Understand 2nd year medicine

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Neuroanatomy

Summary

Nucleus of thalamus

VPM of thalamus - everything to do with head -  nucleus solitarius for taste, trigeminothalamic for face sensation
VPL of thalamus - body (posterior columnar tract -> medial lemniscus)

Trigeminal
supplies contralateral face contralateral and senses touched mandibles. (spinal nucleus → TTT -> VPM of thalamus)


Parasympathetic - salivary stuff

2 salivatory nucleus - facial and glossopharyngeal nerve

  • Facial nerve: Superior salivatory-lacrimal (laCRI - la [taste - glands] and CRI [lacrimal]) nucleus to submandibular ganglion (to sublingual and submandibular glands) and pterygopalatine ganglion to lacrimal gland
  • Glossopharyngeal nerve: Inferior salivatory nucleus to otic ganglion to parotid gland


Parasympathetic ganglion: CPSO community police support officer.. + Vagus
3: EW nucleus: ciliary ganglion to ciliary body and constrictor pupillae
7: superior salivatory-lacrimatory nucleus: submandibular ganglion to sublingual and submandibular, pterygopalatine to lacrimal
9: Inferior salivatory nucleus: glossopharyngeal to otic ganglion to parotid
10: Dorsal nucleus of vagus: vagus to intramural ganglion from heart to rectum
----------

 

Floor of Cranial Cavity
Meninges innervation
Anterior cranial fossa - v1
Middle cranial fossa - v2
Posterior cranial fossa:  c2-3

Crista gali - attachment for falx cerebri
Sphenoid ridge
Petrous ridge

Anterior clinoid process
, sella turcica, dorum sellae and Posterior clinoid process

sphenoid Lesser wing: optic canal
sphenoid Greater wing: superior orbital fissure, rotundum, ovale, spinosum
no foramen in squamous of temporal bone
between sphenoid greater wing and petrous bone: foramen lacerum
petrous bone: internal acoustic meatus, jugular foramen
occipital bone: hypoglossal canal

Inferior view of skull




all the foramens:
cribiform plate, optic canal, superior orbital fissure, rosie often sticks lollipops in jeremy’s hole


Anterior cranial fossa

1: cribiform plate
2: optic canal

Middle cranial fossa:  
Superior orbital fissure - 3, 4, v1, 6
Rotundum - v2
Ovale - v3

ICA internal carotid artery: (from carotid canal) foramen lacerum

Posterior cranial fossa: 2
- Internal acoustic meatus: 7, 8 (quite obvious....)
- Jugular foramen: 9, 10, 11
- Hypoglossal canal: 12

Sinus: Air spaces in skull

  • frontal sinus over eyes
  • maxillary sinus over cheek bone
  • ethmoid behind nose bridge
  • sphenoid behind ethnoid

Each sinus opens into the nose permitting free flow of air

Turbinate = concha
Infection -> opening of sinus blocked - air and secretions trapped in sinus -> pressure on sinus walls -> Pain

Circle of Willis comprises

Anterior cerebral artery (left and right)
Anterior communicating artery
Internal carotid artery (left and right) - NOT middle cerebral artery!
Posterior cerebral artery (left and right)
Posterior communicating artery (left and right)

Posterior communication artery berry aneurysm can compress adjacent occulomotor nerve.

Cranial Nerve and function (s - sensory, b - both, m - motor)
o -  olfactory - some
o - optic (2eyes, 1nose) - say
o - occulomotor - marry
topless- trochlear - money
tiffany - trigerminal (v1 - opthalamic, v2 - maxillary, v3 - mandibular) - but
and - abducens - my
fat- facial - brother
valerie- vestibulocochlear - says
got - glossopharyngeal - big
vaginits- vagus - breasts
and- accessory - matter
hepatitis - hypoglossal - more



Cranial nerve nuclei



sensory (olfactory, optic, vestibulocochlear), or mixed (trigerminal - mastication, facial, glossopharyngeal - posterior 1/3 tongue sensory, parotid gland motor, vagus), purely motor,(occulo, trochlear - SO only, abducens - LR only, accessory - SCM and trapezius (elevate shoulder), hypoglossal - tongue) nerves.

Sensory nuclei: (Side) Lateral brainstem (yellow)
Motor nuclei: Medial brainstem (blue)

Cavernous sinus

  • Lateral: 3, 4, 5 (v1 - opthalmic, v2 - maxillary)
  • Medial: ICA and 6

The cavernous venous sinus lies inferior to frontal lobe, medial to the temporal lobes, superior to sphenois sinus and is separated by pituitary gland that sits in sella turcica (seat - depression in sphenoid bone).



If the pituitary tumor grows sideways (fat tumor) it will compress the cavernous sinus (cranial nerve, carotid artery)

             O                                   O - Occulomotor 3
             T A C         Pit. Gland            C A T -
Carotid Abducens 6 Trochlear 4
             O                                O - Opthalmic (V1)5
             M                         M - Maxillary (V2)5

   Sphenoid bone


V3 (mandibular of trigerminal) is not involved with cavernous sinus as it goes a vertical route down through foramen ovale.-> lingual nerve and mental nerve


Optic chiasm

The optic chiasm crosses in front of the pituitary stalk.
More often, it grows upward start to push on optic chiasm -> tunnel vision. (bitemporal hemianopia)


Eye muscles
- Intraocular: Ciliary body control lens thickness, dilator/constrictor pupillae
- Extraocular: lr6so4 (others = 3 i.e. superior rectus, inf. rectus, medial rectus, inferior oblique)
superior orbital fissure, inferior orbital fissure, and optic canal

Temporal


Superior Orbital Fissure: Live Frankly To See Absolutely No Insult”
-lacrimal (1)
-frontal of V1 (2)
-trochlear (3)
-superior div. of occulomotor  (4)
-abducens (6)
-nasociliary branch of  v1(5)
- inferior div. of occulomotor  (7)

-superior ophthalmic vein (8)
-sympathetic roots of ciliary ganglion (arrow)

Superior orbital fissure trauma can cause 3rd nerve palsy!


