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B&B Part 2 > B&B Week 6 > Flashcards

B&B Week 6 Flashcards

1
Q

what is the relationship between the temporal and infratemporal fossae?

A

composed of the temporal and infratemporal fossae which are separated vertically by the zygomatic arch

the infratemporal fossa is located inferior to the zygomatic arch

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2
Q

what separates the temporal and infratemporal fossae?

A

zygomatic arch

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3
Q

what makes up the floor of the temporal fossa?

A

the four cranial bones which form the pterion: frontal, parietal, temporal and greater wing of the sphenoid–> this floor is then covered by the fan shaped temporal muscle

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4
Q

what are the borders of the infratemporal fossa?

A

the infratemporal fossa is located inferior to the zygomatic arch and is bound anteriorly by the posterior aspect of the maxilla, posteriorly by the tympanic plate, the mastoid and the styloid processes, superiorly by the inferior surface of the greater wing of the sphenoid and inferiorly by the attachment of the medial pterygoid muscle to the angle of the mandible

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5
Q

that muscles are found in the infratemporal fossa?

A

lateral pterygoid and medial pterygoid muscles

both are used as landmarks for locating the other structures in the infratemporal fossa

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6
Q

describe the medial pterygoid muscle

A

found in the infratemporal fossa

quadrilateral muscle which lies deep to the ramus of the mandible and runs from the tuberosity of the maxilla to the ramus of the mandible and the mandibular foramen

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7
Q

describe the lateral pterygoid muscle

A

found in the infratemporal fossa

triangular muscle with its apex attached to the disc of the TMJ and neck of the mandible and its base attached to the greater wing of the sphenoid bone

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8
Q

what artery passes through the infratemporal fossa?

A

maxillary artery

this artery is the larger of the two branches that arises from the external carotid artery (the smaller being the superficial temporal artery which runs as a superior extension of the external carotid artery and enters the temporal fossa by traversing lateral to the zygomatic arch)

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9
Q

describe the pathway of the maxillary artery

A

branches from external carotid artery

as it runs through the fossa from posterior to anterior it gives off several branches and is divided into three parts based on location related to the lateral pterygoid muscle
–> the first part of the maxillary artery gives off several branches, including the middle meningeal artery and the inferior alveolar artery (goes inferiorly to mandible, gingiva and teeth).

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10
Q

what nerve goes through the infratemporal fossa?

A

mandibular nerve (V3 of trigeminal)

mandibular nerve enters the fossa via the foramen ovale and branches off into motor and sensory components

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11
Q

what are the sensory branches of the mandibular nerve (V3) and what is their route?

A
  1. inferior alveolar nerve–> enters mandibular foramen and runs through the mandibular canal where it banches off to form the myohyoid nerve and and the mental nerve
  2. lingual nerve–> runs anterior to the inferior alveolar nerve and exits the fossa between the medial pterygoid and the ramus of the mandible to enter the mouth –> joined in the infratemporal fossa by the chorda tympani nerve (branch of CN VII, facial) which runs anteriorly with the lingual nerve in its sheath –> chorda tympani carries special sensory taste fibres from the anterior 2/3 of the tongue as well as secretomotor fibres for the submandibular and sublingual salivary glands
  3. auriculotemporal nerve–> has two roots (one from otic ganglion and one from mandibular nerve) which run posteriorly and which join once they have encircled the middle meningeal artery–> divides into 3 with the largest of the three passing posterior and medial to the neck of the mandible and going on to supply sensory fibres to the temporal and auricle regions –> second branch goes to parotid gland where it innervates gland secretion
  4. buccal nerve–> branch of V3–> emerges deep the ramus of the mandible as it exits the foramen ovale and then runs anteriorly onto the buccinator muscle
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12
Q

where is the otic ganglion located?

A

just inferior to the foramen ovale and just medial to the mandibular nerve

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13
Q

what does the otic ganglion contain?

A

presynaptic parasympathetic fibres from CN IX (glossopharyngeal) and post synaptic fibres which carry secretory signals to the parotid glands via the auriculotemporal nerve

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14
Q

what bones form the temporomandibular joint?

A

condyle of the mandible, articular tubercle of the temporal bone, and the mandibular fossa

the joint is located just anterior to the opening of the external acoustic meatus and allows for both gliding movements of protrusion and retrusion as well as hinge movements of depression and elevation

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15
Q

what is the temporal fossa?

A

fan shaped space that covers the lateral surface of the skull

upper margin defined by superior and interior temporal lines

lateral margin defined by temporal fascia (aponeurosis)

inferior margin defined by zygomatic arch

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16
Q

what is found in the temporal fossa?

A

temporalis muscle, V2 branches, deep temporal nerves and arteries (motor) and middle temporal artery

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17
Q

name the four muscles of mastication

A

temporalis
masseter
medial pterygoid
lateral pterygoid

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18
Q

what nerve innervates the muscles of mastication?

