2. PRIMARY HEADACHE DISORDERS
• Pain sensitive structures
• Classification of headache.
• Migraine.
• Tension type of headache.
• Trigeminal autonomic cephalalgias.
• Chronic headache.
• Other primary headache.
3. PAIN SENSITIVE STRUCTURE IN HEAD
• Extra-cranial pain sensitive structures:
– Sinuses
– Eyes/orbits
– Ears
– Teeth
– TMJ
– External carotid artery and branches
• Intra-cranial pain sensitive
structures:
– Arteries of circle of willis.
– proximal dural arteries,
– Dural Venous sinuses, veins
– Meninges
– Dura
5,7,9,10 cranial nerves and cervical nerve roots carry pain from this structure.
Afferent pain impulses into the trigeminal nucleus are modulated by descending
facilitatory and inhibitory input from brainstem structures including the
periaqueductal gray matter, rostral ventromedial medulla, locus ceruleus, and
dorsal raphe nuclei.
9. EPIDEMOLOGY
• Migraine affects 10-15% of general population, F>M
• Migraine accounts for 10-20% of all headaches in adults
• 1% chronic migraine (>15 days/months)
• Mean duration 24 h (untreated)
• 10% always with aura, >30% sometimes with aura
• Usual age at onset is 15-35 years
• Family History: 70% of patients have relatives with Headache
• Migraine is now thought of as a genetic disorder of the brain.
10. PATHOPHYSIOLOGY
• Theories on the pathogenesis of migraine include:
The vascular Versus Neuronal.
The cortical spreading depression theory- migraine aura
The Migraine Generator- brainstem and hypothalamus.
The Hyperexcitable Migraine Brain.
The Trigeminocervical System and Migraine Headache-
Trigeminal nucleus caudalis, the trigeminal ganglion, the three branches
of the trigeminal nerve and ascending fibers from the trigeminal nucleus
caudalis to higher order cortical regions.
11.
12.
13.
14. • Dopaminergic mechanisms are likely to mediate some of the symptoms of
migraine in different phases, more notably yawning, nausea, and difficulty
concentrating.
• The orexigenic system has been implicated in the alterations of sleep and fatigue
in migraine. Furthermore, orexin A and B modulate dural nociceptive input.76 In
the locus coeruleus, noradrenergic activity plays a role in sleep-wake regulation
and arousal as well as pain in migraine.
• Multiple neuroendocrine mediators, such as insulin, glucagon, leptin, and
neuropeptide Y, have effects on the trigeminovascular system, linking changes in
appetite, food cravings, and migraine.
• Other emergent neurochemical systems that may be implicated in migraine
include somatostatin, cholecystokinin, antidiuretic hormone, and melatonin.3
• Additional research is needed to confirm their role in migraine pathophysiology.
26. • Aura is complex of neurological symptoms that occurs usually before the
headache but it may begin after the pain phase has commenced, or
continue into the headache phase.
• Visual aura is the most common type of aura, occurring in
over 90% of patients.
• It often presents as fortification spectrum
• Is risk factor for ischemic stroke
54. MIGRAINE IN WOMEN
• Migraine 2-3x more common than in men possibly due to hormonal
association.
• The attacks may occur exclusively during menstruation and at no other
time during the cycle, referred to as pure menstrual migraine occurring
between days −2 and +3 of the menstrual cycle.
• Migraine attacks that occur throughout the cycle but increase in
frequency or intensity at the time of menstruation is called menstrually
related migraine.
• Oestrogen withdrawal before menstruation is a trigger for migraine in
some women due to reduction in central opioid tone, dopamine receptor
hypersensitivity, increased trigeminal mechanoreceptor receptor fields, and
increased cerebrovascular reactivity to serotonin.
55. Migraine in Pregnancy and Menopause
• 70% of women experience improvement or remission of migraine symptoms
during pregnancy.
• Worsening is more common in those with a history of migraine with aura.
• If remission occurs during pregnancy, migraine often recurs in the postpartum
period most often 3 to 6 days after delivery.
• In two-thirds of women with a previous history, migraine decreases with a
physiological menopause, but it can either regress or worsen at menopaus
56. CHILDHOOD MIGRAINE
Prevalence 5%.
Migraine is the most common cause of headaches in children.
Migraine attacks in children are often shorter and occur less often than
those in adults and unilateral location is not a specific feature of juvenile
migraine.
