B&B Week 6 Flashcards
(201 cards)
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
2
Q
what separates the temporal and infratemporal fossae?
A
zygomatic arch
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
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
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
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
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
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)
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).
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
11
Q
what are the sensory branches of the mandibular nerve (V3) and what is their route?
A
- 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
- 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
- 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
- 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
12
Q
where is the otic ganglion located?
A
just inferior to the foramen ovale and just medial to the mandibular nerve
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
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
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
16
Q
what is found in the temporal fossa?
A
temporalis muscle, V2 branches, deep temporal nerves and arteries (motor) and middle temporal artery
17
Q
name the four muscles of mastication
A
temporalis
masseter
medial pterygoid
lateral pterygoid
18
Q
what nerve innervates the muscles of mastication?
A
V3 branch (mandibular) of trigeminal
19
Q
what does the temporalis muscle do?
A
elevation and retraction of mandible
20
Q
what does the masseter muscle do?
A
elevation of mandible
21
Q
what does the medial pterygoid muscle do?
A
elevation and side to side movements of the mandible
22
Q
what does the lateral pterygoid muscle do?
A
protrusion and side to side movements of the mandible
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
24
Q
name the four branches of the maxillary artery
A
- inferior alveolar artery
- middle meningeal artery
- buccal artery
- numerous small muscular branches
25
what does the inferior alveolar artery supply?
supplies all the lower jaw teeth
26
what does the middle meningeal artery supply?
passes thru the foramen spinosum to ENTER the skull, and supplies most of the DURA MATER
27
what does the buccal artery supply?
buccinator muscle and mucosa of the cheek
28
what veins communicate with/feed into the pterygoid plexus of veins?
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
29
where does the maxillary vein receive its blood from and where does it go?
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
30
where does the trigeminal nerve emerge?
mid pons
31
what are the three divisions of the trigeminal nerve?
V1--> ophthalmic
V2--> maxillary
V3--> mandibular
32
through what fissure do the following nerves pass?
1. V1--> ophthalmic
2. V2--> maxillary
3. V3--> mandibular
1. superior orbital fissure
2. foramen rotundum
3. foramen ovale
33
what does V1 (ophthalmic nerve) innervate?
sensory information from upper face, orbit and eye
34
what does V2 (maxillary nerve) innervate?
sensory information from upper teeth and midface
35
what does V3 (mandibular nerve) innervate?
sensory information from lower face and lower teeth
motor to muscles of mastication and proprioception of these muscles
36
list the cranial nerve nuclei associated with CN V (trigeminal)
1. chief nucleus of V
2. spinal nucleus of V
3. mesencephalic nucleus of V
4. motor nucleus of V
37
what nerve fibre modality is associated with the chief nucleus of V?
GSA
38
what nerve fibre modality is associated with the spinal nucleus of V?
GSA
39
what nerve fibre modality is associated with the mesencephalic nucleus of V?
GSA
40
what nerve fibre modality is associated with the motor nucleus of V?
SVE
41
what nerve tracts are associated with the chief nucleus if V?
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
42
what nerve tracts are associated with the spinal nucleus of V?
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)
43
what nerve tracts are associated with the mesencephalic nucleus of V?
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
44
what nerve tracts are associated with the motor nucleus of V?
afferents to motor neurons through bilateral innervation via corticospinal tract
45
what is the function of the chief nucleus of V?
discriminative touch, vibration, conscious proprioception
receives afferents carrying touch and pressure from the head
46
what is the function of the spinal nucleus of V?
pain and temperature from head
also receives afferents from outer ear via CN VII, IX, X
47
what is the function of the mesencephalic nucleus of V?
non-conscious proprioception from muscles of mastication
proprioceptive information from the muscle of mastication
48
what is the function of the motor nucleus of V?
motor to muscles of mastication and tensor tympani
also innervates mylohyoid and anterior belly of the digastric
49
where is the chief nucleus of V located?
it is a sensory nucleus located in the MID-PONS, in the posterolateral area of the tegmentum
50
where is the spinal nucleus of V located?