Inferior Orbital Fissure
- v2  (9)
-pterygopalantine ganglion nerve (10)
-pterygoid nerves (11)
-inferior ophthalmic vein (12)

Optic Canal
-Optic nerve (13)
-Ophthalmic Artery (14)
-Sympathetic fibers from carotid plexus (14a)

Ethmoid: Cribiform plate for olfactory bulb to sit on
Sphenoid: Sphenoid sinus


Eye structure

Lacrimal gland (lateral) makes the aqueous layer of tear film -> Punctua -> Canaliculi -> Common canaliculus -> Lacrimal sac -> Nasolacrimal duct to nose!


Meibomian glands: Sebaceous glands that makes oil to prevent evaporation of eye's tear film
found in the tarsal plate

Superior tarsus: The larger one... where LPS and superior tarsal muscle attaches. Inferior tarsus too!

Dense CT = tarsus
  • medial & lateral angles (7,8)
  • cornea
  • sclera (3)
  • iris (2)
  • pupil (1)
  • lacrimal caruncle (4)
  • lacrimal punctum (5)
  • openings of tarsal glands (6)


Tarsus: Dense CT found in each eyelid (Superior: Superior tarsal muscle and LPS attaches). Meibomian glands in tarsi.

-----------
Rule of 4’s Cranial nerves
12, 11, 10, 9 in medulla
8, 7, 6 (@ medullarypontine junction), 5 in pons

Midbrain
4 just below inferior colliculi (dorsal)
3 in superior colliculi (midbrain-pontine junction)

2 Optic chiasm
1 on cribiform plate of ethmoid

Occulomotor nerve (for pathway see special senses): Ipsilateral for all muscles except SR

Occulomotor nucleus:


Occulomotor nucleus (next to PAG, in front of cerebral aqueduct at level of superior colliculus and exits ventrally in interpeduncular fossa at) -> Cavernous sinus -> Divides at superior orbital fissure
  • Four lateral paired subnuclei that innervate the superior, inferior, and medial rectus, as well as the inferior oblique muscles.
    • Axons from one superior rectus (SR) nucleus cross and pass through the opposite SR subnucleus; thus, a lesion of one SR subnucleus results in bilateral superior rectus palsy.
  • Superior rectus is innervated by a  midline structure (UNPAIRED!!!) called central caudal nucleus. This supplies the LPS on both sides.
    • Lesion -> Bilateral ptosis
  • Edinger-Westphal (parasympathetic)nucleus, which contains preganglionic, parasympathetic neurons whose axons project to the ciliary ganglion and ultimately control pupillary constriction and accommodation

Course of occulomotor
superior and inferior divisions at superior orbital fissure
Course of occulomotor nerve and surrounding nerves.
  • Superior division: LPS (Skeletal muscle) and SR (when one looks upward, the eyelid moves with it!)
  • Inferior division
    • Long ciliary nerve - branch of nasociliary nerve (opthalmic, trigeminal) - NOT FORMED FROM OCCULOMOTOR!!!
  • Post-ganglionic Sympathetic
    • From hypothalamus down to T1 -> Paravertebral ganglion - superior cervical ganglion -> Carotid plexus -> Long ciliary nerve to dilator pupillae)
      • Damage causes Horner’s syndrome...!
  • Short ciliary nerve - branch of ciliary ganglion (occulomotor)
  • Post-synaptic Parasympathetic (ciliary ganglion is where pre and post come together!) : EW nucleus -> Occulomotor nerve -> ciliary ganglion -> short ciliary nerve to supply ciliary body
  • General sensation (from opthalamic) without synapsing in ciliary ganglion



Reflexes
Corneal reflex
Touching the cornea causes BILATERAL blinking.
Afferent: Opthalamic nerve of trigerminal (5) -> Sensory ganglion of trigerminal nerve (Trigerminal is a mixed nerve so mention sensory ganglion!) -> Motor nucleus of facial nerve (again because facial is a mixed nerve!) on both sides (contralateral via medial longitudinal fasciulus)
Efferent: Facial nerve (7) supplying orbicular oculi

Blinking reflex:  Facial nerve
7 like a dumbell pull eyelids down
3 keeps the eys open (LPS)

Light reflex (Direct and consensual light reflex)
Afferent: Optic nerve -> Optic chiasm-> Optic tract -> branches off to synapse with pretectal nucleus of midbrain
Efferent: Pretectal nucleus -> Accessory occulomotor nucleus (aka edinger westphal nucleus) of both sides -> Ciliary ganglion of both sides -> Sphincter pupillae of both sides -> Miosis of both pupils!
  • Pupillary test
  1. Fix on distant object to pupil can dilate (mydriasis)
  2. Lights off
  3. Equal pupil size?
  4. Reaction to light in each pupil
  • RAPD (relative afferent pupillary defect)
    • Swinging light test
    • Lesion on right pupil (Causes: Retinal detachment, central retinal artery/vein ischemia, optic nerve lesion, optic neuritis)
      • Swing to left pupil, both pupil constricts
      • Swing to right pupil - both pupil relatively dilates because right pupil is perceiving less light transmission
        • COMPLETE RAPD defect: No pupil reaction to light
      • Swing to left pupil, both pupil constricts


Accommodation/Convergence
Afferent: Both Optic nerve -> Optic chiasm-> Optic tract -> LGN -> Optic radiation (includes Meyer’s loop) -> Visual cortex
Efferent: Visual cortex -> Frontal eye field (in premotor cortex) ->  both eyes’
  • Accessory occulomotor nucleus: Preganglionic nerve (PS = visceromotor) -> Ciliary ganglion -> Postganglionic Short ciliary nerve -> Sphincter pupillae (Miosis) and ciliary muscle (contract, therefore, suspensory ligaments become relaxed, thus, ROUNDED lens)
  • Occulomotor nucleus: Occulomotor nerve (inferior branch) -> Medial rectus -> Convergence


Trochlear nerve: Contralateral

The only nerve to emerge dorsally

The trochlear nucleus lies in front of the cerebral aqueduct. It winds around the contralateral inferior colliculi and cerebral peduncle to innverate SO4 (intort)