Cyclic vomiting syndrome , Abdominal migraine, Benign paroxysmal
torticollis and Alternating hemiplegia of childhood are some periodic
syndromes that occur in childhood that appear to be variants or precursors
of migraine.
Pharmacological treatment of migraine in children rizatriptan in patients 6–
17 years old and almotriptan, sumatriptan , naproxen, and nasal spray
zolmitriptan in those who are 12 years old and older.
Prophylactic treatment includes Propranolol, Cyproheptadine and Tricyclic
antidepressants.
57. SEVERITY OF MIGRAINE
Severity levels:
• Mild- Patient is aware of a headache but is able to continue
daily routine with minimal alteration.
• Moderate -headache inhibits daily activities but is not
incapacitating.
• Severe -headache is incapacitating.
• Status - severe headache that has lasted more than 72 hours.
58. MANAGEMENT
1. Assess extent of a patient’s disease and disability-
Migraine Disability Assessment Score (MIDAS)
2. NONPHARMACOLOGIC MANAGEMENT-
• Identification and avoidance of specific headache triggers.
• Healthful diet, regular exercise, regular sleep patterns,
avoidance of excess caffeine and alcohol, and avoidance of
acute changes in stress levels.
67. ANALGESICS
• Inhibiting cyclooxygenase (COX) isoforms, resulting in a reduction in the synthesis inflammatory
prostaglandins (e.g. PGE2.
• Caffeine (a methylxanthine) has been shown to produce synergistic analgesic effects when combined with
NSAIDs by reduction in the protein synthesis of COX-2
• Useful in early stages or for mild-moderate migraine
• Only if patient can tolerate oral medication
68. TRIPTANS
• Proven efficacy
– Improvement in 70% in 1 hour, 85% in 2 hours
– Generally well tolerated
• Avoid with MAO-A inhibitors
• Avoid in pts with ischemic heart disease (IHD), angina, myocardial
infarction (MI), uncontrolled hypertension (HT)
– Failure with one triptan does not preclude use of another
• Patients respond variably to different drugs
– Do not combine with ergot agents
– Adverse effects can include chest pressure, flushing, dizziness,
drowsiness, and nausea.
• Action - binds to serotonin 5-HT1B, 5-HT1D and 5-HT1F receptors in
cranial blood vessels (causing their constriction) and subsequent inhibition
of pro-inflammatory neuropeptide release (CGRP and substance P).
69. ERGOT ALKALOIDS
• Ergot alkaloids have agonist effects at numerous 5-HT receptors (5-HT 1A,1B, 1D
& 1F), as well as 5-HT2, adrenergic (alpha-1) and dopamine receptors. They
produce both venous and arterial vasoconstrictor effects.
Ergotamine tartarate
• 2-4 mg per sublingual or rectal
• 1 mg nasal spray
Dihydrergotamine (DHE) (oral & parenteral, nasal spray)
• Should not be used in patients with vascular disease, ischemic
heart disease or hypertension
• Used with caution in patients with vascular risk factors or
prolonged or severe aura
• Avoid ergotamine if triptan used in previous 6 hrs
• Avoid triptan if ergotamine used in previous 24 hrs
70. • Efficacy - 50-70 %
• No longer first-line, superseded by triptans
• Side-effects:
– Ergotamine
– nausea, vomiting, drowsiness, fatigue
– ischaemia
– rebound headache (>3-4 doses per week)
– Dihydrergotamine
– less likely to cause rebound headache
– Low rate of headache recurrence (~17%) due to long
duration of action
– does not prolong aura
– role of caffeine?
– the concurrent administration of caffeine improves both
the rate and extent of absorption of ergotamine
71. ANTIEMETICS
• Prevent and treat nausea
• Improve GI motility
• Enhance absorption of other anti-migraine medications
• Promethazine
– Available PO, IM, PR
– Dose = 25-50 mg
– Blocks dopamine and histamine receptors
• Prochlorperazine
– Available PO, IM, IV, PR
– Dose = 5-10 mg
– Blocks dopamine receptors
72. Alternative Drugs for Acute Treatment
• Not all patients with migraine respond adequately to triptans or
ergot alkaloids.
• Triptans and ergot alkaloids are contraindicated in patients with
vascular disease, risk of MI, stroke, or uncontrolled hypertension. In
such patients, treatment with a gepant or ditan class drug can be of
benefit (Schwedt & Garza, 2021b).
