Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Medicine III > Headache > Flashcards

Headache Flashcards

1
Q

Generally describe a headache

A
  • Symptom for multiple/overlapping causes
  • Difficult to classify several types of headache syndromes
  • Diagnosis of headache syndrome primarily a clinical one, PT’s may be involved ind diagnosis
  • No obvious catastrophic end point but has the potential to erode person’s QOL
  • Rare for any individual to not have experienced headache at any point in life
  • May be difficult to evaluate however intensity, quality, site of pain may provide clues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Classification of headaches

A
  • Primary headaches: not caused by any other disorders; migraine, tension-type (most common), cluster (most severe) headaches
  • Secondary headaches: underlying etiology, less serious (withdrawal from caffeine, increases in BP, fever) to serious (brain tumors, strokes, TBI, infections, hemorrhages); may get resolved if/when underlying cause is treated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Typical patterns of headaches

A
  • Sinusitis: most commonly between the eyebrows
  • Tension: most commonly in a pattern similar to a headband around the forehead/temples
  • Migraine: most commonly the temple, behind the ear (one sided)
  • Trigeminal neuralgia: most commonly from corner of the mouth crossing the cheek toward the ear
  • Cluster: most commonly around/behind the eyeball, half of the face, & below the skull
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define migraine

A
  • often familial disorder characterized by recurrent attacks of headache widely variable in intensity, frequency, & duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe migraines

A
  • derived from Greek word Hemi-crania, commonly unilateral
  • Associated with nausea & vomiting, sensitivity to light/sound, numbness/tingling, anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Incidence/prevalence of migraine

A
  • most cases have onset <40 yrs
  • effects women more
  • Hormonal influences: frequency highest in women during reproductive years, when estrogen levels are higher, & deceases to some extent after menopause
  • Accounts for average 6 lost work days per year
  • 28 million have severe, disabling migraine in US
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Etiology & risk factors

A
  • Neurobiology disorder that increases excitability of the CNS
  • Positive family hx of migraine in 60% of cases
  • Various genes & environmental factors might be involved in the phenotype
  • Pattern of inheritance is complex, APOE and TRESK genes are thought to increase risks
  • These genes are known to regulate excitatory NT concentration in brain & ion channel currents in neurons, specially those related with pain transmission
  • TRESK expression increased in migraine related areas like trigeminal ganglion or nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe triggers

A
  • Migraineurs should avoid certain foods, milk, corn, eggs, wheat, food additives/colors, coffee, alcohol (specially red wine)
  • There are certain triggers: stress levels, tiredness, hormone levels, sleep deprivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe auras (prodromal signs/early ‘warning’ signs)

A
  • Visual auras, somatosensory or vestibular auras
  • Feelings of tiredness, excitement, craving for certain foods (chocolate), sometimes auras can be confused as triggers
  • There may or may not be auras
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can change an episodic migraine to a chronic migraine

A
  • hypertension (HTN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Etiology of migraines related to hormones

A
  • Menstrual migraines occur without auras, more severe, last longer, less responsive to treatment
  • If migraine follows a hormonal pattern, pregnancy can trigger or bring relief periods, can also vary during different periods of pregnancy, also may become severe for months after childbirth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathogenesis of migraines

A
  • Mechanisms of CNS dysfunction appears complex & multifactorial
  • Occurs due to increased excitability in certain groups of neurons in cortex & brainstem due to underlying genetic reasons causing dysfunction in ion channel function & NT activity
  • Hyperexcitability leads to sensitizations of central & peripheral trigeminal pathways that are involved in processing pain sensations known as the trigeminal vascular theory of migraine headaches
  • Triggers might give some clue into the mechanisms
  • Onset of migraine during periods of recovery after prolonged stress might point to the involvement of the autonomic system: switch from sympathetic to parasympathetic dominance can be a trigger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Possible mechanisms involved in migraine headache

A
  • Hyperexcitation: headache starts when excitation of cortical or brainstem neurons cross a certain genetically determined threshold (explains auras but not pain)
  • Dysfunction of brainstem serotonergic antinociceptive centers: up regulation of incoming pain sensations, cannot explain headaches directly but serotonin levels are associated with stress, mood, sleep & it can regulate blood vessels in brain & the meninges
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the trigeminal vascular theory

A
  • Although the brain tissue does not have pain receptors, the meningeal tissue & the arterial walls of cortical vessels have a rich supply of nerve endings from the trigeminal & cervical dorsal roots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe central sensitization in trigeminal vascular theory of migraine

A
  • chronic stimulation of trigeminal pain nucleus -> signals thalamus -> cortical perception of pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe peripheral sensitization in trigeminal vascular theory of migraine

A
  • Dysregulation of serotonergic & autonomic connections to these vessels -> dilation of extra cranial/dural blood vessels -> extravasation -> activation of perivascular trigeminal pain receptors -> release of neuropeptides -> further dilation of vessels -> further stimulation of trigeminal pain receptors -> perpetuation of this cycle -> stimulation of trigeminal pain nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe pain inhibitory GABA-ergic mechanism

