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109 Cards in this Set
- Front
- Back
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3 Primary headaches are? |
Migraine, cluster headache and tension headache |
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Headache involves the activation of what 2 things |
Activation of the trigenminal nerve, and the trigeminal pain pathway |
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Headache involves the trigeminal nerve, trigeminal pain pathway and what two other systems? |
Neurogenic inflammation and Trigeminal autonomic reflex causing parasympathetic outflow |
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Nociceptive afferents within the trigeminal nerve innervate... |
The meninges and the meningeal vessels |
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Trigeminovascular system is the interaction between... |
Trigeminal afferents and meningeal vessels |
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Name the 3 layers of the meninges |
Dura mater, Pia mater, arachnoid |
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Trigeminal nerve has three branches, what are they and what do they serve? |
V1 - Opthalmic - Nasal cavity and upper face. V2 - Maxillary - Meninges and meningeal vessels, and lateral face. V3 - Mandibular Motor for mastication and lower face. |
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Write/talk out the Trigeminal Nociceptive Pathway |
V1, V2, V3 C-fibres and A-delta fibres - Primary afferent to the Trigeminal ganglion - Pons - Drops down and synapses at multiple levels within the Trigeminal Nucleus Caudalis of the medulla with 2nd order afferents - 2nd order afferents decussate and ascend via the contralateral Trigeminothalamic tract to the Thalamus - At the Thalamis 2nd order afferents synapse with tertiary afferents and ascend via the Internal Capsule to the Somatosensory Cortex for perception of pain. |
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Trigeminal ganglion is also called the? |
Gasserion - containing the Somata of the trigeminal nerve branches. |
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During the nociceptive pathways 2nd order afferents also brance off to what two areas of the brain? |
1. The limbic system for emotional repsonse. 2. Hypothalamus for autonomic response to pain. |
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Describe the A-beta pathway |
A-Beta fibres respond to touch/pressure, synapse at the Cheif Sensory Nucleus, 2nd order ascend bilaterally to the thalamus. Involved in gate control. |
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Neurogenic inflammation causes |
Inflammation and sensitisation |
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Neurogenic inflammation causes vasodilation at the |
Meningeal vessels |
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Neurogenic inflammation causes vasodilation by what two methods |
CGRP - NOS - NO - vasodilation. Mast cell degran - Histamine - vasodilation |
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Vasodialtion of the meningeal vessels further irritates? |
Nociceptors and increases pain |
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Neurogenic sensitisation is caused by neuropeptide and what neurotransmitter? |
CGRP, Glutamate |
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Glutamate is a |
Excitatory neurotransmitter |
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The Trigeminal Autonomic Reflex involves 2nd order afferents branching to the |
Superior Salivatory Nucleus in the Pons |
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TAR: 2nd order afferents branche to the Superior Salivatory Nucleus and synapse with |
Efferent parasympathetic fibres of facial nerve CN7 |
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Efferent parasympathetic fibres of facial nerve CN7 causing... |
Parasympathetic outflow, whereby ACH binds to smooth muscle cells causing vasodilation. |
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Parasympathetic outflow, whereby ACH binds to smooth muscle cells causing vasodilation causes... |
Lacrimination, Rhinorrhea, nasal congestion |
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Pos feedback is between what two systems |
Trigeminovascular system and trigeminal autonomic reflex |
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Pos feedback is whereby... |
Vasodilation causes pain which causes vasodilation |
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Pos feedback in more detail is... |
Vasodilation causes irritation of the C-fibres/A-delta fibres of the trigeminal nerve nociceptors innervating the vessels which increases pain, which inturn activates the TAR which causes more vasodilation. |
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Parasympathetic outflow causes vasodilation of what vessles... |
Meningeal vessels |
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Irritating the meningeal vessels does what... |
Increases pain and activates the TAR which further increases vasodilation. |
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What % of migraineurs have aura |
30% |
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MA is associated with |
