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NEURO EXAM #3
CHAPTER 11: VISUAL SYSTEM
PART 1: Components of Visual System
A.) Eyes and Retina
Visual System
 A greater portion of the brain is dedicated to vision versus any other sensory modality
 Pathway of the visual system extends form retina lateral geniculate nuclei of thalamus
primary visual cortex (PVC) of the occipital lobe
 Lesions to the visual association cortex cause disorders of higher-order visual processing
Eyes and Retina
 Light enters eye through lens to form image on the retina (that is inverted (A) and reversed)
o Superior visual field projects onto lower retina and inferior visual field projects onto
upper retina
o Right visual field projects to left side of the retina of each eye, and thus the left visual
field projects to right side of the retina of each eye
 Normal Visual Fields
o Extend ~80°-90° temporally, ~50-60° nasally and superiorly, and ~60-75° inferiorly
 Fovea – central fixation point for each eye (not dead center, a little off to the side)
o Is the area of retina which highest visual acuity
o Corresponds to central 1-2° of visual space
o It is surrounded by the macula, which also has high visual acuity and covers the central
5° of visual space
o What is represented on the fovea is projected to the occipital pole
 Optic Disc- formed by axons leaving the retina where they enter the optic nerve
o No photoreceptors over the optic disc, thus a small blind spot is formed here which is
located ~15° later and slightly inferior to the central fixation point of each eye
o No functional deficit when both eyes are used
o When 1 eye is used, our visual system seems to “fill in” the blind spot
o Blind spot formed by axons and no receptors
 Retina contains 3 main layers
o Photoreceptor- outermost layer of retina
 Respond to light and create synapses onto bipolar cells
 Rods
o For vision in low-level lighting conditions
o Low resolution
o Do not detect color
o Outnumber cones by 20:1
 Cones
o High resolution
o Highly represented in fovea where acuity is highest
o Detect color
o Bipolar cell Layer- Middle Layer
 Receive input via synapses form photoreceptors
o Ganglion cell Layer- Inner layer
 Receive input from bipolar cells and send axons into the optic nerve
 Fire Action Potentials
 Ganglion cell types
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Parasol Cells
 Respond to gross stimulus features and movement, large cell bodies,
large receptive fields
 Their large diameter fibers project to magnocellular layers of LGN of
thalamus
 Midget Cells
 Respond to fine visual detail and colors, small cell bodies, small
receptive fields
 Their small diameter fibers project to parvocellular layers of LGN of
thalamus
 Many neurons in the visual pathways have center-surround receptive fields, which are either
“on center” or “off center”
B.) Optic Nerves/Chiasm/Tracts
Optic Nerves, Optic Chiasm, and Optic Tracts
 Optic Nerve
o Receives input form retinal ganglion cell axons and exits in optic canal
 Optic Chiasm
o Partial crossing of fibers where the optic nerve meets
 Nasal (medial) retinal fibers cross over in chiasm
 Thus nasal (medial) retinal fibers are responsible for temporal (lateral)
hemifields of vision
 Optic Tracts
o Posterior to chiasm carrying visual information form ipsolateral hemiretinas of each eye
 L Hemiretinas of both eyes end up in L optic tract and R hemiretinas of both
eyes end up in R optic
 Thus ipsolateral hemiretinas represent contralateral visual fields
 R hemiretinas represent what visual fields
 Lesions of the eye, retina, or optic nerves produce monocular vision field deficits
 Lesions of optic chiasms therefore often produce bitemporal visual field deficits
 Because of the crossover in the chiasm, lesion posterior to chiasm (optic tracts, LGN, optic
radiations, or visual cortex) will produce homonymous visual field defects
o Visual field defect occurring in the same portion of the visual field for each eye
o Contralateral homonymous hemianopia is most common in stroke patients
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Optic tracts wrap around the midbrain laterally to reach the LGN of thalamus
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Axons of retinal ganglion cells traveling in optic tracts synapse on neurons in LGN, which then
project to primary visual cortex
C.) Lateral Geniculate Nucleus (LGN) & Extrageniculate Pathways
Lateral Geniculate Nucleus
 LGN has layers numbered 1-6 (ventral to dorsal)
o Parvocellular layers- layers 6-3
 Relay information form midget cells of retina
o Magnocellular layers – layers 2-1
 Relay information form parasol cells of retina (motion and spatial analysis)
 Information from left and right eyes remains segregated even after passing through the LGN,
because axons form left and right retinas synapse onto different layers of the LGN
Extrageniculate Pathways
 A minority of fibers in the optic tract bypass the LGN to enter the superior colliculus and
pretectal areas, they form the extrageniculate visual pathways
o Pretectal areas are involved in the pupillary light reflex
o Pretectal areas and superior colliculus are involved in directing visual attention and eye
movements toward visual stimuli (via projections to brainstem and lateral parietal
cortex and frontal eye fields)
D.) Optic radiations
Optic Radiations
 Axons leaving LGN sweep over and around the lateral ventricle to project to the primary visual
cortex
 These axons fan out over a large area as they project back to PVC
 Axons form ipsolateral and contralateral retinal layers of LGN are intermingled in optic
radiations, so lesions of optic radiations cause homonymous contralateral visual field loss
 All fibers of optic (blue and green) radiations pass through parietal and temporal lobes
o Ipsolateral optic radiations carry info form contralateral visual fields
o Lesions of ipsolateral radiations would cause a contralateral homonymous hemianopia
visual field defect
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Fibers of inferior optic radiations arc forward into temporal lobe forming Meyer’s loop
o Inferior optic radiations carry information form inferior retina (or superior visual fields)
o Temporal lobe lesions cause contralateral homonymous superior quadrantanopia “pie in
the sky” visual field defect
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Fibers of superior optic radiations pass just under the parietal lobe
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o Superior optic radiations carry information form superior retina (or inferior visual field)
o Lower parietal lobe lesions cause contralateral homonymous inferior quadrantanopia
(“pie on the floor” visual field defect)
E.) Primary Visual Cortex
Primary Visual Cortex (B1)
 Lies on the upper and lower banks (both sides) of the calcarine fissure in the occipital lobe
(medial view)
 Brodmanns Area (BA): 18- secondary visual cortex
 BA 19- tertiary visual cortex
 Calcarine Fissure
o Cuneus (wedge)- upper bank gyrus
o Lingula (little tongue)- lower bank gyrus
 Superior optic radiations project to upper bank of the calcarine fissure
o Upper bank lesions thus cause contralateral homonymous inferior quadrant defects, pie
on the floor
o Lesion to right upper bank of PVS would cause what visual field defect?
