Neuroscience Week 3: Headaches

Question 1

Be able to recognize the characteristics of the types (tension, cluster, migraine both classical and complicated) and etiologies of headaches.

Question 2

Objective 2

How do we treat these types of headaches?

Question 3

Objective 3

Know how the triptans and ergotamine drugs work, and recognize the major side effects, toxicities & contraindications.

Question 4

Objective 4

Which drugs are used as preventative and which are used abort migraine Recognize the drug classes and prototypes for prophylactic treatment of migraine

Question 5

Objective 5

Recognize the proposed pathophysiologies in a migraine (Trigeminovascular, neurogenic inflammation and cortical spreading depression)

Question 6

Objective 6

Understand what is serotonin syndrome, drug interactions which can produce serotonin syndrome and how we treat it.

Question 7

I thought there are no pain receptors in the brain, so why do we get headaches?

Answer 7

There are several pain sensitive intracranial structures.

Pain signals may arise from

receptors located in the:

1.)dura mater, 2.) meningeal vessels, 3.)intracranial segments of trigeminal CN V, glossopharyngeal CN IX, and vagus CN X, 4.) intracranial segments of the basilar, vertebral, and carotid arteries; all can transmit pain signals to the second-order neurons in the trigeminal nucleus caudalis (TNC) in the medulla and to the dorsal horn of the upper cervical spine.

Question 8

Secondary neuron activity of the TNC

Answer 8

The activity of second-order neurons in those two areas can be modified by inputs from the nucleus raphe magnus (serotonerg ic), periaqueduct al gray area, locus ceruleus (noradrenergic), and rostral trigeminal nuclei, and by descending inhibitory transmissions from the cerebral cortex.

These correspondingly modified signals are then relayed to the contralateral dorsomedial and ventroposteromedial nuclei of the thalamus, a common destination for pain transmissions, and then on to the insular cortex, the anterior cingulate cortex, and the somatosensory cortex.

Question 9

Sensory nerve fibers associated with cranial vasculature

Answer 9

1. Trigeminal sensory nerve fibers : calcitonin gene-related peptide (CGRP), substance P, neurokinin A and pituitary adenylate-cyclase activating peptide (PACAP), as well as nitric oxide synthase (NOS).
2. Parasympathetic nerve fibers: vasoactive intestinal peptide (VIP), PACAP, neuropeptide Y (NPY) and acetylcholine and NOS.
3. Sympathetic nerve fibers: norepinephrine, NPY and adenosine triphosphate (ATP).

Question 10

Potent vasodilators

4 listed

Answer 10

• NOS,
• CGRP
• PACAP
• NPY

are potent vasodilators.

Question 11

Endothelial Vasodilators

Answer 11

ATP is an endothelial vasodilator

Question 12

CGRP AKA

Answer 12

calcitonin gene-related peptide

Question 13

Most headaches occur in this way

Answer 13

With the onset of some headaches, there is an increased release of the vasodilator calcitonin gene-related peptide (CGRP), a potential vasodilator. There is also increased mast cell degranulation and release of histamine, sensitizing the individual to small changes in intracranial pressure, and causing the characteristic throbbing quality of pain.

Question 14

treatment for headaches target

Answer 14

Treatments for a headache may target the pain circuitry peripherally, centrally or both. During the natural course of some types of headache, both initial peripheral sensitization and, in most cases, subsequent central pain sensitization occurs. During peripheral sensitization, primary afferent neurons may become irritable and increase their spontaneous firing because of neurogenic inflammation and dilation of meningeal blood vessels.

Question 15

Central sensitization and cutaneous allodynia

Answer 15

Central sensitization is often marked by the development of cutaneous allodynia (the perception of pain in response to a normally non-painful stimulus), and this may involve the scalp, face, and even the arms. Cutaneous allodynia occurs in 79% of people who get migraine headaches. During central sensitization, the excitatory thresholds of second-order neurons in the TNC and the dorsal horn of the cervical spine is reduced.

Question 16

Classification of Headaches

Answer 16

Classify the headache type (not the patient) by 4 main characteristics

1. ) Quality (pressing throbbing, etc.)
2. ) Intensity (mild, moderate severe)
3. ) Location (unilateral, bilateral, etc.)
4. ) Response to routine physical activities.
5. ) Associated features (nausea, vomiting hypersensitivity to light or noise, auras) and ask about use of analgesics

Question 17

Chronic Tension Headache Description

Answer 17

Occurs equally in women and men

Usually related to musculoskeletal spasm of neck and shoulders

Rebound headaches common from excessive symptomatic medications (ie. OTC preparations, opioid use, barbiturate combination therapies, especially short-acting agents.