Abducens nerve: Ipsilateral

4th ventricle: "roof" dorsally and a "floor" ventrally

Nucleus in caudal pons on floor of 4th ventricle -> Exits at medullary-pontine junction rostral to medullary pyramids
  • Supply LR (ipsilateral)


In relation to cavernous sinus

     o  t       o     m
CN 3, 4, 5 (V1, V2) goes lateral while 6 lies more medially to cavernous sinus and enters superior orbital fissure (3, 4, 5, 6)


Abudcens nerve is very long so easily squeezed if increased ICP
Lesion: Can't abduct


Extraocular muscles

Ipsilateral: Abudcens, occuomotor (others)...
Contralateral: SR (from contralateral occulomotor subnucleus, SO (trochlear)


Annulus of Zinn is a fibrous ring that encircles optic nerve, located orbital apex (where all the nerves, vessels supply the orbit).


When the eye is at 23 (22.5) degrees, superior rectus is aligned with eye axis
  • SR: Elevate, IR: Depress
  • SO: Intort (SO muscle tendon through trochlea - a tendon in the superior nasal aspect of frontal bone), IO: Extort

When the eye is adducted
  • SO: Depress, IO: Elevate
  • SR: Intort, IR: Extort

CN3 lesion: Eye is down (unopposed SO) and out (unopposed LR)
  • Also, because CN3 superior division innervates (LPS), therefore, ptosis
  • CN3 inferior branch - extraocular muscles
    • Loss of convergence
  • Cn3 (short ciliary nerve) is PS.... Cn5 (v1 - hypothalamus -> superior cervical ganglion -> long ciliary nerve -> Superior tarsal muscle, ciliary body and dillator pupiillae) os sympathetic
    • Thus CN3 lesion causes unopposed sympathetics
      • Mydriasis! (dillator pupiillae) and loss of pupillary light reflex
      • Loss of lens accommodation (ciliary body)

CN4 lesion: Ask patient to look medially and down
  • Elevated extorted eye. Vertical dipolopia especially when looking down and to nose Compensate by tilting head slightly down and away from affected side.




Trigeminal nerve: Deals specifically with face, contralateral

Largest cranial nerve
Sensory and motor components


Standing room only - foramen for branches
Sphenoid (sight...)  bone!


v1 - Opthalamic (Superior orbital fissure) - sensory only

  • Sensory for forehead to upper eyelid, medial nose
    • Supraorbital nerve (upper eyelid) in supraorbital foramen

v2 - Maxillary (Foramen rotundum -> Inferior orbital fissure)- sensory only

  • Sensory  for lower eyelid to upper lip
    • Infraoribtal nerve (lower eyelid) in infraorbital foramen
v3 - Mandibular (Foramen ovale) - sensory AND motor (largest branch in trigeminal!)
  • Sensory:
    • Lingual nerve: General sensation for anterior ⅔ of tongue
  • Motor: Muscles of mastication (T - MTPP) - tensor tympani (tea makes you Empty peepee)
    • MTPP: masseter, temporal, lateral and medial pterygoids
      • Lateral Lowers- lateral pterygoid lowers (opens) the jaw
      • Medial pterygoid closes the jaw
    • T: tensor tympani: connects to malleus

 

Masseter: zygomatic arch to mandible (angle/ramus) (close jaw)
temporalis: temporal fossa to coronoid process of mandible (close jaw)






Lateral pons: Where trigeminal nerve enter AND leave!!!

Trigeminal nerve nuclei (3 sensory mss, 1 motor nuclei)

  • Sensory: Mesencephalic nucleus: proprioception of jaw (map - location... proprio!, mandible, maxilla)
    • most top, located on lateral border of cerebral aqueduct
  • Sensory: Main sensory nucleus: 2 point discrimination and others
    • in mid-pons, medial to middle cerebellar peduncle and ventral to superior cerebellar peduncle
    • leave at lateral aspect of pons
  • Sensory: Spinal trigeminal nucleus: Pain/temperature from face (like spinothalamic)
  • Motor: Motor nucleus: Mastication muscles (MTPP) (remember m for medial, s for side for cranial nerve nuclei)
    • Lies medially to the main sensory nucleus
    • leave at lateral aspect of pons next to afferent fiber
    • travels through foramen ovale along with v3 and enter infratemporal fossa


For sensory:

  1. Cell body of trigeminal nerve in trigeminal ganglion which lies in petrous bone in middle cranial fossa. -> enter lateral pons
  2. Descend in brainstem as spinal tract V -> Terminate at spinal nucleus V
  3. Ascend contralaterally as trigeminothalamic tract and terminate at VPM of thalamus
  4. VPM thalamus  to somatosensory cortex

Petrous bone containing in trigeminal is high... above spinal tract lol!

Trigeminal is contralateral and senses touch mandible. (spinal nucleus → TTT -> VPM of thalamus)

 



Lesions along spinal tract V causes ipsilateral deficcit in pain and temperature as it never goes to the spinal nucleus where it decussates.

Lesion in TTT causes contralateral defciit.
Other inputs to Spinal nucleus of V (just different ganglion) -> TTT -> VPM -> Somatosensory cortex

  • CN7 - geniculate ganlgion - pain and temp from ear, taste of 2/3 anterior tongue
  • CN9 - superior ganglion IX (located near jugular foramen) - pain and temp from  posterior 1/3 tongue
  • CN10 - superior ganglion X (located near jugular foramen) - pain and temp from pharynx


 

 

 

 

Special Senses

Mnemonics

distinguish between ganglion and nucleus

mlf - info about direction that eyes should move (tectospinal, 3, 4, 6, vestibulooccular)

Taste: Chorda tympani: GNTP - guts never taste poo - geniculate ganglion (/inferior ganglion X/IX)-> nucleus tractus solitarius -> thalamus (VPM) -> Postcentral gyrus

Visual body reflex: seeing turns necks sideways (contralateral) - Superior colliculus (Seeing turns necks sideways - superior colliculus → tectospinal tract → neck muscles splenius capitus) contralateral

Hearing: SLIM: Superior olivary nucleus → lateral lemniscus → inferior colliculus (midbrain) synapse.. → medial genicular body  of thalamus

Olfactory (olfactory cell) makes (mitral) lasting (lateral olfactory area) memories (hippocampus), recognition (frontal) and emotion (amygdala)


superior ganglion ix/x  - general Sensory (trigeminal)
inferior - taste (chorda tympani of facial)



Sense transduction

REMEMBER: Special senses = BIPOLAR receptor!!!!

