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Chapter 13: Brainstem and Basal Ganglia

Chris RordenUniversity of South CarolinaNorman J. Arnold School of Public HealthDepartment of Communication Sciences and DisordersUniversity of South Carolina

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Muscle

Efferent Fibers

Afferent Fibers

Spinal Ganglia

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Dermatomes

Opthalmic

Mandibular

Maxillary

Branches of Cranial Nerve V (Trigeminal)

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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– Motor Cortex– Basal Ganglia– Cerebellum– Cranial Motor Neurons

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Reticular Formation Function

Arousal Tonal Modulation Pain Processing Regulation of

– 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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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 LimbsExcessive 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

putamencaudate nucleusnucleus accumbens

– globus palliduscaudal

– 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 striatumAcetylcholine

– 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)– 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)– 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 DAParkinsons

Too much DASchizophrenia

‘Normal’