Pain and Temperature System .txt

detection and localization of a stimulated pain receptor (nociceptor)

• involved the emotional (affective) and arousal aspects of such stimulation
• a complex and subjective experience - can arise without nociceptor stimulation --> NO absolute scale for pain

• help guide treatment
• acute vs. chronic pain
• also cancer pain, chronic noncancer pain, chronic pain syndrome, etc.

complex, unpleasant experience with emotional and cognitive, as well as sensory, features that occur in response to tissue trauma

• relate closely to tissue pathology
• resolves with tissue healing
• source: is nociceptor activity

• trauma
• surgery
• labor in pregnancy
• acute disease

signals the extent of or potential for tissue injury

pain that lasts beyond the period of healing and that involves low tissue pathology insufficient to explain the pain

• occurs in relative absence of tissue pathology
• outlasts period of tissue healing
• sour is usually neuropathic

• trauma
• malignancy
• chronic disease
• non-life-threatening disease (arthritis, neuropathy)

• neurological cause unknown
• hypothesis: caused by excess nociceptor activity that outlasts the healing period

serves no useful biological purpose to patient

• recovery from damage to structures involved in pain pathways can result in chronic episodes of spontaneous pain
• Associated with more complex response to the pain: patients may show problems with employment, social relationships, psychological well-being
• examples: headache, back pain, fibromyalgia, neuropathic pain resulting from spinal cord injury, MS, stroke

pharmacological strategies target multiple transmitter systems at specific CNS levels to reduce transmission of pain information

• fast and first: component felt immediately after stimulation = SENSORY-DISCRIMINATIVE COMPONENT linked to nociceptor activation and allows determination of stimulus location, intensity, onset and duration
• Slow and second: component persists after the stimulus has ended
• motivational-emotional component influenced by personal experience, emotional framework, culture and cognitive (attention, anxiety) aspects
• the FAST and SLOW components are due to action potential conduction rates: they have separate, but parallel, pathways through the CNS
• Pain produces: autonomic (b.p. heart rate) and motor (withdrawal reflexes

• Sensory receptors: free nerve endings
• Nociceptors: unique in reposing to physical AND chemical stimuli: mechano, thermal, polymodal- mechano/thermal/chemical stimuli
• Thermal receptors: cool, warm, but not extreme temperatures

• Adelta fibers
• primarily from mechanonociceptors that signal a brief, sharp, pricking sensation

• C fibers
• primarily from polymodal nociceptors that signal a secondary, longer lasting, burning sensation

• several pathways transmit patin information
• spinothalamic tract: for fast pain
• spinoreticulo-thalamic tract: for slow pain
• both of these collectively called ALS = the anterolateral system

located in the dorsal half of the brainstem

• Receptor: Nociceptor
• Axon size: small
• 2 neuron: dorsal horn
• Crossing CNS: spinal cord
• Destinations for info:reticular formation, periaqueductal grey, superior colliculus, hypothalamus, thalamus, cortex
• Relay in Thalamus: VPL, Intralaminar nucleus.
• Cortical area: somatosensory cortex, insula, cingulate gyrus, orbitofrontal
• Modulation: initiates descending activity from brainstem to spinal cord

• Receptor: Meissner's, Merkel, Pacinian, Ruffini
• Axon size: medium/large
• 2 neuron: Caudal medulla
• Crossing CNS: caudal medulla
• Destinations for info: thalamus, cortex
• Relay in Thalamus: VPL
• Cortical area: somatosensory cortex
• Modulation: little

• fast pain component via A-delta fibers
• enables you to distinguish WHERE on the body a painful stimulus arises

Dorsal root ganglion DRG

marginal zone, nucleus proprius

ventral posterior lateral (VPL)

Spinal Nerve/Dorsolateral fasciculus

Spinothalamic Tract/ALS

Posterior limb of Internal Capsule

• this involves multisynaptic connections of primary pain fibers with interneurons and motor neurons at multiple spinal cord levels
• local response in the spinal cord and does not involve the brain

• multisynaptic and multilevel in spinal cord
• contract flexors and inhibit extensors on 1 side
• opposite effect in other leg for postural compensation
• Why is this important: 1) indicates complexity of even "simple" reflexes, 2) shows "wired-in" nature of some actions, 3) for this system indicates a more distributed connectivity

• primary fibers enter the spinal cord at: Dorsolateral fascicles and ascent two levels
• This distributes information from 1 dermatome to several spinal cord levels
• thus, information entering the cord at one level enters spinothalamic tract on opposite side at same level AND for 2 levels above

laminae I (marginal zone) and III-V (nucleus Proprius)

• have long axons that travel to the thalamus
• are located in Marginal zone and Nucleus Proprius

• postcentral gyrus
• conveys information about location/intensity of pain stimulus
• stimulation of postcentral gyrus DOES NOT: elicit painful sensation!