 Left inferior quadrantanopia
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Inferior Optic Radiations project to lower bank of the calcarine fissure
o Lower bank lesions thus cause contralateral superior quadrant defects
o Lesion to right lower bank of PVC would cause what visual field defect
 Left superior quadrantanopia
 Like many other parts of the visual pathway, it is retinotopically organized
 Fovea and macula are represented at the occipital pole
o The fovea occupies about 50% of PVS as the fovea contains the highest density of
photoreceptors and has corresponding high visual acuity
o Thus the five and macula have a disproportionate cortical representation despite the
small retinal area
 More peripheral regions of (ipsilateral) retinas (contralateral visual fields) are represented
more anteriorly along the calcarine fissure
F.) Visual Processing
Parallel Channels for Analyzing Motion, Form, and Color
 3 parallel channels of visual information processing analyze motion form color
 These 3 channels project to different layers of the primary visual cortex
 From the PVC, neurons project to other regions of visual association cortex including areas 18,
19 and other regions of the parieto-occipital and occipitotemporal cortex
 Dorsal Pathways project to parieto-occipital association cortex
o Pathway answers the question, Where? By analyzing motion and spatial relationships
between objects as well as between body and visual stimuli
 Ventral Pathways project to occipitotemporal association cortex
o Pathway answers the question, what? by analyzing form with specific regions
identifying colors, faces, letters, and other visual stimuli
PART 2: KEY CLINICAL CONCEPTS
Assessment of Visual Disturbances- KCC 11.1
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2 major steps needed:
o Time course and any positive phenomena (ex bright colored lights) or negative
phenomena (regions of decreased vision) present
 Visual field
o Description of the regions for each eye involved
 Visual acuity often reported with Snellen notation of 20/x
 “X” is distance at which a normal individual can see the smallest line of the eye chart seen at 20
ft.
 Visual field defects usually do not affect visual acuity
 Distinction between a monocular or binocular visual disturbance is essential for localization
 Pts often describe a disturbance as being “in one eye” when in reality the left or right visual
field is affected for both eyes
 Blurred vision is hard to interpret without further description and examination
 Often divided in positive and negative phenomenon
o Negative phenomena
 Region of vision the person cannot see, including a scotoma or homonymous
defect
o Positive phenomenon
 Simple phenomena
 Include lights colors or geometric shape caused by disturbances located
anywhere form eye to cortex
 Formed phenomena
 Include people animals or complex scenes arising from inferior temporaloccipital visual association cortex
 Formed visual hallucinations arise form the inferior temporal-occipital visual association
cortex
 Can be from many causes: toxic or metabolic disturbances, withdrawal from alcohol or
sedatives focal seizures, complex migraine, neurodegenerative conditions, psychiatric
disorders
 Formed hallucinations can also appear as relapses phenomenon
o Pts with visual deprivation in all or part of their visual fields cause by ocular or CNS
lesions may report seeing objects, people or animals in the region of vision loss,
especially in the early stages of the deficit
 Visual Field Testing- Tests for crude deficits in the visual fields
 Confrontation testing at bedside
 Test each quadrant while making sure patient’s eyes stay centrally fixated
 Test each eye using wiggling fingers and having to count the number of fingers being held up
Localization of Visual Field Defects KCC 11.2
 Testing Visual Fields
o Tests for crude deficits in the visual fields
o Confrontation testing at bedside
o Test each quadrant while making sure patient’s eyes stay centrally fixated
o Test each eye using wiggling fingers and having pt count the number of fingers held up
o Fields recorded as if viewing own visual field
o Blink to threat can be used on lethargic/uncooperative patients
 Visual field defects
 Most important information for localization of problems in the visual pathways
o What is the position and shape of the scotoma?
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o Does it affect one or both eyes?
Know the effects of lesions in the visual pathways form the retina to the PVC (figure 11.5, pg
474)
Monocular Scotoma:
o Can be from lesion of retina
 Area of retina damage would reflect damage to the associated visual filed
 Location, size, and shape will vary depending on location and the extent of the
lesion
 Causes: retinal infarcts, hemorrhage, degeneration, and infection
o Could also be from incomplete damage to optic nerve (ex: trauma, or small accidental
cut of nerve during surgery)
Monocular Vision Loss
o Can be from complete lesions of optic nerve
 All fibers of optic nerve of the respective eye are carrying information from entire
retina of that eye
 Causes: glaucoma, optic neuritis, neuropathy, elevated ICP, tumors, trauma
o A lesion that is severe enough to involve the entire retina would also produce a
monocular vision loss
 Entire retina= all photoreceptors for that eye!
Bitemporal Hemianopia:
o Usually from damage to optic chiasm
 Chiasm is made up of nasal (medial) retinal fibers which carry info for temporal
(lateral) visual fields
 Causes: pituitary adenoma, hypothalamus glioma, other misc tumors
 Optic chiasm lies just in front of pituitary gland thus making it susceptible to
pituitary tumors or other lesions in this area
Contralateral homonymous hemianopia
o Can be from lesions of optic tracts
 Optic tract carries info for contralateral visual field
 For example, right optic tract carries info for left visual field
 Optic tracts: behind the chiasm where nasal (medial) retina fibers for each eye
(responsible for temporal (lateral) hemifields) have crossed over to other side
 Causes: tumors, infarct, demyelination
o Can be from lesions of entire optic radiations
 Entire optic radiations-superior (parietal) and inferior (temporal/Meyer’s loop)
optic radiations carry info for contralateral visual field
 Ex: right optic radiations carry info for left visual field
 Causes: infarcts, tumors, demyelination, trauma, hemorrhage
o Can be form lesions of entire PVC due to termination of optic radiations on lower and
upper banks of calcarine fissure
 Causes: PCA infarcts, tumor, infection
Contralateral superior quadrantanopia (“pie in the sky”)
o Can be caused by lesions in the temporal lobe
 Inferior optic radiations (temporal/Meyer’s loop) carry info for superior
contralateral visual field
 Ex: right inferior optic radiations carry info for left superior visual field
 Cause: MCA inferior division infarcts
o Can be from lesions to lower bank of calcarine fissure
 Inferior optic radiations terminate on lower bank of calcarine fissure
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 Causes: PCA infarcts, hemorrhage, tumors, infections, trauma to occipital pole
Contralateral inferior quadrantanopia (“pie on the floor”)
o Can be caused by lesions in the parietal lobe
 Superior optic radiations (parietal) carry info for inferior contralateral visual
field
 Ex: right superior optic radiations carry info for left inferior visual field
 Causes: MCA superior division infarcts
o Can be from lesions to upper bank of calcarine fissure
 Superior optic radiations terminate on upper bank of calcarine fissure
 Causes: PCA Infarcts, hemorrhage, tumors, infections, trauma to occipital pole
Homonymous Hemianopia
o Is the lesion anterior or posterior to the optic chiasm?
o Which side of the brain is the lesion in?