Hearing: Glutamate

Stapes move: Oval window -> Vibration of endolymph in scale media -> Endolymph shakes basilar membrane (from apex to basilar membrane)-> shearing force between stereocilia and tectorial membrane (remember stereocilia touches tectorial membrane)  -> Sterocilia of IHC moves in the direction of stria vascularis (i.e. direction of kinocilia) -> Sheared hair cell -> Tip open K+ channels on sterocilia -> VDCC open -> Glutamate release from inner hair cell to cochlear nerve -> Increased AP firing

Photoreceptor: Glutamate

Light (HYPERPOLARIZATION due to closed cGMP-gated sodium channel)
  1. Photons get absorbed transforming cis-retinal to trans-retinal. This isomerism makes opsin detach and form enzyme Metarhodopsin II.
  2. Metarhodopsin II activates transducin (G protein that was bound to inactive GDP to active GTP). Tranducin’s G-alpha subunit stimulates cGMP phosphodiesterase.
  3. cGMP PDE converts cGMP to GMP. Thus, with light, there is less cGMP.
  4. Less cGMP to the cGMP-gated channels in the outer membrane of photoreceptors close. No sodium influx.
  5. Voltage-gated calcium channels close
  6. Less glutamate released so hyperpolarization.

Olfactory: glutamate and gaba

Golf (Gprotein) activates AC -> cAMP -> Binds to and activates cation channels -> Depolarize
  • mitral cell: glutamate
  • granule cell: GABA

taste:


Generator/receptor potential is not action potential!

Generator potential found in: olfactory, free nerve endings in skin, merkel's disks in skin, taste buds

Genergraded potential, is the transmembrane potential difference of a sensory receptor caused by inward current flow. They vary in size as opposed to action potential (the peak; all or none). They arise from the summation of the individual actions of ligand-gated ion channel proteins, and decrease over time and space.





Olfactory nerve (e.... ethmoid e similar to o!!!)
  • Shortest cranial nerve
  • The only nerve that doesn’t first synapse in thalamus



Olfactory epithelium
  • Olfactory cell
    • Unmyelinated axon at the basal surface to cribiform plate
    • Bipolar
  • Contain Immotile cilia that has molecule receptors
    • Olfactory cilia - immersed in mucous layer (made by bowman’s glands) that traps molecules and bring them to olfactory receptors
    • Odorant molecule binds to GPCR  on olfactory cell-> G(olf) activation prompts AC activation -> cAMP -> cAMP binds cAMP dependent ion channel -> Na and Ca2+ Influx
    • Ensuing rise in Ca2+ opens Ca2+ gated Cl- channel → Chloride efflux -> Depol
    • Decreased receptor potential
      • cAMP broken down by PDE → no cAMP dependent cation channels open
      • Calcium complexes with calmodulin (ca2+-cam) and binds to cAMP dependent cation channel to reduce its affinity for cAMP
    • Calcium extruded via na+/ca2+ exchanger to return ca2+ back to resting levels

Receptor potential in dendrite..... → Depolarization from axon hillock via voltage gated sodium channels → Mitral cell in olfactory bulb




  • Supporting (sustentacular cell)
  • Basal cell: Transforms to olfactory cell to replace
    • Aging: less replacement - decreased smell sensitivity


Second order neurons... in eye (amacrine, horizontal, bipolar), nose (mitral, tufted, granule, periglomerular)

Olfactory bulb rests on cribiform plate on ethmoid bone, pituitary sits on sphenoid  bone
Olfactory bulb contains 4 types of cells
  • Glomerulus is where synapses form between olfactory nerve terminals and dendrites of mitral cell (main cell)
  • Tufted cells
  • Periglomerular cell: Inhibition of neighbouring glomeruli
  • Granule cell: Between mitral cell - supress neighbouring mitral cell via GABA

Bipolar neuron synapses with either mitral cells or tufted cells in the GLOMERULUS of olfactory bulb.


Pathway (ipsilateral)

Olfactory (olfactory cell) makes (mitral) lasting (lateral olfactory area) memories (hippocampus), recognition (frontal) and emotion (amygdala)

Mitral cells project to lateral olfactory area and also to the anterior olfactory nucleus. The anterior olfactory nucleus crosses in the anterior commissure and synapses in CONTRALATERAL anterior olfactory nucleus

Lateral olfactory stria: Terminate in piriform cortex of anterior temporal cortex (uncus) or frontal cortex (recognition) and limbic system (amygdala etc) - motivation memory (hippocampus - association with memory with food) , emotion (amygdala)

Medial olfactory stria: Axons from anterior olfactory nucleus to
  • Limbic system
  • Cross midline in anterior commissure to inhibit mitral cells contralaterally by stimulating granule cells (GABA) -> directional cue for sourcing smell


Meanwhile, tufted cells project to lateral, intermediate and medial olfactory areas and anterior olfactory nucleus.



Olfactory cell, mitral cell, tufted, lateral, medial olfactory area






Hearing and balance

External ear
External auditory canal (contain ceruminous glands - secrete cerumen - antimicrobial), Pinna, Tympanic membrane

Middle ear: FUNCTIONS to CONCENTRATE SOUND (remember size of tympanic and oval window!)
Hammer (Malleus) -> Anvil (incus) -> Stapes (Stirrup) to Oval window
Filled with air
  • Otitis media: Inflammed middle ear
    • Heals within weeks
    • Cause:  Streptococcus pneumoniae and Pseudomonas aeruginosa, Rhinovirus
    • Acute: Viral, usually accompanied with upper respiratory infection
      • Secretion and inflammation obstructs eustachian tube. Middle ear mucosa no longer able to absorb air in middle ear. Negative pressure generated pulling interstitial fluid into the tube and creates serous effusion (microbial growth!)
    • Serous
    • Chronic suppurative: perforated tympanic membrane
Eustachian tube: Connects to nasopharynx: Allow pressure to equalize

Size of tympanic membrane is 22x bigger than oval window (Pressure = Force / Area -> Sound wave amplification!!!)

