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The Body Senses and Movement

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CHAPTER 11. The Body Senses and Movement. The Body Senses. Movement disorders. Learning disorders – PowerPoint PPT presentation

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Title: The Body Senses and Movement


1
CHAPTER 11
  • The Body Senses and Movement
  • Relation between Movement
  • and Learning Disorders

2
Parkinsons disease
  • Parkinsons disease characterized by
  • motor tremors
  • Rigidity
  • loss of balance and coordination,
  • difficulty in moving, especially in initiating
    movements
  • http//www.youtube.com/watch?vy1dkh2crci4
  • The symptoms are caused by deterioration of the
    substantia nigra.
  • neurons of the substatia nigra send
    dopamine-releasing axons to the striatum.
  • The striatum is composed of the basal ganglias
    caudate nucleus and putamen and the nucleus
    accumbens.
  • Upsets balance between direct and indirect
    pathways

3
etiology
  • Some forms likely genetic
  • recent whole-genome study of Parkinsons patients
    identified 12 genes that likely contribute to the
    disease.
  • Two of the implicated genes may play role in the
    development and programmed death of
    dopamine-producing neurons.
  • Two others result in deviant proteins that are
    components of Lewy bodies
  • Lewy bodies abnormal clumps of protein that form
    within neurons.
  • Lewy bodies found in several brain locations in
    some Parkinsons patients
  • Also found in people with form of dementia,
    dementia with Lewy bodies.
  • Lewy bodies likely contribute to cognitive
    deficits and depression that often accompany
    Parkinsons disease.

4
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5
etiology
  • Some forms likely genetic
  • recent whole-genome study of Parkinsons patients
    identified 12 genes that likely contribute to the
    disease.
  • Two of the implicated genes may play role in the
    development and programmed death of
    dopamine-producing neurons.
  • Two others result in deviant proteins that are
    components of Lewy bodies
  • Lewy bodies abnormal clumps of protein that form
    within neurons.
  • Lewy bodies found in several brain locations in
    some Parkinsons patients
  • Also found in people with form of dementia,
    dementia with Lewy bodies.
  • Lewy bodies likely contribute to cognitive
    deficits and depression that often accompany
    Parkinsons disease.

6
treatment
  • Typically treated by administering levodopa
    (L-dopa),
  • precursor for dopamine.
  • Why use precursor?
  • Dopamine not cross the blood-brain barrier
  • L-dopa will
  • in the brain is converted to dopamine.
  • Problem
  • treatments increase dopamine throughout brain
  • causes side effects including restlessness,
    involuntary movements and hallucinations.
  • As more neurons die, more drug is required,
    increasing the side effects.
  • Eventually, no neurons left

7
Huntingtons chorea
  • Huntingtons disease
  • degenerative disorder of the motor system
  • cell loss in the striatum and cortex.
  • Is genetic dominant gene trait
  • Progressive disorder
  • Onset typically in late 20s, early 30s
  • Years before a diagnosis, begins with jerky
    movements that result from impaired error
    correction.
  • At mid stage
  • involuntary movements appear
  • first as fidgeting
  • then as movements of the limbs
  • Late stage
  • writhing of the body
  • facial grimacing
  • Loss of motor control and death

8
Huntingtons
  • Much more severe symptoms
  • cognitive and emotional deficits are a universal
    characteristic of Huntingtons disease
  • In contrast to other movement disorders such as
    Parkinsons.
  • http//www.youtube.com/watch?vHP9YrOrpt3A
  • Deficits include
  • impaired judgment
  • difficulty with a variety of cognitive tasks
  • depression
  • personality changes
  • Motor symptoms are due to the degeneration of
    neurons in the striatum
  • Defective or degenerated neurons in the cortex
    probably account for the psychological symptoms.

9
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10
etiology
  • Huntingtons disease results for a mutated form
    of the Huntingtons gene.
  • Is dominant trait gene
  • If you have the gene, you will get the disease
  • 50/50 chance of passing it on
  • Ethical dilemma created with identification of
    gene
  • The loss of neurons is probably due to the
    accumulation of the genes protein,
  • Protein called huntington
  • function is unknown.

