Headache: Diagnosis and Treatment – Flashcards
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1 in 4 households in the US has someone that gets migraines 78 percent of people will develop tension-type headaches (usually in 30-50's.
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1 in ___ households in the US has a person that gets migraines What is the prevalence of someone getting tension headaches in their lifetime? When typically?
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It is important to note that the brain feels no pain. The actual stimulus of the heartaches come from other sources, including the large vessels and the dura. The intervention for this pain include (1) CN V - which provides innervation for intracranial structures in the anterior and middle fossa of the skill, above the cerebellar tentorium, (2) CN IX and X - also provide innervation for part of the posterior fossa, and (3) The upper cervical roots, which contain sensory information for the infra-tentorial and the cervical structures
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Does the brain feel pain? Where does the stimulus come from? What nerves provide the innervation for this pain?
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When evaluating headaches, you must distinguish a primary headache from a secondary headache. A primary headache is deteremined largely from ones genetic predisposition for possessing "headache genes." These headaches are migraine, tension-type headaches that occur in clusters. Contrastingly, secondary headaches are headaches that occur as a result of either (a) turmors, (b) blood in the brain, or other causes. People with migraines have an increased likelihood of developing brain tumors.
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What is a "primary" and a "secondary" headache? What do they each occur as results of? What must we look out for in our patients with migraines?
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When trying to determine the origin and characterization of an individual's headaches, it is important to take a headache history. You should ask the person -Occurrence (Are the headaches hyperacute, acute, subacute, or chronic); -Location of the headaches; The DURATION of the headaches; the SEVERITY of the headaches; the CHARACTER of the headaches; -FREQUENCY of the headaches (how often do they occur); -ASSOCIATED SYMPTOMS such as nausea, photophobia. You ALWAYS want to also assess whether the headaches have affected their Sleep, if there are any additional psychiatric comorbidities, and what medications have they been taking.
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Clinically, what are some factors that we should try to determine via questioning the patient to better understand the migraine when collecting a history. What are thee concerns we always want to address
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In your physical examination, you should (1) check that the patient does not have an altered mental status (2) look for papilledema which would indicate high intracranial pressures (3) feel for nuchal rigidity and fever that would be associated with meningitis (4) Assess whether the patient has focal neurologic defects. DON'T FORGET that the vast majority of patients with chronic headaches have a normal neurologic examination
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What are 4 things that we need to test during our physical examination if a patient comes in with headaches? What do we find upon the neurologic assessment/exam in the majority of our patients with chronic headaches?
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The different types of primary headaches include (1) Migraines (2) Tension-type headaches (3) Cluster Headaches (4) MANY other kinds. If you are in doubt of what kind of headache it is, try googling International Classification of Headache Disorders version 3beta (ICHD)
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What are 3 types of chronic headaches? When we are practicing physicians, if we want to determine what kind of migraines are occurring, what website should we go to if we forget.
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You can diagnose a Migraine without an aura if the criteria A-E are satisfied. (A) At least five attacks have occurred filling criteria B-D. (B) If headache attacks last between 4-72 hours. (C ) If at least 2 of 4 characteristics are met (1) The headaches are unilateral in location (2) The headaches have a pulsating quality (3) The headaches have a severity of at least moderate pain or severe (4) The headaches are aggrivated/caused by routine physical activity. (D) During headache, there is at least either (a) nausea or vomiting, or (b) photophobia or phonophobia. (E) The headaches are not accounted for by another ICHD-3 diagnosis
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What types of guidelines should we follow (A-E) to diagnose that a patient has migraines without aura?
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Migraines can be Diagnosed WITH AURA (30% of migraineurs) based on criteria A-D. (A) if the person has at least two attacks fulfilling criteria B-C. (B) If at least one or more of the reversible aura symptoms (1-6) are present (Visual, sensory, speech and/or language, motor, brainstem , retinal). (C ) If at least two of fur characteristics are present (1) at least one aura symptom spreads graually over 5 minutes, and/or two or more symptoms occur in sucession (2) Each individual aura symptom lasts 5-60 minutes (3) At least one aura symptom is unilateral (4) The aura is accompanies, or followed, within 60 minues by headaches. (D) The headache is not better accounter for another ICHD-3 diagnosis and transient ischemic attacks have been excluded.