A
  • activated by stimulation of sensory fibers
  • inhibits pain pathways in dorsal spinal cord
  • If absent can lead to disinhibition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

3 common features of all types of migraines

A
  • Initiated largely by genetically inherited mechanisms
  • Caused by peripheral/central sensitization of pain pathways in head, that also result in abnormal processing of normal sensations
  • Can be initiated by endogenous or exogenous triggers that challenge normal homeostatic biology (stress, HTN, sleep deprivation, hormonal imbalance)
19
Q

Describe migraines with a visual aura

A
  • Begins with aura
  • Can have a visual aura: temporary visual disturbances, loss of focus, dark spots, zigzag flashing lights, hazy spot near the center that will changes into a shape that combines fortification on one side & scotoma
  • Image fades as intense throbbing begins (usually contralateral to visual changes)
20
Q

Describe other kinds of auras

A
  • Paresthesia in hand & face could also occur as aura with tingling & numbness
  • Auras could indicate brain areas affected: speech difficulty reflects dominant hemisphere, vertigo/dizziness reflects brainstem involvement
  • Other auras: muscle weakness, loss of appetite, amnesia, depression, irritability, anxiety, spatial neglect
  • Other symptoms of migraines: throbbing headache, nausea, confusion, blurred vision, mood changes, fatigue, & increased sensitivity to light, sound, or noise
21
Q

Describe migraines without an aura

A
  • No warning signs
  • Headache might be dull or throbbing, may last 4-72 hrs, nausea, photophobia, blurred vision, aggravated by routine physical activity
  • After headache resolves: tender scalp, fatigue, diuresis
22
Q

Describe familial hemiplegic migraine (FHM)

A
  • Mutation in a gene involving voltage gated Ca2+ channel responsible for 50% of FMH
  • Migraine with aura
  • Aura is paresis with impaired coordination in face, arm, or whole one side of body
  • Headache could be on contralateral or ipsilateral side
  • Differential diagnosis with TIA: no infarction
23
Q

Describe basilar type migraine manifestations

A
  • Attack in posterior fossa involving vascular region of basilar artery: brainstem, cerebellum, occipital lobes
  • Auras could be altered mental status, dysarthria, ataxia, vertigo, diplopia, tinnitus
  • Followed by headache
  • Vestibular migraine: dizziness, nausea, vomiting, motion sensitivity, postural instability, may not have headache
24
Q

Describe status migrainosus manifestations

A
  • Persists for > 72hrs
  • Triggers: hormonal changes during menstrual cycle, pregnancy, miscarriage, change in birth control pills can be triggers, respiratory & UTIs
  • Continued vomiting to the pint of dehydration, severe headache, may need hospitalization
  • Ergots, anti-emetics, corticosteroids, opioids may be helpful
25
Q

Diagnosis of a migraine

A
  • Can be mostly determined by hx and symptoms alone
  • Neuro exam is otherwise normal
  • Diagnostic imaging is unnecessary & may be confusing
  • Outcome measures used for assessing disability related to migraine: MIDAS (migraine disability assessment) & HIIT-6 (headache impact test)
26
Q

Treatment for migraines

A
  • Avoidance of triggering factors
  • During attack a dark & quiet place its necessary
  • Pharmacological agents: Triptans, Ergots, Calcitonin Gene-related Peptide (CGRP) receptor antagonist, Botox, NSAIDs
27
Q

Describe the different pharmacological agents used to treat migraines

A
  • Triptans: serotonin receptor agonist, stops throbbing pain by constricting cranial vessels, contraindicated with CAD pts, not helpful with auras
  • Ergots: also relieve severe throbbing pain
  • Calcitonin Gene related Peptide (CGRP) receptor antagonist: better pain relief, do not cause vasoconstriction, safe for CAD patients, also effective with photophobia & nausea
  • Botox: block peripheral & central sensitization of nociceptive receptors
28
Q

Prognosis fo migraines

A
  • Women have higher persistence percentages than men
  • Frequency & intensity determine long term impact of migraine
  • Score low on SF-36 questionnaire specially those who also have depression
  • People with headache & depression are strongly associated with being on disability, welfare, & unemployment
29
Q

Migraine implications for physical therapists

A
  • Biofeedback is widely used & is thought to work by controlling autonomic & somatic nervous systems
  • Both thermal control of finger temp. and EMG control of muscle tone/activity biofeedback are used
  • Modalities or manual treatment one cervical spine sometimes help due to cross connections b/w trigeminal & cervical spinal systems
  • Aerobic endurance exercise may also provide relief of migraine headache
30
Q

Describe pain neuroscience education (PNE)

