Cindy .com Drozda · 2011-11-03 · Cindy Drozda Fabulous Finials! . Cindy Drozda . Cindy Drozda
Cindy Montana's Neuro Exam 2 Review
description
Transcript of Cindy Montana's Neuro Exam 2 Review
By Cindy Montana
WUMS I Neuroscience2006
Pathways
Brainstem Atlas
Brainstem Syndromes
Somatosensory
Pain
Motor
Autonomic Nervous System
Oculomotor / Oculodominance
Hypothalamus
Limbic
Sleep
Memory
Language
References
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
Spinal Cord
C
gracile fasciculus
cuneate fasciculus
dorsalcolumns
sacrallumbarthoraciccervical
afferent Aβ fiber1st order
SLT
dorsal rootganglion
FINE TOUCH
Aβ fibers (large) enter the spinal cord medial to Aδ, C fibers (small)
CLICK
MAIN SECTION
Medullagracile nucleus
cuneate nucleus
mediallemniscus2nd order
sacrallumbarthoraciccervical
CROSS
internalarcuate
fibers2nd order
FINE TOUCH
CLICK
MAIN SECTION
Pons
trigeminal main sensory nucleus
trigeminal ganglion
trigeminal motor nucleus
medial lemniscus2nd order
sacrallumbarthoraciccervicaltrigeminal – sensory
FINE TOUCH
CLICK
MAIN SECTION
Midbrain
mediallemniscus2nd order
inferiorcolliculus
lateral lemniscus
sacrallumbarthoraciccervicaltrigeminal – sensory
FINE TOUCH
CLICK
MAIN SECTION
Midbrainsuperior
colliculus
red nucleus
sacrallumbarthoraciccervicaltrigeminal – sensory
mediallemniscus2nd order
laterallemniscus
FINE TOUCH
CLICK
MAIN SECTION
Forebrain
sacrallumbarthoraciccervicaltrigeminal – sensory
VPM*
VPL*
internal capsule3rd order
click here for horizontal section
primary somato-sensory cortex
click here
FINE TOUCH
CLICK
MAIN SECTION
* These nuclei are slightly displaced in this view, to illustrate that trigeminal input VPM and body input VPL
Internal Capsule – Horizontal Section
anterior limb
posterior limb
sacrallumbarthoraciccervicaltrigeminal – sensory
genu
MAIN SECTION
Spinal Cord
sacrallumbarthoraciccervical
SL
dorsal rootganglion
Aδ fiber1st order
C fiber1st order
interneuron
Lissauer’s tract
substantia gelatinosa (RL II)
nucleus proprius(RL III, IV)
CROSS
2nd order tracts:spinothalamic/spinoreticular/spinomesencephalic
anterior white commissure2nd order
TC
PAIN/TEMP
Aδ, C fibers (small) enter the spinal cord lateral to Aα fibers (large)
posterior marginalis (RL I)
CLICK
MAIN SECTION
RL = Rexed lamina
Medulla
sacrallumbarthoraciccervicaltrigeminal – sensory
trigeminalafferent1st order
trigeminalspinal tract
1st order
trigeminalspinal nucleus CROSS
PAIN/TEMP
2nd order tracts:spinothalamic/spinoreticular/spinomesencephalic
medullary reticularformation
CLICK Show Spinoreticular Tract
MAIN SECTION
Pons
trigeminal ganglion
trigeminalafferent1st order
[to medulla]
sacrallumbarthoraciccervicaltrigeminal – sensory
trigeminal spinal tract
1st order
spinothalamic, spinomesenephalictracts2nd order
PAIN/TEMP
pontine reticularformation
CLICK Show Spinoreticular Tract
MAIN SECTION
Midbrain
spinothalamic/spinomesen-cephalic tracts2nd order
sacrallumbarthoraciccervicaltrigeminal – sensory
inferiorcolliculus
mediallemniscus
PAIN/TEMP
CLICK
MAIN SECTION
Midbrainsuperior
colliculus
red nucleus
sacrallumbarthoraciccervicaltrigeminal – sensory
mediallemniscus
spinothalamic tract2nd order
PAIN/TEMP
periaqueductal gray (PAG)
mesencephalicreticularformation
CLICK Show Spinomesencepahalic
Tract
MAIN SECTION
Forebrain
sacrallumbarthoraciccervicaltrigeminal – sensory
VPM*
VPL*
internal capsule(posterior limb)
3rd order
PAIN/TEMP
Spinothalamic tract (no evidence for orderly topographic cortical map)
primary somato-sensory cortex
click here
CLICK
MAIN SECTION
* These nuclei are slightly displaced in this view, to illustrate that trigeminal input VPM and body input VPL
Spinal Cord - SacralPROPRIOCEPTION
dorsal rootganglion dorsal columns
Aα fibers (large) enter the spinal cord medial to Aδ, C fibers (small)
afferent Aα fiber1st order
CLICK
MAIN SECTION
Spinal Cord - Thoracic
Clarke’s nucleus(dorsal nucleus)
T1-L2
dorsalspinocerebellar
tract2nd order
PROPRIOCEPTION
CLICK
MAIN SECTION
Spinal Cord - Cervical
dorsal rootganglion
dorsal columns
dorsalspinocerebellar
tract2nd order
PROPRIOCEPTION
afferent Aα fiber1st order
CLICK
MAIN SECTION
Medulla
dorsalspinocerebellar
tract2nd order
cuneocerebellar tract2nd order
external (accessory)cuneate nucleus
PROPRIOCEPTION
CLICK
MAIN SECTION
Medullainferior
cerebellar peduncle2nd order
PROPRIOCEPTION
CLICK
MAIN SECTION
Cerebellum
deep cerebellar nuclei (see right)
medial (fastigius)
interposed (globose + emboliform)
lateral (dentate)
mossy fibers
