Headaches Flashcards

e.g. Migraine, Tension Headache

1
Q

Post-Traumatic Headache (PTH)
-> Definition + Etiology

A

PTH = a type of Secondary Headache

PTH =
Headache occurring in the days after a head injury or after regaining consciousness

Etiology:
PTH is a complication of..
- Traumatic Brain Injury (TBI)
- Whiplash injury (= Schleudertrauma)
- Craniotomy

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2
Q

Post-Concussive Syndrome

A
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3
Q

MODERATE or SEVERE Traumatic Brain Injury

A

Associated with:

1) Loss of consciousness for >30min
2) Glasgow Coma Scale (GCS) <13
3) Post-traumatic amnesia for > 24h
4) Altered Level of Consc. for > 24 h
5) Imaging positive for traumat. Head
injury -> e.g:
- Skull fracture,
- Intracranial Haemorrhage
- and/or Brain contusio

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4
Q

MILD Traumatic Brain Injury (mTBI)

A

Associated with NONE of the following
(= S&S of Moderate or Severe TBI):
a) Loss of consciousness for > 30min
b) Glasgow Coma Scale (GCS) <13
c) Post-traumatic amnesia for > 24h
d) Altered Level of Consc. for > 24 h
e) Imaging positive for traumat. Head
injury -> e.g:
- Skull fracture,
- Intracranial Haemorrhage
- and/or Brain contusio

Associated with MIND.1 of the following:
a) Transient confusion, disorientation, impaired consciousness

b) Memory loss for events immediately before / after injury

c) >2 of following Symptoms:
i. nausea
ii. vomiting
iii. visual disturbances
iv. dizziness and/or vertigo
v. gait and/or postural imbalance
vi. impaired memory and/or concentr.

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5
Q

Post-Traumatic Headache (PTH):

Diagnostic criteria & Types

A

PTH-Diagnosis is mostly based on Clinical criteria:

ACUTE PTH
- Onset of Headache within 7d after the head or neck trauma
- Remitting within 3 months after the onset

PERSISTENT PTH
(same as Acute =) Onset of Headache
within 7 d after head or neck trauma,
Persisting for > 3 months after onset

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6
Q

Secondary Headaches:
Venous Thrombosis

A

Symptoms, incl. Headache, depend on:

o Which Venous tract is involved?
-> Cortical veins vs. Venous sinuses

o How many vascular districts are affected?
-> limited vs. diffuse

o How fast does Thrombosis develop?
-> can collateral circuits be activated?

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7
Q

Secondary Headaches: Subarachnoid Hemorrhages (SAH)

A

SAH = dangerous bc autonomic symptoms (brady+tachyk, hypertension, vasospasms)
-> death within 15min

SAH & Headache as symptom:
o Thunderclub Headache in 97% of cases = very sudden / acute onset Headache

o Warning / Sentinel Headache
= Headache that rapidly disappears
-> occurs in case of:
i. Micro-bleeding
ii. Enlargement of the Aneurysm
iii. Intramural bleeding
iv. Vasospasm
v. Micro-embolic phenomena due to Intrasaccular clots

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8
Q

Secondary Headaches:
1. Vascular Intracranial / Cervical disorders

A

1) Hematomas:
-> Intracerebral, Subdural, Epidural

2) Subarachnoid Hemorrhages*

3) Venous Thrombosis*

4) Vascular Malformations in pre-clinical stage:
o Saccular Aneurysms
o AV-Malformations

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9
Q

Secondary Headaches: Vascular malformations in pre-clinical stage

A

o Saccular Aneurysm
o AV-Malformation

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10
Q

Secondary Headaches - Underlying disorders

A

= 9

  1. Vascular Intracranial / Cervical disorders*:
    i. Hematomas
    ii. Subarachnoid Hemorrhage
    iii. Venous Thrombosis
    iv. Vascular malformations in pre-clinical stage
  2. Non-vascular intracranial disorders (= space occupying: Granulomata, Cysts)
  3. Trauma to Head / Neck
  4. Substance abuse / withdrawal
  5. Pathologies of other structures of the head (ears, eyes, teeth etc.)
  6. Infections: Meningitis, Encephalitis
  7. Disorders of Homeostasis:
    Kidney, Liver, Respiratory insufficiency
  8. Psychiatric disorders: Depression, Psychosis
  9. Brain Tumor:
    Headache is an Onset symptom in 35%, but rarely occurs isolated
    = more likely in pts who already have a Primary Headache history
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11
Q