A

V3 branch (mandibular) of trigeminal

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19
Q

what does the temporalis muscle do?

A

elevation and retraction of mandible

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20
Q

what does the masseter muscle do?

A

elevation of mandible

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21
Q

what does the medial pterygoid muscle do?

A

elevation and side to side movements of the mandible

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22
Q

what does the lateral pterygoid muscle do?

A

protrusion and side to side movements of the mandible

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23
Q

from what artery does the maxillary artery branch?

A

external carotid artery–>it is one of two terminal branches of the external carotid artery

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24
Q

name the four branches of the maxillary artery

A
  1. inferior alveolar artery
  2. middle meningeal artery
  3. buccal artery
  4. numerous small muscular branches
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25
Q

what does the inferior alveolar artery supply?

A

supplies all the lower jaw teeth

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26
Q

what does the middle meningeal artery supply?

A

passes thru the foramen spinosum to ENTER the skull, and supplies most of the DURA MATER

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27
Q

what does the buccal artery supply?

A

buccinator muscle and mucosa of the cheek

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28
Q

what veins communicate with/feed into the pterygoid plexus of veins?

A

receives tributaries corresponding with the branches of the maxillary vein

this plexus communicates freely with the FACIAL vein

also communicates with the CAVERNOUS SINUS by branches through the emissary foramina

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29
Q

where does the maxillary vein receive its blood from and where does it go?

A

receives venous blood from the pterygoid plexus and joins to the superficial temporal vein to form the retromandibular vein–> anterior division of the retromandibular vein joins with the facial vein and they drain into the internal jugular vein

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30
Q

where does the trigeminal nerve emerge?

A

mid pons

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31
Q

what are the three divisions of the trigeminal nerve?

A

V1–> ophthalmic

V2–> maxillary

V3–> mandibular

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32
Q

through what fissure do the following nerves pass?

  1. V1–> ophthalmic
  2. V2–> maxillary
  3. V3–> mandibular
A
  1. superior orbital fissure
  2. foramen rotundum
  3. foramen ovale
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33
Q

what does V1 (ophthalmic nerve) innervate?

A

sensory information from upper face, orbit and eye

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34
Q

what does V2 (maxillary nerve) innervate?

A

sensory information from upper teeth and midface

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35
Q

what does V3 (mandibular nerve) innervate?

A

sensory information from lower face and lower teeth

motor to muscles of mastication and proprioception of these muscles

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36
Q

list the cranial nerve nuclei associated with CN V (trigeminal)

A
  1. chief nucleus of V
  2. spinal nucleus of V
  3. mesencephalic nucleus of V
  4. motor nucleus of V
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37
Q

what nerve fibre modality is associated with the chief nucleus of V?

A

GSA

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38
Q

what nerve fibre modality is associated with the spinal nucleus of V?

A

GSA

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39
Q

what nerve fibre modality is associated with the mesencephalic nucleus of V?

A

GSA

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40
Q

what nerve fibre modality is associated with the motor nucleus of V?

A

SVE

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41
Q

what nerve tracts are associated with the chief nucleus if V?

A

second order neurons travel in the CONTRAlateral trigeminal lemniscus and terminate in the VPM of the thalamus

second order neurons from afferents from inside the mouth travel in the IPSIlateral posterior trigeminothalamic tract

**axons cross the midline and ascend as the trigeminal lemniscus to VPM of thalamus

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42
Q

what nerve tracts are associated with the spinal nucleus of V?

A

second order neurons travel in the CONTRAlateral trigeminothalamic tract, collaterals to pain modulating systems terminate in the VPM of the thalamus

**afferents enter pons and descend in the spinal tract of V which runs lateral to the spinal nucleus of V–> the spinal nucleus of V has a position and function similar to the dorsal horn of the spinal cord

**axons from spinal nucleus of V cross the midline and ascend in the trigeminothalamic tract which travels near the medial lemniscus –> this tract terminates in the VPN of the thalamus

**from the thalamus, acons pass through the internap capsule and corona radiata to terminate in the primary somatosensory cortex (post central gyrus)

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43
Q

what nerve tracts are associated with the mesencephalic nucleus of V?

A

central processes travel to the reticular formation, cerebellum, and motor nucleus of V

**peripheral processes bring in proprioceptive info–> central processes project primarily to the motor nucleus of V–> involved in REFLEX CONTROL OF BITE–> can be tested using JAW JERK reflex

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44
Q

what nerve tracts are associated with the motor nucleus of V?

A

afferents to motor neurons through bilateral innervation via corticospinal tract

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45
Q

what is the function of the chief nucleus of V?

A

discriminative touch, vibration, conscious proprioception

receives afferents carrying touch and pressure from the head

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46
Q

what is the function of the spinal nucleus of V?

