Headache

Caffeine and headaches

-130mg Caffeine + two-tabs NSAID relieves tension-type headache pain about 40% better than without caffeine. -Caffeine aids medication absorption- takes about 30mins lasts 3-5 hours -Need 200mg daily( 2 cups) x 2 weeks to develop caffeine withdrawal headache. -Medication overuse headache is constant until med is discontinued.

Migraine epi

-29 million people in the United States suffer from migraines -10% of men and 20% of women (2:1 ratio female to male) -4/5 with family history of migraine -Age at onset more often in 20-30 yrs

WHEN to REFER-neurology

-911 headache- ER -Change in pattern -Focal neurologic symptoms- seizures -Change in personality -Failed first line treatment -High level of disability -Needing abortive therapies more than once a month Neurosurgery referral for CT/MRI lesion

Sleep Apnea

-AM headache -Snoring -Witnessed apnea -BMI>30 - >50 years -Male gender --Stop-Bang criteria

Pt education for MOH

-Acute medication overuse -> increase headache frequency. -When stopped, headache may worsen temporarily or other withdrawal symptoms. -Most patients--long-term HA reduction medication overuse is stopped. -Prophylactic medications may become more effective.

TENSION HEADACHE triggers:

-Alcohol use -Caffeine (too much or withdrawal) -Colds and the flu -Dental problems such as jaw clenching or teeth grinding, TMJ -Eye strain/posture (computers) -Excessive smoking -Fatigue/sleep deprivation -Nasal congestion -Overexertion -Infection/sinus -Environmental & Emotional Stressors (noise, odors, lights....) -allergies

ASSOCIATED FEATURES of HAs

-Aura - broad, scintillating scotoma. -Nausea/vomiting -Dizziness -Numbness Autonomic features: -Nasal stuffiness -Rhinorrhea -Tearing -Eyelid ptosis or edema **•Scintillating scotoma: shimmering light and a fuzzy light •Doesn't create any pain •Can be associated with caffeine, fatigue •Evaluate social stressors in life

PHYSICAL EXAM

-Blood pressure, heart rate -Palpate head -Extracranial structures (eg, sinuses, scalp arteries, temporomandibular joints (TMJ) -Nasal drainage ( CSF) -Range of motion (Nuchal Rigidity) and presence of pain in the cervical spine. -Ears -Eyes- ptosis, pupils = CN111, Visual field exam &conjugation CNV1 /6, cardinal positions- nystagmus , Pupils- papilledema **If the anisocoria is less than 1 mm and remains the same in both the light and the dark and if the pupils are round and reactive, the patient may have physiologic anisocoria Note that even if 1 eye is completely blind, the pupil sizes should be equal in the absence of iris trauma or synechiae. Esotropia ( one or more eyes turns in) Exotropia ( one or more eyes turns out) + diplopia CN111 problem •CSF (rare unless had a recent surgery): sticky, salty and clear.

Prophylactics

-CCB -Anticonvulsants -Sympatholytics -Tricyclic antidepressants -Anti-CGRP/CGRP-R m Abs

MIGRAINE PREVENTION: anti-epilepsy medications

-Divalproex sodium -Neurontin (Gabapentin) -Topiramate (topomax) *

Assessment: Migraine

-Family history -Triggers -Laterality -Aura -Nausea ?

MIGRAINE PREVENTION: 5 HT agonists: SSRIs

-Fluoxetine -Sertraline -Paroxetine -Venlafazine -Nefazodone -Citalopram -Escitalopram

Types of Migraine

-Hemiplegic -Ophthalmoplegic -Retinal -partial or complete loss of vision -Basilar Artery - dizziness, confusion or lack of balance. -Abdominal nausea, vomiting &/or diarrhea -Menstrual -Atypical

Common Less Serious Etiologies of secondary headache: temporomandibular disorder

-If facial pain who have painful jaw clicking, jaw locking, tenderness of muscles of mastication, tenderness of the temporomandibular joints, or limitation of mandibular movement.

Migraine

-Location: Adults: Unilateral in 60 to 70%, bifrontal or global in 30% Children and adolescents: Bilateral in majority -characteristics: Gradual in onset, crescendo pattern; pulsating; moderate or severe intensity; aggravated by routine physical activity Pt appearance: Patient prefers to rest in a dark, quiet room Duration: 4 to 72 hours Associated symptoms: Nausea, vomiting, photophobia, phonophobia; may have aura (usually visual, but can involve other senses or cause speech or motor deficits) ALWAYS ASSOCIATED WITH NAUSEA

Headache Etiology

-Muscle contraction -Vessel engorgement/inflammation -Nerve Activation trigeminal nerve -Amino acid activation -- calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide (PACAP).