Tensor tympani muscle (V3 - 3 words..) attaches to malleus
Stapedius muscle (CN7) attaches to stapes

If loud, the muscles contract, so ossicles vibrate less -> Less conduction  and conduct  less  low frequency (low frequency is the background noise) - protect cochlea

Inner ear
Lie in the petrous portion (hardest skull bone) of temporal bone
Bony labyrinth (continuous with petrous bone - temporal) protects membraneous labyrinth
Membraneous labyrinth
  • Cochlea: Contain perilymph and endolymph (2.5 turns)
  • Vestibular system: Contain endolymph only
    • 3 semicircular canals all at 90 degrees to one another (each canal contains one ampullus - 3 in total): Angular acceleration  (change speed AND direction)
      • superior/anterior: Closest to trochlea - yes
      • lateral/horizontal - no
      • posterior - side to side
    • 2 vestibules - Otolithic organ (utricle and saccule): Linear acceleration (change speed but same direction) and gravity
      • utricle (like UFO)
        • Horizontal plane (like UFO...) - bkwards and fwds
      • saccula
        • vertical plane


Endolymph drained via endolymphatic duct between utricle and saccule into endolymphatic sac -> Blood

Ampullary cupula  (enlarged area in canal) in SC
Anterior -  yes, posterior - side to side, lateral - no

When head is at rest, hair cells are partially depolarized, firing at low frequency
When head is rotating, the bony labyrinth rotates but the endolymph (only endolymph in ampulla) lags behind (inertia). Endolymph pushes cupula, distorting the hairs.
  • If sterocilia in cupula to kinocilia, depolarize -> increased AP firing
  • If away from kinocilia, hyperpolarize -> decreased AP firing

When initially moving, structural components of the corresponding semicircular canal moves immediately since they are attached to the rest of your head. However, the endolymph within that particular semicircular canal would tend to "remain at rest" due to inertia.

When spinning around, if you stop and spin the other way it helps!! If you start spinning the other way, you would be exerting another force trying to push the fluid into the new direction of motion. This means you would be pushing on your cupula even more than if you just stopped. But that would be short lived, as the fluid would eventually succumb to the force from the other direction, bring it to stop more quickly. (and if you keep on spinning you'll get it going in the new direction).


when the head rotates to the left, the fluid in the right horizontal canal moves away from the ampulla (reduced excitation), and the fluid in the left one moves toward it (more excitation).



Otoliths in saccule (up and down) and utricle (bkwards and fwds)

Stereocilia in gelatinous mass whose surface has otoliths (calcium carbonate crystals - increase mass of otolithic membrane to give it more inertia).
Macula - Thickened patch of cells consisting of sensory hair cells and supporting cells

Always firing regardless of whether moving
  • When upright, otoliths sits atop and presses down on hair cell
Same mechanism as above.


Cochlea


Organ of Corti sandwiched between tectorial membrane and basilar membrane.

Vestibular duct begins from oval window to helicotrema?
Vestibular duct continuous with tympanic duct at helicotrema (tip of cochlea)
Tympanic duct begins from helicotrema? to round window

Vibrating oval window shakes the fluid inside the vestibular duct, which passes on the vibrations to the cochlear duct, which passes vibrations to the tympanic duct, and reaches the round window and stops. The hearing receptors are located inside the cochlear duct. Whenever sound hits the cochlear duct, the hearing receptors detect it and send it to the brain.


Basiliar membrane

Wider at the apex than at the base
Waves from base to apex (furthest from oval window)
Basal end: High stiffness (of basilar membrane not HAIR!!!!), low mass of BM- high freq
Apical end: Low stiffness, high mass - low freq


Endolymph: Made by striae vascularis
  • Rich in K+
  • Highly positively charged (high [aa])
Perilymph
  • Similar to plasma/CSF (i.e. high Na+)

Vestibular duct aka scala vestibuli contains perilymph
Scala media aka cochlear duct contains endolymph
Tympanic duct aka scale tympani contains perilymph
Tunnel of corti: Triangular shaped, bound each side by pillar cell which converge to form a hinge

"Outer cells are Out of the brain. Inner cells are Into the brain":

Inner hair cell x 1 row (involved in 95% of afferent cochlear nerve)
Outer hair cell x 3 rows in graded lengths (involved in amplifying): Receive efferent from brain to increase amplitude

Sterocilia: Only the tallest in contact with tectorial membrane
Kinocilia - touches tectorial membrane
The apical ends of the hair cells join to form the reticular lamina.
Supporting hair cell



Tip links involved in mechano-transduction and sterocilia are attached by lateral links.

Tip links attach to K+ channels atop sterocilia. IMPORTANCE OF ENDOLYMPH: High K+!

Stapes move: Oval window -> Vibration of endolymph in scale media -> Endolymph shakes basilar membrane (from apex to basilar membrane)-> shearing force between stereocilia and tectorial membrane (remember stereocilia touches tectorial membrane)  -> Sterocilia of IHC moves in the direction of stria vascularis (i.e. direction of kinocilia) -> Sheared hair cell -> Tip open K+ channels on sterocilia -> VDCC open -> Glutamate release from inner hair cell to cochlear nerve -> Increased AP firing

Sterocilia not regenerable!!!! (e.g. loud noise... the tensor tympani and stapedius contract to allow minimal ossicle movement to prevent their destruction!)

Outer hair cells act to amplify sound via electromotile response
With every soundwave, the OHC shortens and then elongates. This pushes the tectorial membrane, thus amplifying the vibration.