Secondary Headaches Def

A

Headache that is a symptom of an underlying disease*

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12
Q

Other Primary Headache Diseases

A

Arnold-Chiari’s Malformation:
Cerebellar tonsils are positioned more downwards, can penetrate into the Foramen Magnum
-> with time can lead to compression of the
anteriorly located Brainstem -> e.g.
- Bulbar part containing Breathing center
- Swallowing center

S&S:
- very frequent Headaches = bilateral & located posteriorly
- contraction of the Occipital Peri-cranial muscles
- if Brainstem compressed => impaired swallowing, breathing, reduced level of consciousness

Treatment: must be corrected surgically

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13
Q

Migraine Pathophysiology - Further contributions:

A

1) Interplay with Reticular Formation:
 Locus Coerulus = major site of Catecholamine synthesis (wsl. reason for Autonomic symptoms in Migraine)
 Raphe Nuclei → decreased Serotonin levels (→ Depression + Anxiety = common Migraine comorbidities)

2) Hypothalamic activation in the Prodromic Phase → explains associated Symptoms: Polyuria, Mood changes, Appetite changes

3) Activation of Temporal + Occipital Cortex
→ explains Photophobia

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14
Q

Medication Overuse Headache - Treatment

A

=> Withdrawal of overused medication
=> + Preventive medication
Advice itself is effective in > 50%, other possibility is Withdrawal programe (Hospital- / Home based)

Outcomes
in 80%: Resolution of Medication overuse
in 50%: Reduction of monthly Headache days to <50%
in 70%: Reversion to Episodic Migraine (<15 Monthly Migraine Days)
in 35%: Relapse of MOH

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15
Q

Medication Overuse Headache - Diagnosis

A

consider NEUROIMAGING

PSYCHOLOGICAL assessment, bc:
- Med. Overuse Headache has high comorbidity with Anxiety + Depression
- to determine the Overuse-pattern (addiction vs. “simple” overuse)

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16
Q

Medication Overuse Headache - Def

A

= Type of Headache that develops + gets worse with frequent use of Medications = most often Acute Headache Medications, against pain in Migraine- or TTH-pts

-> underlying Headache disorders transform from Episodic conditions to Chronic Daily Headache

-> 15 Headache days / month (i.e. Chronic)

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17
Q

General Pathophysiology of Headaches

A

The Brain parenchyma itself does not have pain receptors!
Instead, pain originates in Algogenic (pain producing) structures in the Head:
● Scalp skin + vessels
● Head + Neck muscles
● Venous sinuses
● Meningeal + large Cerebral Arteries
● Dura Mater at the cranial base
● Nerve fibers: CN V + IX + X
● Non-neurological structures in Head: teeth, oral mucosa, paranasal sinuses, eyes, ears**

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18
Q

Cluster Headache - Treatment

A

● Acute attacks:
o Oxygen administration (FiO2 of 100%)
o Sumatriptan (5-HT1 receptor blocker), via nasal spray or IV

● Prophylactic treatment:
o Short-term (for Episodic CH) – Prednisone, Verapamil (CCB)

o Long-term (episodic + chronic CH) – Verapamil, Lithium
(Verapamil -> ECG monitoring mandatory, bc risk for prolonged PR segment)

● Neurostimulation therapy (DBS)
o when medical therapy fails
o There are less invasive methods by stimulating the occipital nerve, sphenopalatine ganglion or the vagus nerve

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19
Q

Secondary Headaches

A

= Headache is a symptom of an underlying disease:

o Trauma to Head and / or Neck

o intracranial / cervical Vascular disorder: Hemorrhage, Venous Thrombosis

o Non-vascular intracranial disorder: cyst, granuloma (= space occupying)

o Substance Abuse or Withdrawal

o Infections: Meningitis, Encephalitis

o Disorder of Homeostasis = imbalance of ions or metabolites: Liver / Kidney / Respiratory Insufficiency

o Pathologies of structures of Head: eyes, ears, nose, sinuses, teeth, oral mucosa

o Psychiatric disorders: depression, psychosis

o Brain Tumors:
Headache = onset symptom in 30-40% of cases, but it rarely comes isolated;
more common in pts with history of Primary Headaches

