Symptoms and signs caused by neural plasticity
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SYMPTOMS AND SIGNS CAUSED BY NEURAL PLASTICITY. Signs and symptoms of disorders. Not everything can be seen on MRI or other imaging techniques Not everything has positive laboratory tests. Neural plasticity play greater role in generating symptoms and signs than previously assumed.

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SYMPTOMS AND SIGNS CAUSED BY NEURAL PLASTICITY

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Symptoms and signs caused by neural plasticity

SYMPTOMS AND SIGNS CAUSED BY NEURAL PLASTICITY


Signs and symptoms of disorders

Signs and symptoms of disorders

  • Not everything can be seen on MRI or other imaging techniques

  • Not everything has positive laboratory tests


Neural plasticity play greater role in generating symptoms and signs than previously assumed

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


Neural plasticity

Neural plasticity

  • The brain is far from being a fixed system but it is continuously shaped and re-shaped by what it receives from the outside world.

  • Sensory systems provide the input that shapes the brain.


Neural plasticity1

NEURAL PLASTICITY

  • Adjust the nervous system to changing demands (based on sensory input)

  • Compensate for deficits through injury or diseases

  • Cause symptoms and signs of diseases


Promoters of neural plasticity

PROMOTERS OF NEURAL PLASTICITY

  • Deprivation of sensory input

  • Overstimulation


Deprivation

DEPRIVATION

  • “Use it or loose it”


Neural plasticity2

NEURAL PLASTICITY

  • NEURAL PLASTICITY IS AN ABILITY OF THE NERVE CELLS TO CHANGE THEIR FUNCTION OR STRUCTURE

  • THE CHANGES OCCUR WITHOUT DETECTABLE MORPHOLOGIC CHANGES (USING STANDARD CLINICAL METHODS)


Functional changes are caused by

FUNCTIONAL CHANGES ARE CAUSED BY:

  • CHANGE IN SYNAPTIC EFFICACY

  • CHANGE IN NEURAL EXCITABILITY

  • ELIMINATION OF NERVE CELLS (APOPTOSIS)

  • CREATION OR ELIMINATION OF CONNECTIONS (AXONS AND DENDRITES)


Symptoms and signs

SYMPTOMS AND SIGNS

  • HYPERACTIVITY

  • HYPERSENSITIVITY

  • CHANGE IN NEURAL PROCESSING

  • CHANGE IN PERCEPTION OF SENSORY INPUT

  • CHANGE IN MOTOR FUNCTION


Hyperactivity

HYPERACTIVITY

  • MUSCLE SPASM

  • TINNITUS

  • PARESTHESIA (TINGLING)

  • PAIN


Success of treatment supports hypotheses of neural plasticity

Success of treatment supports hypotheses of neural plasticity

  • Pain can be alleviated by electrical stimulation

  • Tinnitus can be alleviated by sound stimulation


Hyperactivity of the vestibular system

Hyperactivity of the vestibular system

  • Ménière's disease

    • Air puffs applied to the inner ear can reverse symptoms


Hypersensitivity

HYPERSENSITIVITY

  • LOWERED THRESHOLD FOR SENSORY STIMULATION

  • EXAGGERATED REACTION ON SENSORY STIMULI


Change in neural processing

CHANGE IN NEURAL PROCESSING

  • ALLODYNIA

    (PAIN FROM INNOCUOUS STIMULATION)

  • HYPERPATHIA

    (LOWERED TOLERANCE TO MODERATE PAIN AND PROLONGED PAIN SENSATION)

    CROSS MODAL INTERACTION


Mechanisms of neural plasticity

MECHANISMS OF NEURAL PLASTICITY

  • CHANGE IN SYNAPTIC EFFICACY

  • NEW CONNECTIONS (SPROUTING)


Unmasking of dormant synapses may cause

UNMASKING OF DORMANT SYNAPSES MAY CAUSE:

  • INCREASE OF SENSORY RESPONSE AREAS

  • SPREAD OF MOTOR ACTIVATION (SYNKINESIS)

  • ACTIVATION OF NEW BRAIN REGIONS MAY (“RE-WIRING”)


Extension of activation of motor areas may cause synkinesis

EXTENSION OF ACTIVATION OF MOTOR AREAS MAY CAUSE SYNKINESIS

  • FACIAL SYNKINESIS AFTER INJURY TO THE FACIAL NERVE

  • LATERAL SPREAD OF BLINK REFLEX IN HEMIFACIAL SPASM


Activity dependent synaptic plasticity

ACTIVITY DEPENDENT SYNAPTIC PLASTICITY

  • LONG TERM POTENTIATION (LTP)

  • LONG TERM DEPRESSION (LTD)

    • HIGH-FREQUENCY TRAINS ARE EFFECTIVE IN INDUCING LTP

      (IS THE “NOVEL STIMULATION” OFTEN REFEREED TO IN NEURAL PLASTICITY A HIGH FREQUENCY TRAIN?)


