Somatic Sensations

PHYSIOLOGY: Neurophysiology of Somatic Sensations

Discussion Outline: i. Overview of somatic sensations ii. Cutaneous Sensory Physiology

a. Skin Mechanoreceptors b. Thermoreceptors

iii. Proprioceptors –also are somatosensory (will be discussed during the Reflex Lecture)

a. Muscle spindle b. Golgi tendon organs

*these two are the most studied proprioceptors, though they are also somatosensory receptors *There are also other proprioceptors in skin and joint/muscle, but we will not be dealing with them much anymore

iv. Cutaneous & Visceral Pain Receptors (Nociceptors & Intro to Pain Physiology) - Pain receptors and various ascending fibers which may take the fast pain / slow pain, and recent advances in introductory pain physiology

Two Well Studied Endogenous Pain Control Systems:

1. Gate control system by Dr. Walden Melzack discovered in 1960’s

- know the lateral inhibition mechanism behind this GCC/spinal gating - you may read more about this in your book

2. Descending pain inhibition system (late 1970-

1980’s) **these two are briefly described in handout diagram

Objectives: Know the features & functions of receptors Know how adequate stimuli is converted to changes

membrane conductance (receptor potential) Know the size of receptive field (small/large;

contribution in characterizing sensory stimuli Know how increasing stimulus intensity is expressed

in terms of increasing spike discharges Know the Central & Peripheral Mechanisms of pain

and analgesia distinguish fast pain, slow pain, referred pain,

projected pain gating theory, opiod and non-opiod mechanism of

endogenous pain control short definitions: hyperalgesia, allodynia, muscle

radiating spasm, congenital insensitivity to pain,

phantom limb/phantom pain and peripheral and central mechanisms theories to explain this phenomenon

itch vs. tickle vs. pain

Review:

Dorsal Root Ganglion (DRG)

1st order neuron of the somatosensory system, whether it is for crude touch, pressure, pain, temperature, proprioception, fine touch, 2 point determination)

If from face region, what is the 1st order sensory neuron?

2 general classes of DRG neurons

(innervate various somatosensory receptors):

1. Large DRG neurons Large soma, large axon (from single

branching from soma, divides into 2 processes)

o Peripheral – innervates the sensory receptors

o Central – enter the dorsal horn (posterior gray horn) of spinal cord

they are myelinated (not all myelinated are large, refer to Type A delta fibers described below)

Ex. Neurons that give rise to Type A beta, Type A delta, and Type A gamma fibers

Sensory modalities involved: Proprioception, Fine Touch, Pacinian Corpuscles, etc.

2. Small DRG Neurons Neurons that give rise to:

o C Fibers o Type A delta fibers (myelinated)

= if compared with other Type A

afferent fibers, A delta are

smaller

Sensory Modalities involved: Most from Anterolateral system (but not all, only majority) – some experimental literatures state that fine touch afferents send ‘some’ collateral to ALS; also, pain too sends ‘some’ collaterals to the medial lemniscal pathway.

* keyword: “some”

SUBJECT: PHYSIOLOGY

TOPIC: Neurophysiology of Somatic Sensations

LECTURER: DR. SIMBULAN

DATE: FEBRUARY 2011


Fast Pain = generally part of small DRG, with Type A

delta fibers, myelinated but smaller in diameter (smaller,

as compared with large DRG axons)

Slow pain = C fibers innervated

Crude Touch = difficulty to localize; innervated by C

fibers

Fine Touch = uses vibratory sensors, those specialized

for precise stimulus localization such as Merkel’s disks,

Meissners, Ruffini’s, Pacinian, Hair Cells

*however based on actual experimental observation (ex:

histological), fine touch modalities are discovered to

have ‘some’ Type A delta fibers (but still, mostly have

larger diameters)

*thermal receptors = predominantly a delta and c fibers

Dr. Simbulan: this can be confusing in terms of

innervation. Generally, small myelinated and

unmyelinated C fibers predominate nociceptors;

proprioception generally A beta and A alpha

Still Confused? Just remember this:

Proprioceptors:

o large diameter, myelinated

o Aβ, Aα

Crude touch, pain, temperature:

o small, unmyelinated

o Group 4 or Type C fibers

Fine touch, vibration, pressure:

o large, myelinated

o Group 2, or the rest of Type A

A few Thermoreceptors:

o Aδ, C

*somatic motor neurons (ventral horn):

o Aα

Lecture Proper:

I. Overview

Ascending Tracts

AAnntteerroollaatteerraall SSyysstteemm, composed of :

1. Lateral Spinothalamic Tract – pain and temperature

2. Anterior (Ventral) Spinothalamic Tract – touch and pressure

*recall their sites of decussation, thalamic nuclei destination, cerebral cortex destination, also, look at images of the sensory homunculus

Sensory Homunculus – regional specification can

change (amputees developing the remaining limb’s

capabilities); Size of cortical receptive fields =

proportional to the density of receptors in the

representative region. (Fingers: have high density of ss

receptors)

DDoorrssaall CCoolluummnn // MMeeddiiaall LLeemmnniissccaall SSyysstteemm

–fine touch, proprioception

Effects of Damage to Somatosensory cortex

> Severely damaged Area 312 = contralateral loss of

sensation; however, based on experiments, actually:

tactile sensations – all fine tactile is generally abolished (esp. at contralateral side); crude touch is recovered after a period of time

Pain, temperature – left generally intact

Hence, we can conclude that:

• in fine touch: cortex is very important

• in pain, temp: awareness center is below

cortex (can even be at thalamus), though there

are no definite studies as to where it is exactly.

It is just somewhere below the cortex. The role

of cortex perhaps is mainly on the localization

of the pain or temperature stimulus.

> Lesions to Area 5 AND 7

= Sensory Association Cortex Lesion)

= astereognosis; inability to identify an object if

touched when blindfolded

Diameter

(μm)

Type Modality

12-20 Aα Proprioception

5-12 Aβ Fine touch, Pressure

3-6 Aγ Muscle Spindles

2-5 Aδ Pain, Cold, crude touch

<3 B Preganglionic Autonomic

0.4-1.2 C Pain, Temperature, etc.

Guyton further divided the spinothalamic tract into:

a. Paleospinothalamic – connecting mostly to brainstem, then to intralaminar thalamic nuclei before going to Cerebral Cortex; generally related to affective/emotional aspects of pain

b. Neospinothalamic – associated to fast pain


In short:

“Increase stimulus intensity, increase amplitude of

receptor potential, increase discharge frequency of

sensory nerve.”

II. Sensory Receptors of Skin

Cutaneous Receptors

– can be found in both hairy/hairless skin

– studied via microneurography (thus, it was

studied in isolated nerves from animals/humans,

without actually exposing the nerves. They just

stimulate nerve ending above skin with some pressure

stimuli (or other stimuli). Microelectrodes are inserted

to actually impinge on the isolated nerve itself. Action

potentialns are recorded. It is with this technique that

we were able to identify the thresholds for various

mechanoreceptors, as well as their receptive fields, and

whether the receptors are slowly or rapidly adapting.

Receptor potentials as stimulus intensity is increased

(ex: from 0.1 to 0.6 Newton) = increasing amplitude.

When the action potentials were recorded from the

axon itself where checked, they have increasing

discharge frequency

Scientists were also able to identify via

microneurography whether the receptors have small or

large receptive fields.

Which size of receptive field gives more exact

information about the location of the stimulus? Small!

FA = Fast Adapting

SA = Slowly Adapting

I = small receptive field

II = large receptive field

>>>>>Slowly vs. Fast Adapting Receptors

- see last page

(want tabular form? See final page)

1. Pacinian Corpuscle (FA-II) Rapidly adapting Studied well via microneurographic

techniques Onion-like lamellar capsule (about 1mm in

diameter)

✪ Speed of Adaptation: very rapid

✪ Receptive Field: Large (hence, not accurate in localizing stimulus source)

✪ Encoded Sensation: touch, vibration (acceleration detector)

✪ Afferents, location: generally Aβ (some Aα); skin Aβ = large, myelinated, group 2