Assessment:Tension Headaches

-No abnormal findings on a neurological exam -May have tender points (trigger points) in the muscles are often seen in the neck and shoulder areas -Usually have historical triggers

RESCUE meds

-Non narcotic- Tramadol -Narcotics -DHE -dihydroergotamine mesylate- IV -Anti-emetics

Headache Treatments

-Preventive-avoid triggers -Abortive (use this if regular medications don't work) -rescue (narcotics, used very infrequently)

MIGRAINE PREVENTION: Beta-Blockers

-Propranolol - *Timolol -*Nadolol -Metoprolol -Atenolol* *FDA approved

Other therapies for HA

-Psychotherapy -Guided imagery -Relaxation techniques -Biofeedback -Physical and massage therapy -Acupuncture/acupressure -Aromatherapy -Diaphragmatic breathing

Indications for Diagnostic test

-S -systemic symptoms/fever -S -Secondary factors -N -neurologic S&S -O -New onset -O -Older age -P- Progressive

WHEN to IMAGE ?

-SUDDEN ONSET -SEVERE HEADACHE -Onset during exertion -First in a middle-aged patient (>50) -Accompanied by loss of consciousness or systemic illness -Headache associated with meningeal signs (fever, stiff neck, rash) -An accelerating pattern of headache -New onset in immunocompromised patients or h/0 cancer -Accompanied by signs of disease or focal neurologic symptoms- new onset seizures -Atypical aura *•Vasalving increases ICP and that's a red flag •HAs with sexual activity can be a problem •Starting to have frequent HAs and never had them before •Accelerating pattern: getting worse over time •Atypical aura: a new different aura they've never had before

EXCERBATING FACTORS -triggers

-Stress -Fatigue -Noise -Extreme Changes in temperature/wind -Foods- chocolate, red wine, beer, whiskey, aged cheeses, food additives (monosodium glutamate) -Exertion -Infection/inflammation/fever **Histamines in cheese MSG: associated with Chinese food bc it enhances flavor •Exertional HAs

Trigeminal autonomic cephalagias: Cluster HA epi

-The prevalence of cluster headache is <1 percent and mostly affects men -family hx of cluster HA -Hx of head trauma (still unsure) •Usually develops in 3rd-4th decade •80% have sleep apnea •Almost exclusively (thin) males 9:1 (♂:♀) •Increased incidence with smoking •May be seasonal (spring and fall most common)

MIGRAINE PREVENTION: other antidepressants

-Trazodone -Bupropion -Phenelzine (MAOI — Monoamine Oxidase Inhibitor)

MIGRAINE PREVENTION: Calcium channel blockers

-Verapamil -Diltiazem -Nicardipine -Nifedipine -Nimodipine

Common Less Serious Etiologies of secondary headache: Cervicogenic HA

-consider if neck and occipital head pain, with or without pain radiation to other head regions (or face) -pain is precipitated or aggravated by neck movements or sustained neck postures - (+) abnormalities on examination of the neck (abnormal movement, muscle tone, or muscle tenderness). -"chronic headache attributed to whiplash injury": If HA after neck trauma and persists > 3 months •Caution: Patients with migraine often complain of neck discomfort during a headache and may have muscular tender points. These appear to be secondary to the migraine pain, and do not necessarily indicate a neck disorder as cause of the headache.

MOH presentation

-is typically preceded by an episodic headache disorder, typically migraine or tension-type headache, that has been treated with frequent and excessive amounts of acute symptomatic medications -In clinical practice, MOH often manifests as a headache that is present or develops upon awakening -acute symptomatic treatment only provides transient relief, which leads to more acute symptomatic medication use.

Common Less Serious Etiologies of secondary headache: Post-traumatic headache

-new headache disorder begins within 7 days of a head injury. These may occur even after a mild head injury. If the headache persists for more than 3 months, it is termed a chronic post-traumatic headache.

Trigeminal autonomic cephalagias: Paroxysmal hemicrania epi

-rare condition - Paroxysmal hemicrania may begin at any age, although onset usually occurs during adulthood. The mean age of onset ranges from 34 to 41 year

Characteristics of migraine, tension type and cluster HA syndromes

1) migraine 2) tension -type 3) cluster

Most common migraine diagnoses in clinical practice

1) migraine without aura 2) Migraine w aura 3) Migraine w typical aura

Headaches characteristics with brain tumors

111 consecutive patients with primary or metastatic brain tumor -Classic early morning headache is uncommon -Primary symptom in only - 44% -Worse with bending over - 33% -Similar to TTH in 77%; migraine in 9% -Nausea and vomiting - 40%

Diagnostic criteria for tension-type HA

A. Headache lasting from 30 min to 7 d B. ≥2 Of the following pain characteristics: 1. Pressing or tightening (nonpulsating quality) 2. Mild or moderate intensity that does not prohibit activity 3. Bilateral location 4. No aggravation by walking stairs or similar routine activity C. Both of the following: 1. No nausea or vomiting (anorexia may occur) 2. Photophobia and phonophobia are absent, or only 1 is present -Triggered by stress or hunger Although the number of patients studied is small, the available data suggest that the frequency of menses as a trigger of tension-type headache is similar to that of migraine. Food triggers occur in only 14% of patients with tension-type headache and should prompt consideration of the diagnosis of migraine.

