Term
| three major types of sensation |
|
Definition
| exterioceptive, proprioceptive (kinesthesia), interoreceptive |
|
|
Term
|
Definition
| external, acting on the body surface |
|
|
Term
|
Definition
| (kinesthesia) internal, deals with balance, position, and motion of the body |
|
|
Term
|
Definition
| also internal, but it deals with subconscious stimuli (e.g., blood pressure) |
|
|
Term
| four major sensory modalities |
|
Definition
| tactile, thermal, proprioceptive, nociceptive. these modalities have submodalities based on kind of stimulus or strength of the sensation |
|
|
Term
|
Definition
mechanical stimulation of the skin—
touch, pressure, vibration |
|
|
Term
|
Definition
| temperature changes of skin—cold, warm |
|
|
Term
|
Definition
| mechanical displacement of muscles, tendons, joints—static, dynamic |
|
|
Term
|
Definition
| pain; destructive insults to tissue—mechanical, thermal, chemical |
|
|
Term
|
Definition
What you have here is a cross-section of the spinal cord, and what you have in the center that looks like a letter H is the gray matter. And around it, you have white matter. The big chunks of white matter we call funiculi. Inside of the funiculi, you have a faciculi. In the middle here, for instance, you have the faciculus gracilis, and on the side you have the faciculus cuneatus.
The dorsal root ganglia are over here. This is the dorsal part. That's why we have dorsal columns. Dorsal root ganglia contain the somata of the sensory neurons. The sensory neuron has an action that it splits into two main components. A proximal component enters the gray matter and brings information about pain or sensation, pleasure, and so on. The distal part of the action is what goes to the different parts of the skin, different parts of the body, to the muscles and so on. This ending is going to have a specialized type of receptor according to the sensation that it's going to feel.
In the ventral part here you have motor neurons, and they will be able to give you a motor command. [INAUDIBLE], remember, is what is motor. [INAUDIBLE] is central information coming in. So the motor will go out via the ventral roots and will form this pathway. |
|
|
Term
|
Definition
|
|
Term
| Four Major Types of Encapsulated Mechanoreceptors Specialized to Receive Tactile Information |
|
Definition
| Meissner corpuscle, Pacinian corpuscle, Ruffini’s corpuscle, Merkel’s disk, + Free endings |
|
|
Term
|
Definition
| defined distributions in different types of skin (hairy vs. glabrous) and at different depths in the skin (superficial vs. deep). |
|
|
Term
|
Definition
| sensation—touch/pressure—dynamic |
|
|
Term
|
Definition
sensation—deep pressure/
vibration—dynamic |
|
|
Term
|
Definition
| sensation—stretching of the skin |
|
|
Term
|
Definition
| sensation—touch/pressure—static |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
If:
Receptor is superficial
Than: |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| a discrete surface area of skin to which a receptor is responsive |
|
|
Term
|
Definition
| larger stimuli activate a greater number of receptors |
|
|
Term
|
Definition
| longer stimuli cause receptor to fire multiple action potentials |
|
|
Term
|
Definition
| receptors specialize in responding to a particular stimulus |
|
|
Term
| receptor activation diagram |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| respond to high mechanical and chemical stimulation, but have very high threshold for heat |
|
|
Term
|
Definition
| have lower threshold for heat and high threshold for mechanical stimulation |
|
|
Term
|
Definition
| polymodal with some, especially sensitive to chemical irritants, acids, cold, etc. |
|
|
Term
|
Definition
|
|
Term
|
Definition
Again, the same idea. Nothing new. The same thing that I've been telling you about. Just another diagram to show you specificity. In here you have the cell body for the essential information in the dorsal root ganglia. This one is in the dorsal root ganglia as well. And then the specialized receptors.
In this case, free endings; in this case some type of Merkel disc, let's say, mechanical receptor; and in here, what looks to me like a hair cell. So it will be for a different type of sensory modality, like sound. But the concepts are exactly the same. Concept of receptive field, stimulus, and the receptors being specialized.
Conduction velocity when taking place in myelinated fibers is very fast for many reasons that we will review when we do neurophysiology. But for right now, suffice it to tell you that this gives rise to what we call saltatory conduction. At the nodes of Ranvier, which is where there is no myelin, is the places where very quick ionic exchange can take place between the in and the outside of the cell.