Naming Convention for Mechanoreceptors

Tactile Receptor Adaptation Receptive Field Code

1. Pacinian Corpuscle

2. Meissner’s Corpuscle

3. Merkel’s Disk

4. Hair Follicle Endings

5. Ruffini’s Endings

Fast

Fast

Slow

Fast

Slow

large

small

small

small

large

FA-II

FA-I

SA-I

FA-I

SA-II

Somatic Senses Pathways

(ALS or Medial Lemniscus)

Ventrobasal Nuclei

(VPM – if from head, neck)

(VPL – if from rest of the body)

Area 312

(Anterior Parietal Cortex)

Sensory Association Cortex

(Posterior Parietal Cortex)

- helps identify objects only by touching via higher

order processing (stereognosis)

- makes holistic image of the object

Stimulus intensity

maintained constant.

There is only discharge only

when there is increase in

intensity. After that, there

is no more response

Increase in stimulus intensity (skin

deformation is the stimulus)

Discharge


Pacinian Corpuscles only become really active (with

higher discharge frequency) when stimulus frequency is

increased within this frequency range: 200-300 Hz.

(Create stimulus within this range, and this is the only

time the sensory nerve will have higher discharge

frequency)

2. Meissner’s Corpuscle (FA-I) Rapidly adapting Studied well via microneurographic

techniques

✪ Speed of Adaptation: very rapid

✪ Receptive Field: small (hence, accurate in localizing stimulus source)

✪ Encoded Sensation: speed of stimulus application, low freq vibration sensors (like pacinian, though meissner’s have lower sensibility: 30-40Hz)

✪ Afferents, location: Aβ (group2); fingertips, lips, skin, even at sexual erectile tissues, glans penis, etc.

3. Ruffini Endings (SA-II)

Slowly adapting Studied well via microneurographic

techniques

✪ Speed of Adaptation: slow

✪ Receptive Field: large (hence, not accurate in localizing stimulus source)

✪ Encoded Sensation: magnitude and duration of stimulus (touch pressure); because it is slowly adapting, it can give accurate description magnitude and duration… unlike those that are rapidly adapting

✪ Afferents, location: Aβ (group2), with some Aα according to some literature ; covered by liquid filled collagen

4. Merkel’s Disk (SA-I)

Slowly adapting Studied well via microneurographic

techniques An independent cell; a specialized epithelial

cell that releases a chemical messenger (which acts like a neurotransmitter), activating sensory nerve endings that synapse with them.

✪ Speed of Adaptation: slow


✪ Encoded Sensation: localization of stimulus (touch pressure)

✪ Afferents, location: Aβ (group2); high density in fingertips, lips, many skin areas

5. Hair Follicle Endings

Rapidly adapting Studied well via microneurographic

techniques Practical example: when you wear your

clothes, at first you feel them on you, but as time passes, you won’t even feel them (you won’t be constantly conscious of it) Of course, when you move, you stimulate these hair endings a bit to produce some spike discharges so you can feel it as you move

✪ Speed of Adaptation: rapid


✪ Encoded Sensation: light touch flutter; low vibration sensors (30-40 Hz, like Meissner’s)

✪ Afferents, location: Aβ (group2)

6. Tactile Discs 7. Other Cutaneous Receptors

Two point threshold

Two point discrimination threshold

Using a compass, or any tool with 2 points

Smallest tip separation for which the subject can tell that there are two stimulus source points without looking at them

>> High two point threshold = low sensitivity

(ex: scapular region, back of neck)

>> Low two point threshold = high sensitivity

(ex: fingertips)


Spatial resolution

Can be extracted using the values of the two point threshold

the inverse/reciprocal of the two point threshold

if two point threshold is 70; spatial threshold is 1/70

the higher the two point threshold; the lower the spatial resolution

more sensitive areas will have higher spatial resolution

*The ones with highest spatial resolution (low 2 pt

threshold) = fingertip; also has high density of

mechanoreceptors with small receptive field and low

density of mechanoreceptors with large receptive field.

