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MSY2 Neuro > Headaches > Flashcards

Headaches Flashcards

1
Q

*Red Flag*

DDX…HA +

split second onset, unexpected, WOSRT HA EVER/never previously encountered, LOC, vertigo, vomiting

A

Consider DDX:

Aneurysmal Subarachnoid Hemorrhage

Cerebellar Hematoma

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2
Q

*Red Flag*

DDx to consider: HA +

Fever and skin rash

A

DDx:

Meningitis

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3
Q

*Red Flag*

DDx to consider: HA in immunosuppressed state

A

Crypto meningitis

Toxoplasmosis

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4
Q

*Red Flag*

DDx to consider: HA with coagulopathy/anticoagulation

A

Subdural hematoma

intradural hematoma

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5
Q

What type of drugs should never be used to treat a headache?

(1 example)

A

Opiods and narcotics

DO NOT USE: butalbital-acetaminophen combination therapy

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6
Q

[True/False]

Severity of the HA is key to clinically diagnose a migraine hHA

A

FALSE

Severisty is NOT A FEATURE of migraines

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7
Q

What are the three key clinical questions that would highly point to Migraines?

A
  1. Do you have NAUSEA or feel SICK to your STOMACH with your HA?
  2. Does LIGHT BOTHER you more than with a HA than withouth a HA?
  3. Does the HA LIMIT YOU from working, studying or doing what you need to do?

*IF yes to all three: sensivity 0.81, specificity 0/75

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8
Q

Typical clinical symtopms of a migraine (6):

Risk Factors (3):

A

a migraine POUNDS:

P: pulsatile

O: one-day duration

U: unilateral

N: nausea

D: disabling

S: stereotypical

INC Risk Factors: females, young, + family history

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9
Q

What are some typical triggers of migraines (8):

A

Stress

Lack of sleep

Hunger

Hormonal fluctuations

Foods (+/-)

Alcohol/nitrates

Weather changes

Smokes, scents, fumes

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10
Q

Name the 4 phases of a migraine:

A

PAPP

    1. PROdrome*
    1. AURA*
    1. Pain*
    1. POSTdrome*
  • (PAPPs give me migraines)*
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11
Q

Phase 1 of Migraines:

When could the pt experience it?

What are signs the pt could experience?

A

Phase 1: Prodrome

Occurs: 6 hours to 48 hours before the HA (60% of patients)

SX: depression, irritability, drowsiness, fatigue, yawning, rhinorrhea/lacrimation, hunger/third (cause or reaction?)

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12
Q

Phase 2:

When can it occur?

How long can it last?

What are the different types?

A

Phase 2: Aura, due to spreading cortical depression

BEFORE > during >> after the HA

develops over 5-20 minutes and lasts usually <60 minutes

you can expect the HA within 60 minutes

Types: VISUAL (most common), sensory, motor, brainstem (dizziness/diplopia) or cortical (aphasia)

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13
Q

What is an acephalgic migraine?

A

An aura not associated with headache symptoms

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14
Q

A person experiencing a visual aura…

near the center of vision, the patient has a ____ _____ that prohibits reading

in the periphery, the person experiences ____ and pulsating ____ of light across the visual field

A

near the center of vision, the patient has a BLIND SPOT that prohibits reading

in the periphery, the person experiences FLASHING and pulsating BANDS of light across the visual field

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15
Q

Phase 3:

Three main locations where it can occur:

Onset timing:

Duration:

Associations (5 main categories)

A

Phase 3: Pain

Locations: Head (most common), abdomen (abdominal migraine) or chest (precordial migraine)

Onset: gradual, minutes –> hours

Duration: hours to days

Associations: Phobia to light, sound, odor, temp, N/V

Photophobia, phonophobia

Nausea/vomiting

Osmophobia, Termophobia

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16
Q

Spreading Cortical Depression:

A genetically susceptible patient has a multifactoria defect in brain metabolism leading to a ______ in _______ receptor function.

This receptor is ________ (inhibitor/excitatory)

Activation of the receptor leads to a burst of focal _____ activity causing local _______ (INC/DEC of blood) and ______ (+/-) symptoms

It is usually in the ______ lobe of the brain

Burst is then followed by a ______ (gain/loss) of neuronal activity = ___ ___

Moves at _____ mm/min and advances until there is a ______ in ____ _____.

A

Spreading Cortical Depression:

A genetically susceptible patient has a multifactorial defect in brain metabolism leading to GAIN in NMDA receptor function.

This receptor is EXCITATORY (inhibitor/excitatory)

Activation of the receptor leads to a burst of focal cerebral activity causing local HYPEREMIA (INC/DEC of blood) and POSITIVE (+/-) symptoms (probably why you see lights, etc) = WAVE FRONT

It is usually in the OCCIPITAL lobe of the brain

Burst is then followed by a LOSS (gain/loss) of neuronal activity = CEREBRAL DEPRESSION

Moves at 3 mm/min and advances until there is a CHANGE in CORTICAL ARCHITECTURE

17
Q

*What are ways to optimize the treatment of acute attacks of migraines (5):

A

treat EARLY in the attack when the pain is still mild

NSAIDS are first line, followed by triptans

Use effective DOSES

AVOID butalbital-containing medications

RX associated symptoms

18
Q

*What is the first line medication effective for migraine HA?

