory nuclei?
III. What happens with lesion?
CN VI - Abducens
I. Nucleus is in pons surrounded by facial axons (below facial colliculus), exits in midline ponto-medullary junction ventrally
II. GSE - Innervates lateral rectus eye muscle –> abduction
III. CN VI lesion –> esotropia (eye sitting inwards), eye cannot move past midline
Can occur with increased ICP –> brainstem pushed downwards and VI is stretched
main central connection of II, IV, and VI is the medial longitudinal fasciculus (MLF) i.e. ascending medial vestibulospinal tract (descending for head movements)
Describe the 6 systems to control eye movements to place an image on the fovea
- Active fixation
- Saccadic system
- SPEM
- Vergence
- Vestibulo-ocular reflexes
- Optokinetic
- Active fixation - works best if eyes are still, those with nystagmus have poor vision
- Saccadic system - extremely fast movements to point eye to an object
- SPEM - smooth pursuit eye movement for following moving objects, convergence; requires moving object works with saccades when target moves
- Vergence - for targets at different depths, mediated by MR and LR muscles; vergence center in midbrain and thus convergence preserved with MLF lesion (–> INO)
- Vestibulo-ocular reflexes - hold images still on retina during head movements; elicited by vestibular inputs
- Optokinetic - hold images still on retina during translation/rotation; elicited by visual field movements e.g. watching trees go by when on the train
Describe horizontal gaze center of brainstem
PPRF = Paramedian pontine reticular formation in pons; produces excitatory burst to CN VI nucleus:
- CN VI LMNs –> lateral rectus
- interneurons in medial longitudinal fasciculus MLF –> contralateral CN III –> contralateral medial rectus
- see pictures for 6 possible lesions
Describe vertical gaze center of brainstem
What is Parinaud’s Syndrome
Diffuse areas cerebral cortex –> rostral interstitial nucleus of Cajal (midbrain vertical gaze center):
- CN III and IV
- posterior commissure –> CN III and IV for upwards gaze
Parinaud’s syndrome - -increased pressure on dorsal, rostral midbrain due to tumors, herniations, hydrocephalus:
- paralysis of upward gaze
- hydrocephalus (cerebral aqueduct), headaches (ICP) nystagmus (MLF - which extends to nucleus of cajal)
- large irregular pupils (because Edinger-Westphal fibers also go through posterior commissure)
- Describe pathways for vestibulo-ocular reflexes
- Conditions that affect VOR and symptoms
- Doll’s eye maneuver with coma patient
- Vestibulo-ocular reflexes (VOR) - gaze stabilization
detects brief head movements via vestibular system and generates eye movements in opposite direction
For example, if head turns left:
L vestibular inputs through VIII –> synapse on L medial vestibular nucleus –> stimulates R abducens nucleus and inhibits L –> R lateral rectus and L medial rectus (through MLF)–> Eyes turn right
- Conditions - injury to vestibular system (peripheral or central), cerebellar deficits, anxiety disorders, vestibular cortex lesions in parietal lobe prevent VOR suppression
- Symptoms - inability to read while walking or driving, oscillopsia (feeling that environment is moving) - Doll’s eye = oculocephalic reflex to test integrity of brainstem
- Vestibular input causes eyes to move in opposite direction of head turn if someone is in coma
- impaired doll’s eye reflex –> brainstem dysfunction
Describe cortical control of gaze. Types of lesions and their effects on eye movements: 1. Cortical lesion 2. Superior colliculus lesion 3. Brainstem lesion
Frontal eye field = Brodman Area 8; used for voluntary movements to the contralateral side
Projects through superior colliculus in midbrain to the contralateral PPRF (horizontal gaze center) in the pons
Lesions:
- FEF (cortical) lesion - transient loss of horizontal gaze to contralateral side
- -> eyes point towards the lesion e.g. eyes point L if there is a stroke in L cortex (would cause R paralysis) - Superior colliculus lesion - transient loss in accuracy, frequency of saccades; permanent loss of reflexive saccades
- PPRF (brainstem) lesion - longer lasting deficit in horizontal gaze to the ipsilateral side
- -> eyes point away from lesion e.g. eyes point R if there is a stroke in L pons (would cause R paralysis) *bc corticospinal fibers decussate in medulla
What are the components of the near response triad?