Activity dependent synaptic plasticity1

ACTIVITY DEPENDENT SYNAPTIC PLASTICITY

  • ACETYLCHOLINE IS IMPORTANT IN DEVELOPMENT

  • NICOTINIC ACETYLCHOLINE RECEPTORS MAY MODULATE GLUTAMATE RECEPTORS

    • MEDIATE LONG TERM CHANGES IN SYNAPTIC EFFICACY

    • AFFECT MATURATION OF THE NERVOUS SYSTEM


Activity dependent synaptic plasticity2

ACTIVITY DEPENDENT SYNAPTIC PLASTICITY

  • SYNCHRONOUS PRE AND POST-SYNAPTIC ACTIVATION PROMOTE NEURAL PLASTICITY

    • HEBB’S PRINCIPLE: “NEURONS THAT FIRE TOGETHER WIRE TOGETHER”


Activity dependent synaptic plasticity3

ACTIVITY DEPENDENT SYNAPTIC PLASTICITY

  • THE TEMPORAL PATTERN OF NEURAL ACTIVITY IS IMPORTANT


New brain regions may become activated

NEW BRAIN REGIONS MAY BECOME ACTIVATED

  • DISORDERS OF THE VESTIBULAR SYSTEM

    • AWARENESS OF HEAD MOVEMENTS

    • DIZZINESS

    • NAUSEA AND VOMITING


New brain regions may become activated1

NEW BRAIN REGIONS MAY BECOME ACTIVATED

  • CHRONIC PAIN

    • ALLODYNIA

    • INVOLVEMENT OF THE SYMPATHETIC NERVOUS SYSTEM; RSD*)

      *) REFLEX SYMPATHETIC DYSTROPHY


New brain regions may become activated2

NEW BRAIN REGIONS MAY BECOME ACTIVATED

  • ACTIVATION OF NON-SPECIFIC PATHWAYS THROUGH SUBCORTICAL ROUTES

  • INVOLVEMENT OF THE LIMBIC SYSTEM


Severe tinnitus is often associated with affective mood disorders

Severe tinnitus is often associated with affective (mood) disorders

  • Depression

  • Phonophobia


The amygdala is involved in fear and other mood disorders

The amygdala is involved in fear and other mood disorders


Symptoms and signs of neuropathic pain

Symptoms and signs of neuropathic pain

  • Strong emotional components

  • Depression

  • High risk of suicide


The amygdala is involved in fear and other mood disorders1

The amygdala is involved in fear and other mood disorders

  • Subcortical connections to the amygdala may induce emotional response unconsiously

    • uncontrollable fear and rage


Involvement of limbic system structures

INVOLVEMENT OF LIMBIC SYSTEM STRUCTURES

  • AFFECTIVE DISORDERS

    • DEPRESSION IN PAIN AND TINNITUS


Involvement of limbic system structures1

INVOLVEMENT OF LIMBIC SYSTEM STRUCTURES

  • EMOTIONAL REACTIONS TO STIMULI THAT NORMALLY DO NOT CAUSE SUCH REACTIONS

  • EXAMPLES:

    • CHRONIC PAIN (HYPERPATHIA)

    • SEVERE TINNITUS (PHONOPHOBIA)


Connections from the auditory system to the amygdala

Connections from the auditory system to the amygdala

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

  • Subcortical connections

    (the “low route”)


How can pain information reach the amygdala

How can pain information reach the amygdala?