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
51
where would you find the cell bodies of the afferent fibres to the chief and spinal nuclei of V?
in trigeminal ganglion in the middle cranial fossa
52
where is the motor nucleus of V located?
in MID-PONS, medial to main sensory nucleus
53
name the 4 nuclei associated with CN VII (facial) nerve
1. facial nucleus
2. superior salivatory nucleus
3. chief sensory trigeminal nucleus/spinal trigeminal nucleus
4. nucleus of the solitary tract
54
what nerve fibre modality is associated with the facial nucleus?
SVE
55
what nerve fibre modality is associated with the superior salivatory nucleus?
GVE
56
what nerve fibre modality is associated with the chief sensory trigeminal nucleus/spinal trigeminal nucleus?
GSA
57
what nerve fibre modality is associated with the nucleus of the solitary tract?
SVA
58
what is the special sensory component of CN VII?
TASTE afferents from the anterior 2/3 of the tongue
terminate in the rostral part of the nucleus solitaris
59
what is the function of the nucleus of the solitary tract?
taste from anterior 2/3 of tongue
60
what is the function of the facial nucleus?
motor innervation to muscle of facial expression
61
where would you find the main motor nucleus of VII/the facial nucleus?
lies in anterolateral part of the pontine tegmentum in the caudal pons
62
what is the "genu of the facial nerve"?
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
63
what is the facial colliculus?
the slight bulge in the floor of the fourth ventricle caused by fibres of VII looping over VI nerve nucleus
64
what is the function of the superior salivatory nucleus/secretomotor nucleus of VII?
parasympathetic innervation to the lacrimal, submandibular and sublingual glands
efferent fibres travel with fibres of the nevus intermedius
65
where would you find the superior salivatory nucleus/secretomotor nucleus of VII?
medial to the main motor nucleus of VII (facial nucleus)
66
what artery supplies the pons?
basilar artery
67
what artery supplies the midbrain?
posterior cerebral arteries
68
what artery supplies the medulla?
anterior spinal artery, vertebral arteries, posterior spinal arteries
69
what nerve innervates tensor veli palatini?
V3 (mandibular branch of V)
70
what nerve innervates levator veli palatini?
X
71
what is the function of levator veli palatini muscle?
only muscle in the pharynx that lifts the soft palate
72
name the major muscles of the soft palate
1. tensor veli palatini (V3)
2. levator veli palatini (X)
3. palatopharyngeus (X)
4. palatoglossus (X)
73
what is the soft palate?
essentially a valve that either swings up to prevent food from entering the nasopharynx while swallowing, or swings down to allow food to pass
74
define pain
unpleasant sensory and emotional experience associated with actual or potential tissue damage
75
define chronic/neuropathic pain
pain that persists longer than the temporal course of natural healing, associated with a particular type of injury or disease process
76
name the four types of pain
1. superficial pain
2. dull, burning pain
3. deep, visceral pain
4. referred pain
77
```
what are the characteristics of superficial pain?
1. sensation
2. timing
3. fibre type
4. AP speed
5 stimulus
```
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
78
what are the characteristics of dull, burning pain?
1. sensation
2. timing
3. fibre type
4. simuli
1. sensation of soreness
2. longer lasting
3. small, slow conducting, unmyelinated pain fibres (C fibres)
4. mechanical, thermal, chemical
79
what are the characteristics of deep, visceral pain?
1. sensation
2. localization
3. fibre type
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
80
what are the characteristics of referred pain? what fibre type?
pain perceived at a site adjacent to or at a distance from the site of an injury's origin
unmyelinated C fibres
81
what is adaptive pain? what are the two types?
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
what is maladaptive pain? what are the two types?
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
what is chronic pain?
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
what is meant by the term "peripheral sensitization"?
a reduction in the threshold, and an increase in the responsiveness of nociceptors (i.e change in heat sensitivity after a sunburn)
85
why does peripheral sensitization occur?
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
what are some processes implicated in peripheral sensitivity?
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
what is meant by the term "central sensitization"?
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
what are the 4 phases involved in central sensitization?
1. acute phase
2. persistent phase (gene regulation)
3. persistent phase (disinhibition)
4. persistent phase (structural reorganization)
89
what happens int he acute phase of central sensitization?