Near response to moving eye to see a near object:
- Convergence (controlled by neurons in midbrain near oculomotor nerve)
- Accommodation (increased curvature of the lens)
- Constriction (increase depth of field)
Describe the types of gliomas including key characteristics and histology: 1. Astrocytoma A. Pilocytic astrocytoma B. Diffuse astrocytoma C. Glioblastoma *role of MGMT
- Astrocytoma - tumor arising from astrocytes (BBB, physical support, removes neurotransmitter, reactive gliosis; GFAP marker positive)
A. Pilocytic astrocytoma - Grade I (potentially curable with surgery), usually suprasellar or cerebellar
- most common CNS tumor in children
- Classic MRI = cyst with mural nodule
- histology: elongated cells with hairlike processes, tumor makes eosinophilic Rosenthal fibers
B. Diffuse astrocytoma - Grades II, III, or IV; infiltrate normal brain
- histology: irregular, elongated, crowded darkly-stained nuclei; fibrillary background
C. Glioblastoma - Grade IV astrocytoma; Glioblastoma multiforme (GBM) is most common malignant CNS tumor in adults
- histology: microvascular endothelial cell proliferation, palisading necrosis
- frequent amplification of receptor tyrosine kinases
- classic gross autopsy “butterfly lesion”
- classic ring-enhancing lesion on MRI
- patients with methylated MGMT promoter do better bc MGMT is not transcribed (MGMT can remove chemo drug from tumor DNA)
Describe the types of gliomas including key characteristics and histology:
- Oligodendroglioma
- Ependymoma
- Oligodendroglioma - tumor of oligodendrocytes
- Grade II or III (III called anaplastic), usually cerebral hemisphers and often hemorrhagic
- genetics - co-deletion of 1p and 19q
- histology: “fried egg” nuclei (artifact of fixation), chickenwire vasculature, heavily calcified - Ependymoma - tumor of ependymal cells (epithelial lining of ventricular system of CNS)
- Grade II or III
- most commonly in 4th ventricle (in kids, aggressive) or spinal cord (in adults, treatable)
- histology: perivascular pseudorosettes (tumor cells surrounding blood vessels)
Describe the following including key characteristics and histology:
- Pituitary adenoma
- Craniopharyngioma
- Pituitary adenoma - low grade neuroendocrine tumor
- most common doesnt produce hormone (null cell)
- most common hormone-producing type os prolactinoma
- symptoms: bitemporal hemianopsia (lose peripheral vision bc tumor squishes optic chiasm), prolactinomia (amenorrhea, galactorrhea) - Craniopharyngioma - tumor of very young kids, from rathke pouch –> supratentorial mass –> bitemporal hemianopsia
- histology: squamous epithelium, wet keratin, cholesterol clefts w/out tumor in them
Tumor predisposition syndromes with CNS manifestations:
- NF1
- NF2
Tumor predisposition syndromes - mutant gene (either inherited or de novo)
- NF1- Neurofibromatosis Type 1
- lose neurofibromin, which normally negatively regulates Ras
- bodies covered with neurofibromas, cafe au lait spots; nerve sheath tumor is usually cause of death - NF2 - Neurofibromatosis Type 2
- lose merlin, which normally negatively regulates pro-proliferation signal with actin cytoskeleton
- hallmark bilateral vestibular schwannoma
- tumors surgically treatable but there are so many / recurrent –> not good prognosis
Tumor predisposition syndromes with CNS manifestations:
- Schwannoma
- Meningioma
- Schwannoma - tumor of Schwann cells
- Grade I
- bi-allelic inactivation of NF2 –> bilateral vestibular schwannoma (tinnitus, deafness)
- histology: spindle-shaped cells with rod-like nuclei, hyper (Antoni A) and hypo (Antoni B) cellular areas, and Verocay bodies (nuclei lined up) - Meningioma - dural-based tumor of meningothelial arachnoid cells
- Grade I-III
- 50% have NF2 mutation; more common in adult females
