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Recent Research Findings:
Implications for Interventions
• Paradoxical Kinesia (“motion”)
– A deficit to execute movements can be overcome
in the presence of external sensory cues (e.g.
visual, auditory, proprioception)
– Rationale: distinct contribution of the corticostriatal (implicit) and cortico-cerebellar (explicit)
systems to motor learning and control (Doyon,
2003)
– Provide external sensory cues to bypass the
defected cortico-striatal system
– Cycling (Bloem, 2010); Kick and Rush (Asmus,
2008)
PTP 512
Neuroscience in Physical Therapy
Sensation and Perception
Min H. Huang, PT, PhD, NCS
Reading Assignments
S & W: 131-132, 134-135
L-E: 108, 109, 113, 114, 136-141, 286-293
Objectives
• Compare somatosensory receptor neurons
relative to their size and myelination
• Describe the sensory function controlled by
neurons in each of the sensory pathways
• Sketch the sensory homunculus
• Describe the role of posterior parietal cortex
(areas 5 & 7) in sensory perception
• Apply knowledge of the sensory and perceptual
pathways to determine expected sensory loss or
impairment with injury to the peripheral nerve,
spinal cord, brainstem, or cortex
FUNCTION OF SENSORY RECEPTORS
AND PATHWAYS
Receptive Field for Cutaneous
Sensation
• Receptive field is the area that innervated
by a single afferent neuron.
• Where you may find the smallest receptive
field in the body?
Discuss at your table group
End
1. Identify the regions with impaired
sensation following injury to the C8 root of
brachial plexus vs. ulnar nerve distal to the
wrist vs. medial brachial cutaneous nerve
distal at the shoulder.
2. Are the affected regions the same or
different and why?
• Lundy’s Fig 6-4
Discuss at your table group
1. What is dermatome?
2. Compare and contrast the regions
innervated by the dermatomes vs.
cutaneous nerves. Why are they
different?
• Lundy’s Figure 6-5
End
End
Discussion at your table group
1. Compare and contrast somatosensory
receptor neurons relative to their axon
size and myelination
2. Describe the sensory function controlled
by neurons in each of the sensory
pathways
Lundy’s Table 6-1
Produced by Dave Foord
End
Large Diameter Neurons
• Large diameter axons conduct faster than small
diameter axons
– less resistance to electrical current in larger
axons
• Large diameter axons are myelinated
– allows “saltatory” conduction of action
potentials
• Large diameter axons are affected before small
diameter axons in nerve compression injuries
like carpal tunnel syndrome
End
Discussion at your table group
Describe the sensory function controlled by
neurons in each of the sensory pathways
Sensory Pathways
• Discriminative touch
– Where does it cross?
– Lundy’s CD: Touch
• Fast pain
– Where does it cross? Is it the same for the fast
pain pathways innervating the trunk vs. face?
– Lundy’s CD: Fast pain
PNS LESIONS
Types of Peripheral Nerve Injuries
Commonly Seen in Clinical Practice
• Stretch injuries
– Most common
– PN are inherently elastic
(20% stretch is OK, will
not injure nerve)
– e.g. Brachial plexus
birth-related injuries
• Laceration/severance
– e.g. injury caused by a
knife blade
http://orthoinfo.aaos.org/topic.cfm?topic=a00077
Types of Peripheral Nerve Injuries
Commonly Seen in Clinical Practice
• Compression injuries
– Due to mechanical
compression and ischemia
– Larger myelinated nerve
fibers are more susceptible
than smaller unmyelinated
nerve fibers.
– e.g. carpal tunnel syndrome,
Saturday night palsy
(entrapment of the nerve)
Compression Injuries: Changes in
Sensory Function
• Large myelinated fibers are affected first with
initial sparing of smaller pain, thermal, and
ANS fibers
• Sensory loss typically occurs in this sequence
1.
2.
3.
4.