  • Through the thalamus

  • Through routes that are enhanced by expression of neural plasticity (re-routing of information)


Main connections to the amygdala

MAIN CONNECTIONS TO THE AMYGDALA:

  • THALAMUS (MEDIODORSAL)

  • PREFRONTAL CORTEX

    • (VIA MEDIODORSAL THALAMUS)

  • SEPTAL NUCLEI

  • PERIAQUEDUCTAL GRAY (PAG)

  • TEMPORAL ASSOCIATION CORTEX

  • MOST CONNECTIONS ARE RECIPROCAL


Symptoms and signs caused by neural plasticity

The “high route” and the “low route” to the amygdala

Auditory cortex

Thalamus

Connections from the amygdala

From: Møller: Sensory Systems, 2002


Symptoms and signs caused by neural plasticity

Connections from a sensory system to the amygdala

“the high route”

From: Møller: Sensory Systems, 2003


High route

SLOW

CARRIES HIGHLY PROCESSED INFORMATION

“SLOW AND ACCURATE”

HIGH ROUTE


Symptoms and signs caused by neural plasticity

Connections from a sensory system to the amygdala

“the low route”

From: Møller: Sensory Systems, 2003


Low route

LOW ROUTE

  • IS FAST

  • CARRIES UNPROCESSED INFORMATION

    • “FAST AND AND DIRTY”


Symptoms and signs caused by neural plasticity

Connections from the amygdala

From: Møller: Sensory Systems, 2003


Conclusion

CONCLUSION

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


Symptoms and signs caused by neural plasticity

MANY REGIONS OF THE BRAIN ARE CONNECTED

Which routes are active?

Depends on synaptic efficacy


Sensory input causes abnormal emotional reactions

SENSORY INPUT CAUSES ABNORMAL EMOTIONAL REACTIONS

  • TINNITUS

  • PHONOPHOBIA AND HYPERACUSIS

  • DIZZINESS

  • ALLODYNIA

  • CHRONIC PAIN

  • AUTISM


Involvement of the limbic system in hearing

INVOLVEMENT OF THE LIMBIC SYSTEM IN HEARING:

  • UNMASKING OF CONNECTIONS FROM THE CLASSICAL AUDITORY SYSTEM TO COMPONENTS OF THE LIMBIC SYSTEM INVOLVING:

    • MEDIO-DORSAL MEDIAL GENICULATE BODY

    • ASSOCIATION CORTICES

    • AMYGDALOID NUCLEI


Symptoms and signs caused by neural plasticity

Classical auditory

pathways

Non-classical

auditory pathways

From: Møller: Sensory Systems, 2003


Escapable and inescapable fear

ESCAPABLE AND INESCAPABLE FEAR


Autism

AUTISM

  • ABNORMAL PERCEPTION OF SENSORY INPUT

  • MAY BE CAUSED BY ABNORMAL INVOLVEMENT OF THE AMYGDALA


Autism1

AUTISM

  • Kluver-Bucy wrote in 1939 regarding the effect of bilateral amygdalectomy in monkeys:

  • “Monkeys are no longer capable of functioning as members of social groups. They cannot recognize the social significance of the exteriorceptive (especially visual, auditory and olfactory) signals that regulate social behavior, or relate then to their own affective states (moods), which regulate approach to or avoidance of other members of the group and are thus the building blocks of social interactions. They avoid other members of the group and seem anxious and insecure”.


Autism2

AUTISM

  • Similarities with the Klüver-Bucy syndrome


Autism3

AUTISM

  • SPECULATION:

  • Insufficient pruning or apoptosis is involved in autism

    • THE AMYGDALA IN AUTISTIC CHILDREN SEEMS TO HAVE A HIGHER DENSITY OF CELLS THAN NORMAL.


Autism4

AUTISM

  • SPECULATION:

    • NONSPECIFIC SENSORY PATHWAYS MAY BE HYPERACTIVE CAUSING TOO MUCH INPUT TO ASSOCIATION CORTICES AND LIMBIC STRUCTURES.

    • SPECIFIC SENSORY PATHWAYS MAY BE HYPOACTIVE SO THAT LESS INPUT REACHES PRIMARY CORTICES.


How can we test if nonspecific pathways are involved

HOW CAN WE TEST IF NONSPECIFIC PATHWAYS ARE INVOLVED:

  • NONSPECIFIC SENSORY PATHWAYS ARE POLYMODAL

  • EXAMPLE: STIMULATION OF THE SOMATOSENSORY SYSTEM CHANGE PERCEPTION OF TINNITUS


How can nonspecific pathways become activated

HOW CAN NONSPECIFIC PATHWAYSBECOME ACTIVATED?

  • UNMASKING OF DORMANT SYNAPSES

  • CREATION OR ELIMINATION OF NERVE CELLS


How can nonspecific pathways become activated1

HOW CAN NONSPECIFIC PATHWAYSBECOME ACTIVATED?

