Created by Cindy Montana at Washington University in St. Louis

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Created by Cindy Montana at Washington University in St. Louis Hosted at MedStudentBooks.

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Pathways Oculomotor / Oculodominance

Brainstem Atlas Hypothalamus

Brainstem Syndromes Limbic

Somatosensory Sleep

Pain Memory

Motor Language

Autonomic Nervous System

Note: If a slide says CLICK, click outside the buttons to advance the animation until CLICK disappears.
Otherwise, use the arrow buttons (top right) to navigate between slides.
Pathways

• Fine Touch
• Pain/Temperature
• Proprioception
• Corticospinal/Corticobulbar
• Rubrospinal/Tectospinal
• Reticulospinal
• Vestibulospinal

MAIN
FINE TOUCH
CLICK Spinal Cord
dorsal root
ganglion
gracile fasciculus dorsal
columns
cuneate fasciculus

S
T L Aβ fibers (large)
C enter the spinal
afferent Aβ fiber cord medial to
1st order Aδ, C fibers
(small)

sacral
lumbar
thoracic
cervical

MAIN SECTION
FINE TOUCH
CLICK Medulla
gracile nucleus

cuneate nucleus

internal
arcuate
fibers
2nd order medial
lemniscus
2nd order
CROSS

sacral
lumbar
thoracic
cervical

MAIN SECTION
FINE TOUCH
CLICK Pons
trigeminal
motor
nucleus

trigeminal
ganglion

trigeminal main
sensory nucleus

sacral
lumbar
medial lemniscus
thoracic
2nd order
cervical
trigeminal – sensory
MAIN SECTION
FINE TOUCH
CLICK Midbrain
inferior
colliculus

lateral lemniscus

medial
sacral
lemniscus
lumbar
2nd order
thoracic
cervical
trigeminal – sensory
MAIN SECTION
FINE TOUCH
CLICK Midbrain
superior
colliculus
lateral
lemniscus

red nucleus medial


lemniscus
2nd order

sacral
lumbar
thoracic
cervical
trigeminal – sensory
MAIN SECTION
FINE TOUCH
CLICK Forebrain
primary somato-
sensory cortex
internal capsule click here
3rd order
click here for
horizontal section

VPL*

VPM*

* These nuclei are slightly displaced in this


view, to illustrate that trigeminal input 
VPM and body input  VPL

sacral
lumbar
thoracic
cervical
trigeminal – sensory
MAIN SECTION
Internal Capsule – Horizontal Section

anterior limb

genu

posterior limb

sacral
lumbar
thoracic
cervical
trigeminal – sensory
MAIN SECTION
PAIN/TEMP
CLICK Spinal Cord
RL = Rexed lamina

Aδ fiber
dorsal root
1st order
ganglion posterior marginalis (RL I)
substantia gelatinosa (RL II)
C fiber
1st order nucleus proprius
(RL III, IV)
Aδ, C fibers
(small) enter the Lissauer’s tract
spinal cord
lateral to Aα
fibers (large)
interneuron

CROSS
S
C T L
sacral 2nd order tracts:
lumbar spinothalamic/
thoracic spinoreticular/
spinomesencephalic
cervical
anterior white commissure
2nd order MAIN SECTION
PAIN/TEMP
CLICK Medulla Show Spinoreticular Tract

trigeminal
afferent
1st order

trigeminal medullary reticular


spinal tract formation
1st order

trigeminal
spinal nucleus
CROSS

2nd order tracts:


spinothalamic/
spinoreticular/
sacral spinomesencephalic
lumbar
thoracic
cervical
trigeminal – sensory
MAIN SECTION
PAIN/TEMP
CLICK Pons Show Spinoreticular Tract

pontine reticular
formation

trigeminal
ganglion

trigeminal
spinal tract
1st order

spinothalamic,
trigeminal
sacral spinomesenephalic
afferent tracts
lumbar 1st order 2nd order
thoracic [to medulla]
cervical
trigeminal – sensory
MAIN SECTION
PAIN/TEMP
CLICK Midbrain
inferior
colliculus

spinothalamic/
spinomesen-
cephalic tracts
2nd order

medial
sacral
lemniscus
lumbar
thoracic
cervical
trigeminal – sensory
MAIN SECTION
PAIN/TEMP
CLICK Midbrain Show
Spinomesencepahalic Tract

spinothalamic tract
superior
2nd order
colliculus

periaqueductal
gray (PAG)
mesencephalic
reticular
formation

red nucleus medial


lemniscus

sacral
lumbar
thoracic
cervical
trigeminal – sensory
MAIN SECTION
PAIN/TEMP
CLICK Forebrain
primary somato-
sensory cortex
internal capsule Spinothalamic tract click here
(posterior limb) (no evidence for
3rd order orderly topographic
cortical map)
VPL*

VPM*

* These nuclei are slightly displaced in this


view, to illustrate that trigeminal input 
VPM and body input  VPL

sacral
lumbar
thoracic
cervical
trigeminal – sensory
MAIN SECTION
PROPRIOCEPTION
CLICK Spinal Cord - Sacral
dorsal root
ganglion dorsal columns

afferent Aα fiber
1st order

Aα fibers (large)
enter the spinal
cord medial to
Aδ, C fibers
(small)

MAIN SECTION
PROPRIOCEPTION
CLICK Spinal Cord - Thoracic

dorsal
spinocerebellar
tract
nd
2 order

Clarke’s nucleus
(dorsal nucleus)
T1-L2

MAIN SECTION
PROPRIOCEPTION
CLICK Spinal Cord - Cervical
afferent Aα fiber
1st order dorsal columns

dorsal root
ganglion

dorsal
spinocerebellar
tract
2nd order

MAIN SECTION
PROPRIOCEPTION
CLICK Medulla
cuneocerebellar tract
2nd order

dorsal
spinocerebellar
tract
2nd order

external (accessory)
cuneate nucleus

MAIN SECTION
PROPRIOCEPTION
CLICK Medulla
inferior
cerebellar peduncle
2nd order

MAIN SECTION
PROPRIOCEPTION
CLICK Cerebellum
medial (fastigius)

interposed (globose +
deep cerebellar nuclei (see right) emboliform)

lateral (dentate)

mossy fibers

inferior cerebellar
peduncle (restiform body)

MAIN SECTION
PROPRIOCEPTION
CLICK
afferent Aα fiber
Pons
(from masseter, temporalis)
mesencephalic ganglion

trigeminal motor nucleus

trigeminal
ganglion

efferent α-MN in CN V3
(to masseter, temporalis)

MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Forebrain
CLICK
corona Precentral,
radiata prefrontal,
postcentral gyri
internal capsule
(posterior limb)

cerebral
peduncle

to lumbar spinal cord


to cervical spinal cord
to CN motor nuclei
MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Midbrain
CLICK

superior
colliculus

oculomotor
nucleus

red nucleus
cerebral
peduncle

to lumbar spinal cord


to cervical spinal cord
to CN motor nuclei
MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Midbrain
CLICK

inferior
colliculus

trochlear
nucleus

to lumbar spinal cord cerebral


to cervical spinal cord peduncle
to CN motor nuclei
MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Pons
CLICK
trigeminal (CN V)
motor nucleus

middle
cerebellar
peduncle

corticospinal
tract
to lumbar spinal cord
to cervical spinal cord
to CN motor nuclei
MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Pons
CLICK
abducens (CN VI) middle
nucleus cerebellar
peduncle

facial (CN VII)


nucleus
This nucleus is
complicated – click here
corticospinal
tract

to lumbar spinal cord


to cervical spinal cord
to CN motor nuclei
MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Medulla
CLICK
hypoglossal (CN XII)
nucleus

nucleus
ambiguous

to lumbar spinal cord


corticospinal
to cervical spinal cord
tract
to CN motor nuclei
MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Medulla
CLICK

trigeminal (CN V)
spinal nucleus

CROSS

pyramidal
decussation

to lumbar spinal cord


to cervical spinal cord pyramid

MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Spinal Cord - Cervical
CLICK

ventral white
commissure
lateral
corticospinal
tract

CROSS PF DF
PE DE Regions of the ventral horn
that innervate…
- proximal flexors = PF
- distal flexors = DF
- proximal extensors = PE
ventral horn - distal extensors = DE

anterior
to lumbar spinal cord corticospinal
to cervical spinal cord tract

MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Spinal Cord - Thoracic
CLICK