Genetic abnormailities |
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MO is associated with |
Environmental issues |
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Gene mutations cause an alteration in |
gene expression |
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Write or talk through CSD |
I'm not going there |
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Neuronal hyperexcitability spreads how quickly |
2-5mm/sec |
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Increased rCBF lasts for |
a few seconds |
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Depression phase is what and last for how long |
Reduced synaptic activity, lasting 5-10mins |
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Cellular hypoxia lasts for and due to... |
1-2 hrs, due to reduced rCBF due to vasoconstriction |
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Following CSD you get... |
Extra cellular accumulations of ions and solutes |
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What are the extracellular ion and solutes after CSD... |
Ions - Na+/K+. Solutes - NO, adenosine/ATP, glutamate |
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Headache is exac by |
Neurogenic inflammation, meningeal vessel vasodilation and meningeal vasodilation from TAR. |
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Hypoxia in CSD is caused by what two things... |
1. 1-2hrs reduced rCBF /vasoconstriction, reduced perfusion, reduced 02 supply. 2. Available 02 used by Na+/K+ ATPase pumps to restore RMP (anaerobic gylcolysis - bi-product lactase and H+). |
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The extracellular solutes and neuronal hypoxia stimulate... |
Visual disturbances |
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Post CSD extracellular solutes irritate |
Ipsilateral trigeminal nociceptors activating the TNP and causing headache. |
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What activates Pannexins 1 megachannels |
During intense depolarisation and overactivation of NMDARS activates Panx1 megachannels |
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Two things Panx1 megachannels do? |
1. Increase neurotransmitters that sustain CSD. 2. Stimulate release of IL-1, CGRP, inflam mediators, together they sustain trigeminal stimulation beyond the removal of ions and solutes. |
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How many ion channelopathies are associated with migraine |
112 |
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If ion channels are dysfunctional there can be |
changes in the ionic profile that cause neuronal excitability and CSD, meaning they open more readily. |
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Detailed process in Neurolimbic theory... |
Even in the interictal state migraineurs have areas of spontaneous depolarisation that causes neuronal excitability and CSD - Due to central sensitisation in the Periaqueductal grey and rostral ventromedial medulla - interneurons in the descending modulating pathway known as ON/OFF switches change from being anti-nociceptive to pro-nociceptive - the Periaqueductal grey and rostral ventromedial medulla have close links with the hypothalamus and limbic system - so triggers such as emotions trigger spontaneous depolarisation. |
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Non-detailed steps to Neurolimbic theory |
Interictal migraineurs - neuronal excitability - spontaneous depolarisation and CSD - PAG and RVM - descending modulation pathway - interneurons - neuronal links - hypothalamus and limbic system |
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Details of CGRP and central/peripheral sensitisation |
CGRP is a neurokinin - exocytosed from pre-synaptic membranes - binds to post synaptic CGRP receptors - via cAMP and Protein kinase A phosphorylates NMDAR's and AMDAR's which sensitises them - CGRP also increases Glutamate release by binding to astrocytes which increases the amount of Glutamate bought back to the synapse. |
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Detainled involvement of Seotonin (5-HT)... |
Increased levels from released plts in migraine - serotonin stimulates NO - NO stimulates CGRP - CGRP stimulates NO = vasodilation and sensitisation |
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NO binds to what receptors to stimulate CGRP secretion? |
TRP receptors |
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CGRP stimulates NOS in vascular endothelia cells and astrocytes causing |
vasodilation |
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Extended periods of hypoxia cause |
increased levels of serotonin |
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Breif: How do you get hypoxia in migraine |
reduced regional blood flow - reduced perfusion - reduced 02 supply - increased use of available 02 for ATP, RMP increases demand for 02 = hypoxia. |
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To be hypoxic levels must be below |
90mmHg |
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HYpoxia causes vasodilation - increased cerebral blood flow due to |
NO, CGRP and adenosine |
