This presentation offers a structured and practical guide to the clinical approach to headache, one of the most common neurological complaints. It covers headache classification, red flags, key history-taking elements, physical examination tips, and a step-by-step diagnostic framework. Whether you're a medical student, clinician, or healthcare provider, this slide deck provides essential tools to differentiate between primary and secondary headaches and manage patients effectively.

1. Approach To Headache
A Presentation By:
CYUBAHIRO KARANGWA VERITE, Medical student.
Supervised By:
Dr. Longin, Neurology resident.
16/05/2025

2. INTRODUCTION:
• Headache, or cephalalgia, is defined as diffuse pain in
various parts of the head, with the pain not confined to
the area of distribution of a nerve.
• The term headache should encompass all aches and
pains located in the head, but in practice its applications
is restricted to discomfort in the region of the cranial
vault.
• Headache is usually a benign symptom but occasionally
it is the manifestation of a serious illness.

3. Common causes of headache:
There are mainly two causes of headache:
1. Primary headache:
• Primary headache often results in considerable disability and a
decrease in the patient's quality of life. It can be:
• i. Benign
• ii. Recurrent
• iii. No organic disease as their cause

4. i. Underlying organic disease.
ii. Headache associated with head trauma.
iii. Headache associated with vascular disorders.
• Acute ischemic cerebrovascular disorder
• SAH
• Un-ruptured vascular malformation
• Arterial HTN
• Arteritis (e.g. temporal arteritis, sinusitis )
iv. Headache associated with nonvascular intracranial disorder:
• Benign intracranial HTN ( pseudotumor cerebri –presence with headache papilledma, diplopia and
elevated CSF pressure > 20 cm of H2O in relaxed lateral decupitus position).
• Low CSF pressure (e.g., headache subsequent to LP)
• Intracranial infection
2. Secondary Headache:

6. Classification:
• Primary headache syndromes include migraines with (classic) or without
(common) aura, the hemicranias and indomethacin-responsive headaches,
tension headaches, chronic daily headaches, and cluster headaches.
• Secondary headaches have specific etiologies, and symptomatic features
vary depending on the underlying pathology (i.e., SAH, tumor,
hypertension, posterior reversible encephalopathy syndrome [PRES],
analgesic overuse, iatrogenic).
• Migraine without aura (common): At least five attacks that last 4 to 72
hours.Symptomsshouldincludeatleasttwoofthefollowing:unilaterallocation,p
ulsatingorthrobbing,moderatetosevereinintensity,aggravatedbyactivity,anda
tleastone of these associated features: nausea/vomiting, photophobia,
and/or phonophobia.
• Migraine with aura (classic): Same as the aforementioned, except at least
two attacks with an associated aura that lasts from 4 minutes to 1 hour
(longer than 60 minutes is a red flag). The aura should have a gradual
onset, be fully reversible, and can occur before, with, or after headache
onset

7. • Cluster headache: Unilateral orbital or temporal pain with
lacrimation, conjunctival injection, nasal congestion, rhinorrhea,
facial swelling, miosis, ptosis, and eyelid edema.
• Rebound headache (analgesic overuse headache) occurs in the
setting of chronic use of analgesics or narcotics.
• Trigeminal neuralgia presents as episodic sharp stabbing pain
that is unilateral. Rule out multiple sclerosis.
• Temporal arteritis presents as a dull unilateral headache with a
thick tortuous artery over temporal region. The disease is almost
exclusively limited to individuals over 60 years of age with jaw
claudication, low-grade fever, and an elevated ESR and C-
reactive protein (CRP).

