NMS
6/24/1999
Sympatheticotonia
Asthma
- NE is neurotransmitter
- Catacholamine
- Epinephrine is another catacholamine (a
and b
)
- Only place you find NE is neurotransmitter is postganglionic sympathetic nerves
- Found in certain areas of the brain and cord—highly concentrated in highly active areas
- Specific neurotransmitter
- a
-adrenergenic
- some tissues do not have a
receptors and are not affected by NE
- the lungs are an example—they only have b
receptors and E is the affector
- sympathetics affect the adrenals from about T9
- only through circulation does adrenaline affect the body
- How does the heart rate goes up when they need it to?
- SA node controls the rate
- Parasympathetics (CNX) slows it down
- Sympathetics do not directly innervate the SA node
- The SA node is a b
receptor and only reacts to E
- Sympathetics have a direct affect to the ventricles
- Adrenaline that gets to dilate the cardiopulmonary system (b
receptors)
- Ephedra—stimulant—have dangerous side affects
- Sympatominmetic—mimics sympathetics—have dangerous side affects
- Bradycardia
- Parasympatheticotonia—increase output, decrease the heart rate
- Sympathetic atonia—loss of sympathetic tone
- Tx depends upon which one of these you decide is the problem
- Increase sympathetics through adjusting—inhibiting the nerve outflow, catacholamines must be low in the pt
Vagus Nerve
- Nodose ganglion
- C1 and C2 pass through Nodose area
- Parasympatheticotonia is related to upper cervical subluxation
- Sensory receptors is cough receptors—key role in the tissues
- Goes up to the nucleus in the brain motor portion which will cause the muscles in the bronchi to constrict in the lungs
- NE lands in the area of the irritant receptors and lowers their threshold
Hyperesthesia appears w/CES
RSD—reflex sympathetic dystrophy (causalgia)—intractable pain in an extremity, occurs sometimes after a surgery, trauma—unknown reasons the pt recovers then complains of pain in the arm and leg—drugs were not effective—cutting away part of the cord came from this—sympathtetica—destroy several of the ganglion that went into those areas—60-75% received relief
- Anxiety from the hypothalamus that releases NE
Imbalances b/w Para and Sympathetics
- Sympatheticotonia and sympathetic atonia
- Parasympatheiticotonia and parasympathetic atonia
- Atonia is damage to the nerves
- -otonia is a hyperexcitation of the nerves
- pupilary reflex
- pupils should dilate when turn off the lights (sympathetics come in from the superior cervical ganglion)
- bilateral dilation occurs from increased sympathetic state
- shine light source towards the right eye—it should constrict (parasympathetics, CNIII, Edenger-Westfall Nucleus) Optic Nerve told it that the light source was there
- both should constrict if the nerves are healthy
- direct light reflex—the right constricts when light is shone on it
- consensual reflex—the left constricts do to the increased parasympathetic response
- dark room w/right dilated and left constricted
- Anisocoria (not the same cornea)—neurologic lesion
- Could not take a drug that could stimulate only one side
- The left is not dilating—it is not doing what it is supposed to be doing
- Either has too much parasympathetic or not enough sympathetic
- Sympathetic atonia is a neurologic lesion
- Horner's syndrome
- Neuropathies can be very selective in there destruction of a nerve
- Miosis—pupil that will not dilate
- Light room w/right eye dialted and left constricted
- Not enough parasympathetics
- CNIII lesion
- Mydriasis—pupil that won't constrict