Somatic Sensations: II. Pain, Headache, and Thermal Sensations Flashcards
fast pain
Fast pain is also described by many alternative names, such as sharp pain, pricking pain, acute pain, and electric pain. This type of pain is felt when a needle is stuck intothe skin, when the skin is cut with a knife, or when the skin is acutely burned. It is also felt when the skin is subjected to electric shock. Fast-sharp pain is not felt in most deep tissues of the body
slow pain
Slow pain also goes by many names, such as slow burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain. This type of pain is usually associated with tissue destruction. It can lead to prolonged, almost unbearable suffering. Slow pain can occur both in the skin and in almost any deep tissue or organ.
pain receptors are
free nerve ending which are superficially present in the skin and in some deep tissues as well like atrial wall, joint surfaces periosteum falx and tentorium of the cranial vault
why deep tissue transmit slow pain
they are sparsely populated with free nerve endings so they transmit slow chronic aching type of pain
what type of stimuli excite pain receptors (both type)
Pain can be
elicited by multiple types of stimuli, which are classified
as mechanical, thermal, and chemical pain stimuli. In
general, fast pain is elicited by the mechanical and thermal
types of stimuli, whereas slow pain can be elicited by all
three types.
Some of the chemicals that excite the chemical type of
pain are
bradykinin, serotonin, histamine, potassium ions,
acids, acetylcholine, and proteolytic enzymes. In addition,
prostaglandins and substance P enhance the sensitivity of
pain endings but do not directly excite them.
hyperalgasia
pain receptors
adapt very little and sometimes not at all. In fact, under
some conditions, excitation of pain fibers becomes progressively greater, especially for slow-aching-nauseous
pain, as the pain stimulus continues. This increase in sensitivity of the pain receptors is called hyperalgesia
the pain is corellated to
the rate at which the damage is occurring and also the intensity of the pain is directly related to the damage occurring in the tissue
what is extracted from damaged tissues or seen an increase in when tissues are being damaged
you can extract brandykinin which is a substance that causes most amount of pain
also an increase in potassium ions or proteolytic enzymes that attack the nerve endings
what other 2 factors can be a cause of pain in muscles
muscle ischemia which is due to the accumulation of lactic acid due to anaerobic respiration and also could be due to release of bradykinin and proteolytic enzymes in the damaged tissues.
muscle spasm which directly induce mechanosensitive receptors and indirectly compress blood vessels causing muscle ischemia and increasing metabollic rate which furthur upsets the situation
fast pain and slow pain pathway to spinal cord
The fast-sharp pain signals are elicited by either mechanical or thermal pain stimuli. They are transmitted in the
peripheral nerves to the spinal cord by small type Aδ
fibers at velocities between 6 and 30 m/sec. Conversely,
the slow-chronic type of pain is elicited mostly by chemical types of pain stimuli but sometimes by persisting
mechanical or thermal stimuli. This slow-chronic pain is
transmitted to the spinal cord by type C fibers at velocities
between 0.5 and 2 m/sec.
Neospinothalamic Tract for Fast Pain.
The fast type
Aδ pain fibers transmit mainly mechanical and acute thermal pain. They terminate mainly in lamina I (lamina marginalis) of the dorsal horns, and there they excite second-order neurons of the neospinothalamic tract. These second-order neurons give rise to
long fibers that cross immediately to the opposite side of the cord through the anterior commissure and then turn upward, passing to the brain in the anterolateral columns.
Termination of the Neospinothalamic Tract in the
Brain Stem and Thalamus.
few fibers of the neospinothalamic tract terminate in the reticular areas of the
brain stem, but most pass all the way to the thalamus without interruption, terminating in the ventrobasal complex along with the dorsal column–medial lemniscal tract for tactile sensations A few fibers also terminate in the posterior nuclear group of the thalamus.
type of nerutransmitter released for fast pain fibers
glutamate
Paleospinothalamic Pathway for Transmitting SlowChronic Pain
In this pathway, the peripheral fibers terminate in the spinal cord almost entirely in laminae II and III of the
dorsal horns, which together are called the substantia
gelatinosa, as shown by the lateral most dorsal root type
C fiber. nerve signals then pass through addditional short fibers within the dorsal horn and then lastly through long fibers and are transmitted to the other side of the cord through anterior commisure and then upward to the brain through anterolateral pathway
neurotransmitter released from type C fibers
substance P which sends slow signals to cns and also glutamate which sends fast signals
thats why you have double pain sensation one by glutamate which is fast pain and other is the lagging signal send by slow pain send by type c through substance p
Projection of the Paleospinothalamic Pathway (Slow-Chronic Pain Signals) into the Brain Stem and Thalamus
The slow-chronic paleospinothalamic pathway terminates widely in the brain stem very less terminate in thalamus
1) the
reticular nuclei of the medulla, pons, and mesencephalon;
(2) the tectal area of the mesencephalon deep to the
superior and inferior colliculi; or (3) the periaqueductal
gray region surrounding the aqueduct of Sylvius. These
lower regions of the brain appear to be important for
feeling the suffering types of pain,
slow type of pain terminates in what areas and it has what effect on body
reticular area of the brain stem and the interlaminar nuclei of the thalamus cause overall arousal and spread excitability in the whole cns thats why you cant sleep when in chronic pain
anaglesia system
This variation results partly from a capability
of the brain itself to suppress input of pain signals to the
nervous system by activating a pain control system, called
an analgesia system
The analgesia system, consists
of three major components:
(1) The periaqueductal gray
and periventricular areas of the mesencephalon and
upper pons surround the aqueduct of Sylvius and portions of the third and fourth ventricles. Neurons from
these areas send signals to (2) the raphe magnus nucleus,
a thin midline nucleus located in the lower pons and upper medulla, and the nucleus reticularis paragigantocellularis, located laterally in the medulla. From these
nuclei, second-order signals are transmitted down the
dorsolateral columns in the spinal cord to (3) a pain inhibitory complex located in the dorsal horns of the spinal
cord. At this point, the analgesia signals can block the pain
before it is relayed to the brain.
enkephalin
is the substance released by nerve endings in mostly periventricular periaqueductal gray area which transmits signs to gray horns of spinal cord to produce enkephalin locally which blocks transmission of type c and fast pain fibers
referred pain
Often a person feels pain in a part of the body that is fairly
remote from the tissue causing the pain. This phenomenon is called referred pain
why referred pain takes place
In the figure, branches of visceral pain fibers are shown to
synapse in the spinal cord on the same second-order
neurons (1 and 2) that receive pain signals from the skin.
causes of true visceral pain are
ischemia chemical stimula muscle spasm of hollow viscera overdistention of hollow viscus insensitive viscera