Diagnostic criteria for Migraine without aura

A. ≥ 5 Attacks lasting 4-72 h each with ≥2 of the following characteristics: 1. Unilateral location 2. Pulsating quality 3. Moderate or severe intensity that inhibits or prohibits daily activities 4. Aggravation by walking stairs or similar routine physical activity B. ≥ 1 Of the following: 1. Nausea and/or vomiting 2. Photophobia and phonophobia

Diagnostic criteria for Migraine with aura

A. ≥2 Migraine attacks with ≥3 of the following: 1. ≥1 Fully reversible aura symptoms 2. ≥1 Aura symptom develops gradually over ≥4 min 3. No aura symptom lasts > 60 min 4. Headache begins simultaneously with aura or follows aura with an interval of < 60 min

Diagnostic criteria for Cluster HA

A. ≥5 Attacks of severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 min and associated with ≥1 of the following on the pain side: 1. Conjunctival injection 2. Lacrimation 3. Nasal congestion 4. Rhinorrhea 5. Forehead and facial sweating 6. Miosis 7. Ptosis 8. Eyelid edema B. Attacks occur from 1 every other day to 8 per day

CSF leak MOA

An underlying connective tissue disorder may result in dural weakness and play a role in the development of spontaneous low CSF pressure A potential contributing factor to the development of spontaneous low CSF pressure is that of minor trauma or an inciting event, including a fall, a sudden twist or stretch, sexual intercourse or orgasm, a sudden sneeze, sports activity, or "trivial trauma" In addition, degenerative disc disease, osseous spurs, and microspurs may lead to spontaneous intracranial hypotension by causing dural tears

Secondary Headache

Any headache that has secondary pathological process. Includes: brain mass, trigeminal neuralgia, closed head injury, subarachnoid hemorrhage, temporal arteritis, medication induced, infection, acute angle closure glaucoma, aneurysm, AVM, angina, metabolic, cervical,TMJ, poisoning -trauma -infection -expanding lesion

Diagnostic criteria for migraine w typical aura:

B. ≥1 Of the following aura features establishes a diagnosis of migraine w typical aura 1. Homonymous visual disturbance 2. Unilateral paresthesias and/or numbness 3. Unilateral weakness 4. Aphasia or unclassifiable speech difficulty

Other labs to order

BMP/CMP CBC (infection) INR Focused *ferritin with significant fatigue

Migraine prevention: neurotoxins

BOTOX (Botulinum neurotoxin) $300 to $600 q 3 mths

New Migraine therapies for Migraine prevention:

CGRP inhibitors : Calcitonin gene-related peptide receptor antagonist : monoclonal antibody that competitively binds at the CGRP receptor sites. -SQ once monthly or quarterly -Prefilled autoinjection syringes - < HA intensity and frequency ( 4-8/mth) -Erenumab (Aimovig) FDA and EMA approved May 2018. -Fremanezumab (Ajovy) $575 per monthly dose and $1,725 per quarterly dose -Galcanezumab (Emgalaity) FDA approval September 2018 -Ubrogepant (Ubrelvy) immediate CGRP antagonist

If concerned for a bleed for imaging

CT scan

CT vs MRI

EMERGENT CT -NEW abnormal findings in a neurologic exam -focal deficit -altered mental status/ cognitive function (non-contrast) URGENT CT or MRI ( MRI/MRA for suspected aneurysm) -NEW SUDDEN -onset severe headache ->50 years age -NEW type of headache but with a normal neurologic examination - -Glasgow coma scores greater than 13- CT or MRI

Headache Physical Exam

First time HA or different than usual HA? Physical including: 1) a screening neurological examination; 2) a neck examination; 3) a blood pressure measurement; 4) a focused neurological examination, if indicated; 5) an examination for temporomandibular disorders, if indicated. Screening Neurological Examination •General assessment of mental status. •Cranial nerve examination: fundoscopy, examination of pupils for symmetry and reaction to light, eye movements, visual field examination, and evaluation of facial movement for asymmetry and weakness. •Assessment of all four limbs for unilateral weakness, reflex asymmetry, and evaluation of coordination in the upper limbs. Assessment of gait, including heel-toe walking (tandem gait) Meningismus=symptoms of brain/spinal cord irritation, but without actual inflammation Pheochromocytoma: can have elevated BP and significant HA

Treatment plan

Goal is to decrease by 50% Negotiate goals with pt bc won't be able to get rid of HA entirely -Diary -Treat early <2/week or 9 days/month -Treat 2-3 headaches with the same therapy -Start with NSAID- naproxen + alternate tx -Educate re risks of NSAIDs and rebound -3,000 mg acetaminophen, 2400mg ibuprofen

CSF leak time course

Headache attributed to spontaneous intracranial hypotension may be of sudden or gradual onset. The headache ordinarily develops within two hours, and in most cases within 15 minutes, of sitting or standing . Rarely, it starts as a thunderclap headache During the course of the illness, the orthostatic features may disappear, and a chronic daily headache may develop. On occasion, the postural component may not be present at al

Tension-type HA (IHS criteria)