Transduction Mechanism of Mechanoreceptors

Simply stretching the extracellular matrix of the skin

would stretch the cytoskeletal structures which open up

the mechanically gated ion channels allowing cation

influx, causing initial depolarization (receptor potentials

form)

Temperature = generally group a delta and c fibers;

Thermal Spots

Hairy skin has larger thermal spots than hairless skin

A Monkey Experiment using Braille (to evaluate

various mechanoreceptors)

Pattern recorded closely resembles Braille: SA-I (Merkel’s disc)

More or less resembles the Braille: FA-I (Meissner’s Corpuscle)

The CNS cannot describe it, no idea at all: SA-II (Ruffini’s Endings), FA-II (Pacinian Corpuscles)

*the characteristic common with Merkel’s and

Meissner’s = both have small receptive field, that’s why

they are good in localizing stimulus (hence, creating a

closer image of it)

**You may try to look for the image related to the

monkey-braille experiment, if you are having a hard

time visualizing it.

Recent findings on temperature sensation

transduction mechanisms

There are receptors for ATP (ATP is released by surrounding tissues, exciting the free nerve endings that are sensitive to warm stimulus) o P2X receptors = purinergic receptors

which are activated ATP released from surrounding tisssues; mediate moderate heat sensations

There are also receptors found in cold receptor free nerve endings o CMR (cold and methol sensitive

receptor) ‘

I cannot find the image that Dr.

Simbulan flashed during his

lecture. Sorry


The opposite occurs when the

temperature is increased

*if you go higher (temp), the activity of the cold

receptors will dive down (same happens for warm

receptors)

*If temperature is increased beyond 45 degrees, before

sensory nerves become denatured, there will be an

increase in discharge frequency… results to paradoxical

cold sensation. (Principle: cold receptors are briefly

active before they are inactivated; the pain sensation is

from the pain receptors) Prolong the exposure to high

temperature, and the cold receptors will be destroyed.

Pain receptors will be activated (slow pain if there will

be swelling and blisters forming)

*example: accidentally touching a hot iron, you will feel

brief coldness, then pain (try it!)

>>Thermal Stimulus (34 degrees30 degrees34

degrees)

>>Cold Fiber = Cold sensitive free nerve endings

>>Warm Fiber = Heat sensitive free nerve endings

*However, these two cannot give any responses to

absolute temperature, only to transient changes in

temperature

There are specific types of nociceptors for every

damaging stimulus:

Cold nociceptors Hot nociceptors Mechanonociceptors Chemonociceptors

Are “receptors” used in different ways? Cold receptor? Pain Receptor?

The word “Receptor” can describe:

1. a part of a sensory nerve ending, or specialized epithelial cell that causes changes to membrane conductance in response to an adequate stimulus

2. a transmembrane protein in the cell membrane that may have different function (can be an enzyme, an ion channel, binds to chemical messenger)

*don’t be confused when the word “receptor” is used in

a statement to describe different things

* Hence, the CNS uses both warm and cold fibers to

respond to cold or warm stimulus (if stimulus is cold,

heat sensitive free nerve endings also acts, v/v.)

Trivia:

According to new version of Ganong: ipsilateral insular

cortex is a possible new sensory cortex for thermal

sensation


Questions:

1. Difference of pain receptors from others: signals potential threat/damage

2. The importance of pain receptors? They lead to the eventual removal of damaging stimuli

3. When is pain harmful? If it is chronic in nature that it already disturbs personal and social life, or even causes loss of sensation leading to self mutilation

Chronic Pain related to illnesses

Diabetes = leads to peripheral neuropathies; leads to hyperactivity and degeneration of sensory nerves, causing chronic pain

Whiplash syndrome = from injury arising from neck, complains for a long period of time

Spinal Nerve Problems = if vertebrae is degenerating; may cause chronic pain

Chronic Headache experiences = like migraine Onset of changes of physiologic states =

dysmenorrhea (possibly with headache)

III. Cutaneous and Visceral Nociceptors

Cutaneous Nociceptors (Skin receptors) o A delta (fast pain) group III o C fibers (slow pain) group IV

*Specific for damaging mechanical,

chemical, or thermal stimuli

Question: If you are to isolate touch receptors: merkel’s,

meissner’s, ruffini’s, pacinian (assuming you can isolate

them) –then increase stimulation intensity. What will

be the sensation felt (touch only, or both touch and

pain)?