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How do we diagnose migraines with an aura? What are criteria (A-D) that must be fulfilled?
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Migraine with aura" is a relatively new name for the less common type of migraine headache. Aura refers to feelings and symptoms you notice shortly before the headache begins. These early symptoms are also called a prodrome. Migraines with aura account for less than 20% of all migraines. But that's little comfort when you are the one who falls victim to this painful headache.
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What is a migrane aura? What are examples? How common in comparison are migraines with and without aura?
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A person is considered to have CHRONIC migraines if their symptoms fulfill at least 3 criteria. (1) migraines must occur at least 15 days in a given month, (2) the migraines must last at least 4 hours a day (3) the migraines must have migrainous features at least 8 days per month.
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What criteria must be fulfilled after you confirm that a patient has migraine headaches to also illustrate they are chronic migraines?
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The migraine pathogenesis is always at least in part due to a genetic susceptibility gene, causing a dysfunction of the brain-stem nuclei that are involved in the sensory/nociceptive modulation of the craniovascular afferents. If there is a genetic suspectivility to migraines, there are several things that could worsen or trigger the headaches. These include (1) skipping meals, fasting, and dehydration (2) changes in sleeping patterns (3) stress (4) menses, ovulation, or irregular cycles (5) head trauma. Depression and anxiety also commonly co-occur with, but do not cause headaches.
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Do genetics contribute to migraine pathogenesis? What part of the brain can contribute to migraine activity when dysfunctioning? If you have a genetic susceptibility to experience migraines, what could put your over the edge and cause you to get them? Can Depression and anxiety cause headaches?
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Activation of the trigeminal nucleus caudalis can cause release of vasoactive peptides (including calcitonin gene-related peptide (CGRP) and substance P). These vasoactive peptides can stimulate further infalammatory response of the trigeminovascular system. This nociceptor activation can cause central and peripheral sensitization.
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How can the trigeminal nucleus contribute to migraine headaches?
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The activation of the nociceptive pathway may begin with a wave of neuronal excitation in the neuronal gray matter, with local blood flow changes, followed by spreading cortical depression (CSD). There is probably bidirectinal activation both from the cortex to the brainstem and from the brainstem to the cortex.
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How do migraine headaches usually begin?
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We can take abortive medication at the time of the headache to releive the pain. We can also take preventative medication daily, whether the headache is present or not, to decrease the overall frequency and severity on average. This does not actually "prevent" headaches.
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What are two ways that medications can help migraines
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Therapy to prevent migraines should be considered if: (1) the frequency of headaches is greater than 1-2 days/week with disabling headaches at least 3 days/month. (2) If the patient feels that the recurrent headaches significantly interferes with their daily routines. (3) If the patient already uses acute medications more than 2x/week (4) If the acute medications are contraindicated or not well tolderated or affected
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When should we consider starting one of our patients on migraine preventive therapy?
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Abortive medication for primary migraine treatments are medications that are taken at the time of the headache to relieve the headache episode. These include (1) NSAIDS, (2) Anti-emetic, (3) Dihydroergotamines (can be given intranasal and IV) (4) Triptants
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What are abortive migraine medications? Name 4 types? can you list any examples in each type?
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NSAIDs include (Naproxen, Ibuprofen and combination analgesics like Excedrin
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What are 3 examples of NSAIDS that can be given to people with migraines?
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Anti-emetics include (Prochlorprezine "Compazine" and Metoclopramide "Reglan") These both have migraine-specific actions in addition to treating nausea because they are dopamine antagonists and serotonin receptor antagonists
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What are 2 examples of anti-emetic drugs that can be used to treat migraines? What else do they treat?
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Triptan medications are part of the abortive therapy. They work primarily by selectively agonizing the serotonin 1B, 1D receptor, acting as a trigeminal nucleus caudalis and peripherally on blood vessels. This causes neuronal inhibition and blockage of CGRP release. They can be combined with NSAIDS and antiemetics. Triptans should be avoided during pregnancy because they have the potential to cause Serotonin Syndrome. It has found that Long-acting triptans are best for menstrual related migraines.
