Created by Cindy Montana at Washington University in St.

Louis

Hosted at MedStudentBooks.com

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.

Pathways

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

MAIN

FINE TOUCH

Spinal Cord

CLICK
dorsal root
ganglion

dorsal
columns

gracile fasciculus
cuneate fasciculus

afferent A fiber
1st order

T L

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

sacral
lumbar
thoracic
cervical

MAIN

SECTION

FINE TOUCH

Medulla

CLICK
gracile nucleus

cuneate nucleus

internal
arcuate
fibers
nd
2 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
thoracic
cervical
trigeminal sensory

medial lemniscus
2nd order

MAIN

SECTION

FINE TOUCH
CLICK

Midbrain

inferior
colliculus
lateral lemniscus

medial
lemniscus
2nd order

sacral
lumbar
thoracic
cervical
trigeminal sensory

MAIN

SECTION

FINE TOUCH

Midbrain

CLICK
superior
colliculus
lateral
lemniscus

red nucleus

medial
lemniscus
2nd order

sacral
lumbar
thoracic
cervical
trigeminal sensory

MAIN

SECTION

FINE TOUCH
CLICK

internal capsule
3rd order

Forebrain
primary somatosensory cortex
click here

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

Spinal Cord

CLICK
A fiber
1st order

dorsal root
ganglion

posterior marginalis (RL I)

substantia gelatinosa (RL II)

C fiber
1st order
A, C fibers
(small) enter the
spinal cord
lateral to A
fibers (large)

RL = Rexed lamina

nucleus proprius
(RL III, IV)
Lissauers tract
interneuron

CROSS
C T
sacral
lumbar
thoracic
cervical

S
2nd order tracts:
spinothalamic/
spinoreticular/
spinomesencephalic

anterior white commissure

2nd order

MAIN

SECTION

PAIN/TEMP
CLICK

Medulla

Show Spinoreticular Tract

trigeminal
afferent
1st order
trigeminal
spinal tract
1st order

trigeminal
spinal nucleus

sacral
lumbar
thoracic
cervical
trigeminal sensory

medullary reticular
formation

CROSS
2nd order tracts:
spinothalamic/
spinoreticular/
spinomesencephalic

MAIN

SECTION

PAIN/TEMP

Pons

CLICK

Show Spinoreticular Tract

pontine reticular
formation
trigeminal
ganglion
trigeminal
spinal tract
1st order

trigeminal
afferent
1st order
[to medulla]

sacral
lumbar
thoracic
cervical
trigeminal sensory

spinothalamic,
spinomesenephalic
tracts
2nd order

MAIN

SECTION

PAIN/TEMP

Midbrain

CLICK
inferior
colliculus

spinothalamic/
spinomesencephalic tracts
2nd order

medial
lemniscus

sacral
lumbar
thoracic
cervical
trigeminal sensory

MAIN

SECTION

PAIN/TEMP

Midbrain

CLICK
superior
colliculus

Show Spinomesencepahalic
Tract

spinothalamic tract
2nd order

periaqueductal
gray (PAG)

red nucleus

mesencephalic
reticular
formation

medial
lemniscus

sacral
lumbar
thoracic
cervical
trigeminal sensory

MAIN

SECTION

PAIN/TEMP

Forebrain

CLICK

internal capsule
(posterior limb)
3rd order

Spinothalamic tract
(no evidence for
orderly topographic
cortical map)

primary somatosensory cortex

click here

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 A fiber
1st order
A fibers (large)
enter the spinal
cord medial to
A, C fibers
(small)

MAIN

SECTION

PROPRIOCEPTION
CLICK

Spinal Cord - Thoracic

dorsal
spinocerebellar
tract
nd
2 order

Clarkes nucleus
(dorsal nucleus)
T1-L2

MAIN

SECTION

PROPRIOCEPTION
CLICK

Spinal Cord - Cervical

afferent A 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)

deep cerebellar nuclei (see right)

interposed (globose +
emboliform)
lateral (dentate)

mossy fibers

inferior cerebellar
peduncle (restiform body)

MAIN

SECTION

PROPRIOCEPTION
CLICK
afferent A fiber
(from masseter, temporalis)

Pons
mesencephalic ganglion
trigeminal motor nucleus

trigeminal
ganglion

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

MAIN

SECTION

CORTICOSPINAL/
CORTICOBULBAR
CLICK

corona
radiata

Forebrain
Precentral,
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
CLICK