Many patients have “mixed headaches”

Question 18

Chronic tension headache Treatment

Answer 18

Physical therapy – Stretching- Relaxation techniques- Posture correction

Muscle relaxants

Tricyclic antidepressants

Non-steroidal anti-inflammatory medications

Question 19

REBOUND OR MEDICATION OVER-USE HEADACHES Description

Answer 19

Rebound headaches (medication-overuse headaches) are caused by regular, long-term use of medications, often those used to treat headaches, such as migraine. Pain relievers offer relief for occasional headaches. But if you take them more than a couple of days a week, they may trigger rebound headaches. Any medication taken for pain relief can cause rebound headaches. Rebound headaches usually stop when you stop taking the pain medication. Signs and symptoms of rebound headaches may differ according to the type of original headache being treated and the medication used

Question 20

Rebound headaches Common features

Answer 20

Occur every day or nearly every day, often waking you in the early morning

Improve with pain relief medication but then return as your medication wears off

Other signs and symptoms may include:

• Nausea
• Listlessness
• Restlessness and difficulty concentrating
• Memory problems
• Irritability

Question 21

Rebound Headaches (a Complication)

Answer 21

Rebound headaches are usually a complication of Migraine or another headache disorder, a complication that can present huge obstacles to headache treatment.

Question 22

Cluster headache Description

Answer 22

Cluster headache is a primary headache syndrome that is characterized by excruciatingly severe, strictly unilateral attacks of orbital, supraorbital or temporal pain, which last 15–180 min and are accompanied by ipsilateral autonomic manifestations (e.g. lacrimation and rhinorrhea). Hypothalamic dysregulation plays a key role in this type of primary headache

Question 23

Cluster headache Clinical Presentation

Answer 23

• Occurrence males > females
• Usually no family history Headaches can occur up to 3 times a day over a several month period, orbital supraorbital or temporal
• Pain – abrupt onset, unilateral and usually remains on the same side of the head from attack to attack.
• Attacks can last for 15-180 min The attacks typically occur with circadian rhythmicity, being experienced at fixed hours of the day or night Ipsilateral eye injected, nostril blocked
• Partial Horner syndrome can occur (miosis, ptosis and anhidrosis) hemifacial sweating CGRP and VIP are released

Question 24

Cluster headache Treatment

Answer 24

• Oxygen works in many cases but why is not known.
• Short course of corticosteroids
• lidocaine intranasal ipsilateral to the headache
• “Triptans”
• Ergotamine-DHE
  *

Question 25

Cluster headache Prophylactic Treatment

Answer 25

* Verapamil –calcium channel blocker * Lithium * mood stabilizer Valproate, Topiramate etc * antiseizure drugs * Ergotamines * BoTox

Question 26

Classical Migraine Headache

Answer 26

1. With visual aura, such as scintillating scotoma (diminished vision within a field) or fortification spectra (zig zag lines at outer edge of visual field) – thought to represent neuronal spreading depression within the occipital lobe 2. The remainder of clinical presentation is the same as with common migraine

Question 27

Complicated Migraine Headache

Answer 27

Involves significant neurological deficits (cranial nerve palsy, paresthesia, hemiopia, hemiparesia, dysphasia, seizure, etc) Neurological symptoms tend to persist into the headache phase Recovery may take hours to days or weeks Rarely may represent a **stroke** if neurological symptoms are due to vasoconstriction or spasm then treatment should **NOT** include ergotamines or “Triptans”

Question 28

Rare Forms of Migraine 3 listed

Answer 28

* Familial Hemiplegic Migraine * Basilar migraine (BM) * Retinal migraine

Question 29

Migraine Headaches Common Clinical Presentation

Answer 29

1. No aura 2. With nausea, vomiting, photophobia 3. Sleep alleviates symptoms 4. Positive familial history frequent 5. Unilateral, throbbing quality of pain

