Educational Purpose Only

2. Do you know Emotional Pain and Physical Pain are the
Same to your Brain. In both cases Natural Chemical
(Painkiller mu-opioid) is Released. Means When you’re
emotionally hurt, the Reaction in your Brain will be
Similar to Physical Pain.
INTERESTING NEUROSCIENCE FACT

3. Sakit palo boh…!!!
Gie mano nie…?!!!
Less go into the brain…
DR. VASU NALLALUTHAN
MS. NEUROSURGERY (USM)
SUPERVISOR: DR. SANIHAH BT ABD HALIM

4. INTRODUCTION
• Thought PROCESS
• What MEDICATION is this?
• Can it MANAGE the Headache???
• Is it the correct DIAGNOSIS?
• Which STRUCTURE involve?
• Any SIGN?
• SYMPTOMS at presentation?

5. HEADACHE
• Headache pain is referred to a cutaneous territory area on the scalp,
sharing supply with a nerve innervating the intracranial area, which might
be the actual source of pain.
• Can be referred to a different territory than the actual nerve receiving the painful
stimulation.
• CONVERGENCE  a process if the two nerves share a high-order neuron.

6. EPIDEMIOLOGY
• Prevalence 96% of people during their lifetime.
• Female predominant
• More than 50% of outpatient visits for headache occur in primary care
• Headache is the 4th leading cause of emergency department visits.
• International Classification of Headache Disorders  updated
• Diagnostic criteria for headache disorders
• International Headache Society

7. CLASSIFICATIONS - AETIOLOGY
• Primary headache disorders
• Headaches that are not caused by an underlying medical condition
• Believed to have a genetic etiology.
• Categorized into 4 types:
• Migraine
• Tension-type headache (TTH)
• Trigeminal autonomic cephalalgias (TACs) including cluster headache
• Other disorders  new daily persistent headache and other rare disorders
• Secondary headache disorders
• Due to an underlying medical disorder

8. CLASSIFICATIONS - DURATION
• Duration of headache
• Acute – hours to days
• Subacute – days to weeks
• Chronic – months or years
Rizzoli P and Mullally WJ. Headache. Am J Med. 2018 Jan;131(1):17-24.
THE
INTERNATIONAL
CLASSIFICATION
OF
HEADACHE
DISORDERS,
3RD
EDITION

9. PATHOPHYSIOLOGY
• STRUCTURES  HEAD AND NECK
– PAIN SENSITIVE
• EXTRACRANIAL TISSUES
• CERVICAL AND INTRACRANIAL ARTERIES
• VENOUS SINUSES
• VEINS
• THE MENINGES
• CRANIAL NERVES (V, VII, IX, X)
• UPPER CERVICAL NERVES
HEAD PAIN OR DISCOMFORT
ANY ETIOLOGY
PRESSURE
TRACTION
IRRITATION
INFLAMMATION
RELEASE OF VASOACTIVE, INFLAMMATORY
SUBSTANCES - CALCITONIN GENE–RELATED PEPTIDE
DURAL NOCICEPTIVE AXONAL TERMINALS.
TARGETS FOR PHARMACOLOGIC
THERAPY
- SUBSTANCE
- RECEPTORS
Diagnosing headache begins with distinguishing secondary from primary headache
disorders.

10. RIGHT QUESTION AT THE RIGHT TIME
• History and examination  for evaluation of
headache(s), the goal of the is to answer 2 questions:
• Is there an underlying cause of headache(s)
• Need of further laboratory/neuroimaging evaluation
 SECONDARY HEADACHE?
• If there is no underlying cause of headache(s),
• PRIMARY HEADACHE Syndrome best describes the headache (e.g.,
migraine, tension, cluster)?