lateral
corticospinal
tract

anterior
to lumbar spinal cord corticospinal
tract

MAIN SECTION
CORTICOSPINAL/
CORTICOBULBAR
Spinal Cord - Sacral
CLICK

lateral ventral white


corticospinal commissure
tract

CROSS

ventral horn
anterior
to lumbar spinal cord corticospinal
tract

MAIN SECTION
RUBROSPINAL/
TECTOSPINAL
Midbrain
CLICK input from forebrain

dorsal tegmental superior colliculus


decussation

ventral tegmental
decussation
red nucleus

rubrospinal
tectospinal

MAIN SECTION
RUBROSPINAL/
TECTOSPINAL
Pons
CLICK
tectospinal tract

rubrospinal tract
pontine reticular
formation

rubrospinal
tectospinal

MAIN SECTION
RUBROSPINAL/
TECTOSPINAL
Medulla
CLICK tectospinal
MLF
tract

medullary
reticular
formation
rubrospinal
tract

rubrospinal
tectospinal

MAIN SECTION
RUBROSPINAL/
TECTOSPINAL
Medulla
CLICK

trigeminal (CN V)
spinal nucleus

rubrospinal
tract

pyramidal
decussation
tectospinal
tract
rubrospinal
tectospinal pyramid

MAIN SECTION
RUBROSPINAL/
TECTOSPINAL
Spinal Cord - Cervical
CLICK

rubrospinal
tract

rubrospinal tectospinal
ventral horn
tectospinal tract

MAIN SECTION
RUBROSPINAL/
TECTOSPINAL
Spinal Cord - Lumbar
CLICK

rubrospinal
tract

ventral horn

rubrospinal

MAIN SECTION
RETICULOSPINAL
CLICK Pons
medial longitudinal pontine reticular
fasciculus (MLF) formation

medial reticulospinal tract


lateral reticulospinal tract

MAIN SECTION
RETICULOSPINAL
CLICK Medulla
MLF

medial reticulospinal tract


lateral reticulospinal tract

MAIN SECTION
RETICULOSPINAL
CLICK Medulla

MLF

medial reticulospinal tract


lateral reticulospinal tract

MAIN SECTION
RETICULOSPINAL
CLICK Spinal Cord - Cervical

medial reticulospinal tract


lateral reticulospinal tract

MAIN SECTION
RETICULOSPINAL
CLICK Spinal Cord - Thoracic

medial reticulospinal tract


lateral reticulospinal tract

MAIN SECTION
RETICULOSPINAL
CLICK Spinal Cord - Lumbar

medial reticulospinal tract


lateral reticulospinal tract

MAIN SECTION
VESTIBULOSPINAL
CLICK Pons
medial longitudinal fasciculus (MLF)
lateral vestibular
nucleus

medial vestibular
nucleus

medial vestibulospinal tract


lateral vestibulospinal tract

MAIN SECTION
VESTIBULOSPINAL
CLICK Medulla
MLF

medial vestibulospinal tract


lateral vestibulospinal tract

MAIN SECTION
VESTIBULOSPINAL
CLICK Spinal Cord - Cervical

medial vestibulospinal tract


lateral vestibulospinal tract

MAIN SECTION
VESTIBULOSPINAL
CLICK Spinal Cord - Thoracic

lateral vestibulospinal tract

MAIN SECTION
VESTIBULOSPINAL
CLICK Spinal Cord - Lumbar

lateral vestibulospinal tract

MAIN SECTION
Brainstem Atlas

• Open Medulla
• Lower Pons
• Middle Pons
• Upper Pons
• Midbrain

MAIN
Medial Syndrome
Lateral Syndrome Open Medulla
medial vestibular nucleus
CN XII medial longitudinal
nucleus fasciculus dorsal motor nucleus
medial lemniscus of the vagus

nucleus of
the solitary
spinal trigeminal tract
tract
inferior
cerebellar
spinal trigeminal peduncle
nucleus
solitary tract

inferior olivary
fibers nucleus
ambiguus

inferior olivary
pyramids nucleus

nucleus raphe magnus

MAIN SECTION
Medial Syndrome
Lateral Syndrome Lower Pons
medial vestibular nucleus
medial medial longitudinal
CN VI
lemniscus fasciculus lateral vestibular nucleus
nucleus

lateral CN VII motor nucleus


lemniscus

raphe
nuclei

middle
superior olivary
cerebellar
nuclear complex
peduncle

pontine fibers spinothalamic tract

pontine nuclei
corticospinal tract

MAIN SECTION
Medial Syndrome
Lateral Syndrome Middle Pons
CN V
mesencephalic
CN V main CN V motor nucleus
sensory nucleus nucleus
CN V
mesencephalic
tract

lateral
lemniscus

MAIN SECTION
Medial Syndrome
Lateral Syndrome Upper Pons
medial longitudinal
fasciculus

central tegmental locus coeruleus


bundle

parabrachial region
medial lemniscus

periaqueductal gray

corticospinal
tract

pontocerebellar fibers

MAIN SECTION
superior [inferior is caudal] colliculus
Midbrain
periaqueductal gray
superior cerebellar
peduncle
Click here to expand this
region
medial
lemniscus

red nucleus

cerebral peduncle

CN III

Tegemental Syndrome
Ventral Syndrome

MAIN SECTION
Brainstem Syndromes

• Medial Medullary
• Lateral Medullary
• Medial Inferior Pontine
• Lateral Inferior Pontine
• Medial Mid-Pontine
• Lateral Mid-Pontine
• Medial Superior Pontine
• Lateral Superior Pontine
• Tegmental
• Ventral

MAIN
Medial Medullary Syndrome
CN XII medial longitudinal
nucleus fasciculus
medial lemniscus

Loss of vestibuloocular reflex*


Tongue paralysis
Loss of fine touch (contralateral)
Cerebellar ataxia
Limb paralysis (contralateral)
inferior olivary
fibers

pyramids * VOR might be preserved


because this is below the level of
the vestibular nuclei

ARTERY: anterior spinal artery MAIN SECTION


Lateral Medullary Syndrome
CN V spinal
nucleus

nucleus
ambiguus

descending
symapthetic
tract Loss of facial pain/temp sensation
(ipsilateral)
Hoarseness, difficulty swallowing
Horner’s syndrome, ipsilateral loss of
sweating
dorsal Cerebellar ataxia
spinocerebellar Loss of body pain/temp sensation
tract (contralateral)

spinothalamic tract

ARTERY: posterior inferior cerebellar artery (PICA) MAIN SECTION


Medial Inferior Pontine Syndrome
medial
CN VI
longitudinal
medial nucleus
fasciculus
lemniscus

Loss of vestibuloocular reflex


Loss of lateral rectus (ipsilateral)
Loss of fine touch (contralateral)
Cerebellar ataxia
Limb paralysis (contralateral)
pontine fibers

corticospinal tract

ARTERY: paramedian branches of the basilar artery MAIN SECTION


Lateral Inferior Pontine Syndrome
CN V spinal
nucleus
spinothalamic
tract

Loss of facial pain/temp sensation


(ipsilateral)
Loss of body pain/temp sensation
CN VIII (contralateral)
Hearing deficit (ipsilateral), vertigo
Facial paralysis (ipsilateral)

CN VII

ARTERY: anterior inferior cerebellar artery (AICA) MAIN SECTION


Medial Mid-Pontine Syndrome

Limb paralysis (contralateral)


corticospinal
tract Facial paralysis
Cerebellar ataxia

corticobulbar
tract

corticopontine/
pontocerebellar fibers

ARTERY: paramedian branches of the basilar artery MAIN SECTION


Lateral Mid-Pontine Syndrome
CN V main CN V motor
sensory nucleus nucleus

lateral
lemniscus

Weakened mastication
Loss of facial sensation (ipsilateral)
No deficit reported

ARTERY: circumferential branches of the basilar artery MAIN SECTION


Medial Superior Pontine Syndrome
medial longitudinal
fasciculus

central tegmental
bundle

medial lemniscus

Loss of vestibuloocular reflex


Soft palate temor
Loss of fine touch (contralateral)
Limb paralysis (contralateral)
Cerebellar ataxia

corticospinal
tract

pontocerebellar fibers

ARTERY: paramedian branches of the upper basilar artery MAIN SECTION


Lateral Superior Pontine Syndrome
superior cerebellar
peduncle

spinothalamic tract

medial lemniscus
Cerebellar ataxia
Loss of body pain/temp sensation
(contralateral)
Loss of fine touch (contralateral)

pontocerebellar
fibers

ARTERY: superior cerebellar artery MAIN SECTION


Tegmental Syndrome
superior cerebellar
peduncle

medial
lemniscus

Cerebellar ataxia
Loss of fine touch to body and face
(contralateral)
red nucleus
No deficit reported
Loss of pupil constriction; lateral
strabismus

CN III

ARTERY: paramedian branches of the basilar a. / posterior cerebral a. MAIN SECTION


Ventral Syndrome

Paralysis (contralateral)
Loss of pupil constriction; lateral
strabismus

cerebral peduncle

CN III

ARTERY: paramedian branches of the basilar a. / posterior cerebral a. MAIN SECTION


Somatosensory
• Ascending Somatic Pathways
– Fine Touch
– Pain/Temperature
– Proprioception
• Lesions
– Peripheral
– Spinal Cord
– Forebrain
• Peripheral Receptors
• Somatosensory Cortex
• Somatosensory Plasticity

MAIN
Lesions - Peripheral

Lesion location Sensory loss Distribution


Peripheral nerve All sensation Distribution of the nerve
Peripheral neuropathy Large myelinated fibers Bilateral, “stocking-glove”
first
Single dorsal root None
Several dorsal roots All Ipsilateral dermatomal
(fine touch less affected
than pain/temp)

MAIN SECTION
Lesions - Spinal Cord

Lesion location Sensory loss Distribution


Central cord, early Pain/temp Bilateral, at level of lesion
Dorsal column Fine touch, position Ipsilateral, from lesion on
down
Anterolateral column Pain/temp Contralateral, from lesion
on down
Hemi-transection of cord Fine touch, position Ipsilateral, lesion on down
Pain/temp Contralat., lesion on down
Complete cord All sensation Lesion on down
transection