• Gepants and ditans are newer anti-migraine medications with less
efficacy compared to triptans, but lack the potentially harmful
vasoconstrictive side effects of triptans and ergot alkaloids (Yang et al,
2021).
73. Gepants
• CGRP antagonists are currently recommended options for patients
with more severe migraine whose headaches respond poorly to
NSAIDs, triptans or combination analgesics (Schwedt & Garza,
2021b).
• Both rimegepant and ubrogenpant are FDA approved for acute
treatment of migraine. Zavegepant FDA approved in 2023.
Ditan
• Lasmiditan is selective 5-HT1F receptor agonist.
• It does not act by causing vasoconstriction.
74.
75.
76. Prophylactic Drugs of 2nd Choice or Treatment
Resistant Migraine
Gepants :-
• In contrast to other gepants , atogepant have been approved for acute treatment of migraine.
• Patients with marked disability from frequent migraine who either do not respond to, or cannot
tolerate other options.
• As a class, gepants are generally considered drugs of second choice due to high cost.
CGRP Monoclonal Antibodies :-
• CGRP monoclonal antibodies has become a new target in the prophylaxis of migraine headache.
• They act by binding to CGRP, which prevents it from binding to its receptor.
• These drugs are given by subcutaneous injection twice a month.
• These drugs are currently reserved for use in patients whose migraine headaches are not controlled
by oral agents.
• CGRP monoclonal Antibodies currently available include: erenumab, fremanezumab, galcanezumab,
and eptinezumab.
77.
78.
79.
80.
81.
82.
83.
84. TRIGEMINAL AUTONOMIC CEPHALALGIAS
• TACs are characterized by relatively short lasting attacks
of head pain associated with cranial autonomic
symptoms, such as lacrimation, conjunctival injection, or nasal Congestion.
• Includes:
• Cluster headache,
• Paroxysmal hemicrania, and
• SUNCT/SUNA
• Hemicrania continua
85. CLUSTER HEADACHE
Diagnostic criteria:
• A. At least five attacks fulfilling criteria B–D
• B. Severe or very severe unilateral orbital, supraorbital and/or
temporal pain lasting 15–180 minutes (when untreated)
• C. Either or both of the following:
1. at least one of the following symptoms or signs, ipsilateral to headache:
a) conjunctival injection and/or lacrimation
b) nasal congestion and/or rhinorrhoea
c) eyelid oedema
d) forehead and facial sweating
e) forehead and facial flushing
f) sensation of fullness in the ear
g) miosis and/or ptosis
2. a sense of restlessness or agitation
• D. Attacks have a frequency 1-2/day to 8/day
• E. Not better accounted for by another ICHD-3 diagnosis.
86. Pathophysiology of cluster headache
• Pain is likely mediated by activation of the trigeminal nerve pathways, the autonomic
symptoms are due to parasympathetic outflow and sympathetic dysfunction.
• Parasympathetic activation is believed to be responsible for the ipsilateral conjunctival
injection, lacrimation, nasal congestion, rhinorrhoea, and/or eyelid oedema.
• Trigeminal parasympathetic overactivity may result in perivascular oedema
compromising the carotid canal, leading to neurapraxic injury of postganglionic
sympathetic fibers and hence a Horner syndrome manifest by ptosis and miosis.
87. Pain afferents from the trigeminovascular system traverse the ophthalmic division of the trigeminal nerve, taking signals
from the cranial vessels and dura mater. These synapse in the trigeminocervical complex, trigeminal nucleus caudalis
(TNC), and dorsal horns of C1 and C2, and then project to the thalamus and lead to activation in cortical areas, including
frontal cortex, insulae, and cingulate cortex, resulting in pain. There is reflex activation of the parasympathetic outflow
from the superior salivatory nucleus (SSN) via the facial (VIIth cranial) nerve, predominantly through the pterygopalatine
(sphenopalatine) ganglion, which acts as a positive feedback system to dilate the vessels and irritate trigeminal endings
further. This autonomic activation leads to lacrimation, reddening of the eye, and nasal congestion, and a local third-
order sympathetic nerve lesion due to carotid swelling results in a partial Horner’s syndrome. The key site in the CNS for
triggering the pain and controlling the cycling aspects is in the posterior hypothalamic grey matter region
89. 3.1 Cluster headache
3.1.1 Episodic cluster headache
A. Attacks fulfilling criteria A-E for 3.1 Cluster headache
B. At least two cluster periods lasting 7-365 d and separated by
pain-free remission periods of ≥1 mo
3.1.2 Chronic cluster headache
A. Attacks fulfilling criteria A-E for 3.1 Cluster headache
B. Attacks recur over >1 y without remission periods or with
remission periods lasting <1 mo
90. 'Chronic'
In pain terminology, chronic denotes persistence over
a period of more than 3 months
For primary headache disorders that are more usually
episodic, chronic is used whenever headache occurs
on more days than not over more than 3 months
The trigeminal autonomic cephalalgias are an
exception:
in these disorders, chronic is not used until the
condition has been unremitting for more than 1 year
93. The most striking feature of CH – the feature from which its name is
derived – is the unmistakable periodicity of the attacks.
