CNS Regulation of the ANS

1. CNS Regulation of the ANS Thomas H. McNeill, PhD Dept. Cell and Neurobiology March 25, 2014 tmcneill@usc.edu

2. Lecture Objectives • Describe the “top-down” control of ANS function from the brainstem and hypothalamus • Describe the basic anatomical pathways of the CNS that control heart rate • Describe the clinical deficits associated CNS lesions that sympathetic function in the face • Describe the clinical deficits associated CNS lesions that effect parasympathetic function of CN lll, Vll, lX and X.

3. What is the Function of the ANS? • The ANS helps maintain homeostasis by regulating bodily functions & responses not under voluntary or cognitive control • The ANS is regulates the activity of cardiac and smooth muscles and exocrine glands • ANS is regulated in part by higher centers in the hypothalamus and cortex • ANS activity is dependent on sensory information provided by internal organs (viscera), blood vessels and sensory systems including sight, sound smell ect.

4. Some Things That Might Stimulate an ANS Response

5. Regulation of the ANS from Cortex/Limbic System to the Hypothalamus NEOCORTEX Provides cognitive/sensory input to: SEPTAL NUCLEI AMYGDALA HIPPOCAMPUS Links cognitive info with emotion and memory and communicates this with: HYPOTHALAMUS Integrates this input with the ANS and endocrine function for: NEOCORTEX Integrates input and causes motor activity for: SURVIVAL - ANS RESPONSES Individual (behavior, fight or flight, homeostasis)

6. Hypothalamic Regulation of the ANS • Hypothalamus, in particular, the Paraventricular Nucleus (PVN) is the “Master Controller” of the ANS • The PVN receives input regarding homeostasis including body temperature, blood pressure, fluid and electrolyte balance, body weight from brainstem regulatory centers and sensory stimuli from cortex and limbic system. • It sends neural signals to the autonomic nervous system, to coordinate the activity of the parasympathetic and sympathetic nervous system.

7. Hypothalamic control of ANS occurs via descending fibers tracts from hypothalamic nuclei to brainstem regulatory centers in reticular formation • Medial Forebrain Bundle (MFB) • Dorsal Longitudinal Fasciculus (DLF) • Mammillotegmental tract (MTegT) • Hypothalamospinal tract to T1, T2

8. Example is Regulation of Heart Rate by ANS • Cells of the SA node have the fastest rate of depolarization and thus, coordinates the overall rate of contraction • The intrinsic rate of contraction for the SA node is 100-110 “beats” per min. • Innervation from sympathetic nerves will increase heart rate and force of contraction • Innervation from parasympathetic nerves (CN X, vagus) will decrease heart rate

9. CNS Regulation of Heart Rate Regulation of ANS is Top down parasympathetic X sympathetic

10. Resting HR At rest vagal influences are dominant over sympathetic reducing the heart rate down to 60-80 beats per min. Key Point However, as we go about our daily activities sensory receptors in the vasculature (blood pressure) as well information from the cortex and hypothalamus (emotions - anger, fear, surprise) provide feedback to cardiovascular regulatory centers in the brain stem allowing us to adapt to changes in the environment and maintain homeostasis.

11. Medullary Control of Cardiovascular Function DMN NTS NA Location of medullary regulating centers in cross section of rostral medulla Schematic of neural circuit for regulation of CV function NTS – nucleus tractus solitarius DMN – dorsal motor nucleus of vagus NA – nucleus ambiguus

12. Sympathetic Medullary Regulating Center hypothalamus 1. Neurons in the NTS in the medulla assess changes in blood pressure from afferent baroreceptor fibers via CN IX and X and top down input from the hypothalamus. 2. Increased input to NTS in response to high blood pressure or stress will inhibit activity in RVLM and decrease sympathetic tone to heart or 3. Decreased input to NTS will reduce inhibition at RVLM and increase sympathetic tone in response to low blood pressure 2 3 1 4 5

13. Parasympathetic Medullary Regulating Center hypothalamus 1. Other excitatory neurons in the NTS project to the DMN and NA of the CN X to modulate parasympathetic innervation to the heart 2. Increased input from NTS to DMN or NA will increase parasympathetic tone and decrease heart rate in response to increased blood pressure 3. Decreased input from NTS to NA and DMN will decrease parasympathetic tone in response to low blood pressure Baroreceptor afferents 1 DMN 2 NA 3