A

pain and temperature from head

also receives afferents from outer ear via CN VII, IX, X

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47
Q

what is the function of the mesencephalic nucleus of V?

A

non-conscious proprioception from muscles of mastication

proprioceptive information from the muscle of mastication

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48
Q

what is the function of the motor nucleus of V?

A

motor to muscles of mastication and tensor tympani

also innervates mylohyoid and anterior belly of the digastric

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49
Q

where is the chief nucleus of V located?

A

it is a sensory nucleus located in the MID-PONS, in the posterolateral area of the tegmentum

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50
Q

where is the spinal nucleus of V located?

A

it is a sensory nucleus located as a column of cells extending from MID-PONS to C2

spinal tract and nucleus of V cause a bulge or raised area on the surface of the brainstem just lateral to the fascicular cuneatus

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51
Q

where would you find the cell bodies of the afferent fibres to the chief and spinal nuclei of V?

A

in trigeminal ganglion in the middle cranial fossa

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52
Q

where is the motor nucleus of V located?

A

in MID-PONS, medial to main sensory nucleus

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53
Q

name the 4 nuclei associated with CN VII (facial) nerve

A
  1. facial nucleus
  2. superior salivatory nucleus
  3. chief sensory trigeminal nucleus/spinal trigeminal nucleus
  4. nucleus of the solitary tract
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54
Q

what nerve fibre modality is associated with the facial nucleus?

A

SVE

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55
Q

what nerve fibre modality is associated with the superior salivatory nucleus?

A

GVE

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56
Q

what nerve fibre modality is associated with the chief sensory trigeminal nucleus/spinal trigeminal nucleus?

A

GSA

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57
Q

what nerve fibre modality is associated with the nucleus of the solitary tract?

A

SVA

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58
Q

what is the special sensory component of CN VII?

A

TASTE afferents from the anterior 2/3 of the tongue

terminate in the rostral part of the nucleus solitaris

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59
Q

what is the function of the nucleus of the solitary tract?

A

taste from anterior 2/3 of tongue

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60
Q

what is the function of the facial nucleus?

A

motor innervation to muscle of facial expression

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61
Q

where would you find the main motor nucleus of VII/the facial nucleus?

A

lies in anterolateral part of the pontine tegmentum in the caudal pons

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62
Q

what is the “genu of the facial nerve”?

A

the efferent fibres of VII from the motor/facial nucleus curve over the abducent nucleus, forming a loop known as the genu of the facial nerve

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63
Q

what is the facial colliculus?

A

the slight bulge in the floor of the fourth ventricle caused by fibres of VII looping over VI nerve nucleus

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64
Q

what is the function of the superior salivatory nucleus/secretomotor nucleus of VII?

A

parasympathetic innervation to the lacrimal, submandibular and sublingual glands

efferent fibres travel with fibres of the nevus intermedius

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65
Q

where would you find the superior salivatory nucleus/secretomotor nucleus of VII?

A

medial to the main motor nucleus of VII (facial nucleus)

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66
Q

what artery supplies the pons?

A

basilar artery

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67
Q

what artery supplies the midbrain?

A

posterior cerebral arteries

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68
Q

what artery supplies the medulla?

A

anterior spinal artery, vertebral arteries, posterior spinal arteries

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69
Q

what nerve innervates tensor veli palatini?

A

V3 (mandibular branch of V)

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70
Q

what nerve innervates levator veli palatini?

A

X

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71
Q

what is the function of levator veli palatini muscle?

A

only muscle in the pharynx that lifts the soft palate

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72
Q

name the major muscles of the soft palate

A
  1. tensor veli palatini (V3)
  2. levator veli palatini (X)
  3. palatopharyngeus (X)
  4. palatoglossus (X)
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73
Q

what is the soft palate?

A

essentially a valve that either swings up to prevent food from entering the nasopharynx while swallowing, or swings down to allow food to pass

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74
Q

define pain

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage

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75
Q

define chronic/neuropathic pain

A

pain that persists longer than the temporal course of natural healing, associated with a particular type of injury or disease process

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76
Q

name the four types of pain

A
  1. superficial pain
  2. dull, burning pain
  3. deep, visceral pain
  4. referred pain
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77
Q 
what are the characteristics of superficial pain?
1. sensation 
2. timing
3. fibre type
4. AP speed 
5 stimulus
A
  1. sharp, prickling
  2. sense with little delay, short duration
  3. myelinated pain fibres (A fibres)
  4. AP speed is 5-30 m/sec (medium conducting speed)
  5. mechanical, temperature
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78
Q

what are the characteristics of dull, burning pain?

  1. sensation
  2. timing
  3. fibre type
  4. simuli
A
  1. sensation of soreness
  2. longer lasting
  3. small, slow conducting, unmyelinated pain fibres (C fibres)
  4. mechanical, thermal, chemical
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79
Q

what are the characteristics of deep, visceral pain?