Midbrain

superior
colliculus
oculomotor
nucleus

red nucleus
cerebral
peduncle

to lumbar spinal cord

to cervical spinal cord
to CN motor nuclei

MAIN

SECTION

CORTICOSPINAL/
CORTICOBULBAR
CLICK

Midbrain

inferior
colliculus
trochlear
nucleus

cerebral
peduncle

to lumbar spinal cord

to cervical spinal cord
to CN motor nuclei

MAIN

SECTION

CORTICOSPINAL/
CORTICOBULBAR
CLICK

Pons

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
CLICK

Pons

abducens (CN VI)

nucleus

middle
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
CLICK

Medulla

hypoglossal (CN XII)

nucleus

nucleus
ambiguous

to lumbar spinal cord

to cervical spinal cord
to CN motor nuclei

corticospinal
tract

MAIN

SECTION

CORTICOSPINAL/
CORTICOBULBAR
CLICK

Medulla

trigeminal (CN V)
spinal nucleus

CROSS
pyramidal
decussation

to lumbar spinal cord

to cervical spinal cord

pyramid

MAIN

SECTION

CORTICOSPINAL/
CORTICOBULBAR
CLICK

Spinal Cord - Cervical

ventral white
commissure

lateral
corticospinal
tract

CROSS

PF DF
PE DE

ventral horn
to lumbar spinal cord
to cervical spinal cord

Regions of the ventral horn

that innervate
- proximal flexors = PF
- distal flexors = DF
- proximal extensors = PE
- distal extensors = DE

anterior
corticospinal
tract

MAIN

SECTION

CORTICOSPINAL/
CORTICOBULBAR
CLICK

Spinal Cord - Thoracic

lateral
corticospinal
tract

to lumbar spinal cord

anterior
corticospinal
tract

MAIN

SECTION

CORTICOSPINAL/
CORTICOBULBAR
CLICK

Spinal Cord - Sacral

lateral
corticospinal
tract

ventral white
commissure

CROSS

ventral horn
to lumbar spinal cord

anterior
corticospinal
tract

MAIN

SECTION

RUBROSPINAL/
TECTOSPINAL
CLICK
dorsal tegmental
decussation

Midbrain
input from forebrain

superior colliculus

ventral tegmental
decussation
red nucleus

rubrospinal
tectospinal

MAIN

SECTION

RUBROSPINAL/
TECTOSPINAL
CLICK

Pons
tectospinal tract

rubrospinal tract
pontine reticular
formation

rubrospinal
tectospinal

MAIN

SECTION

RUBROSPINAL/
TECTOSPINAL
CLICK

Medulla
MLF

tectospinal
tract

medullary
reticular
formation
rubrospinal
tract

rubrospinal
tectospinal

MAIN

SECTION

RUBROSPINAL/
TECTOSPINAL
CLICK

Medulla

trigeminal (CN V)
spinal nucleus

rubrospinal
tract

pyramidal
decussation
tectospinal
tract
rubrospinal
tectospinal

pyramid

MAIN

SECTION

RUBROSPINAL/
TECTOSPINAL
CLICK

Spinal Cord - Cervical

rubrospinal
tract

rubrospinal
tectospinal

ventral horn

tectospinal
tract

MAIN

SECTION

RUBROSPINAL/
TECTOSPINAL
CLICK

Spinal Cord - Lumbar

rubrospinal
tract

ventral horn

rubrospinal

MAIN

SECTION

RETICULOSPINAL
CLICK

Pons
medial longitudinal
fasciculus (MLF)

pontine reticular
formation

medial reticulospinal tract

lateral reticulospinal tract

MAIN

SECTION

RETICULOSPINAL

Medulla

CLICK
MLF

medial reticulospinal tract

lateral reticulospinal tract

MAIN

SECTION

RETICULOSPINAL

Medulla

CLICK

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
lateral vestibular
nucleus

Pons
medial longitudinal fasciculus (MLF)

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 n
ucleus
medial lemniscus

medial longitudinal fasciculu

s

dorsal motor nucleus

of the vagus
nucleus of the
solitary trac
t

spinal trigeminal
tract

inferior cer
ebellar pedu
ncle

spinal trigeminal
nucleus

solitary tract
inferior olivary
fibers

pyramids

nucleus am
biguus

inferior olivary
nucleus
nucleus raphe magnus

MAIN

SECTION

Medial Syndrome
Lateral Syndrome

medial lemnisc
us
lateral lemnisc
us

Lower Pons
CN VI nucl
eus

medial longitudinal
fasciculus

medial vestibular nucleus

lateral vestibular nucleus
CN VII motor nucleus

raphe nucl
ei

middle ce
rebellar
peduncle

superior olivary nu
clear complex

pontine fibers

spinothalamic tract

pontine nuclei
corticospinal tract

MAIN

SECTION

Medial Syndrome
Lateral Syndrome

CN V main sensory
nucleus

Middle Pons
CN V motor nu
cleus

CN V mesencephal
ic nucleus
CN V
mesencephalic
tract

lateral lemni
scus

MAIN

SECTION

Medial Syndrome

Upper Pons

Lateral Syndrome

medial longitudinal
fasciculus
central tegmental
bundle

locus coeruleus

parabrachial region
medial lemniscus
periaqueductal gray

corticospinal
tract

pontocerebellar fibers

MAIN

SECTION

superior [inferior is caudal] colliculus

Midbrain
periaqueductal gray

superior cerebellar pe
duncle

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
nucleus

medial longitudinal
fasciculus

medial lemniscus

Loss of vestibuloocular reflex*

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

pyramids

ARTERY: anterior spinal artery

* VOR might be preserved

because this is below the level of
the vestibular nuclei

MAIN

SECTION

Lateral Medullary Syndrome

CN V spinal
nucleus
nucleus
ambiguus

descending
symapthetic
tract

dorsal
spinocerebellar
tract

Loss of facial pain/temp sensation

(ipsilateral)
Hoarseness, difficulty swallowing
Horners syndrome, ipsilateral loss of
sweating
Cerebellar ataxia
Loss of body pain/temp sensation
(contralateral)

spinothalamic tract

ARTERY: posterior inferior cerebellar artery (PICA)