MAIN SECTION
Lesions - Forebrain

Lesion location Sensory loss Distribution


Thalamus All sensation Contralateral (peri-oral
facial sparing from ipsi
fibers)
Cortex Varies by location of Contralateral
lesion

MAIN SECTION
Peripheral Receptors

Click on a receptor:

Merkel’s disk
Epidermis

free nerve ending

Dermis
Meissner’s corpuscle

Pacinian corpuscle

Ruffini ending

MAIN SECTION
Merkel’s Disk
Discriminative Touch Mechanoreceptor

Location: Epidermis
Specificity: Steady skin indentation – form, texture
Dynamics: Slow-adapting
Spatial Range: Small receptive field (3-4 mm fingers, 30-40 cm trunk)
2-point discrimination threshold = 1 mm fingers, 10 cm trunk
Conduction: Aδ fiber – 25 m/s

MAIN SECTION RECEPTORS


Meissner’s Corpuscle
Discriminative Touch Mechanoreceptor

Location: Dermis
Specificity: Flutter; contact and movement
Dynamics: Fast-adapting
Spatial Range: Small receptive field (3-4 mm fingers, 30-40 cm trunk)
2-point discrimination threshold = 1 mm fingers, 10 cm trunk
Conduction: Aδ fiber – 25 m/s

MAIN SECTION RECEPTORS


Pacinian Corpuscle
Discriminative Touch Mechanoreceptor

Location: Subcutaneous tissue


Specificity: Non-localized vibration
Dynamics: Fast-adapting
Spatial Range: Large receptive field
Conduction: Aδ fiber – 25 m/s

MAIN SECTION RECEPTORS


Ruffini Ending
Discriminative Touch Mechanoreceptor

Location: Dermis
Specificity: Low frequency stimulation
Dynamics: Slow-adapting
Spatial Range: Large receptive field
Conduction: Aδ fiber – 25 m/s

MAIN SECTION RECEPTORS


Free Nerve Ending
Pain/Temperature Receptor

Aδ C
Specificity Cold or fast pain Warmth or slow pain

Conduction 25 m/s (myelinated) <1 m/s (unmyelinated axon, 1-2 um


diameter)

MAIN SECTION RECEPTORS


Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

3a
M1
lateral sulcus
S2 posterior
parietal lobule

Click here for S1 topography


Click here for S1 histology

MAIN SECTION
Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

3a
M1
lateral sulcus
S2 posterior
parietal lobule

Click here for S1 topography


S1 – Area 3a
Click here for S1 histology
• Input from thalamic shell (muscles, joints, deep
mechanoreceptors)
• RFs similar to periphery
MAIN SECTION
Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

3a
M1
lateral sulcus
S2 posterior
parietal lobule
S1 – Area 3b
• Input from thalamic core (VPM/VPL - cutaneous) Click here for S1 topography
• Each column within 3b is specific for one type of Click here for S1 histology
cutaneous receptor
• Smallest RFs
MAIN SECTION
Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

3a
M1
lateral sulcus
S1 – Area 1 S2 posterior
• Input from 3b and thalamic core (cutaneous) parietal lobule
• Large, complex RFs – combine info from multiple
receptor types Click here for S1 topography
• Sensitive to motion, direction, orientation Click here for S1 histology
• Primarily tactile info
• LESION  trouble describing texture
MAIN SECTION
Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

3a
M1
lateral sulcus
S1 – Area 2 S2 posterior
• Input from 3a, 3b and thalamic core (cutaneous) + parietal lobule
shell (muscle)
• Large, complex RFs Click here for S1 topography
• Combines tactile and muscle info Click here for S1 histology
• LESION  poor stereognosis, can’t pick up small
objects or maneuver hand through tight places
MAIN SECTION
Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

S2 3a
• Input from S1 and thalamus
lateral sulcus
M1

• Two complete maps S2 posterior


• Complex RFs with influence of behavioral state parietal lobule
• Collosal connections:
– Bilateral RFs Click here for S1 topography
– Interhemispheric transfer of learned info Click here for S1 histology
• LESION  problems with tactile discrimination,
interhemispheric transfer of learned info
MAIN SECTION
Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

3a
M1
lateral sulcus
S2 posterior
parietal lobule
Area 5
• Input from area 2 (S1) Click here for S1 topography
• Cutaneous plus movement Click here for S1 histology
• Very complex RFs: Multi-joint, multi-limb
• Responds differently to active and passive movement
MAIN SECTION
Somatosensory Cortex
postcentral gyrus intraparietal sulcus Click on an area:
central sulcus
posterior
parietal lobule central intraparietal
postcentral gyrus – S1
sulcus sulcus

1 7

2
3b
4 5

3a
M1
lateral sulcus
S2 posterior
parietal lobule

Area 7 Click here for S1 topography


• High order visual area Click here for S1 histology
• Activity reflects spatial properties of visual stimuli
• Large RFs, prominent effects of behavioral relevance
MAIN SECTION
Somatosensory Topography

• Face lies near fingers, not neck


and head

• Area devoted to each body part


reflects the density of sensory
innervation

• Extremely distorted

• All areas of S1 (3a, 3b, 1, 2) have


complete maps

• S2 has two complete maps

MAIN SECTION
Somatosensory Cortex

I
II

III

IV small granule cells

precentral gyrus postcentral gyrus


MOTOR SENSORY V

VI

MAIN SECTION
Somatosensory Plasticity
• Finger amputated  corresponding cortical areas are
taken over by adjacent finger representations

• Limb amputated  (1) smaller “phantom limb” is


perceived; (2) tactile acuity on stump increases, and its
stimulation results in sensation on the phantom limb
– Possibly due to the stump taking over cortical territory

• Better recovery if nerve is crushed rather than


severed/reattached
– Regenerating axons might follow their Schwann cell tubes

• Plasticity does not require damage


MAIN SECTION
Pain

• Types of Pain
– Nociceptive
– Inflammatory
– Neuropathic
• Central Pain Modulation
• Sensitization
– Peripheral
– Central

MAIN
Nociceptive Pain
TISSUE ACTIVATE
INJURY NOCICEPTORS

Types of Nociceptors

MAIN SECTION
Inflammatory Pain
INFLAMMATORY
MEDIATORS
INSULT

NOCICEPTOR
ACTIVATION

MAIN SECTION
Neuropathic Pain
REPETITIVE STRESS
LESION
INJURY (TO NERVES)

PAIN

MAIN SECTION
Types of Nociceptors
Fiber type
Channel types
Nociceptor Responds to… Myelination Type of pain
(Transduction)
Conduction

Thermal Extreme temperature Aδ Sharp, stinging, well TRP (Transient Receptor


Potential)
(>45oC or < 5oC) Light myelin localized
5-30 m/s
Mechanical Intense pressure Aδ Sharp, stinging, well DEG/ENaC (ASIC
Light myelin localized - Acid Sensing Ion Channel)

5-30 m/s Maybe TRP

Polymodal Extreme temperature C fibers Dull aching or DEG/ENaC (ASIC)


Intense pressure No myelin burning, prolonged,
Noxious chemicals 1 m/s poorly localized

• Location: Everywhere but the CNS


• Neurotransmitters:
– All are excitatory glutamatergic (AMPA, NMDA, kainate, metabotropic)
– Some express peptide NTs like substance P, CGRP, NPY
MAIN SECTION
CLICK Central Pain Modulation
PAG
Electrically stimulate
or apply opiates here

nucleus raphe
magnus (NRM)

via dorsolateral funiculus

NOTE:
1) Dorsal horn neuron also receives dorsal horn
descending pain-facilitation inputs.
2) Serotonin has other indirect effects,
involving opiate receptors and
enkephalins.

inhibits
5-HT

dorsal horn neuron NRM projection


(ascending pain afferent) terminus

MAIN SECTION
CLICK Sensitization - Peripheral
Injury Sensitization can occur via:
1) Potentiation of sensory transduction channel function
2) Enhancement of neuronal excitability

Release bradykinin, prostaglandins


dorsal root ganglion
activate/
sensitize

dorsal horn

nociceptor /
peripheral ending excite

histamine

degranulation

stimulate

mast cell

MAIN SECTION
CLICK Sensitization - Central
Limbic augmentation Repeated stimulation
(anxiety, anticipation, etc.) + (e.g., by nociceptors)

Hyperphosphoryl-
ation of ion channels
nociceptor in dorsal horn
terminus neurons

dorsal horn .. .
.
P
P P Increased
excitability of dorsal
horn neurons
P P
P

dorsal horn ion


neuron channels

Chronic
pain

MAIN SECTION
Motor

• Motor Pathways
• Deficits/Lesions
• Motor Cortex
• Reflexes
• Posture
• CN VII
• Basal Ganglia
• Cerebellum

MAIN
Motor Pathways
• Motor input to CN nuclei: Corticobulbar tract

• Lateral descending motor pathway


– Corticospinal tract
– Control of voluntary limb movements (distal body parts)

• Medial descending motor pathway


– Vestibulospinal, tectospinal, reticulospinal tracts
– Control of postural movements (proximal body parts)