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How do Triptan medications work? Where in the body do they work (CNS and PNS)? What does their action cause? Do we usually give any drugs with them? When shouldnt we give Triptans? Why? What types of migraines are long lasting Triptans vest for?
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The choice of the agent will depend on the co-morbidities and acceptable side effects for the specific patient. Preventative treatment is usually started with a low dose and slowly increased to assess efficacy and side effects, and effectiveness can be adequately judged after 2-3mo. During this time you can continue abortive treatments.
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If we were to start a person on preventative migraine treatment, should we take them off their abortive treatment? How should we dose? How long must they be on this new treatment before we can really assess treatment effectiveness? How do we determine which agent to give?
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Antidepressants such as tricyclics and SNRI Beta blockers Anti-convulsants ACE inhibitors Botulinum toxin A (Botox) -FDA approved for chronic migraines (also monoclonal Ab Tx's).
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Whate are 5 different types of preventative therapies for primary migraines? Whats the only one thats FDA approved for chronic migaines?
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Level A = Established efficacy Level B = Probably effective Level C = possibly effective Level U = inadequate or conflicting data Level A drugs -Beta blockers (propranolol, metroprolol, and timolol) -AEDs (divalproex sodium, and topiramate) Level B drugs -Antidepressants (amitryptyline, and venlafixine) -Supplements: Riboflavir, Mg Level C - Cyproheptadine, candesartan, lisinopril
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What do levels A, B, and C refer to in terms of drug effectiveness?
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31 injections! Onabotulinum toxin A (Botox) is the only FDA approved treatment for chronic migraines, and the recommended dose for treating chronic migraines is 155 units. This should be administered intramuscularly. It can be given by a provider in office every 1-2 weeks. This should be given by the provider in the office every 12 weeks. There is no pregnancy data.
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If you wanted to get botox for migraines, how many injections would you typically get? How is it injected? What about with pregnancY?
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Pregnant women usually get less headaches because of their higher estogren levels. 5-30% have no improvement or worsening? Symptoms could also be due to secondary headaches due to (1) disseciton, (2) pituitary apoplexy, (3) venous sinus thrombosis (4) pre-eclampsia (5) reversible cerebral vasoconstrictive syndrome.
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Do pregnanct women usually get more or less headaches than normal? Why? What percent doesnt show change? What are some causes of secondary headaches during pregnancy?
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The FDA Risk Categories to migraine medications can be grouped into Group A, B, C, D, and X risks. Category A: Controlled human studies show no risk. Category B: No evidence of risk in humans but there are no controlled human studies. Category C: Risk to humans have not been ruled out Category D: Positive evidence of risk in human or animal studies Category X: Contraindicated in pregnancy
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Explain the A-D + X risk categories for migraine meds made by the FDA
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Abortive medications in Pregnancy risk category B include (1) acetaminophen (2) caffeine (3) metoclopramine. Preventative category B meds include (1) memantine and (2) magnesium oxide Preventative meds in Pregnancy risk category A include (1) magnesium gluconate Magnesium sulfate (IV) is now a Category D medication
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When should migraine medications be used during pregnancy? What are some abortive and preventative meds that are OK during pregnancy? Both group A and B.
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There are many cautions that must be taken during pregnancy when considering ABORTIVE MEDS. In particular, during the first trimester NSAIDS can cause inc risk of spontaneous aborption. During the third trimested they can also decrease the amnionic fluid volume, inhibit labor, cause bleeding or closure of ductur arteriorsis prematurely. Additionally Caffeine (more than 300mg/day) can increase risk of spontaneous absorption and cause low birth weight.
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What abortive migraine meds should we take caution with during pregnancy? Name two that many people use all the time during normal life that we need to keep an eye out for. (One dietary and one OTC drug)
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Triptans should be avoided (period!) because they change placentral blood flow. Butalbital containing analgesics can cause "rebound headaches" and severe neonatal withdrawl syndrome if use if prolonged. Amitryptaline and Dihydroergotamine (DHE) should also be avoided Atenlolol may be associated with perinatal beta blockage and growth retardation Valproic acid should be avoided to prevent neural tubular defects days 17-30.