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Fovea has a relatively large representation (beginning in optic nerve and continuing to the PVC)
given its actual size in the retina
 Thus, it would take a large lesion of the primary visual cortex to affect the entire fovea and
macula
 Thus, partial lesions of the visual pathways sometimes result in the central visual field being
spared (because partial lesions would not usually affect entire fovea and macula representation
in PVC)
 Macular Sparing- the visual field represented by macula is intact (“macula is spared”)
 However, a partial lesion to the PVC specifically to the occipital pole, would primarily involve
the area represented by fovea and macula and could result in visual loss in the center of the
visual field, which would be called a central acotoma
o Ex: a head injury involving hitting the back of the head at the bottom of the occiput could
involve the area representing the central visual filed in the PVC on both sides of the
posterior occipital lobe
Blood Supply and Ischemia in the Visual Pathways- KCC 11.3
 Retina receives blood supply mainly form branches of opthalamic artery
 Impaired blood flow can be caused by emboli, stenosis, and vasculitits
 Central retinal artery (branch of the opthalamic artery) supplies inner retinal layers
 Retinal artery has 2 main brancheso Superior= one covering superior half
o Inferior= covering the inferior half
 Occlusion of one of these arteries can cause an altitudinal scotoma in one eye
 An altitudinal scotoma in one eye can result form occlusion to one of these branches
o Occlusion of the superior or inferior branch of the right central retinal artery (branch of
opthalamic) would cause the defect below?
o Answer: superior branch because it supplies superior retina which represents inferior
visual field
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Transient occlusion of the superior or inferior branch of the retinal artery caused by emboli
results in a TIA of the retina called amaurosis fagax with “browning out” or loss of vision in 1
eye for ~10 min
Is sometimes described as “like a window shade” moving down or up over the eye
This symptom should be treated like any TIA and should e considered a warning sign or
impending retinal or cerebral infarct!
Common cause in ipsilateral ICA stenosis causing artery-to-artery emboli
Optic tracts, optic chiasm and optic nerves receive blood supply form numerous small branches
of anterior cerebral artery (ACA) and middle cerebral artery (MCA)
Clinically significant infarcts of these are therefore rarely seen
LGN has a variable blood supply form several vessels including anterior choroidal (branch of
ICA) , thalamogeniculatem and posterior choroidal arteries (branches of PCA)
o Could be associated contralateral hemiparesis (due to involvement of nearby posterior
limb of internal capsule) and/or associated hemisensory loss (due to involvement of
nearby thalamic somatosensory radiations)
Infarcts of the LGN would cause what type of deficit?
o Contralateral homonymous hemianopia
Optic radiations passing through parietal lobe receive blood supply form superior divisions of
MCA
o Damage/infarct to parietal (superior) optic radiations cause what type of visual field
deficit?
 Contralateral inferior quadrantanopia “pie on floor”
o Damage to left parietal optic radiations causes what?
 Right inferior quadratanopia
Optic radiations passing through temporal lobe 9Meyer’s loop) receive blood supply form
inferior divisions of MCA
o Damage/infarct to the temporal (inferior/Meyer’s Loop) optic radiation cause what type
of visual field deficit?
 Contralateral superior quadratanopia “pie in sky”
o Damage to left temporal optic radiations causes what?
 Right superior quadratanopia
Primary visual cortex is supplied by PCA
Large infarcts involving the entire ipsilateral PVC will cause what visual field defect?
o Contralateral homonymous hemianopia
R PCA infarct of entire PVC would cause what?
o Left homonymous hemianopia
CHAPTER 12 Brainstem I: Surface Anatomy & Cranial Nerves
Anatomical & Clinical Review
 Brainstem- compact area that carries nearly all information between brain & remainder of
body
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o Contains numerous important nuclei
Surface features of brainstem, course & function of cranial nerves- Chapter 12
Cranial nerves & central pathways mediating eye movement- Chapter 13
Vascular supply & internal structures including ascending & descending tracts, reticular
formation- Chapter 14
Surface Features of the Brainstem
 Midbrain, pons, & medulla
 Rostral limit= midbrain-diencephalic junction
 Midbrain-pons= pontomesencephalic junction
 Pons-medulla= pontomedullary junction
 Caudal limit= cervicomedullary junction
 Dorsal View
o Tectum Roof
 Superior colliculi
 Inferior colliculi
 Ventral View
o Cerebral peduncles
 Interpeduncular fossa
o Pyramidal Decussation
 Rostral
 Caudal
 Lateral View
o Pons
 4th ventricle
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 Superior, middle, & inferior cerebellar peduncles
Skull Foramina & Cranial Nerve Exit Points
 Olfactory nerve (CN1)- cribriform plate
 Optic Nerve (CN2)- optic canal
 Oculomotor (CN3), Trochlear (CN4), Abducens (CN6), & Trigeminal V1 (CN5) – superior orbital
fissure into orbit
 Trigeminal V2- foramen rotundum
 Trigeminal V3- foramen ovale
 Facial nerve (CNVII) internal auditory canal to enter auditory canal then exits skull via
stylomastoid foramen
 Vestibulocochlear nerve (CNVIII)- internal auditory canal to enter auditory canal
 Glossopharyngeal (CNIX), Vagus (CNX), Spinal Accessory (CNXI) – jugular foramen
 Hypoglossal (CNXII)- hypoglossal foramen
Sensory & Motor Organization of Cranial Nerves
 Analogous to spinal nerves
o Sensory-dorsal
o Motor-ventral
 More specialized due to anatomy of head & neck
 Embryological development-adjacent to ventricular system
 Mature nervous system
o 3 motor columns
o 3 sensory columns
Functions & Course of Cranial Nerves
 Know Table 12.4: exception omit functional categories
 CN sections
o Function
o Course
o Common clinical disorders
CN I: Olfactory Nerve
 How important is the sense of smell?