5.
conscious proprioception / discriminate touch
cold
fast pain
heat
slow pain
• When compression is relieved, paresthesia
often develops
Compression Injuries: Changes in
Motor Function
• Difficult to identify the lesion in non-severe
cases because of extensive intermingling of
muscle fibers of different motor units in
compression injuries
• Innervated muscles become fatigue faster
than normal
– A patient with partial denervation lesion may
be able to recruit enough motor units to
generate a single max voluntary contraction to
be graded as "normal" on MMT
– Need to test for muscle fatigue
Compression Injuries: Changes in ANS
Function
• ANS symptoms are rare. Usually single
nerve is involved unless the nerve is
completely severed
• Symptoms include:
– lack of sweating
– loss of sympathetic control of smooth muscle
fibers leading to edema
– if multiple nerves are involved, may have
difficulty regulating BP, HR, sweating, bowel &
bladder function
PNS Structure
http://missinglink.ucsf.edu/lm/IDS_101_histo_resource/images/141Cx1_copy.jpg
Pathology of PNS Injury: Neurapraxia
(Class I)
• Temporary impairment of a local nerve
conduction. Mild mechanical disruption of
a nerve (e.g. carpal tunnel syndrome)
• Very subtle and localized demyelination
without loss of axonal continuity may be
present, typically without Wallerian
degeneration
http://harvester.lib.utah.edu/
Pathology of PNS Injury: Neuroapraxia
(Class I)
• Larger fibers are affected (e.g. efferent
fibers to αMN).
• Small sensory fibers are not affected
• Clinical features
– Marked reduction in muscle strength in a
specific distribution distal to the lesion
– Sensation may be similarly affected
– Nerve conduction across the lesion site is
slowed or absent, whereas above and below
the lesion it is normal
– Recovery in hours to weeks
Pathology of PNS Injury: Axonotmesis
(Class II)
• Caused by severe compression or stretching
that results in a loss of axonal continuity
but endoneurial, perineurium, and
epineurium are intact
• Leading to Wallerian degeneration (i.e.
axons and myelin degenerate) distal to the
site of injury within 48 hours of a severe
injury
http://harvester.lib.utah.edu/
Pathology of PNS Injury: Axonotmesis
(Class II)
• Axonal regeneration may occur at a rate of
about 1 mm/day
• Clinical features
– Muscle weakness or paralysis
• Up to 50% atrophy in 2 weeks
– Sensory loss in a specific distribution
– Conduction velocities across lesion site are
lost immediately
• Distal to the lesion are lost within a few days
A. Normal
B. Injury
C. Anterograde
degeneration
D. Loss of
connection
with muscle
E. Total
degeneration
F. Axons resprout using
remaining
Schwann cells
as guides and
re-innervate
the muscle.
Wallerian Degeneration
http://www.medscape.com/viewarticle/480071_4
Two alternative
models explaining
the greater axon
degeneration distal
to the lesion
(center). ‘Dying
back' model (top):
axonal degeneration
starts at the distal
end. Focal lesion
model (bottom):
focal lesions can
trigger Wallerian
degeneration of
distal axons.
http://www.nature.com/nrn/journal/v6/n11/fig_tab/nrn1788_F1.html
Pathology of PNS Injury: Neurotmesis
(Class III)
• A nerve injury characterized by loss of
axonal and all connective tissue continuity
• Usually results from a rapid stretch/avulsion
injury or complete severance of the nerve
• Clinical features
– Similar to axontomesis but more severe. The
prognosis is poor
– Surgical repair is necessary for any chance of
recovery
Patterns of somatosensory
impairments
• Peripheral nerve: nerve distribution
• Nerve root: dermatome
• Spinal cord: may involve different sensory tracts,
loss of sensation usually begins one or two
segments below the level of the lesion because of
branching of the afferent fibers in the spinal cord
• Brainstem: may have mixed ipsilateral/contralateral
sensory loss of the body and the face
• Cortical and subcortical structure above midbrain:
contralateral body/face
• Thalamus: contralateral body/face
• Somatosensory cortex: contralateral body/face
Blumefeld, 2010
Blumefeld, 2010
Blumefeld, 2010
SENSATION AND PERCEPTION
Sensation vs. Perception
Sensation
Perception
• The process of integrating,
• “Picking up” sensory
organizing and interpreting
information
sensations.
• The process of
• Creating meaningful
detecting a stimulus
patterns from sensory
(e.g. light waves-vision,
information
sound waves-heating,
• Require attention,
chemical moleculesmemory, integration of
taste, heat or pressurestimuli, motivation,
touch).
expectations etc.
Thalamus
“inner chamber” or “bedroom” in Greek
“egg-shaped” grey matter structure
The last synaptic site before sensory information
reaches cerebral cortex
Thalamic Connections
• In addition to processing sensory
information, thalamus is a major sensory
relay station
• Each sensory modality (except for
olfactory), including vision, hearing, taste,
and somatic sensation, has a different
nuclear area in the thalamus, where
synapses occur before the information is
relayed to the cerebral cortex.
