Transmission and perception-- The brain receives the information for further processing and action

Contact with stimulus -- Stimuli can be mechanical (pressure, punctures and cuts) or chemical (burns)

Conduction -- A nerve sends the signal to the central nervous system. The relay of information usually involves several neurons within the central nervous system

Yes, this can occur in patients with trauma or other physical injuries including both a nociceptive and neuropathic pain classification. For example, a football player has just fractured their fibula. The physical fracture would be classified as somatic nociceptive pain and the swelling or burning would be classified as neuropathic inflammatory pain. Nociceptive pain causes neuropathic pain more often than the other way around

The perception pathway is relatively the same in both cases. However, when communicating nociceptive pain, sensory receptors (nociceptors) in the skin are activated by external noxious stimuli in order to communicate the signal, and with neuropathic pain, the same pathway is used, but the pain signal comes from damage to the nerve fibers themselves. When a nerve fiber is damaged, it tends to release an excessive amount of signals or increase the amount of sodium channels.

There are many tools that are currently used to classify pain. The primary one is the pain numeric rating scale, but this tool is one of many. There is also the pain inventory, Mcgill's pain questionnaire, the explanatory models approach and the wong-baker FACES pain rating scale. Each of the previously mentioned tools was designed and developed with all people of different ethnicities, languages and upbringings in mind.

Chronic pain lasts more than 3-6 months and persists past acute disease, even after tissue healing is complete. Acute pain lasts less than 6 weeks, has a rapid onset and could be a medical condition or symptom of noxious stimuli.

No, but if one is experiencing acute pain symptoms but it is lasting longer than 6 weeks, their pain can be classified as sub-acute pain.

Referred Pain - pain felt in a part of the body other than its actual source

Musculoskeletal Pain - injury to the bones, joints, muscles, tendons, ligaments, or nerves

Vascular Pain - develops when there is interruption in blood flow to a tissue, organ or nerves

Post herpatic neuralgia - most common complication of shingles. The condition affects nerve fibers and skin, causing burning pain that lasts long after the rash and blisters of shingles disappear.

Trigeminal neuralgia - A chronic pain condition affecting the trigeminal nerve in the face, causes extreme pain and hypersensitivity

Casualgia - severe burning pain in a limb caused by injury to a peripheral nerve

Dysfunctional Pain - pain that persists due to errors in our pain processing abilities

Mono-neuropathy Multiplex - Damage to multiple nerves

Polyneuropathy - a general degeneration of peripheral nerves that spreads toward the center of the body

Neuritis - inflammation of a peripheral nerve or nerves, usually causing pain and loss of function

Analgesia - Absence of pain in response to stimulation which would normally be painful

Hyperpathia - normally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold

Hypoalgesia - Diminishd pain in response to a normally painful stimulus

Hyperalgesia - Increased pain from a stimulus that normally provokes pain

Mechanical Allodynia - Caused by innocuous stimuli (light tough), no protective role

Yes, to a certain extent. Especially with neuropathic pain, one can become desensitized (not immune) to the pain they experience. Nerves fire a signal that is constant and respond to a wide range of input with varying intensity. If a nerve signal doesn’t change, the brain might get used to it. Becoming desensitized to nociceptive pain, through repeated experience, is much harder.

Yes, in most cases. Impairment or damage to any sensory nerves involved in pain perception leads to neuropathic pain. Each category of neuropathic pain causes noxious signals to be perceived in an entirely different way (whether no pain at all, intensified pain, or somewhere in between). This nerve damage can be biological or can also occur as a result of conditions throughout the lifespan. Neurologically speaking, all humans have the same general layout of nerves, so differences in "neurological makeup" as a potential nociception threat does not necessarily exist.

I would not go as far as to say that one's pain is MORE psychogenic (meaning that pain has a psychological origin or cause rather than a physical one) than physical. Our physical perception of pain will always come first, without it our physical pain would not exist. However, psychological factors definitely have an affect on how we interpret and respond to our pain. Anxiety and depression can have a large effect on the emotional and cognitive dimensions of pain perception and our symptoms vary depending on our mood, pleasure, excitement, mental distraction, worry, or fatigue. Additionally, the influence of a negative schema for pain from past symptoms greatly increases our negative outlook towards future symptoms. Therefore, our psychological state does augment the pain we perceive by clouding our interpretation.