inferior cerebellarpeduncle (restiform body)
PROPRIOCEPTION
CLICK
MAIN SECTION
Pons
trigeminal ganglion
efferent α-MN in CN V3(to masseter, temporalis)
mesencephalic ganglion
trigeminal motor nucleus
afferent Aα fiber(from masseter, temporalis)
PROPRIOCEPTIONCLICK
MAIN SECTION
Forebrain
internal capsule(posterior limb)
Precentral, prefrontal, postcentral gyri
cerebral peduncle
to lumbar spinal cordto cervical spinal cordto CN motor nuclei
CORTICOSPINAL/CORTICOBULBAR
corona radiata
CLICK
MAIN SECTION
Midbrain
to lumbar spinal cordto cervical spinal cordto CN motor nuclei
cerebral peduncle
superiorcolliculus
red nucleus
oculomotor nucleus
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
Midbrain
trochlear nucleus
inferiorcolliculus
cerebral peduncle
to lumbar spinal cordto cervical spinal cordto CN motor nuclei
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
Pons
corticospinal tract
middle cerebellar peduncle
trigeminal (CN V) motor nucleus
to lumbar spinal cordto cervical spinal cordto CN motor nuclei
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
Ponsabducens (CN VI)
nucleus
facial (CN VII) nucleus
This nucleus is complicated – click here corticospinal
tract
middle cerebellar peduncle
to lumbar spinal cordto cervical spinal cordto CN motor nuclei
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
Medullahypoglossal (CN XII)
nucleus
nucleus ambiguous
corticospinal tract
to lumbar spinal cordto cervical spinal cordto CN motor nuclei
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
Medulla
CROSS
trigeminal (CN V) spinal nucleus
pyramidal decussation
pyramidto lumbar spinal cordto cervical spinal cord
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
Spinal Cord - Cervical
ventral horn
lateral corticospinal
tract
anterior corticospinal tract
to lumbar spinal cordto cervical spinal cord
ventral white commissure
PF DF
PE DE Regions of the ventral horn that innervate…- proximal flexors = PF- distal flexors = DF- proximal extensors = PE- distal extensors = DE
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
CROSS
Spinal Cord - Thoracic
to lumbar spinal cord
lateral corticospinal
tract
anterior corticospinal tract
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
Spinal Cord - Sacral
lateral corticospinal
tract
anterior corticospinal tract
ventral horn
to lumbar spinal cord
ventral white commissure
CORTICOSPINAL/CORTICOBULBAR
CLICK
MAIN SECTION
CROSS
Midbrain
rubrospinaltectospinal
superior colliculus
red nucleus
RUBROSPINAL/TECTOSPINAL
dorsal tegmental decussation
ventral tegmental decussation
input from forebrainCLICK
MAIN SECTION
Ponstectospinal tract
pontine reticular formation
rubrospinal tract
rubrospinaltectospinal
RUBROSPINAL/TECTOSPINAL
CLICK
MAIN SECTION
Medullatectospinal tract
rubrospinal tract
medullary reticular formation
MLF
rubrospinaltectospinal
RUBROSPINAL/TECTOSPINAL
CLICK
MAIN SECTION
Medulla
tectospinal tract
rubrospinal tract
trigeminal (CN V) spinal nucleus
pyramidal decussation
pyramidrubrospinaltectospinal
RUBROSPINAL/TECTOSPINAL
CLICK
MAIN SECTION
Spinal Cord - Cervical
rubrospinaltectospinal
tectospinal tract
rubrospinal tract
ventral horn
RUBROSPINAL/TECTOSPINAL
CLICK
MAIN SECTION
Spinal Cord - Lumbar
rubrospinal
rubrospinal tract
ventral horn
RUBROSPINAL/TECTOSPINAL
CLICK
MAIN SECTION
Pons
medial reticulospinal tractlateral reticulospinal tract
pontine reticular formation
medial longitudinal fasciculus (MLF)
RETICULOSPINALCLICK
MAIN SECTION
MedullaMLF
medial reticulospinal tractlateral reticulospinal tract
RETICULOSPINALCLICK
MAIN SECTION
Medulla
MLF
medial reticulospinal tractlateral reticulospinal tract
RETICULOSPINALCLICK
MAIN SECTION
Spinal Cord - Cervical
medial reticulospinal tractlateral reticulospinal tract
RETICULOSPINALCLICK
MAIN SECTION
Spinal Cord - Thoracic
medial reticulospinal tractlateral reticulospinal tract
RETICULOSPINALCLICK
MAIN SECTION
Spinal Cord - Lumbar
medial reticulospinal tractlateral reticulospinal tract
RETICULOSPINALCLICK
MAIN SECTION
Ponslateral vestibular
nucleus
medial vestibular nucleus
medial longitudinal fasciculus (MLF)
medial vestibulospinal tractlateral vestibulospinal tract
VESTIBULOSPINALCLICK
MAIN SECTION
Medulla
medial vestibulospinal tractlateral vestibulospinal tract
MLF
VESTIBULOSPINALCLICK
MAIN SECTION
Spinal Cord - Cervical
medial vestibulospinal tractlateral vestibulospinal tract
VESTIBULOSPINALCLICK
MAIN SECTION
Spinal Cord - Thoracic
lateral vestibulospinal tract
VESTIBULOSPINALCLICK