Question 30

Familial Hemiplegic Migraine

Answer 30

A hemiplegic migraine is a very rare but well-described form of migraine. Tends to run in families with 60-80% have an affected family member. A recurrent headache associated with temporary unilateral hemiparesis or hemiplegia, at times accompanied by ipsilateral numbness or tingling, with or without a speech disturbance. Attacks typically the last one to three days- severe, incapacitating, unilateral, pulsating headache. The focal neurologic deficit may precede or accompany the headache, which is usually less dramatic than a motor deficit. Other migraine symptoms may variably be present. Patients may also experience disturbance of consciousness, and rarely coma. The neurologic deficit is transient and usually clears in minutes to hours, or resolves with the beginning of the headache phase. Hemiplegic migraines are associated with four different mutations in the gene encoding the P/Q voltage-gated calcium channel. The point mutation produces a missense mutation that codes for a substitution at a residue that is highly conserved among the Ca2+ channel 1-subunits

Question 31

Basilar migraine (BM)

Answer 31

also known as Bickerstaff syndrome, consists of headache accompanied by dizziness, ataxia, tinnitus, decreased hearing, nausea and vomiting, dysarthria, diplopia, loss of balance, bilateral paresthesias or paresis, altered consciousness, syncope, and sometimes loss of consciousness. BM is observed most frequently in adolescent girls and young women. Localized vertebrobasilar vasoconstriction leading to transient posterior circulation ischemia may contribute to the symptomatology of the disorder. A novel mutation in the ATP1A2 gene, similar to FHM, has been reported in members of one family with BM. Differential diagnosis includes various causes of syncopal, inner ear disease, intoxication, and posterior fossa pathologies.

Question 32

Basilar migraine (BM) AKA

Answer 32

Bickerstaff Syndrome

Question 33

Retinal migraine

Answer 33

recurrent attacks of unilateral visual disturbance or blindness lasting mins to 1 hour, associated with minimal or no headache.

Question 34

Migraine Pathophysiology

Answer 34

Trigemnial Reflex Pathology Migraine dysfunction of the trigeminal-autonomic reflex via brain stem pathways that normally modulate sensory input. Migraine is thought to be a dysfunction of the sensory input modulation within the diencephalon (Thal. & hypothal) and the brain stem. (Locus ceruleus & Periaquiductal gray) The extra and intracranial vessels are innervated with small unmyelinated fibers from the trigeminal nerve. The trigeminal nociceptive input from the meningeal vessels passes through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex these neurons project through the quintothalamic tract and then decussating in the brain stem they form synapses with neurons in the thalamus. There is a reflex connection between neurons in the pons in the superior salivatory nucleus which results in a cranial parasympathetic outflow through the pterygopalatine ganalion, Activation of the Trigeminovascular system is thought to be responsible for the pain. Vasoconstriction due to 5HT while over active vasodilation is linked to CGRP. . Ophthalmic division of the Trigeminal nerve innervates the meningies and the large intracranial vessels, densely innervated with nociceptive fibers.-Activation of these fibers releases CGRP and substance P leads to migraine The initial vasoconstriction is followed by a rebound vasodilation in intracranial arteries. CGRP acts on smooth-muscle cells to cause potent dilation CGRP-containing sensory nerve fibers act to counter vasoconstrictor influences. CGRP is thought to be a major player in migraine pain. Rebound vasodilation leads to plasma protein extravasation in dura mater, leading to “neurogenic” inflammation (resident macrophages and mast cells. 2. Cortical Spreading depression- is another phenomenon seen in migraine. CSD is a slow propagating wave of sustained strong neuronal depolarization. Transient intense spike activity followed by neuronal suppression that can last for minutes. It is associated with increase regional cerebral blood flow and depressed cortical activity. This is followed by a sustained hyperpolarization. CSD Activates trigeminal afferents and causes inflammation of pain sensitive meninges that generates aura. Blocking CSD prevents the aura but does not stop the pain. About 20-30% of episodic migraine have auras

Question 35

Cortical Spreading depression

Answer 35

is another phenomenon seen in migraine. CSD is a slow propagating wave of sustained strong neuronal depolarization. Transient intense spike activity followed by neuronal suppression that can last for minutes. It is associated with increase regional cerebral blood flow and depressed cortical activity. This is followed by a sustained hyperpolarization. CSD Activates trigeminal afferents and causes inflammation of pain sensitive meninges that generates aura. Blocking CSD prevents the aura but does not stop the pain. About 20-30% of episodic migraine have auras