• Other:
– Rubrospinal tract is involved in voluntary limb movements

MAIN SECTION
Motor Deficits

Negative Deficit Positive Deficit


Severing a Fibrillation
Weakness or paralysis
motor nerve (spontaneous firing of single muscle fibers)

Disease of Fasciculation
Weakness or paralysis (spontaneous firing of an axon  twitch of
motor neurons all fibers in the motor unit)

Damage to the descending pathways

MAIN SECTION
Damage to Descending Pathways
• Effect on stretch reflexes
– Autonomous and overactive (exaggerated)
– Claspknife reaction
• Passively extend limb  spindle stretch-induced contraction (resistance) 
activate GTO  sudden relaxation
– Clonus
• Rhythmic contraction-relaxation tremor
• Occurs when you suddenly stretch a muscle and hold at a longer length
• Due to cyclic alternations of stretch reflex, GTO, and Renshaw inhibition

• Effect on pain-sensing reflexes


– Flexor spasms
• Extreme maintained flexion of leg at foot, knee, and hip
• Due to hyperactive pain reflexes
– Babinski response
• Big toe moves up when sole of foot is sharply stimulated
• Normal in infants
• In adults, is the first sign of hyperactive pain reflexes

MAIN SECTION
Cortical Regions
Area 6 M1 (Area 4) central sulcus
PMA SMA
S1
Area 5 posterior
prefrontal parietal
cortex cortex
Area 7

PMA = premotor area


Click: SMA = supplementary motor area
Primary motor cortex
Secondary motor cortical areas
Somatosensory cortical areas

MAIN SECTION
Primary Motor Cortex (M1)
• Motor cortical neurons fire to cause voluntary movement (via corticospinal/
corticobulbar pathways)
– Lesions in this pathway (prior to synapse in the spinal cord ventral horn) result in
“upper motor neuron” deficits
• Impaired movement at individual joints
• Weakness
• Increased sensitivity and magnitude of spinal reflexes (stretch & nociceptive)
– Irritation in the cortex can cause seizures
• Focal (face or arm or leg) or “marching” (face  arm  leg)

• Columnar organization
– Different neurons code for muscle force, joint position, movement direction

• Specialty: Moving single digits – must actively hold other digits still (digits 3, 4,
5 have individual tendons but just one muscle)

• Access M1 by conscious thought over pathways from frontal and parietal


cortex

M1 topography M1 histology

MAIN SECTION CORTEX


Motor Cortex Topography

• Distal body parts have greater


representation than proximal
body parts

• Map is over-detailed – in reality,


cortical lesions affect entire body
regions (face, arm, leg) and not
smaller parts

• Corticospinal neurons are the


largest in the leg area

• M2 map is more diffuse than M1

MAIN SECTION CORTEX


Motor Cortex

I
II

III

contains large
V pyramidal Betz cells

precentral gyrus postcentral gyrus


MOTOR SENSORY

VI

Gigantocellular pyramidal cells of Betz (layer V)


• Cells of origin of the corticospinal fibers
• Provide much of the direct projection onto MNs
• Present in M1 only

MAIN SECTION CORTEX


Secondary Motor Cortical Areas
SMA, PMC, PFC

• High level planning of movements

• Thinking about movements without actually


making them

• Arm the transcortical reflexes – click here for more info

MAIN SECTION CORTEX


Reflexes

• Muscle Spindle
• Golgi Tendon Organ
• Reciprocal Inhibition
• “Crossed Extension” Flexor Reflex
• Locomotion
• Transcortical Reflex

MAIN SECTION
CLICK Muscle Spindle
chain fiber bag fiber
1a or II
afferent

γ1- or 1a*
γ2-MN to spinal
quadriceps
cord

α-MN II*

from
spinal
muscle spindle cord
γ1-MN*

biceps tendon
γ2-MN*
1) Hit tendon
2) Spindle stimulated (1a, II)
3) α-MN fires  muscle contracts
Renshaw cell stimulated α-MN * * click on label for details
γ-MN fires  spindle fibers contract
Muscle spindle is involved in…
4) Renshaw cell inhibits α-MN
(click here)

MAIN SECTION REFLEXES


CLICK Golgi Tendon Organ (GTO)
Ib
afferent GTO

inhibitory interneuron

to spinal
α-MN
cord Ib afferent
1) High muscle tension (force)
2) GTO stimulated (Ib)
3) Interneuron inhibits α-MN
from
4) α-MN decreases firing
spinal
5) Decreased muscle tension
cord α-MN

Roles of the GTO:


GTO is involved in:
• Protect against hurtful muscle stretch
• Clonus
• Servo-control force (e.g., combat
weakness due to muscle fatigue) • Claspknife reflex

MAIN SECTION REFLEXES


CLICK Reciprocal Inhibition
1a afferent

muscle spindle
α-MN to
agonist
agonist muscle
(flexor)
inhibitory ACTIVATED
interneuron

α-MN to
antagonist

antagonist muscle
(extensor)
INHIBITED

MAIN SECTION REFLEXES


“Crossed Extension” Flexor Reflex

• Involves the spinal cord bilaterally


• Flexion of one limb evokes extension of the opposite
limb

Applications
• Spinal withdrawal reflex
– Hurtful stimulus  withdraw stimulated limb + extend opposite
limb
• Locomotion
– Brainstem activity  oscillation of leg flexion and extension

MAIN SECTION REFLEXES


Locomotion Modulation
motor cortex

midbrain locomotor
region (MLR)

corticospinal tracts

reticulospinal tract

Modify locomotory
Initiate locomotory activity activity for voluntary
in spinal cord circuits corrections of gait
(obstacle avoidance)

MAIN SECTION REFLEXES


CLICK Transcortical Reflexes
SMA pyramidal tract
neuron (PTN)

1) SMA “sets” PTN by low-level firing


- Conscious intent (willing the reflex to occur)

2) Muscle is stretched (or skin is touched)

3) Muscle spindle sends 1a afferent to thalamus  PTN

4) PTN fires and stimulates MNs in the ventral horn

5) α-MN and γ-MN fire

6) Muscle contracts  length is restored

Prefrontal lesion  “set signal” is lost 


motor cortex is hyperactive

1a afferent Hyperactive Hyperactive long


palpatory reflex loop stretch reflex
(“involuntary (“Gegenhalten” –
grasp reflex”) resistance to limb
γ-MN displacement)
These are involuntary
α-MN
MAIN SECTION REFLEXES
Normal Postural Reflexes
Vestibulospinal reflexes can act ALONE if you tilt your head up/down without extending/flexing your neck.
Tonic neck reflexes can act ALONE if you extend/flex your neck without tilting your head up/down.

If you combine head tilt with neck flexion/extension, either… Tips for learning this chart
- the tonic neck reflex will CANCEL the vestibulospinal reflex, or
- the tonic neck reflex will ADD to the vestibulospinal reflex. Abnormal Posture

Head up Head normal Head down


Neck extended

The TNR involves…


- the reticulospinal pathway
for somatosensory input.
VSR alone - the tectospinal pathway
TNR alone for visual input.
VSR – TNR
Neck normal

VSR + TNR To maintain balance, you must


have two of the following:
- Somatosensory input
- Visual input
- Vestibular input
Neck flexed

VSR = vestibulospinal reflex


TNR = tonic neck reflex

MAIN SECTION
Normal Postural Reflexes
1) Vestibulospinal
Know that for VSR alone
reflexes can(head movement
act ALONE only),
if you head
tilt your up 
head forelimbs
up/down flex &extending/flexing
without hindlimbs extendyour(andneck.
opposite
Tonic neckifreflexes
head is can
down).act ALONE if you extend/flex your neck without tilting your head up/down.
2) Know that for TNR alone (neck movement only), neck extended  forelimbs extend & hindlimbs flex (and
If opposite
you combineif neck is flexed).
head tilt with neck flexion/extension, either…
3) - Combining a head movement
the tonic neck reflex will CANCEL and neck movement: reflex, or
the vestibulospinal
• If the limb positions resulting from VSR and TNR agree, then the reflexes add (limb hyper-extension/flexion).
- the tonic neck reflex will ADD to the vestibulospinal reflex.
• If the limb positions resulting from VSR and TNR disagree, then the reflexes cancel (no limb movement).