14. CNS Regulation of Sympathetics of Head Regulation of ANS is Top down parasympathetic sympathetic

15. Clinical Syndromes Associated with Sympathetic Nerve Lesions Can Occur from Peripheral or Central Lesions Peripheral Lesion (review from Dr. Albrecht’s lecture • Horner’s Syndrome (unilateral) • typically results from damage to superior cervical ganglia • “little” Ptosis: drooping of upper eyelid (superior tarsal muscle – smooth muscle) • Miosis: constriction of pupil due to loss of innervation to dilator muscles of the pupil • Facial anhydrosis: inability to sweat Patient with Horner’s Syndrome

16. Central Lesion • Spinal cord injury to cervical spinal cord - Horner’s syndrome (usually bilateral due to trauma) • Medullary vascular lesion • - Lateral medullary syndrome • - unilateral lesion of PICA Indicates location of hypothalmospinal tract that provides top-down regulation of sympathetic function

17. CNS Regulation of Parasympathetics Regulation of ANS is Top down parasympathetic sympathetic

18. CNS Regulation of Parasympathetics in CN lll, Vll, lX, X Vagus Nerve (X) – anatomy • Parasympathetic preganglionic cell bodies – dorsal motor nucleus and nuc. ambiguous in the brainstem • Somatomotor cell bodies are located in the nucleus ambiguus and innervate skeletal muscles of the pharynx and larynx

19. Vagus Nerve Lesion – pathology • Vagus nerve does not innervate the head region • UMN lesions typically have little effect on vagal functions below the neck because of the bilateral distribution from the vagus nerve to the target (example cardiac plexus) • However, unilateral lesions in the brain stem that involved nuc. ambiguous can lead to difficulty swallowing and speaking due to lost innervation to the larynx and pharynx from the recurrent laryngeal nerve.(see lateral medullary syndrome)

20. Oculomotor Nerve (III) - anatomy • Preganglionic cell bodies- Edinger-Westphal nucleus in brainstem adjacent to somatomotor neurons • Para-pre and somatomotor axons exit the midbrain together medial to the crus cerebri • Postganglionic cell bodies in ciliary ganglion • Postganglionic fibers travel via short ciliary nerves to sphincter muscles of pupil (constriction) and ciliary muscles of eye for accommodation (thickening lens)

21. Weber’s Syndrome Weber’s Syndrome -Vascular lesion of the posterior cerebral artery and top of the basilar artery involving the crus cerebri and LMN axons of CN lll ipsilateral to lesion. • Parasympathetic Symptoms • Mydriasis: dilated pupil • Loss of light reflex -- Loss of accommodation of lens to adjust for near vision Lesion Normal

22. Weber’s Syndrome con’t • Somatomotor Symptoms • Loss of ability to move eye medial • “big” ptosis due to loss of innervation to levatorpalpebrae • Eye is deviated laterally (i.e abducted) ptosis

23. Facial Nerve (VII) Lesions- clinical symptoms • The constellation of clinical symptoms that result from damage to the facial nerve depends on the site of injury • Central lesions may result in both parasympathetic and somatomotor problems • Peripheral lesions typically are somatomotor because the lesion site is after it leaves the stylomastoid foramen (Bell’s Palsy)

24. Central Lesions of Facial Nerve (VII) Lesion – pathology parasympathetic pathology resulting from lesion in pons or tumor at the internal acoustic meatus - Causes dry eye or loss of tears - Dry mouth somatomotor pathology - facial paralysis on one side of lower face, drooping corner of mouth - frontalis and obicularis oculi remain intact due to bilateral innvervation of UMNs.

25. Glossopharyngeal Nerve (IX) – anatomy • Preganglionic cell bodies – inferior salivatory nucleus • Preganglionic fibers travel via the lesser petrosal nerve to postganglionic neurons • Postganglionic cell bodies – otic ganglia • Postganglionic fibers travel along side of V3 to the parotid gland Otic ganglia V VII IX Lesser petrosal n.

26. Glossopharyngeal Nerve (IX) Lesion – clinical symptoms • UMN lesions have little effect on the function of the glossopharyngeal nerve because of the bilateral innervation • Injury to the LMN’s of IX from infections or tumors is usually associated with damage to lX, X and XI because all three nerves pass together through the jugular foraman i.e. jugular foramen syndrome • Non-parasympathetic symptoms might include: • Loss of taste posterior 1/3 of tongue • Loss of gag reflex on side of lesion • Unilateral weakness in swallowing

27. Questions?