1. 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

2. Afferent Fibers
Spinal Ganglia
Muscle
Efferent Fibers

3. Dermatomes Branches of Cranial Nerve V (Trigeminal) Opthalmic
Maxillary
Mandibular

4. Chickenpox
Shingles

5. Brainstem Motor Mechanism
Pyramidal
Corticospinal tract and corticobulbar tract
Extrapyramidal
Facilitatory, inhibitory, and/or regulatory
Red Nucleus
Part of midbrain
Cranial Nerve Nuclei
Reticular Formation

6. Brainstem Anatomy Red Nucleus Cranial Nerve Nuclei Reticular Formation
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

7. Reticular Formation Located between caudal diencephalon & spinal cord
Network of Overlapping Dendrites and Axons
Input From
Motor Cortex
Basal Ganglia
Cerebellum
Cranial Motor Neurons

8. Reticular Formation Function
Arousal
Tonal Modulation
Pain Processing
Regulation of
Vomiting
Coughing
Cardiovascular Functions
Respiration
Speech Functions

9. Reticular Nuclei Reticularis Gigantocellular Pontis Oralis and Cudalis
Lateral Reticular Nucleus
Ventral Reticular Nucleus
Paramedial Reticular Nucleus
Interstitial
Raphe
Ceruleus

10. 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

11. 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
ascending reticular formation
descending reticular formation

12. 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

13. Modify cortically initiated motor movements (speech)
Basal Ganglia
Modify cortically initiated motor movements (speech)
Caudate Nucleus
Putamen
Globus Pallidus
Related Brainstem Structures
Substantia Nigra
Subthalamic Nucleus

14. 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

15. Basal Ganglia rostral caudal striatum globus pallidus
putamen
caudate nucleus
nucleus accumbens
globus pallidus
caudal
subthalamic nucleus (STN)
substantia nigra (SN)

16. Neostriatum or Striatum Pallidum
Aliases
Lenticular Nucleus
Putamen and Globus Pallidus
Neostriatum or Striatum
Caudate Nucleus and Putamen
Pallidum
Globus Pallidus

17. Globus Pallidus Next to Putamen
Structures
Caudate Nucleus
Elongated C Shaped Mass With Head and Tail
Bordered by Ventricles, Internal Capsule and Temporal Lobe
Globus Pallidus Next to Putamen
Putamen Connected to Head of Caudate Nucleus

18. The Basal Ganglia

19. Gamma-Aminobutyric Acid
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

20. 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.

21. 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

22. 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

23. 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.

24. 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

25. 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

26. 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)

27. Basal Ganglia Disease Not enough DA Parkinsons ‘Normal’ Too much DA
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