Individual cluster attacks occur during attack phases known as
“cluster periods.”
Most patients have one or two annual cluster periods, each lasting
between one and three months.
Some patients have a seasonal propensity for attacks related to the
duration of the photoperiod, with the highest incidence of attacks
occurring in January or July.
Kudrow demonstrated that the most likely times for a cluster period
to begin were associated with the number of daylight hours; that is,
more exacerbations occur within two weeks following the summer
and winter solstices, with fewer exacerbations beginning within two
weeks of the onset and offset of daylight savings time.
1. .
99. Therapy of Cluster HA
Acute
therapy
Preventive
therapy
Transitional
therapy
Avoid triggers: Alcohol, nitroglycerin, altitude, sildafenil
100.
101. ACUTE ATTACK TREATMENT
1. OXYGEN- 100% oxygen at 10–12 L/min for 15–20 min.
High flow and high oxygen content are important.
2. TRIPTAN- Sumatriptan 6 mg SC is rapid in onset and
usually shorten attack to 10–15 min;
• Sumatriptan (20 mg) and zolmitriptan (5 mg) nasal sprays are
both effective in acute cluster headache.
3. DHE – IV provide prompt and effective relief.
102.
103.
104.
105.
106.
107.
108. Paroxysmal Hemicrania
ICHD-3 Diagnostic Criteria
A. At least 20 attacks fulfilling B-E
B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain
lasting 2-30 minutes
C. Either or both of the following
1. At least one of the following, ipsilateral to the pain:
A. Conjunctival injection and/or lacrimation
B. Nasal congestion and/or rhinorrhoea
C. Eyelid oedema
D. Forehead and facial sweating
E. Miosis and/or ptosis
2. A sense of restlessness or agitation
D. Occurring with a frequency >5 per day
E. Attacks are prevented absolutely by therapeutic doses of indomethacin
F. Not attributed to another disorder
110. PH: Episodic vs. Chronic
• Episodic Paroxysmal Hemicrania (35%)
A. Attacks of PH occurring in bouts
B. At least 2 bouts lasting 7-365 days, separated by
pain-free periods lasting at least 3 months
• Chronic Paroxysmal Hemicrania (65%)
A. Attacks meeting criteria for PH
B. Occurring for > 1 year without remission periods or
remission periods lasting < 3 months
111. The pathophysiology of paroxysmal hemicrania
is believed to be similar to that of cluster
headache with an important distinction:
functional imaging studies indicate
hypothalamic dysfunction contralateral, rather
than ipsilateral, to the expression of pain and
autonomic features
112. Secondary PH-
• Reported with lesions in the region of sella turcica, including arteriovenous
malformation, cavernous sinus meningioma, and epidermoid tumor.
• Secondary PH is more likely if the patient requires high doses (>200 mg/d) of
indomethacin.
• In patients with apparent bilateral PH, raised CSF pressure should be
suspected.
• When a diagnosis of PH is considered, MRI is indicated to exclude a pituitary
lesion.
• Occasionally PH can coexist with trigeminal neuralgia.
113. Paroxysmal Hemicrania
Evidence-Based Treatment
• Acute: none
• Prophylactic:
• Indomethacin (treatment of choice)
• 25mg tid with meals or 75mg SR qday; 150mg often required
• Dose can be lowered to find lowest effective dose
• Intermittent discontinuation useful as remissions occur
• Other prophylactic options:
• Verapamil
• NSAIDs and COX-2 inhibitors
• Topiramate
• Occipital nerve block
• Gabapentin
• Acetazolamide
• Sumatriptan SQ – can help some patients with longer attack duration
114. PH: Indomethacin
• ICHD-3: “In an adult, oral indomethacin should be used initially at a
dose of at least 150 mg daily and increased if necessary up to 225 mg
daily. The dose by injection is 100-200 mg. Smaller maintenance doses
are often employed.”