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
what happens in the persistent phase (gene regulation) of central sensitization?
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
what happens in the persistent phase (disinhibition) of central sensitization?
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
what happens in the persistent phase (structural reorganization) of central sensitization?
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
what are the first line pharmaceutical agents used in the treatment of chronic pain?
tricyclic antidepressants and anticonvulsants
94
what are the second line pharmaceutical agents used in the treatment of chronic pain?
SSNRIs and topical lidocaine
95
what are the third and fourth line treatments used in the treatment of chronic pain?
opioid analgesics, tramadol, SSRIs, IV lidocaine and mexilitine, topical capsaicin, cannabinoids, NMDA receptor antagonists
96
name four TCAs
secondary amines--> nortriptyline and desipramine
tertiary amines--> amitriptyline and imipramine
97
in what types of pain are TCAs most effective?
most effective in DIABETIC NEUROPATHY and POST-HERPETIC NEURALGIA as well as relief of concomitant symptoms like sleep disorder, anxiety disorder and depression
98
what is the MOA of TCAs when used in the tx of chronic pain?
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
what are some side effects of TCA use for chronic pain?
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
which are generally better tolerated, secondary or tertiary amines?
secondary
| nortriptyline and desipramine
101
name two drugs used in the tx of chronic pain that are calcium channel alpha 2-delta ligands
gapapentin
pregabalin
102
what is the MOA of the calcium channel alpha 2-delta ligands gapapentin and pregabalin?
binds to alpha 2 and delta 1 calcium channels--> reduces the release of glutamate, NE, substance P and CGRP
103
in what types of pain would you use calcium channel alpha 2-delta ligands gapapentin and pregabalin as treatment?
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
what are some side effects of calcium channel alpha 2-delta ligands gapapentin and pregabalin?
generally well tolerated
few SEs: dizziness, somnolence (drowsiness), confusion, ataxia
105
what type of drug is carbamazepine?
anticonvulsant
106
what is the drug of first choice in the tx of trigeminal neuralgia (tic doloreux)?
carbamazepine
107
in what type of pain is carbamazepine the drug of first choice?
tic doloreux/trigeminal neuralgia
108
what is the MOA of carbamazepine in the tx of chronic pain?
unclear
may act by blocking Na+ channels
109
SEs of carbamazepine
dizziness, ataxia, nausea, hepatitis, aplastic anemia, Stevens-Johnson syndrome
110
name 3 other anticonvulsants that can be used in the tx of chronic pain
lamotrigine
valproic acid
topiramate
111
how do anticonvulsants work to treat chronic pain?
MOA is unclear
may work by blocking Na+ channels
112
other than in trigeminal neuralgia, when should you use anticonvulsants int he tx of chronic pain?
in other pain syndromes, do not use until other interventions have been tried
113
MOA of lidocane?
inhibits fast Na+ channels
114
what is the MOA of tramadol?
it is a synthetic opioid with weak u-agonist activity--> inhibits serotonin and NE re-uptake --> peripheral LOCAL anaesthetic
115
in what types of pain is tramadol effective?
post-herpetic neuralgia, diabetic neuropathy, polyneuropathies and POST-AMPUTATION pain
116
what are some advantages of tramadol?
relative lack of respiratory depression, major organ toxicity, depression of GI motility
relatively low abuse potential
117
what is the disadvantage of tramadol?
reduces seizure threshold
118
what is capsaicin?
active ingredient in red hot chilli peppers
119
in what types of pain is capsaicin effective?
diabetic neuropathy and post-herpetic neuralgia
120
MOA of capsaicin in the tx of pain?
depletion of substance P in C fibres--> nociceptor desensitization
121
what is an adverse event associated with capsaicin?
local burning sensation and erythema (cessation after 3-4 weeks of analgesic effect)
122
what is the drug derived from cannabinoids used in the treatment of chronic pain?
delta-9-tetrahydrocannabinol (buccal spray)
123
in what type of pain are cannabinoids used?
effective in reducing pain and sleep disturbance in the central pain of MS
124
SEs of cannabinoids?
dizziness, fatigue, nausea, euphoria and potential for the precipitation of psychosis
*causes urine to be positive in cannabinoids drug tests
125
what are primary headaches?