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In hypoxia there are intracellular changes, they are?... |
Increased glycolysis disrupts the BBB and stimulates ROS generation. 2 Anearobic glycolysis results in lactate and H+ instead of pyrvate. 3. Hypoxia causes CSD and MO. |
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Lactates stimulates the release of what solute from the cell? |
Adenosine |
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What times do you get cluster headache |
0100 - 0200, 1300 - 1500, 2100 |
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CH is linked |
seasonally July and Jan and circadianly |
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Hypothalamic grey contains the |
Suprachiasmatic nucleus (SCN) |
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CH: The Suprachiasmatic Nucleus receives light signals from the retina via the ? |
Retinohypothalamic tract |
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In response to light the hypothalamus stimulates the release of? and suppresses? |
Cortisol and suppresses Melatonin |
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Cortisol release pathway? |
Hypothalamus - Cortisol Releasing Hormone. Anterior pituitary - Adrenocorticotropin Hormone - Adrenal cortex - cortisol. |
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Melatonin is released from the? |
Pineal gland |
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Two causes CH |
1. The hypothalamus grey is enlarged - so too much cortisol is released and melatonin suppressed. 2 Suprachiasmatic Nucleus can be dysfunctional leading to abnormal levels of cortisol and melatonin. |
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What causes unilateral temperol/ orbitol pain in CH? |
Hypothalamus - TNC - stimulates CN5 and Superior Salivatory Nucleus - activation of CN7 - this activates the TVS leading to vasodilation of meningeal vessels and neurogenic inflammation and sensitisation of trigeminal nociceptors. |
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What causes pain in CH |
Input CN5 - SSN - activate CN7 - activation of the TVS leading to vasodilation of meningeal vessels and neurogenic inflammation and sensitisation of trigeminal nociceptors. |
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Tension Type Headache is |
Episodic or chonic |
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How often does TTH need to be to be episodic? |
10 episodes <15days of the month |
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How often does chronic headache need to be to be chronic? |
>15days/ for at least 6months |
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What muscles are firm or tight even when theres no headache in TTH |
Pericranial myofacial and trapezius muscles |
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In TTH the myofacial muscle has |
Increased activity and contraction in myofacial trigger points |
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A sentence to explain the cause of TTH |
Hyperirritable areas associated with tight bands of skeletal tissue. |
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Why do we get pain in TTH |
Frequent input from pericranial muscles sensitises primary and 2ndry afferents in the TNC and dorsal horn - activates the TVS - neurogenic inflammation and vasodilation of meningeal vessles causing pain. |
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Episodic TTH changing to chronic involves the |
sensitisation and long-term potentiation of synapses at every level |
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TTH is linked to multiple genetic factors known as |
Polygenic |
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In sensitisation there maybe be 'stepwise' sensitisation due to? |
the secretion of neuropeptides at the synapses in the TNC and Thalamus |
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Stepwise sensitisation may effect trigenminal branches causing |
Allodynia and hyperaesthesia |
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In long term potentiation of synapses acute/episodic and switch to? |
Chronic |
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Due to central sensitisation there can be |
Ipsilateral hyperalgesia, allodynia, photophobia, phonophobia |
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Ipsilateral hyperalgesia, allodynia, photophobia, phonophobia is caused by |
Synaptic sensitisation of other ipsilateral trigeminal branches |
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Contralateral hyperalgesia, allodynia, or referred pain in head or upper limbs is caused by? |
Convergent 3rd order neurons at the thalamus level or alterations in the descending modulatory pathway. |
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Activation of the SSN causes |
Parasympathetic efferent pathway of CN7 activation |
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Primary headache syndromes that demonstrate TAR symptoms is called |
Trigeminal autonomic cephalgia |
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Trigeminal autonomic cephlagia can be? |
Lacrimination, conjunctival injection, tarsal oedema, nasal congestion, rhinorrhoea, salivation. |