Headache lasting from 30 minutes to 7 days. Both of the following: •1. No nausea or vomiting (anorexia may occur) •2. Photophobia and phonophobia are absent, or only 1 is present ≥2 of the following: •1. Pressing or tightening (nonpulsating quality) •2. Mild or moderate intensity that does not prohibit activity •3. Bilateral location •4. No aggravation by walking stairs or similar routine activity •Episodic < 15/month •Chronic > 15/month (may also have nausea) Tightness/pressure. "hat band" Dull, pressure-like (not throbbing) No evidence of temporally related, structural or metabolic disease

pheochromocytoma

Intermittent headache with generalized sweating, tachycardia, and/or sustained or paroxysmal hypertensio

Cluster syndrome

Location: Always unilateral, usually begins around the eye or temple Characteristics: Pain begins quickly, reaches a crescendo within minutes; pain is deep, continuous, excruciating, and explosive in quality Patient appearance: Patient remains active Duration: 30 minutes to 3 hours Associated symptoms: Ipsilateral lacrimation and redness of the eye; stuffy nose; rhinorrhea; pallor; sweating; Horner syndrome; restlessness or agitation; focal neurologic symptoms rare; sensitivity to alcohol Another clinical landmark of the cluster headache syndrome is the circadian rhythmicity of the relatively short-lived (15 to 180 minutes) painful attacks. In the episodic form of cluster headache, attacks occur daily for some weeks followed by a period of remission. In the chronic form, attacks occur without significant periods of remission. On average, a cluster period lasts 6 to 12 weeks while remissions can last up to 12 months or longer. The episodic form is the most common, affecting 80 to 90 percent of patients with cluster headache. It is characterized by periods of attacks (clusters or bouts) and periods of remission. In a bout, patients may experience one to eight attacks per day, and bouts may last from seven days to 12 months. When not in a bout, patients are usually asymptomatic. The chronic form of cluster headache lacks remissions and is diagnosed after a year without remission, or if remission has lasted less than three months. Chronic cluster may arise de novo (primary chronic cluster headache) or evolve from the episodic type (secondary chronic cluster headache).

Danger signs

May be the presenting symptom of a space-occupying mass or vascular lesion, infection, metabolic disturbance, or a systemic problem SNNOOP10 ●Systemic symptoms including fever ●Neoplasm history ●Neurologic deficit (including decreased consciousness) ●Onset is sudden or abrupt ●Older age (onset after age 50 years) ●Pattern change or recent onset of new headache ●Positional headache ●Precipitated by sneezing, coughing, or exercise ●Papilledema ●Progressive headache and atypical presentations ●Pregnancy or puerperium ●Painful eye with autonomic features ●Post-traumatic onset of headache ●Pathology of the immune system such as HIV ●Painkiller (analgesic) overuse (eg, medication overuse headache) or new drug at onset of headache

Traumatic brain injury MOA

Mild TBI results after blunt force, nonpenetrating head trauma, and it is most often defined as mild by a Glasgow Coma Scale (GCS) score of 13 to 15, 30 minutes after head injury

Medication oversuse HA (MOH) epi

Multiple factors play a role into whether MOH will occur -The prevalence of medication overuse headache (MOH) in the general population is approximately 1 to 2 percent in most studies, and is higher in women than in men - Among patients who are seen at specialized headache centers, the prevalence of MOH is near 50 percent. -Migraine is the most common primary headache disorder associated with MOH. Among those with migraine, the odds of medication overuse are increased with older age, smoking, symptoms of anxiety and depression, cutaneous allodynia (experience of pain from stimuli that isnt normally painful), greater migraine symptom severity, and more intense head pain

diagnosis of paroxysmal hemicrania

Must have all of the following criteria: ●At least 20 attacks ●Severe unilateral orbital, supra-orbital, and/or temporal pain lasting 2 to 30 minutes ●Either or both of the following: (1) At least one of the following symptoms or signs, ipsilateral to the headache: -Conjunctival injection and/or lacrimation -Nasal congestion and/or rhinorrhea -Eyelid edema -Forehead and facial sweating -Miosis and/or ptosis (2) A sense of restlessness or agitation ●Attacks have a frequency >5 per day for more than half of the active time course ●Prevented absolutely by therapeutic doses of indomethacin ●Not better accounted for by another ICHD-3 disorder

Primary Headaches

No underlying abnormality. -99.5% of headache. Includes: Migraine, tension, cluster, trigeminal autonomic cephalgias Other : stabbing ,cough, exertional, sexual activity, thunderclap, hypnic, hemicrania continua

MIGRAINE PREVENTION: Tricyclic antidepressants

Non-sedating -Protriptyline -Desipramine Sedating -Amitriptyline -Doxepin -Nortriptyline -Imipramine

CSF leak presentation

Postural headache is usually but not always the major manifestation of spontaneous intracranial hypotension The neurologic examination is often normal The headache with this syndrome is often described as throbbing or dull pain that may be generalized or focal. Headache relief is typically obtained with recumbency, usually within minutes. The headache is seldom relieved with analgesics. Exacerbating factors include erect posture, head movement, coughing, straining, sneezing, jugular venous compression, and high altitude ●Neck pain or stiffness ●Nausea ●Vomiting

Trigeminal autonomic cephalagias: Paroxysmal hemicrania presentation

Pts typically have unilateral, brief, severe attacks of pain associated with cranial autonomic features that recur several times per day. -The pain is most often in the ophthalmic trigeminal distribution (V1), but it can be extratrigeminal. -Attacks of paroxysmal hemicrania typically occur in association with ipsilateral cranial autonomic features: Lacrimation, conjunctival injection, rhinorrhea, nasal congestion, ptosis, or facial flushing frequently accompany the headache

Lumbar Puncture?