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What are 6 meds that are prescribed and should be avoided during pregnancy
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During pregnancy we should limit abortives to no more than 2 days of use per week. Typically we want to substitute acute meds and start good preventitive meds. Stop (NSAIDS, Opiates, Triptns, Barbituates, and Caffiene).
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By how much should we limit abortive medications during pregnancy? What in particular shoudl they try to stop using? How much coffee can a pregnant woman have per day? How we we wanna try to compensate for this?
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Primary tension-type headaches are defined as headaches that (A) last from 30minutes to 7 days (B) have at least 2 of 4 criteria (1) Bilateral location (2) pressing or tightening (non-pulsating) quality (3) mild or moderate intensity (4) not aggravated by routine physical activity such as walking or climbing stairs . (C ) There is neither nausea or vomiting assocaited, and not (both) photophobia or phonophobia (if just 1 it could still be a tension headache). (D) Not better accounted for by another ICHD-3 diagnosis.
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What are the characteristics (A-D) that one must excibit to be classified as having tension type headaches?
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Tension Type headaches (TTH) can occur with or without pericranial tenderness, they occur in episodic and chonic forms, and are the most common headache type.
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How common are tension type headaches? Do they occur with pericranial tenderness? Are they episodic?
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There are abortive therapies and preventative therapies that can be given to people that experience tension type headaches. As an abortive therapy, NSAIDS and OTC combinations (Excedrin) are often given. As preventative medications Tricyclic antidepressants (Amitriptyline is best), and SNRI (Venlafixine) are helpful. As additional treatments, biofeedback, PT, and cognitive behavioral therapy measures can also be explored.
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What are some teatments that exist for people that have tention type headaches?
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Cluster headaches are rather rare, with a prevalence of 0.1%, predominantly seen in males, lasting only 15mins-2 hours of unilateral periorbital pain, side locked only to one side. Associated concurrent synmptoms are with ipsalateral lacrimation, nasal stuffiness, conunctival injection and Horner syndrome commonly associated. They usually occur in clusters lasting from weeks to months. Between these periods the patient is headache free for months-years. During a cluster, they get the pain during the same time each day. Headaches can be triggered by alcohol during an active cluster. There is a high association between Cluster headaches and SUICIDE.
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What are cluster headaches? Are they common? Are they seen in men or women more? Is it unilateral or bilateral? Where do we usually feel the pain in the head? What are associated symptoms? Why do we call them "cluster headaches?" What is 1 substance that can trigger headaches in these patients? What are these patients likely to do?
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To be classified as Cluster headaches, criteria A-D must be fulfilled. (A) There must have been at least 5 attacks fulfilling (B-D). (B) There was severe or very servere unilateral orbital, supraorbital and temporal pain lasting 15-180 minutes when untreated. (C ) At least one of the following symptoms or signs was experienced ipsalateral to the headache (1) conkunctival injection (2) lacrimation (3) nasal congestion and rhinorrhea (4) eyelid edema (5) forehead and facial sweating (6) forehead facial flushing (7) sensation of fullness in ear (8) miosis or photophobia. (D) Attacks have a frequence between one every day and eight per day for more than half of the time when the disorder is active.
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What criteria must be fulfilled for a patient to be diagnosed with cluster headaches?
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Two abortive therapies during an active cluster headache crisis are (1) Sumatriptan, which is subcutaneous (2) 100% oxygen using a NON-REBREATHER. Preventative therapies for cluster headaches include (1) verapamil, (2) lithium carbonate Bridge therapies of (1) greater occipital nerve blocks given with steroids, as well as (2) prisone taper, are also considered.
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What are abortive therapies done for people with cluster headaches? What are preventative therapies? What are bridge therapies?
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Trigeminal Neuralgia 2-3% of patients feel the pain bilaterally The pain can be spontaneous or triggered by chewing, talking, or touching face, or from the wind or cold. This could cause facial spasm "tic doroeaux" and usually the person is pain free between attacks, but might have chronic dull aches in the region. The incidence increases with increasing age.