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Details of Horners syndrome |
Activation of the TAR causes parasympathetic vasodilation of the internal carotid artery - CN3 and internal carotid artery pass through the same cavernous sinus - this vasodilation compresses CN3 - sympathetic input is decreased and parasympathetic dominates = facial flushin, Horners sydrome - pupil constriction and ptosis. |
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In headache N+V is stimulated by |
Dopamine (D2) and Serotonin (5-HT) |
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In headache what vomiting centres are triggered? |
CTZ and vomiting centre in the medulla |
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Pathway of the descending modulation pathway |
Cortex sends AP - Periaqeuductal grey enkephalin is exocytosed - Enkephalin stimulates a series of interneurons resulting in activation of the modulation pathway - Periaqueductal grey - AP - Restroventromedial of the medulla - AP via efferent modulatory neuron - Dorsal horn - Neuron from medulla exocytoses Serotonin - Serontonin can be EPSP or IPSP depending on the receptor. Serotonin 1. Directly inhibits the 2nd order afferent by creating IPSP's. 2. Stimlates an interneuron EPSP which expcytoses Encephalin which creates IPSP's that inhibit the 2nd order afferents. |
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In the descending modulatin pathway neurons from the medulla exocytose what? and modulates the pathway in what two ways... |
Serotonin. 1. Directly inhibits the 2nd order afferent by creating IPSP's. 2. Stimlates an interneuron EPSP which expcytoses Encephalin which creates IPSP's that inhibit the 2nd order afferents. |
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In the descending modulating pathway the cortex sends an AP to the?... |
Periaqueductal grey |
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In the descending modulating pathway the Periqueductal grey sends an AP to the |
Rostroventromedial of the medulla |
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In the descending modulating pathway the AP from the RVM goes to the... where is exocytoses? |
Dorsal horn... Serotonin |
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In the descending modulating pathway the Cortex sends an AP to the Periaqueductal grey, what is then exocytosed in the Periaqueductal grey? |
Enkephalin. |
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In the descending modulating pathway what does Enkephalin do? |
Stimulates a series of interneurons resulting in activation of the modulation pathway. |
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Inflammatory mediators that stimulate nocicpetors are? |
Histamine, bradykinin, prostaglandins, nerve groth factor, serotonin, H+ via ASIC's, Adenosine/ATP via purinergic receptors. |
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Nocicpetors of C-fibres and A-delta fibres also secrete neuropeptides |
CGRP and Sub P |
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In regards to inflam pain how does CGRP cause this |
stimulates NOS - NO - Vasodilation - swelling, vascular leakage - hyperanaemia due to increased vascualr perfusion |
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How does Substance-P cause inflammation |
Degranulates mast cells - histamine release - vasodilation - increase in vasoactive changes |
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Long-term potenitation and frequent neurogenic inflammtion does what to the receptors and channels? |
Alters expression of genes that code for that receptor and channels of the pathway. Can enhance transmission of the AP, and stimulate synaptic sensitisation. |
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How do inflam mediators cause pain? |
Inflam mediators bind to nerve endings - opens ligand-gated ion channels - TRP receptors are triggered - AP generated |
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Describe the Modulation Pathway: Gate control. |
Non-noxious stimuli/touch, pressure - AP primary A-Beta fibres - At spinal level synapses with inhibitory interneuron - IPSPs are summated with EPSP's from the first order C-fibre = inhibited or reduced AP reaching the thalamus and somatosenosry cortex. |
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What 3 types of sensory neurons are there? |
Chemical, thermal, mechanical. |
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Sensory neurons are |
Polymodal |
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In a sensory neuron the noxious stimuli triggers the nerve endings that trigger the? |
Transient Receptor Potential |
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In a sensory neuron spatial and temporal EPSP's are summated at the |
Trigger Zone |
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Transduction is starts at what to what |
Noxious stimuli to the trigger zone |
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Transmission is from the what |
Trigger zone to Somatosensory cortex |
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A sensory neuron is what polar |
Unipolar, meaning dendrites at either end and soma in dorsal horn |
