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
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
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
4
Q
Define migraine
A
- often familial disorder characterized by recurrent attacks of headache widely variable in intensity, frequency, & duration
5
Q
Describe migraines
A
- derived from Greek word Hemi-crania, commonly unilateral
- Associated with nausea & vomiting, sensitivity to light/sound, numbness/tingling, anorexia
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
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
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
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
10
Q
What can change an episodic migraine to a chronic migraine
A
- hypertension (HTN)
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
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
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
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
15
Q
Describe central sensitization in trigeminal vascular theory of migraine
A
- chronic stimulation of trigeminal pain nucleus -> signals thalamus -> cortical perception of pain
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
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
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)
