Transcript Temporal Aspects of Visual Extinction

Chapter 13: Brainstem and Basal Ganglia
 Chris Rorden
University of South Carolina
Norman J. Arnold School of Public Health
Department of Communication Sciences and Disorders
University of South Carolina
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Afferent Fibers
Spinal Ganglia
Muscle
Efferent Fibers
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Dermatomes
Branches of Cranial Nerve V (Trigeminal)
Opthalmic
Maxillary
Mandibular
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Chickenpox
Shingles
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Brainstem Motor Mechanism
Motor
– Pyramidal
Corticospinal tract and corticobulbar tract
– Extrapyramidal
Facilitatory, inhibitory, and/or regulatory
– Red Nucleus
Part of midbrain
– Cranial Nerve Nuclei
– Reticular Formation
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Brainstem Anatomy
 Red Nucleus
– Rubrocerebellar Tract
– Important for gait in animals
without significant corticospinal
tract
– Humans: upper arm and
shoulder
 Cranial Nerve Nuclei
– Will Be Discussed With Cranial
Nerves
 Reticular Formation
– Focus in This Chapter
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Reticular Formation
 Located between
caudal diencephalon &
spinal cord
 Network of Overlapping
Dendrites and Axons
 Input From
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Motor Cortex
Basal Ganglia
Cerebellum
Cranial Motor Neurons
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Reticular Formation Function
 Arousal
 Tonal Modulation
 Pain Processing
 Regulation of
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Vomiting
Coughing
Cardiovascular Functions
Respiration
Speech Functions
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Reticular Nuclei
 Reticularis Gigantocellular
 Pontis Oralis and Cudalis
 Lateral Reticular Nucleus
 Ventral Reticular Nucleus
 Paramedial Reticular
Nucleus
 Interstitial
 Raphe
 Ceruleus
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Reticular Motor Functions (1)
Examined in anencephalic children who have
no cortex or cerebellum
- Expel
food
- Eat
- Suck
- Cry
- Yawn
- Breathe
-Swallow
- Vomit
- Sleep
- Awaken
Muscle Tone Regulation - Maintains Balance of
Stimulation
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descending reticular formation
ascending reticular formation
Reticular Motor Functions (2)
 Facilitatory Reticular Areas
– Upper and Lateral Brainstem
– Increases Muscle Tone in
Extremities
– Sleep wake cycle, alertness
 Inhibitory Reticular Areas
– Lower and Medial Region of Medulla
– Decreases Muscle Tone in
Extremities
– Posture, equilibrium, motor control
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Clinical considerations
Disconnection of cortex and basal ganglia from
reticular formation
– Decerebrate Rigidity
Extensor posturing of all Limbs
Excessive facilitatory impulses
Transection Below Vestibular Nucleus
– Flaccid Paralysis
– Similar to degeneration of the lower neuron
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Basal Ganglia
Modify cortically initiated motor movements
(speech)
– Caudate Nucleus
– Putamen
– Globus Pallidus
– Related Brainstem Structures
– Substantia Nigra
– Subthalamic Nucleus
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Results of Basal Ganglia Impairment
 Involuntary Motor Movements
 Bradykinesia (slow) or Hypokinesia (slow or
diminished)
 Altered Posture
 Changes in Muscle Tone
 Implicate Neurotransmitters
 All Result in Dysarthria and Dysphagia
 Parkinson’s Disease
 Huntington’s Disease
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Basal Ganglia
rostral
– striatum
putamen
caudate nucleus
nucleus accumbens
– globus pallidus
caudal
– subthalamic nucleus (STN)
– substantia nigra (SN)
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Aliases
Lenticular Nucleus
– Putamen and Globus Pallidus
Neostriatum or Striatum
– Caudate Nucleus and Putamen
Pallidum
– Globus Pallidus
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Structures
1. Caudate Nucleus
 Elongated C Shaped Mass With Head and Tail
 Bordered by Ventricles, Internal Capsule and
Temporal Lobe
2. Globus Pallidus Next to Putamen
3. Putamen Connected to Head of Caudate
Nucleus
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The Basal Ganglia
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Neurotransmitters
Dopamine
– Inhibitory Neurotransmitter
– Produced in the substantia nigra and secreted in
the striatum
Acetylcholine
– Facilitatory/Inhibitory Neurotransmitter
Gamma-Aminobutyric Acid
– GABA Regulates Adjacent Structures
– e.g. thalamus
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Clinical Considerations
 Athetosis
– Involuntary slow writhing (twisting) movement
– Continuous stream of slow, sinuous, writhing movements,
typically of the hands and feet.
– Varying degrees of hypertonia
– Usually seen in lesions of the globus pallidus
 Ballism (Subthalamic Nuclei – Diencephalon, chapter 6)
– Violent Forceful Flinging of Arms and Legs
– Most violent form of dyskinesia (movement disorder)
– Usually associated with lesions in the sub-thalamic nucleus
(which regulates the globus pallidus)
– Hemiballism: unilateral ballism (e.g. unilateral stroke)
– Can be treated with dopamine blockade or resection of GP.
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Clinical Considerations
 Chorea
– Series of rhythmic involuntary movements
– Predominantly in the distal extremities and muscles of the
face, tongue, and pharynx
– Chorea is characterized by brief, irregular contractions that
are not repetitive or rhythmic, but appear to flow from one
muscle to the next.
– These 'dance-like' movements of chorea (from the same
root word as "choreography")
– often occur with athetosis and more severe cases present
with ballism
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Forms of Chorea
 Sydenham’s Chorea (rheumatic fever 5-15 years old)
– Secondary to streptococcal infection
– Most recover completely (with problems for a few months)
 Huntington’s Chorea (aka Huntington’s Disease)
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1872, George Huntington
Treated families with same characteristics
Heredity, Adult Onset, Chorea, Cognitive Loss
Autosomal Dominant
5 in 100,000 prevalence
Equal in Men and Women
Loss of Cholinergic and GABAnergic neurons in Caudate
Nucleus
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Autosomal Dominant Traits
the trait, half the children will have the trait.
Example: being a boy. Your father has one copy of
the Y chromosome, and one X. Each child has a
50% chance of being a boy.
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Clinical Considerations
Dyskinesia
– Generalized Disorder of Involuntary and Voluntary
Movement
– Masked Face, Infrequent Blinking, Slow
Movement, Disturbed Equilibrium, Stooped
Posture, Impaired Speech, Impaired Swallowing
Tremors
– Alternating Movement of Opposing Muscles
– Resting Tremor
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Basal Ganglia Diseases
 Parkinson’s Disease (1817, James Parkinson)
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Tremor at Rest
Cogwheel Muscular Rigidity
Bradykinesia (Slow execution of body movements)
Akinesia (Slow beginning or inability to initiate a movement)
Shuffling Gate
Expressionless Face
Flexed Posture
Dysarthria
30% have Cognitive impairment
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Parkinson’s Disease Treatment
Lack of Dopamine
(Inhibitor)
Tx: L-Dopa or Other
Dopamine Enhancers
Prolonged L-Dopa Tx
can result in tardive
dyskinesia (increased
facial and lingual
movements)
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Basal Ganglia Disease
 Parkinson's disease: loss of dopamine in the
neostriatum
– Treatment: increase dopamine
 Schizophrenia: Too much dopamine
– Treatment: Block some (D2) dopamine receptors.
– Problem: Prolonged treatment using Chlorpromazine and
Haloperidol leads to Parkinson's disease-like tremors
(tardive dyskinesia)
Not enough DA
Parkinsons
‘Normal’
Too much DA
Schizophrenia 27