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

Afferent Fibers Spinal Ganglia Muscle Efferent Fibers

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

Chickenpox Shingles

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

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

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

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

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

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

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

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

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

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

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

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

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

The Basal Ganglia

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

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.

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

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

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.

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

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

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)

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