  1. sensation
  2. localization
  3. fibre type
A
  1. gives rise to aching sensation that is hard to localize
  2. arises from joints, muscles, bones, connective tissue–> produces contraction of nearby skeletal muscle generating pain
  3. unmyelinated C fibres
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80
Q

what are the characteristics of referred pain? what fibre type?

A

pain perceived at a site adjacent to or at a distance from the site of an injury’s origin

unmyelinated C fibres

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81
Q

what is adaptive pain? what are the two types?

A

adaptive pain is coupled with a noxious stimulus or healing tissue

  1. nociceptive (acute) pain–> acute pain caused by a noxious stimulus
  2. inflammatory pain–> increased sensitivity to prevent contact with or movement of the injured part until repair is complete
82
Q

what is maladaptive pain? what are the two types?

A

maladaptive pain is pain uncoupled from noxious stimuli or healing

  1. neuropathic pain–> pain occurring in response to damage to the nervous system (can be central or peripheral)
  2. functional pain–> pain occurring in response to abnormal operation of the nervous system
83
Q

what is chronic pain?

A

typically represented as INFLAMMAORY or NEUROPATHIC in origin

characterized by enhanced PERCEPTION of pain to a nociceptive stimulus (i.e hyperalgesia) and the novel perception of a normal innocuous stimulus as being painful (i.e allodynia)

84
Q

what is meant by the term “peripheral sensitization”?

A

a reduction in the threshold, and an increase in the responsiveness of nociceptors (i.e change in heat sensitivity after a sunburn)

85
Q

why does peripheral sensitization occur?

A

occurs due to the action of inflammatory chemicals or modulators (i.e bradykinin, ACh, serotonin, substance P) released around the site of tissue damage or inflammation

86
Q

what are some processes implicated in peripheral sensitivity?

A
  1. changes to existing nociceptive receptors (post translational processing) –> involves addition of a PHOSPHATE group to receptors which lowers the threshold at which they open and makes the channel open for longer (so any stimulus will evoke a greater response)
  2. changes to proteins being made by the nociceptor (altered transcription and thus gene expression)–> signals are transported back to the cell body of sensory neurons in the DRG where they either change transcription or change translation –> increase proteins are shipped back down to the terminals where they contribute to increase responsiveness of the terminal to peripheral stimuli
87
Q

what is meant by the term “central sensitization”?

A

an increase in the excitability of neurons WITHIN the CNS, so that normal inputs begin to produce abnormal responses

contributes to hyper-responsive conditions of post-operative pain, migraine, neuropathic pain, fibromyalgia, GI tract pain

88
Q

what are the 4 phases involved in central sensitization?

A
  1. acute phase
  2. persistent phase (gene regulation)
  3. persistent phase (disinhibition)
  4. persistent phase (structural reorganization)
89
Q

what happens int he acute phase of central sensitization?

A

normal synaptic transmission occurs via the activation of AMPA channels by GLUTAMATE, while NMDA receptors (that also bind to glutamate) are typically BLOCKED by Mg

following injury–> summation of synaptic inputs from
activation of nociceptors results in REMOVAL OF THE Mg BLOCK of NMDA receptors increasing the sensitivity to glutamate

during central sensitization, POSTSYNAPTIC receptors are PHOSPHORYLATED–> this increases their recruitment to the synaptic membrane, enhances receptor kinetics (channel is open longer) and decreases receptor threshold (requires lower stimulus to open)

together, you get a WIND-UP–> progressive increase in the discharge of dorsal horn neurons in response to repeated low-frequency activation of nociceptors

90
Q

what happens in the persistent phase (gene regulation) of central sensitization?

A

upregulation of genes encoding receptors locally

upregulation of genes globally (i.e COX2 is expressed in neurons in many areas of the CNS several hours after a localized peripheral tissue injury… this expression is initiated by a circulating factor released by inflammatory cells… results in increase of PGE2 which facilitates synaptic transmission and excitability)

91
Q

what happens in the persistent phase (disinhibition) of central sensitization?

A

inhibitory interneurons in the spinal cord act pre and post synaptically to focus sensory input so it produces a limited, appropriate, and brief response to any input

loss of inhibition can also lead to increased excitability and pain

92
Q

what happens in the persistent phase (structural reorganization) of central sensitization?

A

after nerve injury, the central nerve terminals of C-fibres atrophy creating vacant synaptic sites

interneurons also die

AB fibres sprout and form novel synapses in lamina which creates inappropriate functional connections leading to persistent hypersensitivity and phenotype conversion (i.e touch leads to pain sensation)

93
Q

what are the first line pharmaceutical agents used in the treatment of chronic pain?

A

tricyclic antidepressants and anticonvulsants

94
Q

what are the second line pharmaceutical agents used in the treatment of chronic pain?

