Exam 4 Part III Flashcards
A. The pain receptors and their stimulation: Pain receptors are:
all free nerve endings
sensitive to: mechanical stress or damage, extremes of hot or cold, and/or chemical substances (bradykinin: produced upon injury, histamine, acids, prostaglandins, leukotrienes, K+, etc.).
relatively non adapting
Conditions in which pain is produced:
chemicals released from tissue damage (inject bradykinin under skin,
tissue ischemic damage from lack of blood flow. Who are the culprits?Lactic acid? Other chemicals from injury as above?
Muscle spasm is a common cause, directly stimulating receptors & causing ischemia.
Two pathways exist corresponding to the 2 types of pain:
acute, sharp pain (Aδ) and chronic slow or aching pain (C fiber). Burn, for example: instantly remove your finger from that stove! Then a sec. later, you know how badly you have hurt yourself (the ache or throbbing comes).
The anterior and lateral spinothalamic tracts both are part of the
anterolateral system.
Most of the pain fibers terminate in the
reticular formation (RF) in the medulla, pons and midbrain. Then other neurons transmit this information upward to the thalamus, etc.
. Some fast fibers go directly to the
. Some fast fibers go directly to the thalamus and then on to other areas, particularly somatosensory cortex. These are for pain localization.
The significance of having all the slow fibers terminate in the RF is that
The significance of having all the slow fibers terminate in the RF is that this is part of the reticular activating system, which activates the nervous system, promoting defense and aversion in the case of pain.
C. A pain control (“analgesia”) system in the brain and spinal cord.
Experimental pain thresholds tend to be very much the same for different people. How people react to pain and pain tolerance are very different for different people. Part of this probably has to do with the ability of the nervous system to control what pain signals make it all the way in in different circumstances.
periaquaductal gray area of the midbrain and upper pons
decrease-> enkephalin secreted
raphe magnus of lower pons and medulla
decrease -> 5 – HT secreted
a pain inhibitory complex in the dorsal horns of the spinal cord [substantia gelatinosa] Enkephalin secreted also here. These 2 places for enkephalin secretion show that
endorphins or endogenous opiates are important in endogenous pain-management.
“Pain–gating”?
“Pain–gating”? 40% of people with severe injury are unaware of injury, feel no pain. Part of the concept of pain-gating is that other kinds of stimuli can block pain.
Another way in to the analgesia system is by
tactile stimulation which causes blockade at the spinal cord. Tactile stimulation near the site of pain or many segments away can cause pain suppression.
Physical therapy emphasizes now
Physical therapy emphasizes now stimulating other parts of the nervous system than the areas of pain.
Acupuncture for pain: at least part of its effect to reduce pain is
endorphin release from periaquaductal gray area
H2O – can wash away
H2O – can wash away pain–promoting substances (Also does it
Visceral pain can come from
overdistension of a hollow organ, injury, ischemia, spasm of a hollow organ (can result from mechanical stimulation of the pain endings, diminished blood flow). Pain often comes in the form of a cramp.
Visceral pain is often diffuse because
Visceral pain is often diffuse because there are very few receptors in the viscera. According to Guyton, the only sensation in the viscera is pain.
Visceral pain can often be felt as
Visceral pain can often be felt as referred pain on the surface of the body or in some other deep area of the body than the origin. Each spinal nerve innervates an area on the skin called a dermatome. Referred pain tends to follow dermatomes.
Referred pain”
Referred pain” (not the usual meaning) can be caused secondarily by reflex muscle spasm. The painful stimulus may originate in a ureter and that can cause reflex spasm of the lumbar muscles.
Hyperalgesia =
Hyperalgesia = hypersensitivity to pain
Hyperalgesia primary
Primary: excessive sensitivity of the pain receptors themselves,
hyperalgesia secondary
Secondary: facilitation of sensory transmission. It can result from lesions of the spinal cord or of the thalamus (“thalamic pain syndromes”).
herpes zoster
It infects a dorsal root ganglion & causes pain in that dermatome = shingles. (Also tend to have blistering, usually at the thorax.) Immunosuppression later → virus moves down axons and can cause skin infection. Can have postherpetic neuralgia.
A headache is not due to direct pain in the brain, but
A headache is not due to direct pain in the brain, but stretching the dura or the blood vessels of the dura can cause intense pain.
meningitis –
meningitis – inflammation of the meninges
sub-arachnoid hemorrhage:
sub-arachnoid hemorrhage: “the worst headache a person has ever had”
low CSF pressure – removal of 20 ml prevents normal
low CSF pressure – removal of 20 ml prevents normalflotation of the brain and the weight of the brain stretches the dural surfaces.
Migraine –
Migraine – only theories: often seems to involve vasoconstriction followed by more long-lasting vasodilation, both of which can cause pain.
Alcoholic headache –
Alcoholic headache – toxicity (irritates the tissue) and dehydration (reduced brain flotation): reduced ADH effects → ↑ urine
Constipation headache –
occurs even when the spinal cord is severed. Perhaps either due to toxic products or loss of fluid into the tissues (distension causes venous pooling) resulting in reduced brain floatation.
extracranial muscle spasms
From muscle spasm – emotional or physical tension causes muscles of the head and neck to become spastic, “tension headaches”
extracranial irritation of nasal structures
Irritation of nasal structures including sinuses – “not an intense type of pain”
extracranial irritation of the eye
Eye disorders – attempts to focus can cause strain or spasm, UV can burn the conjunctiva or retina
extracranial causes of headaches
muscle spasms
irritation of nasal structures
irritation of the eye
G. Thermal sensations –
G. Thermal sensations – all free nerve endings
thermal sensations
Freezing cold = cold receptors and pain receptors.