MAIN SECTION
Spinal Cord - Lumbar
lateral vestibulospinal tract
VESTIBULOSPINALCLICK
MAIN SECTION
Brainstem Atlas
• Open Medulla• Lower Pons• Middle Pons• Upper Pons• Midbrain
MAIN
Open MedullaCN XII nucleus
medial longitudinal fasciculus
medial lemniscus
inferior olivary fibers
pyramids
dorsal motor nucleus of the vagus
medial vestibular nucleus
nucleus of the solitary tract
solitary tract
spinal trigeminal tract
spinal trigeminal nucleus
nucleus ambiguus
inferior olivary nucleus
inferior cerebellar peduncle
nucleus raphe magnus
Medial Syndrome
Lateral Syndrome
MAIN SECTION
Lower PonsCN VI nucleus
medial longitudinal fasciculusmedial
lemniscus
pontine fibers
corticospinal tract
CN VII motor nucleus
medial vestibular nucleus
lateral vestibular nucleus
superior olivary nuclear complex
pontine nuclei
middle cerebellar peduncle
lateral lemniscus
spinothalamic tract
raphe nuclei
Medial Syndrome
Lateral Syndrome
MAIN SECTION
Middle PonsCN V main sensory nucleus
CN V motor nucleus
lateral lemniscus
CN V mesencephalic nucleus
CN V mesencephalic tract
Medial Syndrome
Lateral Syndrome
MAIN SECTION
Upper Pons
central tegmental bundle
medial longitudinal fasciculus
medial lemniscus
corticospinal tract
pontocerebellar fibers
locus coeruleus
parabrachial region
periaqueductal gray
Medial Syndrome
Lateral Syndrome
MAIN SECTION
Midbrain
medial lemniscus
superior cerebellar peduncle
red nucleus
CN III
cerebral peduncle
superior [inferior is caudal] colliculusperiaqueductal gray
Click here to expand this region
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
ARTERY: anterior spinal artery
Loss of vestibuloocular reflex*Tongue paralysisLoss of fine touch (contralateral)Cerebellar ataxiaLimb paralysis (contralateral)
CN XII nucleus
medial longitudinal fasciculus
medial lemniscus
inferior olivary fibers
pyramids
MAIN SECTION
* VOR might be preserved because this is below the level of the vestibular nuclei
Lateral Medullary Syndrome
ARTERY: posterior inferior cerebellar artery (PICA)
Loss of facial pain/temp sensation (ipsilateral)Hoarseness, difficulty swallowingHorner’s syndrome, ipsilateral loss of sweatingCerebellar ataxiaLoss of body pain/temp sensation (contralateral)
nucleus ambiguus
CN V spinal nucleus
descending symapthetic
tract
dorsal spinocerebellar
tract
spinothalamic tract
MAIN SECTION
Medial Inferior Pontine Syndrome
ARTERY: paramedian branches of the basilar artery
Loss of vestibuloocular reflexLoss of lateral rectus (ipsilateral)Loss of fine touch (contralateral)Cerebellar ataxiaLimb paralysis (contralateral)
CN VI nucleus
medial longitudinal fasciculusmedial
lemniscus
pontine fibers
corticospinal tract
MAIN SECTION
Lateral Inferior Pontine Syndrome
ARTERY: anterior inferior cerebellar artery (AICA)
Loss of facial pain/temp sensation (ipsilateral)Loss of body pain/temp sensation (contralateral)Hearing deficit (ipsilateral), vertigoFacial paralysis (ipsilateral)
spinothalamic tract
CN V spinal nucleus
CN VIII
CN VII
MAIN SECTION
Medial Mid-Pontine Syndrome
ARTERY: paramedian branches of the basilar artery
Limb paralysis (contralateral)Facial paralysisCerebellar ataxia
corticobulbar tract
corticospinal tract
corticopontine/ pontocerebellar
fibers
MAIN SECTION
Lateral Mid-Pontine Syndrome
ARTERY: circumferential branches of the basilar artery
Weakened masticationLoss of facial sensation (ipsilateral)No deficit reported
CN V main sensory nucleus
CN V motor nucleus
lateral lemniscus
MAIN SECTION
Medial Superior Pontine Syndrome
ARTERY: paramedian branches of the upper basilar artery
Loss of vestibuloocular reflexSoft palate temorLoss of fine touch (contralateral)Limb paralysis (contralateral)Cerebellar ataxia
central tegmental bundle
medial longitudinal fasciculus
medial lemniscus
corticospinal tract
pontocerebellar fibers
MAIN SECTION
Lateral Superior Pontine Syndrome
ARTERY: superior cerebellar artery
Cerebellar ataxiaLoss of body pain/temp sensation (contralateral)Loss of fine touch (contralateral)
spinothalamic tract
superior cerebellar peduncle
medial lemniscus
pontocerebellar fibers
MAIN SECTION
Tegmental Syndrome
ARTERY: paramedian branches of the basilar a. / posterior cerebral a.
Cerebellar ataxiaLoss of fine touch to body and face (contralateral)No deficit reportedLoss of pupil constriction; lateral strabismus
medial lemniscus
superior cerebellar peduncle
red nucleus
CN III
MAIN SECTION
Ventral Syndrome
ARTERY: paramedian branches of the basilar a. / posterior cerebral a.