11
Myasthenia gravis
  • Myasthenia gravis
  • disorder or muscular weakness
  • caused by reduced numbers of sensitivity of
    acetylcholine receptors.
  • http//www.youtube.com/watch?v4lRBB-CFAn0feature
    related
  • Drugs that inhibit the action of AChe give
    temporary relief from the symptoms of myasthenia
    gravis.
  • Remember AChe breaks down Ach in synapse.
  • Inhibitors increase amount of neurotransmitter
    available at the neuromuscular junction.

12
Multiple sclerosis
  • motor disorder with many varied symptoms
  • caused by deterioration of myelin (demyelination)
    and neuron loss in the central nervous system.
  • Demyelination causes slowing or elimination of
    neural impulses
  • This reduces the speed and strength of movements.
  • As the disease progresses, unmyelinated neurons
    die, leaving areas of sclerosis, or hardened scar
    tissue.
  • muscular weakness, tremor, impaired coordination,
    urinary incontinence, and visual problems.
  • Symptoms may wax and wane autoimmune reactions
  • Several drugs are available modify immune
    activity in multiple sclerosis patients
  • Slow the progress of the disease
  • Do not repair the harm already done.

13
Figure 11.23 The brain of a deceased MS
patient The arrows indicate areas of sclerosis,
or hardened scar tissue.
14
Learning and motor disruptions
  • Strong link between descending motor pathway
    abnormalities and a variety of genetic,
    behavioral, learning and psychological disorders.
  • Learning and psychological disorders linked to
    descending motor pathway disturbances include
  • dyslexia,
  • Tourettes syndrome,
  • several genetic forms of mental retardation,
  • autism
  • ADHD.
  • The common link between all of these disorders
    Inability to appropriately inhibit some
    behavioral patterns while disinhibiting others.

15
distonia
  • Primary dystonia
  • movement disorder resulting from basal ganglia
    dysfunction,
  • may be related to ability to detect different
    emotional facial expressions.
  • Patients with primary dystonia show
  • isolated deficits in the recognition of disgust
  • not happiness surprise, sadness or anger.
  • Dystonia resulting from basal ganglia
    dysfunction
  • not only motor dysfunction
  • Also demonstrates role of the basal ganglia in
    cognitive behavior such as emotion recognition.

16
22q11.2 deletion syndrome
  • 22q11.2 deletion syndrome (22qDS).
  • children show a wide spectrum of disabilities
  • cognitive and motor deficits
  • physical anomalies
  • ADHD,
  • poor executive visual attention,
  • poor sensorimotor processing,
  • learning disabilities with primary impairment in
    working memory.
  • up to 25 times more likely to develop autism,
    pervasive developmental disorders, and
    schizophrenia.
  • may have early functional abnormalities in
    corticostriatal pathways linking the prefrontal
    cortex and basal ganglia structures.

17
Lesch-nyan syndrome
  • Rare genetic disorder
  • linked to descending motor pathway dysfunction
  • caused by a mutation in the gene coding for the
    enzyme hypoxanthine-quanin phosphoribosyltransfera
    se
  • characterized by
  • hyperuricemia,
  • motor disorders,
  • severe and compulsive self mutilation.

18
Lesch-nyan syndrome
  • Why? disconnect between the prefrontal cortex
    and the basal ganglia
  • caused by DA dysfunction
  • results in a dysfunctional DA signal
    accidentally reinforces early injurious behavior
  • Initial injurious behavior occurs because motor
    dysfunction resulting in clumsiness and awkward
    movements incidentally produce self injury.
  • Behavior becomes well learned and automated
  • Result Pattern of severe self mutilation.