Head up Head normal Head down


Neck extended

The TNR involves…


- the reticulospinal pathway
for somatosensory input.
VSR alone - the tectospinal pathway
TNR alone for visual input.
VSR – TNR
Neck normal

VSR + TNR To maintain balance, you must


have two of the following:
- Somatosensory input
- Visual input
- Vestibular input
Neck flexed

VSR = vestibulospinal reflex


TNR = tonic neck reflex

MAIN SECTION
Abnormal Posture
• Flexion of upper limb,
DECORTICATE

extension of lower limb, When the head is passively


slight intorsion of legs turned to one side, the
looked-at limbs will extend
• Hyperactive vestibulo-
and the others will flex.
spinal AND tonic neck
reflexes (see right)
This is normal in infants but is
• Caused by a lesion of a sign of corticospinal lesion
the internal capsule in adults.
(corticospinal pathway)

• Extension of all four limbs, extension of neck, slight intorsion of legs


DECEREBRATE

• Used normally when riding a bike


• Hyperactive vestibulospinal reflexes – no tonic neck reflex
• Caused by a lesion of the upper pons or midbrain (medial descending
motor pathways)
– Damage the tectospinal and corticospinal pathways
– Vestibulospinal pathway remains intact
• Usually more serious than internal capsule injury (decorticate posture)

MAIN SECTION
CN VII Innervation
R L

to upper facial muscles (left)

to lower facial muscles (left)

CN VII nuclei

NORMAL
Click on a lesion site (circled in purple)

MAIN SECTION
CN VII Innervation
R L

to upper facial muscles (left)

X
to lower facial muscles (left)

CN VII nuclei

Lesion of left peripheral CN VII


- Left UPPER and LOWER facial weakness
- Cannot wrinkle forehead, brow droops, nasolabial fold diminished, mouth droops

MAIN SECTION
CN VII Innervation
R L

to upper facial muscles (left)

to lower facial muscles (left)

CN VII nuclei

Lesion of right motor cortex, internal capsule, midbrain, or upper pons


- Left LOWER facial weakness only
- Upper facial muscles still have innervation from the left corticobulbar tract
- Nasolabial fold diminished, mouth droops

MAIN SECTION
Basal Ganglia
ROSTRAL
Lenticular nucleus = Globus pallidus + Putamen
Striatum = Globus pallidus + Putamen + Caudate

Connections NTs
Selection-Brake
Diseases
CAUDAL

Caudate

Putamen

Nucleus accumbens Subthalamic nucleus (STN)

Globus pallidus, externa (GPe) Substantia nigra – click here


- pars reticulata (SNpr)
Globus pallidus, interna (GPi) - pars compacta (SNpc)
Amydala (part of lymbic system)
MAIN SECTION
Substantia Nigra - Histology

SNpc SNpr
dopaminergic GABAergic

MAIN SECTION BG
Basal Ganglia Neurotransmitters

• Dopamine
• GABA
• Enkephalin
• Substance P
• Glutamate
• ACh

NOT norepinephrine

MAIN SECTION BG
CLICK Basal Ganglia Connections
cerebral cortex
= excitatory (Glu)
= inhibitory (GABA)
= mixed (DA)
= unknown
SC = superior colliculus
caudate / putamen
PPPA = peri-pedunculo-pontine area
VA/VL = ventroanterior/ventrolateral
nuclei of thalamus VA/VL

SNpc
GPe STN

The caudate and putamen receive most of the basal gangia


input from the cerebral cortex.

The caudate/putamen send some info to the SNpc, which GPi


sends info back.

But most of the caudate/putamen output goes to the GP and SNpr. SNpr PPPA
The SNpr projects outside the basal ganglia to control head/eye movements.

The GP (GPi, specifically) sends most of the inhibitory input to the


thalamus.
GPi also projects to the PPPA, probably for postural control. SC brainstem/
The globus pallidus (GPe and GPi) are both in communication with the STN. spinal cord
Show selection-brake mechanism
MAIN SECTION BG
CLICK Basal Ganglia Connections
cerebral cortex
= excitatory (Glu)
= inhibitory (GABA)
= mixed (DA)
= unknown
SC = superior colliculus
caudate / putamen
PPPA = peri-pedunculo-pontine area
VA/VL = ventroanterior/ventrolateral
nuclei of thalamus VA/VL
= excitatory SNpc
= inhibitory GPe STN
Person wants to make a voluntary movement
Premotor/motor cortex excite STN
STN excites GPi GPi
GPi inhibits MPGs
SNpr PPPA
DIRECT path from caudate/putamen to GPi INHIBITS GPi
 Release the MPGs (those desired for the movement)

INDIRECT path from caudate/putamen  GPe  GPi SC brainstem/


DISINHIBITS GPi
spinal cord
 Shut down the MPGs (those interfering with the movement)

MAIN SECTION BG
Selection-Brake Hypothesis

• Basal ganglia outputs are inhibitory to the


thalamus and motor pattern generators (MPGs)

• When a movement is made…


– the BG outputs to the desired MPGs decrease their
firing rate (take off the brake).
– the BG outputs to interfering MPGs increase their
firing rate (put on the brake).

Click here for the selection brake mechanism

MAIN SECTION BG
Basal Ganglia Diseases
General Pathophysiology

• Damage to BG output cells removes tonic


inhibition from all motor pattern generators
(MPGs)
– Results in sustained contraction in all muscles,
agonist and antagonist
– MPGs operate independently and intermittently,
resulting in spontaneous involuntary movements

• Bradykinesia: slow movement

• Akinesia: lack of movement


Parkinson’s Disease Huntington’s Disease

MAIN SECTION BG
Parkinson’s Disease
• Caused by degeneration of the SNpc (dopaminergic)
– SNpc modulates putamen and caudate
– Putamen/caudate can no longer “focus” the GPi output

• Symptoms
– Rigidity, bradykinesia, akinesia, pill-rolling tremor
– Can be mimicked by taking dopamine receptor blockers

• Treatment
– Give oral L-dopa, a precursor to dopamine
• Too much L-dopa  develop chorea/hemiballismus (involuntary,
gesture/dance-like movements)
– Ablate or electrically stimulate the STN
• This causes chorea in normal subjects, but restores normal function
to Parkinson’s patients

MAIN SECTION BG
Huntington’s Disease
• Caused by damage of the caudate/putamen or
STN
– Results in excessive activity in the caudate/putamen

• Symptoms
– Chorea, athetosis, hemiballismus
• Writhing, purposeful-looking but involuntary movements
• Hemiballismus is specifically caused by STN lesion

• Treatment
– Drugs that block dopamine receptors in the putamen
– Is worsened by L-dopa or dopamine agonists (unlike
in Parkinson’s)

MAIN SECTION BG
Cerebellum

• Folium
• Cortical Cells
• Deep Nuclei
• Connections

MAIN SECTION
Cerebellar Folium
Click here to overlay cell
types/connections
molecular layer

Purkinje cell layer

granule cell layer

white matter

MAIN SECTION CB
Cerebellar Folium
Click on a cell type:
Purkinje cell
Climbing fiber
dendrite Granule cell
parallel fiber
Mossy fiber

dendrite synapse

Not shown (can click):


Stellate cell
terminal Basket cell
terminal (synapse)
Golgi cell

axon

to the deep nuclei

MAIN SECTION CB
Purkinje Cell
• One Purkinje cell receives
molecular layer

input from…
– One climbing fiber
Purkinje cell – Many parallel fibers (up to a
dendrite
million)
• Inter-Purkinje cell
connections via parallel fibers
granule cell layer

Purkinje allow motor coordination to


cell body occur

• Projects to and inhibits the


deep nuclear cells

MAIN SECTION CB
Climbing Fiber
• Cell bodies reside in the inferior
molecular layer

olive

• Projects to the Purkinje cell layer,


where one climbing fiber
synapses with one Purkinje cell
– Excitatory
– Climbing fiber input weakens the
granule cell layer

excitatory effect of parallel fibers


climbing
on the Purkinje cell
fiber

• Fire at high rates when learning


movement, low rates during
learned movement

MAIN SECTION CB
Granule Cell
• Receives input from mossy fibers
molecular layer

in the granule cell layer


parallel fiber – Extends “claws” to grab the
mossy fiber terminus

• Projects to molecular layer,


where the fiber then runs parallel
to the folia surface
– These “parallel fibers” synapse
granule cell layer

granule cell on and excite Purkinje cell


dendrites
• One synapse per Purkinje cell
• One parallel fiber connects many
Purkinje cells
– The coincidence of parallel and
climbing fiber excitation of the
Purkinje cell results in learning
related to coordination

MAIN SECTION CB
Mossy Fiber
• Originates in the…
molecular layer

– Spinocerebellar pathway
• Ascending (from spinal cord)
• Fibers do not cross
• Enters cerebellum through the
inferior cerebellar peduncle
– Pons
• Descending (from cerebral
cortex)
granule cell layer

mossy • These fibers must cross in the


fibers cerebral peduncles
(corticopontine fibers)
• Enter cerebellum through the
middle cerebellar peduncle

• Projects to the granule cell layer,


where it synapse on the “claws”
of the granule cells
– Excitatory

MAIN SECTION CB
Inhibitory Interneurons

Stellate cell
• Molecular layer

Basket cell
• Cell body in molecular layer
• Projections wrap around Purkinje cell
Purkinje cell
basket cell
body

Golgi cell
• Granule cell layer

MAIN SECTION CB
Cerebellar Deep Nuclei
• Receive inhibitory input from Purkinje cortical cells Click on a nucleus:
• Project to brainstem and thalamus – click here
Fastigial (medial) nucleus
• Each nucleus has a separate body map
• Help initiate movement – click here Globose/emboliform
(intermediate) nuclei
Dentate (lateral) nucleus

MAIN SECTION CB
Deep Nuclei and Movement

Deep nuclei probably help initiate movement


because…

• their stimulation results in movement.


• their damage delays movement initiation.
• they send excitatory projections to their targets.

MAIN SECTION CB
Nuclear Functions/Lesions
Nucleus Input Function Lesion results in…

Fastigial (medial) Vestibular Control upright stance Falls to the side of the
against gravity lesion
Globose/ Cerebral cortex Balance agonist and Ipsilateral action tremor
emboliform Spinal cord antagonist muscles at a during voluntary
(interposed) single joint movements (e.g. reaching)
Dentate (lateral) Cerebral Cortex (1) Combined digit (1) Incoordination of digits
movements (2) Overshoot targets in
(2) Arm/leg reaching to reaching with arm/leg
a visual target

• Movements involving multiple joints are more impaired than those


involving a single joint.
• Patients may try to compensate by moving more slowly or moving
one joint at a time.
• Lesions prevent several types of motor learning.

MAIN SECTION CB
Cerebellar Connections

All cerebellar projections are excitatory ventrolateral


thalamus

red nucleus

vestibular
nuclei

reticular
formation

MAIN SECTION CB
Autonomic Nervous System

• Efferents/Afferents
• Circumventricular Organs
• Functions
– Baroreceptor
– Respiration
– Micturition
• Periaqueductal Gray (PAG)

MAIN
Viscero-Motor Efferents / Visceral Afferents
Sympathetic Efferents
• Output arises from the intermediolateral (IML) cell column from T1 to L2
• Relay through sympathetic trunk
Parasympathetic Efferents
• Sacral output
– From cells similar to the IML in the sacral cord
– Relays through ganglion cells in the pelvic plexus
• Cranial output
– Runs in CN III, CN VII, CN IX, CN X
– Arises in nuclei associated with the CNs

Visceral Afferents
• Return to the CNS with sympathetic & parasympathetic efferent fibers
• Cell bodies are in dorsal root or CN ganglia
• Sympathetic afferents: Pain (synapse on cells of spinothalamic tract)
• Parasympathetic afferents: State of the viscera
– CN VII, CN IX, CN X
MAIN SECTION
CN III Parasympathetics
Pupillary Constriction and Accommodation

Edinger-Westphal nucleus

to pupilloconstrictor
and ciliary muscles

CN III nucleus

CN III
ciliary ganglion

MAIN SECTION
CN VII and IX Parasympathetics

Viscero-motor
• Parasympathetic fibers in CN VII and IX arise from
“salvatory/lacrimal nuclei”
– Scattered cells in the pons and upper medulla
– Relay through submandibular, pterygopalatine, otic ganglia
• Responsible for secretion from salvatory glands, lacrimal gland, and
other glands in mouth and nasal cavity

Visceral afferents
• Synapse in the nucleus of the solitary tract
• CN VII: Taste info
• CN IX: Info from carotid body/sinus, pharynx

MAIN SECTION
CN X Parasympathetics
dorsal nucleus of CN X nucleus of the solitary tract GUT

HEART

nucleus ambiguus

PHARYNX/
= secretomotor efferents LARYNX
= vasomotor efferents
= visceral afferents

MAIN SECTION
Circumventricular Organs
nucleus of the
solitary tract
area postrema

dorsal nucleus solitary


of CN X tract

CN XII
nucleus

• Area postrema, subfornical organ, organum vasculosum of the lamina terminalis


(OVLT)
– Small areas around the 3rd and 4th ventricles
• LACK a blood brain barrier
– Chemosensitive neurons detect circulating molecules/ hormones (AII, insulin,
vasopressin)
MAIN SECTION
= inhibitory
Baroreceptor Reflex
= excitatory
= parasympathetic
= sympathetic

rostral carotid sinus baroreceptors


ventrolateral
medulla aortic arch baroreceptors

nucleus of the
solitary tract

caudal
ventrolateral
medulla
nucleus
ambiguus

tonic

intermedio-
lateral column

peripheral arterioles
MAIN SECTION
Respiration = excitatory
= inhibitory
Lung stretch receptors
Carotid body chemoreceptors Forebrain Intrinsic chemoreceptors

Nucleus of the solitary tract Parabrachial nucleus

VENTROLATERAL Pre-Botzinger cells


MEDULLA
Respiratory rhythm

Ventral respiratory pre-motor cells

Rostral inspiratory Botzinger complex Caudal expiratory


Excitatory Reciprocal inhibition Excitatory

Phrenic motorneurons Int. intercostal motorneurons


Ext. intercostals Abdominal muscles

MAIN SECTION
= afferent
Micturition
= efferent
Hypothalamus, PAG

pontine micturition center Short loop reflex


(parabrahial region)
Long loop reflex

sacral spinal cord

bladder

MAIN SECTION
= afferent
Micturition
= efferent
Hypothalamus, PAG

pontine micturition center


(parabrahial region)

Short loop reflex


- Bladder stretch triggers bladder contraction
- Used by infants

sacral spinal cord

bladder

MAIN SECTION
= afferent
Micturition
= efferent
Hypothalamus, PAG

pontine micturition center


(parabrahial region)

Long loop reflex


- Hypothalamic/PAG input plus bladder stretch
info control bladder contraction
- Used by adults for better control of micturition
- GABAergic neurons play a role

sacral spinal cord

bladder

MAIN SECTION
Periaqueductal Gray (PAG)
• Integrates several autonomic reflexes

• Receives visceral afferent projections (like the parabrachial nuclei)

• Outputs: hypothalamus, amygdala, other forebrain areas

PAG region stimulated Evokes… In response to…


Lateral Fight or flight Superficial (escapable) pain
Ventrolateral Quiescence Deep (inescapable) pain

PAG

MAIN SECTION
Eye Movements / Ocular Dominance

Goal Eye movement Function


Vestibulo-ocular Use vestibular input to hold images stable on
Stabilize the eye when the head retina during brief/fast head movement
moves (reflexive) Optokinetic Use visual input to hold images stable on
retina during sustained/slow head movement
Saccade Bring new objects of interest into the fovea

Keep the fovea on a visual Smooth pursuit Hold image of a moving target on the fovea
target (volitional control)
Vergence Adjust the eyes for viewing distances in depth
(converge for near, diverge for far)

Ocular Dominance Columns

MAIN
CLICK Vestibulo-Ocular Reflex (VOR)
If the head moves left quickly, VOR causes the eyes to move right.

eye muscles But the VOR can get “out of tune” if it


operates alone. Therefore, a secondary
pathway (long latency, multisynaptic,
involving the visual system and cerebellum)
synapses on ocular motorneurons and
adjusts the gain of the reflex.
Secondary pathway motor nuclei to
(visual cortex  eye muscles
cerebellar flocculus) The VOR depends on the stimulation of
kinocilium in the vestibular labyrinth.

vestibular
semicircular
nuclear
canal
complex

MAIN SECTION
Optokinetic Reflex
• Senses motion of the visual background
(involves the extrastriate cortex)
• Nystagmus
– Slow phase: Compensatory tracking movements
(smooth pursuit)
– Fast phase: Anticipatory fast movement to reposition
eyes after they reach the edge of the orbit (saccade)
Eye position (degrees)

Time (sec)

MAIN SECTION
Ocular Dominance Columns (ODCs)
• Features of ODCs
– Located in V1
– Develop prenatally
– Visual input to each ODC is monocular (by looking out of one
eye, you drive just one set of ODCs)

• Development of binocular vision


– Requires visual experience and development of inter-ODC
connections
– Occurs during the critical period (60-90 days postnatally)

• Conditions that result in binocular vision impairment


– Strabismus: Misaligned eyes
• If subject becomes accustomed to using just one eye at a time, left
and right ODCs will never be co-stimulated and no inter-ODC
connections will develop
– Anisometropia: One eye more nearsighted than the other, due
to unilateral amblyopia (poor visual acuity)
• There is more metabolic activity in the non-amblyopic columns
MAIN SECTION
Click on a zone, nucleus, or button
Hypothalamus
Hypothalamic Inputs Anterior Pituitary
Physiological Regulation
Hypothalamic Outputs Posterior Pituitary

ZONE STRUCTURE(S)

Periventricular nucleus
PVZ Arcuate nucleus
Paraventricular nucleus
(not shown)

Dorsomedial nucleus
MHA Ventromedial nucleus

fornix
LHA Lateral hypothalamic area

PVZ = Periventricular zone


MHA = Medial hypothalamic zone
LHA = Lateral hypothalamic zone

OTHER
Supraoptic nucleus
Suprachiasmatic nucleus (not shown) median eminence

MAIN
Hypothalamic Nuclei

paraventricular nucleus

lateral
hypothalamic
area
fornix ventromedial
nucleus

fornix

arcuate
orexin cells? nucleus

median eminence
median eminence

MAIN SECTION
Hypothalamic Nuclei
anterior commissure

anterior
hypotha-
lamic area

fornix

median eminence

supraoptic nucleus suprachiasmatic nucleus

MAIN SECTION
Hypothalamic Nuclei
paraventricular nucleus

dorsomedial
nucleus
lateral
hypothalamic
area ventromedial
nucleus

fornix

optic tract
arcuate
nucleus
(dopa-
minergic
median eminence cells)