A

SSNRIs and topical lidocaine

95
Q

what are the third and fourth line treatments used in the treatment of chronic pain?

A

opioid analgesics, tramadol, SSRIs, IV lidocaine and mexilitine, topical capsaicin, cannabinoids, NMDA receptor antagonists

96
Q

name four TCAs

A

secondary amines–> nortriptyline and desipramine

tertiary amines–> amitriptyline and imipramine

97
Q

in what types of pain are TCAs most effective?

A

most effective in DIABETIC NEUROPATHY and POST-HERPETIC NEURALGIA as well as relief of concomitant symptoms like sleep disorder, anxiety disorder and depression

98
Q

what is the MOA of TCAs when used in the tx of chronic pain?

A

serotonin and NE reuptake inhibition

increases endogenous inhibition by increasing descending pathway transmission

analgesia dose is lower than the antidepressant dose–> analgesia effect is almost immediate (unlike the several week wait for antidepressant effect)

99
Q

what are some side effects of TCA use for chronic pain?

A

anticholinergic effects–> dry mouth, blurred vision, constipation, urinary retention

CVS effects–> postural hypotension (due to alpha adrenoreceptor blockage–> avoid in the elderly), conduction delay and myocaridal depression

100
Q

which are generally better tolerated, secondary or tertiary amines?

A

secondary

nortriptyline and desipramine

101
Q

name two drugs used in the tx of chronic pain that are calcium channel alpha 2-delta ligands

A

gapapentin

pregabalin

102
Q

what is the MOA of the calcium channel alpha 2-delta ligands gapapentin and pregabalin?

A

binds to alpha 2 and delta 1 calcium channels–> reduces the release of glutamate, NE, substance P and CGRP

103
Q

in what types of pain would you use calcium channel alpha 2-delta ligands gapapentin and pregabalin as treatment?

A

used in chronic neuropathic pain (diabetic neuropathy, post herpetic neuralgia, MS, cancer related neuropathic pain)

pregabalin has a more linear pharmacokinetic profile than gabapentin

104
Q

what are some side effects of calcium channel alpha 2-delta ligands gapapentin and pregabalin?

A

generally well tolerated

few SEs: dizziness, somnolence (drowsiness), confusion, ataxia

105
Q

what type of drug is carbamazepine?

A

anticonvulsant

106
Q

what is the drug of first choice in the tx of trigeminal neuralgia (tic doloreux)?

A

carbamazepine

107
Q

in what type of pain is carbamazepine the drug of first choice?

A

tic doloreux/trigeminal neuralgia

108
Q

what is the MOA of carbamazepine in the tx of chronic pain?

A

unclear

may act by blocking Na+ channels

109
Q

SEs of carbamazepine

A

dizziness, ataxia, nausea, hepatitis, aplastic anemia, Stevens-Johnson syndrome

110
Q

name 3 other anticonvulsants that can be used in the tx of chronic pain

A

lamotrigine
valproic acid
topiramate

111
Q

how do anticonvulsants work to treat chronic pain?

A

MOA is unclear

may work by blocking Na+ channels

112
Q

other than in trigeminal neuralgia, when should you use anticonvulsants int he tx of chronic pain?

A

in other pain syndromes, do not use until other interventions have been tried

113
Q

MOA of lidocane?

A

inhibits fast Na+ channels

114
Q

what is the MOA of tramadol?

A

it is a synthetic opioid with weak u-agonist activity–> inhibits serotonin and NE re-uptake –> peripheral LOCAL anaesthetic

115
Q

in what types of pain is tramadol effective?

A

post-herpetic neuralgia, diabetic neuropathy, polyneuropathies and POST-AMPUTATION pain

116
Q

what are some advantages of tramadol?

A

relative lack of respiratory depression, major organ toxicity, depression of GI motility

relatively low abuse potential

117
Q

what is the disadvantage of tramadol?

A

reduces seizure threshold

118
Q

what is capsaicin?

A

active ingredient in red hot chilli peppers

119
Q

in what types of pain is capsaicin effective?

A

diabetic neuropathy and post-herpetic neuralgia

120
Q

MOA of capsaicin in the tx of pain?

A

depletion of substance P in C fibres–> nociceptor desensitization

121
Q

what is an adverse event associated with capsaicin?

A

local burning sensation and erythema (cessation after 3-4 weeks of analgesic effect)

122
Q

what is the drug derived from cannabinoids used in the treatment of chronic pain?

A

delta-9-tetrahydrocannabinol (buccal spray)

123
Q

in what type of pain are cannabinoids used?

A

effective in reducing pain and sleep disturbance in the central pain of MS

124
Q

SEs of cannabinoids?

A

dizziness, fatigue, nausea, euphoria and potential for the precipitation of psychosis

*causes urine to be positive in cannabinoids drug tests

125
Q

what are primary headaches?

A

no structural or pathological cause

126
Q

what are the three types of primary headache?