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20
Q

Cranial Neuralgia

A

= Nerve Pain
-> Pain follows CN territories (eg. CN V) or Roots of C1 / C2

Neuropathy refers to nerve damage Neuralgia is a type of Nerve pain. Neuralgia can be a symptom of neuropathy

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21
Q

Types of Headache

A

Primary H.
Secondary H*
Painful Cranial Neuropathies (e.g. Cranial Neuralgias*), other Facial pains

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22
Q

Comorbidities & Epidemiology in Primary Headache Types

A

Bild

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23
Q

Characteristics of the different Types of Primary Headache

A
  1. Duration*
  2. Pain features (siehe Bild)
    İ. intensity
    ii. quality
    iii. side
    iv. location
    v. Autonomic symptoms?
    vi. Other accompanying symptoms
    vii. Aggravated by physical activity?
  3. Comorbidities*
  4. Epidemiology
  5. Treatment
  6. Other additional characteristics
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24
Q

Diagnosis Primary Headaches

A
  1. Diagnostic Algorithm: Primary vs. Secondary Headache (KK)
  2. HISTORY
    i. Family History -> in Migraine usually parents are affected
    ii. Medical History
    o Past -> TTH: Hypertension, Mood disorders
    o Recent: Stroke, Trauma, Intracranial surgery

iii. Natural History: was the Headache present/absent during important developmental periods?
(eg. females -> puberty, menopause)

  1. Pain features*
  2. General Medical examination
  3. Neurological examination
  4. İnstrumental examination
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25
Q

Primary Headaches - Diagnostic Algorithm

A

Primary Headache = when there are..
1. NO Alarm signs =>
i. Fever
ii. Focal Neurological Deficits
(->mein Notion)
iii. Seizure
iv. Meningeal signs (e.g. Nuchal rigidity)
v. Elevated ICP - signs (e.g. Papilledema)
vi. Decr. Level of Consciousness

  1. NO Abnormal examination
    => Medical & Neurological examination
  2. NO Unusual features =>
    e.g. we visit pt later and now they show Somatosensory dysfunction
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26
Q

DD Cluster Headache

A

Trigeminal Neuralgia => attacks are localized more in the Maxillary / Mandibular area

Sinusitis => is as well a disease with seasonal occurrence, but pain is less severe& worsens while bending forward

Migraine => as well unilateral, but Migraine pts prefer not to move and stay in a dark room, attacks last longer (4-72h), different Autonomic symptoms

Parosysmal Hemicrania (another TAC Type) = very similar to Cluster, but there have to be mind. 20 attacks for Diagnosis, lasting 2-30 min (vs. 15-180 min in CH)

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27
Q

Pathophysiology Trigem. Autonomic Cephalgias (TACs) PERIPHERAL component 1/2

A
  • Peripheral component
    = Activation of the following Nerve Fibres in the Cavernous Sinus:

İ. Fibers running from the Sphenopalatine ganglion to the Superior Salivary Nucleus (Brainstem)
ii. Fibers running from the Trigemınal ganglion to the Trigeminal Nuclei (Pons)
iii. Fibers running to Super. Cervical ganglion, then to the Medio-lateral Columns in Spinal Cord

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28
Q

Pathophysiology Trigeminal Autonomic Cephalgias (TACs)
- CENTRAL component 2/2 -

A
  • CENTRAL component = Chronopathological aspect of TACs

There is an activation of the Hypothalamic Gray = the part of the Hypothalamus controlling Pain& Circadian rhythm, İ.e. there is a dysfunction of the Hypothalamic Pacemaker cells

This results in a Circadian cycle dysfunction: the circadian release of certain Hormones is abnormal, they are not released as they should
=> decreased levels of Testosterone, LH, nocturnal Melatonin
=> increased levels of Cortisol

=>

29
Q

Cluster Headache vs. Paroxysmal Hemicrania (= both are TACs)

A

Paroxysmal Hemicrania is very close to CH:
Headache has exactly the same features as in CH

*But the Diagnosis requires:
o 20 attacks (vs CH = 5 attacks)
o lasting 2-30 min
o occuring >5 times per day

Paroxysmal Hemicrania can be prevented 100% by daily dosis of 100-200 ml Indomethacin (NSAID)
[vs CH=unresponsive to Indomethacin]