Answer: Only touch sensation will be generated; no

pain sensation will be felt. (See Mullerian Doctrine of

Specific Nerve Energies). Overstimulation will only lead

to pain if the touch receptors are not isolated and are

adjacent to pain receptors. Thus, the overstimulation

hypothesis is countered.

Mullerian Doctrine of Specific nerve energies.

- The sensation which is generated by stimulating a sensory pathway or receptor is due to the fact that there is a specialized receptor for that particular sensation. And of course, the sensation generated is basically due to the central connections of this sensory pathway

- for one specific type of sensation there is one type of sensory receptor with its own sensory ascending pathway to a part of the brain

Overstimulation hypothesis

- when you stimulate a receptor lightly, you only cause touch and when you stimulate it at higher intensity, temperature at higher still, possibly tickle and more, pain.

Labeled Line Mechanism

- No matter how specialized sensory receptor is, if there are no central connections no sensory experience. That kind of central connection component is called labeled line mechanism—it is a little bit of an extension of this older doctrine.

Visceral Nociceptors o Primarily innervated by C fibers (slow) o Periosteum, joint Surfaces, dura mater,

tentorium, cranial vault o Most are associated with Referred pain

Referred Pain - there are corresponding surfaces of the body wherein pain is referred to by various injuries or some inflammatory conditions of internal organs. Muscle nociceptors

o Primarily A delta (III) and C type (IV) o Ischemic pain (blood unable to cope with

contraction o Basically, much of these receptors are

activated as a result of occlusion of blood supply in the muscle tissue contributing to relief of other sensitizing chemicals like potassium in a so-called Louis factor so this can either be experienced in skeletal or cardiac muscles which can activate these muscle pain receptors.

o the adequate stimuli in transduction mechanisms involved for pain pathways, generally speaking, damaged cells can induce the release of various neurochemicals or other tissue chemicals of non-neural nature which would sensitize or activate numerous nerve endings. So in addition to histamine, you have potassium, and hydrogen ions.

Activators (Tissue Chemicals) that activate nociceptors

o In addition to histamine or bradykinin, which are released from damaged tissues and can activate these damaged nociceptors, there are other tissue chemicals of both neural and nonneural nature which can activate various pain nerve ending.

o Synthesized by polypeptides

Cholecystokinin Opiods Neurokinin


o Non neural Histamine Bradykinin Acetylcholine ATP Etc.

o Neural What are they?

= And they bind to their corresponding receptors on pain nerve endings so it seems the pain system is really a primitive system which can respond to various chemicals. So even if you fail to synthesize one kind of chemical due to gene mutation, still, there are other chemicals released from damaged tissue which can activate the pain system. So they are not as highly specialized as the other pain systems. Other neurobiological findings will be specialized receptors which can activate some endings. For example, the sili.

The component of some chili sauce is a capsaicin, a molecule which activates your vanilloid, your vr1 receptor. The receptor itself is activated by temperature beyond 43 degrees centigrade. Probably some kind of hot nociceptors.

In addition, there are also other kinds of membrane receptors called vrl1 receptor which is non-capsaicin sensitive and is also activated by changes of thermal stimulus beyond 50 degrees centigrade.

So these vrl1 is supposed to be found in c fibers. However, data does not actually discuss whether they come from a delta or c fibers.

Activation of Pain System

- as long as there is damage to the tissue - a nerve ending can stimulate itself

(autostimulation of pain)by releasing chemicals such as substance P. Interaction of Bradykinin with other neurochemicals and tissue chemicals in sensitizing joint tissue during inflammation (such as arthritis) 1. Damaged tissue releases bradykinin. 2. Bradykinin will stimulate a corresponding receptor

(like B2, a metabotropic receptor) 3. Other sensitizing chemicals will be released 4. How bradykinin interacts with them determines the

excitation of the sensory endings (complex cocktail of chemicals + prostaglandins)

Question: if prostaglandins are the predominant chemicals, what kind of analgesics would be most effective? Answer: Your aspirin-like drugs. They are prostaglandin synthesis inhibitors. They actually inhibit the synthesis of prostaglandin. 5. histamine is released from mast cells, activating

histamine receptors 6. Serotonin is also released. It is a known active

ingredient in inflammatory tissues, in inflamed joints.