11. STRUCTURES HEAD AND NECK
HEADACHE

12. THE TRIGEMINOVASCULAR SYSTEM
• PRIMARY headache pathophysiology
• The vascular system of the head, face, meninges and the brain
• variable innervation of autonomic and sensory nerves.
• The arterial system is richly supplied with sensory nerves
• The veins are weakly innervated.
• For the cerebral vasculature, it is different;  once the vessels penetrate
into the brain parenchyma their autonomic and sensory fibres disappear (at
the level of the space of Virchow)

13. STRUCTURE INVOLVED IN HEADACHE
• TRIGEMINAL NERVE
• TRIGEMINAL GANGLION
• TRIGEMINOCERVICAL COMPLEX (TCC)
• TRIGEMINAL NUCLEUS CAUDALIS (TNC)
• TRACT
• TRIGEMINOHYPOTHALAMIC
• PARABRACHIAL-LIMBIC

14. THE OPHTHALMIC BRANCH (V1)
• First branch of the trigeminal Nerve
• TG it crosses the sidewall of the
cavernous  superior orbital
fissure  orbit  divides into 3
terminal branches:
• The lacrimal nerve
• The frontal nerve
• Supratrochlear nerve
• The nasociliary nerve
• Infratrochlear nerve
• Anterior ethmoidal nerve, the latter
further forming external nasal nerves
Fillmore EP and Seifert MF. Chapter 22: Anatomy of the Trigeminal Nerve. In: Nerves and Nerve Injuries. 2015,
Pages 319-350.

15. THE OPHTHALMIC BRANCH (V1)
• V1 provide
• Somatic sensation from the eye structures  terminal branches of the
lacrimal and nasociliary
• Damage of these nerves impair the corneal reflex.
• Superficial and autonomic sensory innervation  Ciliary body, lacrimal
gland, iris, conjunctiva and cornea
• Not from TRIGEMINAL GANGLION
• Originate from
• Superior cervical ganglion  sympathetic fibres  dilatator pupillae  run in the
nasociliary branch
• Sphenopalatine ganglion (SPG)  parasympathetic fibres  lacrimation  partially
running in the lacrimal branch of V1

16. THE OPHTHALMIC BRANCH (V1)
Nerves of the left orbit,
ophthalmic nerve (CN V1)
branches.
Fillmore EP and Seifert MF. Chapter 22: Anatomy of the Trigeminal Nerve. In: Nerves and Nerve Injuries. 2015,
Pages 319-350.

17. THE OPHTHALMIC BRANCH (V1)
• Distribution
• Extracranial
• Upper part of the face and the two thirds of the anterior scalp
• From the level of the palpebral fissures to the area of the coronal suture.
• Intracranial
• Superior part of the nasal cavity
• Medial orbital roof
• Crista galli
• Dura mater meninges
• Cerebral arteries in the circle of Willis
• Tentorial nerve of Arnold
• Traverse and straight venous sinuses.
Maxillary and mandibular branches, or
cervical dorsal root ganglia  provide the
innervation of only a limited extent of the
meninges.
Explanation for painful sensation in this
territory

18. THE MAXILLARY BRANCH (V2)
• 2nd branch of the CN V
• Distribution
• Extracranial
• Skin of the lower eyelid, the sides of
the nose, nasolabial fold, upper lip and
the cheek.
• Intracranial
• Dura of the middle cranial fossa
• Upper teeth and the related oral
gingiva
• Palate and mucous membranes of the
maxillary sinuses and nasal cavity.
• Connection with CN VII
• Postganglionic parasympathetic
neurons from the SPG (innervated by
TG fibres) reach the lacrimal gland via
V2 branches  mix with homologous
fibres from V1.
• Sphenopalatine branches supply
intramural glands of the nose and the
hard palate.

19. THE MAXILLARY BRANCH (V2)
Fillmore EP and Seifert MF. Chapter 22: Anatomy of the Trigeminal Nerve. In: Nerves and Nerve Injuries. 2015,
Pages 319-350.
Maxillary nerve (CN V2) branches.

20. THE MAXILLARY BRANCH (V2)
Fillmore EP and Seifert MF. Chapter 22: Anatomy of the Trigeminal Nerve. In: Nerves and Nerve Injuries. 2015,
Pages 319-350.
Trigeminal ganglion reflected,
pterygopalatine ganglion
showing connections

21. THE MANDIBULAR BRANCH (V3)
• Largest of the three branches
• V3 passes between tensor veli palatini and lateral pterygoid  Gives off
• Meningeal branch (nervus spinosus  passes through the foramen spinosum)
• Nerve to medial pterygoid from its medial side.
• Then, splits into an anterior and a posterior trunk.
• Anterior trunk gives off:
• 3 major muscles of mastication
• Buccal branch (provides sensory innervation to the cheek)
• Posterior division gives off:
• Sensory  3 main branches the auriculotemporal, lingual and inferior alveolar nerves
• Motor fibres  mylohyoid and the anterior belly of the digastric muscle.

