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CNS regulation of the ANS Flashcards

1
Q

Control of ANS

A
  • Much of the ANS is controlled by the CNS, by top-down tracts that begin in the CNS and end on ANS lateral horn cells (in the intermediolateral column) of the SC (for sympathetics) in the region of T1-L2
  • For parasympathetics much of the regulation is directly from brainstem nuclei of cranial nerves (III, VII, IX, X) and from top-down tracts of the CNS that end on the lateral horns of the sacral SC region (S2-S4)
  • The cortex, diencephalon (thalamus and related structures), and brainstem all contribute to regulating the ANS
  • Tissue innervated by ANS: smooth muscle, cardiac muscle, or glands
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2
Q

Hypothalamus regulation of ANS

A
  • The hypothalamus, in particular the paraventricular nucleus (PVN- just lateral to the 3rd ventricle in the hypothalamus), is the master controller of homeostasis
  • The hypothalamus regulates homeostasis by sending multiple signals to different parts of the body
  • It sens neural and hormonal signals to the pituitary gland to modulate endocrine function
  • It also sends neural signals to the ANS to coordinate the activity of the SNS and PsNS
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3
Q

Hypothalamic pathways to ANS

A
  • Descending fiber tracts originating in hypothalamus travel to the brainstem to initiate the ANS, these are mostly reciprocal to the afferent systems to the hypothalamus
  • These tracts include the medial forebrain bundle (MFB- in the dorsolateral tegmentum), the dorsal longitudinal fasciculus (DLF), and the mammillotegmental tract (MTegT)
  • There is also a tract from the hypothalamus that descends to the SC: the hypothalamospinal tract (HTST)
  • The HTST descends through the lateral part of the medulla then through the lateral column of the SC to end on lateral horn cells of sympathetic pre ganglion cells
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4
Q

Example of CNS control of ANS 1

A
  • Intrinsic rate of SA node firing in heart is 100-110 BPM, but this is affected by both sym and para
  • Sympathetic innervation comes from the sym/post cell bodies in the sympathetic trunk (some to superior cervical ganglion), coming thru cardiac splanchnics
  • These cells received input from the sym/pre neurons in the lateral horn of the SC from segments T1-T4/5
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5
Q

Example of CNS control of ANS 2

A
  • The sym/pre cell bodies received input from the HTST, thus some of the sympathetic action on the heart is controlled in the brainstem
  • The para sympathetic innervation of the heart is simply from the vagus (X), which has its cell body in the medulla
  • Therefore both the sym and para innervation of the heart receive instructions from the brainstem
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6
Q

CV regulatory centers 1

A
  • The CV centers (CVCs) are located in the nucleus tractus solitarius (NTS) in the medulla
  • Sensory receptors in vasculature (sensing BP) and information from the cortex and hypothalamus (emotions/senses and other stimuli) all feedback to the NTS
  • The NTS will respond appropriately, depending on what the situation requires, and either increase SNS/decrease PsNS to heart or decrease SNS/increase PsNS to heart
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7
Q

CV regulatory centers 2

A
  • The other nuclei at this same level are nucleus ambiguus (NA), where the motor nucleus for X is (SM cells that will run in the recurrent laryngeal nerve to larynx/pharyngeal muscles), but also conveys some para/pre fibers
  • Also there is the dorsal motor nucleus of X (DMN), which is the para/pre origin (cell bodies) of most parasympathetic fibers from the vagus nerve
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8
Q

Sympathetic medullary control of heart

A
  • Neurons in NTS receive info from afferent fibers of IX and X that communicate the BP level
  • When BP is high there is increased firing of baroreceptors and increased input to NTS
  • NTS sends out GABA (inhibitory) fibers to the rostral ventrolateral medulla (RVLM), thus higher NTS input increases inhibition of the RVLM
  • Inhibition of the RVLM decreases input onto the sym/pre cell bodies in the lateral horns of the SC in T1-T4/5
  • This causes a decrease in SNS activity on the heart, to lower the BP
  • If there was low BP the RVLM will be disinhibited (due to lower input to NTS and thus less inhibition from NTS to RVLM) and it would increase the sympathetic tone to the heart
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9
Q

Parasympathetic medullary control of heart

A
  • For the parasympathetic system, neurons from NTS to the DMN and NA are excitatory
  • A higher BP will cause more NTS firing and more activation of the DMN and NA
  • Para/pre axons come from both DMN and NA and go directly to heart thru X
  • Low BP causes less firing from NTS, thus less firing from DMN/NA para/pre and thus less parasympathetic tone to heart thru X, raising the BP
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10
Q

Sympathetic nerve dysfunction

A
  • Can get sympathetic dysfunction if there is a lesion in the descending HTST, in the preganglionic cells (lateral horns of T1-L2), in the postganglionic cells (sympathetic trunk), or from splanchnic nerve
  • Sympathetics never decussate, always remain ipsilater and only innervate unilaterally
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11
Q

Horner’s syndrome

A
  • Dysfunction of SNS due to peripheral or central lesion
  • Peripheral: unilateral lesion of the superior cervical ganglion (damaging the postganglionics) or damage to lateral horn cell bodies from T1-T4 (preganglionics)
  • Central: Cervical SC damage (bilateral or unilateral) or lateral medullar syndrome (both destroy the HTST descending to supply the preganglionics innervation)
  • Lateral medullary syndrome due to lesion of PICA
  • This causes little ptosis (drooping of upper eyelid due to lack of sympathetic innervation of the superior tarsal smooth muscle)
  • Also causes miosis (constriction of pupil- lack of SNS), and anhydrosis (inability to sweat due to lack of SNS)
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12
Q