- Classic MRI sign = dural tail –> does NOT invade the cortex
- histology: whorls and psammomatous calcifications (layering of calcium)
Tumor predisposition syndromes with CNS manifestations:
- Tuberous sclerosis complex (TSC)
- Von Hippel Landau (VHL)
- TSC - multiple benign tumors grow in multiple systems
- SEGA - subependymal giant cell astrocytoma - see tumors jutting out into the ventricles (most commonly lateral)
- inactivation mutation in TSC1 or TSC2 - normally negatively regulate mTOR - Von Hippel Landau (VHL)
- associated with hemangioblastoma (Grade I) - blood vessel tumors in cerebellum
- histology: foamy stromal cells and dense capillary network
- also get retinal angiomas, renal cell carcinoma
- inactivation mutation in VHL - normally negatively regulates HIF –> too much angiogenesis
Tumor predisposition syndromes with CNS manifestations:
- Medulloblastoma
- Metastasis
- Medulloblastoma - malignant tumor of primitive neurons (from neuroectoderm) that affects young children
- Grade IV - poor prognosis and spreads via CSF
- only arises in cerebellum
- synpatophysin positive (normal neurons don’t normally make this)
- form true rosettes (wrap around neuritic processes, not bv like the pseudorosettes from ependymoma) - Metastasis - most common reason for neoplastic lesion / tumor in CNS
- most common primary cancers - lung
- most likely to go to brain - melanoma, breast, renal
- most likely to go to grey-white junctions
- well circumscribed, usually several of them
Describe the vascular supply of the medulla
Contrast to vascular supply of pons
- Medulla
- Anterior spinal artery –> midline (pyramids, medial lemniscus, hypoglossal nucleus)
- Vertebral artery –> medial olivary nucleus
- PICA –> lateral (anterolateral system, nucleus solitarius, ambiguus, vestibular nuclei) - Pons
- Basilar artery –> median parts of pons –> corticospinal tract, pontine nuclei, abducens nuclei, facial nerve fascicles, MLF, PPRF, medial lemniscus
- AICA –> lateral pons –> motor V, spinal V, auditory nerve, vestibular nuclei, middle cerebellar peduncle, VII nucleus/nerve,
Describe lateral medullary syndrome including lesion and associated symptoms
Lateral medullary syndrome = Wallenberg’s, due to infarct of PICA
Symptom (lesion):
1. contralateral loss of pain and temp on body (spinothalamic anterolateral tract)
2. ipsilateral loss of pain and temperature on face (spinal nucleus of V)
3. nystagmus, vertigo, ataxia (vestibular nuclei)
4. ipsilateral ataxia, nystagmus (inferior cerebellar peduncle)
5. ipsilateral Horner’s (descending autonomics)
- ipsilateral decreased taste (bc of n. solitarius)
- hoarseness and dysphagia (trouble swallowing), contralateral uvula deviation (n. ambiguus)
Describe medial medullary syndrome including lesion and associated symptoms
Medial medullary syndrome = Dejerine, due to infarct of ASA (anterior spinal)
Symptom (lesion):
- contralateral loss of position and vibration sense (bc medial lemniscus is composed of internal arcuate fibers post decussation of DCMLS)
- contralateral hemiparesis/hemiplegia (bc fibers of lateral CST decussate after pyramids)
- ipsilateral tongue weakness/same side tongue deviation (LMN lesion of hypoglossal nerve)
* pain and temperature spared (bc STT is on lateral side)
Describe lateral pontine syndrome including lesion and associated symptoms
Lateral pontine syndrome, due to AICA infarct
Symptom (lesion): vary depending on level
- contralateral loss of p/t on body (STT)
- ipsilateral loss of p/t on face (spinal tract of CN V)
- vertigo, nystagmus, ataxia (vestibular nuclei/nerve)
- ipsilateral ataxia, nystagmus (middle cerebellar peduncle)
- ipsilateral Horner’s (descending autonomics)
- ipsilateral deafness, tinnitus (auditory nerve)