no structural or pathological cause
126
what are the three types of primary headache?
tension type
migraine
cluster
also: sinus headache, paroxysmal headaches, chronic daily headache, medication overuse headache and cervicogenic headache
127
what are the symptoms of a migraine?
unilateral
worse with exertion
throbbing
moderate to severe intensity
may have nausea or symptoms sensitivity
128
what is aura?
can be associated with migraine
duration of less than 60 min, followed by headache
visual (central scotoma), sensory and cognitive manifestations
129
what are some migraine triggers?
menstruation
food (chocolate, cheese)
weather
oversleeping
odours
post-stress
130
who generally gets migraines?
females in the western world
131
how "serious" are migraines?
considered to be one of the most disabling chronic disorders
132
what are the symptoms of a tension type headache?
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
what is a sinus headache?
a type of migraine characterized by recurrent frontal headache and nasal stuffiness
134
how common is cluster headache?
very rare
135
what are the symptoms of cluster headache?
unilateral orbital pain of short duration
nocturnal episodes occurring in clusters
may also have red eyes, tearing, nasal congestion, ptosis
136
what is the treatment for cluster headache?
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
what are paroxysmal headaches?
short lasting
cough, post-coital, exercise induced
chronic hemicrania all different types
138
what is chronic daily headache?
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
what is a medication overuse headache?
tolerance to pain meds with withdrawal headache, diffuse, bilateral, daily
treatment involves drug withdrawal, behavioural modification, regimented plan and prophylaxis
140
what is a cervicogenic headache?
pain in neck with referred pain to head
141
what is the vascular theory of migraine pathophysiology?
vasoconstriction produces aura with rebound vasodilation and nociceptive activation causing headache
142
what is the neurovascular theory of migraine pathophysiology?
baseline neuroexcitability in occipital cortex leading to vulnerability to develop migraines
143
what is cutaneous allodynia?
migraine produces stimulation of secondary pain pathways in the trigeminothalamic pathway, mainly due to central sensitization
144
what is cortical spreading depolarization?
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
how is brainstem activation related to migraine pathophysiology?
PET has shown brainstem activation just before migraine onset
146
what might the mechanism of the vasoconstriction suspected in migraine pathophysiology happen?
magnesium deficiency--> glutamate release--> 5-HT release--> vasoconstriction
147
how are dopamine and migraines related?
dopaminergic hypersensitivity has been linked to migraine
148
what are secondary headaches?
trauma, vascular disease, tumour, infection, CSF pressure, drugs, metabolic disorders
149
what are the steps in migraine management and treatment?
1. identification and avoidance of triggering factors
2. safe and effective acute therapy
3. migraine prophylaxis
150
what are some non-pharmacological acute therapies for migraine?
cold and pressure to cause vasoconstriction and decrease blood flow
rest in quiet, dark atmosphere to reduce environmental stimuli
151
what are some symptomatic agents used for acute migraine tx?
simple and combination analgesics, NSAIDs, opioids
152
what are some specific agents used for acute migraine tx?
1. ergotamine--> vasoconstrictor
2. dihydroergotamine (DHE)--> vasoconstrictor
3. triptans--> decreases transmission, vasoconstriction, modulation at the trigeminal nucleus caudalis in the brain stem
153
what is ergotamine?
vasoconstrictor used as acute tx for migraines
154
what is dihydroergotamine (DHE)?
vasoconstrictor used as acute tx for migraines
155
what are triptans?
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
name two triptans
sumatriptan and naratriptan
157
what is the step-wise drug therapy model for migraine tx?
1. mild attacks--> aspirin or NSAIDs
2. moderate attacks--> triptans, combination analgesics/opioids
3. severe attacks--> triptans, opioids for rescue
158
why are migraine prophylaxis attempts a last resort?
because they typically do not work very well
159
what are some non pharmacological methods of migraine prophylaxis?
relaxation training
biofeedback (i.e neuromuscular)
CBT
160
what are some pharmacological agents that can be used as migraine prophylaxis?
beta blockers
calcium channel blockers
TCAs
serotonergic agents
anticonvulsants
neurotoxins (for chronic migraines)
161
How do you treat cluster headaches?