30
Q

TACs - full name & 2 Types

A

= Trigeminal Autonomic Cephalgia

Types (we talked about):
1. Cluster Headache
2. Paroxysmal Hemicrania

31
Q

Cluster Headache -
further Manifestations & Characteristics

A
  • 80% of pts have Leonine Face characteristics: pronounced orbital roofs, tough skin
  • Pain location (orbital, periorbital, tempoal regions) resembles region of 1st Trigeminal N. branch
  • CH attack can be induced by Nitroglyceride administration (= vasodilator!)
  • Seasonal occurrence (more often during transition periods of the year)
  • Symptoms of Autonomic dysfunction are present

-

32
Q

Cluster Headache occurs typically..

A

During the time transitional btw. Summer and Winter (april, october)
= Seasonal occurence

33
Q

Cluster Headache Epidemiology

A

Male > Female 3:1

34
Q

Cluster Headache Types

A

1) EPISODIC Cluster H. (85%)

II—cluster p.—II II~~remission p.~~II II–cluster p:–II II~~remission p.~~II

Cluster period (7d - 1 year)
Remission period = painfree ( > 3 months)

2) CHRONIC Cluster H. (15%) -> 2 Options:

  • Option A:
    Cluster period (7d - 1y)
    Remission period < 3 months
  • Option B:
    Cluster period > 1 year
35
Q

Cluster Headache - Diagnostic Criteria

A

Mind. 5 attacks fulfilling the following:

  1. pain intensity: severe - very severe (‘stabbing’ pain)
  2. unilateral
  3. pain location: orbital / peri-orbital / temporal (!) areas
  4. accompanied by Cranial Autonomic symptoms (i.e. symptoms of Autonomic dysfunction):
    i. conjunctival injections / lacrimation (red eye)
    ii. Eyelid edema
    iii. Sweating on forehead / face (ipsilat. to pain)
    iv. Flushing (ipsilat. to pain)
    v. Rhinorrhea / Nose congestion
    vi. Sensation of full Ear
    vii. Ptosis / Myosis

AND/ OR
5. Restlessness / Agitation

  1. Attack lasts 15-180 min
  2. Headache attacks (within one Cluster period) occur 1- 8 times per day (or >50% of active time)
36
Q

Treatment TTH

A

Episodic: NSAIDs, Paracetamol

Chronic: Prophylactic Treatment (the same drugs as for Migraines)

37
Q

TTH Diagnosis

A

Physical examination -> Palpation (tenderness)

Instrumental examination ->
o Electromyography (at rest or during cognitive activtiy)
o Algometry (measures pain threshold)
o Electronic Palpation (using glove with electrodes)

38
Q

TTH prevalence

A

86% lifetime prevalence

39
Q

Characteristics of the Headache in TTH

A
  1. lasts 30min - 7 days
  2. constrictive or compressing (not pulsating)
  3. mild-moderate pain intensity
  4. bilateral
  5. more in frontal area (“band around head”)
  6. some cases = accompanied by Pericranial Tenderness
  7. only occasional + wenn dann mild and only one of the two! Photo-& Phonophobia
  8. pain not aggravated by physical activity
  9. Comorbidities - TTH is associated with: Stress, Anxiety, Depression, Oro-Mandibular dysfunction, Muscle stress, Hypertension
40
Q

TTH Types

A

*TTH Types are classified according to Frequency: *

Infrequent episodic TTH:
>10 episodes for in total 1-12 d/year

Frequent episodic TTH
>10 episodes with 1-14 d/month for >3 months
= in total 12-180 d/year

Chronic TTH:
> 180 d/year or >15 d/month for >3 months

41
Q

TTH Epidemiology

A

Tension Type Headache
= 84% life time prevalence
(vs. Migraine 10%)

42
Q

Chronic Migraine
- def
- pathophys.
- treatment

A

> 15 Monthly Migraine Days (MMDs)

Chronic Migraine is due to Peripheral & Central (!) Sensitization

Treatment by (u.a) Botox = decreases sensitization*

43
Q

Migraine attack: Postdrome

A

-> until 1-2 after attack

= “Hangover-like” feeling:
o Tiredness
o Prostration (extreme weakness)
o Mood changes
o Appetite reduced