- ipsilateral facial weakness (facial nucleus/nerve)
- jaw weakness, dysarthria (motor nucleus V)
Describe medial pontine syndrome including lesion and associated symptoms
Medial pontine syndrome, due to infarct of paramedian branches of basilar artery
Symptom (lesion)
- contralateral loss of touch, vibration, position (DCMLS)
- contralateral hemiparesis of face AND body (but not forehead, since its UMN); dysarthria/ trouble speaking bc of UMN effects on IX, X (CST, corticobulbar)
- contralateral ataxia (pontine nuclei and pontocerebellar fibers)
- ipsilateral facial weakness (facial nerve fascicles)
- ipsilateral horizontal gaze palsy, diplopia (PPRF, abducens nucleus/nerve)
- Internuclear Ophthalmoplegia INO (MLF) - conjugate horizontal gaze palsy with normal convergence
Describe types of midbrain syndrome and including lesion and associated symptoms:
- Midbrain base (Weber’s)
- Red nucleus (Claude’s)
- Midbrain syndrome (Benedikt)
- Midbrain base (Weber’s) - infarct of paramedian branches at top of basilar artery
Symptom (lesion):
- contralateral hemiparesis (UMN syndrome) of body and face (CST, corticobulbar)
- ipsilateral CN III palsy (oculomotor nerve and fascicles) - mydriasis, eyes down and out - Red nucleus (Claude’s) - infarct of proximal PCA
- contralateral tremor and ataxia (Red nucleus)
- contralateral loss of position vibration (DCMLS) - Weber + Claude = Benedikt syndrome
- all symptoms combined
Where is the cerebellum located?
What are the main subdivisions of the cerebellum and their functions and deep cerebellar nuclei ?
What is the somatotopy
Cerebellum located in posterior fossa, covered by tentorium cerebelli , and is the roof of the fourth ventricle (the floor being pons and medulla)
Functions - motor planning (feedforward), execution (feedback), and learning (adjustments)
Subdivisions:
- Cerebrocerebellum (dorsal lateral) –> lateral hemisphere –> planning, cognition execution of skilled and complex spatio-temporal sequences e.g. speech
- dentate nucleus
- superior cerebellar peduncle connects to midbrain - Spinocerebellum (dorsal medial) –> midline vermis + intermediate hemisphere –> gross limb movement e.g. touching nose; vermis in particular is eye movements, proximal muscles
- intermediate hemisphere –> emboliform + globusus nuclei (= interposed nuclei)
- vermis –> fastigial nucleus - Vestibulocerebellum (ventral) –> flocculonodular lobe –> posture, equilibrium affected by alcohol
- Vestibular nuclei
- fastigial nucleus
Deep cerebellar nuclei: “Don’t Eat Greasy Food” (lateral to medial)
Somatotopy = midline/vermis represents midline structures (eyes) whereas intermediate hemisphere is the limbs
Role of red nucleus and tectum in conveying cerebellar output pathways
Both contain pathways from the midbrain
- Red nuclei are within midbrain tegmentum (ventral part of midbrain)
A. caudal magnocellular red nucleus is origin of rubrospinal tract –> voluntary contralateral upper arm flexor muscles
-lateral motor system that runs with the lateral CST
-ventral tegmental decussation in midbrain
B. rostral parvocellular red nucleus is origin of central tegmental tract to inferior olivary nucleus, which feeds back to cerebellum
-Guillan Mollaret triangle - Superior and inferior colliculi are within the tectum (“roof,” dorsal part of midbrain) –> tectospinal tract (coordinates head and eye movements)
- Fastigial nucleus in vermis –> superior colliculus –> immediately decussates –> tectospinal tract
*inferior colliculus has to do with hearing
Describe and identify the cerebellar peduncles and the types of inputs and outputs for each of its functions:
Superior Cerebellar Peduncle
1. Output - Motor learning, cognition, planning
2. Output - Motor coordination