Question 36

Abortive treatment of Migraine

Answer 36

5-HT 1d/b, receptor agonists -“Triptans” Triptans are inhibitory autoreceptor agonists at the 5hT1B/D receptor. Triptans cause vasoconstriction thereby blocking further CGRP and Sub P release from the trigeminal nerve terminal release (inhibits neurogenic inflammation) in the vessel wall during the activation of the trigeminovascular system. Sumatriptan and ergotamine block the development of neurogneic plasma extravasation in dura by blocking neuropeptide release. The triptans can be used for cluster headache as well. Sumatriptan (Imitrex) Rizatriptan (Maxalt) Zolmitriptan (Zomig) Naratriptan (Amerge) Frovatriptan (Frova) Eletriptan (Relpax) Almotriptan (Axert) Ergot alkaloids Dihydroergotamine Ergotamine Opioid analgesics Barbiturates NSAIDS- naproxen, ibuprofen Antiemetics/ antipsychotic-chlorperazine (compazine), chlorpromazine (thorazine) This later group of pharmacotherapies just relieve the nausea component.

Question 37

5-HT1B/1D auto-receptors in migraines

Answer 37

This figure shows the sites which have 5-HT1B/1D auto-receptors which are activated by the “triptans” leading vasoconstriction and a decrease in CGRP release. Remember auto-receptors hyperpolarize the presynaptic terminal leading to decreased neurotransmitter release. CGRP is found throughout the trigeminovascular system and in central brain regions regarded as important in migraine pathogenesis. CGRP serum concentrations can be reversed with triptan administration—an effect that coincides with migraine symptom relief

Question 38

Antagonists to the Calcitonin gene-related peptide

Answer 38

* Antagonists to the calcitonin gene related peptide receptors are being developed for migraine. * There are several anti-CGRP drugs which are in late stage clinical trials which may be available in 2018 Most are monocolonal antibodies like erenumab and fremanezumab and glacanezumab. * Telcagepant (a CGRP receptor antagonist, Merck, this drug was halted in phase 3 trials due to liver toxicity).

Question 39

Sumatriptan-Pharmacokinetics & side effects

Answer 39

97% bioavail. subQ , 14% from oral. ½ life is 2 hours metabolized by MAOA isozyme. * Side effects mostly associated with injection … Lightheadedness muscle aches nausea or vomiting * Rare side effects: Severe chest pain Shortness of breath Convulsions Swelling of the eyelids * Can cause atrial and ventricular arrhythmias, myocardial infarction and transient myocardial ischemia * Contraindicated-coronary vasospasms, so avoid with patients with ischemic heart disease or coronary artery spasm, vasospasms, * or in combination with on other 5HT elevating drug

Question 40

Ergotamine

Answer 40

* Nonselective, partial 5HT agonist at some blood vessels, nonselective 5HT antagonist at smooth muscle. Causes smooth muscle contraction. variant ergonovine that has selecitvity for uterine smooth muscle * DiHydroE is a vasoconstrictor. Used in cluster and abortive for migraine • Inhibits neuropeptide release and blocks neurogeneic inflam. * Some antagonist effects at DA & alpha adrenergic receptors. * Nausea by direct action on CTZ. Leg weakness and muscle pain, numbness in fingers and toes. Constricts arteries and veins. * Can cause coronary vasospasm. coronary artery vasoconstriction, angina, and with frequent use: myocardial infarction, coronary artery disease and stroke * Contraindication: pregnancy (fetal damage), peripheral vascular and coronary heart diseases. Raynaud’s syndrome Severe or uncontrolled hypertension Hyperthyroidism Sepsis Porphyria Hepatic or renal disease * Can cause serotonin syndrome when used in combination with other serotonin elevating drugs.

Question 41

Prophylactic Treatments of Migraines

Answer 41

Question 42

WHAT IS SEROTONIN SYNDROME?

Answer 42

A clinical triad of abnormalities brought on by an elevation of serotonin levels due to drug interactions: 1. Cognitive effects: hypervigilance, mental confusion, hallucinations, agitation, headache, coma. 2. Autonomic effects: shivering, sweating, fever, hypertension, tachycardia, nausea, diarrhea. 3. Somatic Neuromuscular effects: myoclonus/clonus (muscle twitching), hyperreflexia, incoordination tremor. Other effects: metabolic acidosis, rhabdomyolysis, renal failure, and disseminated intravascular coagulation (DIC)

Question 43

Drugs causing serotonin syndrome

Answer 43

SSRIs, second generation antidepressants, MAOIs, linezolid, tramadol, meperidine, fentanyl, ondansetron, MDMA, LSD, St. John's wort, ginseng (this is not a complete listing)

Question 44

Treatment for serotonin syndrome

Answer 44

Sedation (benzodiazepines), intubation and ventilation; consider 5-HT2 block with cyproheptadine (serotonin receptor antagonist) or chlorpromazine (greater antagonistic effect on 5HT than D2)

Question 45

Does sumatriptan lead to serotonin syndrome?