A
  • newer non-invasive approach for treating migraines
  • educational strategies to teach patients about how they think about their pain
  • explains the neurophysiological processes involved in pain
  • known to increase pain thresholds, decrease fear-avoidance behaviors, decrease activation of brain areas that are involved in chronic pain conditions
31
Q

Generally describe tension type headaches

A
  • Most common type of primary headache
  • Episodic TTH occurs < 12 days/year
  • Frequent TTH occurs b/w 12 to 180 days/year
  • Chronic TTH occur > 180 days/year
  • Episodic TTH is caused by peripheral sensitization of the pericardial myofascial nociceptive afferents possibly due to increased release of neuropeptides like serotonin, bradykinin
  • In chronic TTH there is central sensitization at the level of trigeminal nucleus which alters non-painful stimuli around head to noxious stimuli
32
Q

Clinical manifestations of tension type headache (TTH)

A
  • Increased hardness of muscle tissue in the upper cervical area
  • Increased tenderness to palpation of tissues around head, level of tenderness is proportional to intensity of headache
  • Pain is reported as pressure or tightness in whole head
  • Pain is dull & not throbbing with associated mild photo- and phono-phobia
  • Triggers are stress, irregular eating pattern, high coffee intake
33
Q

Diagnosis of tension type headaches (TTH)

A
  • Exam should include palpation of pericardial muscles to identify tender & trigger points, specifically in temporal, pterygoid, mass ester, SCM, traps
  • Referred pain should also be noted
  • Chronic medication use is associated with TTH, so diagnosis should be made after 15 days free of meds
  • Needs to exclude other causative factors
34
Q

Treatment of tension type headaches (TTH)

A
  • Patient should be educated, frequent to chronic TTH may not be cured but significant improvements in QOL can happen
  • Analgesics are most typical meds, tricyclic antidepressants
35
Q

Implications for physical therapists related to tension type headaches (TTH)

A
  • PT is the most used non-pharmacologic treatment for TTH: manual therapy techniques, stretching & relaxation techniques, massage, cervical exercise programs, spinal mobs, dry needling can be used
  • Number of active myofascial trigger points are correlated with intensity & duration of headache, trigger point therapies might work
  • EMG biofeedback to reduce pericardial muscle tension for relaxation training
  • Cognitive behavioral therapy to identify & cope with thoughts & beliefs that aggravate headache
36
Q

Generally describe cluster headaches

A
  • Rare type but most painful & most disabling of primary headaches
  • 20% of cluster headache patients have lost their jobs & 8% are on disability
  • Suicidal thoughts are substantial in about 55% cases
  • Occurs in clusters called cluster periods when headache happens daily or several times daily for a period of several weeks
  • can be episodic (remission lasts several months) or chronic (remission lasts <14 days)
37
Q

Incidence of cluster headaches

A
  • Occurs in about 1-4% of population predominantly in males between 27-30 years
  • Black males have higher incidence than males of other races
  • Beer is the most common type of alcohol trigger, other triggers are weather changes & smells
  • Second hand cigarette exposure during childhood increases risk
38
Q

Pathogenesis of cluster headaches

A
  • May be a result of cranial vasodilation due to stimulation of the trigeminal complex
  • Serotonergic & histamine levels also go up during headaches & come down in the absence of headache
  • The cyclic pattern of cluster periods could be due to disturbances in the hypothalamic regulation of neuroendocrine system & hypothalamus is associated with the circadian rhythm
39
Q

Clinical manifestations of cluster headaches

A
  • Onset is sudden with excruciating pain, remains always on one side of the head usually localized to one eye & surrounding frontotemporal region
  • Boring & non-throbbing pain
  • Autonomic changes could be same side or opposite side
  • During headaches person prefers to assume erect rather than reclining posture
  • Attacks occur mostly awakening from afternoon nap or sleep during night (90 minutes after falling asleep)
40
Q

Diagnosis of cluster headaches

A
  • Based on symptoms & hx
  • Diagnostic criteria: strictly unilateral, severe intensity, orbital localization
  • Needs differential diagnosis from migraine, trigeminal neuralgia, sinusitis, SAH, etc.
  • Significant diagnostic delay
41
Q

Treatment for cluster headaches

A
  • Melatonin therapy can be useful during attacks with remission in 3-5 days
  • O2 and triptans can be used during attacks
  • In chronic clusters: lithium, ergots, topiramate can be used prophylactics
  • In drug resistant types deep brain stimulation of the hypothalamus
42
Q

Describe cervicogenic headaches

A
  • Unilateral pain that starts in the neck/base of skull & can come up & around your head to your forehead and behind your eye (Ram’s Horn)
  • Can occur as a result of degenerative problems in cervical vertebrae, joints, or neck muscles that happen over time: secondary to fall, sports injury, whiplash, or arthritis
43
Q

Signs and symptoms of cervicogenic headaches

A
  • Limited cervical ROM
  • Headache with sudden cervical movement or when neck remains ion the same position for extended time (FHP in dentists, carpenters)

Clinical Medicine III (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions