CHAPTER 3 SENSORY SYSTEMS

CHAPTER 3SENSORY SYSTEMS

Disorders of sensory systems• Deficits

– Sensory organ– Sensory nerves– Central nervous system

• Hyperactivity– Central neuropathic pain– Tinnitus– Tingling

• Normal response that is redirected– Pain from touch – Dizziness and vertigo from head movements

Disorders of sensory systems

• Reduced sensitivity– Hearing loss– Visual impairment

• Incorrect response– Hyperacusis– Distorted sounds– Allodynia– Hyperpathia

Disorders of sensory systems

• Impaired conduction of the physical stimulus to the receptors

• Impaired function of receptors

• Impaired function of sensory nerves

• Impaired or changed function of the central nervous system

Reduced sensitivity

• Often caused by disorders of the sense organs

• Injury to afferent nerves

Hyperactive sensory disorders

• Increased sensation of physical stimuli

• Altered sensation of physical stimuli

• Sensation without any physical stimulation

General organization of sensory systems

• Conduction of the physical

stimulus to the receptors

• Sensory receptors

• Sensory nerves

• Central nervous system

Sensory transduction

• A physical stimulus generates a receptor potential

• The receptor potential is a graded potential

• The receptor potential is conducted electrotonically to the spike generation site

Bipolar receptor cells (taste)

Initiation of nerve impulses

• Occurs at the first node of Ranvier

Two different types of receptors, with bipolar nerve fibers

Sensory transduction (mechanoreceptor in a muscle)

Central nervous system

HUMAN

Mouse

Chick

Cochlea

Reticularformation

Cochlearnucleus

MGB

Primary auditory cortex

Midline

Inferiorcolliculus

Ventralthalamus

AN LL

Auditory nervous systemAscending auditory pathways

From: Møller, 2005

Two different ascending sensory pathways have been identified:

• The classical systems

• The non-classical systems

From: Møller: Sensory Systems, 2003

Classical auditorypathways

Non-classical auditory pathways


Receive input from the somatosensory system

Use the dorsal part of the MGB

From: Møller, 2005

The classical ascending pathways

• The number of nuclei is different in different sensory systems

• Use ventral thalamic nuclei that project to primary sensory cortices

• Neurons processes only input from of one sensory modality

Midline

LGN

Primary visual cortex

LGN

Primary visual cortex

Thalamus

Retinalganglion cells

Retinalganglion cells

SCN andhypothalamus

Pretectalnucleus

Superiorcolliculus

Externaleye muscles

Thalamus

Thalamus

Pulvinar

Lightreflexes

Other regionsof the CNS

Extrastriatecortex

A B

From: Møller, 2005

Visual systemClassical ascending pathways Non-classical ascending pathways

The nonclassical pathways

• Use dorsal and medial thalamic nuclei that project to secondary cortices and to other parts of the CNS

• Receive input from more than one sense

Fig 3.3

Reticular formation

Thalamusventral

Limbic system Association cortex

Anteriorlateral tract

Mediallemniscus

Thalamusdorsal

SII

AROUSAL

"WHERE""WHAT"

Pain pathways

cortex SI

Somatosensory pathways

Classical pathways Non-classical pathways

From: Møller, 2005

Trigeminalganglion

Thalamus

Cerebralcortex

Motornuclei

RF

Brainstem

Midbrain

Spinalcord

Processing after primary sensory cortices

• Integration of input from different sensory systems occurs in association cortices

• Parallel processing• Stream segregation

The neocortex has six layers

Simplified diagram of the connections to and from the different layers of the cerebral cortex


Maps

Tonotopic

Somatotopic

SURFACE VIEW

LOWER BODY IS REPRE-SENTED NEAR THE MIDLINE

Tonotopic organization in the CN of a cat, as an example of tonotopic organization in the auditory system

Tonotopic organization in the CN of a cat, as an example of tonotopic organization in the auditory system

Parallel processingStream segregation

Parallel processing:Cochlear nucleus

Function of sensory nervous systems

• Processing of sensory input at the peripheral level– Convergence (spatial integration)– Interplay between inhibition and excitation

Spatial integration: Receptive field of a dorsal column nucleus cell

Convergence of input to a secondary neuron

Lateral inhibition

Central processing of sensory information

• Each stage enhances or suppress specific Information

Parallel processing:The same information is

processed in different structures

Stream segregation:Different kinds of information is processed in different structures

(“What” and “Where”)

Processing after primary sensory cortices

• Integration of input from different sensory systems occurs in association cortices


Stream segregation Cortical circuitry

Dorsal stream“where”

Ventral stream“what”

Sensory information can reach other regions than sensory

regions

Motor systems

Memory

Emotional brain (limbic system)

Fig 3.7

DorsalmedialMGB

AII

VentralMGB

Thalamus

AAF

Endocrine

Behavioral

Autonomic

AI

ICXDC

ICC

Amygdala

Associationcortices

AL ABL ACE

Nucleusbasalis

Arousaland

plasticity

Cortex

"High Route"

"Low Route"

Polymodalassociation

cortex

Other corticalareas

From: Møller, 2005

Two different routes to the Amygdala from a sensory system


Connections from a sensory system to the amygdala “the high route”

Connections from a sensory system to the amygdala “the low route”



Connections from the amygdala

Hypoactive sensory disorders

• Loss of sensitivity– Hearing loss– Poor vision– Numbness– Loss of vestibular (balance) function

Frequency in kHz

0

0.250.125 0.50.75 1 1.5 3 4 6 82

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HE

AR

ING

LE

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T 4

kH

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NOISE IMMISSION LEVEL

Courtesy of M. Charles Liberman

Genetic, epigenetic and environmentalCauses (and a stochastic component ?)

Age-related hearing loss

0

10

Left Ear

4000 Hz. Women

Right Ear

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Number

Normal variations in hearing loss of 70 year old individuals

0

N=179

Men 70 years old

25

50

75

100

≥92%76-88%<76%<48% deaf

%

0

N=197

Women 70 years old

25

50

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100

≥92%76-88%<76%<48% deaf

%

Left EarRight Ear

Left EarRight Ear

Variations in speech discrimination in 70 year old individuals

0

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Frequency in kHz

0.250.125 0.5 0.75 1 1.5 3 4 6 82

Hearing loss in Ménière's disease

I: Pre-op Discr.=96% ASII: 5 days post-op Discr.=0% AS

II

I

Frequency in kHz

0

0.250.125 0.50.75 1 1.5 3 4 6 82

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I: Pre-op Discr.=80% ASII: 7 days post-op Discr.=30% AS

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B

A

Frequency in kHz

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0.250.125 0.5 0.75 1 1.5 3 4 6 82

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Effect of surgical injuries to the auditory nerve:

Large decrease in speech discrimination

Hyperactive sensory disorders

• Tinnitus

• Paresthesia

• Phosphenes

• Phantom sensations

• Central neuropathic pain

Subjective and objective tinnitus

• Different forms of tinnitus have very different effects on an individual’s life

Similarities between chronic pain and severe tinnitus

There are many forms of tinnitus

• Mild tinnitus:

Does not interfere noticeably with everyday life• Moderate tinnitus:

May cause some annoyance and may be perceived as unpleasant • Severe tinnitus:

Affects a person’s entire life in major ways

Patients’ own perception varies between mild, moderate and severe (disabling)

Important to have words for disorders

• We cannot think about matters that do not

have names

• The same words is used to describe very different forms of tinnitus and pain

• Using the same names for fundamentally different disorders is a disadvantage in treating these disorders

How prevalent is severe tinnitus?

Some statistics show 50 million people

have tinnitus in the USA

The prevalence of severe (bothersome) tinnitus is infrequent at young age; it reaches 12-14% for people at age 65 according to one study

How prevalent is severe pain?