22. THE MANDIBULAR BRANCH
(V3)
Fillmore EP and Seifert MF. Chapter 22: Anatomy of the
Trigeminal Nerve. In: Nerves and Nerve Injuries. 2015, Pages
319-350.
Mandibular nerve (CN V3) distribution.

23. THE MANDIBULAR BRANCH (V3)
• Distribution:
• Extracranial
• Posterior part of the temporal region
• Anterior part of the earlobe
• Anterior and superior walls of the
external ear canal
• Lower lip and the chin.
• Intracranial
• Mucosal territory - Ant 2/3 of the
tongue
• Medial aspect of the cheek
• The floor of the oral cavity
• The gingiva
• The mandibular alveoli and teeth.
Trigeminal motor fibres
• Innervate the masticatory muscles
• Masseter
• Temporal
• Internal and external pterygoid
• Mylohyoid
• Anterior body of the digastric
• Tensor palati
• Controlling biting and chewing
mechanisms.

24. DISTRIBUTION
OF
CN
V
Cutaneous
distribution of the
trigeminal nerve.

25. DISTRIBUTION
OF
CN
V
Trigeminal ganglion
and innervation of
cranial meninges

26. THE TRIGEMINAL GANGLION
• CN V protrudes from each side of
the superior lateral pons
• Trigeminal ganglion (TG)
• Residing in each of Meckel’s caves.
• A “central hub” in the
trigeminovascular transmitting
pathway
• Contains the soma of the peripheral
nerves  pseudo-unipolar neurons
• Most sensory fibres from the
intracranial and the extracranial tissues
Malhotra A et al. Neuroimaging of Meckel's cave in normal and disease conditions. Insights Imaging.
2018 Aug;9(4):499-510.

27. NEUROCHEMICAL
• Neurotransmitters and Neuropeptides
• Glutamate (most prominent)
• Dynorphins
• Calcitonin Gene-Related Peptide (CGRP)
• Serotonin
• Amylin
• Substance P
• Neurokinin A/B
• Pituitary Adenylate Cyclase Activating Polypeptide (PACAP).
• Receptors for these signalling molecules are expressed on peripheral and
central structures, and importantly on the TG neurons themselves
Pivotal in cellular communication
for pain processes (e.g. induction
or central/peripheral sensitization)
 headache perception.

28. TRIGEMINAL NUCLES

29. THE TRIGEMINOCERVICAL COMPLEX (TCC)
• In the brainstem  receive the first order sensory neurons - project centrally to the
trigeminocervical complex (TCC).
• The Second order neurons of the trigeminal sensory pathway
• TRIGEMINAL NUCLEUS CAUDALIS (TNC)
• C1 and C2 segments of the cervical spinal region.
• Third-order neurons
• Afferents from the TNC terminate at the THALAMUS (mainly posterior and ventral posteromedial
thalamic nuclei).
• TCC also responsible for conveying sensory and nociceptive signaling from the meninges and
craniovascular structures to several higher order relays.
• Direct ascending connections within the
• Medulla (e.g. medullary pontine nuclei including the rostral ventromedial medulla)
• Brainstem (e.g. nucleus raphe magnus, parabrachial nucleus and locus coeruleus)
• Midbrain nuclei (e.g. ventrolateral periaqueductal gray and cuneiform nucleus)
• Diencephalon (e.g. hypothalamus and thalamus).