44
Q

Migraine attack: Resolution phase S&S

A
  • somnolence + sleeping
  • asthenia
  • nausea
  • muscle pain
45
Q

Migraine attack: Headache phase

A
  • lasts 4-72 h

Headache =
- pulsating
- unilateral
- pain intensity moderate-severe
- worsens with physical activity

  • with Autonomic symptoms:
    i. Nausea, Vomiting
    ii. Photophobia, Phonophobia
46
Q

Migraine attack: Prodrome

A
47
Q

Phases of a Migraine attack

A
  1. Predrome = up to 24 h before attack
  2. Aura (only in 25%) = 5-60 min
    (before / or contempor. with Headache)
  3. Headache = 4-72 h
  4. Resolution
  5. Postdrome = 1-2 d after attack
48
Q

Epidemiology Migraine

A

3:1 women&raquo_space;> men
highest incidence btw 21-54 y.

Migraine = 2nd most disabling, 3rd most prevalent disorder

49
Q

Comorbidities Migraine

A

Comorbidities can be both
Risk factor for Migraine (Comorbidity → Migraine) & Consequence of Migraine (Migraine → Comorbidity)
Symptoms of Migraine + Comorbidity can overlap (eg. Episodic Headache = Depression, Depression = daily Headache)
Migraine + Comorbidity can be caused by the same Risk factor (e.g. environment, genes, age)
-> eg. incidence of both Migraine & Depression increase with Age

Bsp. of Migraine comorbidities:
- Depression
- Cerebral Ischemia: Migraine v.a. with Aura, increases the risk for it (v.a. in young women)

50
Q

Factors contributing to Migraine development

A

Genes:
Migraine is a polygenic disease => Gene mutations can affect:
- Dopamine + Serotonin receptors
- Enzymes in cardiovascular functions (NO, ACE)

Comorbidities:
can be both Risk factor + Consequence of Migraine (e.g. Depression)

51
Q

Headache characteristics

A
52
Q

Central sensitization

A

= Condition of the NeSy causing + maintaining chronic pain; it plays a significant role in progression from Episodic to Chronic Migraines

In central sensitization the NeSy is in a persistent state of high reactivity:
Nociceptors have low threshold = increased responsiveness to pain stimuli (e.g. Neuropeptides)

Result: even minor irritations induce severe pain ⇒ Chronic + Severe Migraines

53
Q

Peripheral sensitization

A

= Perivascular Trigem. N. Terminals have become hypersensitive to Stimuli (= inflamm. mediators that are released around Nerves + blood vessels during a Migr. attack)

→ Perivascular Trigem. N. Terminals send more signals to Trigem. N. Sensory Nuclei → Neurons here release a lot of Neuropeptides (= pain signals)in response to the normally not painful stimulus
(i.e. stimulus would normally lead to way less Neuropept. release)
⇒ Allodynia & Incr. pain intensity

54
Q

Migraine Progression over lifetime - Natural History

A

Migraine is exacerbated during
- Puberty
- Surgery
- Working
- Menopause

Migraine is alleviated during
- Pregnancy
- Travelling
- > 70 y

55
Q

Aura Pathophysiology

A
  1. Aura-pt brain is in a state of Hyperexcitability = increased neural response to sensory stimuli
  2. Cortical Spreading Depression
    = slowly propagating wave of cortical Neuron- & Glia cell depolarization, startıng in the Occipital lobe followed by a phase of depression (no electrical activity)
  3. In Cortical Spreading Depress. there is massive
    o Influx of Na, Ca, Water
    o Efflux of K, Protons, Glutamate, ATP
    o Release of
     Vasodilators
     Inflammatory mediators ⇒ same as above: Inflamm. Med. stimulate perivascular Trigem. N. Terminals → Trigem. N. Sens. Nuclei → Neuropeptides
    → Nociceptors ⇒ Pain
56
Q