Vagus nerve parasympathetics 1

A
  • Preganglionics are in the DMN and the DA in the medulla
  • These preganglionic fibers travel on X to reach the postganglionic cell bodies located close to the target
  • Isolated unilateral lesions of preganglionics (DMN/NA/X) have little effect on parasympathetic function b/c of bilateral innervation of the vagus nerve from the other side
  • Only the parasympathetics from X are innervating bilaterally
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13
Q

Vagus nerve parasympathetics 1

A
  • Proximal lesions that involve SM components (DMN/NA/proximal X before it turns into recurrent laryngeal/recurrent laryngeal) will lead to difficulty swallowing and speaking
  • This is b/c the SM in proximal X/recurrent laryngeal only innervate ipsilaterally (not bilaterally)
  • Thus the loss of one side of the SM from X will result in speaking/swallowing deficits in the larynx and pharynx
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14
Q

Occulomotor nerve (III) parasympathetics

A
  • Preganglionics in the edinger-westphal nucleus (EWN) in upper midbrain (level of red nucleus/superior colliculi) sit right next to the SM nucleus of III (thus CN III as it leaves the midbrain just medial to the crus cerebri contains both para/pre and SM)
  • These fibers travel w/ III to eye, where they synapse on postganglionics in the cilliary ganglion
  • Then travel on short cilliary nerves to reach sphincter muscles (for pupillary constriction) and cilliary muscles (for accommodation of lens)
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15
Q

Pathology of parasympathetics of III

A
  • Since III innervates ipsilateral eye to the EWN, all deficits will be ipsilateral to lesion
  • Lesions in III result in weber’s syndrome: cause by vascular lesions of PCS and top of basilar artery, this KOs the crus cerebri and III since III exits the midbrain just medial to crus cerebri (both share common blood supply)
  • Results in mydriasis (dilation) of pupil, loss of light reflex, and loss of accommodation, all from loss of para
  • Will also see loss of SM to levator palpebrae causing big ptosis
  • Loss of SM to MR means ipsilateral eye will be abducted, due to presence of LR (from contralateral VI) but loss of ipsilateral SM of III
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16
Q

Facial nerve parasympathetics

A
  • Preganglionics in the superior salivatory nucleus (VII), and travel w/ VII very briefly before branching off VII and hitchhiking on other nerves to reach destination
  • VII as it leaves the stylomastoid foramen does not have any parasympathetics
  • Therefore damage (peripheral) to VII after exiting the stylomastoid foramen will only affect SM, and not para
  • But central damage to VII (before it exits stylomastoid foramen) will affect para
  • Since bell’s palsy is defined by compression of VII as it exits (or after) the stylomastoid foramen, there cannot be any para deficits in bell’s palsy
17
Q

Parasympathetic pathology of VII

A
  • Central lesion in pons or tumor at the internal acoustic meatus will affect the parasympathetics from VII
  • Must be before VII leaves stylomastoid foramen
  • This causes dry eyes/loss of tears, and dry mouth (para’s only innervate glands)
18
Q

Somatomotor pathology from central lesions of VII

A
  • Central lesions: destroying the cortex, internal capsule, crus cerebri, or descending CBT above the level of the lower pons (where VII motor nucleus is)
  • UMNs from cortex bilaterally innervate motor nucleus of VII for UPPER facial muscles only
  • UMNs from cortex contralaterally innervate motor nucleus of VII for lower facial muscles
  • Therefore we see facial paralysis on one side of the face (contralateral) and only affecting the lower face (below the eyes)
  • Frontalis and obicularis oculi remain intact due to bilateral innervation
19
Q

Somatomotor pathology from peripheral lesions of VII

A
  • Called bell’s palsy if the lesion is after VII exits the stylomastoid foramen (before it exits could also affect para and is not bell’s palsy)
  • This results in paralysis of all facial muscles (upper and lower): obicularis oculi + frontalis (upper) and obicularis oris (lower)
  • This is b/c once in VII (now LMNs) the SM components only innervate the ipsilateral muscles of the face
  • The bilateral innervation from the cortex (UMNs) doesn’t matter since UMNs already synapsed on the motor nucleus of VII in the lower pons
20
Q

Glossopharyngeal (IX) parasympathetics

A
  • Preganglionic cell bodies in inferior salivatory nucleus, travel on IX and hitchhike their way to the parotid gland (only gland in head not innervated by VII)
  • Since parotid gland is not the only supplier of saliva for the mouth, lesions to para fibers from IX have little effect on function
21
Q

Pathology in IX SM

A
  • Lesions of UMNs (to nucleus of IX) have no effect b/c of bilateral innervation of the nucleus by both cortices
  • LMN lesions of IX can have large effects when there is compression of jugular foramen since this also effects X and XI
  • Symptoms would include loss of taste to posterior 1/3rd of tongue on ipsilateral side, loss of gag reflex, difficulty swallowing and speaking, and paralysis of SCM and trapezius on ipsilateral side
  • This lesion would not include any para fibers from IX since they use a different pathway

Neuro (62 decks)

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