 Chemoreceptors detect odor& are located in nasal epithelium
 Short olfactory nerves head up through the cribriform plate
 Synapse in olfactory bulb, then information travels via olfactory tract to specific locations that
will be discussed in chapter 18
KCC 12.1 Anosmia (CN1)
 Anosmia-olfactory sensory loss
 Unilateral deficits- pts are rarely aware because contralateral nostril compensates
 Bilateral deficits are often accompanied with decreased taste
 Causes: head trauma, viral infections, PD, Az, intracranial lesions
 Loss of smell
CN II: Optic Nerve
 Optic Nerve- from retina to lateral geniculate of thalamus to the extrageniculate pathways
 Before chiasm- optic nerve
 After chiasm- optic tract
 Optic nerve travels from orbit to intracranial cavity via optic canal
CN III, IV, VI: Oculomotor, Trochlear, Abducens Nerve
 Control extraocular eye muscles- main discussion will be in chapter 13
 CN VI: abducts eye laterally in horizontal direction
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CN IV: rotates top of eye medially & moves it downward
CN III: subserves all other eye movements
Nuclei location
o CN III & CN IV: nuclei are in midbrain
o CN VI: nucleus is in pons
 Intracranial course
o CN III: exits brainstem ventrally in interpeduncular fossa (also carries parasympathetic
to pupillary constrictor & cilliary muscle of lens)
o CN IV- dorsally form inferior Tectum
o CN VI- ventrally at pontomedullary junction
 Skull exit points
o Superior orbital fissure to reach muscles in orbit
CN V: Trigeminal Nerve
 3 major divisions
o opthalamic division V1
o Maxillary division V2
o Mandibular division V3
 Sensory to face
 Small motor root- travels with V3 for muscles of mastication
 Exits brainstem form ventrolateral pons
o Enters small fossa-Meckel’s cave
o Trigeminal ganglion- sensory ganglion of nerve
 Opthalamic V1- inferior part of cavernous sinus to exit skull via superior orbital
fissure
 Maxillary division V2- exits via foramen rotundum
 Mandibular division V3- exits via foramen ovale
o Mnemonic- Single Room Occupancy
KCC 12.2- Trigeminal Nerve Disorders (CN V)
 Trigeminal neuralgia- Tix Douloureux
o Brief severe pain lasting seconds to minutes
o Episodes provoked by chewing, shaving, etc
o Cause: usually unknown, can occur in MS pts
o Initial treatment with medications
CN VII: Facial Nerve
 Main Function: control muscles of facial expression
 Other functions include: tear production, salivation, taste-anterior 2/3 tongue
 Facial nucleus located in caudal pons
 Exits brainstem ventrolaterally at pontomeduallry junction- lateral to CN VI
o Traverses subarachnoid space then enters internal auditory meatus, joins VIII
o Main portion of CN VII exits skull at stylomastoid foramen
KCC 12.3- Facial Nerve Lesions (CN VII)
 Facial weakness: UMN vs. LMN
 UMN face area of primary motor cortex control LMN in contralateral face muscle of pons
 Superior regions of face controlled by projections descending from ipsilateral & contralateral
motor cortex
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*lesion is on right side, Lesion A spared the forehead because UMN work as pair so there is still
function
 Bell’s Palsy: division of the nerve are impaired & then gradual recovery
 Clinical presentation: unilateral LMN facial weakness
 Cause: unknown; possibly viral or inflammatory
 MRI: will yield normal results
 Medical management: oral steroids
 Evidence: ~80% of pts will have full recovery within 3 weeks
CN VIII: Vestibulocochlear Nerve
 Dual Purpose: hearing & vestibular sense from inner ear
 Exits brainstem at pontomeduallary junction just lateral to CN VII
o Enters subarachnoid space to enter internal auditory meatus
o Together with CN VII travels in auditory canal through petrous portion of temporal bone
to enter the cochlea & vestibular organs
 Auditory anatomy-outer ear
o Pinna
o External auditory meatus tube brings the sound to the tympanic membrane
o Tympanic membrane
 Auditory anatomy- Middle Ear
o Cavity in temporal bone
o Ossicles
o Oval & round windows
o Eustachian tube
o Malleus (hammer) attaches to the tympanic membrane
o Incus (anvil)
o Stapes (stirrup) attaches to the oval window
o Tensor tympani & stapedius are the muscles that attach to the ossicles & regulate the
sound energy that is then transmitted to the inner ear
 Auditory anatomy-inner ear
o Bony Labyrinth
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o Membranous Labyrinth
 Cochlea (contains Organ of Corti)
 Vestibule (saccule & utricle)
 Semicircular canals
o Membranous Labyrinth
 Cochlea-coiled tube:
 2 main tucts
o Scala Vestibuli: sound vibrations enter here form the oval window
o Scala tympani found at apex, spirals around and ends at Round
Window
 Central Duct: Scala Media: surround by scala vestibule above and scala
tympani
o Tonotopic representation
 Higher frequencies activate hair cells near oval window
 Lower frequencies activate hair cells near apex of cochlea
o Scala Media
 Triangle in diagram
 Bound by 2 membranes
 Basilar membra
 Reisner’s membrane
 Contains the organ of corti: the receptor organ for hearing
o Organ of Corti
 Contains the Hair cells (sensory receptors)
 Outer hair cells- have sterocillia embedded in tectorial membrane
 Inner hair cells (with spiral ganglia make up 95% of the auditory nerve)free float in endolymph
 Deflection of hair cells occurs with vibrations of basilar membrane leads to
depolarization of hair cells
 Leads to nerve impulses
 Auditory Pathway
o Air pressure waves causes tympanic membrane to vibrate (OUTER EAR)
o Oscillatory movements of stapes against oval window (MIDDLE EAR)
 Endolymph inside cochlea causes vibration of basilar membrane (INNER EAR)
o Organ of corti hair cells deflected and spiral ganglion axons form CN VIII
o Synapse @ dorsal & ventral cochlear nuclei (2nd order)
 Heads upwards in lateral lemniscuses tract
 Ascend to inferior colliculus (MIDBRAIN): the major auditory center
o On to medial geniculate body (THALAMUS): auditory radiations
o Auditory cortex: Herschel’s Gyri- Areas 41, 42
 Secondary auditory cortex: Wernicke’s Area- Area 22
o Central pathway for hearing form cochlear nuclei to primary auditory cortex
o Collaterals
 Contralateral- reticular activating system to cortex & to SC in response to loud
sounds, cerebellum in response to sudden noise
 From inferior colliculus to superior collicuus to synapse with tectospinal tract to
mediate audiovisual reflexes
CN VIII: Vestibulocochlear Nerve
 Auditory information ascends bilaterally with Decussation at multiple levels, unilateral hearing
is not seen with lesions in CNS proximal to cochlear nuclei
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Vestibular anatomy
o 3 anatomical components
 peripheral sensory apparatus
 location-inner ear
 bony labyrinth – 3 semicircular canals (SCC), vestibule& contains
perilymph
 membranous labyrinth- 3SCC & 2 otoliths & contains endolymph
 Receptors- Semicircular Canals
o Dynamic receptors
o Position Right and left lateral