Paralysis (contralateral)Loss of pupil constriction; lateral strabismus
cerebral peduncle
CN III
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 DistributionPeripheral 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 DistributionCentral 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, positionPain/temp
Ipsilateral, lesion on downContralat., lesion on down
Complete cord transection
All sensation Lesion on down
MAIN SECTION
Lesions - Forebrain
Lesion location Sensory loss DistributionThalamus All sensation Contralateral (peri-oral
facial sparing from ipsi fibers)
Cortex Varies by location of lesion
Contralateral
MAIN SECTION
Peripheral Receptors
Merkel’s disk
Meissner’s corpuscle
Pacinian corpuscle
Ruffini ending
Dermis
Epidermis
Click on a receptor:
free nerve ending
MAIN SECTION
Merkel’s DiskDiscriminative Touch Mechanoreceptor
Location: EpidermisSpecificity: Steady skin indentation – form, textureDynamics: Slow-adaptingSpatial Range: Small receptive field (3-4 mm fingers, 30-40 cm trunk)
2-point discrimination threshold = 1 mm fingers, 10 cm trunkConduction: Aδ fiber – 25 m/s
MAIN SECTION RECEPTORS
Location: DermisSpecificity: Flutter; contact and movementDynamics: Fast-adaptingSpatial Range: Small receptive field (3-4 mm fingers, 30-40 cm trunk)
2-point discrimination threshold = 1 mm fingers, 10 cm trunkConduction: Aδ fiber – 25 m/s
Meissner’s CorpuscleDiscriminative Touch Mechanoreceptor
MAIN SECTION RECEPTORS
Location: Subcutaneous tissueSpecificity: Non-localized vibrationDynamics: Fast-adaptingSpatial Range: Large receptive fieldConduction: Aδ fiber – 25 m/s
Pacinian CorpuscleDiscriminative Touch Mechanoreceptor
MAIN SECTION RECEPTORS
Location: DermisSpecificity: Low frequency stimulationDynamics: Slow-adaptingSpatial Range: Large receptive fieldConduction: Aδ fiber – 25 m/s
Ruffini EndingDiscriminative Touch Mechanoreceptor
MAIN SECTION RECEPTORS
Free Nerve EndingPain/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
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
S2
M1
Click on an area:
Click here for S1 topographyClick here for S1 histology
MAIN SECTION
Somatosensory Cortex
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
M1
Click on an area:
S1 – Area 3a• Input from thalamic shell (muscles, joints, deep
mechanoreceptors)• RFs similar to periphery
S2
Click here for S1 topographyClick here for S1 histology
MAIN SECTION
Somatosensory Cortex
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
M1
Click on an area:
S1 – Area 3b• Input from thalamic core (VPM/VPL - cutaneous)• Each column within 3b is specific for one type of
cutaneous receptor• Smallest RFs
S2
Click here for S1 topographyClick here for S1 histology
MAIN SECTION
Somatosensory Cortex
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
M1
Click on an area:
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
Click here for S1 topographyClick here for S1 histology
MAIN SECTION
Somatosensory Cortex
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
M1
Click on an area:
S1 – Area 2• Input from 3a, 3b and thalamic core (cutaneous) +
shell (muscle)• Large, complex RFs• Combines tactile and muscle info• LESION poor stereognosis, can’t pick up small
objects or maneuver hand through tight places
S2
Click here for S1 topographyClick here for S1 histology
MAIN SECTION
Somatosensory Cortex
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
S2
M1
Click on an area:
S2• Input from S1 and thalamus• 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
Click here for S1 topographyClick here for S1 histology
MAIN SECTION
Somatosensory Cortex
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
M1
Click on an area:
Area 5• Input from area 2 (S1)• Cutaneous plus movement• Very complex RFs: Multi-joint, multi-limb• Responds differently to active and passive movement
S2
Click here for S1 topographyClick here for S1 histology
MAIN SECTION
Somatosensory Cortex
4
3a
3b
1
2
5
7
lateral sulcus
central sulcus
postcentral gyrus intraparietal sulcus
posteriorparietal lobule central
sulcus postcentral gyrus – S1intraparietalsulcus
posteriorparietal lobule
M1
Click on an area:
Area 7• High order visual area• Activity reflects spatial properties of visual stimuli• Large RFs, prominent effects of behavioral relevance
S2
Click here for S1 topographyClick 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
precentral gyrusMOTOR
postcentral gyrusSENSORY
I
II
III
IV 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 damageMAIN SECTION
Pain
• Types of Pain– Nociceptive– Inflammatory– Neuropathic
• Central Pain Modulation• Sensitization
– Peripheral– Central
MAIN
Nociceptive Pain
TISSUEINJURY
ACTIVATENOCICEPTORS
Types of Nociceptors
MAIN SECTION
Inflammatory Pain
INSULTINFLAMMATORYMEDIATORS
NOCICEPTORACTIVATION
MAIN SECTION
Neuropathic Pain
REPETITIVE STRESSINJURY (TO NERVES) LESION
PAIN
MAIN SECTION
Types of Nociceptors
• Location: Everywhere but the CNS• Neurotransmitters:
– All are excitatory glutamatergic (AMPA, NMDA, kainate, metabotropic)– Some express peptide NTs like substance P, CGRP, NPY
Nociceptor Responds to…Fiber typeMyelinationConduction
Type of painChannel types(Transduction)
Thermal Extreme temperature (>45oC or < 5oC)
Aδ Light myelin5-30 m/s
Sharp, stinging, well localized
TRP (Transient Receptor Potential)
Mechanical Intense pressure AδLight myelin5-30 m/s
Sharp, stinging, well localized
DEG/ENaC (ASIC - Acid Sensing Ion Channel)Maybe TRP
Polymodal Extreme temperatureIntense pressureNoxious chemicals
C fibersNo myelin1 m/s
Dull aching or burning, prolonged, poorly localized
DEG/ENaC (ASIC)
MAIN SECTION
Central Pain ModulationPAGElectrically stimulate or apply opiates here
nucleus raphe magnus (NRM)
NRM projectionterminus
5-HTinhibits
dorsal horn neuron(ascending pain afferent)
NOTE:1) Dorsal horn neuron also receives
descending pain-facilitation inputs.2) Serotonin has other indirect effects,
involving opiate receptors and enkephalins.
via dorsolateral funiculus
dorsal horn
CLICK
MAIN SECTION
Sensitization - Peripheral
Injury
Release bradykinin, prostaglandins
subs
tance
P
stimulate
mast cell
degranulation
histamine
dorsal horn
dorsal root ganglion
excite
activate/sensitize
Sensitization can occur via:1) Potentiation of sensory transduction channel function2) Enhancement of neuronal excitability
nociceptor /peripheral ending
MAIN SECTION
CLICK
Sensitization - Central
dorsal horn
nociceptorterminus
dorsal hornneuron
Limbic augmentation(anxiety, anticipation, etc.)
