PAIN Flashcards
1. Peripheral afferent nociceptive pathways 2. Central processing of nociceptive information 3. Mechanisms of action of drugs used for the treatment of neuropathic pain. 4. Biopsychosocial model of pain
What other symptom correlates best with pain intensity during recent onset low back pain?
Poor sleep quality increases pain intensity and the duration of pain intensity after new onset low back pain.
A&R 5/14
What is the medical definition of pain?
Pain is a somatic perception with quality like those causing tissue damage, experienced as a threat, associated with unpleasantness or other negative emotions.
What is the definition of chronic pain?
Chronic pain is defined as lasting beyond the ordinary duration required for healing-three months. ACR criteria for generalized pain-bilateral, above and below the waist, involving the spine-chest, thorax, low back, cervical. DSM-IV requires 6 months.
What pathways conduct pain?
Multiple ascending pathways relay nociceptive information including spinocervical, spinomesencephalic, spinal-diencephalic, and spinotelencephalic. These combined to form the contralateral spinothalamic tract which synapse in the thalamus. The thalamus projects to multiple brain areas in the primary and secondary somatosensory cortex, cingulate cortex, prefrontal cortex, insular cortex, amygdala, and the cerebellum.
What types of neurons provide pain transmission to the anterior horn?
Nociceptors are a specialized subset of primary sensory neurons that respond only to pain stimuli. Myelinated nociceptors include A-delta fibers which respond to heat (MTR) or high-pressure mechanoreceptors (HTM) and are responsible for immediate sharp pain. Unmylinated C fibers classified as C-polymodal nociceptors (C-PMN) reduce dull pain. Response threshold may be wide-wide dynamic range (WDR) or narrow, responding only to noxious stimuli (NS).
What are some specific ion channels in nociceptive pathways?
Na(v1, 7) is the sodium channel isoform found in nociceptive and sympathetic ganglion neurons. Calcium-permeable nonselective cation channels (TRPV1, capsation receptor) may produce transient receptor potentials which are gated by heat, low pH, or chemical mediators.
What descending pathways generates central pain inhibition?
descending pathways that inhibit or facilitate nociceptive transmission include ones from the somatosensory cortex prefrontal, cingulate, hypothalamus, periaqueductal gray, and the pons. Fibers in the dorsolateral funiculus of the spinal cord synapse in the dorsal horn with nociceptive neurons.
What sort of cell membrane receptors modify nociceptive transmission.
Other systems influencing nociceptive transmission includes the opioid system, noradrenergic system, and serotonergic system.
What peripheral stimuli sensitize nociception?
Peripheral sensitization may be due to cytokines (IL-1 beta), chemokins, bradykinin, histamine, prostaglandins (leukotriene B4), growth factors, and acidic environment. These may stimulate or reduce the threshold of nociceptor stimulation.
What does the NMDA receptor work?
N-methyl-D-aspartic acid (NMDA) receptor is responsive to glutamate, more so if phosphorylated which increases its distribution. Increased responsiveness follows removal of voltage-dependent magnesium block of the NMDA channel.
What substances increase during transcription dependent sensitization?
Transcription dependent sensitization occurs due to brain derived neurotrophic factor (BDNF), substance P, neurokinin 1, dynorphin, and prostaglandin-endoperoxide synthase 2.
What causes ectopic excitability?
Ectopic excitability may affect neurons at the site of injury, in a neuroma, or in the dorsal root ganglion. This happens because of upregulated sodium channels, channel subunits, receptors in myelinated neurons, or down regulation of potassium channels. GABA or glycine mediated inhibition might also be decreased.
What changes occur in the spinal cord during chronic pain?
Chronic pain may result in sensory fibers normally activated by light touch, pressure, or vibration and ending superficially within the spinal cord moving deeper into the area where pain fivers normally connect. These fibers may also start producing BDNF, and substance P, normally produced only by C-fibers.
How are sodium channels classified?
Ion channels are classified in general as ligand-gated, light gated, voltage-gated, and stretch-activated. Sodium channels are classified as constitutively active, proton-gated, and voltage-gated. The voltage gated sodium channels are classified as Nav alpha (1.1 through 1.9) and Nav beta (1-4). These channels are expressed by SCNA or B* genes (sodium channel neuronal type) A or B. Various combinations account for differences in conduction in central neurons, peripheral neurons, cardiac myocytes, uninnervated skeletal muscle, smooth muscle, interstitial cells of Cajal, dorsal root ganglia, glial cells, sympathetic neurons, Schwann cells, neuroendocrine cells, astrocytes, and ganglion cells.
What sorts of conditions result from mutations affecting sodium channels
Mutations cause assorted channelopahies, resulting in epilepsy, myoclonus, hemiplegic migraine, encephalitis, hyperkinetic periodic paralysis, long QT syndrome, ventricular fibrillation, erythromelalgia, and insensitivity to pain.