• significant only in the spinal cord and cortex
• ALS is divided medial to lateral: C to T to L to S

• Slow pain component: transmitted via C fibers
• Carries information about UNPLEASANT QUALITIES of pain: burning, long-lasting
• MULTISYNAPTIC PATHWAY: NOT a 3-nouron sensory pathway!! via reticular formation in medulla and pons to intralaminar nuclei in thalamus to cortex
• travels parallel to Lateral Spinothalamic Tract

• Cell body/nucleus: Dorsal root ganglion (DRG)
• Axon/Tract: spinal nerve/dorsolateral fasciculus

• Cell body/nucleus: marginal zone, substantia gelatinosa (lamina II)
• Axon/Tract: ALS - spinoreticular fibers

• Cell body/nucleus: Reticular formation
• Axon/Tract: reticular formation

• Cell body/nucleus: Intralaminar thalamic Nuclei
• Axon/Tract: Posterior limb of Internal Capsule

• lamina II
• neurons are interneurons, which do not send axons into the ALS
• It provides the opportunity for more connections and thus more modulation of pain signals

• location of cell bodies of last neuron in spino-reticular thalamic tract
• intralaminar nuclei project to several cortical areas associated with emotion and attention aspects of pain
• Orbitofrontal cortex:
• Insula:
• Cingulate Gyrus:

periaqueductal Gray (PAG) and Superior Colliculus

pain modulatory center part of the anti-pain pathway

a visual reflex center that mediates head and eye turning toward pain stimuli

• relays information from the PAG in the midbrain to the reticular formation in the medulla and then to spinal cord to terminate in the dorsal horn where it inhibits transmission os pain signals from primary to secondary pain neurons
• This descending pathway is activated by: 1) ascending pain (spinoreticular fibers) and 2) cortex

• Visceral pain is transmitted by SYMPATHETIC nerve fibers (mixed sensory/motor nerves)
• poorly localized: dur to low nociceptor density and pathway convergence

• Cell Body: Dorsal root Ganglia (T1-L2)
• Axon: splanchnic nerve to spinal nerve

• Cell Body: dorsal horn; central grey
• Axon: ALS

• Cell Body: VPL
• Axon: Internal Capsule

• 1) a deep body sensation: stomach ache; pain info is transmitted with fidelity to the cortex where it terminates in the visceral area of the postcentral gyrus located ventrally within the lateral sulcus.
• 2) referred pain to a dermatome: left arm for heart attack; some primary sympathetic pain fibers converge onto secondary SOMATIC ALS neurons in segments T1-T2, causing visceral pain information to MERGE with body dermatome information. The ALS carries information to the cortex (postcentral gyrus), where it is interpreted as originating n the associated dermatome

C3-C4

Left T1-T4

Left T6-T9

Right T10

L1-L2

• can cause neuropathic pain
• e.g. phantom limb pain

ALS lesions cause loss of pain on contralateral body;

• complete damage causes a pure sensory loss of tactile and pain sensation
• If recovery occurs, thalamic pain syndrome can result!
• pain episodes involving all or part of the contralateral body with butning, unpleasant quality, triggered spontaneously, or by touch

impairs ability to LOCALIZE: source of pain, but pain is still experienced due to other cortical areas that receive pain info

• formation of a cavity around central canal of spinal cord
• Due ti its position: crossing spinothalamic fibers are affected
• commonly occurs at cervical levels
• can be caused by developmental abnormalities (chiari malformation), trauma, spinal cord tumors

• produced by spinal cord damage
• results in loss of sensation on one side of body and loss of pain/temperature sensation on opposite side
• these are key symptoms characteristic of damage to the spinal cord due to the pathways these sensory stimuli travel along in the CNS