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A patient has sharp, stabbing, burning pain like that of an electrick shock in the distribution of one ore more branches of the trigeminal nerve in the chin and cheek area that is unilateral and lasts for seconds but occurs multiple times per day. What does this patient have? What can cause the pain? What could this cause them to experience? Does the incidence change as we age?
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Trigeminal neuralgia could be idiopathic or could be symptomatic due to structural lesions (either a tumor, aneurysm, or trauma) that involve the trigeminal root. MRI is required to determine involvement. When Trigeminal Neuralgia is seen in younger individuals, it is often associated with MS. Idiopathic trigeminal neuralgia is also thought to result from microvascular compromise of the trigeminal nerve by abnormal or tortuous blood vessels such as vessels found in 90% at surgery.
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What are some potential causes of trigeminal neuralgia and how can we decide whats causing an individual case? What should we think if a young individual has trigeminal neuralgia
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Medical: Carbamazepine (first choice), as well as Lamotrigine and gabapentin Surgical: Microvascular decompression, Percutaneous sterotactic radiofrequency ablation, thermal rhizotomy, and gamma knife therapy.
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What are some medical and surgical treatment options for someone with trigeminal neuralgia?
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Based on the patient's history, red flags for headaches include (1) if it was the worst headache you ever had (2) if you have headaches and have cancer, HIV, or are IC'ed (3) if you are over 50 and have never had headaches before and now you do (4) if you also have seizures (5) if you also have focal symptom (6) the location of your headache changes over time. PE findings --- papilledema, cognitive impairment, fever, stiff neck, and focal signs
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When should we think of a secondary headache being the cause of a headache? List examples both obtained from patients history and PE presenation
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Secondary headaches can be due to blood present in areas where it should not be. This can be caused by (1) intra-parenchymal hemorrhage due to (HTN, vascular malformation, trauma, anticoagulation, intracranial tumor, amyloid) (2) intra-ventricular hemorrhage (which can cause hydrocephalus) (3) epidural hematomas (which are usually from the arterial supplyassociated with linear skull fracture skull fractures or tears in the middle meningeal artery (4) subdural hemorrhage, appearing crescent shaped and caused by sheaaring of the bridging veins into the subdural space and more common in the young and elderly and assciated with anticoagulation or closed head trauma (5) subarrachnoid hemorrhage into the CSF
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What are 4 causes of secondary headaches?
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Subarachnoid hemorrhage We treat these patients by reducing the Intracerebral pressure, controlling the BP, giving them CCBs like nimodipone to reduce ischemic sequelae from cerebral vasospacm, and surgery to secure the aneurysm.
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The typical presentation for a patient with ______________ includes (1) spontaneous onset (usually due to rupture of aneurysm) (2) Presents with "the worse headache of my life" and altered mental status, vomiting, and nuchal rigidity, (3) CT scan of brain demonstrates blood in >90% of patients if done in the first 24 hours. There are usually focal neurological defects within 7-14 days after the bleed. How do we treat?
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If there is blood in the CSF, it will be pink for first 24 hours then the CSF will turn yellow due to enzyatic breakdown of Hb after subarachnoid hemorrhage. If we see yellow CSF, think subarachnoid hemorrhage.
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What would Xanthochromic CSF indicate?
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(1) carotid artery dissection, which can cause headaches and facial pain ipsilateral to the dissecting artery and can be complicated by arterial infarction in the anterior circulation (2) Vertebral artery dissection, which can cause headache and neck pain ipsolateral to the dissecting artery, and can be complicated by arterial infarction in the posterior circulation, (3) Venous sinus thrombosis, which can occur with hypercoaguable states (pt is taking oral contraceptives) and can cause lethal venous infarction from not allowing tissue to drain properly, as well as (4) Temporal arteritis, or Giant Cell Arteritis, which is an indicator of granulomatous inflammation.
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What are some arterial or venous problems that could cause secondary headaches?
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Arterial dissection carotid dissection Horner's syndrome
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______________ is a common cause stroke in patients less than 40 years old. About 50% of patients with _______________ have ipsilateral ______________ due to stretchng or compression of sympathetic fibers traveling with the vessel.