12. Migraine
 1. Migraine
 1.1 Migraine without aura
 1.2 Migraine with aura
1.2.1 Migraine with typical aura
 1.2.1.1 Typical aura with headache
 1.2.1.2 Typical aura without headache
1.2.2 Migraine with brainstem aura
1.2.3 Hemiplegic migraine
 1.2.3.1 Familial hemiplegic migraine (FHM)
 1.2.3.1.1 Familial hemiplegic migraine type 1 (FHM1)
 1.2.3.1.2 Familial hemiplegic migraine type 2 (FHM2)
 1.2.3.1.3 Familial hemiplegic migraine type 3 (FHM3)
 1.2.3.1.4 Familial hemiplegic migraine, other loci
 1.2.3.2 Sporadic hemiplegic migraine (SHM)
 1.2.4 Retinal migraine
 1.3 Chronic migraine
1.4 Complications of migraine
1.4.1 Status migrainosus
1.4.2 Persistent aura without
infarction
1.4.3 Migrainous infarction
1.4.4 Migraine aura-triggered seizure
1.5 Probable migraine
1.5.1 Probable migraine without aura
1.5.2 Probable migraine with aura
1.6 Episodic syndromes that may be
associated with migraine
1.6.1 Recurrent gastrointestinal
disturbance
1.6.1.1 Cyclical vomiting
syndrome
1.6.1.2 Abdominal migraine
1.6.2 Benign paroxysmal vertigo
1.6.3 Benign paroxysmal torticollis
Cephalalgia 2018, Vol. 38(1) 1–211

13. STAGES OF MIGRAINE
Adapted from Cady RK. Clin Cornerstone. 1999;1(6):21-32.
Phases of a Migraine Attack
Premonitory/
Prodrome
Aura Mild Moderate to
Severe HA Postdrome
Pre-HA Post-HA
Headache
Time
Intensity

16. Pathophysiology
• The neurovascular theory:

17. PATHOPHYSIOLOGY OF HEADACHE:
• Pain sensitive structures in brain
 Intracranial:
1. Cranial venous sinuses with afferent veins
2. arteries at base of brain and arteries of dura including middle meningeal
artery
3. Dura around venous sinuses and vessels
4. Flax cerebri
 Extracranial:
1. Skin
2. Scalp appendages
3. Periosteum
4. Muscles
5. Arteries
6. Mucosa
 Nerves:
1. Trigeminal nerve(fifth)
2. Facial nerve ( seventh)
3. Vagal nerve (tenth)
4. Glossopharyngeal nerve (ninth)
5. Second and third cranial nerve( optic
and oculomotor)

18. HISTORY:
FIRST OR WORST HEADACHE:
1.Age, Sex, Occupation:
• Migraine headache – more frequent in teenagers & young adults, higher
occurrence in female.
• Cluster headache – almost exclusively in males.
• Cranial arteritis – more frequently in late middle age & in elderly.
2. Duration:
• Tension headache -often has long duration.
• Headache due to expanding of intracranial disease – usually short duration.
• Headache due to meningeal cause – acute in onset.
• Migraine headache – recur over a long period of time, with symptoms free interval
between attacks

19. 3. Location:
• As a general rule localized headache is of greater significance than diffuse
headache.
• Tension headache – typically generalized, band like or bi-occipital.
• Migraine with aura – often unilateral & frequently more prominent interiorly.
• Migraine without aura – frequently bilateral.
• Cluster headache – invariably limited to the same side of the head in any given
attacks & usually periorbital.
4. Prodromal symptoms:
• Migraine headache – commonly precede by systemic complaints as euphoria,
anorexia, nausea.
• Migraine headache – often precede by neurological symptoms as scintillating
scotoma, transient hemianopia, hemi-motor or hemi-sensory disturbance &
dysphasia.

20. 5. Associated symptoms:
• Tension headache – often associated with other psycho-physiologic
disturbances.
• Cluster headache – typically associated with ipsilateral
lacrimation, Conjunctival injection, Rhinorrhea, & Facial Flushing.
6. Quality of pain:
• Tension headache – Pressing, Squeezing, Tight or Heavy.
• Migraine headache – Throbbing or Pounding.
• Headache due to intracranial lesion – Relatively Mild.
• Acute SAH- Pain tends to be explosive & intense.

