Autonomic Nervous System (ANS) Clinical Correlations

Clinical Correlations

• horner’s syndrome (sympathetic nervous system)

• peripheral nerve lesions

• spinal cord lesions

• autonomic dysreflexia

This is just a partial list of ANS deficits

Horner’s Syndrome

• if a lesion affects the sympathetic pathway to the head, sympathetic activity on one side of the head (ipsilateral side) is defective

• can occur with lesions of the:

  • descending sympathetic fibers from the hypothalamus (central lesion: CNS)

  • upper thoracic spinal cord (T1-T4) (preganglionic lesion: spinal cord)

  • superior cervical ganglion (from cervical sympathetic chain) (postganglionic neuron cell body)

• can also be the result from another injury, disorder (head injury, lung tumor, etc)

Horner’s Syndrome: Clinical Signs

Signs are on the same side (ipsilateral) as the lesion

• ptosis: partial drooping of the eye lid (superior tarsal muscle)

• miosis: pupillary constriction

• anhidrosis (Hypohidrosis): lack (or decrease) of sweating

• enophthalmos: eye appears to sink into the orbit

Peripheral Nerve Lesions

• if peripheral nerve is severed, interruption of sympathetic efferents can cause loss or decrease of sympathetic functions in the areas supplied by that nerve or nerves

  • vascular control (sympathetic efferents control diameter of blood vessels)

  • temperature regulation

  • sweating

Spinal Cord Lesions

• complete spinal cord lesion interrupts all communication between the brain and the spinal cord region located below the lesion

• effects of spinal cord lesions on bladder, bowel, ad sexual functions depend on the location of the lesion along the levels (C, T, L, S) of the spinal cord

  • it could affect both sympathetic and parasympathetic innervation

  • it could just involve the sympathetic or parasympathetic innervation

• sexual function is a significant issue for many following SCI

• with SCI, the effects of spinal cord lesions on bowel control and sexual organ functions are similar to bladder function

  • so, as an example we will discuss bladder dysfunctions following a SCI

Types of bladder dysfunctions after spinal cord injury

• lower motor neuron (LMN) bladder, aka:

  • flaccid bladder

  • atonic or hypotonic bladder

  • underactive bladder

• Upper Motor Neuron (UMN) bladder, aka:

  • spastic neurogenic bladder

  • hyper-reflexive bladder

Levels of SCI for bladder dysfunctions

• LMN bladder (flaccid bladder) due to complete lesion of:

  • Cauda Equina

  • spinal cord levels S2-S4 (located in the conus medullaris)

• UMN Bladder (spastic bladder) due to complete lesion of:

  • spinal cord above S2 (above the conus medullaris)

LMN bladder: cauda equina lesion

flaccid bladder due to a complete lesion of:

• the cauda equina (L2-S4 ventral and dorsal roots)

  • all neural connections with the bladder are severed, except the sympathetic efferents

  • interruption of the reflexive bladder emptying circuit. Results:

    • the bladder keeps filling up

LMN bladder: S2-S4 spinal cord lesion

flaccid bladder due to a complete lesion of:

• spinal cord levels S2-S4

  • all neural connections with the bladder are severed, except the sympathetic efferents

  • interruption of the reflexive bladder emptying circuit. Results:

    • the bladder keeps filling up

UMN bladder: Lesion above S2 spinal cord level

Spastic/Hypertonic bladder

• the reflexive connective between bladder and spinal cord are sill intact, so

  • reflexive emptying of the bladder can still take place

  • spastic emptying because gets no control from higher centers

  • sympathetic input does not override “reflex” response

Autonomic Dysreflexia (hyperreflexia)

• sudden over-active autonomic nervous system

  • potentially life threatening (medical emergency)

  • can result in stroke, heart attack, seizures, death

• who is at risk for autonomic dysreflexia?

  • people with SC injury at T6 or above is most common cause

  • other factors:

    • brain injury, stroke, multiple sclerosis, Guillain-Barre syndrome, side effects of medication

• triggers: irritation, noxious stimuli (painful or not)

  • bladder — over-distention, kink in a catheter, bladder spasms, infection

  • bowel — constipation, hemorrhoids, gas, diarrhea

  • skin — constrictive clothing (jeans, socks, shoes), bed sores, ingrown toenails, cuts, bruises

• results in uncoordinated autonomic responses

Autonomic Dysreflexia (hyperreflexia) cont’d

• a noxious afferent stimulus (distended bladder, bed sore, etc) below SC lesion triggers excessive peripheral sympathetic response below lesion

  • results in: vasoconstriction to viscera and muscles below the level of the lesion

  • causes: abrupt increase in blood pressure

• baroreceptors in blood vessels detect this hypertensive crisis and signal the brain via cranial nerves IX and X

• descending inhibitory singals respond to counteract the rise in blood pressure with slowed heart rate and vasodilation

• however, vasodilation is blocked at the level of the spinal cord injury and below

• results:

  • uncoordinated autonomic control responses (high BP)

  • above lesion: flushed/warm skin (vasodilation), profuse sweating and pounding headache, reduced heart rate

  • below the lesion: vasoconstriction, cold/pale extremities, goose bumps

Autonomic Dysreflexia (hyperreflexia): Treatment

• stroke can be an immediate life-threatening concern associated with this

• treatment/management

  • first step:

    • sit the patient upright with their legs dangling

    • remove source of noxious stimulus (tight clothing, constrictive devices, ask about bladder or bowel issues)

  • this will help lower their blood pressure by inducing the pooling of blood in the abdominal and lower extremity vessels

• if the source of noxious stimuli cannot be found, emergency medical services should be contacted

ANS dysfunctions at various levels of spinal cord injury