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MHD Neuro > Headaches > Flashcards

Headaches Flashcards

1
Q

What Causes HA: Pain Pathways

A
  • The brain parenchyma itself DOES NOT produce pain
  • An intracranial lesion (tumor, hemorrhage) does not produce headache pain by itself—the swelling around it may cause headache by stretching or compressing blood vessels or CN
  • What produces pain?
    • Skin, subcutaneous tissue, muscles, extracranial arteries, periosteum of the skull
    • Delicate structures of the eye, ear, nasal cavities & paranasal sinuses
    • Intracranial venous sinuses & tributaries
    • Dura at the base of the brain & arteries within the dura and pia-arachnoid (ACA, MCA, ICA)
    • Optic, oculomotor, trigeminal, glossopharyngeal, vagus, first three cervical nerves
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2
Q

What are the two main types of HA?

A
  1. Primary HA (majority of HA in clinic)
    1. Condition in which HA=primary manifestation
    2. NO underlying disease process=BENIGN
    3. Types:
      1. MG
      2. Cluster
      3. Tension
      4. Trigeminal Neuralgia
      5. Pseudotumor Cerebri
      6. Primary Exertional HA
  2. Secondary HA-often more serious and concerning!!
    1. HA is a secondary manifestation of an underlying disease process
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3
Q

What are the most common HA?

A
  • Tension-type
  • Migraine & variants
  • Fever or Hunger provoked
  • Nasal/paranasal, ear, tooth, eye disease
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4
Q

Aneurysmal subarachnoid hemorrhage

A

Vignette: 24 year old female presents for the sudden onset of the “worst headache of her life.” Her neurologic examination is notable for an enlarged and poorly reactive right pupil. What is the most likely diagnosis?

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5
Q

A. What are the RED FLAGS for Rapid HA Evaluation?

B. Signs and Symptoms/Diagnosis to Consider

A
  1. split second, unexpected, worst/not previously encountered, LOC, vertigo vomiting
    1. D2C: aneurysmal SAH, cerebellar hematoma
  2. Fever and skin rash
    1. D2C: meningitis
  3. Immunosuppressed state
    1. D2C: crypto meningitis, toxoplasmosis
  4. Coagulopathy/anticoaulation
    1. D2C: subdural or intradural hematoma
  5. Acute cranial neuropathy
    1. D2C: carotid artery aneurysm
  6. Carotid bruit in the young:
    1. D2C: carotid artery dissection
  7. Shock, Addison’s
    1. Pituitary apoplexy

Note: Also have raid HA Eval: NON-Neurologic causes:

  • acute angle glaucoma
  • temporal arteritis
  • acute sinusitis
  • pheochromocytoma
  • Herpes zoster
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6
Q

Vignette and Tx for a Classic Migraine HA

A
  • A 28 year old male presents for complaint of visual problems and headaches. He reports the development of a shimmering light in his left visual field that gets bigger over the course of about 30 minutes, followed by a pounding left sided headache lasting several hours, associated with an upset stomach, light and sound sensitivity.
  • Tx: SUMATRIPTAN 100 mg=migraine specific medication
    • do NOT use BUTALBITAL-ACETAMINOPHEN combo therapy–may worsen HA
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7
Q

What are the “Key Clinical Questions” for a Migraine?

Sn/Sp?

A
  1. Do you have nausea or feel sick to your stomach with your HA?
  2. Does light bother you more with a headache than w/o?
  3. Does the HA limit you from working, studying, or doing what you need to do?

**Sn=0.81, Sp=0.75 for migraine headache if all 3 are positive

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8
Q

Migraine Epidemiology/Genetics

A
  • genetic condition in which a person has a predisposition to:
    • episodic headaches
    • GI dysfunction
    • –OR– neurologic dysfunction
  • Severity NEED NOT BE a feature
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9
Q

What are typical clinical symptoms for Migraines?

A
  • Periodic, usually unilateral pulsatile
  • **Begin in late childhood or early adult life (“From menarche to menopause.”)
    • Peaks around age 40 (wont be 75 yo pt with first-time HA)
    • 16% of women, 6% of men
  • Recur with diminishing frequency throughout life
  • It is unusual to develop late in life
  • Usually stereotypical (pt can accurately describe)
  • Most patients will limit activities due to/during the headache

The POUND of Migraine: Pulsatile, One-Day duration, Unilateral, Nausea, Disabling

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10
Q

Typical Triggers of Migraines

A
  • Stress
  • Lack of sleep
  • Hunger
  • Hormonal fluctuations
  • Foods (+/-)
  • Alcohol/nitrates
  • Weather changes
  • Smokes, scents, fumes
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11
Q

What are the Migraine Phases?