Pathway



Input to cochlear nuclei: C.N. VIII - cell body in spiral/cochlear ganglion (for vestibular alias to scarpa’s) which lies in the modiolus [bony core] of the cochlea)

2 cochlear nuclei in medulla
  • more common pathway: dorsal lateral (dorsal cochlear nucleus) - ipsilateral
    • SLIM: Superior olivary nucleus → lateral lemniscus → inferior colliculus (midbrain) synapse.. → medial genicular body  of thalamus
  • ventral lateral (ventral cochlear nucleus) - opposite
    • Superior olivary nucleus to contralateral superior olivary nucleus via trapezoid body -> LIM

M for music!!
Medial geniculate body of thalamus to primary auditory cortex in the temporal lobe.

lesion of the auditory portion of the C.N. VIII (nerve) results in deafness in the IPSILATERAL ear



Vestibulocochlear  nerve - UNCROSSED for lateral, biliateral for medial (middel.. both!)!!!


Vestibular nerve: Info from hair cells in semicircular canal and otolith organs (utricle and saccule)
  • Vestibular (Scarpa’s) ganglion in internal acoustic meatus
  • Terminate in the vestibular nuclei and cerebellum



Semicircular canal - angular acceleration (everything in same direction. right rotation -> right SC canal -> right vestibular nuclei)
  1. head rotate to right → hair cells in ampullary cupula of the RIGHT horizontal SC canals stimulated and those in the LEFT horizontal SC canals inhibited
  2. Action potentials in right vestibular nerve to right vestibular nuclei
  3. Right vestibular nuclei affects RIGHT SIDE
    • ipsilateral limb musculature via right lateral vestibulospinal tract in ventral funiculus (eg when fall to right side -> right vestibular nuclei -> right arm and leg) … lateral - limbs
    • bilateral neck musculature via right medial vesetibulospinal tract in ventral funiculus

    Utricle (horizontal plane) and saccule (vertical plane) - linear acceleration



    Sight

    Cornea - dericed from surface ectoderm

    Eye Embryology
    • surface ectoderm - cornea and lens
    • mesoderm - sclera and uveal tunics
      • The only embryonic tissue that has angiogenic (BV) properties
    • neuroectoderm - retina proper and its pigment cell layer


    Begins at 22 days
    1. Optic grooves in neural tube
    2. Neural tube closes and Optic vesicle forms as evagination of forebrain and connection to brain narrows and become more stalk like
    3. Induction: As the vesicle grows and touches ectoderm, it transforms the surface ectoderm and cauases it to thicken to form lens placode
    4. Distal optic vesicle invaginates to form optic cup, at the same time forming two distinct layers
      1. Inner layer: Retinal tunic - light-sensitive
      2. Intraretinal space obliterates when inner and outer layer fuses
      3. Outer layer: Pigment epithelium layer
      4. Neuroectoderm -> Muscle
        1. Mouth of optic cup eventually becomes the pupil (dilaltor and constrictor pupillae)
    5. Optic vesicle folds along a centerline choroid fissure and invaginates mesenchyme
      1. Angiogenic
        1. Forms the hyaloid artery and vein (in the hyaloid canal) which later becomes central artery and vein of retina
      2. Muscle
        1. Ciliary muscle
      3. Choroid fissure closes at 7 week
    6. Lens pit and detach from lens placode to form lens vesicle to lie in the mouth of optic cup (future pupil)
      1. Lens vesicle (future lens) Supplied by hyaloid artery

      2. The remaining lens placode form the cornea
      3. The mesoderm beneath it makes the eylid



    Retinal detachment
    • Congenital: Failure of fusion between inner and outer optic cup
    • Acquired: Trauma

    Defect in closure of choroid fissure
    - Coloboma

    Since mesoderm is the only embryonic tissue with angiogenic potential, i.e., the capacity to form blood vessels, its participation in the formation of the uveal tunic and the sclera is necessary. The cornea is from ectoderm, and it is therefore avascular  - privileaged state for transplant.



    sight... (superior orbital fissure made by sphenoid bone!)
    Inner: Retina
    Bruch’s membrane (BM of pigmented epithelium)
    Middle: Choroid (loose CT, vascular, melanocytes which produce melanin to absorb any lighs rays that passes through the retina to prevent internal reflection)
    Outer: Sclera

    Uvea: iris, ciliary body, choroid







    Sclera

    Choroid

    Bruch’s membrane


    Retina
    Inner limiting membrane separates the optic fiber layer from vitreous body: Basment membrane of Muller cells
    Muller cell: Glial cell that spans from inner limiting membrane to outer limiting membrane
    Plexiform layers: Contain synapse
    Nuclear layers: Contain cell body
    • Inner nuclear layer: Bipolar or horizontal or amacrine
    • Outer: Of photoreceptor
    External limiting membrane: Tight junctions between photoreceptors and Muller cells (Muller cells end here)
    Photoreceptor layer: Rod and cone processes
    Pigmented epithelium lies on Bruch’s membrane
    Bruch’s membrane separates choroid from retina


    Cone bipolar neurone (Bipolar neurons synapsing cones) -> Ganglion neuron of same type
    • ON (depolarized by light) CB -> ON GC
    • OFF (hyperpolarize by light) -> OFF GC

    Rod bipolar neurone
    - ALWAYS hyperpolarized by light
    - Activate ON and OFF galgnion cells by way of amacrine


    Input to ganglion cell
    70% Amacrine
    30% Bipolar

    Amacrine x ganglion

    Amacrine cell: Works at the inner plexiform layer, (NO AXONS), dendrites contacts ganglion and bipolar cells by releasing GABA/glycine to ganglion (i.e. ganglion receive input from either bipolar or amacrine)

    Horizontal x photoreceptor

    Horizontal cell (on the floor): Works at the outer plexiform layer, dendrites connects to photoreceptor (i.e. photoreceptors either connect to horizontal cell or bipolar cell), axons to inhibit bipolar

    When light is shone, the photoreceptor hyperpolarizes and reduces the release of glutamate. Horizontal cells gets hyperpolarized and reduces GABA release to bipolar. The reduction of inhibition causes the bipolars to be depolarized.


