Académique Documents
Professionnel Documents
Culture Documents
Alteration in sensory function dysfunctions of the general or special senses Dysfunctions of the general senses chronic pain, abnormal temperature regulation, tactile dysfunction
Definitions of pain
Pain is a complex unpleasant phenomenon composed of sensory experiences that include time, space, intensity, emotion, cognition, and motivation
Pain categories
1. Somatogenic pain is pain with cause (usually known) localised in the body tissue a/ nociceptive pain b/ neuropatic pain 2. Psychogenic pain is pain for which there is no known physical cause but processing of sensitive information in CNS is dysturbed
Acute and chronic pain Acute pain is a protective mechanism that alerts the individual to a condition or experience that is immediately harmful to the body Onset - usually sudden
Relief - after the chemical mediators that stimulate the nociceptors, are removed
This type of pain mobilises the individual to prompt action to relief it Stimulation of autonomic nervous system can be observed during this type of pain (mydriasis, tachycardia, tachypnoe, sweating, vasoconstriction) Responses to acute pain - increased heart rate - diaphoresis
Psychological response to chronic pain Intermittent pain produces a physiologic response similar to acute pain. Persistent pain allows for adaptation (functions of the body are normal but the pain is not reliefed) Chronic pain produces significant behavioural and psychological changes The main changes are: - depression - an attempt to keep pain - related behaviour to a minimum - sleeping disorders - preoccupation with the pain - tendency to deny pain
Pain tolerance is generally decreased: - with repeated exposure to pain, - by fatigue, anger, boredom, apprehension, - sleep deprivation Tolerance to pain may be increased: - by alcohol consumption, - medication, hypnosis,
Neuroanatomy of pain
The portions of the nervous system responsible for the sensation and perception of pain may be divided into three areas: 1. afferent pathways 2. CNS 3. efferent pathways The afferent portion is composed of:
system
The portion of CNS involved in the interpretation of the pain signals are the limbic system, reticular formation, thalamus, hypothalamus and cortex The efferent pathways, composed of the fibers connecting the reticular formation, midbrain, and substantia gelatinosa, are responsible for modulating pain sensation
describing
localising
of pain
The reticular formation and limbic system: - control the emotional and affective response to pain
The role of the afferent and efferent pathways in processing of pain information
Nociceptive pain
Nociceptors: Endings of small unmyelinated and lightly myelinated afferent neurons
Stimulators: Chemical, mechanical and thermal noxae Mild stimulation positive, pleasurable sensation (e.g. tickling) Strong stimulation pain These differences are a result of the frequency and amplitude of the afferent signal transmitted from the nerve endings to the CNS In muscles, tendons, epidermis, subcutanous tissue, visceral organs - they are not evenly distributed in the body
(in skin more then in internal structures)
Location:
Nociceptive pain:
Afferent pathways:
From nociceptors transmitted by small A-delta fibers and C- fibers to the spinal cord form synapses with neurons in the dorsal horn(DH) From DH transmitted to higher parts of the spinal cord and to the rest of the CNS by spinothalamic tracts *The small unmyelinated C- neurons are responsible for the
Enk enkefalinergic PAG paraaqueductal gray EAA excitatory amino acids RVM rostral ventro-medial medulla
2nd afferent neurons transmit the impulse from the substantia gelatinosa (SG) and laminae through the ventral and lateral horn,
PAG periaqueductal gray PB parabrachial nucleus in pons VMpo ventromedial part of the posterior nuclear complex MDvc ventrocaudal part of the medial dorsal nucleus VPL ventroposterior lateral nucleus ACC anterior cingulate cortex PCC posterior cingulate cortex HT hypothalamus S1, S2 first and second somatosensory cortical areas PPC posterior parietal complex SMA supplementary cortical areas AMYG amygdala PF prefrontal cortex
Stimulation of small fiber input inhibits cells in SG and "open the gate". An open gate increases the stimulation of T-cells transmission of impulses enhances pain perception In addition to gate control through large and small fibers stimulation, the central nervous system, through efferent pathways, may close, partially close, or open gate. Cognitive functioning may thus modulate pain perception
Action of endorphins(ED)
All ED act by attaching to opiate receptors on the plasma membrane of the afferent neuron. The result than is inhibition of releasing of the neurotransmitter, thus blocking the transmission of the painful stimulus
Neuropathic pain
It occurs as a result of injury to or dysfunction of the
nervous system itself, peripheral or central Deaferentation pain - form of neuropathic pain: a term implying that sensory deficit in the painful area is a prominent feature (anesthesia dolorosa) Phantom pain- pain localizei into non-existing organ (tissue)
involved in the pain processing Hyperalgesia increased the pain sensitivity to noxious stimuli
Most peripheral neuralgias are the result of trauma or surgery. Such a conditions does not necessary occur as a result of damageing a major nerve trunk but may be caused by an incision involving only small nerve branches
(incisional pain)
Mechanism: the pain is due to neuroma formation in the scar tissue (?)
3. deafferentation pain
5. Hemiagnosia
is a loss of ability to identify the sorce of pain on one side
MP is not a prominent feature of the serious progressive diseases affecting muscle, e.g. the muscular dystrophies, denervation, or metabolic myopathies, but it is a feature of rhabdomyolysis Muscles are relatively insensitive to pain when elicited by needle prick or knife cut, but overlying fascia is very sensitive to pain. Events, processes which may lead to muscular pain are: metabolic events: metabolic depletion ( ATP muscular contracture) accumulation of unwanted metabolities (K+, bradykinin)
It is clear that painful stimulation of visceral structures evokes a visceromuscular reflex, so that some muscles
of somatic structures.
Possible mechanisms: - onset of self-maintaining vicious circle impulses: peripheral tissue afferent fibers central nervous system peripheral tissue somatic and sympathetic efferent fibres
Intricate conditions - in some types of pain, e.g. chest pain, is difficult to distinguish the true cause of pain because such kind of pain may be related to cervical osteoarthrosis, esophageal hernia, or cholecystitis. It is
Mechanisms of SMI
a) Lack of the pain is, in part, related to the duration and severity of MI. Episodes shorter than 3 min, and those accompanied by a modest impairment of left ventricle ( in end-diastolic pressure inferior to 6 mm Hg) are always painless. Longer and more severe episodes are acccompanied by chest pain in some instances but not in others. b) Pacients with predominantly SMI appear to have a generalized defective perception of pain (threshold and tolerance). Mechanism: level of circulating -endorphin (?)