1.

​ ​Berdasarkan sumber nyeri, maka nyeri dibagi menjadi : 5​

a. Somatic pain can be further classified as superficial or deep. Superficial somatic pain is

due to nociceptive input arising from skin, subcutaneous tissues, and mucous membranes.

It is characteristically well localized and described as a sharp, pricking, throbbing, or

burning sensation. Deep somatic pain arises from muscles, tendons, joints, or bones. In

contrast to superficial somatic pain, it usually has a dull, aching quality and is less

well-localized. An additional feature is that both the intensity and duration of the stimulus

affect the degree of localization. For example, pain following brief minor trauma to the

elbow joint is localized to the elbow, but severe or sustained trauma often causes pain in

the whole arm.

b. The visceral form of acute pain is due to a disease process or abnormal function of an

internal organ or its covering (eg, parietal pleura, pericardium, or peritoneum). Four

subtypes are described: (1) true localized visceral pain, (2) localized parietal pain, (3)

referred visceral pain, and (4) referred parietal pain. True visceral pain is dull, diffuse,

and usually midline. It is frequently associated with either abnormal sympathetic or

parasympathetic activity causing nausea, vomiting, sweating, and changes in blood

pressure and heart rate. Parietal pain is typically sharp and often described as a stabbing

sensation that is either localized to the area around the organ or referred to a distant site.

The phenomenon of visceral or parietal pain referred to cutaneous areas results from

patterns of embryological development and migration of tissues, and the convergence of

visceral and somatic afferent input into the central nervous system. Thus, pain associated

with disease processes involving the peritoneum or pleura over the central diaphragm is

frequently referred to the neck and shoulder, whereas disease affecting the parietal

surfaces of the peripheral diaphragm is referred to the chest or upper abdominal wall.
2. Berdasarkan jenisnya nyeri juga dapat diklasifikasikan menjadi : 5​

a. Nyeri nosiseptif

Nociceptive pain is caused by the ongoing activation of A-! and C-nociceptors in response to

a noxious stimulus (e.g., injury, disease, inflammation). Pain arising from visceral organs is

called visceral pain, whereas that arising from tissues such as skin, muscle, joint capsules,

and bone is called somatic pain​. (NPC)

b. Nyeri neuropathy

Neuropathic pain is caused by aberrant signal processing in the peripheral or central

nervous system. In other words, neuropathic pain reflects nervous system injury or

impairment. Common causes of neuropathic pain include trauma, inflammation,metabolic

diseases (e.g., diabetes), infections (e.g., herpes zoster), tumors, toxins, and primary

neurological diseases. Neuropathic pain can be broadly categorized as peripheral or central in

origin. Painful peripheral mononeuropathy and polyneuropathy, deafferentation pain,

sympathetically maintained pain, and central pain are subdivisions of these categories.

Neuropathic pain is sometimes called “pathologic” pain because it serves no purpose. A

chronic pain state may occur when pathophysiologic changes become independent of the

inciting event. Sensitization plays an important role in this process. Although central

sensitization is relatively short lived in the absence of continuing noxious input, nerve injury

triggers changes in the CNS that can persist indefinitely. Thus, central sensitization explains

why neuropathic pain is often disproportionate to the stimulus (e.g., hyperalgesia, allodynia)

or occurs when no identifiable stimulus exists (e.g., persistent pain, pain spread). Neuropathic

pain may be continuous or episodic and is perceived in many ways (e.g., burning, tingling,
prickling, shooting, electric shock-like, jabbing, squeezing, deep aching, spasm, or cold).

(NPC)

3. Berdasarkan timbulnya nyeri dapat diklasifikasikan menjadi: 5​

a. Nyeri akut

Acute pain can be defined as pain that is caused by noxious stimulation due to injury, a

disease process, or the abnormal function of muscle or viscera. It is usually nociceptive.