7. The role of sympathetic system in pain, especially if there’s nerve injury, is induced.

Uninjured Nerve What is known is that many pain nerves as well as ordinary somatosensory pain nerves are not highly excitable at the basal state, if they are not injured. Injured Nerve But when they are injured, what has been found out is that many of these pain nerves as well as ordinary pain nerve endings upregulated their membrane molecular receptors for norepinephrine (either in the soma or in the peripheral nerve endings).

The alpha adrenoreceptor is a receptor subtype for norepinephrine. When they upregulate this receptor, they become sensitive to circulating or basal concentrations of norepinephrine in the blood, in the plasma. And then they would possibly reach these free nerve endings. So upregulation of these norepinephrine receptors can make them excitable and that is why many of these nerve injuries are very difficult to suppress the pain so what some pain doctors would do is to use blocking agents for some alpha norepinephrine receptor. Role of norepinephrine receptors in nerve endings of pain system

Again, another important polypeptide is substance P which is not only released in the soma of dorsal horn, but they’ve been found to be released in free nerve endings in inflamed tissue and they can also cause sensitization of pain afferents. Then hydrogen ions when the tissues become more acidic as a result of damaged tissue so there are protons here and then of course the release of free radicals like H2O2 from damaged tissue can also cause activation of nerve endings.

H2O2 – increases pain sensitivity H+ – acidity also increases pain sensitivity Bradykinin cascade – metabotropic; uses G protein and Phospholipase C

Remember: o VR1 = capsaicin sensitive o VRL1 = non capsaicin sensitive


Fast Pain vs. Slow Pain

Neospinothalamic = associated with fast pain Paleospinothalamic = associated with slow pain Here possibly acute injuries let’s say bullet wound. Initially, sharp pain. Also like thumbtack. Stimulating c fiber for short periods of time can stimulate release of glutamate and aspartate. For acute responses to painful stimuli, glutamate ad aspartate will be released but in this experiment c fibers also induce this release to activate second order neuron in dorsal horn. However, for chronic responses, for prolonged stimulation of c fibers, other polypeptides like substance P, cholecystokinin, g-related peptide, neurokinin is co-released with glutamate and aspartate. This is more complex than Guyton saying that: A delta will be for glutamate and c fibers will be for substance P. ALS which mediate your pain signals. Referred Pain o One well accepted theory now is the convergence

of afference from somatic structure and visceral nociceptor which converges in the spinal cord and since there is no cortical representation of your viscera, most of the excitation of your visceral receptors is reflected on various body surfaces at the same dermatome as your visceral receptors.

o For example, in cardiac pain, you would find it in the inner aspect of left arm.

o When you have dysmenorrhea (assuming that you are a female), do you experience referred pain?

Projected Pain o Phenomenon of projected pain which arises from

the so-called law of projection. o In this law, when you excite a sensory pathway,

sensation generated will always be projected to the site of the receptors for that particular ascending pathway

o Eg. Ulnar nerve excitation: sensation projected to fingertips.

o Phenomenon of projected pain can be used to understand phantom pain.

Phantom Pain o In phantom pain, (having phantom limb) pain is

arising from the body part which is absent/amputated.

o Earlier hypothesis about phantom pain- even in amputating it, severed nerve will regenerate. There will be a kind of neuronal regeneration which will contribute to hyperactivity of regenerated axonal stump.

o The cortex will always project it to area of body even if it is missing.

o What clinicians try to do is to inject with local anaesthetics, sometimes they succed, but for some, they don’t. Thus, phantom pain comes back.

o Dr. Ramachandran from india, a neurologist, found out that many of his patients would report phantom pain sensations on their upper arm. Digits can be reflected in upper arm as well as in face region. Follow-up studies in animals verify same observations e.g. in monkeys.