A

tension type

migraine

cluster

also: sinus headache, paroxysmal headaches, chronic daily headache, medication overuse headache and cervicogenic headache

127
Q

what are the symptoms of a migraine?

A

unilateral

worse with exertion

throbbing

moderate to severe intensity

may have nausea or symptoms sensitivity

128
Q

what is aura?

A

can be associated with migraine

duration of less than 60 min, followed by headache

visual (central scotoma), sensory and cognitive manifestations

129
Q

what are some migraine triggers?

A

menstruation

food (chocolate, cheese)

weather

oversleeping

odours

post-stress

130
Q

who generally gets migraines?

A

females in the western world

131
Q

how “serious” are migraines?

A

considered to be one of the most disabling chronic disorders

132
Q

what are the symptoms of a tension type headache?

A

mild, non-pulsating, generalized pressure, not aggravated by activity, no nausea or photophobia

episodic synonymous with mild migraine

chronic may be due to central sensitization

133
Q

what is a sinus headache?

A

a type of migraine characterized by recurrent frontal headache and nasal stuffiness

134
Q

how common is cluster headache?

A

very rare

135
Q

what are the symptoms of cluster headache?

A

unilateral orbital pain of short duration

nocturnal episodes occurring in clusters

may also have red eyes, tearing, nasal congestion, ptosis

136
Q

what is the treatment for cluster headache?

A

aggressive

use preventative drugs (verapamil) with or without steroids until two weeks of headache free

acute therapy is provided by DHE, sumatriptan or oxygen inhalation

137
Q

what are paroxysmal headaches?

A

short lasting

cough, post-coital, exercise induced

chronic hemicrania all different types

138
Q

what is chronic daily headache?

A

lasts more than 4 hours, more than 15 days a month for more than 6 months

can be a transformational migraine, post-traumatic, chronic tension type, new daily persistent

139
Q

what is a medication overuse headache?

A

tolerance to pain meds with withdrawal headache, diffuse, bilateral, daily

treatment involves drug withdrawal, behavioural modification, regimented plan and prophylaxis

140
Q

what is a cervicogenic headache?

A

pain in neck with referred pain to head

141
Q

what is the vascular theory of migraine pathophysiology?

A

vasoconstriction produces aura with rebound vasodilation and nociceptive activation causing headache

142
Q

what is the neurovascular theory of migraine pathophysiology?

A

baseline neuroexcitability in occipital cortex leading to vulnerability to develop migraines

143
Q

what is cutaneous allodynia?

A

migraine produces stimulation of secondary pain pathways in the trigeminothalamic pathway, mainly due to central sensitization

144
Q

what is cortical spreading depolarization?

A

associated with migraine pathophysiology

wave of neuronal excitation spreads through grey matter producing aura followed by a wave of neurosuppression–> wave of excitement activates trigeminal nucleus caudalis causing headache–> CN V activation causes vasodilation with release of substance P, CGRP (peripheral sensitization) leading to further dilation–> central sensitization occurs secondary to peripheral sensitization

145
Q

how is brainstem activation related to migraine pathophysiology?

A

PET has shown brainstem activation just before migraine onset

146
Q

what might the mechanism of the vasoconstriction suspected in migraine pathophysiology happen?

A

magnesium deficiency–> glutamate release–> 5-HT release–> vasoconstriction

147
Q

how are dopamine and migraines related?

A

dopaminergic hypersensitivity has been linked to migraine

148
Q

what are secondary headaches?

A

trauma, vascular disease, tumour, infection, CSF pressure, drugs, metabolic disorders

149
Q

what are the steps in migraine management and treatment?

A
  1. identification and avoidance of triggering factors
  2. safe and effective acute therapy
  3. migraine prophylaxis
150
Q

what are some non-pharmacological acute therapies for migraine?

A

cold and pressure to cause vasoconstriction and decrease blood flow

rest in quiet, dark atmosphere to reduce environmental stimuli

151
Q

what are some symptomatic agents used for acute migraine tx?

A

simple and combination analgesics, NSAIDs, opioids

152
Q

what are some specific agents used for acute migraine tx?

A
  1. ergotamine–> vasoconstrictor
  2. dihydroergotamine (DHE)–> vasoconstrictor
  3. triptans–> decreases transmission, vasoconstriction, modulation at the trigeminal nucleus caudalis in the brain stem
153
Q

what is ergotamine?

A

vasoconstrictor used as acute tx for migraines

154
Q

what is dihydroergotamine (DHE)?

A

vasoconstrictor used as acute tx for migraines

155
Q

what are triptans?

A

used for acute tx of migraines

decreases transmission (i.e decreases release of vasoactive peptides CGRP, substance P etc)

vasoconstriction

modulation at the trigeminal nucleus caudalis in the brainstem

156
Q

name two triptans

A

sumatriptan and naratriptan

157
Q

what is the step-wise drug therapy model for migraine tx?