 Left anterior & right posterior
 Left posterior & right anterior
o Ampulla- bulge at base of SCC, contains primary sensory structure,
crista ampullaris
o Ampulla
o Crista Ampullaris
o Cupula
 Receptors- Otoliths
o Static receptors- utricle & saccule
o Location-hair cells embedded in macula
 Receptors- Otolithic Membrane
o Cilia from hair cells are embedded in gelatinous matrix of the
membrane containing calcium carbonate crystals
 Hair Cells- sensors that convert displacement of head movement into
neural firing via fluid
o Depolarization- when sterocilia bent towards kinocilia
o Hyperpolarization- when sterocilia bent away form kinocilia
 central processor
 CNVIII innervates the labyrinths
 Scarpa’s ganglion- vestibular ganglion
 Information can take several paths to the vestibular nuclei or to the
cerebellum
 Vascular supply
 Vestibular nuclear complex- primary processor of vestibular information
o 4 major nuclei
o 7 minor nuclei
 From vestibular nuclei
o Cerebellum
 Adaptive processor
 Direct afferent signals
 Outflow form vestibular nuclei
 Input goes form vermis to flocculus
o Spinal cord via vestibulospinal tract
o Motor nuclei or extraoccular eye muscles
o Input to CN X
o Input to thalamus & then to parietal lobe
 Mechanism for motor output
14
 VOR- purpose to keep vision stable while the head is being moved
 VSR- purpose is to keep head & body stabilized
Functions of the Vestibular System
 Head stability
 Muscle tone & postural control
 Awareness of body position & movement in space
 Contributes to balance
 Contributes to integration of 2 sides of body
 Ocular function
 Influences proprioception
 Auditory processing
KCC 12.5- Hearing Loss (CN VIII)
 Unilateral hearing loss caused by disorders of external auditory canal, middle ear, cochlea, CN
VIII, or cochlear nuclei
o Conductive hearing loss: abnormalities of external auditory canal or middle ear
 Causes include: otitis, tympanic membrane perforation
o Sensorineural hearing loss: disorders of cochlea or CN VIII
 Causes: exposure to loud sounds, Meniere’s disease, tumor
 Assessment- Video #42
o Gold Standard: Audiometry
o Clinical tests: Hearing of different frequencies
 Rinne Test
 More sensitive to determine conductive hearing test
 Comparing air conduction to bone conduction
o In normal individual air should be louder than bone
 Weber test
 Better for sensorineural loss
 Middle of pts head touching skull
 Compare one side to other
o In normal should be some on both sides
o If sensorineural loss then one side is quieter
KCC 12.6- Dizziness & Vertigo (CN VIII): Peripheral Causes
 Dizziness vs. vertigo
15



Vertigo can be caused by lesions anywhere along vestibular pathway
Determine central vs. peripheral disorders
BPPV- Benign paroxysmal positional vertigo
o Presence of otoconia in SCC
o Assessment
 Dix-Hallpike for A/P SCC
 Roll Test for horizontal SCC
o Treatment:
 Canalith repositioning maneuvers
 Semont Liberatory maneuver
 Vestibular neuritis inflammation of vestibular ganglia or nerve
o Intense vertigo for days & loss of postural control for weeks to months
 Meninere’s disease- excess fluid & pressure in endolymphatic system
o Recurrent episodes of vertigo accompanied by fluctuating hearing loss & tinnitus
 Acoustic neuroma- vestibular schwannoma
o Hearing loss, tinnitus, vertigo, & LOB
CN IX: Glossopharyngeal Nerve
 Named for its role in sensation for posterior tongue & pharynx
 Additional functions include: salivation, carotid body reflexes
 Exits brainstem as several rootlets along the upper ventrolateral medulla between inferior
olive & inferior cerebellar peduncle
 Traverses subarachnoid space & exits skull via jugular foramen
CN X: Vagus Nerve
 Vagus- wandering
 Parasympathetic innervation to organs
o Heart, lungs, digestive tract
 Motor
o Pharyngeal, upper esophageal, & larynx muscles
o Heart, lungs, digestive tract
 Exits ventrolateral medulla as several rootlets just below CN IX between inferior olive &
inferior cerebellar peduncle
 Crosses subarachnoid space & leaves cranial cavity via jugular foramen
CN XI: Spinal Accessory Nerve
 As name implies, a rises form upper 5 or 6 cervical segments
 Spinal accessory nucleus protrudes laterally between dorsal & ventral horns of spinal cord gray
matter
 Nerve rootlets leave nucleus & exit lateral aspect of spinal cord between the dorsal & ventral
roots just dorsal to the dentate ligament & ascend through foramen magnum
 Exits cranium again via jugular foramen to supply sternomastoid & upper trapezius muscles
o Sternomastoid turns head opposite direction
o Upper trapezius elevates shoulder
 LMN impairments
CN XII: Hypoglossal Nerve
 Function: tongue movement
 Exits ventral medulla as multiple rootlets between pyramid & inferior olivary nucleus in
hypoglossal foramen
 Contralateral weakness of tongue- UMN lesion
 Ipsilateral weakness of tongue- hypoglossal nucleus or below
16
KCC 12.8- Dysarthria & Dysphagia
 Dysarthria- abnormal articulation of speech
o Common causes include: infarct, MS, BS lesions, lesions of cerebellar & BG pathways
 Dysphagia is impaired swallowing
o Common causes include: neoplasms, esophageal structures, neural components
o Red flags for PT/OT: aspiration pneumonia
THIS REVIEW WILL NOT BE TESTED BUT COULD HELP UNDERSTANDING
Review: Cranial Nerve Combinations
 Sensory & motor innervation to face
 Taste & other sensorimotor functions of tongue & mouth
 Sensory & motor innervation to pharynx. Larynx
Review: Cranial Nerve Combinations
 Sensory & motor innervation of ear
 Sensation form meninges
 General visceral sensation
 Effects of unilateral cortical lesions
ONLINE ASSIGNMENT
 Case 12.5 Hearing loss and dizziness
 41 y.o. woman dizzy and hearing loss in left ear
CHAPTER 13: Brainstem II: Eye Movements and Pupillary Control
Anatomical and Clinical Review
 2 levels of control:
o Nuclear and infranuclear pathways
 Brainstem nuclei of CN III, IV, VI
 Peripheral nerves arising form these nuclei
 Eye movement muscles
o Supranuclear pathways
 Brainstem and forebrain circuits that control eye movements through
concentrations with the nuclei of CN III, IV, VI
Extraocular muscles
 There are 6 muscles for each eye
 Muscle names corresponds with movements
 Horizontal movement:
o Lateral rectus
o Medial rectus
 Vertical movements
o Superior rectus
o Inferior rectus
 The oblique muscles provide torsional movements
 Superior obliqueo Inserts on superior surface of eye to produce intorsion (movement of the upper pole of
the eye inward (nasally)
 Inferior Obliqueo Inserts on inferior surface to produce extorsion (movement of the upper pole of the eye
outward (temporally)
17
Extraocular Muscles Dual Action
 Movement depends on direction the muscle pulls relative to the axis of the eye
 Actions depend on eye position as the eye moves in the orbit
 Both the rectus muscles and oblique muscles are involved in vertical and torsional eye
movements
Extraocular Nerves
 Eye muscles control is like a molecular equation!