PPP
PP
P
Hyperphosphoryl-ation of ion
channels in dorsal horn neurons
Increased excitability of dorsal
horn neurons
Chronic pain
+ Repeated stimulation (e.g., by nociceptors)
....
ion channels
MAIN SECTION
CLICK
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 amotor nerve
Weakness or paralysis Fibrillation (spontaneous firing of single muscle fibers)
Disease ofmotor neurons
Weakness or paralysisFasciculation (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
prefrontal cortex
PMA SMA
M1 (Area 4) central sulcus
S1
Area 6
Area 5
Area 7
posterior parietal cortex
Primary motor cortex
PMA = premotor areaSMA = supplementary motor area
Somatosensory cortical areas
Secondary motor cortical areas
Click:
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 (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
precentral gyrusMOTOR
postcentral gyrusSENSORY
III
III
V
VI
contains large pyramidal Betz cells
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
• High level planning of movements
• Thinking about movements without actually making them
• Arm the transcortical reflexes – click here for more info
SMA, PMC, PFC
MAIN SECTION CORTEX
Reflexes
• Muscle Spindle• Golgi Tendon Organ• Reciprocal Inhibition• “Crossed Extension” Flexor Reflex• Locomotion• Transcortical Reflex
MAIN SECTION
Muscle Spindle
muscle spindle
quadriceps
biceps tendon
1a or IIafferent
α-MN
γ1- or
γ2-MN
1) Hit tendon
2) Spindle stimulated (1a, II)
3) α-MN fires muscle contracts
γ-MN fires spindle fibers contract
* click on label for details
chain fiber bag fiber
4) Renshaw cell inhibits α-MN
Renshaw cell stimulated
1a*
II*
to spinalcord
γ2-MN*
γ1-MN*
α-MN *
fromspinal
cord
Muscle spindle is involved in…(click here)
MAIN SECTION REFLEXES
CLICK
Golgi Tendon Organ (GTO)
α-MN
α-MN
Ibafferent
Ib afferent
to spinalcord
fromspinal
cord
inhibitory interneuron
1) High muscle tension (force)2) GTO stimulated (Ib)
3) Interneuron inhibits α-MN 4) α-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)
GTO is involved in:• Clonus• Claspknife reflex
GTO
MAIN SECTION REFLEXES
CLICK
Reciprocal Inhibition
agonist muscle(flexor)
muscle spindle
1a afferent
α-MN to agonist
α-MN to antagonist
antagonist muscle(extensor)
inhibitoryinterneuron
INHIBITED
ACTIVATED
MAIN SECTION REFLEXES
CLICK
“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 Modulationmotor cortex
midbrain locomotorregion (MLR)
corticospinal tracts
reticulospinal tract
Initiate locomotory activity in spinal cord circuits
Modify locomotory activity for voluntary corrections of gait (obstacle avoidance)
MAIN SECTION REFLEXES
Transcortical ReflexesSMA
α-MN
γ-MN
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
Hyperactive palpatory reflex
(“involuntary grasp reflex”)
Hyperactive long loop stretch reflex (“Gegenhalten” – resistance to limb displacement)
These are involuntary
1a afferent
MAIN SECTION REFLEXES
CLICK
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.
Normal Postural Reflexes
Head up Head normal Head downN
eck
exte
nded
Nec
k no
rmal
Nec
k fle
xed
VSR aloneTNR aloneVSR – TNRVSR + TNR
VSR = vestibulospinal reflexTNR = tonic neck reflex
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
Tips for learning this chart
MAIN SECTION
Abnormal Posture
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.
Normal Postural Reflexes
Head up Head normal Head downN
eck
exte
nded
Nec
k no
rmal
Nec
k fle
xed
VSR aloneTNR aloneVSR – TNRVSR + TNR
VSR = vestibulospinal reflexTNR = tonic neck reflex
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
1) Know that for VSR alone (head movement only), head up forelimbs flex & hindlimbs extend (and opposite if head is down).
2) Know that for TNR alone (neck movement only), neck extended forelimbs extend & hindlimbs flex (and opposite if neck is flexed).
3) Combining a head movement and neck movement: • If the limb positions resulting from VSR and TNR agree, then the reflexes add (limb hyper-extension/flexion).• If the limb positions resulting from VSR and TNR disagree, then the reflexes cancel (no limb movement).
MAIN SECTION
Abnormal Posture
When the head is passively turned to one side, the looked-at limbs will extend and the others will flex.
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)– Damage the tectospinal, and corticospinal pathways– Vestibulospinal pathway remains intact
• Usually more serious than internal capsule injury (decorticate posture)
• Flexion of upper limb, extension of lower limb, slight intorsion of legs
• Hyperactive vestibulo-spinal AND tonic neck reflexes (see right)
• Caused by a lesion of the internal capsule (corticospinal pathway)D
EC
OR
TIC
ATE
DE
CE
RE
BR
ATE
MAIN SECTION
CN VII Innervation
to lower facial muscles (left)
to upper facial muscles (left)
R L
CN VII nuclei
Click on a lesion site (circled in purple)NORMAL
MAIN SECTION
CN VII Innervation
to lower facial muscles (left)
to upper facial muscles (left)
R L
CN VII nuclei
X
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
to lower facial muscles (left)
to upper facial muscles (left)
R L
CN VII nuclei
X
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
Caudate
Putamen
Nucleus accumbens
Globus pallidus, externa (GPe)
Globus pallidus, interna (GPi)
Amydala (part of lymbic system)
Subthalamic nucleus (STN)
Substantia nigra – click here- pars reticulata (SNpr)- pars compacta (SNpc)
Lenticular nucleus = Globus pallidus + Putamen
Striatum = Globus pallidus + Putamen + Caudate
ROSTRAL
CAUDAL
Connections
Diseases
Selection-Brake
NTs
MAIN SECTION
Substantia Nigra - Histology
SNpcdopaminergic
SNprGABAergic
MAIN SECTION BG
Basal Ganglia Neurotransmitters
• Dopamine• GABA• Enkephalin• Substance P• Glutamate• ACh
NOT norepinephrine
MAIN SECTION BG
Basal Ganglia Connections
SNpcGPe
GPi
SNpr
STN
VA/VL
PPPA
SC brainstem/spinal cord
cerebral cortex
caudate / putamenSC = superior colliculusPPPA = peri-pedunculo-pontine areaVA/VL = ventroanterior/ventrolateral nuclei of thalamus
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.
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.
The globus pallidus (GPe and GPi) are both in communication with the STN.