Specifically, when referring to the afferent pain perception pathway via the spinothalamic tract (the most common pathway)... Pain information is first carried by rapidly conducting myelinated A delta fibers and slowly conducting unmyelinated C fibers (both nociceptive fibers). The axon containing these fibers extends from the free nerve endings (external or internal) to the dorsal root of the spinal cord (unless the information is coming from the face). Their nociceptor axons synapse with the second order neurons in the substantia gelatinosa (or the loose aggregate of neurons at the end of the dorsal horn). Then, the second order neurons cross the midline (to the opposite side) and ascend the spinal cord in the anterolateral quadrant, making up the spinothalamic tract (in the white matter of the spinal cord). The pain information is then communicated to the thalamus when the second and third order neurons synapse. The thalamus, playing the role of sorting station, causes third order neurons to terminate the somatosensory cortex (homunculus), where the pain is localized, the frontal cortex (in charge of thinking), and the limbic system (linked to emotions).

Whether you are experiencing pain from a bruise in your arm, an ache in your stomach, or nerve damage as a result of shingles, your nervous system will perceive your pain in relatively the same way. Starting in either internal or external free nerve endings, traveling to the substantia gelatinosa in the dorsal root of the spinal cord, making its way up the spinothalamic tract and finally communicating the pain information to the brain (see previous response for more details). However, this process differs when your pain is localized in your face. Face pain utilizes the trigeminal pathway. Let's say that you just were hit in the cheek. Immediately after impact, the pain information is detected by free nerve endings belonging to the cranial trigeminal nerves. The signal then travels along the axon of these nerves to the main sensory trigeminal nucleus (within the medulla) where the sensory neurons synapse with second order neurons. The nerve fibers then cross the midline and ascend to innervate the ventral posteromedial (VPM) nucleus of the thalamus on the contralateral side (the area of the thalamus where information is transmitted regarding touch and pressure). From the thalamus (where the second order neurons synapse with third order neurons), the signal travels along the axons of the third order neurons which take the pain information to the postcentral gyrus of the parietal lobe, the reception center for the somatosensory cortex.

The pathway used in pain perception differs from any other form of perception. For example, the nerve fibers used (A delta fibers and C fibers) are specific to pain perception (for the most part), and the receptor type used to perceive the initial impact and begin the chain reaction of synapses between neurons (for pain the free nerve endings are used, opposed to the Pacinian corpuscles for example, which sense vibration) is also different. The perception of temperature is the pathway with the closest relation (because extreme temperatures can cause pain). Temperature perception pathways also utilize the free nerve endings and the A delta and C fibers, however your brain is able to differentiate signals through the presence of ion channels that respond to particular temperatures. But overall, each type of perception utilizes nerve fibers, some type of receptor, and eventually takes the signal to the brain.

It is important to differentiate between "good pain" and "bad pain" when understanding the idea that pain can seem like a mental weakness in SOME cases. In sports or any other form of physical activity, we often put our bodies through motions that utilize muscles we have not used or rarely use. Pain due to soreness or tightness is different than pain due to a pulled muscle, sprain or tear. In the case that one's pain is due to soreness, tightness or exhaustion, a negative response to the pain may be labeled as a "mental weakness." With most physical activities, one must go through some form of pain to reach an intended goal or to get stronger. Without a mindset that adversity is a part of the process, that goal may never be attained... therefore causing the lack of determination to be considered a mental weakness. However, if one's pain results from an injury, then reducing activity is necessary (an act which should not be considered a "mental weakness").

As psychology and neurology explain, the use of more than one sense enhances the accuracy of what we perceive. For example, being able to smell the freshly baked cookie you are eating generally enhances the taste. Though pain is not considered one of our senses, the same principle can be used. With additional input communicating what happened to the brain, we gain a better understanding of the state we are in. In the event that seeing the injury occur increases the severity of the pain, the visual input more than likely provoked a feeling of fear. Fear stands to be a psychological influence known to intensify pain. Other psychological influences or emotions can occur in response to visual input and all have the potential to influence the severity of the pain we perceive.

First pain is the quick, sharp pain communicated by A Delta Fibers. These fibers are myelinated, causing signals to transmit quickly. Second pain is the prolonged, aching pain communicated by the C fibers. These fibers are not myelinated, causing them to transmit pain signals slower than the A Delta fibers. It is because of the difference in transmission rates that you first feel a quick, sharp pain, followed by a dull ache. When experiencing nociceptive pain, first and second pain are not necessarily interdependent, meaning that they respectively rely on the other to cause signals to fire. However, both A Delta and C Fibers activate when noxious stimuli is detected. So, rather, they are both dependent on pain itself, not each other (though they do always fire together).