SUDDEN-ONSET, SEVERE HEADACHE -negative noncontrast head CT scan -Subarachnoid hemorrhage/Apoplexy (bleeding into pituitary) SIGNS OF INCREASED INTRACRANIAL PRESSURE -papilledema -absent venous pulsations on Fundoscopic exam -altered mental status -focal neurologic deficits -signs of meningeal irritation- should undergo a neuroimaging study before having a lumbar puncture. **•Do not want to herniate someone thus should indergo a neuroimaging study before LP

Post-concussive HA treatment

Simple reassurance is often the major treatment, since most patients will improve within three months. -Cognitive or physical rest -HA management -Managementment of sleep-wake disorders -

Sinus headache vs. Migraine

Sinus-related HA commonly confused with migraine •Prevalence of overlapping sinus symptoms in people diagnosed with migraine (IHS criteria) -Facial or maxillary pain 39% -Nasal discharge 12% -Sensitive to weather changes 33% -Sinus problems 40% -Any of the above 72% •Other reasons -Decongestants can "take the edge off" of migraine -Withdrawal from decongestants can precipitate migraines

Treatment of TBI

Some form of observation is recommended for at least 24 hours after a mild TBI because of the risk of intracranial complications; while the incidence is low, sequelae are potentially life threatening. Some patients may be safely monitored at home by a responsible caregiver, while inpatient observation is recommended for others Patients who have suffered loss of consciousness or have persistent symptoms should be referred to an emergency departmen

Medication oversuse HA (MOH) MOA

Still uncertain but multiple factors play a role into whether MOH will occur -Genetic predisposition: MOH is restricted to individuals who already have other headache disorders -Central sensitization: In humans, chronic exposure to triptans and other analgesics could lead to downregulation of serotonin receptors and changes in central inhibitory pathways that translate to an impairment of antinociceptive activity and a permanent feeling of head pain -Biobehavioral factors: It has been proposed that MOH is a biobehavioral disorder . Some patients may have compulsive drug seeking and drug taking behavior despite negative consequences, as the basis of MOH. Other patients may use opiates or other drugs with sedative/anxiolytic effects to treat both pain and a coexistent anxiety disorder

Diagnosing mild TBI aka concussion

The diagnosis of concussion or mild TBI is made in an individual with a head injury due to contact; brief loss of consciousness may or may not have occurred. The patient typically has neurologic symptoms, including confusion or memory loss as described above, but does not have neurologic deficits that are associated with a Glasgow Coma Scale (GCS) score of less than 13, measured at approximately 30 minutes after the injur

CSF leak diagnosis

The diagnosis of spontaneous intracranial hypotension should be considered in patients who present with positional orthostatic headache, with or without associated symptoms, perhaps in the setting of minor trauma, and in the absence of a history of dural puncture or other cause of cerebrospinal fluid (CSF) fistula. Confirmation of the diagnosis requires evidence of low CSF pressure, most often by magnetic resonance imaging (MRI; eg, pachymeningeal enhancement) or by radioisotope cisternography, and/or evidence of a CSF leak on other neuroimaging studies, mainly computed tomographic (CT) myelography. Diagnostic criteria for headache attributed to spontaneous intracranial hypotension, as delineated by the International Classification of Headache Disorders, 3rd edition (ICHD-3), are as follows [78]: ●A) Any headache fulfilling criterion C ●B) Either or both of the following: •Low CSF pressure (<60 mmH20) •Evidence of CSF leakage on imaging ●C) Headache has developed in temporal relation to the low CSF pressure or CSF leakage, or has led to its discovery ●D) Not better accounted for by another ICHD-3 diagnosis

Trigeminal autonomic cephalagias: Paroxysmal hemicrania time course

The headache usually lasts 2 to 30 minutes, but may go on for up to two hours. -the attacks tend to occur at a high frequency, with a range from 1 to 40 daily. The diagnosis is confirmed by an optimum response to a therapeutic trial of indomethacin.