30. THE SPINAL TRIGEMINAL NUCLEUS
• A sensory tract
• Located lateral medulla of the brain stem
• Descends to the caudal end of the medulla and into the spinal cord
• As far as the third or fourth cervical level
• Becomes continuous with Lissauer’s tract
• Takes sensory information from different cranial nerves  Trigeminal nerve
and its branches

31. TRIGEMINAL NUCLEUS CAUDALIS (TNC)
• Runs medial to the spinal trigeminal tract
• Has an onion skin somatotopy ÷ into 3 different cytoarchitectural regions:
• Pars Oralis (PO) most superior nucleus (Pons to the mid-medulla)
• Pars Interpolaris (PI) middle nucleus (spanning in the mid-medulla)
• Pars Caudalis (PC) most inferior nucleus (lower medulla to the upper cervical SC)
• Dedicated to pain perception
• Extends from C2 or C3 rostrally to the level of the obex
• Cytoarchitectural similarities with the posterior horn of SC.
• Termed as “medullary posterior horn”  divided into layers  Rexed SC laminae.
• Most superior area  inferior medulla
• Most inferior area  upper cervical spinal cord
* Rostral parts are mainly deputed to tactile perception
Mainly temp, deep
or crude touch

32. TRIGEMINAL NUCLEUS CAUDALIS (TNC)
• Area of lips and perioral  outermost layer of the onion
• Lie within the most superior area of the TNC.
• Nose, eyes, and outer oral areas  innermost layer
• Lies inferiorly within PC .
• The V1 branch  most ventral part of the spinal tract and extends caudally.
• The V2 branch  most dorsal part of the trigeminal nucleus caudalis and
terminates in the most rostral level.
• The lowest  areas reserved to cheeks and forehead
• The vertical  area of the ears
• The partial sensory innervation of the external ears (from cranial nerves VII, IX,
and X).

33. THE TRIGEMINOCERVICAL COMPLEX (TCC)

34. THE TRIGEMINOCERVICAL COMPLEX (TCC)
Onion skin pattern of facial sensory loss
with intramedullary lesions

35. THE TRIGEMINOCERVICAL COMPLEX (TCC)
• Activation of these structures are believed to contribute to the perception of
pain during migraine, and also to autonomic, endocrine, cognitive and
affective symptoms that last throughout the migraine episode.
• Furthermore, the second order neurons receive inputs from the occipital
nerve.
• This convergence may have treatment implications for some primary
headache conditions as well as referred pain.

36. Composition:
1. Neuron-glia unit (NGU)
2. Nerve bundles and extracellular matrix with microvessels
3. Nerve fibres
4. Occasional mast cells and stromal cells
THE PAIN PROCESS MEDIATED BY CN V
Mechanical, chemical and thermal INPUTS
Small neurons PROCESS the action potentials
CONVEY the nociception of HEADACHE
Pseudo-unipolar neurons
TRIGEMINAL GANGLION
PERIPHERAL NOXIOUS STIMULI
• Afferent C-(unmyelinated)
• Aδ-fibres (thinly myelinated
1
2
3
TRIGEMINAL PAIN PATHWAY
V1
V2
V3
THALAMUS
CEREBRAL CORTEX
CN V NUCLEUS (TNC)
TRIGEMINOCERVICAL COMPLEX TCC
BRAINSTEM
• CEREBRAL ARTERIES
• PIAL DURAL
• BLOOD VESSELS
• SINUSES
* No BBB
REFLECT ALTERED SENSORY, AUTONOMIC, AFFECTIVE, AND COGNITIVE PROCESSING

37. PAIN AND TEMPERATURE PATHWAYS
ACTIVATION
• Limbic system
• Hypothalamus
• Sensory Cortex
• Cingulate Cortex

38. TRIGEMINOHYPOTHALAMIC TRACT
• Originates from specific nociceptive, multimodal intensity-coding wide dynamic
range (fundamental for pain “gating effects”) and non-nociceptive neurons
• But 80% of its fibres are AXONS FROM NOCICEPTIVE NEURONS.
• Ascends contralaterally in the brainstem
• 50% of the fibres present a decussation in the lateral hypothalamus  lateral and medial
structures of hypothalamus (e.g. prefornical, suprachiamatic, supraoptic nuclei).
• While non-nociceptive information are transmitted only by direct pathway
• Nociception is carried both directly and indirectly (i.e. trigeminoreticular tract) 
hypothalamus
• Receiver areas of the hypothalamus  regulating homeostasis and integrating
pain with visceral afferent input.