A
  1. PRO-drome
  2. Aura
  3. Pain
    1. SCD (spreading cortical depression)
    2. Trigeminovascular Reflex and SCD
  4. POST-drome
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12
Q

Migraine-Step 1: PRO-drome

A
  1. Prodrome: occurs hours (6hrs) to days (48hrs) BEFORE the headache (in 60% of patients)
  • Depression
  • Irritability
  • Drowsiness
  • Fatigue
  • Yawning
  • Rhinorrhea/lacrimation
  • Hunger/thirst
  • Cravings for chocolate, nuts, bananas (controversy as to cause or effect)
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13
Q

Migraine-Step 2: Aura

A

AURA can be:

  1. visual (most common)
    1. ​blind spot near center of vision prohibits reading, as peripheral, flashing, pulsating bands of light spread out across the visual field.
  2. sensory (numbness/tingling)
  3. motor, brainstem (dizziness/diplopia)
  4. cortical (aphasia)
  • Can occur BEFORE (most common)> during >> or after the HA
  • Usually develop over 5-20 minutes
    • NOT seconds–that would be a detached retina
  • Usually last <60 minutes
  • HA usually occurs within 60 minutes
  • May not be associated with HA (acephalgic migraine)
  • May not be present (common migraine; migraine without aura)
    • BUT, characteristics and associated features are otherwise identical to migraine with aura.
  • Due to “spreading cortical depression”
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14
Q

Migraine-Step 3: PAIN

A
  1. PAIN may be:
  2. in the head (most common, by far)
  3. abdomen (abdominal migraine)
  4. chest (precordial migraine)
  • Onset: gradual over minutes to hours
  • Duration: hours to days
  • Can be associated with:
    • Photophobia, phonophobia
    • Nausea/vomiting
    • Osmophobia (fear, aversion or psychological aversion to odors)
    • Thermophobia
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15
Q

Migraine-Step 3.1: Spreading Cortical Depression (SCD)

A
  • A genetically susceptible pt has a multifactorial defect in brain metabolism leading to a gain in NMDA-receptor function (an excitatory receptor)
    • NMDA activation leads to a burst of focal cerebral activity causing:
      • local hyperemia
      • “positive” symptoms
  • Usually in the occipital lobe
  • Burst followed by a loss of neuronal activity (“cortical depression”)
  • Slow, deliberate march forward at around 3 mm/min
  • Advances until there is a change in cortical architecture
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16
Q

Migraine-Step 3.2: Trigeminovascular Reflex & SCD

A
  • …with the fwd advance: Trigeminal nerves:
    1. ​ wrap around pain sensitive structures
    2. release local neuropeptides
    3. convey information to the trigeminal nucleus in the brainstem
  • Associated with release of neuropeptides (CGRP, Substance P, and Neurokinin A)
    • May lead to “neurogenic inflammation”
    • Evoke vasodilation of pain-producing structures
    • Creates a (postitive) feedback loop with the trigeminal pathway
      • gets progressively worse
17
Q

Migraine-Step 4: POST-drome

A
  1. POST-drome: present for several hours after the event
  • Mood changes (euphoria, fatigue)
  • Impaired concentration
  • Scalp/muscle tenderness
18
Q

Migraine Treatment

A

Optimizing the Tx of ACUTE Attacks of Migraine:

  1. Treat early in the attack when the pain is still mild (don’t “wait it out”!!!)
  2. Simple analgesics (OTC NSAIDs)=first-line tx for mild to moderate MG
    1. second-line=TRIPTANS
  3. Use effective doses! (doctors and patients often underdose)
  4. Avoid medications with high medication overuse potential (MOH): especially butalbital-containing medications
  5. Tx the associated symptoms when needed (ie, nausea)
  6. Consider SE & CI
  7. Less is more: try to minimize the use of medications as much as possible
19
Q

MG specific Therapies (A): TRIPTANS

A

If a patient fails to respond to simple analgesics –OR– has moderate to severe MG pain, MG-specific therapies are recommended

  • All triptans are agonists at 5HT1B/D receptors
  • May lead to vasocostriction
  • Range of agents available (currently 7), half-lives 3-26 hours, and routes of delivery
    • Inadequate response to one does not mean an inadequate response to all
  • Most provide approx 66% headache response at 2 hours
  • Most provide approx 30% pain-free response at 24
20
Q