Migraine aura

The two important historical features of the aura are the subjective description and its duration -The IHS criteria require each aura feature to be longer than 4 minutes and shorter than 60 minutes in duration -Aura that lasts more than 1 hr are classified as complicated migraine -Migraine w aura=more likely indicator of vascular issues (do not prescribe oral contraceptives w estrogen) -•Visual symptoms: (most common) haziness, shimmering heat waves, bright or dark holes in visual field to frank hemianopia •Sensory symptoms: 20% tingling paresthesias- facial circumoral and UE, 11% dysphasia, 4% unilateral weakness Can have both sensory and visual aurae

Traumatic brain injury epi

Traumatic insult d/t external physical force that may produce a diminished or altered state of consciousness

Trigeminal autonomic cephalagias

a group of primary headache disorders characterized by unilateral trigeminal distribution pain that occurs in association with prominent ipsilateral cranial autonomic features . The trigeminal autonomic cephalalgias include: - cluster headache - paroxysmal hemicrania - short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) - short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA) - hemicrania continua The most widely accepted theory is that the trigeminal autonomic cephalalgias are due to an abnormality in the hypothalamus leading to hypothalamic activation with secondary activation of the trigeminal autonomic reflex, probably via a trigeminal-hypothalamic pathway.

If concerned for solids (ie lesion or mass)

contrast MRI

Post-concussive HA diagnosis

functional injury-Makes it difficult to diagnose •Neuroimaging is normal -Requires establish temporal relationship to head trauma •direct blow to the head, face, neck, or elsewhere on the body with an "impulsive" force transmitted to the head

MIGRAINE PREVENTION: Glucocorticoids

hydrocortisone, prednisone, dexamethasone (HPA axis suppression)

tension-type headache

location: Bilateral -Characteristics: Pressure or tightness which waxes and wanes -patient appearance: Patient may remain active or may need to rest -Duration: variable -Associated symptoms: none

Most HAs are caused by what?

muscle contraction or blood flow problems •Distrubution of muscles (for example TTH are everywhere). Distribution of vessels and nerves travel along the same pathways.

chronic tension type HA diagnostic criteria

occurring more than 180 days each year

MIGRAINE PREVENTION: Methysergides

refractory ...SE valvulop/retro peritoneal fibrosis

Medication oversuse HA (MOH)

term applied to headache occurring on 15 or more days per month developing as a consequence of regular overuse of acute headache medication for more than three months It usually, but not invariably, resolves after the overuse is stopped

The principal diagnostic features of migraine

throbbing pain unilateral pain (least sensitive criterion) duration from 4 to 72 hours nausea photophobia phonophobia exacerbation by routine physical activity.

Premonitory phase

•12 to 24 hours prior to headache •May include: anxiety, tension, fatigue, depression, altered sleep, carbohydrate craving, difficulty concentrating, neck stiffness, nausea, pallor, sensitivity, etc. •Prophylaxis works at this stage (Triptans: such as Imitrex or sumatriptan) •Treatment: exercise, limit caffeine, limit carbohydrates, increase water intake, avoid ETOH, rest, avoid tobacco smoke.

Headache: Low-Risk Indicators

•< 30 years •Features typical of primary headaches •History of similar headache •No abnormal neurologic findings •No concerning change in usual headache pattern •No high-risk comorbid conditions (e.g.,HIV) •No new, concerning H&P findings

Head Injury/Concussion Physical Exam

•ABCs •Cardiovascular •Respiratory •HEENT •Neuro (mental status with Glascow, CN, etc) •MS (c-spine, back) •Change in clinical status since the time of injury? • This may involve seeking additional information from parents, coaches, teammates and eyewitness to the injury. •Assess need for emergent neuroimaging in order to exclude a more severe brain injury involving a structural abnormality •Repeat exam frequently •Other systems if indicated/based upon injury

Drugs causing MOH

•Butalbital containing combination products, 48 percent •Acetaminophen, 46 percent •Opioids, 33 percent •Aspirin 32 percent •Triptans, 18 percent •Ergotamine tartrate, 12 percent •NSAIDS other than aspirin, 10 percent

When You Do Need to Get a Scan

•Extremely abrupt onset of headache • Persistent unremitting headache • New onset of headache in patient >50yo • Fever • Papilledema • Abnormal neurological examination Cluster-type HA who hasn't had it before should get a scan. Very abrupt onset is not uncommon in cluster HA.

Head Injury: Indicators of increased ICP

•Headache increasing in severity •Decreased level of consciousness •Restlessness, irritable •Vital signs- bradycardia, hypertension •Papilledema

Am. Acad. Neuro: 4 effective questions for HA screening

•How often do you get severe headaches (ie, without treatment it is difficult to function)? •How often do you get other (milder) headaches? •How often do you take headache relievers or pain pills? •Has there been any recent change in your headaches?