  • CREATION OR ELIMINATION OF NERVE CELLS

    • REQUIRES TIME TO DEVELOP

    • AGE RELATED


Unmasking of dormant synapses

UNMASKING OF DORMANT SYNAPSES

  • ACTS INSTANTLY

  • DEPENDS ON INPUT

  • DEPENDS ON TEMPORAL INTEGRATION

  • DEPENDS ON AVAILABILITY OF NEURAL TRANSMITTERS

  • CAN BE MANIPULATED BY DRUGS


How do synapses become dormant

HOW DO SYNAPSES BECOME DORMANT?

  • DURING (NORMAL) CHILDHOOD DEVELOPMENT

  • THROUGH STIMULATION (SENSORY INPUT)


Synaptic receptors undergo changes during maturation

SYNAPTIC RECEPTORS UNDERGO CHANGES DURING MATURATION

  • GABA CAN BE EXCITATORY IN IMMATURE TISSUE.

  • GABA SYNTHESIS DECREASES WITH AGE

  • ONLY NMDA RECEPTORS IN IMMATURE TISSUE


Conclusion1

CONCLUSION

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


Ontogenetic development depends on

ONTOGENETIC DEVELOPMENT DEPENDS ON:

  • GENETICS (AND EPIGENETICS)

  • STIMULATION (SENSORY INPUT) “NEURONS THAT FIRE TOGETHER WIRE TOGETHER” (HEBB, 1949).

  • OTHER ENVIRONMENTAL FACTORS

  • CHEMICAL FACTORS (DRUGS, ALCOHOL ETC.)

  • UNKNOWN FACTORS


Ontogenetic childhood development shapes the nervous system by

ONTOGENETIC (CHILDHOOD) DEVELOPMENT SHAPES THE NERVOUS SYSTEM BY:

  • APOPTOSIS

  • PRUNING OF AXONS AND DENDRITES

  • CHANGE IN SYNAPTIC EFFICACY


Normal development of the central nervous system involves

NORMAL DEVELOPMENT OF THE CENTRAL NERVOUS SYSTEM INVOLVES:

  • APOPTOSIS

  • ADJUSTMENT OF SYNAPTIC EFFICACY


Abnormal development of the central nervous system may be caused by

ABNORMAL DEVELOPMENT OF THE CENTRAL NERVOUS SYSTEM MAY BE CAUSED BY:

  • FAILURE TO BLOCK SYNAPSES

  • INADEQUATE PRUNING OF THE NERVOUS SYSTEM

    MAY PLAY A ROLE IN:

  • DEVELOPMENTAL DISORDERS

  • OCULAR DOMINANCE

  • AUTISM


What cause plastic changes of the cns

WHAT CAUSE PLASTIC CHANGES OF THE CNS?

  • DEPRIVATION OF INPUT

  • NOVEL INPUT

  • ACTIVITY GENERATED BY INJURY

  • UNKNOWN FACTORS


Plastic changes of the nervous system are reversible

PLASTIC CHANGES OF THE NERVOUS SYSTEM ARE REVERSIBLE

  • THE ASSOCIATED DISORDERS ARE TREATABLE

    • DEPENDING ON CORRECT DIAGNOSIS


Disorders caused by neural plasticity are treatable

DISORDERS CAUSED BY NEURAL PLASTICITY ARE TREATABLE

  • EXAMPLES:

    • ELECTRICAL STIMULATION (TENS) CAN ALLEVIATE NATUROPATHIC PAIN

    • TRAINING CAN REDUCE SYNKINESIS

    • TRAINING CAN REDUCE TINNITUS


Examples of reversal of neural plasticity

EXAMPLES OF 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

Stimulation of somatosensory system can relieve tinnitus

  • Electrical stimulation of the ear or the skin behind the ears have been used to treat tinnitus

  • Few systematic studies of efficacy have been published


Conclusion disorders caused by functional changes of the central nervous system

CONCLUSIONDISORDERS CAUSED BYFUNCTIONAL CHANGES OF THE CENTRAL NERVOUS SYSTEM:

  • FEW AND OFTEN AMBIGUOUS SYMPTOMS AND SIGNS

  • OFTEN DIAGNOSED INCORRECTLY

  • OFTEN TREATED INEFFECTIVELY IF AT ALL


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