= excitatory (Glu)= inhibitory (GABA)= mixed (DA)= unknown
Show selection-brake mechanismMAIN SECTION BG
CLICK
Basal Ganglia Connectionscerebral cortex
SC = superior colliculusPPPA = peri-pedunculo-pontine areaVA/VL = ventroanterior/ventrolateral nuclei of thalamus
= excitatory (Glu)= inhibitory (GABA)= mixed (DA)= unknown
SNpcGPe
GPi
SNpr
STN
VA/VL
PPPA
SC brainstem/spinal cord
caudate / putamen
Person wants to make a voluntary movement
Premotor/motor cortex excite STN
STN excites GPi
GPi inhibits MPGs
DIRECT path from caudate/putamen to GPi INHIBITS GPi
INDIRECT path from caudate/putamen GPe GPi DISINHIBITS GPi
Release the MPGs (those desired for the movement)
Shut down the MPGs (those interfering with the movement)
= excitatory= inhibitory
MAIN SECTION BG
CLICK
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
• 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
General Pathophysiology
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
molecular layer
Purkinje cell layer
granule cell layer
white matter
Click here to overlay cell types/connections
MAIN SECTION CB
Cerebellar Folium
Purkinje cell
Granule cell
Climbing fiber
Mossy fiberparallel fiber
terminal(synapse)
dendrite
terminal
dendrite synapse
axon
to the deep nuclei
Click on a cell type:
Stellate cell
Basket cell
Golgi cell
Not shown (can click):
MAIN SECTION CB
Purkinje Cell• One Purkinje cell receives
input from…– 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
Purkinje cell body
mol
ecul
ar la
yer
gran
ule
cell
laye
r
Purkinje cell dendrite
MAIN SECTION CB
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
• Fire at high rates when learning movement, low rates during learned movement
mol
ecul
ar la
yer
gran
ule
cell
laye
r
climbing fiber
MAIN SECTION CB
Granule Cell• Receives input from mossy fibers
in the granule cell layer– 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
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
granule cell
parallel fiber
mol
ecul
ar la
yer
gran
ule
cell
laye
r
MAIN SECTION CB
Mossy Fiber• Originates in the…
– Spinocerebellar pathway• Ascending (from spinal cord)• Fibers do not cross• Enters cerebellum through the
inferior cerebellar peduncle– Pons
• Descending (from cerebral cortex)
• These fibers must cross in the 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
mossy fibers
mol
ecul
ar la
yer
gran
ule
cell
laye
r
MAIN SECTION CB
Inhibitory Interneurons
Stellate cell• Molecular layer
Basket cell• Cell body in molecular layer• Projections wrap around Purkinje cell
Golgi cell• Granule cell layer
basket cell Purkinje cell body
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
Fastigial (medial) nucleusDentate (lateral) nucleusGlobose/emboliform (intermediate) nuclei
Click on a 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
• 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.
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) Combined digit movements
(2) Arm/leg reaching to a visual target
(1) Incoordination of digits(2) Overshoot targets in
reaching with arm/leg
MAIN SECTION CB
Cerebellar Connections
ventrolateral thalamus
red nucleus
vestibular nuclei
reticular formation
All cerebellar projections are excitatory
MAIN SECTION CB
Autonomic Nervous System
• Efferents/Afferents• Circumventricular Organs• Functions
– Baroreceptor– Respiration– Micturition
• Periaqueductal Gray (PAG)
MAIN
Viscero-Motor Efferents / Visceral AfferentsSympathetic 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 XMAIN SECTION
CN III Parasympathetics
Edinger-Westphal nucleus
CN III nucleus
CN IIIciliary ganglion
to pupilloconstrictor and ciliary muscles
Pupillary Constriction and Accommodation
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 Parasympatheticsdorsal nucleus of CN X nucleus of the solitary tract
nucleus ambiguus
= secretomotor efferents= vasomotor efferents= visceral afferents
GUT
HEART
PHARYNX/ LARYNX
MAIN SECTION
Circumventricular Organs
area postrema
dorsal nucleus of CN X
nucleus of the solitary tract
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
Baroreceptor Reflex
nucleus of the solitary tract
nucleus ambiguus
caudal ventrolateral medulla
rostral ventrolateral medulla
intermedio-lateral column
peripheral arterioles
aortic arch baroreceptors
carotid sinus baroreceptors
tonic
= inhibitory= excitatory= parasympathetic= sympathetic
MAIN SECTION
RespirationForebrain
Parabrachial nucleus
Lung stretch receptorsCarotid body chemoreceptors Intrinsic chemoreceptors
Nucleus of the solitary tract
Rostral inspiratoryExcitatory
Caudal expiratoryExcitatory
Botzinger complexReciprocal inhibition
Phrenic motorneuronsExt. intercostals
Int. intercostal motorneuronsAbdominal muscles
Ventral respiratory pre-motor cells
= excitatory= inhibitory
Pre-Botzinger cellsRespiratory rhythm
VENTROLATERALMEDULLA
MAIN SECTION
MicturitionHypothalamus, PAG
pontine micturition center (parabrahial region)
sacral spinal cord
bladder
= afferent= efferent
Short loop reflex
Long loop reflex
MAIN SECTION
MicturitionHypothalamus, PAG
pontine micturition center (parabrahial region)
sacral spinal cord
bladder
= afferent= efferent
Short loop reflex- Bladder stretch triggers bladder contraction- Used by infants
MAIN SECTION
MicturitionHypothalamus, PAG
pontine micturition center (parabrahial region)
sacral spinal cord
bladder
= afferent= efferent
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
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
Stabilize the eye when the head moves (reflexive)
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
Keep the fovea on a visual target (volitional control)
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
Vestibulo-Ocular Reflex (VOR)
Secondary pathway (visual cortex cerebellar flocculus)
semicircular canal
vestibular nuclear complex
motor nuclei to eye muscles
eye muscles
If the head moves left quickly, VOR causes the eyes to move right.