 LR6SO4R3
o Meaning LR by CN 6, SO by CN4, all the rest by CN3
 The Oculomotor nerve splits into 2 major branches
o Superior division- supplies levator palpebrae superioris (elevates eyelid)
18
o Inferior division- carries preganglionic parasympathetic fibers to pupillary constrictor
muscles and cilliary muscles of the lens
6 Cardinal Directions of gaze
Extraocular Nerves and Nuclei
 CN III
o Superior division
 Superior rectus
 Levator palpebrae
o Inferior division
 Medial rectus
 Inferior rectus inferior oblique
19
o Parasympathetics to pupil constrictor and cilliary muscle of lens
o Susceptible to compression of PCA
Occulomotor nucleus consists of several nuclei
 Edinger-Westphal
o Parasympathetic preganglionic
 Unilateral lesions of Oculomotor nucleus & contralateral eye since some axons cross in the
brainstem before the nerve exits

A unilateral nuclear lesion in CN III does not cause:
o Unilateral ptosis
o Unilateral dilated unresponsive pupil
o Unilateral superior rectus palsy
 Ipsilateral fibers travel to the contralateral SR cross directly over the contralateral
Oculomotor nucleus
 CN IV- Trochlear Superior Oblique
o Trochlear nerves are the only CNs to
 Exit the dorsal surface of the brainstem
 Only CN that cross over each other to exit
o Susceptible to cerebellar tumors
o Very thin, thus very easily damaged from shearing forces with head trauma
 CN IV- Abducens
o Lateral rectus
o Abducens nuclei lie on the 4th ventricle of mid to lower pons
o Axons travel ventrally to exit at the pontomedullary junction
o Highly susceptible to downward traction injury produces by elevated intracranial
pressure
KCC 13.1- Diplopia (double vision)
 Possible etiologies
o Mechanical problems – orbital fx
o Disorders of Extraocular muscles
 Thyroid disease
o Disorders of the neuromuscular junctions
 Myasthenia gravis
20
o Disorders of CN III, IV, VI and their pathways
o In young children where visual pathway is still developing, congenital eye muscle
weakness can produce strabismus that over time causes suppression of one image
resulting amblyopia (decreased vision in one eye)
 Early correction is critical for proper function of both eyes
KCC 13.2- CN III (Oculomotor) palsy
 Damage of Oculomotor nerve or nucleus causes paralysis of all Extraocular muscles except for
lateral rectus and superior oblique
 Only movement remaining is abduction, depression, and intorsion
 Results is the eye may take the “down and out position”
 Paralysis of levator palpebrae will cause eyelid closure (ptosis)
 Common causes of Oculomotor palsy
o Diabetic neuropathy
o Head trauma
o Compression of CN III by P-communicating aneurysm
KCC 13.3- Trochlear Palsy (CN IV)
 Trochlear nerve innervates superior oblique muscle
 CN IV Palsy produces elevation of eye
o Patients often tuck in chin and tilt head away form the affected eye to correct diplopia
 Because these maneuvers compensate for the hypertropia and extorsion
o With a CN IV palsy there is vertical diplopia
o Commonly injured CN in
 Head trauma, tumor, infection and aneurysm
KCC 13.4- Abducens Palsy (VI)
 CN VI innervates lateral rectus
 Produces horizontal diplopia
o Patients often turn head toward the affected eye
 Abducens palsy is susceptible to traction caused by elevated ICP, also is often early sign of
tumors
o Also caused by hydrocephalus, infection, inflammation, aneurysm, and diabetic
neuropathy
The pupils and other ocular autonomic pathways : the Pupillary Light Reflex
 Pupils under both parasympathetic (constriction) and sympathetic (dilation) control
 Light reflex: optic nerve>optic tract>pretectal area
o Pretectal neurons>bilateral Edinger Westphal nuclei>cilliary ganglion>constrictor
muscles
o Direct response and consensual response
 See also You Tube: the consensual Pupillary Light Reflex, bobmcpac, 2:39 or neuro exam #29
Accommodation Response
 Bilateral pupillary constriction occurs through a slightly different circuit during the
accommodation response
 Accommodation responses included pupillary constriction, accommodation of the lens of the
cilliary muscle and convergence of the eye
 Accommodation requires activation of the visual cortex (recognize closer objects)
 Contraction of the cilliary muscle of the lens is parasympathetically mediated
 Lens is normally under tension form suspensory ligament
 Ciliary muscle acts as sphincter and when contracted causes the suspensory ligament to relax,
producing a rounder lens for near focus
21
Sympathetic Pathway for Pupillary Dilation
 Connections form the hypothalamus via lateral brainstem to spinal cord T1-T2
o Sympathetic preganglionic neurons whose axons go to superior vertical ganglion
 Neurons to the SCG project to the pupillary dilator muscles of the eye
 Sympathetic also controls
o Superior tarsal muscle (upper eyelid elevation giving wide eyed stare)
o Sweat gland to the face and neck, when damaged this gives Horner’s Syndrome
KCC 13.5- Pupillary Abnormalities
 Can be caused by peripheral or central lesions, by sympathetic or parasympathetic lesions or
disorders of the iris muscle or visual pathways
 Pupillary abnormalities can be bilateral or unilateral, in which case anisocoria (pupillary
asymmetry) is present
 Oculomotor lesions
o Unilateral dilated pupil (when large= blown up pupil)
o Decreased or absent direct and consensual light response
 Horner’s Syndrome
o Disruption of sympathetic path to eye and face
o Ptosis, miosis (constriction) , and anhydrosis
o Impaired dilation response
o Direct and consensual light response intact
 Following dilation slowed
KCC 13.6- Ptosis
 Eye opening involves levator palpebrae superior (CN III) and Muller’s smooth muscle in upper
eyelid (sympathetic control)
o Frontalis muscle of forehead (CN VII) also plays an accessory role
 Eye closure is performed by the orbicularis oculi muscle (CN VII)
 Common causes of ptosis
o Horner’s Syndrome
o Oculomotor nerve palsy
o Myasthenic gravis
o Redundant skin folds that occur with aging (pseudoptosis)
Cavernous Sinus & orbital apex
 CN III, IV, & VI pass through CS and lesions produce characteristic syndromes that often affect
eye movements
 CS is a group of venus sinusoids on either side of pituitary that receive venous blood form the
eye and adjacent cortex
 5 CN branches run through
o CN III, VI, and V (opthalamic and maxillary divisions)
22
o Sympathetics going to the pupil travel through the CS
 Orbital Apex
o Region caudal to the eye where most all of the nerves, arteries, and veins of the orbit
converge before passing into the optic canal and superior orbital fissure
Supranuclear Control of Eye Movements
 Brainstem, cerebellum, and forebrain all contribute to control of eye movements via effects on
CN nuclei III, IV, VI
 3 main types of eye movements
o horizontal, vertical, and vergence eye movements
 types of eye movement
o saccades- rapid eye movements directed at targets in visual field
 reach velocities of up to 700 degrees/sec
 is the only type of eye movement that can be easily performed voluntarily, but
can also be elicited by reflexes as well
 neuroexam.com #33
o Smooth pursuit- slower movements following objects in visual field
 Reach velocities of 100 degrees/sec
 Neuroexam.com #32
o Vergence- movements to maintain visual fixation of objects moving toward or away
from the viewer
 Neuroexam.com- end of #32
o Reflex Eye Movements
 Optokinetic Nystagmus (OKN)
 Vestibulo-Ocular (VOR)
 Reflex eye movements- include optokinetic Nystagmus (OKN) and vestibule-ocular reflex (VOR)
 Nystagmuso Composed of slow eye movements in one direction interrupted repeatedly by fast,
saccade-like eye movements in the opposite direction
 Normal nystagmus occurs during attempts to view a visual scene or a series of
stripes moving in front of the eyes and is called optokinetic nystagmus (OKN)
 Nystagmus is abnormal when it occurs at rest (without changing visual or