39. THE PARABRACHIAL-LIMBIC TRACT
• The trigeminoparabrachial tract  polysynaptic pathway connecting CN V to
the limbic system
• Direct tracts ending amygdala, lenticular nucleus, nucleus accumbens
• The transmission of visceral pain and the emotional value of pain sensations.
• The parabrachial nucleus
• Contains a large share of neurons expressing both CGRP and PACAP (lateral portion)
 activated by painful stimulation.
• The transmission of CGRP is thought to reach directly the limbic system, where it can
mediate aversive behaviour or freezing
• Migraine and cluster headache pain  rely on the CGRP pathway in the
trigeminovascular system

40. HISTORY AND EXAMINATION
Rizzoli P and Mullally WJ. Headache. Am J Med. 2018 Jan;131(1):17-24.
ESSENTIAL ELEMENTS OF THE HEADACHE HISTORY

41. -Unknown etiology
PRIMARY HEADACHE DISORDERS

42. MIGRAINE
• 2nd most common form of headache  prevalence 10%
• Age 25 – 55 yrs old
• 3x > common in female
• Recurrent throbbing or pulsating Moderate to severe
• Often unilateral pain that lasts 4–72 hours with complete freedom between the
attacks (episodic).
• Associated with nausea, vomiting and/or sensitivity to light, sound or smell.
• Prefers to lie still in a dark and quiet room, and to avoid physical activity.
• The main subtypes are migraine
• with aura
• without aura.

43. Migraine Headaches. Available at https://my.clevelandclinic.org/health/diseases/5005-migraine-headaches
“washout”

44. MIGRAINE
• International Classification of Headache Disorders, 3rd Ed (ICHD-III)
criteria
• Migraine attacks should last between 4 and 72 h
• At least two of the four following criteria:
1. Unilateral location
2. Pulsating pain
3. Moderate to severe intensity
4. Aggravated by routine physical activity
• There must also have at least one of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia

45. • An aura is a fully reversible set of nervous system symptoms
• Visual/ sensory aura  form of zigzag lines or spreading scintillating
scotoma (diminished sight)
• most common
• Unilateral sensory disturbances and/or dysphasia  same time or sequentially.
• Evolves over a few minutes and marches from one area to the other
• Develops gradually, recedes, and is then followed by headache
• Accompanied by nausea, vomiting, photophobia, and phonophobia.
• Less common symptoms of aura
• Speech/ language symptoms
• Motor or brainstem symptoms
• Retinal symptoms.
• Aura phenomena  linked to a characteristic spreading cortical
depression
• Start posterior and moving slowly across the brain surface  producing orderly
progression of neurologic symptoms.
AURA

46. MIGRAINE WITH AURA
• If an aura contains multiple features
• Symptoms usually occur in succession of at
least 5 or so minutes each
• Total symptom complex of 5-60 minutes.
• Headache  begins within 60 minutes
after the resolution of the neurologic
symptoms.
• Hemiplegic migraine
• Rare subtype of migraine
• Aura that is characterized by unilateral
weakness
• May be familial or sporadic.
• Usual manifestation
• Start with both visual symptoms 
typically noted at the outset
• Positive, such as scintillations
• Negative, such as scotomata
• Followed by development of sensory
complaints
• Then a mixed dysarthric/aphasic
language disorder
• Followed by gradual clearing.

47. AURA WITHOUT HEADACHE
• Migraine equivalent
• Patients will experience an aura  usually visual, without an accompanying
headache
• Older individuals
• Must be differentiated from TIA.

48. CHRONIC MIGRAINE
• Headaches on 15 or more days in a month of which 8 or more days have
migrainous features for a period of more than 3 months
• The most disabling form of migraine with substantial impact on
• Health-related quality of life
• Co-morbities
• Frequent accompaniment of medication overuse.
• Approximately 3% of the population
• Characteristics of the patients
• More likely to be unemployed
• Have relationship difficulties and family problems
• Refractory to conventional acute and preventive treatments.

49. TENSION-TYPE HEADACHE
• Prevalence 80%
• Featureless headache
• because of the lack of associated symptoms that accompany migraine.
• Commonly episodic and rarely impacts on activities of daily living.
• The condition is often diagnosed but very poorly understood.
• A dull, bilateral, mild- to moderate-intensity pressure–pain without striking
associated features that may be categorized as infrequent, frequent, or
chronic and is easily distinguished from migraine.
• Patient described as aching or pressure, and as feeling as if the head is in a
vice or has a tight band around it.