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.
The VOR depends on the stimulation of kinocilium in the vestibular labyrinth.
MAIN SECTION
CLICK
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
pos
ition
(deg
rees
)
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
Periventricular nucleus
Lateral hypothalamic area
Dorsomedial nucleus
Supraoptic nucleus
Ventromedial nucleus
Arcuate nucleus
fornix
median eminence
PVZ
MHA
LHA
ZONE STRUCTURE(S)
Paraventricular nucleus (not shown)
OTHER
PVZ = Periventricular zoneMHA = Medial hypothalamic zoneLHA = Lateral hypothalamic zone
Hypothalamus
Suprachiasmatic nucleus (not shown)
Hypothalamic Inputs
Hypothalamic OutputsAnterior Pituitary
Click on a zone, nucleus, or button
Posterior PituitaryPhysiological Regulation
MAIN
Hypothalamic Nuclei
fornix
median eminence
lateral hypothalamic area
ventromedial nucleus
fornix
arcuate nucleus
median eminence
paraventricular nucleus
orexin cells?
MAIN SECTION
Hypothalamic Nuclei
fornix
median eminence
supraoptic nucleus
anterior hypotha-lamic area
anterior commissure
suprachiasmatic nucleus
MAIN SECTION
Hypothalamic Nuclei
fornix
median eminence
lateral hypothalamic area ventromedial
nucleus
arcuate nucleus (dopa-minergic cells)
paraventricular nucleus
optic tract
dorsomedial nucleus
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 tractParabrachial nucleus
Taste, visceral sensation
Olfactory cortex Food, sexual attractants
Amygdala, hippocampus, prefrontal cortex (limbic input)
Cognition
Circumventricular organs Osmolality of bloodPeptide 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… EffectLateral hypothalamusParaventricular nucleus
Autonomic nuclei in spinal cord, brainstem(PAG, parabrachial nuclei, nucleus of the solitary tract, dorsal vagal nucleus, ventrolateral medulla, IML)
Control body temp (sweating, shivering, vasoconstriction)
Releasing hormone neurons in periventricular zone (arcuate nucleus and part of the paraventricular nucleus)
Median eminence Control of anterior pituitary
Supraoptic and paraventricular nuclei
Posterior pituitary Secrete ADH, oxytocin
Scattered large neurons Cerebral cortexLimbic structures
Not clear; presumably contribute to hypothalamic control of behavior
MAIN SECTION
Anterior Pituitary
CRHTRHGnRHGHRHSomatostatinDopamine
ACTHTSHLH/FSHGHGH/TSHMSH
median eminence
periventricular zone of the hypothalamus(arcuate nucleus and part of the paraven-tricular nucleus)
hypothalamic releasing hormones
corresponding anterior pituitary hormones
Hypothalamic cell axons terminate in the median eminence and secrete hormones into the fenestrated pituitary portal capillaries
MAIN SECTION
Posterior Pituitary
supraoptic nucleus / paraventricular nucleus
Posterior pituitary hormones:- oxytocin- ADH (vasopressin)
median eminence
Hypothalamic cell axons terminate in the posterior pituitary and secrete hormones into the fenestrated pituitary capillaries
MAIN SECTION
The hypothalamus regulates…
• Body temperature• Body weight• Ionic balance• Blood pressure (chronic)• Circadian rhythm• Reproduction• Response to stress
MAIN SECTION
Body Temperature
spinal cord
reticular formation
intrinsic thermoreceptors
releasing hormone neurons
anterior hypothalamus
TSH, GH, somatostatin
lateral hypothalamus
autonomic nuclei
sweating, shivering, etc.
cerebral cortex
behavior?
inputs
outputs/effects
MAIN SECTION REG
Body Weightviscera (gut)
food intake, gut distension
NTS / parabrachial nuclei
tonguetaste
NTS
olfactory cortexsmell
fat cells leptin(receptors in dorsomedial nucleus)
gut ghrelin
orexin
suppress food intake / increase metabolism
promote food intake / decrease metabolism
promote food intake / stabilize sleep
autonomic nuclei
pituitary
inputs
outputs/effects
MAIN SECTION REG
Ionic Balance
circumventricular organs
blood osmolality, peptide hormones
intrinsic osmorecptors
CSF tonicity
vena cava / R atriumblood volume
NTS
posterior pituitary
ADH
alter urine tonicity, Na+ and H2O intake
inputs
outputs/effects
MAIN SECTION REG
Blood Pressure (Chronic)
baroreceptors
NTS
angiotensin II
circumventricular organs
autonomic nuclei
vasoconstriction
inputs
outputs/effects
posterior pituitary
ADH
vasoconstriction, anti-diuretic action
on kidney
MAIN SECTION REG
Circadian Rhythm
retina
inputs
outputs/effects
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.
suprachiasmatic nucleus
MAIN SECTION REG
Reproduction
olfactory system
gonadal steroids
inputs
outputs/effects
reproduction
amygdala / hippocampus
emotion, memory
MAIN SECTION REG
Response to Stress
ascending catecholamine
systems
limbic system
inputs
outputs/effects
CRH
ACTH
glucosteroid release from adrenal cortex
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 Systemcingulate gyrus / cingulum
amygdala
fornix
hippocampus
parahippocampal gyrus
dentate gyrus
mammillary body
stria terminalisolfactory bulb
anterior commissure
hypothalamus
orbital/medial prefrontal cortex
Not shown: olfactory cortex
MAIN
Amygdala
central nucleus
basal nucleus
accessory basal nucleus
lateral nucleus
medial nucleus
PAC
PAC = periamygdaloid complex
Dorsal nuclei
Deep nuclei
nucleus basalis of Meynert
amydala
entorhinal cortex
Role
Inputs/Outputs
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
ascending sensory system
vision, olfactory, auditory, somatosensory
inputs
outputs/effects
autonomic cell groupslateral hypothalamus, PAG,
parabrachial nucleus, NTS, dorsal nucleus of CN X, ventrolateral medulla
influence HR, BP, gut/bowel/respiratory/bladder function, etc.