vestibular inputs)
 Vestibulo-Ocular Reflex (VOR)
o Stabilizes the eyes on a visual image during head and body movements
Brainstem Circuits for Horizontal Eye Movements
 Controlled by lateral rectus (VI) & medial rectus (III)
 MLF interconnects nuclei of CN III, IV, VI & vestibular nuclei
o Allows bilateral fixation on a single object (conjugate movement)
 Nucleus VI acts as horizontal gaze center
o Controls movement of both eyes by projecting to ipsilateral rectus and contralateral CN
III nucleus
 Pontine reticular formation
o Additional horizontal gaze center
o Projects to nucleus VI lateral gaze
KCC 13.8- Brainstem Lesions Affecting Horizontal Gaze
23
Brainstem Circuits for Vertical Eye Movements
 Vertical eye movements
o Mediated by superior & inferior rectus superior& inferior oblique muscles
o Centers for controlling vertical eye movements located rostral midbrain reticular
formation and pretectal area
o Ventral portion
 Mediates downgaze
o Dorsal portion
 Mediates up gaze
o Locked in syndrome
 Caused by large ventral pontine infarct/hemorrhage often damages CST
bilaterally and nucleus VI (corticobulbar), thus eliminating body movement and
horizontal eye movement (gaze)
 Patient can only communicate via vertical eye movement
Brainstem circuits for Vergence Eye Movements
 Convergence is produced by medial recti muscles and divergence of eyes is produced by lateral
recti muscles
 Exact anatomical locations of vergence centers not known but neurons in midbrain reticular
formation appear to be involved
 Visual cortex and parietal cortex involved as part of the accommodation response
Forebrain Control of Eye Movements
 Multiple paths descend form forebrain and affect eye movement
 Paths project
o Directly to brainstem nuclei involved with eye movement
o Or relay via the superior colliculus
 Frontal eye fields (FEF) appear to be in area 6
24
o The generate contralateral saccades via connections with PPRF (paramedian pontine
reticular formation)
 Parieto-occipital-temporal cortex function in smooth pursuit eye movements
 Inputs from visual association cortex and visual association cortex influence FEF activity
 Basal ganglia also appears to play a role in eye movements
Cerebellar, Vestibular, and Spinal Control of Voluntary and Reflex Eye Movements
 The cerebellum, vestibular nuclei, and cervical spinal proprioceptors influence eye movements
and contribute to several forms of reflex eye movements
 Optokinetic Nystagmus (OKN)
o Slow phase (smooth pursuit phase)
o Fast Phase (saccades phase)
o Neuroexam.com #34
 Vestibulo-Ocular Reflex (VOR)
o Stabilizes the eyes on a visual image during head and body movements
o Inputs from vestibular nuclei (especially the medial vestibular nuclei) travel in the MLF
to control the Extraocular eye muscle nuclei
o VOR demonstration
 Focus on your finger in front of you and turn your head side to side, noting the
stable image of your finger
 Compare this to when you keep your head still and move your finger form side to
side at the same rate
 In a comatose pts, the integrity of the brainstem circuits mediating the VOR is often tested with
the oculocephalic test to elicit “doll’s eyes”
o + Doll’s Eyes- eye move opposite head rotation
 indicates brainstem circuits likely intact
o _ Doll’s eyes- eyes move in same direction as head rotation
 indicates likely brainstem damage or brain death
o IN the normal, awake individual, cerebellar circuits enable visual fixation to overcome
the VOR
 This is why oculocephalic testing does not produce “doll’s eyes” in the normal
awake individual
 Ex: intact VOR will cause visual fixation
Summary
 Damage to the eye movement pathways can interfere with normal vision and can also affect
pupil and eyelid control
 Understanding brainstem circuits, nerves and muscles involved in movement of the eye,
eyelids, and pupils will assist the rehab professional determining the effects of lesions and
illness on these functions
CHAPTER 14: Brainstem III: Internal Structures and Vascular Supply
Main Components of the Brainstem
 Main functional groupings:
o Cranial nerve nuclei
o Long tracts
o Cerebellar circuitry
o Reticular formation (RF) and related structures
 Brainstem lesions are often associated with:
o CN abnormalities
o Long tract findings
25
o Ataxia
o Impaired RF function such as impaired loss of consciousness
o Autonomic dysfunction
 Terms Used
o Tectum (roof)
 In the midbrain
 Consists of inferior and superior colliculi
o Tegmentum (covering)
 Makes up main bulk brainstem nuclei and reticular formation
o Basis
 Most ventral corticospinal and corticobulbar tracts
 Rostral midbrain
o At the level of the superior colliculi
 Includes oculomotor nuclei (CN III) and red nuclei
 Caudal Midbrain
o Level of inferior nuclei
 Includes trochlear nuclei (CN IV) and Decussation of superior cerebellar
peduncles
 Rostral to Mid Pons
o Pons (bridge)
 Between middle cerebellar peduncles
o Basis Pontis (CS and CB tracts)
 Pontine nuclei (cerebellar function)
 Rostral Medulla
o Inferior olivary nucleus
 Inferior cerebellar peduncles, pyramidal tracts, anterolateral system, medial
leminiscus
 Caudal medulla
o Posterior columns and nuclei
 Pyramidal tracts, anterolateral system, medial lemniscus
Reticular Formation
 Nuclei that run through the entire length of brainstem
 Rostral RF
o Key Functions: midbrain and upper pons work with diencephalic nuclei to maintain
alert, conscious state in forebrain
 Caudal RF
o Key Functions: pons and medulla work with CN nuclei & spinal cord to carry out motor,
reflex and autonomic functions
 Numerous nuclei in RF have projection patterns to reach practically every part of the CNS
 Roles in postural control, cardiovascular pain, sleep and consciousness, habituation
 Consciousness system
o Regulates level of consciousness and sleep wake transitions
 Formed by cortical and subcortical networks
 Upper brainstem
 Diencephalon
 Basal forebrain
 Medial & lateral frontoparietal association cortex
 Congulate gyrus
26



Normal consciousness= an individual fully awake and aware of self and environment
AAA (alertness, attention, awareness)
Loss of consciousness
o Is a continuum (ex: form being awake to in a coma)
 Alertness
o Conscious, aware of environment, keenly responsive
 Where in the brain can a lesion cause a coma?
o Upper brainstem reticular formation and related structures
o Bilateral regions of cerebral cortex (extensive damage)
o Bilateral lesions of the thalamus
Brainstem Projection Systems
 In addition to the RF, there are other widespread projection systems that contribute to
alertness
o NE, Dopamine, Histamine
 Ach- attention, memory, and learning (antagonist caused delirium)
 Serotonin- depression, anxiety, obsessive compulsive disorders, aggressive
behavior and eating disorders
 These NT
o Mediate communication between neurons (EPSP and IPSP)
o Neuromodualtion- can facilitate or inhibit transmission
 Signaling cascades, synaptic regulation
o Essential for maintaining attention, the sleep wake cycle and emotional balance
The Sleep-Wake Cycle
 Circuits are located in the brainstem
 The 5 Stages of Sleep
o NonREM (non rapid eye movement) sleep
 Makes up to 75% of sleep
 Begins the sleep cycle
 Stages 1- drowsiness
 Stage 4- most difficult to awake a person form
o REM (rapid eye movement) sleep
 Dreaming occurs
 Periods become longer
o Cycles repeat several times during the night
 Sleep in not a passive process- it is generated by neural circuits
 NonREM sleep
o Governed by regions in lower medulla
o Inhibition of ascending activating systems
 REM sleep
o Governed by regions in the pons
o Pontine circuits inhibit tonic lower motor neuron muscle activity during sleep
o Some brief phasic movements occur (eyes and limbs)
 What would you expect to see with transection at the lower pons or at the medulla?