Answer 45

Triptans do not produce it on their own (as a monotherapy). SSRIs can produce Serotonin syndrome on their own. The data suggest that the combination of Triptans and serotonin reuptake inhibitors does not lead to serotonin syndrome. But some examiners may still think triptans and SSRIs are contraindicated and ask a question based on this assumption.

Question 46

Secondary Headache type examples

Answer 46

Systemic infection (e.g. meningitis) Medication overuse Head injury Vascular disorders Subarachnoid hemorrhage Brain tumor

Question 47

Pain-sensitive intracranial structures

Answer 47

* Great venous sinuses * Dural arteries * Arteries forming the circle of Willis * Pain-sensitive fibers of intracranial segments of CN: V, IX, X * Dura Matter (at skull base)

Question 48

Pathways of Headache pain

Answer 48

Question 49

Triggers of migraine

Answer 49

* caffeine * wine * chocolate * change of routine * lack of sleep * menstruation

Question 50

Case 1 1. What type of headache is this? 2. Is it a primary or secondary headache? 3. What is the cause of this headache? 4. How would you treat this headache?

Answer 50

Medication-overuse headache is a secondary headache because it is caused by something else

Question 51

How to Treat a Medication-overuse headache

Answer 51

Question 52

Question : Which of the following medications are implicated in causing medication overuse headache? A. Analgesics B. Caffeine C. Antiepileptics D. Triptans E. Ergotamine F. Opiates/narcotics/barbiturates G. All of the above

Answer 52

All of the Above

Question 53

Case 2 1. What type of headache is this? 2. What are the key findings leading to the diagnosis? 3. What is your abortive medication plan? 4. How do these drugs work? 5. What side effects or contraindications are there to consider?

Answer 53

* Common Migraine Headache * key patient findings; nausea, triggers such as chocolate or wine, no aura, +FHx, photophobia and phonophobia, usually throbbing and unilateral and is a female * abortive medication are triptans such as sumatriptan

Question 54

What are the Triptan drugs and how do they work?

Answer 54

act on the serotonin 5ht1b,1e,1d receptors as agonists these receptors sit mostly presynaptically

Question 55

What are the key patient findings that lead you to the diagnosis of common migraine?

Answer 55

Question 56

Mrs. Zhang needs acute (abortive) medications. What is your proposed treatment?

Answer 56

Question 57

overview of migraine physiology

Answer 57

Question 58

Sumatriptan as

Answer 58

CGRP inhibitor

Question 59

disregulation of the trigeminal nerve in the brain stem can?

Answer 59

be like allodynic where a touch of the hand can become quite painful

Question 60

What happens during a migraine

Answer 60

Question 61

Nerve involved in migraines

Answer 61

Trigeminal nerve is disregulated

Question 62

Sumatriptan is generally contraindicated in?

Answer 62

* Postpartum Yes * uncontrolled HTN Yes * Coronary vasospasm Yes * Ischemic cardiac disease Yes

Question 63

What preventative medications are there for migraines?

Answer 63

Question 64

Botox in migraines

Answer 64

SNAP-25 complex involved in CGRP release or any neurotransmitter so they are injected in the sinus where needed

Question 65

neural mechanism of aura

Answer 65

Question 66

Case 3 1. What type of headache is this? 2. What are the key findings leading to the diagnosis? 3. What is your abortive medication plan? 4. How do these drugs work? 5. What side effects or contraindications are there to consider?

Answer 66

Question 67

Key features of cluster headache

Answer 67

Conjunctival injection Lacrimation Nasal congestion Rhinorrhoea Forehead and facial sweating Miosis Ptosis Eyelid edema

Question 68

Treatment of Cluster headache

Answer 68

Methylprednisolone, (Correct) Oxygen (Correct) Sumatriptan, (Correct) 4% lidocaine solution intranasal (Correct)

Question 69

Partial Horner Syndrome can occur with what head ache type

Answer 69

Cluster headaches

Question 70

Partial Horner Syndrome Clinical Features

Answer 70

Partial Horner syndrome can occur (miosis, ptosis and anhidrosis) hemifacial sweating

Question 71

During your examination of Mr. Bibs, he develops a severe headache consistent with his cluster headaches. Which of the following is the best therapy to offer him as an acute treatment of his current headache? A. Promethazine B. Methylprednisolone C. Oxygen D. Sumatriptan E. 4% lidocaine solution intranasal

Answer 71

c, d, e

Question 72

Simplest acute treatment of cluster headaches

Answer 72

Oxygen

Question 73

After have managed Mr. Bibbs acute pain you discuss with him the plan for managing his cluster headaches and reducing the frequency of their occurrence. What are options for Mr. Bibbs?