Post-concussive HA epi

•Less than 10% will have had LOC -Previously was considered hallmark

aura

•Likely caused by wave of short-lasting cortical excitation followed by prolonged depression of cortical neuron activity •Affects 1/3 of migraine sufferers •Lasts >4 min but <60minutes. 70% <30min -Fades after 15-30 minutes -Replaced with HA, N/V, photophobia, phonophobia •Visual symptoms: (most common) haziness, shimmering heat waves, bright or dark holes in visual field to frank hemianopia •Sensory symptoms: 20% tingling paresthesias- facial circumoral and UE, 11% dysphasia, 4% unilateral weakness Aura that lasts more than 1 hr are classified as complicated migraine Migraine w aura=more likely indicator of vascular issues (do not prescribe oral contraceptives w estrogen

Traumatic brain injury presentation

•May begin days or weeks after MTBI and persist for weeks to years •Common Sx: -Headaches -Dizziness -Fatigue -Irritability -Anxiety -Insomnia -loss of concentration and memory -noise sensitivity The hallmark symptoms of concussion are confusion and amnesia, sometimes with, but often without, preceding loss of consciousness These symptoms may be apparent immediately after the head injury or may appear several minutes later Clinical findings NOT consistent with mild, uncomplicated TBI include focal neurologic findings such as limb weakness or hemiparesis, visual field deficit, pupillary abnormality, or Horner syndrome. These should be evaluated independently. A stroke syndrome, in particular, raises suspicion for traumatic vascular injury, while paraparesis or paraplegia suggests spinal cord inju

Headache: Physical exam Red Flags

•Meningismus (Meningismus=symptoms of brain/spinal cord irritation, but without actual inflammation) •Papilledema •Focal neurologic signs •Fever •Altered mental status

Headache: Tension-type (TTH)

•Mild to moderate intensity, bilateral, nonthrobbing headache without other associated features -relatively featureless HA ->least distinct of all the primary headache phenotypes -Least studies/understood •3 subtypes of TTH: helps determine treatment approach -Infrequent episodic TTH, with headache episodes less than one day a month -Frequent episodic TTH, with headache episodes 1 to 14 days a month -Chronic TTH, with headaches 15 or more days a month

Headaches and Children

•Much the same distribution of HA: -But variable presenting sx -> difficulty diagnosing -Migraine #1 primary HA type -Shorter duration—usually < 1 hour -More often bilateral (bifrontal or bitemoporal) than in adutls May present w/ hemiplegia, ophthalmoplegia, tinnitus, vertigo, ataxia, weakness, confusion, and paresthesias -requires workup to exclude tumor •Young children respond to pain differently than older children -> may not be apparent -crying, rocking, or hiding -Chronic pain may cause developmental regression, anxiety, depression, and behavior problems -affect the child's ability to eat, sleep, or play. Older children are better able to perceive, localize, and remember pain

Headache: High-Risk Indicators [Red Flags]

•New onset before 5 yo and after age 50 •Sudden onset of new/severe HA -i.e. Subarachnoid hemorrhage •Onset with Onset exertion (strain, cough, sex) or increase with strenuous exercise -IC hemorrhage or Cart. dissection •Progressive worsening -mass lesion, subdural hematoma, or medication overuse headache •Change in cognition, focal neuro deficits or systemic features (fever, myalgia, weight loss etc) •Any abnormality on neuro or physical exam •"Worst" HA ever -"Thunderclap headache" (that reaches maximal intensity within a few seconds or less than one minute after the onset of pain) -intracranial hemorrhage or CNS infection

Secondary Headache: H&P "Can't Miss"

•Nuchal rigidity—meningitis or SA bleed •Pain or cords over temporal artery—temporal arteritis •Headache, fatigue, generalized aches and pain, and night sweats > 55 yo--temporal arteritis •Sudden, severe, unilateral vision loss --optic neuritis •Intermittent HA with elevated BP--pheochromocytoma. •nausea, vomiting, worsening of headache with changes in body position (particularly bending over), an abnormal neurologic examination, and/or a significant change in prior headache pattern --tumor

Headache: Additional Red Flags

•Pain in middle of night •Seizure •Maximal intensity in few seconds-minutes or worsening of normal HA pattern •New HA during pregnancy or postpartum •New HA in patient with CA, HIV or Lyme disease •Elderly patient with new headache and subacute cognitive change -subacute or chronic subdural hematoma. -Head injury not always present Pain in the middle of the night: mostly in tension type HA. Will be more concerned. -Maximal intensity in few seconds-minutes or worsening of normal HA pattern: cluster HA, but not a typical type of HA -Hx if head injury: assess in elderly with HA and subacute and cognitivie change

When Don't You Need to Get a Scan?

•Patient with established history of episodic headache • Current headache is consistent with previous headaches or is consistent with different manifestation of a primary headache. • Normal neurological exam

Headache Physical Exam: Neck exam

•Physical examination of patients with headache should include an assessment of neck posture and range of motion, and palpation for muscle tender points. Focused Neurological Examination •A focused neurological examination should be added if indicated by patient symptoms and/or abnormal signs on the screening examination (e.g., dysarthria would lead to more detailed assessment of lower cranial nerves; reflex asymmetry would lead to assessment of plantar responses). Examination for Temporomandibular Disorders •If headache and associated jaw complaints, include clinical assessment of jaw movements and palpation of the muscles of mastication for tender points.

Post-concussive HA MOA

•Postconcussion syndrome controversial—pathophys unclear •Functional rather than structural injury that can affect somatic, cognitive, and affective domains most often described in the setting of mild TBI, but it may also occur after moderate and severe TBI, and similar symptoms are described after whiplash injuries as well the severity of injury does not clearly correlate with the risk of PCS.