Caveats (CI) in use of TRIPTAIN

A

**Common Theme: Avoid in those with vascular risk factors

  • Avoid if patient has/is at risk for, ischemic heart disease
  • Avoid with uncontrolled hypertension, renal disease
  • Should not be used during pregnancy
  • Avoid in cases of basilar migraine, hemiplegic migraine
    • Debatable contraindication in the literature
  • Avoid within 24 hrs of use with ergotamine
  • Avoid if patient on MAO inhibitor
21
Q

TRIPTAN Sensations (SE)-A

A
  • Warm/Hot sensations
  • Tightness (alarming for pts)
  • Tingling
  • Feelings of heaviness or pressure
  • Occur in nearly any part of the body
    • Most commonly reported in face, limbs, and chest
  • Occur with ALL 5-HT1B/1D agonists (hence the name “sensations”)
  • typically short in duration and resolve spontaneously
22
Q

TRIPTAN Serotonin Syndrome (SE)-B

A
  • Caused by excessive activation of 5-HT1a and 5-HT2 receptors
  • CP:
    • Severe leg-predominant rigidity
    • dysautonomia (diarrhea, excessive lacrimation, hyperactive bowel sounds)
    • encephalopathy characterized by myoclonus, hyper-reflexia & seizures
  • Usually within 24hr of med exposure/change
  • No reports of SS in triptan clinical trials.
    • Cases reports of it occurring with monotherapy.
    • Dual therapy is a risk but use is not prohibited.
23
Q

MG specific Therapies (B): ERGOT ALKALOIDS (Ergot & DHE)

A

Ergotamine

  • rarely used in US since introduction of TRIPTANS
  • available in US only in suppository form
  • potent arterial vasoconstrictor
  • extremely nauseating
  • causes uterine contractions

DHE (Dihydro-ergotamine)

  • more powerful than TRIPTAN, but more SE
  • IV, SC and nasal spray formulations
  • arterial and venous vasoconstrictor
  • less emetic
  • less uterine contractions than ergotamine
24
Q

MG specific Therapies (B.1): ERGOT ALKALOIDS (Ergot & DHE); CI/Precautions

A
  • STRONGER VASOCONSTRICTOR than TRIPTAN…
    • Ischemic cardiac, cerebrovascular, or peripheral vascular disease,
    • Collagen vascular disease or vasculitis
    • Cardiac valvular disease
    • Uncontrolled hypertension
  • Use within 24hrs of triptan therapy
  • Hemiplegic/basilar migraine
  • Prior evaluation of patients with risk factors for CAD
  • Renal or hepatic impairment
  • Pregnancy, breastfeeding
  • Age > 60
25
Q

When to consider a preventive therapy for MA

A
  1. Incidence of attacks ≥2-3 per month
  2. Attacks are severe and impair normal activity
  3. Patient is psychologically unable to cope with attacks
  4. Optimal abortive therapies have failed or produced serious side effects

Note:

  • some therapies (AMITRIPTYLINE) are indicated for depression BUT also tx MG
  • Valproic acid v. Topiramate v. PropranOLOL/MetoprOLOL; consider dosing other medical conditions, SIDE EFFECTS, and dosing regimen when selecting therapies
    • V-SE: weight gain, teratogenic, hair loss, liver and hematologic abnormalities
    • T-SE: lose weight, renal stones, angle closure glaucoma
    • OLOL: 2-for2
26
Q

MG Alternative Therapies

A
  • Avoid triggers
  • Relaxation, biofeedback, acupuncture
  • Physical therapy
  • Dietary/vitamin supplementation (no scientific research):
    • Petadolex type of Butterbur
    • Vitamin B2, B6
    • St.John’s Wort
    • Ginger
    • Gingko biloba
    • Fever few
    • Magnesium supplementation (+/-)
    • Coenzyme Q10
  • **Botulinum Toxin
    • Indicated only for CHRONIC MG HA
    • Usually approved only after a patient has failed multiple medications and has multiple headache days per month
    • Effective after 7-10 days up to 12 weeks
27
Q

“Other” HA-Cluster; Vignette

A

A 48 year old male presents for a severe boring pain in the left eye. What duration of symptoms is most consistent with cluster headaches…>30 minutes