MAIN SECTION
Inputs to Hypothalamus

Type Structure Carries info about…


Extrinsic Reticular formation Temperature
Retina Light/dark cycle (to suprachiasmatic nucleus)
Nucleus of the solitary tract Taste, visceral sensation
Parabrachial nucleus
Olfactory cortex Food, sexual attractants
Amygdala, hippocampus, Cognition
prefrontal cortex (limbic input)
Circumventricular organs Osmolality of blood
Peptide hormones in blood (AII, atrial natiuretic factor)
Intrinsic Thermoreceptors Local blood temperature
Osmoreceptors Local CSF ionic strength
Chemoreceptors Hormones (e.g., leptin, ghrelin)

MAIN SECTION
Outputs from Hypothalamus

From… To… Effect


Lateral hypothalamus Autonomic nuclei in Control body temp (sweating, shivering,
Paraventricular nucleus spinal cord, brainstem vasoconstriction)
(PAG, parabrachial nuclei,
nucleus of the solitary tract,
dorsal vagal nucleus,
ventrolateral medulla, IML)
Releasing hormone neurons Median eminence Control of anterior pituitary
in periventricular zone
(arcuate nucleus and part of the
paraventricular nucleus)
Supraoptic and Posterior pituitary Secrete ADH, oxytocin
paraventricular nuclei
Scattered large neurons Cerebral cortex Not clear; presumably contribute to
Limbic structures hypothalamic control of behavior

MAIN SECTION
Anterior Pituitary
median periventricular
eminence zone of the
hypothalamus
(arcuate nucleus and
part of the paraven-
tricular nucleus)
Hypothalamic cell
axons terminate in the
median eminence and
secrete hormones into
the fenestrated pituitary CRH
portal capillaries TRH hypothalamic
GnRH releasing
GHRH
Somatostatin hormones
Dopamine

ACTH corresponding
TSH
LH/FSH anterior
GH pituitary
GH/TSH hormones
MSH

MAIN SECTION
Posterior Pituitary

supraoptic nucleus /
paraventricular nucleus

median
eminence

Hypothalamic cell
axons terminate in the
posterior pituitary and
secrete hormones into
the fenestrated pituitary Posterior pituitary hormones:
capillaries
- oxytocin
- ADH (vasopressin)

MAIN SECTION
The hypothalamus regulates…

• Body temperature
• Body weight
• Ionic balance
• Blood pressure (chronic)
• Circadian rhythm
• Reproduction
• Response to stress

MAIN SECTION
inputs

outputs/effects
Body Temperature
releasing hormone neurons
spinal cord
anterior hypothalamus
reticular formation
TSH, GH, somatostatin

lateral hypothalamus

autonomic nuclei

sweating, shivering, etc.

intrinsic cerebral cortex


thermoreceptors
behavior?

MAIN SECTION REG


inputs

outputs/effects
Body Weight
viscera (gut)
food intake, gut distension autonomic nuclei

NTS / parabrachial
nuclei

pituitary
tongue
taste

NTS

olfactory cortex
smell

fat cells  leptin suppress food intake /


(receptors in dorsomedial nucleus) increase metabolism

promote food intake /


gut  ghrelin decrease metabolism

orexin promote food intake /


stabilize sleep

MAIN SECTION REG


inputs

outputs/effects
Ionic Balance

circumventricular
organs
blood osmolality, peptide hormones

intrinsic posterior pituitary


osmorecptors
CSF tonicity
ADH

alter urine tonicity,


Na+ and H2O intake
vena cava / R atrium
blood volume

NTS

MAIN SECTION REG


inputs

outputs/effects
Blood Pressure (Chronic)

posterior pituitary
angiotensin II
ADH
circumventricular
organs vasoconstriction,
anti-diuretic action
on kidney

baroreceptors autonomic nuclei

NTS vasoconstriction

MAIN SECTION REG


inputs

outputs/effects
Circadian Rhythm
suprachiasmatic nucleus

couple the
circadian rhythm to
retina
the light/dark cycle

The suprachiasmatic nucleus of the hypothalamus (and the surrounding region) sets the circadian rhythm.
Input from the retina allows the cycle to be coupled to the light/dark cycle.

MAIN SECTION REG


inputs

outputs/effects
Reproduction

gonadal steroids

olfactory
system reproduction

amygdala /
hippocampus
emotion, memory

MAIN SECTION REG


inputs

outputs/effects
Response to Stress

CRH

ascending ACTH
catecholamine
systems glucosteroid release
from adrenal cortex
limbic system
change glucose
metabolism and
energy use

Glucosteroids can inhibit the hypothalamus to terminate the stress response.


Chronic glucocorticoids can cause neuronal and other damage, possibly contributing to post-traumatic
stress disorder, depression, and other disorders.

MAIN SECTION REG


Limbic System
Not shown: olfactory cortex
cingulate gyrus / cingulum

anterior
fornix
commissure

orbital/medial
prefrontal cortex

olfactory bulb stria terminalis

hippocampus
hypothalamus
amygdala
dentate gyrus
mammillary body
parahippocampal gyrus
MAIN
Amygdala
nucleus basalis of Meynert
central nucleus
Dorsal nuclei
medial nucleus

basal nucleus
amydala

Deep nuclei
accessory
basal nucleus PAC

entorhinal cortex lateral nucleus

Role

Inputs/Outputs
PAC = periamygdaloid complex

MAIN SECTION
The amygdala is involved in…
• Making cortical cells more responsive to other synaptic
inputs
– Most cells of the amygdaloid nuclei are cholinergic
– Help activate (desynchronize) cortex during waking state

• Fear conditioning
– Modulate brainstem reflexes in response to emotional status

• Recognizing fear in others


• Depression (may show increased activity)
• Kluver-Bucy Syndrome
– Associated with temporal lobe ablation
– Cannot recognize the significance of objects; loss of fear; failure
to learn

MAIN SECTION AMYG


inputs

outputs/effects
Inputs/Outputs
Amygdala
autonomic cell groups
ascending sensory lateral hypothalamus, PAG,
parabrachial nucleus, NTS, dorsal
system nucleus of CN X, ventrolateral medulla
visual, olfactory, auditory,
somatosensory
influence HR, BP,
MAJOR SHORTCUT
gut/bowel/respiratory/
bladder function, etc.
thalamic relay
nucleus

primary sensory
cortex

orbital/medial
secondary posterior prefrontal cortex
association intralaminar
cortex thalamic nuclei
determine whether
sensory stimulus is
rewarding or
The shortcut afferent pathway produces your initial “gut reaction” to a potentially aversive; set mood
threatening situation, before the major pathway kicks in.

MAIN SECTION AMYG


Olfactory Bulb
olfactory nerves

glomerular formations

mitral cells

granule cells

Mitral cells
• Principal relay cells
• Dendrites extend to the glomerular formations and synapse with olfactory receptor
neurons (reciprocal, dendritodentritic synapses)

Granule cells
• Deep
– Processes interact with mitral cell dendrites in the external plexiform layer
– GABAergic
• Superficial
– Synapse with mitral cell dendrites
– GABA (most), dopamine, neuropeptides (enkephalin, substance P, neurotensin)

MAIN SECTION
Olfactory Cortex
putamen
• At the junction of frontal and lateral striate
temporal cortices nucleus accumbens / arteries
olfactory tubercle
• Axons of mitral cells run in
olfactory tract to primary
olfactory tract
olfactory cortex

• Olfactory cortex is the major primary olfactory


center for odor detection and cortex
discrimination

• Efferent info is integrated with


other sensory modalities in the
orbital part of the frontal cortex

• Other outputs: amygdala,


hippocampus, hypothalamus,
mediodorsal thalamic nucleus

MAIN SECTION
Olfactory Cortex
putamen
• At the junction of frontal and lateral striate
temporal cortices nucleus accumbens / arteries
olfactory tubercle
• Axons of mitral cells run in
olfactory tract to primary
olfactory tract
olfactory cortex

• Olfactory cortex is the major primary olfactory


center for odor detection and cortex
discrimination

• Efferent info is integrated with Nucleus accumbens


- “Reward” center
other sensory modalities in the
- Contains mostly GABAergic neurons
orbital part of the frontal cortex - Receives input from the amygdala and hippocampus

• Other outputs: amygdala,


hippocampus, hypothalamus,
mediodorsal thalamic nucleus

MAIN SECTION
Hippocampus
tail of
caudate
Role
dentate gyrus
CA3
pre-subiculum
Inputs/Outputs
para-
CA1 subiculum
subiculum

Information Flow
inferior temporal area
entorhinal
cortex
Alzheimer’s Disease

MAIN SECTION
The hippocampus is involved in…
• Memory processing (especially for spatial orientation)
– Hippocampal “place cells” fire when animal is in a particular spatial
location, related to surrounding sensory stimuli

• Formation of new memories


– Hippocampal lesion  inability to form new memories (old memories
remain intact)

• Memory deficits following ischemia or seizures


– CA1 is the most commonly damaged brain area after ischemia or
epileptic seizures
• Ischemia  cells are depolarized  NMDA receptors allow Ca2+ and Na+ to
enter cell  more depolarization  excitotoxicity

• Kluver-Bucy Syndrome
– Associated with temporal lobe ablation
– Cannot recognize the significance of objects; loss of fear; failure to learn

• Alzheimer’s Disease

MAIN SECTION HIPP


inputs

outputs/effects
Inputs/Outputs
Hippocampus
hypothalamus

info from
multisensory
association cortical
areas prefrontal / cingulate
visual, auditory areas of inferior cortical areas
and superior temporal cortex

perirhinal/entorhinal
cortex

basal ganglia
(ventral)