50. TENSION-TYPE HEADACHE
• Often a degree of associated disability, and this, combined with the high
frequency, produces significant socioeconomic impact
• Typically does not require medical management
• Factors
• Genetic element
• Tenderness of pericranial muscles
• Co-existing mood disorders
• Mechanical disorders of the spine and neck
• May be associated with medication overuse  chronic variant

51. CLUSTER HEADACHE
• Most prevalent headache disorder among TAC.
• Prevalence 0.1%
• More common in young men (3.5:1) who smoke (65%)
• A specific subtype of primary headache disorders
• The pain is excruciating, often described as ‘suicidal headaches’.
• The attacks
• last between 15 minutes and 3 hours
• Frequency  from once every other day to up to eight per day.
• The striking feature is the circadian rhythmicity with attacks occurring at the same time every day.
• Alcohol triggers an attack in almost all cases.
• It is episodic in 80–90% of cases, with attacks occurring daily for a few weeks to a few months,
followed by a gap of a few months to a few years.
• The chronic variety has continuous attacks for a year or longer with no symptom-free interval or a
remission period that lasts for less than a month.

52. CLUSTER HEADACHE
• Most prevalent headache disorder among TAC.
• A specific subtype of primary headache disorders
• Characterized by headaches that are of short duration, are strictly unilateral and
have accompanying autonomic features of lacrimation, rhinorrhea, conjunctival
injection and ptosis.
• More common in young men (3.5:1) who smoke (65%) and the pain is excruciating,
often described as ‘suicidal headaches’.
• The attacks last between 15 minutes and 3 hours, occurring from once every other
day to up to eight per day.
• The patient is extremely restless and agitated and often sweats profusely.
• The other TAC include paroxysmal hemicrania and short-lasting unilateral
neuralgiform headache with conjunctival tearing, which are extremely rare and
beyond the scope of this article.

53. MEDICATION-OVERUSE HEADACHE (MOH)
• Often complicates primary headache disorders
• Common accompaniment to various CDH disorders.
• Affects 1–1.5% of the general population
• Women are affected 3x times more often than men.
• Around two-thirds of patients overusing analgesics have migraine and 27% have
tension-type headache.
• Any painkilling medicine can cause MOH although combination analgesics,
particularly those with opioids, barbiturates and caffeine, carry a high risk.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) are least
• MOH develops faster and on a much lower dose intake with triptan
• Withdrawal symptoms are much shorter and milder with triptans than with other painkillers.

54. - Result of another condition causing traction on or inflammation of pain-sensitive structures
- Have numerous etiologies
- Intracranial pressure disorders
Idiopathic intracranial hypertension (IIH)
Spontaneous intracranial hypotension (SIH)
SECONDARY HEADACHE DISORDERS

55. IDIOPATHIC INTRACRANIAL HYPERTENSION (IIH)
• Pseudotumor cerebri syndrome is defined as intracranial hypertension without a
structural or vascular cause.
• A diagnosis of IIH  exclude drug-induced, metabolic, or hormonal causes of
intracranial hypertension.
• Annual incidence of 1 to 2 per 100 000
• Individuals with obesity.
• Women aged 20 to 40 years
• Most common symptom Headache
• Other symptoms 
• Visual - persistent blurred vision, transient visual obscurations, and horizontal diplopia
• Pulsatile tinnitus are frequent
• if untreated can lead to irreversible visual loss.

56. IDIOPATHIC INTRACRANIAL HYPERTENSION (IIH)
• Ix:
• Fundoscopy  optic disc edema.
• Brain MRI and MR venography  exclude other causes such as neoplasm and cerebral
venous thrombosis.
• Additional  LP - to confirm an elevated opening pressure (typically >25 cm of CSF) and
ensure CSF constituents are normal and neuroophthalmological evaluation.
• Rx goals  vision preservation
• Weight loss
• Prescription of acetazolamide to reduce CSF production.
• Patients with more severe visual loss may require surgery to lower intracranial pressure.
• Prognosis
• Headache improvement may not accompany visual improvement
• May require treatment with migraine therapies.