115. Short-lasting Unilateral Neuralgiform headache attacks
(SUNCT & SUNA): ICHD-3 Diagnostic Criteria
A. At least 20 attacks fulfilling B-D
B. Moderate-severe unilateral orbital, supraorbital, temporal and/or other
trigeminal distribution head pain, lasting 1-600 seconds, and occurring as
single stabs, series of stabs, or in a saw-tooth pattern
C. Headache is accompanied by at least one of the following, ipsilateral to the
pain:
1. Conjunctival injection and/or lacrimation
2. Nasal congestion and/or rhinorrhoea
3. Eyelid oedema
4. Forehead and facial sweating
5. Miosis and/or ptosis
D. Attacks have a frequency at least 1 per day
E. Not attributed to another disorder
117. SUNCT vs SUNA: ICHD-3 criteria
SUNCT:
1. Meets criteria for short-lasting unilateral neuralgiform headache attacks
2. Both of conjunctival injection and lacrimation (tearing)
SUNA:
1. Meets criteria for short-lasting unilateral neuralgiform headache attacks
2. Only one or neither of conjunctival injection and lacrimation (tearing)
120. TREATMENT
ABORTIVE THERAPY-
• IV lidocaine, which arrests the symptoms, can be used in hospitalized patients.
PREVENTIVE THERAPY-
• Lamotrigine, 200– 400 mg/d.
• Topiramate and gabapentin may also be effective.
• Carbamazepine, 400–500 mg/d
Surgical approaches-
• microvascular decompression or destructive trigeminal procedure
• Greater occipital nerve injection
• Occipital nerve stimulation
• deep-brain stimulation of the posterior hypothalamic region
122. SUNCT/SUNA vs Trigeminal Neuralgia
• Location:
• V1 vs V2/V3
• Refractory period:
• SUNCT/SUNA can be triggered without a refractory period
• TN usually has a refractory period after each attack
• Some patients have overlapping symptoms, and should be diagnosed with both
• SUNCT/SUNA vs PSH: look for autonomic symptoms!
123. Hemicrania Continua:
ICHD-3 Diagnostic Criteria
A. Unilateral headache fulfililng B-D
B. Present for > 3 months, with exacerbations of moderate or greater
intensity
C. Either or both of the following:
A. At least one of the following, ipsilateral to the pain:
A. Conjunctival injection and/or lacrimation
B. Nasal congestion and/or rhinorrhea
C. Eyelid oedema
D. Forehead and facial sweating
E. Miosis and/or ptosis
B. A sense of restlessness or agitation, or aggravation of the pain by
movement
D. Responds absolutely by therapeutic doses of indomethacin
E. Not attributed to another disorder
124. Hemicrania Continua: Pain
Exacerbations
• Migrainous features
• Nausea: 53%
• Vomiting: 24%
• Photophobia: 59%
• Phonophobia: 59%
• Autonomic features (74% - at least one autonomic sx)
• Lacrmiation: 53%
• Nasal congestion: 21%
• Ptosis: 18%
• Other key features: eyelid edema, eyelid twitching, foreign body sensation
in eye ipsilateral to headache
125. Hemicrania Continua:
Remitting vs Unremitting
• Hemicrania Continua, remitting subtype (12%)
• Headache is not daily or continuous, but interrupted
by remission periods of > 1 day without treatment
• Hemicrania Continua, unremitting subtype (88%)
• Headache is daily and continuous for at least 1 year,
without remission periods of at least 1 day
.
126. Hemicrania Continua: Treatment Options
• Indomethacin
• ICHD-3: “should be used initially in an oral dose of at least
150 mg daily and increased if necessary up to 225 mg
daily. Smaller maintenance doses are often employed.”