MAIN

SECTION

Medial Inferior Pontine Syndrome

medial
lemniscus

CN VI
nucleus

medial
longitudinal
fasciculus

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
(contralateral)
Hearing deficit (ipsilateral), vertigo
Facial paralysis (ipsilateral)

CN VIII

CN VII

ARTERY: anterior inferior cerebellar artery (AICA)

MAIN

SECTION

Medial Mid-Pontine Syndrome

corticospinal
tract

Limb paralysis (contralateral)

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
sensory nucleus

CN V motor
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)
No deficit reported
Loss of pupil constriction; lateral
strabismus

red nucleus

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

first

Bilateral, stocking-glove

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

Pain/temp

Ipsilateral, lesion on down

Contralat., lesion on down

Complete cord
transection

All sensation

Lesion on down

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
lesion

Contralateral

MAIN

SECTION

Peripheral Receptors
Click on a receptor:

Merkels disk

Epidermis

free nerve ending

Dermis

Meissners corpuscle

Pacinian corpuscle
Ruffini ending

MAIN

SECTION

Merkels Disk
Discriminative Touch Mechanoreceptor

Location:
Specificity:
Dynamics:
Spatial Range:
Conduction:

Epidermis
Steady skin indentation form, texture
Slow-adapting
Small receptive field (3-4 mm fingers, 30-40 cm trunk)
2-point discrimination threshold = 1 mm fingers, 10 cm trunk
A fiber 25 m/s
MAIN

SECTION

RECEPTORS

Meissners Corpuscle
Discriminative Touch Mechanoreceptor

Location:
Specificity:
Dynamics:
Spatial Range:
Conduction:

Dermis
Flutter; contact and movement
Fast-adapting
Small receptive field (3-4 mm fingers, 30-40 cm trunk)
2-point discrimination threshold = 1 mm fingers, 10 cm trunk
A fiber 25 m/s
MAIN

SECTION

RECEPTORS

Pacinian Corpuscle
Discriminative Touch Mechanoreceptor

Location:
Specificity:
Dynamics:
Spatial Range:
Conduction:

Subcutaneous tissue
Non-localized vibration
Fast-adapting
Large receptive field
A fiber 25 m/s

MAIN

SECTION

RECEPTORS

Ruffini Ending
Discriminative Touch Mechanoreceptor

Location:
Specificity:
Dynamics:
Spatial Range:
Conduction:

Dermis
Low frequency stimulation
Slow-adapting
Large receptive field
A fiber 25 m/s

MAIN

SECTION

RECEPTORS

Free Nerve Ending

Pain/Temperature Receptor

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
central sulcus

Click on an area:

intraparietal sulcus
posterior
parietal lobule

central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

3a
lateral sulcus

M1

S2

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

MAIN

SECTION

Somatosensory Cortex
postcentral gyrus
central sulcus

Click on an area:

intraparietal sulcus
posterior
parietal lobule

central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

3a
lateral sulcus

M1

S2

S1 Area 3a
Input from thalamic shell (muscles, joints, deep
mechanoreceptors)
RFs similar to periphery

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

MAIN

SECTION

Somatosensory Cortex
postcentral gyrus
central sulcus

Click on an area:

intraparietal sulcus
posterior
parietal lobule

central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

3a
lateral sulcus

M1

S2
S1 Area 3b
Input from thalamic core (VPM/VPL - cutaneous)
Each column within 3b is specific for one type of
cutaneous receptor
Smallest RFs

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

MAIN

SECTION

Somatosensory Cortex
postcentral gyrus
central sulcus

Click on an area:

intraparietal sulcus
posterior
parietal lobule

central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

3a
lateral sulcus

M1

S1 Area 1
Input from 3b and thalamic core (cutaneous)
Large, complex RFs combine info from multiple
receptor types
Sensitive to motion, direction, orientation
Primarily tactile info
LESION trouble describing texture

S2

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

MAIN

SECTION

Somatosensory Cortex
postcentral gyrus
central sulcus

Click on an area:

intraparietal sulcus
posterior
parietal lobule

central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

3a
lateral sulcus

M1

S1 Area 2
Input from 3a, 3b and thalamic core (cutaneous) +
shell (muscle)
Large, complex RFs
Combines tactile and muscle info
LESION poor stereognosis, cant pick up small
objects or maneuver hand through tight places