19
Lesch-nyan syndrome
20
Tourettes syndrome
  • Tourette syndrome (TS) characterized by
  • stereotyped involuntary movements, or tics.
  • Result of structural and functional abnormalities
    of the basal ganglia
  • Link between motor system and limbic system is
    disturbed
  • Result is spontaneous disinhibiton of competing
    motor and limbic system
  • http//www.youtube.com/watch?vqjWdnQZGScs
  • Treatment
  • Typically antipsychotic medication (Dopamine D2
    antagonists) because reduce available DA in
    system
  • Unfortunately, compound learning deficits
  • Alternative biofeedback and learned control of
    tics

21
Language disorders
  • Language disorders may be due to poor regulation
    by the basal ganglia and related structures.
  • May be Language disorder due to abnormal
    development of the basal ganglia
  • Basal ganglia modulates Procedural memory
  • modulates learning and execution of motor and
    cognitive skills
  • Also critical for aspects of grammar.
  • Lexical and declarative memory not affected
  • these behaviors depend on other brain structures
  • not affected by abnormalities in the
    frontal-subcortical network.

22
Speech apraxia
  • Speech apraxia
  • Difficulty with pronunciation, production of
    speech
  • particular phonemic characteristics of speech
    apraxia may be due to subcortical dysfunction.
  • observations of those with speech apraxia reveal
  • greater phoneme substitution errors
  • errors occurred significantly more often in the
    initial rather than the medial or final word
    position.
  • The speech errors likely due to disinhibition of
    competing phonemes during speech
  • Suggests speech motor planning occurs at
    subcortical and cortical brain levels.

23
stuttering
  • link between stuttering and basal ganglia
    dysfunction.
  • stuttering similar to other basal ganglia
    disorders such as Parkinsons disease and
    dystonia.
  • stuttering is alleviated with interventions such
    as rhythm effects, chorus speech, and singing
    retraining brain

24
stuttering
  • Basal ganglia-thalamocortical motor circuits
    through the putamen likely play a key role in
    stuttering.
  • Stuttering due to impaired ability of basal
    ganglia to produce timing cues for the initiation
    of the next motor segment in speech.
  • Dysfunction due to abnormalities in the dopamine
    error-detection feedback system,
  • Pharmacologic interventions such as DA
    antagonists thus effective in alleviating
    stuttering
  • Also behavioral training programs

25
adhd
  • Descending motor system plays strong role in
    attention deficit disorder/hyperactivity disorder
    (ADHD).
  • Neuropsychological studies show a pattern of
    cognitive deficits consistent with prefrontal
    executive problems
  • Individuals with ADHD exhibit
  • inattention,
  • difficulty with self regulation,
  • response inhibition deficits (impulsivity),
  • restlessness or hyperactivity, and even apathy
  • Individuals may show all or some of these
    behavioral deficits.

26
adhd
  • Exist at least two subtypes, according to the
    DSM-IV
  • the inattention dimension
  • hyperactive or impulsive dimension
  • symptoms appear to be related to a latent trait
    of disinhibition,
  • inattentive symptoms impact cognitive behaviors
    more than the impulsive subtype.

27
ADHD
  • ADHD disorder of self-regulation stemming from
    dysfunction of frontal-subcortical system.
  • Total cerebral volume smaller in ADHD children
    than controls.
  • Small, but significant reductions in mean total
    cerebral volume also found.
  • Frontal lobe volume small is smaller in ADHD
    children
  • Regions of the basal ganglia, particularly
    caudate nucleus, shown to be smaller in ADHD
    children

28
ADHD
  • Studies with typical children show that caudate
    size decreases as child matures- result of normal
    pruning of neurons.
  • Children with ADHD appear to start out with
    smaller caudate nuclei,
  • With maturation decline significantly greater
  • The size differential of caudate nuclei between
    ADHD and typical children may increase with age.
  • Right hemisphere structures more affected than
    left hemisphere structures for children with
    ADHD.
  • Typically, right frontal area gtleft frontal area
  • Right hemisphere important in regulating
    attention.
  • May explain lack of attention regulation found in
    ADHD children

29
ADHD
  • Several other related structures appear to be
    abnormal in children with ADHD.
  • relative decrease in size of cerebellum
  • reduction in area of anterior or posterior corpus
    callosum
  • ADHD may be due to a dysfunction of the
    prefrontal-subcortical system
  • evidence points to greater dysfunction in right
    hemisphere.
  • children with ADHD may have delayed development
    in their frontostriatal circuits.
  • Why do DA agonists (ritalin, adderall) work
    speed up system!
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