• One suggestion for dosing: 25mg PO TID and increase
every 5 days to 50mg-75mg TID, once remission achieved
taper down to lowest effective dose
• PPI for GI prophylaxis
• Non-indomethacin options:
• Melatonin
• Topiramate
• Occipital nerve block
• Gabapentin
127. Trigeminal Autonomic Cephalgias
Feature PH SUNCT Cluster
Sex F:M 2:1 1:2 1:3
Attack
duration
~15 mins ~ 1 min 60 mins
Attack
frequency
11 ~ 30 1
Treatment
of choice
Indomethacin Lamotrigine Verapamil
128. TAC vs Migraine
TAC Migraine
Autonomic Symptoms • Prominent
• Lateralized to side of
pain
• Consistent symptoms
with every attack
• Bilateral
• Mild
• Do not always parallel
the severity of the
attacks
Photophobia/Phonophobia Ipsilateral to the side of pain Bilateral even when pain is
lateralized
129. Pituitary Tumors and TACs
• Increased prevalence of TACs in patients with pituitary
tumors and headache
• 86 patients with headache and pituitary tumor
• SUNCT (5%) and cluster headache (4%)
• 40 cases of symptomatic TACs in the literature
• Pituitary tumors (16)
• 7/10 SUNCT; 2/3 PH; 7/27 cluster
• MRI brain imaging with pituitary views & pituitary
function tests are an important part of the
evaluation in all patients with TACs.
130.
131. TENSION-TYPE HEADACHE
• Tension-type headache (TTH) is chronic head-pain syndrome
characterized by bilateral tight, band like discomfort.
• Pain typically builds slowly, fluctuates in severity, and may
persist more or less continuously for many days.
• Headache may be episodic or chronic
• Headaches are completely without accompanying features
such as nausea, vomiting, photophobia, phonophobia,
osmophobia, throbbing, and aggravation with movement.
• Prevalence - 30% and 78%
133. Pathophysiology
• Peripheral pain mechanisms are most likely to play a role in
Infrequent episodic tension type headache and Frequent
episodic tension-type headache.
• Central pain mechanisms play more important role in Chronic
tension-type headache.
• Increased pericranial tenderness may be recorded by manual palpation.
• Tenderness is typically present interictally, is further increased
during actual headache and increases with intensity and
frequency of headaches.
134.
135. Infrequent episodic tension-type headache
Description:
• Infrequent episodes of headache, typically bilateral, pressing
or tightening in quality and of mild to moderate intensity,
lasting minutes to days.
• Pain does not worsen with routine physical activity and is not
associated with nausea, but photophobia or phonophobia may be present.
136. Diagnostic criteria
• A. At least 10 episodes of headache occurring on <1 day per month
on average (<12 days per year) and fulfilling criteria B-D
• B. Lasting from 30 minutes to 7 days
• C. At least two of the following four characteristics:
1. bilateral location
2. pressing or tightening (non-pulsating) quality
3. mild or moderate intensity
4. not aggravated by routine physical activity such as walking or climbing stairs
• D. Both of the following:
1. no nausea or vomiting
2. no more than one of photophobia or phonophobia
• E. Not better accounted for by another ICHD-3 diagnosis
137. Frequent episodic tension-type headache
• A. At least 10 episodes of headache occurring on 1-14 days per
month on average for >3 months (12 and <180 days per year) and
fulfilling criteria B-D
• B. Lasting from 30 minutes to 7 days
• C. At least two of the following four characteristics:
1. bilateral location
2. pressing or tightening (non-pulsating) quality
3. mild or moderate intensity
4. not aggravated by routine physical activity such as walking or climbing stairs
• D. Both of the following:
1. no nausea or vomiting
2. no more than one of photophobia or phonophobia
• E. Not better accounted for by another ICHD-3 diagnosis.
138. MANAGEMENT
Acute Treatment-
• Simple analgesics such as acetaminophen, aspirin, or NSAIDs.
• Behavioural approaches including relaxation can also be effective.
• High risk of rebound headaches.
• Limit acute treatment to 2-3 days per week.
141. CHRONIC DAILY HEADACHE
• Headache occurring on 15 or more days per month for more than 3 months
• 4% of adults have daily or near-daily headache.
• Daily headache may be primary or secondary
142.
143. NEW DAILY PERSISTENT HEADACHE
• Presents with headache on most if not all days and the patient can clearly, and
often vividly, recall the moment of onset.
• Headache usually begins abruptly, but onset may be more gradual;
• Evolution over 3 days has been proposed as the upper limit for this syndrome.
• Primary NDPH occurs in both males and females.
• Some patients have a previous history of migraine.