S2

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

MAIN

SECTION

Somatosensory Cortex
postcentral gyrus
central sulcus

intraparietal sulcus
posterior
parietal lobule

Click on an area:
central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

4
S2

3a
M1
Input
from S1 and thalamus
lateral sulcus
Two complete maps
Complex RFs with influence of behavioral state
Collosal connections:
Bilateral RFs
Interhemispheric transfer of learned info
LESION problems with tactile discrimination,
interhemispheric transfer of learned info

S2

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

MAIN

SECTION

Somatosensory Cortex
postcentral gyrus
central sulcus

Click on an area:

intraparietal sulcus
posterior
parietal lobule

central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

3a
lateral sulcus

M1

S2
Area 5
Input from area 2 (S1)
Cutaneous plus movement
Very complex RFs: Multi-joint, multi-limb
Responds differently to active and passive movement

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

MAIN

SECTION

Somatosensory Cortex
postcentral gyrus
central sulcus

Click on an area:

intraparietal sulcus
posterior
parietal lobule

central
sulcus

intraparietal
sulcus

postcentral gyrus S1

1
2
3b

3a
lateral sulcus

M1

S2
Area 7
High order visual area
Activity reflects spatial properties of visual stimuli
Large RFs, prominent effects of behavioral relevance

posterior
parietal lobule

Click here for S1 topography

Click here for S1 histology

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
precentral gyrus
MOTOR

postcentral gyrus
SENSORY

small granule cells

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
INJURY

ACTIVATE
NOCICEPTORS

Types of Nociceptors

MAIN

SECTION

Inflammatory Pain
INSULT

INFLAMMATORY
MEDIATORS
NOCICEPTOR
ACTIVATION

MAIN

SECTION

Neuropathic Pain
REPETITIVE STRESS
INJURY (TO NERVES)

LESION

PAIN

MAIN

SECTION

Types of Nociceptors
Fiber type
Myelination
Conduction

Responds to

Thermal

Extreme temperature
(>45oC or < 5oC)

A
Light myelin
5-30 m/s

Sharp, stinging, well

localized

TRP (Transient Receptor

Mechanical

Intense pressure

A
Light myelin
5-30 m/s

Sharp, stinging, well

localized

DEG/ENaC (ASIC
- Acid Sensing Ion Channel)
Maybe TRP

Polymodal

Extreme temperature
Intense pressure
Noxious chemicals

C fibers
No myelin
1 m/s

Dull aching or
burning, prolonged,
poorly localized

DEG/ENaC (ASIC)

Type of pain

Channel types
(Transduction)

Nociceptor

Potential)

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

Central Pain Modulation

CLICK

PAG
Electrically stimulate
or apply opiates here
nucleus raphe
magnus (NRM)

via dorsolateral funiculus

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

inhibits

dorsal horn neuron

(ascending pain afferent)

dorsal horn

5-HT

NRM projection
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

excite

histamine

stimulate

an
ce

degranulation

su
bs
t

nociceptor /
peripheral ending

mast cell

MAIN

SECTION

CLICK

Sensitization - Central

Limbic augmentation
(anxiety, anticipation, etc.)

Repeated stimulation
(e.g., by nociceptors)
Hyperphosphorylation of ion
channels in dorsal
horn neurons

nociceptor
terminus

dorsal horn

.. .
P
P

Increased
excitability of dorsal
horn neurons

P P
P

dorsal horn
neuron

ion
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
Severing a
motor nerve
Disease of
motor neurons

Weakness or paralysis
Weakness or paralysis

Positive Deficit
Fibrillation
(spontaneous firing of single muscle fibers)

Fasciculation
(spontaneous firing of an axon twitch of
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
PMA

SMA

prefrontal
cortex

Click:

M1 (Area 4)

central sulcus
S1

Area 5
Area 7

posterior
parietal
cortex

PMA = premotor area

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
V
precentral gyrus
MOTOR

contains large
pyramidal Betz cells

postcentral gyrus
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

Muscle Spindle

CLICK

chain fiber

bag fiber

1a or II
afferent

1- or
2-MN

quadriceps

to spinal
cord

1a*

II*

-MN

muscle spindle

from
spinal
cord
1-MN*

biceps tendon
2-MN*

1) Hit tendon
2) Spindle stimulated (1a, II)
3) -MN fires muscle contracts
Renshaw cell stimulated
-MN fires spindle fibers contract
4) Renshaw cell inhibits -MN

MAIN

-MN *

* click on label for details

Muscle spindle is involved in

(click here)

SECTION

REFLEXES

CLICK

Golgi Tendon Organ (GTO)

Ib
afferent

GTO

inhibitory interneuron

-MN

to spinal
cord

Ib afferent

1) High muscle tension (force)

2) GTO stimulated (Ib)
3) Interneuron inhibits -MN
4) -MN decreases firing
5) Decreased muscle tension

Roles of the GTO:

Protect against hurtful muscle stretch

Servo-control force (e.g., combat

weakness due to muscle fatigue)

from
spinal
cord

-MN

GTO is involved in:

Clonus

Claspknife reflex

MAIN

SECTION

REFLEXES

Reciprocal Inhibition

CLICK

1a afferent

muscle spindle
-MN to
agonist
agonist muscle
(flexor)
ACTIVATED

inhibitory
interneuron

-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
activity for voluntary
corrections of gait
(obstacle avoidance)

Initiate locomotory activity

in spinal cord circuits

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) -MN and -MN fire
6) Muscle contracts length is restored

Prefrontal lesion set signal is lost

motor cortex is hyperactive
1a afferent

Hyperactive
palpatory reflex
(involuntary
grasp reflex)

-MN

Hyperactive long
loop stretch reflex
(Gegenhalten
resistance to limb
displacement)

These are involuntary

-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
- the tonic neck reflex will CANCEL the vestibulospinal reflex, or
- the tonic neck reflex will ADD to the vestibulospinal reflex.

VSR = vestibulospinal reflex

TNR = tonic neck reflex

Neck normal

Head normal

Abnormal Posture

Head down
The TNR involves
-

the reticulospinal pathway

for somatosensory input.

the tectospinal pathway

for visual input.

To maintain balance, you must

have two of the following:
-

Somatosensory input
Visual input
Vestibular input

Neck flexed

VSR alone
TNR alone
VSR TNR
VSR + TNR

Neck extended

Head up

Tips for learning this chart

MAIN

SECTION

Normal Postural Reflexes

1) Vestibulospinal
Know that for VSR
alone
movement
only),
head
up
forelimbs
flex &extending/flexing
hindlimbs extendyour
(andneck.
reflexes
can(head
act ALONE
if you
tilt your
head
up/down
without
opposite
head is can
down).
Tonic
neckifreflexes
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
opposite head
if neck
flexed).
If (and
you combine
tiltiswith
neck flexion/extension, either
3) - Combining
a head
movement
and neck
movement: reflex, or
the tonic neck
reflex
will CANCEL
the vestibulospinal

If theneck
limb positions
resulting
from
and TNR agree,
then the reflexes add (limb hyper-extension/flexion).
- the tonic
reflex will
ADD to
theVSR
vestibulospinal
reflex.

If the limb positions resulting from VSR and TNR disagree, then the reflexes cancel (no limb movement).

VSR = vestibulospinal reflex

TNR = tonic neck reflex

Neck normal

Head normal

Head down
The TNR involves
-

the reticulospinal pathway

for somatosensory input.

the tectospinal pathway

for visual input.

To maintain balance, you must

have two of the following:
-

Somatosensory input
Visual input
Vestibular input

Neck flexed

VSR alone
TNR alone
VSR TNR
VSR + TNR

Neck extended

Head up

MAIN

SECTION

DECEREBRATE

DECORTICATE

Abnormal Posture

Flexion of upper limb,

extension of lower limb,
slight intorsion of legs
Hyperactive vestibulospinal AND tonic neck
reflexes (see right)
Caused by a lesion of
the internal capsule (
corticospinal pathway)

This is normal in infants but is

a sign of corticospinal lesion
in adults.

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

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)

When the head is passively

turned to one side, the
looked-at limbs will extend
and the others will flex.

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

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

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
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)
- pars compacta (SNpc)

Globus pallidus, interna (GPi)

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

caudate / putamen

SC = superior colliculus
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
sends info back.
But most of the caudate/putamen output goes to the GP and SNpr.

GPi
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/
spinal cord

The globus pallidus (GPe and GPi) are both in communication with the STN.

Show selection-brake mechanism

MAIN

SECTION

BG

CLICK

Basal Ganglia Connections

cerebral cortex

=
=
=
=

excitatory (Glu)
inhibitory (GABA)
mixed (DA)
unknown

caudate / putamen

SC = superior colliculus
PPPA = peri-pedunculo-pontine area
VA/VL = ventroanterior/ventrolateral
nuclei of thalamus
= excitatory
= inhibitory

VA/VL
SNpc

GPe

STN

Person wants to make a voluntary movement

Premotor/motor cortex excite STN
STN excites GPi
GPi inhibits MPGs

GPi
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
DISINHIBITS GPi

SC

brainstem/
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
Parkinsons Disease

Huntingtons Disease

MAIN

SECTION

BG

Parkinsons 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 Parkinsons patients

MAIN

SECTION

BG

Huntingtons 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 Parkinsons)
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
(synapse)

terminal

Basket cell
Golgi cell

axon

to the deep nuclei

MAIN

SECTION

CB

granule cell layer

molecular layer

Purkinje Cell
One Purkinje cell receives
input from
Purkinje cell
dendrite

Purkinje
cell body

One climbing fiber

Many parallel fibers (up to a
million)
Inter-Purkinje cell
connections via parallel fibers
allow motor coordination to
occur