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
what is acute therapy for cluster headaches?
sumatriptan (gold standard), oxygen therapy, DHE
163
what is preventative tx for cluster headaches?
verapamil (calcium channel blocker), prednisone
164
how do you manage and treat a medical overuse headache?
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
name two drugs used in the prophylaxis of chronic migraines
topiramate (anticonvulsant)
onabotulinumtoxin A (blocks peripheral sensitization)
166
what are some important aspects to ask about on the history of a patient with chronic or neuropathic pain?
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
what are the usual signs and symptoms of neuropathic pain?
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
what type of nerve fibres carry superficial pain that feels sharp and pricking?
A-delta fibres (so its fast because these fibres are myelinated, unlike other types of pain)
169
what are the two types of superficial pain?
sharp and pricking (carried by myelinated A-delta fibres)
dull and burning (carried by unmyelinated C fibres)
170
what type of pain is easiest to localize? why?
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
what is fibromyalgia?
"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
what are the two major challenges in pain management?
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
what does "sensitization" mean in the context of pain?
an increase in the excitability of neurons i.e neurons are more sensitive to stimuli or sensory inputs
174
what are the most potent pain producing substances?
kinins
i.e bradykinin
produced by proleolytic breakdown of kininogens in area of wound
175
what is the gate theory of pain transmission?
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
what is transcutaneous electrical stimulation (TENS)?
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
what is phenotype conversion?
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
what are causes of primary headache?
migraine (episodic and chronic)
tension type headache
trigeminal autonomic cephalgia (TACs)
179
what are causes of secondary headache?
head and neck trauma
extra cranial
vascular disease
tumour
infection
abnormal CSF pressure
drugs
180
what are some important factors to find out on history for headache?
age of onset
headache characteristics
associated sx
neuro symptoms
trigger factors
changes over time
181
if a patient has symptoms of migraine and no seizures, do you need to do imaging?
no because you wont find anything
182
what symptoms do you need to be diagnosed with episodic migraine?
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
what are visual aura symptoms?
photopsia
scintillations
central scotoma
peripheral field loss
184
if a headache is associated with menstruation, what is it?
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
what sex is more affected by migraines?
women
186
what % of people with chronic migraines are overusing medications?
50%
187
what are trigeminal autonomic cephalgias? (TACs)
cluster headache
ice pick headache
cough headache
coital headache
benign exertional headache
chronic paroxysmal hemicrania
188
list the associated autonomic symptoms (unilateral) associated with cluster headache
1. conjunctival injection
2. tearing
3. rhinorrhea and nasal congestion
4. ptosis and miosis
189
what is calcitonin gene-related peptide (CGRP)?
main sensory neuropeptide released (along with glutamate) by activated trigeminal neurons
physiological actions:
vasodilation
mast cell degranulation
sensory transmission
190
how is CGRP related to migraine?
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
list emotional stress triggers for migraine
```
stress
relaxation
anxiety
depression
emotion
excitement
```
192
list physical stress triggers for migraine
```
exercise
fatigue
hunger
lack of sleep
oversleeping
```
193
list external stimuli triggers for migraine
```
climate
high altitude
heat
odours
noise
glare
```
194
list dietary and hormonal triggers for migraine
```
chocolate
cheese
alcohol
OCPs
menstruation
pregnancy
menopause
```
195
what drugs may be given as adjuctive therapy in addition to triptans in the treatment of migraine?
NSAID (naproxen)
anti-emetic (metoclopramide)
196
how does botox/onabotulinumtoxin A work to treat chronic migraine?
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
define chronic pain
pain lasting greater than 3-6 months
pain of any etiology not directly related to neoplastic involvement, associated with a chronic medical condition or extending in duration beyond the expected temporal boundary of tissue injury and normal healing, and adversely affecting the function or wellbeing of the individual
-----
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
what is the economic impact of chronic pain?
chronic and acute pain cost our society more than cancer and heart disease combined
199
what is causalgia?
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
what is neuralgia?
pain in the distribution of a nerve or nerve
201
briefly describe the pathophysiology of central sensitization
*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