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Temporal arteritis, or Giant Cell Arteritis, is an indicator of granulomatous inflammation, most prominent along the internal elastic lamina of the arterial wall. It usually affects branches of the external carotid artery (superficial temporal artery). The scalp tenderness is due to decreased blood flow. The opthalmic artery involvement can result in visual changes or sudden loss of vision, leading to blindness in 60% of patients.
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Symptomatically a patient has malaise, fever, weight loss, myalgia, arthralgias as well as claudication, stiffness, as well as scalp tenderness. They also have opthalmis artery involvement that progresses to blindness. What does the patient have?
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The American College of Rheumatology developed Diagnostic criteria for Temporal Arteritis. These criteria include (1) Age >50 (2) New onset localized headache (3) Temporal artery tenderness or decreased pulsation (4) increase in SED rate over >50mm/hr (5) Arterial biopsy showing necrotizing artheritis. If the patient meets 3 out of 5 the diagnosis can be established with a 93% sensitivity and 91.2% specificity. You treat this with high dose steroids, and don't wait for biopsy results before treatment.
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What age of people are usually affected by Temporal arteritis? Will their temporal artery be tender? Will it be heavily pulsating? What will the SED rate be like? What will Bx of the artery demonstrate? Who established diagnostic criteria based on the above features?
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Secondary Headaches could be due to Meningitis or Meningo-encephalitis. In this scenario, pain can be due to inflammation caused by (viral, granulomatous, neplastic, autoimmune antibodies, or chemical irritant causes).
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Meningitis and Meningo-encephalitis caused pain from inflammation that is due to what 5 causes?
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The headaches usually develop over a period of hours/days, and seizures may occur. The diagnosis can be made based on CSF examination, and the treatment is specific to the causative agent. We can make the diagnosis based on CSF examination, and we usually treat the causative agent.
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How are the headaches usually onset in the case of meningitis? What else might occur with their presentation? How can we make the diagnosis?
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(1) arterial hypertension, such as a hypertensive emergency (2) intracranial hypertension seen with morning-predominant headaches. With this you would expect to see elevated pressure due to mass/tumor/or abscess. It could also be idiopathic.
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What are two kinds of high pressure caused secondary headaches and in what scenarios would we see these?
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The are possible risk factors for development include: young obese women, pregnancy, oral contraceptives, corticosteroids, hypervitaminosis of vitamin A, Tetracycline (infants), and obstruction of intracranial venous drainage. Obstruction can either be due to venous sinus thrombosis or from polycythemia, or thrombocytosis.
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What are some risk factors for idiopathic intracranial hypertension?
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(IIH) can cause increased resistance to CSF reabsorption at arachnoid granulations, high intracranial pressure contributing to papilledema, as well as other symptoms including blurry vision, intermittent visual obscurations, horizontal diplopia, "pulsatile tinnitus," and pressure on the optic nerve resulting in optic atrophy and blindness, which these patients MUST be followed up with an ophthalmologist. When examining by CT/MRI "slit-like" ventricles can be seen.
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What are some symptoms of a patient with idiopathic intracranial hypertension? What must we do once we diagnose these patients?
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These can be treated by acetazolamide or lomboperitoneal shunting, and optic nerve sheath fenestrations.
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How can we treat people with secondary headaches caused by idiopathic intraceranial hypertension?
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(1) Post LP headaches (wet epidrural headache may be experienced after pregnancy) - this is caused by (a) persistent spinal subarachnoid fluid leak causing traction on pain sensitive structures at the base of the brain. OR (b) the meningeal contrast enhancement producing "sagging brain" with pontine flattening (2) Spontaneous intracranial hypotension - usually due to trauma, small tears in the dura and around the spine, or form CT disorders.
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What are two ways that people could get secondary headaches due to intracranial hypotension?
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they should be primarily affecting the occipital region, should be precipitated by standing and relieved by laying down, should improve with caffeine, and blood patching may help patients with lingering symptoms.
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If we think a patient has intracranial hypotention headaches that are causing their secondary headaches, what should we think about to prove this is the cause?
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Thinderclap headache These are bad!
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What types of headaches can occur from sex especially?