Projects to and inhibits the

deep nuclear cells

MAIN

SECTION

CB

granule cell layer

molecular layer

Climbing Fiber

Cell bodies reside in the inferior

olive

Projects to the Purkinje cell layer,

where one climbing fiber
synapses with one Purkinje cell
Excitatory
Climbing fiber input weakens the
excitatory effect of parallel fibers
on the Purkinje cell

climbing
fiber

Fire at high rates when learning

movement, low rates during
learned movement

MAIN

SECTION

CB

molecular layer

Granule Cell

parallel fiber

Extends claws to grab the

mossy fiber terminus

granule cell layer

granule cell

Receives input from mossy fibers

in the granule cell layer

Projects to molecular layer, where

the fiber then runs parallel to the
folia surface
These parallel fibers synapse
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
molecular layer

Originates in the
Spinocerebellar pathway
Ascending (from spinal cord)
Fibers do not cross
Enters cerebellum through the
inferior cerebellar peduncle

granule cell layer

Pons
Descending (from cerebral
cortex)
These fibers must cross in the
cerebral peduncles
(corticopontine fibers)
Enter cerebellum through the
middle cerebellar peduncle

mossy
fibers

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
basket cell

Purkinje cell
body

Golgi cell
Granule cell layer
MAIN

SECTION

CB

Cerebellar Deep Nuclei

Receive inhibitory input from Purkinje cortical cells

Project to brainstem and thalamus click here
Each nucleus has a separate body map
Help initiate movement click here

Click on a nucleus:
Fastigial (medial) nucleus
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

against gravity

Falls to the side of the

lesion

Globose/
emboliform
(interposed)

Cerebral cortex
Spinal cord

Balance agonist and

antagonist muscles at a
single joint

Ipsilateral action tremor

during voluntary
movements (e.g. reaching)

Dentate (lateral)

Cerebral Cortex

(1)

(1)
(2)

(2)

Combined digit
movements
Arm/leg reaching to
a visual target

Incoordination of digits
Overshoot targets in
reaching with arm/leg

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

= secretomotor efferents
= vasomotor efferents
= visceral afferents

PHARYNX/
LARYNX

MAIN

SECTION

Circumventricular Organs
nucleus of the
solitary tract

area postrema
dorsal nucleus
of CN X

solitary
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
excitatory
parasympathetic
sympathetic
rostral
ventrolateral
medulla

Baroreceptor Reflex
carotid sinus baroreceptors
aortic arch baroreceptors
nucleus of the
solitary tract
caudal
ventrolateral
medulla
nucleus
ambiguus

tonic

intermediolateral column

peripheral arterioles
MAIN

SECTION

Respiration
Lung stretch receptors
Carotid body chemoreceptors

Forebrain

= excitatory
= inhibitory

Intrinsic chemoreceptors

Nucleus of the solitary tract

Parabrachial nucleus

VENTROLATERAL
MEDULLA

Pre-Botzinger cells
Respiratory rhythm

Ventral respiratory pre-motor cells

Rostral inspiratory
Excitatory

Phrenic motorneurons
Ext. intercostals

Botzinger complex
Reciprocal inhibition

Caudal expiratory
Excitatory

Int. intercostal motorneurons

Abdominal muscles

MAIN

SECTION

= afferent
= efferent

Micturition
Hypothalamus, PAG

pontine micturition center

(parabrahial region)

Short loop reflex

Long loop reflex

sacral spinal cord

bladder

MAIN

SECTION

= afferent
= efferent

Micturition
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
= efferent

Micturition
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
Stabilize the eye when the head
moves (reflexive)

Keep the fovea on a visual

target (volitional control)

Eye movement

Function

Vestibulo-ocular

Use vestibular input to hold images stable on

retina during brief/fast head movement

Optokinetic

Use visual input to hold images stable on

retina during sustained/slow head movement

Saccade

Bring new objects of interest into the fovea

Smooth pursuit

Hold image of a moving target on the fovea

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

Secondary pathway
(visual cortex
cerebellar flocculus)

semicircular
canal

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.
motor nuclei to
eye muscles

The VOR depends on the stimulation of

kinocilium in the vestibular labyrinth.
vestibular
nuclear
complex

MAIN

SECTION

Optokinetic Reflex
Senses motion of the visual background
(involves the extrastriate cortex)
Nystagmus

Eye position (degrees)

Slow phase: Compensatory tracking movements

(smooth pursuit)
Fast phase: Anticipatory fast movement to reposition
eyes after they reach the edge of the orbit (saccade)

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
SECTION
MAIN

Click on a zone, nucleus, or button

Hypothalamus

Hypothalamic Inputs
Hypothalamic Outputs

ZONE

PVZ

Anterior Pituitary
Physiological Regulation

Posterior Pituitary

STRUCTURE(S)
Periventricular nucleus
Arcuate nucleus
Paraventricular nucleus
(not shown)

Dorsomedial nucleus

MHA

Ventromedial nucleus

LHA

Lateral hypothalamic area

fornix

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
nucleus

orexin cells?