Phanotom limb

o not necessarily pain, can merely be an awareness that there still remains a certain part of our body, even if it was already removed.

o animal studies: it can be due to cortical neurons from the regions receiving activated synaptic connections from adjacent regions of the body.

o Neuron 2 (the one once innervated by the amputated limb) upregulates receptors, causing denervation hypersensitivity

o Example, your forearm hand region receiving sensory inputs from limb. Putol na yung sensory signals, what could happen is that there are axonal projections from adjacent regions e.g. upper arm, face. Probably, there may still be long term memories of amputated arm in cortical neuron so that when upper arm or face are activated, they activate also the cortical neurons which were receiving signals originally form the amputated region. This is the central mechanism of phantom pain.

Cortical plasticity Some functions of a cortical region will connect with other cortical regions. If there is a sensory deafferentation or cutting off of sensory signals, there will be upregulation of synaptic receptors on the postsynaptic neuron. If there are upregulation of these receptors, they become sensitive to circulating neurotransmitters which was described originally in Phenomenon of denervation hypersensitivity.

FAST (First) PAIN “initial”

SLOW (Second) PAIN “delayed”

Aδ fibers C fibers

Discrete Burning sensation

Sharp dull

Well localized Poorly localized


Withdrawal reflex o generally sympathetic autonomic response o There are some individuals who may report

opposite response. o Generally, however, associated with

sympathetic response along with fight or flight response.

o Slow pain, generally activated by c fiber stimulation produce autonomic response associated behavioral experiences like nausea and thermoregulatory responses like profuse sweating and deduction in muscle tone.

Rigidity

o We experience when visceral nociceptors are activated e.g. appendicitis, diarrhea, dysentery, severe stomach pain—doctors touch muscles, rigid upon touch due to protective reflex.

o When visceral nociceptors are activated, polysynaptic reflex can excite alpha motor neurons in ventral horn which will activate overlying muscles. This is a viscerosomatic guarding reflex.

Chronic vs Acute pain

Chronic Pain Acute Pain

C fibers

A delta fibers

How chronic pain works and how to manage it?

o it has been assumed that it will be passing through ALS system

o thus, treatment may be via spinal cord transsections focusing on anterolateral quadrant.

o Mostly for patients with terminal cancer to manage pain. Transecting ascending pathways passing through ventral and lateral spinothalamic tracts. They do transections of anterolateral quadrant by surgery. They found out that even surgery is not very successful for chronic pain relief:

there can be central structures, supraspinal structures, above the thalamus which become already sensitive as a result of chronic pain conditions or some types of chronic denervations, or some reverberating circuits.

there can be some pathways which can send collaterals through dorsal column.

Guyton’s reverberating circuit theory—inputs will cause action of higher reverberating circuit but what present studies actually discovered is that synaptic neurotransmitters can be upregulated in cases of denervation causing activation of supraspinal pain centers.

Itch and tickle usually innervated by C fibers a number are also activated by similar tissue

chemicals like histamine, kinine, elevated number of bile cells, etc. and the same type of afferent C fibers.

Clinical Correlations Hyperalgesia = oversensitivity to noxious stimulus Allodynia = pain caused by the non noxious movement of sensitized skin e.g. boils on skin (when touched, painful) “Normally, when you touch skin, no pain. If you have a pin and you touch it lightly on skin, it can sometimes activate threshold of nociceptor and cause pain, but if you do that to skin adjacent to a boil = very painful hyperalgesia.” Previously, noxious stimuli to normal skin can cause more sensitive response to inflamed tissues. That’s a hyperalgesic condition. In fact, there are discussions or experimental conditions of primary and secondary hyperalgesia.

o Secondary will be brought about by sensitization of structures at spinal cord and above spinal cord centers for pain processing.

o Primary it is only peripheral nerve endings that are sensitized. Removal of the inflammatory condition can result in absence of pain but in secondary even removal of main source of activation can still result in chronic pain condition as result of sensitization of higher pain order processing centers.