MAIN SECTION HIPP


CLICK Hippocampus
tail of
caudate
Role
dentate gyrus
CA3
pre-subiculum
Inputs/Outputs
para-
CA1 subiculum
subiculum

Hide Information Flow


inferior temporal area
entorhinal
sensory inputs from cortex
Alzheimer’s Disease cerebral cortex

to the
neocortex

to frontal cortex, anterior


thalamus, hypothalamus

MAIN SECTION HIPP


Alzheimer’s Disease
β-amyloid plaques
CA1
CA3

DG
ParaSub
PreSub
Sub

CA1
EC

tangles (intracellular)

• Entorhinal cortex and CA1 are severely damaged during early Alzheimer’s
– High amounts of tangles in these areas
• Tangles develop before plaques, but plaques mark beginning of the disease
– Plaques are prevalent in the cerebral cortex outside the hippocampal formation

MAIN SECTION HIPP


Orbital/Medial Prefrontal Cortex (OMPC)
Orbital prefrontal cortex Medial prefrontal cortex

hypothalamus, PAG
assessment of food
control visceral
functions
reward/aversion
appropriate
choices

control
of mood

multimodal amygdala /
inputs
sensory inputs hippocampus
outputs/effects

MAIN SECTION
Sleep

• Electroencephalogram (EEG)
• Stages
• Ascending Reticular Activating System

MAIN
Electroencephalogram (EEG)

Synchronized waves Desynchronized waves

• High amplitude, low frequency • Low amplitude, high frequency

• Represent wave summation • Represent wave subtraction

• Result when similar events • Result when disparate events


coincide coincide

• Ex: δ waves of sleep • Ex: wakefulness, REM

MAIN SECTION
Stages of Sleep

• Stage 1: Alpha waves (still relatively desynchronized)


• Stage 2: Sleep spindles
• Stage 3-4: Delta waves (synchronized) – deep sleep, slow waves
• REM (Rapid Eye Movement):
– Very desynchronized but person is still asleep (“paradoxical”)
– No movement except for the extraocular and middle ear muscles, and penile erection
– Loss of thermoregulation
– Dreaming, sleep apnea occur; dreaming often reflects experiences over the past few days
– Initiated in the rostral pons, LGN, and occipital cortex
– Depends on cholinergic inputs from the upper pons to thalamus

These stages cycle several times throughout the night.

MAIN SECTION
Ascending Reticular Activating System
Nucleus basalis of Meynert (ACh) [not shown]
- Implicated in sleep and wakefulness
- Projects to all parts of forebrain except basal ganglia
- Histology

Laterodorsal tegmental nucleus (LDT) (ACh)

Pedunculopontine tegmental nucleus


(PPT) (ACh)

Locus coeruleus (norepinephrine)


- Contributes to changes in thalamocortical activity
- Histology thalamus

Raphe nucleus (5-HT)


- Caudal  spinal cord
- Rostral  all parts of forebrain
- Atlas

Thalamic relay nuclei (e.g., LGN)

Reticular nucleus (GABA)


- Receives synapses from thalamocortical, cortico-
thalamis axons (connect cortex and principal thalamic
nuclei) This system is active during wakefulness (and its stimulation causes
- Project back onto the principal thalamic nuclei waking). It is inactive during sleep (and its transection causes coma).
- Histology
Neurotransmitters Sleep Initiation

MAIN SECTION
Ascending Reticular Activating System
RAT BRAIN – Stained for GABA
Nucleus basalis of Meynert (Ach) [not shown]
- Implicated in sleep and wakefulness
- Projects to all parts of forebrain except basal ganglia
- Histology

Laterodorsal tegmental nucleus (LDT) (Ach)


reticular nucleus
Pedunculopontine tegmental nucleus
(PPT) (ACh)
ventrolateral
Locus coeruleus (norepinephrine)
thalamic nucleus
- Contributes to changes in thalamocortical activity
- Histology

Raphe nucleus (5-HT)


- Caudal  spinal cord
- Rostral  all parts of forebrain
- Histology

Thalamic relay nuclei (e.g., LGN)

Reticular nucleus (GABA)


- Receives synapses from thalamocortical, cortico-
thalamis axons (connect cortex and principal thalamic
nuclei) This system is active during wakefulness (and its stimulation causes
- Project back onto the principal thalamic nuclei waking). It is inactive during sleep (and its transection causes coma).

MAIN SECTION SYS


Neurotransmitter Systems
Ascending Reticular Activating System

Wakefulness Slow wave sleep REM sleep


Norepinephrine
ACTIVE INACTIVE INACTIVE
(locus coeruleus)
Serotonin
ACTIVE INACTIVE INACTIVE
(raphe nuclei)
ACh
ACTIVE INACTIVE ACTIVE*
(LDT/PPT)

Both norepinephrine and ACh facilitate the responsiveness of post-synaptic neurons.

* The ACh input here is responsible for the paradoxical situation in REM sleep.

MAIN SECTION SYS


CLICK
Sleep Initiation
SLEEP INITIATION
WAKEFULNESS

Add ascending
Remove ACh,ACh,
ascending NE, NE,
5-HT5-HT
inputinput
CORTEX
released  RN bursting
RN inhibition of TRN is blocked

respondrespond
TRN cells cannot to sensory input with
to sensory input
a tonic
and firefiring pattern (
in a rhythmic wakefulness)
bursting pattern thalamocortical
( sleep spindles in early sleep stages) neuron

RETICULAR
NUCLEUS

THALAMIC
RELAY
ACh
NUCLEUS
NE (TRN)
5-HT

= Excitatory (glutamate)
= Inhibitory (GABA)
sensory afferents
eye, spinal cord, etc.
MAIN SECTION SYS
Memory
Types of amnesia
• Anterograde
– Inability to form new memories post-trauma
– May be able to form short-term working memories (minutes), but
cannot hold them
• Retrograde
– Loss of memories from a few seconds to a couple years pre-trauma
– May have more distant memories

Types of memory Memory Disorders


• Implicit (e.g., procedural) • Alzheimer’s Disease
• Explicit (a.k.a declarative) • Lewy Body Dementia
• Working • Korsakov’s Syndrome

MAIN
Implicit Memory
Procedural

• Subconscious
– Skills/procedures/habits
– Simple classical conditioning

• Learned by repetition
• Examples: riding a bike, playing an instrument
• Brain regions involved:
– Striatum, cortex, cerebellum
– Not the hippocampus

MAIN SECTION
Explicit Memory
Declarative

• Conscious
– Episodic: places and events
– Semantic: names and facts

• Brain regions involved


– Medial temporal lobe (hippocampus and associated areas)
– Entorhinal and perirhinal cortices project to the hippocampus and are
especially important in memory

• Memory storage: Sensory association cortical areas


– Lateral temporal, parietal, posterior insular cortex
– Memory consolidation depends on the interaction between these areas
and the limbic structures

• Is affected in Korsakov’s Syndrome and most cases of amnesia

MAIN SECTION
Working Memory

• Short term (i.e., seconds to minutes)


• Example: holding a conversation
• Brain regions involved
– Prefrontal cortex, areas of the parietal and temporal
lobes (relatively unknown)
• Lesion to dorsolateral prefrontal cortex disrupts performance
on short delay tasks
– Not the hippocampus

MAIN SECTION
Korsakov’s Syndrome
• Lack of vitamin B1  damage along 3rd ventricle
– Seen in alcoholics due to vitamin deficiency
• Presentation
– Anterograde amnesia
– Patients do not have a good awareness of their amnesia (unlike patients
with medial temporal lobe lesion)
• Involves the mammillary bodies, dorsal thalamus, anterior thalamus

NORMAL KORSAKOV’S

3rd ventricle

mammillary bodies no mammillary bodies

MAIN SECTION
Lewy Body Dementia
• Closely related to Parkinson’s Disease
• Intracellular inclusions of protein α-synuclein 
neuronal dysfunction
• Dementia is similar to that found in Alzheimer’s

Lewy bodies

MAIN SECTION
Language Processing
CODES: Aphasia
• Visual / orthographic
• Auditory / phonological Note: This is not a thorough treatment of language
• Syntactic / grammatical processing, but these are the only questions I’ve
seen on past exams…
• Semantic / meaning
• Articulatory / speech motor planning

Evidence against the Wernicke-Gershwind model:


Existence of phonological and surface dyslexia

Dual route model:


Damage to lexical, whole-word route leads to problems reading irregular
words like “have”

MAIN
Aphasia
Loss or impairment of language function (caused by brain damage) during
speech, hearing, reading, or writing

Click on Broca’s Wernicke’s


an aphasia

MAIN SECTION
Broca’s Aphasia
• Aphasia with difficulty in language expression
• Caused by lesion to the left frontal lobe
– Note the proximity of Broca’s area to the motor cortex, specifically
the region controlling the mouth and lips

control of mouth/lips

MAIN SECTION
Wernicke’s Aphasia
• “Receptive aphasia” with language comprehension difficulty
• Caused by lesion to the left posterior temporal lobe
– Note the proximity of Wernicke’s area to the auditory cortex

MAIN SECTION

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