57. SPONTANEOUS INTRACRANIAL HYPOTENSION
• Headache is an important symptom of low intracranial pressure (intracranial
hypotension)
• Precipitated by a spinal CSF leak  lower ICP or volume  downward brain
sagging with traction on intracranial structures  compensatory venous
engorgement.
• Can be secondary to post-dural puncture headache after a diagnostic lumbar
puncture, lumbar anesthesia, another spine procedure, or SIH.
• Annual incidence of 2 to 5 per 100,000
• Onset of SIH is often associated with an inciting event such as a Valsalva maneuver.
• SIH can be caused by 3 types of CSF leaks:
• Focally weakened dura often in a nerve root sleeve
• Osteophytic or discogenic ventral tears
• CSF-venous fistulas.

58. SPONTANEOUS INTRACRANIAL HYPOTENSION
• The classic presentation of post-dural puncture headache or SIH
• Orthostatic headache
• Developing within minutes of standing and disappearing within minutes of becoming supine
• Other headache characteristics (exertional, “second-half-of-the-day headache”)
• Non-headache symptoms muffled hearing
• Rx 
• Hydration, nonspecific analgesics, and caffeine
• The underlying cause may require more definitive therapy if no improvement
• Lumbar or targeted autologous epidural blood patches
• Surgical repair of the leak or fistula site

59. HEAD INJURIES
• Traumatic headache  over several
days, weeks, or months.
• Acute setting  any focal neurological
symptoms or signs a CT head and CT
angiogram of the head and neck vessels
• Subdural or epidural hematoma
• Carotid or vertebral artery dissection
• Cerebrospinal fluid leak
• CVST or carotid-cavernous fistula (rare).
• Bone windows  assess for fractures
at the vault or base of the skull.
• If absence of findings on the
neurological examination  CT head
rules.
• Canadian, Percan
• Chronic setting (weeks, months, or
years)
• No diagnostic evaluation guidelines
exist.
• MRI can be done  more sensitive
• Should include a gradient weighted
sequence to identify  presence of
hemosiderin deposition.

60. SECONDARY HEADACHE
Micieli A and Kingston W (2019) An Approach to Identifying Headache Patients That Require
Neuroimaging. Frontier in Public Health 7:52

61. NEUROIMAGING
• When is it appropriate to order neuroimaging?
• Does the patient with chronic migraine require a magnetic resonance
imaging (MRI) study?
• What imaging does a patient with a thunderclap headache require in the
emergency department?
• When is vascular imaging indicated?
• What are characteristics of neurological symptoms to suggest it is
secondary to a focal cerebral lesion as opposed to a migraine aura?

62. NEUROIMAGING
Micieli A and Kingston W (2019) An Approach to Identifying Headache Patients That Require
Neuroimaging. Frontier in Public Health 7:52
Approach to neuroimaging in a patient with headaches.
TACS, trigeminal autonomic cephalalgias

63. TAKE HOME MESSAGE
Robbins MS. Diagnosis and Management of Headache - A Review. JAMA. 2021;325(18):1874-1885

64. TAKE HOME MESSAGE
Robbins MS. Diagnosis and Management of Headache - A Review. JAMA.
2021;325(18):1874-1885

65. TAKE HOME MESSAGE
Robbins MS. Diagnosis and Management of Headache - A Review. JAMA. 2021;325(18):1874-1885

66. REFERENCES
• Robbins MS. Diagnosis and Management of Headache - A Review. JAMA.
2021;325(18):1874-1885
• Edvinsson JCA et al. The fifth cranial nerve in headaches. J Headache Pain. 2020
Jun 5;21(1):65.
• Micieli A and Kingston W (2019) An Approach to Identifying Headache Patients
That Require Neuroimaging. Frontier in Public Health 7:52
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67. "Mental pain is less dramatic than physical pain,
but it is more common and also more hard to bear.
The frequent attempt to conceal mental pain
increases the burden: it is easier to say "My tooth
is aching" than to say "My heart is broken."
-C.S. Lewis