orbital/medial prefrontal cortex
determine whether sensory stimulus is
rewarding or aversive; set mood
direct OR via mediodorsal thalamus
thalamic relay nucleus
primary sensory cortex
secondary association
cortex
posterior intralaminar
thalamic nuclei
MAJOR SHORTCUT
The shortcut afferent pathway produces your initial “gut reaction” to a potentially threatening situation, before the major pathway kicks in.
feedback
OR via the ventromedial striatum
Amygdala
MAIN SECTION AMYG
Olfactory Bulbolfactory 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
primary olfactory cortex
olfactory tract
putamen
nucleus accumbens /olfactory tubercle
lateral striate arteries
• 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
MAIN SECTION
Olfactory Cortex
primary olfactory cortex
olfactory tract
putamen
nucleus accumbens /olfactory tubercle
lateral striate arteries
• 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
Nucleus accumbens- “Reward” center- Contains mostly GABAergic neurons- Receives input from the amygdala and hippocampus
MAIN SECTION
Hippocampus
tail of caudate
dentate gyrus
CA1
CA3
subiculum
pre-subiculum
para-subiculum
entorhinal cortex
inferior temporal area
Role
Inputs/Outputs
Alzheimer’s Disease
Information Flow
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
info from multisensory
association cortical areas
visual, auditory areas of inferior and superior temporal cortex
perirhinal/entorhinal cortex
inputs
outputs/effects
hypothalamus
Hippocampus
feedback prefrontal / cingulate cortical areas
basal ganglia (ventral)
direct O
R via ant. t
halamic nuc. /
mammillary
nuclei
MAIN SECTION HIPP
Hippocampus
tail of caudate
dentate gyrus
CA1
CA3
subiculum
pre-subiculum
para-subiculum
entorhinal cortex
inferior temporal area
to frontal cortex, anterior thalamus, hypothalamus
to the neocortex
sensory inputs from cerebral cortex
Role
Inputs/Outputs
Alzheimer’s Disease
Hide Information Flow
MAIN SECTION HIPP
CLICK
Alzheimer’s Disease
CA1
Sub
PreSubParaSub
EC
CA3
DG
β-amyloid plaques
tangles (intracellular)
CA1
• 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
inputs
outputs/effects
multimodal sensory inputs
assessment of food
amygdala / hippocampus
hypothalamus, PAG
control visceral functions
appropriate choices
reward/aversion
control of mood
MAIN SECTION
Sleep
• Electroencephalogram (EEG)• Stages• Ascending Reticular Activating System
MAIN
Electroencephalogram (EEG)
Synchronized waves
• High amplitude, low frequency
• Represent wave summation
• Result when similar events coincide
• Ex: δ waves of sleep
Desynchronized waves
• Low amplitude, high frequency
• Represent wave subtraction
• Result when disparate events coincide
• 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
thalamus
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
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)- Project back onto the principal thalamic nuclei- Histology
This system is active during wakefulness (and its stimulation causes waking). It is inactive during sleep (and its transection causes coma).
Neurotransmitters Sleep Initiation
MAIN SECTION
Ascending Reticular Activating SystemNucleus 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
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)- Project back onto the principal thalamic nuclei
This system is active during wakefulness (and its stimulation causes waking). It is inactive during sleep (and its transection causes coma).
reticular nucleus
ventrolateral thalamic nucleus
RAT BRAIN – Stained for GABA
MAIN SECTION SYS
Neurotransmitter Systems
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.
Ascending Reticular Activating System
MAIN SECTION SYS
Sleep Initiation
depolarizeAChNE
5-HT
depo
larize
hyperpolarize
sensory afferentseye, spinal cord, etc.
CORTEX
RETICULARNUCLEUS
THALAMICRELAY
NUCLEUS(TRN)
Add ascending ACh, NE, 5-HT input
RN inhibition of TRN is blocked
TRN cells respond to sensory input with a tonic firing pattern ( wakefulness)
Remove ascending ACh, NE, 5-HT input
RN inhibition of TRN is released RN bursting
TRN cells cannot respond to sensory input and fire in a rhythmic bursting pattern ( sleep spindles in early sleep stages)
thalamocortical neuron
= Excitatory (glutamate)= Inhibitory (GABA)
WAKEFULNESSSLEEP INITIATION
MAIN SECTION SYS
CLICK
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• Implicit (e.g., procedural)• Explicit (a.k.a declarative)• Working
MAIN
Memory Disorders• Alzheimer’s Disease• Lewy Body Dementia• Korsakov’s syndrome
Implicit Memory
• 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
Procedural
MAIN SECTION
Explicit Memory
• 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
Declarative
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
3rd ventricle
mammillary bodies
NORMAL KORSAKOV’S
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
MAIN SECTION
Lewy bodies
Language ProcessingCODES:• Visual / orthographic• Auditory / phonological• Syntactic / grammatical• 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”
Aphasia
MAIN
Note: This is not a thorough treatment of language processing, but these are the only questions I’ve seen on past exams…
AphasiaLoss or impairment of language function (caused by brain damage) during speech, hearing, reading, or writing
Broca’s Wernicke’sClick on 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
References
Bear, M.F., Connors, B.W., and Paradiso, M.A. Neuroscience: Exploring the Brain (2nd ed.). Baltimore: Lippincott Williams & Wilkins, 2001.
“Digital Anatomist: Interactive Brain Atlas.” http://www9.biostr.washington.edu/da.html.
Molavi, D.W. “Neuroscience Tutorial.” http://thalamus.wustl.edu/course/.
Monroe, Eric. “Brainstem Lesions,” 2006.
Neuroscience 2006 Course Notes, Part II. Washington University School of Medicine, St. Louis.
Woolsey, T., Hanaway, J., and Gado, M.H. The Brain Atlas (2nd ed.). New Jersey: John Wiley & Sons, Inc., 2003.
MAIN