A
  1. mild attacks–> aspirin or NSAIDs
  2. moderate attacks–> triptans, combination analgesics/opioids
  3. severe attacks–> triptans, opioids for rescue
158
Q

why are migraine prophylaxis attempts a last resort?

A

because they typically do not work very well

159
Q

what are some non pharmacological methods of migraine prophylaxis?

A

relaxation training

biofeedback (i.e neuromuscular)

CBT

160
Q

what are some pharmacological agents that can be used as migraine prophylaxis?

A

beta blockers

calcium channel blockers

TCAs

serotonergic agents

anticonvulsants

neurotoxins (for chronic migraines)

161
Q

How do you treat cluster headaches?

A

aggressive approach

start preventative agent, with or without prednisone

use acute agents from breakthrough headaches

treat until two weeks headache free then start to wean off drugs

162
Q

what is acute therapy for cluster headaches?

A

sumatriptan (gold standard), oxygen therapy, DHE

163
Q

what is preventative tx for cluster headaches?

A

verapamil (calcium channel blocker), prednisone

164
Q

how do you manage and treat a medical overuse headache?

A

stop causative drug

break headache cycle and treat withdrawal

modify behaviours to prevent patient from taking inciting drug to treat headache

offer a clear acute treatment plan, prophylaxis and follow up

165
Q

name two drugs used in the prophylaxis of chronic migraines

A

topiramate (anticonvulsant)

onabotulinumtoxin A (blocks peripheral sensitization)

166
Q

what are some important aspects to ask about on the history of a patient with chronic or neuropathic pain?

A
  1. quality–> burning, hot or cold, “icy hot”, “pins and needles”, stinging, lancinating, sharp, shooting
  2. distribution of symptoms may aid in localization–> i.e stocking and glove in generalized neuropathy, numbness in a peripheral nerve territory in focal neuropathy
  3. large fibre neuropathy–> coexisting numbness, hyporeflexia, or weakness may be seen, usually worse distally
  4. spinal cord sx–> coexisting spasticity, bowel or bladder involvement, sensory level
  5. nerve root–> coexisting neck or low back pain that radiates along a specific dermatome–> most common cause distally
  6. prior history of thalamic stroke in central thalamic pain syndrome (dejerine-roussy syndrome)
  7. family hx may suggest a genetic cause
167
Q

what are the usual signs and symptoms of neuropathic pain?

A

typically has an unusual burning, tingling or electric shock like quality and may be triggered by very light touch

these features are rare in other types of pain

on exam a sensory deficit is characteristically present in the area of the patients pain–> hyperalgesia and allodynia may be noted

168
Q

what type of nerve fibres carry superficial pain that feels sharp and pricking?

A

A-delta fibres (so its fast because these fibres are myelinated, unlike other types of pain)

169
Q

what are the two types of superficial pain?

A

sharp and pricking (carried by myelinated A-delta fibres)

dull and burning (carried by unmyelinated C fibres)

170
Q

what type of pain is easiest to localize? why?

A

the sharp, fast type (mediated by A-delta fibres) can be localized much more exactly in the different parts of the body than the slow-long-lasting pain (mediated by C fibres)

if only pain receptors are stimulated, without simultaneous stimulation of tactile receptors, the pain is very poorly localized (even pain mediated by A-delta fibres can only be localized within 10 cm of the stimulated area) –> when tactile receptors are also stimulated, the localization can be very exact

171
Q

what is fibromyalgia?

A

“functional maladaptive pain”

medically unexplained syndrome with no cure or universally-accepted treatment

characterized by chronic widespread pain and allodynia

muscle and connective tissue pain (but with a wide range of symptoms

  • myofascial pain, fatigue, twitches
  • chest pain
  • nausea
  • problems urinating
  • dysmenorrhea
  • pain, weight gain, cold sx, multiple chemical sensitivity
  • chronic headaches, sleep disorders, dizziness, cognitive impairment, memory impairment, anxiety, depression
  • vision problems
172
Q

what are the two major challenges in pain management?

A
  1. to ID the mechanisms responsible for producing hypersensitivity to pain
  2. to find a means of normalizing sensitivity or preventing hypersensitivity from becoming established
173
Q

what does “sensitization” mean in the context of pain?

A

an increase in the excitability of neurons i.e neurons are more sensitive to stimuli or sensory inputs

174
Q

what are the most potent pain producing substances?

A

kinins

i.e bradykinin

produced by proleolytic breakdown of kininogens in area of wound

175
Q

what is the gate theory of pain transmission?

A

states that the transmission of pain from the peripheral nerve through the spinal cord can be modulated by

  1. other afferent neurons
  2. controls emanating from the brain

the effect of transcutaneous electrical stimulation (TENS) presumably is due to this effect–> in these devices, weak electrical current is applied to the skin near the site of pain–> believed to stimulate the A-beta fibres and reduce the flow of pain information to the brain

176
Q

what is transcutaneous electrical stimulation (TENS)?