median eminence

median eminence

MAIN

SECTION

Hypothalamic Nuclei
anterior commissure

anterior
hypothalamic 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
(dopaminergic
cells)

median eminence

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

Parabrachial nucleus

Taste, visceral sensation

Olfactory cortex

Food, sexual attractants

Amygdala, hippocampus,
prefrontal cortex (limbic input)

Cognition

Circumventricular organs

Osmolality of blood
Peptide hormones in blood (AII, atrial natiuretic
factor)

Thermoreceptors

Local blood temperature

Osmoreceptors

Local CSF ionic strength

Chemoreceptors

Hormones (e.g., leptin, ghrelin)

Intrinsic

MAIN

SECTION

Outputs from Hypothalamus

From

To

Effect

Lateral hypothalamus
Paraventricular nucleus

Autonomic nuclei in
spinal cord, brainstem

Control body temp (sweating, shivering,

vasoconstriction)

Releasing hormone neurons

in periventricular zone

Median eminence

Control of anterior pituitary

Supraoptic and
paraventricular nuclei

Posterior pituitary

Secrete ADH, oxytocin

Scattered large neurons

Cerebral cortex
Limbic structures

Not clear; presumably contribute to

hypothalamic control of behavior

(PAG, parabrachial nuclei,

nucleus of the solitary tract,
dorsal vagal nucleus,
ventrolateral medulla, IML)

(arcuate nucleus and part of the

paraventricular nucleus)

MAIN

SECTION

Anterior Pituitary
median
eminence

Hypothalamic cell
axons terminate in the
median eminence and
secrete hormones into
the fenestrated pituitary
portal capillaries

periventricular
zone of the
hypothalamus
(arcuate nucleus and
part of the paraventricular nucleus)

CRH
TRH
GnRH
GHRH
Somatostatin
Dopamine

hypothalamic
releasing
hormones

ACTH
TSH
LH/FSH
GH
GH/TSH
MSH

corresponding
anterior
pituitary
hormones

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
capillaries

Posterior pituitary hormones:

- 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

spinal cord
reticular formation

Body Temperature
releasing hormone neurons
anterior hypothalamus
TSH, GH, somatostatin

lateral hypothalamus
autonomic nuclei
sweating, shivering, etc.

intrinsic
thermoreceptors

cerebral cortex
behavior?

MAIN

SECTION

REG

Body Weight

inputs
outputs/effects

viscera (gut)

autonomic nuclei

food intake, gut distension

NTS / parabrachial
nuclei
pituitary

tongue
taste

NTS
olfactory cortex
smell

fat cells leptin

suppress food intake /

increase metabolism

(receptors in dorsomedial nucleus)

promote food intake /

decrease metabolism

gut ghrelin

promote food intake /

stabilize sleep

orexin

MAIN

SECTION

REG

inputs
outputs/effects

Ionic Balance

circumventricular
organs
blood osmolality, peptide hormones

intrinsic
osmorecptors

posterior pituitary

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
circumventricular
organs

ADH
vasoconstriction,
anti-diuretic action
on kidney

baroreceptors

autonomic nuclei

NTS

vasoconstriction

MAIN

SECTION

REG

inputs
outputs/effects

Circadian Rhythm
suprachiasmatic nucleus

retina

couple the circadian

rhythm to 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
catecholamine
systems

ACTH
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
commissure

fornix

orbital/medial pr
efrontal cortex

stria terminalis

olfactory bulb
hippocampus
hypothalamus

amygdala
mammillary body

dentate gyrus
parahippocampal gyrus

MAIN

Amygdala
nucleus basalis of Meynert

central nucleus
Dorsal nuclei

medial nucleus
basal nucleus

amydala

Deep nuclei

accessory
basal nucleus

PAC

lateral nucleus

entorhinal cortex

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

inputs
outputs/effects

Amygdala
autonomic cell groups

ascending sensory
system
visual, olfactory, auditory,
somatosensory
MAJOR

SHORTCUT

thalamic relay
nucleus

primary sensory
cortex
secondary
association
cortex

posterior
intralaminar
thalamic nuclei

lateral hypothalamus, PAG,

parabrachial nucleus, NTS, dorsal
nucleus of CN X, ventrolateral medulla

fee
dba

ck

di
re
ct
O
O
R
vi R v
a
t h ia m
e
ve edi
o
nt
ro dor
m
s
ed al
th
ia
a
ls
tri lam
at
u
um s

influence HR, BP,

gut/bowel/respiratory/
bladder function, etc.

orbital/medial
prefrontal cortex
determine whether
sensory stimulus is
rewarding or
aversive; set mood

The shortcut afferent pathway produces your initial gut reaction to a potentially
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

At the junction of frontal and

temporal cortices
Axons of mitral cells run in
olfactory tract to primary
olfactory cortex

Olfactory cortex is the major

center for odor detection and
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

putamen
nucleus accumbens /
olfactory tubercle

lateral striate
arteries

olfactory tract
primary olfactory
cortex

MAIN

SECTION

Olfactory Cortex

At the junction of frontal and

temporal cortices
Axons of mitral cells run in
olfactory tract to primary
olfactory cortex