Burning hot = hot and pain and sometimes cold receptors. Burning hot can sometimes feel cold at the same time.
thermal sensations are
rapidly adapting, thus the misperception after holding one hand in cold water and one in hot and then both in tepid. The previously hot hand feels the water as cold and the previously cold one feels the water as hot. These receptors signal changes in T not absolute T.
the stretch reflex is
monosynaptic and ipsilateral.
the stretch reflex
The stretch reflex (= myotatic reflex), e.g., the knee jerk
The mallet hits the tendon which stretches the quadriceps femoris muscle which causes the intrafusal fiber to be stretched. This causes the midportion of the muscle spindle to be stretched which excites the IA afferent (labelled proprioceptive nerve). This excites a synapse onto the alpha motor neuron. The extrafusal muscle (the quadriceps in this case) contracts and the leg kicks. This is the stretch reflex. It is a monosynaptic reflex. Its purpose is to “oppose sudden changes in muscle length.”
The stretch reflex is used to assess
The stretch reflex is used to assess the degree of facilitation coming from other places in the spinal cord and from higher areas.
If facilitation is greatly increased, the muscle jerks can
If facilitation is greatly increased, the muscle jerks can be exacerbated. If facilitation is lessened or gone, the jerks can be gone. This happens immediately following spinal cord injury, is called spinal shock..
clonus
Muscle jerks can oscillate = clonus.
clonus can be used to
Can be used clinically to test for damage, as in contralateral motor cortex.
Signals from γ efferents would
Signals from γ efferents would increase muscle tone.
During exercise, coactivation of γ efferents when α motor neuron is firing keeps
During exercise, coactivation of γ efferents when α motor neuron is firing keeps muscle spindle in right range to keep stretch reflex working. (Without coactivation of γ efferents, main muscle contraction shortens spindle, so no A.P.s from it.)
If tension on the muscle is increased, the tendon organ is
If tension on the muscle is increased, the tendon organ is stretched. This activates an inhibitory interneuron that inhibits the alpha motor neuron, and the muscle relaxes
the nociceptive or pain reflex,
it is most powerfully elicited by painful stimuli. But it can also be elicited by a cutaneous sense in a decerebrate or chronic spinal animal.
reflex is reciprocal inhibition
reflex is reciprocal inhibition between 2 groups of muscles. When the flexor is excited, the extensor is inhibited.
C. The crossed extensor reflex
This allows the body to be supported while one limb is being withdrawn. It is a spinal reflex, polysynaptic and crossed = contralateral. Reciprocal inhibition is also a component of this reflex: when the flexor of one limb is excited, the flexor of the opposite limb is inhibited.
The positive supporting reaction.
Supportive pressure on the footpad of a decerebrate animal (sectioning at the middle of the midbrain) results in the limb extending against the pressure being supplied.
Rhythmic stepping motions can be observed in
Rhythmic stepping motions can be observed in a spinal animal or even if the lumbar cord is separated from the rest and cut down the center to prevent interaction between the 2 limbs. Forward flexion occurs and then backward extension and then this repeats itself. No sensory input is needed for it to occur.
rhythmic stepping involves
It involves reciprocal inhibition (one group of neurons inhibits another and vice versa), i.e., the flexors inhibit the extensors. The flexor stimulus dies out and the extensors rebound from inhibition.
Pain stimuli can cause
Pain stimuli can cause reflex muscle spasm (not known exactly how). Relief of pain relieves the spasm, as, for example, with local anaesthetic
spinal shock
At first when the spinal cord is transected, all spinal reflexes cease = spinal shock. They lose their source of excitability from above. (Continual or tonic discharge from reticulospinal, vestibulospinal and corticospinal tracts.)
After a few hours, days or weeks of spinal cord transsection (longer in humans),
After a few hours, days or weeks (longer in humans), excitability returns.
It seems to be a property of neurons that, after they lose their source of excitability from without, they
It seems to be a property of neurons that, after they lose their source of excitability from without, they increase their own excitability to make up for the loss.
spinal shock symptoms
arterial P drops – to 40 or so, due to loss of sympathetic tone sacral reflexes (parasym.) for bladder and bowel evacuation are lost skeletal muscle reflexes are lost. The simplest return first (stretch, flexor, postural antigravity, stepping)
. In a chronic spinal animal, often all the spinal reflexes are facilitated. So then if a painful stimulus or overdistension occurs, there is a mass reflex involving large portions of the cord. The pattern is:
flexor spasm of the body
colon and bladder evacuation
arterial P increase, so that the mean P may be 200mmHg
profuse sweating
The triple response to injury:
The triple response to injury:
1) the red reaction: pressure on the capillary from the injuring object causes immediate capillary dilation,
2) the flare: redness spreading out from the injury due to arteriolar dilation and
3) the wheal: swelling spreading out with slight delay from increased permeability of capillaries, maybe due to histamine, etc..