A

n these devices, weak electrical current is applied to the skin near the site of pain–> believed to stimulate the A-beta fibres and reduce the flow of pain information to the brain

177
Q

what is phenotype conversion?

A

i.e when touch leads to sensation of pain

likely due to structural reorganization phase of central sensitization as A-beta fibres sprout and form novel synapses in lamina II which creates inappropriate functional connections (replace C fibres that have atrophied)

178
Q

what are causes of primary headache?

A

migraine (episodic and chronic)

tension type headache

trigeminal autonomic cephalgia (TACs)

179
Q

what are causes of secondary headache?

A

head and neck trauma

extra cranial

vascular disease

tumour

infection

abnormal CSF pressure

drugs

180
Q

what are some important factors to find out on history for headache?

A

age of onset

headache characteristics

associated sx

neuro symptoms

trigger factors

changes over time

181
Q

if a patient has symptoms of migraine and no seizures, do you need to do imaging?

A

no because you wont find anything

182
Q

what symptoms do you need to be diagnosed with episodic migraine?

A

2 of:

  • unilateral location
  • throbbing quality
  • worse with exertion
  • moderate to severe intensity

1 of:

  • nausea or vomiting
  • stimulus sensitivity

5 attacks plus 1 year history plus normal exam–> migraine without aura

183
Q

what are visual aura symptoms?

A

photopsia

scintillations

central scotoma

peripheral field loss

184
Q

if a headache is associated with menstruation, what is it?

A

MIGRAINE

you dont even have to ask about associated symptoms–> many women will also get one with ovulation, associated with the drop in estrogen

185
Q

what sex is more affected by migraines?

A

women

186
Q

what % of people with chronic migraines are overusing medications?

A

50%

187
Q

what are trigeminal autonomic cephalgias? (TACs)

A

cluster headache

ice pick headache

cough headache

coital headache

benign exertional headache

chronic paroxysmal hemicrania

188
Q

list the associated autonomic symptoms (unilateral) associated with cluster headache

A
  1. conjunctival injection
  2. tearing
  3. rhinorrhea and nasal congestion
  4. ptosis and miosis
189
Q

what is calcitonin gene-related peptide (CGRP)?

A

main sensory neuropeptide released (along with glutamate) by activated trigeminal neurons

physiological actions:
vasodilation
mast cell degranulation
sensory transmission

190
Q

how is CGRP related to migraine?

A

released during and triggers migraine attacks

CGRP infusion triggers migraine

CGRP levels are normalized by triptans

CGRP blockade at key sites (i.e TNC, PAG, thalamus) is effective in preclinical models of migraine pain

there are currently 4 MAbs in development against CGRP

191
Q

list emotional stress triggers for migraine

A 
stress
relaxation
anxiety 
depression
emotion
excitement
192
Q

list physical stress triggers for migraine

A 
exercise
fatigue
hunger
lack of sleep
oversleeping
193
Q

list external stimuli triggers for migraine

A 
climate
high altitude
heat
odours
noise
glare
194
Q

list dietary and hormonal triggers for migraine

A 
chocolate
cheese
alcohol
OCPs
menstruation
pregnancy
menopause
195
Q

what drugs may be given as adjuctive therapy in addition to triptans in the treatment of migraine?

A

NSAID (naproxen)

anti-emetic (metoclopramide)

196
Q

how does botox/onabotulinumtoxin A work to treat chronic migraine?

A

when used for the phrophylaxis of headaches in adults with chronic migraine, botox acts as an inhibitor of neurotransmitters associated with the genesis of pain

presumed mechanism for headache prophylaxis works by blocking the peripheral signals to the CNS, which inhibits central sensitization and this is confirmed by pre-clinical and clinical studies

197
Q

define chronic pain

A

pain lasting greater than 3-6 months

pain that persists beyond what would reasonably be expected from an injury, surgery or other disease

persistent pain that is not amenable to treatments based on specific remedies or to the routine methods of pain control

198
Q

what is the economic impact of chronic pain?

A

chronic and acute pain cost our society more than cancer and heart disease combined

199
Q

what is causalgia?

A

a syndrome of sustained burning pain, allodynia and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes

200
Q

what is neuralgia?

A

pain in the distribution of a nerve or nerve

201
Q

briefly describe the pathophysiology of central sensitization

A

from dr. schwartz notes

  1. sensitization of nociceptors
  2. unmasking of silent nociceptors
  3. collateral sprouting
  4. increased activity of damaged axons and their sprouts
  5. abnormal firing of damaged axons and their sprouts
  6. DRG invasion by sympathetic fibres
  7. phenotype switch

B&B Part 2 (5 decks)

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