28
Q

“Other”: Cluster HA Epidemiology + CP

A
  • One of the most severe headaches
  • More common in men (4.5:1)
  • Peak incidence 40-49y
  • Often heavy smokers & excessive alcohol use
  • More common in the spring & autumn
  • Commonly occur at night
  • Symptoms usually “side locked” during cluster but can switch sides in subsequent attacks
  • Clusters last 6-12 weeks
    • Typically occur every year or two
    • 85% episodic, 15% chronic/unremitting
    • 1-4 attacks/day lasting 20m to 3hrs
    • Rapid onset over usually 15-30 minutes (not seconds)
    • Invariably unilateral
  • Alcohol nearly always triggers attacks
  • Can be associated with a partial Horner’s & unilateral rhinorrhea
29
Q

Cluster HA-Acute Therapies

A
  • Limited by headache duration 30- 90 minutes
  • Oral medications of little use
  • Effective medications
    • Inhaled oxygen 100% by rebreather at 10-15 L/min
    • Injectable sumatriptan
    • Nasal spray triptans
    • Intranasal lidocaine
    • Intranasal DHE
  • Prednisone (last choice)
    • 60-100 mg Qdaily for 5-7 days
30
Q

“Other”: TENSION-type HA

A. CP

B. Tx

A
  • The most common form of HA (occurs in 35-75% of adults)
    • Rarely severe & thus account for <5% of visits
  • Clinical features
    • Bilateral pain lasting >30 minutes, usually 4-6 hours
    • Band-like head pain with a “pressing” or “tightening” quality
    • Mild-to-moderate intensity
    • Not aggravated by routine activity
    • No N/V
    • Phonophobia & photophobia can occur but not both
  • Treatment is both pharmacologic & non-pharmacologic
    • Screen for depression and sleep disorders
    • May be responsive to TCAs (amitriptyline)-helps ppl fall asleep
    • Physiotherapy, biofeedback–adjust day-to-day activity
31
Q

“Other”: TRIGEMINAL Neuralgia

A
  • Buzzwords: “SEVERE shooting/lightning pain radiating down the jaw” (vs. cluster HA usually behind the EYE and last MUCH longer)
    • Paroxysmal attacks of pain lasting from a fraction of a second to two minutes, affecting one or more divisions of the TN (trigeminal nerve)
    • worse with coughing, talking, chewing
  • Peak incidence 60-70, CTN unusual before 40
  • MS is the most common assoced disease (idiopathic most common)
  • Often end up at the dentist first for a root canal
  • Treatment:
    • CARBAMAZEPINE effective for controlling pain (200-1200 mg/d)=first line therapy
    • Oxcarbazepine is probably effective (600-1800 mg/d)
    • Baclofen & Lamotrigine are possibly effective
32
Q

“Other”: PSEUDO-tumor CEREBRI

A
  • most common in obese female pts on OCP with generalized HA
    • weight increasing intra-abdo pressure, decreases outflow, increases intracranial pressure–risk of BLINDNESS
  • Clinical Features:
    • ICP ≥250 mm H20
    • No localizing features
    • No mass lesion or enhancement
    • Normal CSF content
    • No CVT (cerebral vein thrombosis)
    • HA =presenting feature in ≥75%
  • Tx: actezolamide, topiramate, surgical intervention
33
Q

“Other”: PRIMARY Exertional HA

A
  • Pulsating HA last from 5 min to 48 hours, and occurring only during or after physical activity
  • Younger patients (10-48 y/o), usually male
  • Tx:
    • Beta-blockers
    • Indomethacin
    • Can treat for 3-6 months
  • {Jokl & Jokl (1968)
    • Described “effort migraines” during the Olympic Games
    • Athletes developed scotomas, retro-orbital pain, nausea, vomiting and prostration
    • Attributed to high altitude (7000 feet above sea level), heat, & humidity}
  • Note: Take NSAIDS before activity
34
Q

Differentiating Cluster v. Tension v. MG

A
  1. Cluster
    1. Location/Type: UNI-lateral/RETRO-orbital
    2. Duration: 15/20 mins-to-3 hrs
    3. Symptoms:excruciating peri-orbital pain with lacrimation
    4. Tx:inhaled oxygen or injectable SUMATRIPTAN
  2. Tension
    1. Location/Type: BI-lateral
    2. Duration: >30 min (usually hours)
    3. Symptoms: band-like pressure/pain
    4. Tx: sleep, diet, exercise, simple analgesics
  3. MG
    1. Location/Type: UNI-lateral
    2. Duration:4-72 hrs
    3. Symptoms: PULSATING pain with photo/phonophobia
    4. Tx: NSAIDS, Triptans

MHD Neuro (17 decks)

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