Thalamic Connections
• Reciprocal projections between thalamus and
cortex
• Non-sensory pathways also relay their
information in the thalamus before reaching
the cerebral cortex, including motor inputs
from basal ganglia and cerebellum, inputs
from limbic system and brainstem reticular
formation.
What is the clinical implications of this?
Sensory Disturbances Associated with
Thalamic Lesions
• Lesions of the thalamus result in decreased or
lost sensation from the contralateral body or
face.
• Thalamic pain syndrome (central post stroke
pain syndrome)
– People with stroke often develop “thalamic pain
syndrome”
– Burning, pricking, aching, lacerating, shooting pain
– Pain can be spontaneous or evoked by mechanical
or thermal stimuli (e.g. touching a sheet or cold
surface)
Primary Sensory Cortex
Lundy’s
textbook, 2007
Primary Sensory Cortex: Function
Lundy’s
textbook, 2007
Sensory Association Cortex
Lundy’s
textbook, 2007
Sensory Association Cortex: Function
Unimodal sensation (one type of sensory modality)
Higher-order (cortical) sensation
Lundy’s
textbook, 2007
Posterior Parietal Cortex
(Areas 5 & 7)
• Cortical sensation
• Area 5 integrates information from different body
parts
• Area 7 also received processed visual information
• Area 7 combines eye-limb information for visually
guided movements (e.g. reach to grasp)
Primary Sensation
•
•
•
•
•
Pain
Temperature
Vibration
Joint position sense
Two point
discrimination
Cortical or Higher-Order
Sensation
• Graphesthesia
• Stereognosis
• Tactile extinction
 Intact primary sensation with deficits in cortical
sensation such as agraphesthesia or
astereognosis suggests a lesion in the ______
 Note, however, that severe cortical lesions can
cause deficits in primary sensation as well.
Graphesthesia is the
ability of the patient to
identify characters that
are written on the skin
using a dull pointed
object.
Stereognosis is the
ability to identify
objects that are placed
in the hand when the
eyes are closed
Tactile extinction (Double Simultaneous
Stimulation)
•Touching homologous parts of the body on one
side, the other side or both sides at once with the
patient identifying which side or if both sides are
touched with their eyes closed.
•If the patient neglects one side on extinction, it
indicates dysfunction of the contralateral
posterior parietal lobe
http://library.med.utah.edu/neurologicexam/html/sensory_normal.html
Complex Perceptual Dysfunction:
Visual-Spatial Deficits
• Spatial relations disorders encompass a
constellation of impairments that have in common a
difficulty in perceiving the relationship between the
self and two or more objects.
• Research suggests that the right parietal lobe
plays a primary role in space perception.
• Thus, a visual-spatial deficits most commonly
occurs in patients with right-sided brain lesions
with left hemiparesis.
Perceptual Dysfunction:
(a)somatognosia
• Body schema is a postural model of the
body, including the relationship of body
parts to each other and the relationship of
the body to the environment
(a)somatognosia is the failure to recognize
one’s parts and their relationship to each
other. Attitudes towards one’s body can be
indifference, delusion, or critical
– e.g. hemispatial neglect
http://neuroexam.com/neuroexam/content.php?p=10
Hemispatial Neglect
Not absolute but a gradient
of neglect
Eye movements during visual
search in an individual with leftsided neglect attempting to find
letter Ts among Ls. Red dotsvisual fixations. Yellow linessaccadic eye movements.
http://www.scholarpedia.org/article/Hemineglect
Hemispatial Neglect
 Most common in damage
to right posterior parietal
cortex or frontal cortex
From: Neuroscience: Exploring the
Brain by Bear, Connors, Paradeso
Apraxia
• Most common in lesion of the left frontal and
posterior parietal cortex
• Ideomotor apraxia
– Inability to carry out an action in response to
verbal command, in the absence of any
comprehension deficit, motor weakness, or
incoordination
– Patients can make certain gestures/movements
spontaneously but have trouble in making these
same gestures/movements if asked to do so
http://neuroexam.com/neuroexam/content.php?p=9
Apraxia
• Ideational apraxia
– Inability to carry out an action, either
automatically or on command
– Patients are unable to describe verbally how
tooth-brushing is done and unable to brush
the teeth either on command or automatically