Post-concussive HA presentation

•Results in a graded set of clinical symptoms -Symptoms - somatic (e.g. headache), cognitive (e.g. feeling like in a fog) and/or emotional symptoms (e.g. lability) -Physical signs (e.g. loss of consciousness, amnesia) -Behavioural changes (e.g. irritability) -Cognitive impairment (e.g. slowed reaction times) -Sleep disturbance (e.g. drowsiness, insomnia) Most common complaints: -HA -dizziness -fatigue -irritability -anxiety -insomnia -loss of concentration and memory -noise sensitivity

911 HA

•THE WORST HEADACHE OF MY LIFE" • Sudden onset Associated changes •vision, •movement •balance •Mental status • More severe when lying down • Change in headache patterns or pain

Migraine And Pregnancy

•The significant majority of women have an improvement in migraine frequency during the 2nd and 3rd trimesters of pregnancy •There is no consensus or evidenced based approach to treatment of headache during pregnancy •Regular small amounts of caffeine, magnesium supplementation are reasonable non-prescription alternatives •The only adverse event that has been identified with triptans and pregnancy is a slightly increased risk of premature delivery....I.E. Ok to use triptans in severe cases

Migraine Cascade

•Triggers •Premonitory •Aura •Headache •Post- headache •May last 5 days

Cluster headache presentation

•Typically have a long symptom free period •Each episode is more protracted and pain more severe •Cycle repeats over years with increased frequency and severity •Typically awakes during REM sleep at the same time each night -Attacks in groups -Severe pain -Last 30-45 mins -One or > daily. Am & late pm -Cycles can last weeks, months, years -Prevalence 1% pop age 20-45 -May be relieved with O2

Trigeminal autonomic cephalagias: Cluster HA epi MOA

•Unknown etiology- suggested is cyclic neurochemical disturbance that causes periodic spasm, edema or inflammation of internal carotid artery near the skull.

Headache: Tension-type (TTH) Etiology

•Unknown- may result from psychological or environmental stress (anxiety, depression, fatigue, etc). Debate whether stressors are causal or secondary to headache. •Electromyographic studies have shown no sustained muscle contraction or change in blood flow to tender muscles. •May be triggered by stressors, poor posture, anxiety, depression, cervical OA, etc •Theorized pathophys: -Heightened sensitivity of pain pathways in the CNS [and PNS?] -Nitric oxide may be a molecular trigger for pain. •Regulator of cerebral/extra-cerebral blood flow -Genetic factors seem to play a minor role in episodic TTH but may be more important in chronic TTH Nitric oxide (NO) is a very important molecule in the regulation of cerebral and extra cerebral cranial blood flow and arterial diameters. It is also involved in nociceptive processing

Summary- 911 HEADACHE

•Worst •Sudden •Associated •Supine •Change

Diagnostic criteria for chronic cluster headache require the following

●Attacks fulfilling criteria for cluster headache ●Attacks occurring without a remission period, or with remissions lasting less than three months, for at least one year

Diagnostic criteria for episodic cluster headache require the following

●Attacks fulfilling criteria for cluster headache and occurring in bouts (cluster periods) ●At least two cluster periods lasting from seven days to one year (when untreated) and separated by pain-free remission periods of three months or more

With headache subtypes of shorter duration (ie, less than four hours), "chronic" refers to a prolonged duration of the condition itself without remission. The headache subtypes in this category are the following:

●Chronic cluster headache ●Chronic paroxysmal hemicrania, characterized by unilateral, brief, severe attacks of pain associated with cranial autonomic features that recur several times per day with individual headache attacks that usually last 2 to 30 minutes ●Short-lasting unilateral neuralgiform headache attacks, characterized by sudden brief attacks of severe unilateral head pain in orbital, peri-orbital, or temporal regions, accompanied by ipsilateral cranial autonomic symptoms ●Hypnic headache, also known as "alarm clock headache," which occurs almost exclusively after the age of 50 years and is characterized by episodes of dull head pain, often bilateral, that awaken the sufferer from sleep ●Primary stabbing headache, characterized by sudden brief attacks of sharp, jabbing head pain in orbital, peri-orbital, or temporal regions

With headache subtypes of long duration (ie, four hours or more), "chronic" indicates a headache frequency of 15 or more days a month for longer than three months in the absence of organic pathology. These headache subtypes are:

●Chronic migraine headache ●Chronic TTH ●Medication overuse headache, which is typically preceded by an episodic headache disorder (usually migraine or TTH) that has been treated with frequent and excessive amounts of acute symptomatic medications ●Hemicrania continua, a strictly unilateral, continuous headache with superimposed exacerbations of moderate to severe intensity accompanied by autonomic features and sometimes by migrainous symptoms ●New daily persistent headache, characterized by headache that begins rather abruptly and is daily and unremitting from onset or within three days of onset at most, typically in individuals without a prior headache history

CSF leak epi

●The estimated annual incidence is 5 per 100,000 ●The peak incidence is around age 40, but children and older adults are also affected ●Women are affected more frequently than men, with a female to male ratio of 2:1