    Receptive fields (area that when shone on, changes membrane potential)
    • On-center, off-surround: On center: increased firing above baseline, on surround: decreased firing below baseline
    • Off-center, on-surround: vv

    Rods on
    • Center of ganglion cell’s receptive field: direct R - B - G
    • Surround of ganglion cell’s receptive field: R - B - H -G

    Uniform illumination is less effective than activating certain ganglion cells. Ganglion cells sensitive to differences in levels of illumination (luminance contrast). Response rate changes depending on position of receptive field form info about edges and shapes.



    Rod and Cones structure (x horizontal cells / bipolar)


    Cones  are shorter than rods.

    Rhodopsin (visual purple): A pigment in retina
    • Found in photoreceptor’s outer segments only
    • Opsin (Enzyme) + Retinal (Vitamin D derivative)
      • Opsin: With light, it reversible changes (bleaching)
      • Retinal: Produced in retina from vitamin A (from beta-carotene)
    • GPCR
    • In rods, rhodopsin is as disks (lamellae).
      • 1 type of opsin only - 1 wavelength only
    • In cones, rhodopsin is as continuous folds (icecream)
      • 3 different types of opsin, thus interpret 3 different wavelengths
      • L Red cones (74% of cones)
      • M Green cones (10%)
      • S Blue cones (16%)


    Stimulation of the cones in different combinations enables the perception of colours, e.g. the perception of yellow results from a combination of inputs from green and red cones and relatively little input from blue cones. If all three cones are stimulated then WHITEis perceived.

    Photoreceptor transduction

    Light (HYPERPOLARIZATION due to closed cGMP-gated sodium channel)
    1. Photons get absorbed transforming cis-retinal to trans-retinal. This isomerism makes opsin detach and form enzyme Metarhodopsin II.
    2. Metarhodopsin II activates transducin (G protein that was bound to inactive GDP to active GTP). Tranducin’s G-alpha subunit stimulates cGMP phosphodiesterase.
    3. cGMP PDE converts cGMP to GMP. Thus, with light, there is less cGMP.
    4. Less cGMP to the cGMP-gated channels in the outer membrane of photoreceptors close. No sodium influx.
    5. Voltage-gated calcium channels close
    6. Less glutamate released so hyperpolarization.

    No light (DEPOLARIZATION due to closed cGMP-gated sodium channel)
    1. No photons so rhodopsin remains inactive.
    2. Thus transducin remains inactive
    3. Thus cGMP phosphodiesterase remains inactive, Thus no cGMP to GMP, so high levels of cGMP
    4. cGMP keeps the cGMP gated sodium channels open, Na+ influx
    5. Voltage-gated calcium channels open
    6. More glutamate released so depolarization.


    Rods:
    • Located in periphery of retina
    • Scotopic vision (Low light luminance) - used in night vision
    • 3 rods synapse with 1 ganglion, thus, high light senstivity
    • 1 wavelength only - colorless

    Cones:
    • Mainly in the pit of fovea (fovea centralis/pit) is located in the macula of retina
      • Approximately 50% of the optic nerve carries information from fovea.
    • Phototopic vision (high luminance required)
      • Rods become saturated so cones get used
    • 1 cone synapses with 1 ganglion, thus, high visual acuity
    • 3 wavelengths



    Colour blindness is the inability to DISTINGUISH certain colours.

    Trichromatic: all three cone pigments are present and colour vision is normal.
    Dichromatic: the remaining two are normal, depending on which one of the three normal pigments is missing:
    - Protanopes are the most common - lack red sensitive receptors. - - can't tell red from green
    - Deuteranopes lack green receptors - can't tell red from green
    - Tritanopes (rare) lack blue sensitive receptors = cannot distinguish blue from yellow.
    Monochromatic: only one cone pigment.
    Achromatic functioning cones: Complete pigment loss, can only see black, white and shades of grey.

    Most cases of colour blindness are hereditary (X-linked recessive) but are occasionally acquired as a result of optic nerve disease.

    Colorblindness cannot apply for jobs like:
    Certain grades within armed force
    Civil aviation
    Customs and excise officers.
    Railways
    Fire service officers
    Hospital laboratory technicians and pharmacists.

    Fovea
    • No rods
    • Cones in foveal pit have a smaller diameter, so cones can be more densely packed
    • No retinal blood vessels and bipolar and ganglions cells to allow direct passage of light



    Ganglion cells form the optic nerve, optic chiasm, optic tract and finally LGN of thalamus.


    From LGN, optic radiations synapse to primary visual cortex.

    Most fibers travel through parietal lobe, carrying info. from lower visual field.

    A few travel into temporal lobe in the inferior pathway via Meyer's loop which carries information from upper visual field.

    - Pretectal nucleus
    • Pretectal nucleus lies just above superior colliculus
    • Receives afferent from retina
    • Projects to EW nucleus (involved in pupillary light reflex)


    Afferent: Optic nerve -> Optic chiasm-> Optic tract -> branches off to synapse with pretectal nucleus of midbrain
    Efferent: Pretectal nucleus -> Accessory occulomotor nucleus (aka edinger westphal nucleus) of both sides -> Ciliary ganglion of both sides -> Sphincter pupillae of both sides -> Miosis of both pupils!

    Left visual field to right primary visual cortex and vv!
    LGN - light!
    ALWAYS REMEMBER visual field is opposite of retinal field. Trace to the retinal field and draw the opposite (i.e. visual field) that is actually affected.

    LGN to non-Meyer’s loop and Meyer’s loop.

    Remember: Muller’s loop stays the bottom loop - carries upper visual field. If the left meyer’s loop is lesioned, left hemifield is affected.