And so we call it saltatory because the action potential is virtually jumping from one node of Ranvier to the next node of Ranvier. The importance of this for animals such as ourselves is that we are able to react very fast to certain stimulus but no need to react very fast to all kinds of stimuli.
In a giraffe, for instance, it's very important because you can imagine the distance from the brain of the giraffe all the way to the tail as several meters long. And so if you want effective conduction of sensory information and proper motor efferent information to go out for a reaction, the conduction has to be really, really fast. |
|
|
Term
| Dorsal Column-Medial Lemniscal Pathway |
|
Definition
• Touch, pressure, proprioception
• First order cell in DRG; large myelinated fibers
• Second order cell in the gracilis and cuneatus-nuclei; axons of second cell immediately decussate as internal arcuate fibers
• Third order cell is in the VPL nucleus of the thalamus
• *Visceral pain
[image] |
|
|
Term
| Anterolateral or Spinothalamic Pathway |
|
Definition
• Pain and temperature
• First order cell in DRG, axons are small, myelinated and unmyelinated fibers
• Second order cell is in dorsal horn layers I, II, and V
• Third order is in the VPL nucleus of the thalamus
• Crossed at spinal segmental levels
[image] |
|
|
Term
|
Definition
| dermatome- Area of the skin supplied by a single spinal nerve |
|
|
Term
|
Definition
Here you have an examples or a couple of examples of a complete cut of the spinal cord versus a hemicut. Now, let me just concentrate on one of the examples, on this one. When you have a cut of half of the area of the spinal cord, you have cut the sensory information, which is ascending, as well as the motor information, which is descending. And that will give rise to this pattern, the area which is being affected.
Now, understand why would you have lost pain sensation on the contralateral side? Well, this is where you need to remember what is being crossed and what is not being crossed. If you remember for the pain information, pain and temperature, the information came in from this leg. It entered back in here, contacted layers in the gray matter, and the second cell sent its axon to the other side. So the information from this side of the body is traveling on the contralateral side of the spinal cord, and this is the reason why you lose pain sensation on this side.
While the information that is motor information, descending, and then other sensory information, mechanical information, which is ascending, it stays ipsilateral, on the same side, because it doesn't cross until the arcuate fibers cross. It's crossing much higher. This little wedge here, which is sometimes mysterious to students, is on the same side because as the damage was created, the information from this side that was just entering was also caught. And therefore, you get a little bit of a lesion on the same side. |
|
|
Term
|
Definition
| (physiologicalpain):bystimulationof peripheral nerve fibers; can be subdivided into visceral, deep somatic, superficial, etc. Or, according to sensation: thermal, mechanical, chemical |
|
|
Term
|
Definition
| (intractablepain):byperipheraland central lesions, burning, tingling, electrical, stabbing, etc.—an important subtype is phantom pain |
|
|
Term
|
Definition
painthatiscaused,increased,
or prolonged by emotional or mental factors; some authorities challenge this category or attribute it to our lack of knowledge of the processes related
to pain |
|
|
Term
|
Definition
| Aδ~5-30m/s—respond to intense mechanical or mechano-thermal stimuli |
|
|
Term
|
Definition
| C~<2m/s—respond to mild thermal, mechanical, and chemical stimuli |
|
|
Term
| Transduction of Nociceptive Signals |
|
Definition
| A complex task given so many modalities can elicit pain—collection of the signal is done by free endings |
|
|
Term
|
Definition
transient receptor potential
When open Na+ and Ca++ pass
• VR-1 (or TRPV1) vanilloid receptor—sensitive to heat
(>45 °C) and capsaicin—Ad-C
• VRL-1 (or TRPV2)—not sensitive to capsaicin
but sensitive to heat (>52 °C)—C only |
|
|
Term
|
Definition
acid sensing ion channels
• ASIC3: detects the change in pH associated with cardiac ischemia |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Modulation of Pain depends on |
|
Definition
| many different aspects including: type, intensity, localization, etc. |
|
|
Term
|
Definition
| after tissue damage, there is increased sensitivity to stimulus (e.g., increased sensitivity to heat after sunburn) |
|
|
Term
|
Definition
| results from the interaction of nociceptors with inflammatory substances (extracellular protons, arachidonic acid, bradykinin, histamine, serotonin, prostaglandins, nucleotides, NGFs, etc.)—all of which potentiate nociceptors’ response |
|
|
Term
|
Definition
| activity dependent increase in the excitability of neurons in the dorsal horn; if they were recently active, their threshold is now lower; they respond to “smaller” stimulus |
|
|
Term
|
Definition
Discriminative versus affective pain. In the diagram in here, you have, remember, information coming in. The cell is always in the dorsal ganglia. These are your specialized endings. And then this information comes in. And remember, it contacts the second cell in the gray matter. And these second cell, the axon of the second cell, crosses to the other side, locates its cell anterolaterally, hence the anterolateral system, and is going up to inform the ventral posterior lateral nucleus of the thalamus.