Olfactory cortex is the major

center for odor detection and
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

putamen
nucleus accumbens /
olfactory tubercle

lateral striate
arteries

olfactory tract
primary olfactory
cortex

Nucleus accumbens
- Reward center
- Contains mostly GABAergic neurons
- Receives input from the amygdala and hippocampus

MAIN

SECTION

Hippocampus
tail of
caudate
Role

dentate gyrus
CA3
pre-subiculum
Inputs/Outputs

CA1

parasubiculum

subiculum

Information Flow

inferior temporal area

entorhinal
cortex

Alzheimers 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

Alzheimers Disease
MAIN

SECTION

HIPP

Inputs/Outputs

inputs
outputs/effects

Hippocampus
hypothalamus

info from
multisensory
association cortical
areas

f ee

dba
ck

ic
m
a
l
i
ha
. t ucle
t
n
a
yn
via illar
R
m
t O am
c
e
m
dir

c
nu

./

prefrontal / cingulate
cortical areas

visual, auditory areas of inferior

and superior temporal cortex

perirhinal/entorhinal
cortex

basal ganglia
(ventral)

MAIN

SECTION

HIPP

Hippocampus

CLICK

tail of
caudate
Role

dentate gyrus
CA3
pre-subiculum
Inputs/Outputs

CA1

parasubiculum

subiculum

Hide Information Flow

inferior temporal area

Alzheimers Disease

entorhinal
cortex

sensory inputs from

cerebral cortex

to the
neocortex
to frontal cortex, anterior
thalamus, hypothalamus

MAIN

SECTION

HIPP

Alzheimers Disease
-amyloid plaques
CA1
CA3
DG
ParaSub
PreSub
Sub
CA1
EC

tangles (intracellular)

Entorhinal cortex and CA1 are severely damaged during early Alzheimers
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)

Medial prefrontal cortex

Orbital prefrontal cortex

hypothalamus, PAG

assessment of food

control visceral
functions
reward/aversion
appropriate
choices

control
of mood

multimodal
sensory inputs

amygdala /
hippocampus

inputs
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

coincide

Result when disparate events

coincide

Ex: 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, corticothalamis axons (connect cortex and principal thalamic
This system is active during wakefulness (and its stimulation causes
nuclei)
waking). It is inactive during sleep (and its transection causes coma).
- Project back onto the principal thalamic nuclei
- Histology
Neurotransmitters
Sleep Initiation

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

RAT BRAIN Stained for GABA

Laterodorsal tegmental nucleus (LDT) (Ach)

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

reticular nucleus
ventrolateral
thalamic nucleus

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

MAIN

SECTION

SYS

Neurotransmitter Systems
Ascending Reticular Activating System

Wakefulness

Slow wave sleep

REM sleep

Norepinephrine
(locus coeruleus)

ACTIVE

INACTIVE

INACTIVE

Serotonin
(raphe nuclei)

ACTIVE

INACTIVE

INACTIVE

ACh
(LDT/PPT)

ACTIVE

INACTIVE

ACTIVE*

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
WAKEFULNESS

Sleep Initiation

Add ascending
ACh,ACh,
NE, NE,
5-HT5-HT
inputinput
Remove
ascending

CORTEX

blocked RN bursting
RN inhibition of TRN is released

thalamocortical
neuron

riz
e

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

de
p

ola

RETICULAR
NUCLEUS

ize
r
ola
p
er
p
hy

ACh
NE
5-HT

THALAMIC
RELAY
NUCLEUS
(TRN)

ize
depolar

= 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)

Explicit (a.k.a declarative)
Working

Alzheimers Disease
Lewy Body Dementia
Korsakovs 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 Korsakovs 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

Korsakovs 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

KORSAKOVS

3rd ventricle

mammillary bodies

no mammillary bodies

MAIN

SECTION

Lewy Body Dementia

Closely related to Parkinsons Disease
Intracellular inclusions of protein -synuclein
neuronal dysfunction
Dementia is similar to that found in Alzheimers

Lewy bodies

MAIN

SECTION

Language Processing
CODES:

Visual / orthographic
Auditory / phonological
Syntactic / grammatical
Semantic / meaning
Articulatory / speech motor planning

Aphasia

Note: This is not a thorough treatment of

language processing, but these are the only
questions Ive seen on past exams

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
an aphasia

Brocas

Wernickes

MAIN

SECTION

Brocas Aphasia
Aphasia with difficulty in language expression
Caused by lesion to the left frontal lobe
Note the proximity of Brocas area to the motor cortex, specifically
the region controlling the mouth and lips

control of mouth/lips

MAIN

SECTION

Wernickes Aphasia
Receptive aphasia with language comprehension difficulty
Caused by lesion to the left posterior temporal lobe
Note the proximity of Wernickes area to the auditory cortex

MAIN

SECTION