Answer 73

Question 74

Pathophysiology of Cluster Headache

Answer 74

Question 75

CGRP Blockers

Answer 75

Question 76

Ergotamine

Answer 76

Ergotamine Nonselective, partial 5HT agonist at some blood vessels, nonselective 5HT antagonist at smooth muscle. Causes smooth muscle contraction. DiHydroE is a vasoconstrictor. Can cause coronary vasospasm. coronary artery vasoconstriction, angina, and with frequent use: myocardial infarction, coronary artery disease and stroke Contraindication: pregnancy (fetal damage), peripheral vascular and coronary heart diseases. Raynaud’s syndrome Severe or uncontrolled hypertension Hyperthyroidism Sepsis Porphyria Hepatic or renal disease

Question 77

Verapamil-

Answer 77

Calcium Channel antagonist for angina and arrhythmias, Bradycardia, second and third degree atrioventricular block, heart failure, can cause fatal supraventricular tachycardia in ptx with Wolff-Parkinson-White Syndrome.

Question 78

Anticonvulsants

Answer 78

many of the anticonvulsants can produce a rare serious skin reaction called Stevens Johnson syndrome (erythema multiforme, and toxic epidermal necrolysis

Question 79

Your patient comes in to tell you that using his abortive medicine for his cluster headache he felt numbness and tingling in his extremities and blanching and cyanosis in his fingers. Which medicine produces this? A. Lidocaine B. Sumatriptan C. Dihydroergotamine D. Lithium E. Naproxen

Answer 79

C.

Question 80

Serotonin Syndrome

Answer 80

Question 81

Libby Zion Law

Answer 81

Question 82

Pain location of: Sinus Cluster Tension Migraine Headaches

Answer 82

Question 83

A patient presents to your headache clinic complaining of recurring headaches which happen 2-3 times a day and last for about an hour. This has been going on for several weeks and this occurs in the spring and fall. He describes ptosis and miosis on the affected side along with nasal congestion. You give him a prescription but later he returns with a serious skin condition that you identify as Steven Johnson Syndrome. The drug is prescribed was most likely A. Sumatriptan B. NSAID-Caffeine C. Verapamil D. Lidocaine E. Topiramate

Answer 83

E.

Question 84

A 24 year old woman comes into your clinic complaining of extremely painful headaches which she describes as severe throbbing in quality and occurring about 4 times per month lasting for 8 hours at a time. She tells you that the headaches require her to lie down in a darkened room with no noise and she is sometimes nauseated by the pain. What patient history information would most contraindicate an abortive migraine treatment? A. history of type-2 diabetes B. history of atrial fibulation and coronary vasospasms C. genetic history of channelopathy D. history of hypothyroidism E. Substance use disorder

Answer 84

B.

Question 85

In deciding upon a pharmacotherapy for this patient you select an agent to abort these headaches once they begin. The drug you select will most likely produce what therapeutic action in the brain ? A. Increase the release of substance P B. Increase the levels of encephalin C. Decrease the release of calcitonin gene related peptide D. Increase the release of serotonin E. Decrease the activity of nitric oxide synthase

Answer 85

C.

Question 86

A meningitis related headache would be associated most often with which ROS finding? a. stiff neck b. visual aura c. hemiparesis d. Horner’s

Answer 86

Stiff neck

Question 87

Horner’s syndrome would be associated most often with which type of headache a. migraine b. tension c. cluster d. complicated migraine

Answer 87

Cluster

Question 88

A 16 year old female patient being treated for depression with a serotonin selective reuptake inhibitor (SSRI) comes into to your headache clinic seeking prophylactic treatment for classic migraines. Which class of drugs would be **contraindicated** in this patient? A. Propranolol B. Verapamil C. NSAID D. MAOI E. caffeine

Answer 88

MAOI

Question 89

At your headache clinic your patient has a history of hypertension, and a strong family history of MI and A. fib. The migraine treatment which would be contraindicated in this patient is: A. Propranolol B. Caffeine C. Sumatriptan D. Oxycodone E. Naproxen sodium

Answer 89

Sumatriptan