    In order
    1. Left temporal hemianopsia
    2. Left nasal hemianopsia
    3. Left anopsia
    4. Bitemporal hemianopsia (now... after chiasm are all symmetrical!!!!!!!!!!!!!)
    5. Right homonymous hemianopsia (i.e. right side of both eyes affected)
    6. Right homonymous hemianopsia
    7. Meyer’s: Right superior quadrantanopia (Pie in the sky)
    8. Non-meyer’s: Right inferior quandrantopia
    9. Right homonymous hemianopia
    10. Macular sparing (macular area of the cortex is supplied by BOTH post cerebral artery and middle cerebral artery so if there is occlusion of post cerebral artery the macula will spared due to collateral blood supply from middle cerebral artery and vice versa)


    Watershed area - regions of the body that receive dual blood supply from the most distal branches of two large arteries, such as the splenic flexure of the large intestine.[1]



    Artery Defect - Ophthalmologic deficit

    Anterior communicating artery - Bitemporal hemianopia (optic chiasm?)

    Internal carotid artery - Binasal hemianopia (temporal retinal field?)

    Ophthalmic artery - Monocular blindness (temporal and nasal because opthalamic to central artery)

    Posterior cerebral artery - Homonymous hemianopia with macular sparing (optic radiation and macula)

    Posterior communicating artery - Cranial nerve III palsy


    Fibers of the optic radiation are considerably more spread out than those of the optic tract. As a result, damage normally only occurs to a portion of the geniculocalcarine tracts.

    Damage to the fibers of Meyer's loop and/or damage to the temporal lobe portion of the optic radiation results in loss of input from the inferior half (superior visual field) of both contralateral hemiretinas (superior quadrantanopia).

    Damage to the fibers of the parietal lobe portion of the geniculocalcarine tract results in a loss of input from the superior half (inferior visual field) of both contralateral hemiretinas (inferior quadrantanopia).



    LGN

    P
    M


    Magnocellular layer: Layers 1-2
    • Detect motion
    • Used in central
    Parvocellular: Layers 3-6
    • Detect pattern (i.e. shape and form)
    • Used in peripheral

    Input from contralateral eye: 1, 4, 6 (far apart)
    Input from ipsilateral eye: 2, 3, 5 (close together)
    1, 4, 6 is left eye
    2, 3, 5 is right eye

    http://www.sinauer.com/cogneuro/animation_page.html?file=cogneuro_0501.swf&TB_iframe=true&height=450&width=450

    Visual pathways
    • Central visual pathway: Retina -optic nerve> LGN -> Primary visual cortex (V1)
    • Tectospinal tract
      • Retina -optic nerve> Superior colliculus (Seeing turns necks sideways - superior colliculus → tectospinal tract → neck muscles splenius capitus) contralateral
        • Automatic movement of eyes, head, neck to stimuli
        • Protective closing of eyes and raise arm for protection when assault
        • Automatic scanning movements of the eyes & head that are made when reading


    Nucleus of Cajal -> Interstitiospinal tract descends ipsilaterally in the medial longitudinal fasciculus -> Trunk muscles




    Visual cortex:
    Extrastriate visual cortical areas : V2-V5
    5 areas (V’s...)
    V1 has 6 layers
    Optic nerve -> chiasm -> tract -> LGN -> Radiation -> V1 (Layer 4: P of LGN to 4Cβ, M of LGN to 4Cα)
    • Direction-selective
    • Blob: Sensitive to color - receive input from P cells of LGN and project to layer 4Cβ of the primary visual cortex
    • Color-opponent (Red/green: r+ g- or blue/yellow: b+ y-)
      • Color perception depends on adjacent colors
    • Interblobs are areas between blobs sensitive to angle
    Efferents: Dorsal and Ventral stream

    Efferent pathway: Dorsal and ventral stream


    Dorsal stream: Where/how pathway - motion (where) and position (V1 to parietal)
    • Input from M cells of LGN
    Ventral stream: What pathway - object recognition (V1 to temporal)
    • Input from P cells of LGN



    Vestibulo-ocular Reflex (VOR)
    • maintains eye fixation on an object as the head turns
      • MR and LR
    • turning causes movement of hair cells in the horizontal semicircular canals with respect to the fluid → polarizes the hair cells, leading to an altered frequency of action potential discharge in cranial nerve VIII


    If you move your head to the left, you will excite the left horizontal canal, inhibiting the right. To keep your eyes fixed on a stationary point, you need to fire the right lateral rectus and the left medial rectus, to move the eyes to the right.

    left vestibular nerve fires to brainstem and synapses in the vestibular nucleus.
    • medial vestibular nucleus neurons that send their axons to the contralateral (right) abducens nucleus → CN 6 to LR
    • lateral vestibular nucleus neurons to ipsilateral (left) occulomotor nucleus → CN3 to MR
    • inhibit the opposing muscles (in this case, the right medial rectus, and the left lateral rectus).

    VOR axons travel through MLF (medial longitudinal fasciculus


    Taste


    Taste receptors: TAS1 - sweet, TAS2- bitter




    Aldosterone: Upregulates salt receptor
    Sweet, bitter and umami are all GPCR


    Tongue taste Inputs from chorda tympani (anterior ⅔), posterior ⅓ glosspharyngeal and epiglottis - vagus.

    The soft and hard palate are supplied mostly by the maxillary branch of the trigeminal nerve (CNV2) via the pterygopalantine ganglion.


    Chorda tympani: GNTP - guts never taste poo - geniculate ganglion -> nucleus tractus solitarius -> thalamus (VPM) -> Postcentral gyrus

    Solitariothalamic tract shared by...
    GENICULATE GANGLION OF C.N. VII
    INFERIOR GANGLION of C.N. IX
    INFERIOR GANGLION of C.N. X.

    taste information heads for the thalamus  via solitariothalamic tract.- ventral posteromedial nucleus (VPM; the nucleus of the HEAD!; after all, the tongue is in the head). The third neuron in the pathway i.e., the thalamic VPM neuron, then sends its axon to the ventral lateral portion of the postcentral gyrus, areas 3, 1, and 2 UNCROSSED

    A LESION OF THE ROSTRAL NUCLEUS AND TRACTUS SOLITARIUS WILL RESULT IN THE LOSS OF TASTE FROM THE IPSILATERAL ONE-HALF OF THE TONGUE. SO WILL A LESION OF THE SOLITARIOTHALAMIC TRACT