Information leaves cerebellum via peduncles, each associated with one part of the brainstem –> Superior cerebellar peduncle SCP = midbrain
SCP decussates at roof of 4th ventricle (level of inferior colliculus)
- Motor learning, cognition, planning
Dentate nucleus (lateral hemisphere) –> crossed outputs via superior cerebellar peduncle to contralateral:
A. VL ventral lateral nucleus (thalamus) –> motor cortex
B. Parvocellular red nucleus (midbrain) –> central tegmental tract –> inferior olivary nucleus (medulla) –> inferior cerebellar peduncle –> crosses back to cerebellum/dentate nucleus where info is stored this is called Guillan-Mollaret triangle - Motor coordination
Interposed nuclei (intermediate hemisphere) –> crossed outputs via superior cerebellar peduncle to contralateral:
A. VL nucleus (thalamus) –> motor cortex –> pyramidal decussation –> lateral corticospinal tract
B. Magnocellular red nucleus (midbrain) –> ventral tegmental decussation –> rubrospinal tract, runs next to lateral CST and corrects movement
Describe and identify the cerebellar peduncles and the types of inputs and outputs for each of its functions:
Middle Cerebellar Peduncle
1. Inputs from cortex
Middle cerebellar peduncle MCP = pons (on dorsal aspect); afferents ONLY
- largest input to cerebellum from cerebral cortex (frontal and parietal) –> corticopontine axons travel through cerebral peduncles in midbrain –> pontine nuclei –> cross to contralateral side as pontocerebellar fibers –> coalesce to form middle cerebellar peduncle –> cerebellar cortex/deep nuclei
deep nuclei - e.g. dentate, interposed - send info back up to cortex via SCP/VL –> one big loop!
Describe and identify the cerebellar peduncles and the types of inputs and outputs for each of its functions:
Inferior Cerebellar Peduncle
1. Dorsal spinocerebellar tract
2. Cuneocerebellar tract
Inferior cerebellar peduncle ICP = medulla
*No decussation - these pathways are ipsilateral
- DRG have inputs from leg/lower body proprioceptors –> gracile fasciculus –> synapse on nucleus dorsalis of Clark (C8-L3)–> 2nd order neurons ascend via dorsal spinocerebellar tract –> inferior cerebellar peduncle –> cerebellar cortex/deep nuclei
- DRG have inputs from arm/upper body proprioceptors –> cuneate fasciculus –> synapse on external cuneate nucleus –> 2nd order neurons ascend via cuneocerebellar tract –> inferior cerebellar peduncle –> cerebellar cortex/deep nuclei
- Afferents - climbing fibers from olivocerebellar tract from contralateral inferior olivary complex
- Efferents from flocculonodular lobe and fastigial nucleus - to vestibular nuclei
I. Describe the general cellular characteristics of the molecular, Purkinje cell and granular layers of the cerebellar cortex
II. Differentiate between climbing and mossy fibers in stimulating Purkinje cells
III. Describe how overall cerebellar output is excitatory if Purkinje cells are GABA inhibitory
I. Cortex of cerebellum is folded into folia and can be divided into 3 layers:
- Outer - molecular layer –> contains stellate and basket cells
- Middle - Purkinje cell layer –> contains purkinje cells that integrate sensory inputs with motor outputs only output of cerebellar cortex
- Inner - granular layer –> contains granule and golgi cells
IIA. Climbing fibers arise from contralateral inferior olivary nucleus in medulla –> innervates one Purkinje cell but makes multiple connections on it
B. Mossy fibers are pontocerebellar fibers that arise from contralateral pontine nucleus –> synapse with many granule cells (T-shaped axons) –> each granule cell innervates multiple Purkinje cells via glutamate
III. Deep cerebellar nuclei are inhibited by the Purkinje cell output BUT stimulated directly by the mossy and climbing fiber axons –> net output is excitatory