Nociceptive pain serves to detect, localize, and limit tissue damage. Four physiological

processes are involved: transduction, transmission, modulation, and perception. This type of

pain is typically associated with a neuroendocrine stress that is proportional to intensity. Its

most common forms include posttraumatic, postoperative, and obstetric pain as well as pain

associated with acute medical illnesses, such as myocardial infarction, pancreatitis, and renal

calculi. Most forms of acute pain are self-limited or resolve with treatment in a few days or

weeks. on

origin and features.

b. Nyeri kronik

Chronic pain was once defined as pain that extends 3 or 6 months beyond onset or beyond the

expected period of healing. However, new definitions differentiate chronic pain from acute

pain based on more than just time. Chronic pain is now recognized as pain that extends

beyond the period of healing, with levels of identified pathology that often are low and

insufficient to explain the presence and/or extent of the pain. Chronic pain is also defined as a

persistent pain that “disrupts sleep and normal living, ceases to serve a protective function,

and instead degrades health and functional capability. Thus, unlike acute pain, chronic pain

serves no adaptive purpose. Chronic pain may be nociceptive, neuropathic, or both and
caused by injury (e.g., trauma, surgery), malignant conditions, or a variety of chronic

non-life-threatening conditions (e.g., arthritis, fibromyalgia, neuropathy). NPC

Transmission of nociceptive input in the spinal cord can be inhibited by

segmental activity in the cord itself, as well as descending neural activity from

supraspinal centers.

·​ Segmental Inhibition
​

Activation of large afferent fibers subserving epicritic sensation inhibits WDR

neuron and spinothalamic tract activity. Moreover, activation of noxious stimuli in

noncontiguous parts of the body inhibits WDR neurons at other levels; ie, pain in

one part of the body inhibits pain in other parts. These two observations support a

"gate" theory ​for pain processing in the spinal cord. Glycine and -aminobutyric

acid (GABA) are amino acids that function as inhibitory neurotransmitters. They

likely play an important role in segmental inhibition of pain in the spinal cord.

Antagonism of glycine and GABA results in powerful facilitation of WDR

neurons and produces allodynia and hyperesthesia. There are two subtypes of

GABA receptors: GABAA, of which muscimol is an agonist, and GABAB, of

which baclofen is an agonist. Segmental inhibition appears to be mediated by

GABAB receptor activity, which increases K+ conductance across the cell

membrane. The GABAA receptor functions as a Cl– channel, which increases Cl–

conductance across the cell membrane. Benzodiazepines potentiate this action.

Activation of glycine receptors also increases Cl– conductance across neuronal

cell membranes. Strychnine and tetanus toxoid are glycine receptor antagonists.

The action of glycine is more complex than GABA, because the former also has a
facilitatory (excitatory) effect on the NMDA receptor. Adenosine also modulates

nociceptive activity in the dorsal horn. At least two receptors are known: A1,

which inhibits adenylcyclase, and A2, which stimulates adenylcyclase. The A1

receptor mediates adenosine's antinociceptive action. Methylxanthines can reverse

this effect through phosphodiesterase inhibition.

· Supraspinal Inhibition

Several supraspinal structures send fibers down the spinal cord to inhibit pain

in the dorsal horn. Important sites of origin for these descending pathways include

the periaqueductal gray, reticular formation, and nucleus raphe magnus (NRM).

Stimulation of the periaqueductal gray area in midbrain produces widespread

analgesia in humans. Axons from these tracts act presynaptically on primary

afferent neurons and postsynaptically on second-order neurons (or interneurons).

These pathways mediate their antinociceptive action via 2-adrenergic,

serotonergic, and opiate ( mu, ,kappa and gamma) receptor mechanisms. The role

of monoamines in pain inhibition explains the analgesic action of antidepressants

that block reuptake of catecholamines and serotonin. Activity at these receptors

(which are also coupled to G proteins) activates secondary intracellular

messenger, opening K+ channels and inhibiting increases in intracellular calcium

concentration. Inhibitory adrenergic pathways originate primarily from the

periaqueductal gray area and the reticular formation. Norepinephrine mediates this

action via activation of presynaptic or postsynaptic 2-receptors. At least part of the

descending inhibition from the periaqueductal gray is relayed first to the NRM

and medullary reticular formation; serotonergic fibers from the NRM then relay

the inhibition to dorsal horn neurons via the dorsolateral funiculus. The
endogenous opiate system (primarily the NRM and reticular formation) acts via

methionine enkephalin, leucine enkephalin, and -endorphin, which are

antagonized by naloxone. These opioids act presynaptically to hyperpolarize

primary afferent neurons and inhibit the release of substance P; they also appear to

cause some postsynaptic inhibition. In contrast, exogenous opioids may

preferentially act postsynaptically on the second-order neurons or interneurons in

the substantia gelatinosa.