Migraine Pathophysiology

A
  1. Migraine attack is elicited by a Trigger = Sensory stimulus, e.g: emotional stress, alcohol, lack of sleep, noise, altitude, hunger
    Trigger → Migraine attack onset in deep brain structures (e.g. Hypothalamus, Brainstem)
  2. Stimulation of the Endothelium of Blood vessels in the Dura mater
  3. Endothelium releases Serotonin (5-HT) ⇒ Vasodilation → Plasma protein leakage → Macrophage activation → release of Inflammatory mediators
  4. Inflamm. mediators stimulate perivascular Trigeminal Nerve Terminals = Afferent nerve fibers → run to the Trigeminal N. Sensory Nuclei (in Pons)
    → Neurons located here release Neuropeptides: Substance P & Calcitonin Gene Relat. Peptide (CGRP)
    ⇒ act on Nociceptors, i.e. transmit pain = Headache

Peripheral & Central Sensitization → Allodynia, Severe pain, Chronic Migraine

  1. Interplay with Reticular Formation:
    - Locus Coerulus = major site of Catecholamine synthesis (wsl. reason for Autonomic symptoms in Migraine)
    - Raphe Nuclei → decreased Serotonin levels (→ Depression + Anxiety = common Migraine comorbidities)
  2. Efferent stimulus is sent back to the same blood vessel via the Pterygopalatine ganglion
57
Q

Typical Aura - symptoms

A
  1. Visual:
    - scintillating scotoma
    - intense light (continuous / flashing)
    - zig zag lines
  2. Sensory:
    - Paresthesias
    - Hyposthenia (weakness)
  3. Language / speech:
    Motor = Broca’s Aphasia
58
Q

Migraine with Aura - diff. Forms:

A

Typical Aura*
Brainstem Aura*
Hemiplegic (familial or sporadic) Migr.
Retinal Migr.

59
Q

Botulinum Toxin mechanism of action in Migraine treatment

A

→ v.a. in Chronic Migraine
→ intramuscular / intradermal injections across the Head

Botulinum Toxin works by:
1. blocking Peripheral sensitization:
Botox inhibits Receptors on Trigeminal N. Terminals (which are normally activated by inflamm. mediators)
→ This leads to a reduction of Neuropeptide (eg. CGRP) release by Neurons in the Trigem. N. Sensory Nuclei
→ less Neuropeptides means less stimuli binding to Nociceptors, and this means that we have decreased Pain sensation

  1. by this it also indirectly blocks Central sensitization: the hypersensitive Nociceptors do not get enough Stimuli (Neuropeptides), therefore do not elicit Pain
60
Q

Treatment Migraine - Prophylaxis

A

Botulinum Toxin*
b-Blockers (Propanolol)
Tricyclic Antidepressants
anti-CGRP-ABs
Anticonvulsants (Topiramate, Valproate)

61
Q

Treatment Migraine - Acute

A

(4)
o Common Analgesics: combination of Paracetamol, Aspirin, Caffeine (vasoconstrictor)

o NSAIDs: Naproxen, Ibuprofen

o Dopamine receptor Antagonists
→ Antiemetics: Prochlorperazine, Metoclopramide

o 5-HT1 (Serotonin) receptor Agonist
* Triptans
⇒ vasoconstrictors of cerebral blood vessels
// adv. effects: ischemic events in pts w. underlying cardiovascular disease

  • Lasmiditan
    -> blocks 5-HT1 receptors on Trigeminal neurons (wsl in Trig. N. Sensory Nuclei)
    -> by this it inhibits CGRP release (= Neuropeptide transmitting pain)
62
Q

Aura in how many % ?

A

25% of Migraine cases

63
Q

Aura in Migraine - characteristics

A

Aura is present only in 25% of Migraine cases:

  1. Aura symptoms vary according to specif. form of Migraine w. Aura*
  2. Symptom spreads gradually over > 5 min
    or 2 Symptoms occur consecutively
  3. Duration: 5-60 min
  4. unilateral
  5. accompanied / followed within max. 60min, by Headache (<- not always; Migraine w. Aura can be “w.o. Headache” )
64
Q

Brainstem Aura symptoms

A
  • Dysarthria
  • Vertigo
  • Tinnitus
  • Hypoacusis (loss of hearing acuity)
  • Diplopia
  • Ataxia
  • Decreased level of consciousness

(= 7)

65
Q

Migraine Classification

A

= according to Frequency (in Monthly Migraine Days = MMDs)

EPISODIC Migraine:
1-5 Low frequ.
6-8 Moderate frequ.
9-14 High frequ.

CHRONIC Migraine:
>15 MMDs over a period of >3 months

66
Q
A
67
Q
A
68
Q
A