Hyperesthesia = oversensitivity to mechano and thermoreceptive systems to non noxious stimulus Hyperpathia = a pain syndrome characterized by an increase in response with delayed onset, and an after response that outlasts the stimulus; apparent after repetitive stimulation Hypoalgesia = undersensitivity to noxious stimulus Hypoanaesthesia = undersensitivity to all somatosensory modalities *Anaesthesia relates to all somatosensory modalities, even touch. *Analgesia, just pain system. Complete congenital absence of sensitivity to pain due to absence of A delta and C fibers. Complete Congenital Insensitivity = no C fibers&A delta Causalgia and reflex sympathetic dystrophy = Part of neuropathic pain-paindue to nerve injuries; upregulated norepinephrine receptors


Neuralgia = probably similar mechanisms to sympathetic dysreflexia; neuropathic pains Upregulation of norepinephrine receptors either

in soma or in regenerated axonal sprouts which make them sensitive to circulating basal levels of norepinephrine especially in times of stess. In times of stress, fight or flight responses, higher levels of serotonin which can excite nerve-injured areas furthers.

Closest biochemical model for reverberating circuit of Dr. ganong: but this one is brought about by glutamate so there is no such circuit of a circle/pathway of nerves whch have been found experimentally but only expt’l evidence is pathways (pain pathways) which releases glutamates as well as polypeptides like substance Postsynaptic neuron and induces release of nitric oxide which further excites presynaptic neuron.

Nitric oxide, for example, has been known to

diffuse to the presynaptic neuron in central pathways causing positive feedback mechanism-hyperexcitation of this pathway.

Plasticity in normal conditions, may not happen but with

hyperactivation of pathway due to injury to nerve, it can be possible

Eg. Normally, nitric oxide is not produced much but with hyperactivation of this pathway, nitric oxide is formed and would lead to positive feedback of the mechanism.

Another example of plasticity would be regeneration of adjacent neurons in phantom pain. Causes us sensation of a limb which has been cut off as though it is present.

Other examples- you’re blind so your visual cortex is not well used but your somatosensory neurons from anterior parietal and posterior clacarine cortex would be possibly invading (in terms of synaptic connections to your visual cortex). Possibly, visual cortical neurons now will be having synaptic connections with somatosensory cortex in performing work very similar to somatosensory neurons.

Normally, ganito specialized functions niya pero due to changes in environment, they perform either functions.

o For example, left brain, right brainfor young people, infants, with brain damage, left hemisphere is destroyed (language-specialized), right hemisphere still intact, language functions can still be developed in left hemisphere because right hemisphere takes over such functions. Such plasticity gradually decrease

when we’re older.

There are conditions of plasticity in learning. Learning itself is a good model of plasticity.

When we learn/remember there are structural changes happening in our brain. In order for us to remember something/be good at something, we have to do repetitive stimulation (Repetitive stimuli of certain pathway) and Some emotional affective components (you feel well-motivated), emotional cues. At the same time, there are emotional deterrents to further learning e.g. stress.


Characteristic Pacinian Corpuscle

Meissner’s Corpuscle

Merkel’s Disk

Ruffini’s Ending

Hair Follicle Endings

code

FA-II

FA-I

SA-I

SA-II

FA-I??

Adaptation

Fast

Fast

Slow

Slow

Fast

Receptive field size

large

small

small

large

small

Encoded Sensation

Touch, vibration (acceleration

detector)

speed of stimulus application, low

freq vibration sensors (like

pacinian, though meissner’s have lower sensibility:

30-40Hz)

localization of stimulus (touch

pressure)

magnitude and duration of

stimulus (touch pressure);

because it is slowly adapting,

it can give accurate

description magnitude and

duration… unlike those that are

rapidly adapting

Light touch flutter; low

vibration sensors (30-40 Hz, like

Meissner’s)

Afferents

generally Aβ (with some Aα)

Aβ

Aβ

Aβ (with some Aα)

Aβ

Location

Skin

fingertips, lips, skin, even at

sexual erectile tissues, glans

penis, etc.

high density in fingertips, lips,

many skin areas

?? covered by liquid

filled collagen

Notes / Remarks

Onion like lamellar capsule

Aβ = large, myelinated, group2 Small receptive field =accurate in

localizing stimulus source Large receptive field = not accurate in

localizing stimulus source

Somatic Sensations

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