 Narcolepsy
o Abnormal tendency to easily enter REM sleep directly from the waking state
o 4 classical clinical findings of
 excessive daytime sleepiness
 cataplexy (sudden loss of tone)
27
dream like hallucinations- hypnagogic (while falling asleep) or Hypnopompic
(while awaking)
 sleep paralysis (awake, but unable to move for several minutes)
o possibly caused by a deficiency of orexin (neuropeptide)
 prexin tends to stabilize the awake state by stimulating arousal
 inhibited during NonREM and REM sleep
o treated with stimulants, antidepressants, serotonin reuptakes inhibitors
KCC 14.2- Coma and Related Disorders
 Comao Unarousable unresponsiveness in which the pt lies with eyes closed
o Minimum duration of 1 hour (vs. syncope, concussion, etc)
o Due to dysfunction in:
 Upper brainstem- diencephalon activating systems
 Bilateral diffuse regions of cortex


Coma- profoundly impaired function of cerebral cortex and diencephalic- upper brainstem
arousal systems
o Many brainstem reflex activities may occur (ex: VOR, gag reflex, pupillary light reflex,
corneal reflex)
28
o Meaningful or purposeful responses mediated by cortex are absent (limb adduction in
response to pain)
o EEG is abnormal
o Not generally a permanent condition
 Pts either deteriorate or emerge into other states of less profoundly impaired
arousal within 2-4 weeks
 Brain Death- an extreme and irreversible form a coma
o Mo demonstration of forebrain or brainstem function, including brainstem reflexes
o EEG shows “electocerebral inactivity” or a flat pattern
 Vegetative state- usually after coma, where sleep-wake cycle and or reflexes mediated by
brainstem are regained, by pt remains unconscious
o Persistent vegetative state- vegetative state is longer than 1 month
o Prognosis for recovery is very poor if last greater than 3-12 months
o Pts may open their eyes and arouse in response to stimulation
 May produce unintelligible sounds or move their limbs
o Do not have meaningful speech or gestures, do not make purposeful movements, do not
track visual stimuli, and they are incontinent
 Minimally conscious state
o Pts have some minimal or variable degree of responsiveness, including ability to follow
simple commands, say single words, or reach for and hold objects
 Further stage of recovery form vegetative state
 No reliable interactive verbal or nonverbal communication and do not have
reliable functional use of objects
 Appearance of visual tracking may be one of the earliest signs of emergence into
minimally conscious state
Reticular Formation: Respiration
 Respiratory rhythms occur automatically under control of circuits in the medulla
 Other regions have strong modulatory influences on the respiratory system
 Numerous inputs to respiratory circuits
o Chemoreceptors in the blood, project to the nucleus solitaries
o Pre-Botzinger complex is “pacemaker” for respiration
 Inspiration and expiration are controlled by nuclei projecting to LMNs in the spinal cord
Reticular Formation: Heart Rate and Blood Pressure
 Inputs to the caudal nucleus solitaries (cardiorespiratory nucleus) are crucial
o Receives input form baroreceptors in carotid body and aortic arch via CN IX and X
respectively
 Control of HR and BP is mediated by circuits projecting form nucleus solitaries to
parasympathetic and sympathetic preganglionic neurons in brainstem and spinal cord
Reticular Formation: Motor Systems
 Involved in automatic movement and posture
 Posturing reflexes can been seen in pts with damage to these UMN pathways
 Decorticate
o Abnormal flexor
o Lesions at the midbrain or above
o Mnemonic- Lesion is higher, flexed arms pointing up
 Decerebrate
o Abnormal extensor
o Lower down in the brainstem
o Lesion is lower, extended arms pointing down
29

Posturing is largely mediated by brainstem circuits
Reticular formation: Motor, Reflex, and Autonomic Systems
 Circuits in pontomedullary RF contribute
o To behaviors such as coughing, hiccupping, sneezing, yawning, shivering, gagging,
vomiting, swallowing, laughing, and crying
 Lesions can interfere with these behaviors or cause them to emerge abnormally
 Case 12.8
o Episodes of uncontrollable laughter, dysphagia, and absent gag reflex
o Tumor in pons (and into medulla)
Brainstem Vascular Territories


Supply of midbrain
o Superior cerebellar artery
o Posterior cerebral artery
o Paramedian branches at top of basilar artery (interpeduncular fossa)
Supply of Rostral Pons
o Superior cerebellar artery
30
o Basilar Artery (circumferential branches = lateral pontine arteries)
o Basilar Artery (paramedian branches)
 Supply Caudal Pons
o Anterior inferior cerebellar artery
o AICA and basilar artery (circumferential branches= lateral pontine arteries)
o Basilar artery (paramedian branches)
 Supply to Rostral Medulla
o Vertebral artery
o PICA
o Vertebral artery ( paramedian branches)
o Anterior spinal artery
Lateral Medullary Syndromes: (Wallenberg’s Syndrome)
 Aka lateral medullary syndrome and posterior inferior cerebellar artery syndrome
Medial Pontine (Basis) Syndromes
31
Medial Midbrain (Basis) Syndromes: (Weber’s Syndrome)
Summary
 Small lesions in the brainstem can have devastating consequences
 Knowledge of brainstem anatomy is essential for the clinician’s ability to diagnose and treat the
life-threatening disorders of this region
 Vascular territories of brainstem and characteristic syndromes associated with these are also
critical to understand
PG 568 in book
LR6SO4R3
Muscle
Lateral Rectus
Medial Rectus
Superior Rectus
Inferior Rectus
Superior Oblique
Inferior Oblique
CHAPTER 13/14 IN CLASS ACTIVITY
Motion
Abduction
Abduction
Elevation & Intorsion
Depression & Extorsion
Depression & Intorsion
Elevation & Extorsion
Nerve
VI
III Inferior
III Superior
III Inferior
IV
III Inferior
TEST OVERVIEW
Chapter 11
 13 questions (some overlap with chapter 13)
Chapter 12
 +online
 ~13 questions
Chapter 13
 ~12 questions (some overlap with chapter 13)
Chapter 14
 ~12 questions
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