144. • Treatment of migrainous-type primary NDPH- preventive
therapies effective in migraine.
• Featureless NDPH is most refractory to treatment.
145. MEDICATION-OVERUSE HEADACHE
Diagnostic criteria:
• A. Headache occurring on 15 days per month in a patient with a
pre-existing headache disorder
• B. Regular overuse for >3 months of one or more drugs that can be
taken for acute and/or symptomatic treatment of headache
1.Regular intake of ergotamine on 10 days per month for >3 months.
2. Regular intake of one or more triptans, in any formulation, on 10
days per month for >3 months.
3. Regular intake of one or more NSAIDs on 15 days per month for >3 mnths.
4. Regular intake of one or more opioids on 10 days per month for >3 mnths
• C. Not better accounted for by another ICHD-3 diagnosis.
146. Management
• Withdrawal of overused acute medication
- Abrupt except with barbiturates, benzodiazepines and opioids.
-Gradual
• Transitional treatment
- Prednisolone 60-100 mg for 5 days
• Preventive treatment aimed at the underlying primary headache disorder should
be started from the outset.
Opioids, barbiturates containing compounds, and some combination analgesics
appear to have the highest risk; triptans carry moderate risk, and NSAIDs the lowest
risk.
To avoid MOH relapse, in general, it is best to avoid the use of opioids and/or
barbiturates for the regular management of primary headache disorders.
147. Primary cough headache
Diagnostic criteria:
• A. At least two headache episodes fulfilling criteria B-D
• B. Brought on by and occurring only in association with
coughing, straining and/or other Valsalva manoeuvre
• C. Sudden onset
• D. Lasting between 1 second and 2 hours
• E. Not better accounted for by another ICHD-3 diagnosis.
148. Differential diagnosis-
• Chiari malformation or any lesion causing obstruction of CSF
pathways or displacing cerebral structures.
• Cerebral aneurysm, carotid stenosis, and vertebrobasilar disease.
• Benign exertional headache.
TREATMENT
• Indomethacin 25–50 mg two to three times daily .
• Some patients obtain pain relief with LP
149. Primary stabbing headache
Diagnostic criteria:
• A. Head pain occurring spontaneously as a single stab or
series of stabs and fulfilling criteria B–D
• B. Each stab lasts for up to a few seconds
• C. Stabs recur with irregular frequency, from one to many per day
• D. No cranial autonomic symptoms
• E. Not better accounted for by another ICHD-3 diagnosis.
TREATMENT-indomethacin 25–50 mg two to three times daily
150. Primary exertional headache
Diagnostic criteria:
• A. At least two headache episodes fulfilling criteria B and C
• B. Brought on by and occurring only during or after strenuous
physical exercise.
• C. Lasting <48 hours.
• D. Not better accounted for by another ICHD-3 diagnosis.
Differential diagnosis
• cardiac cephalgia, Pheochromocytoma
• Intracranial lesions and stenosis of the carotid arteries.
TREATMENT
• Indomethacin (50 mg), ergotamine (1 mg orally), Dihydrergotamine (2 mg by
nasal spray), or methysergide (1– 2 mg) orally given 30–45 min before exercise
151. Primary thunderclap headache
Diagnostic criteria:
• A. Severe head pain fulfilling criteria B and C
• B. Abrupt onset, reaching maximum intensity in <1 minute
• C. Lasting for 5 minutes
• D. Not better accounted for by another ICHD-3 diagnosis.
Differential diagnosis –
- sentinel bleed of an intracranial aneurysm, cervicocephalic arterial
dissection, cerebral venous thrombosis, subarachnoid hemorrhage, reversible
cerebral vasoconstriction syndromes and hypertensive crisis.
- Ingestion of sympathomimetic drugs or of tyramine-containing foods in a
patient who is taking MAOIs.
- Pheochromocytoma.
152. Hypnic headache
Diagnostic criteria
• A. Recurrent headache attacks fulfilling criteria B-E
• B. Developing only during sleep, and causing wakening
• C. Occurring on 10 days per month for >3 months
• D. Lasting 15 minutes and for up to 4 hours after waking
• E. No cranial autonomic symptoms or restlessness
• F. Not better accounted for by another ICHD-3 diagnosis.
• Begins after age 50 years, but may occur in younger people.
• Attacks usually last from 15 to 180 minutes.
• Most patients are female.