On the way up, it may also inform the periaqueductal gray and areas in the rostro-ventral-medulla. Information going down from the cortex via the thalamus and also directed to the periaqueductal gray via the amygdala, hypothalamus, and so on, all of these descending pathways are ways in which we can modulate pain. I will show you in a second some of the mechanisms. |
|
|
Term
|
Definition
-nociceptive activation
• Tissue damage
• The inflammation “soups” starts forming
• Physical distortion of pain fibers elicits a pain response
• Sensitization:
increase sensitivity of nociceptors |
|
|
Term
|
Definition
| Referred pain (e.g., angina) |
|
|
Term
|
Definition
| Induction of pain by innocuous stimulus |
|
|
Term
|
Definition
| Transcutaneous electrical nerve stimulation |
|
|
Term
|
Definition
For the gating of pain, remember I said a second ago all of those pathways which are descending, let me give examples in here. That applies to here as well. Take, for instance, the C fiber. Remember this, the soma of the cell here. It's in the dorsal root ganglion. And the cell is collecting information from the periphery. It comes, and it's going to inform the cell that is located in the gray matter of the spinal cord, which is the one which is going to project to the thalamus and from the thalamus the projection to the somatosensory cortex.
So in the circuit, if you have only activation of this cell, this cell will strongly activate the one in the gray matter of the spinal cord. And that strong activation will be a strong sensation of pain, if you will, that we call the projection neurons. But this projection neuron is also receiving inputs from interneurons, as well as other types of fibers, like A beta fibers.
If you activate the A beta fiber in the second case, you might also be activating an interneuron. The interplay between these excitatory and inhibitory synapses might result in the reduction of the activity of the cell, which is in charge of sending information about pain. And they overall sensation is a reduction in the sensation of pain.
Part of this, one easy way to understand what is happening here in terms of this mechanism is that when we feel a strong pain, that strong pain may be mediated only by C fibers. And one very innate reaction is immediately to go rub the area. You say, oh, you know. You feel pain, and then you rub the area. What you're actually doing when you do that is you are activating A beta fibers, and they, therefore, activate strongly these interneurons. And therefore, your sensation of pain might be relief. May not disappear completely, but it feels much better. |
|
|
Term
|
Definition
• The nervous system and periphery contain at least three opiate receptors and peptides (enkephalins, endorphins, and dynorphins).
• Activation of these receptors with morphine (which mimics the intrinsic peptides) decreases pain. Blocking these receptors with naloxone blocks both morphine and transcutaneous electrical nerve stimulation (TENS) induced analgesia.
• Systemic administration is undesirable: secondary effects— broad lethargy, constipation, respiratory depression, etc.
• Local administration (an epidural) circumvents the secondary effects and requires lower doses. |
|
|
Term
|
Definition
| increase hot/pain through the release of substance P; can be used for pain control by giving in low doses that deplete substance P and therefore decrease sensitivity to nociceptive stimuli |
|
|
Term
|
Definition
| (non-steroid anti-inflammatory drug) e.g., aspirin: blocks prostaglandins which are released when tissue is damaged |
|
|
Term
|
Definition
| decreases inflammatory reactions, which then limits release of substance P, histamines, etc. |
|
|
Term
| COX and way pain can be modulated |
|
Definition
• In brief: persistent activation of small C fibers yields release of several excitatory transmitters—SP, glutamate (GLU). This results in a depolarization and increased intracellular calcium ([Ca]2+), which in turn results in the activation of a number of intracellular enzymes, including phospholipase A2 (PLA2).
• PLA2 results in an increase in cytosolic arachidonic acid (AA), which then enters the COX cascade, leading to the formation of a variety of PGs that gain access to the extracellular space. |
|
|
Term
|
Definition
| Celebrex: NSAID, Cox-2 inhibitor Vioxx: NSAID, Cox-2 inhibitor |
|
|