A

OTC NSAIDS

19
Q

*What if the patient does not respond to analgesics, pain is too much, what are second line medications?

A

TRIPTAN

agonist of 5HT (1b/d) R

may lead to vasoconstriction

(7 different types with a range of half lives 3-26 hours, and routes of delivery; inadequacy to one doesn’t mean ineffective response to all)

20
Q

Who would NOT be a good candidate for triptan therapy (7)?

A

*AVOID in thsoe with vascular risk factors*

NO: has/at risk for ischemic heart disease

NO: uncontrolled HTN, renal disease

NO: pregnancy

NO: basilar migraine, hemiplegic migraine

AVOID within 24 hours with ergotamine

NO: if pt is on MAO inhibitor

21
Q

What are the TRIPTAN SENSATIONS (aka - side effects) (6)?

A

pressure, pain, tightness, warmth, heaviness and tingling

notify the patient of the potential side effects they could experience; should be okay since they should be screened for vascular disease prior to be prescribed this medication

(ppttw)

22
Q

*What are two other alternative migraine therapies that could be used after Triptan?

A

Ergot Alkaloids: Ergotamine and DHE

more powerful, yet more side effects

Ergotamine: Seratonin syndrome; “triptan on steroids” lots more contraindications and precautin with its use especially on people potentially with ischemic disease.

23
Q

*When should preventative therapy be considered (4)?

A
  1. Incidence of attacks > 2-3 times per month
  2. Attacks are severe and impair normal activity
  3. Patient is psychologically unable to cope with the attacks
  4. Optimal abortive therapies have failed or produced serious side effects
24
Q

What are alternative therapies/aside from medication, that could be considered (5):

A
  • Avoid triggers
  • relaxation, biofeedback, acupuncture
  • physical therapy
  • dietary/vitamin supplementation
  • Botulinum Toxin (only for chronic migraines after many failed attempts)
25
Q

*Cluster Headaches:

Criteria (3)

Risk Factors

Associated Syndromes (2)

Treatment (6)

A

“one of the most severe headaches”

Criteria: 1-4 attacks/day, >30 minutes

rapid onset (15-30 minutes)

clusters lasting 6-12 weeks

INC Risk Factors: M>F, 40s, smokers, drinkers, spring/autumn, nights, unilateral during attack

Associated Syndromes: Horner’s, unilateral rhinorrhea

RX: Inhaled O2 (100% by rebreather at 10-15 L/min)

Injectable sumatriptan

Nasal spray triptans

intranasal lidocaine

intranasal DHE

  • Prednisone (not first line)*
  • [oral medication NOT useful]*
26
Q

*Tension-type Headache:

Clinical Features (6)

Treatment

A

Clinical Features:

Bilateral, >30 minutes, lasting usually 4-6 hours

Band-like head pain with pressing or tightening quality

Mild - moderate intensity

NOT aggravated by routine activity

NO N/V

Phonophobia OR photophobia (either NOT BOTH)

Treatment:

Screen for depression and sleep disorders

TCA may be helpful (amitriptyline)

Physiotherapy, biofeedback

27
Q

Trigeminal Neuralgia

Clinical Featuers:

(most affected area is the _____; with ___ and ___ divisions the TN)

Treatment:

A

Paraoxysmal attacks of pain lasting from a fraction of a second to two minutes, affecting one or more divisions of the trigeminal nerve (V1/V2 usually; affecting the _jaw_ mostly)

Clinical features:

Peak incidence 60-70, worse with talking or eating, often after dentist visit

MS is the most common associated disease

Treatment: Carbamazepine (first line)

[Others: oxcarbazepine, baclofen, Iamotrigine]

28
Q

*Pseudotumor Cerebri:

Clinical Features

Treatment

A

*MEDICAL EMERGENCY*

Clinical Features:

ICP >250 mm H20 (spinal tap)

HA is the presenting feature in >75% of pt​

No localizing features, no mass lesion or enhancement, normal CSF content, no CVT

Fundascope: papilledema (signifying increased pressure)

Treatment: spinal tap to reduce pressure +

actezolamine, topiramate, surgical intervention

29
Q

Primary Exertional Heachache:

Clinical Features

Treatment

A

Clinical Features:

Pulsating HA from 5 minutes to 48 hours

occuring only during or after physical activity

Younger patients, M>F

Treatment:

Beta-blockers, Indomethacin

(prophylaxis before exertion, screen for aneurysms, treat for 3-6 months)

MSY2 Neuro (25 decks)

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