Some pain was reported by 86% of

individuals above the age of 65(Iowa study, 1994)

The prevalence of severe pain was 33% for people at age 77 and above (Swedish study, 1996)

Severe tinnitus affects a person’s entire life in major

ways

• Prevents or disturbs sleep

• Interferes with or prevents

Intellectual work

• Often accompanied by altered perception of sound

Severe pain affects a person’s entire life in major ways

• Prevent or disturb sleep• Interfere with or prevents intellectual work • May cause suicide May involve limbic structures causing affective

reactionsOften accompanied by abnormal sensations

from touch

Severe tinnitus is often accompanied by altered

perception of sound

• Sounds are distorted

• Sounds have exaggerated loudness (hyperacusis)

• Sounds are unpleasant

• Sounds are painful and arouse fear (phonophobia)

Little is known about the cause of subjective tinnitus

• Noise exposure

• Ototoxic antibiotic

• Acoustic tumors

The sympathetic nervous system is involved in some

forms of severe tinnitus

Some forms of tinnitus

can be cured by sympathectomy

Deprivation of sound can cause changes in neural processing such as change in temporal integration

• Expression of neural plasticity

The anatomical location of the abnormality that cause chronic pain and tinnitus may be different from

that to which the pain or the tinnitus is referred

The abnormal neural activity that causes symptoms are not

generated at the location where the symptoms are felt

Examples:

• Phantom pain

• Tinnitus with severed auditory nerve

The tinnitus in some patients can be modulated by stimulation of

the somatosensory systems (such as by electrical stimulation

of the median nerve)“cross-modal” interaction


Receive input from the somatosensory system

Use the dorsal part of the MGB

From: Møller, 2005

Other signs of involvement of the somatosensory system

•Gaze related tinnitus

•Neck muscles and tinnitus

•TMJ and tinnitus

•Sensation of sound from touching the skin

Connections between spinal C2 segment and the dorsal

cochlear nucleus

Can explain why electrical stimulation of the skin behind the

ears can modulate tinnitus

Symptoms and signs of neuropathic pain

and severe tinnitus

• Strong emotional components

• Depression

• High risk of suicide

Severe tinnitus is often associated with affective (mood) disorders

• Depression

• Phonophobia

The amygdala is involved in fear and other mood disorders

Connections from the auditory system to the amygdala

• Cortical-cortical connections (the “high route”)

• Subcortical connections

(the “low route”)

Fig 3.7

DorsalmedialMGB

AII

VentralMGB

Thalamus

AAF

Endocrine

Behavioral

Autonomic

AI

ICXDC

ICC

Amygdala

Associationcortices

AL ABL ACE

Nucleusbasalis

Arousaland

plasticity

Cortex

"High Route"

"Low Route"

Polymodalassociation

cortex

Other corticalareas

From: Møller, 2005

CONCLUSION

ACTIVATION OF NON-CLASSICAL ASCENDING SENSORY PATHWAYS CAN CAUSE SYMPTOMS AND SIGNS OF SEVERAL DISEASES

Neural plasticity play greater role in generating symptoms and

signs than previously assumed

• Plastic changes are reversible

• Treatments without medicine and surgery may alleviate pain and tinnitus

Therapy

There is no treatment for tinnitus that is comparative to common pharmacological treatment of pain. Treatment of tinnitus has been mainly benzodiazepines (GABAA agonists)

Reversal of neural plasticity

• “TENS” (transderm electric nerve stimulation) has been used for many years in treatment of chronic pain

• Recently sound stimulation in various forms have been introduced in treatment of severe tinnitus

Stimulation of somatosensory system can relieve tinnitus

• Electrical stimulation – of the ear and– of the skin behind the ears have been used

to treat tinnitus

• Electrical stimulation of the auditory cortex is in a stage of development

• Few systematic studies of efficacy have been published

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CHAPTER 3 SENSORY SYSTEMS