sensory

heat, pain

crossing over take place in the brain stem, the secondary neurons form the sensory decussation, the primary afferent can be alpha and beta too

Ruffini ending, Pacinian corpuscle, Meissner corpuscle, Merkel disk

It adapts rapidly, Mainly senses vibration, It can be found in deeper layer of the skin

temperature, pain

each hemisphere of somatosensory cortex receives signals from the contralateral side of the body., sensory signals are subject to modification before they reach higher levels of CNS.

pacinian

medial lemniscus, dorsal column, trigeminal nerve

Meissner

inability to accurately asses the texture of objects by touching them, inability to judge the weight of objects, inablilith to discretely localize touch sensations of contralateral limb

proprioception, vibration, fine touch

affect the somatosensory cortex contralateral to the receptor

the ascending sensory tract shows topology in the sensation of vibration, Meissner as are rapidly adapting receptors, the primary afferent cell bodies of the dorsal column are found in DRG

Ruffini endings are found deep in the skin

codes for stimulus strength by changes in receptor potential amplitude, is only stimulated by stimuli within its receptive field

Ruffini ending, Meissner, Hair follicle receptor

Pacinian, Meissner

the cold and warmth receptors are located at discrete separated spots in the skin, paradox cod sensation occurs above 45, free nerve endings detect temperature, the pain receptors can be stimulated only by extreme degrees of heat or cold, transduction of warm temperatures involves transient receptor potential channels, thermoreceptors are slowly adapting receptors

a sensory receptor can be stimulated only by stimuli within its receptive field, the lateral inhibition can be achieved in the brainstem, the primary somatosensory cortex is located in the gyrus postcentralis, the main sensory input of the neocortex is the layer1

the surround inhibition can be achieved in the brainstem

encapsulated nerve endings of Abeta

TRP, capsaicin

Adelta is around 15 m/s, C fibers have polymodal receptors, both c type and A delta may conduct nociceptibe information, prostaglandins can increase their sensitivity, K ions increase their sensitivity

K ions, prostaglandin, Bradylinin

spinothalamic tract, trigeminal nerve

primer hyperaglgesia can be induced by metabolites released from the damaged tissue, both mechanireceptors and nociceptors can end on wide dynamic range neurons, nociceptive pain can be blocked by COX inhibitiors

the acute pain is a protective mechanism, serotonin and histamine can be responsible for secondary hyperalgesia, the referred pain occurs when activation of nociceptors in the viscera results in a perception of pain that is localized to the body surface, the receptors are free nerve endings

transmission of pain may be inhibited by enkephalin, normally results from activation of nociceptors, fibers travel in the spinothalamic tracts, Aδ fibers propagate pain sensation

pain receptors exhibit little or no adaptation, mediated by nociceptors

COX inhibitors are good pain reducers, secondary hyperalgesia can be the result of the axon reflex, hyperemia occurs during secondary hyperalgesia, the threshold of pain sensing receptors is high

80 120

35 75

5 30

3 15