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 cortico-striatal (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 512Neuroscience in Physical Therapy

Sensation and Perception

Min H. Huang, PT, PhD, NCS

Reading AssignmentsS & 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 group1. 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

End

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

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

End

EndProduced by Dave Foord

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

Discussion at your table group

Describe the sensory function controlled by neurons in each of the sensory pathways

End

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 bladehttp://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 sequence1. conscious proprioception / discriminate touch2. cold3. fast pain4. heat5. 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

http://www.medscape.com/viewarticle/480071_4

Wallerian DegenerationA. NormalB. InjuryC. Anterograde

degenerationD. Loss of

connection with muscle

E. Total degeneration

F. Axons re-sprout using remaining Schwann cells as guides and re-innervate the muscle.

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. PerceptionSensation

• “Picking up” sensory information

• The process of detecting a stimulus (e.g. light waves-vision, sound waves-heating, chemical molecules-taste, heat or pressure-touch).

Perception• The process of integrating,

organizing and interpreting sensations.

• Creating meaningful patterns from sensory information

• Require attention, memory, integration of stimuli, motivation, expectations etc.

Thalamus “inner chamber” or “bedroom” in Greek

“egg-shaped” grey matter structureThe 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: FunctionUnimodal 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

Eye movements during visual search in an individual with left-sided neglect attempting to find letter Ts among Ls. Red dots-visual fixations. Yellow lines- saccadic eye movements.

http://www.scholarpedia.org/article/Hemineglect

Not absolute but a gradient of neglect

Hemispatial Neglect

From: Neuroscience: Exploring the Brain by Bear, Connors, Paradeso

Most common in damage to right posterior parietal cortex or frontal cortex

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