153. TREATMENT
• Bedtime dose of lithium carbonate (200–600 mg).
• verapamil (160 mg) or methysergide (1–4 mg at bedtime).
• One to two cups of coffee or caffeine, 60 mg orally, at bedtime may be
effective.
154.
155. Greater Occipital nerve block
• Its used in –
Occipital neuralgia
Migraine (episodic and chronic)
Cluster headache
Cervicogenic headache
Hemicrania continua
• Sites of block are -
1/3 of line between EOP and mastoid.
2cm lateral and inferior to EOP.
• Dose
Lignocaine (1-2%) 0.25-4.5 ml
Bupivacaine (.25-.5%) 1.5-4.5 ml
Steroids to be used only In cluster headache.
• Effects starts in 5 min and last for 4 weeks
The most striking feature of CH – the feature from which its name is derived – is the unmistakable periodicity of the attacks. Individual cluster attacks occur during attack phases known as “cluster periods.” Most patients have one or two annual cluster periods, each lasting between one and three months. Some patients have a seasonal propensity for attacks related to the duration of the photoperiod, with the highest incidence of attacks occurring in January or July. Intriguingly, the attacks occur soon after the shortest and longest days of the year. This may have pathophysiologic implications, which we will discuss later.(1)
Kudrow demonstrated that the most likely times for a cluster period to begin were associated with the number of daylight hours; that is, more exacerbations occur within two weeks following the summer and winter solstices, with fewer exacerbations beginning within two weeks of the onset and offset of daylight savings time.(2)
Cluster periods punctuate longer-lasting remission periods, which usually last six months to two years. During remission periods, neither spontaneous nor provoked attacks occur. Although the duration of cluster and remission periods varies among individuals, these periods remain relatively consistent within the same individual.
Waldenlind E. Biological rhythm in cluster headache. In: Olesen J, Goadsby PJ, eds. Cluster Headache and Related Conditions. London, England: Oxford University Press;1999:171-178.
Kudrow L. The cyclic relationship of natural illumination to cluster period frequency. Cephalalgia. 1987;7 (Suppl 6):76-77.
Cluster headache also has a striking circadian periodicity, with most individuals having one to three attacks per day, although some have up to eight attacks daily. In an individual patient, the attacks usually occur at the same time each day. As shown on this illustration, the most common times for cluster attack onset are 1 a.m. to 2 a.m., 1 p.m to 3 p.m., and 9 p.m.
In addition, cluster headache is characterized by nocturnal attacks that generally occur around the same time each night, with a peak incidence between 1 a.m. and 3 a.m., as seen here in this first clock. This time roughly correlates with the onset of the first period of rapid eye movement (REM) sleep. Although this relationship has been well documented, the significance and exact relationship of this association remains unclear.(1)
There appears to be a relationship in some patients of cluster headache and obstructive sleep apnea (OSA). One possible trigger for cluster headache attacks may be the observed hypoxia or hypercapnia normally associated with OSA.
Trucco M, Waldenlind E. Circadian distribution of episodic cluster headache attacks. Cephalalgia. 1993;13 (Suppl 13):196.
Chervin RD, Zallek SN, Lin X, Hall JM, Sharma N, Hedger KM. Sleep disorder breathing in patients with cluster headache. Neurology. 2000;54(12):2302-2306.
Update references
Patients described the saw-tooth attacks as a single attack each, despite consisting of a volley of several shorter stabs, as the pain did not return to baseline for the duration of the saw-tooth attacks, which could last for up to hours at a time.
Symptomatic forms of SUNCT exist with pituitary lesions, vascular loops compressing the trigeminal nerve, and other intracranial lesions, particularly in the posterior fossa.
To aid the diagnosis of SUNCT, an indomethacin test and oxygen trial can be useful, which can rule out the differential diagnoses of PH and CH, respectively. IV lidocaine is effective for short-term prevention, although its effects can last up to 6 months after the infusion.20% of patients can go into remission with a 10-day course of IV lidocaine. Lamotrigine is the most effective treatment for SUNCT/SUNA, and 2/3rds of patients respond. Gabapentin and topiramate can also be useful as preventatives. Greater occipital nerve injections may play a role as a neuromodulatory procedure, either acting at the trigeminocervical complex or more centrally.
? Female predominance
Often misdiagnosed with migraine
The majority of patients have the unremitting from from onset.