21. 8. Frequency, duration & diurnal variation:
• Tension headache– often persist & may worsen as the day progress.
• Migraine headache – the frequency is variable & unpredictable.
Although usual variation is from 4 - 72 hrs, they may persist for days.
• Cluster headache – occur repetitively over a period of weeks or
months. Often there are 1 or 2 attacks daily. The headache typically
nocturnal & of brief duration (30 min to a few hours).
9. Family History:
• Migraine headache – strong family history.
• Cluster headache – are not familial.
10. Intracranial Mass Lesion:
• Associated symptoms are more prominent than headache.
• Some intra-cerebral lesion may exhibit seizure or vomiting.

22. 11. Cranial arteritis:
• Systemic symptoms as fever, anorexia & rheumatic symptoms.
12.Tension headache & Vascular Headache:
• Induced or aggravated by emotional factors.
• Intraventricular & posterior fossa tumor – may be
accentuated by change in the head position, coughing &
Valsalva maneuver

24. Approach to Headache
1. PHYSICAL EXAMINTAION:
• The primary purpose of the physical examination is to identify
causes of secondary headaches.
• General physical examination:
• VS (BP, temperature)
• Fundoscopic examination (papilledema)
• CV assessment (assess risk of CVA)
• Palpation of the head and face (R/O sinusitis).
• Systemic sign (fever, weight loss, anemia) – infectious disease,
specific infection of CNS, metastatic disease of brain &/or
meninges

25. Complete Neurologic Examination:
• focal neurologic signs
• Mental status
• Level of consciousness
• Cranial nerve testing
• Motor strength testing
• Deep tendon reflexes
• Pathologic reflexes (e.g. Babinski’s sign)
• Cerebellar function
• Gait testing
• Signs of meningeal irritation ( Kernig’s and Brudzinski’s signs).

26. 2. Neurological examination:
• No neurological abnormality – tension headache.
• Evidence of cerebral ischemia – small percentage of migraine
(permanent residual damage).
• Horner’s syndrome – sometimes during migraine headache(rarely
permanent). Localizing sign – expanding ICSOL.

• Papilledema - ICP due to ICSOL.
• Bruits over the eyes/cranium – vascular malformation.
• Sign of meningeal irritation – lesion affecting the meninges.

28. INVESTIGATION:
• Laboratory:
• Random use of laboratory testing in the
evaluation of acute headache is not warranted.
• CBC when systemic or intracranial infection is
suspected
• ESR when temporal arteritis is a possibility.

29. Neuroimaging:
• Neuroimaging is not usually warranted in patients
with primary headaches.
• CT scanning is recommended to identify acute
hemorrhage.
• MRI studies are recommended to evaluate the
posterior fossa.

30. Lumbar Puncture:
• CT scanning without contrast medium, followed by LP if the
scan is negative, is preferred to rule out SAH within the first
48 hours.
• LP is useful for assessing the CSF for blood, infection and
cellular abnormalities.
• Headaches are associated with low CSF pressure (e.g.
posttraumatic leakage of CSF) and elevated CSF pressure
(e.g. idiopathic intracranial HTN and CNS space-occupying
lesions)

31. Indication For Scan:
• First or worst headache, particularly if of sudden onset.
• Headache of increasing frequency or severity.
• Increased frequency of vomiting and headache on waking.
• Headache triggered by coughing, straining or postural changes.
• Persistent physical symptoms or signs after attack (neurological or
endocrine)

32. When to refer to a neurologist????
• Physician has inadequate level of comfort in diagnosing or treating
patient’s headache.
• Patient requests a referral.
• Patient does not respond to treatment.
• Patient’s condition or disability continues or worsens.
• Physician is unable to classify patient’s headache according to diagnostic
criteria for primary or secondary headache disorders.
• Habituation or rebound headaches limit outpatient management.
• Patient has intractable or daily headaches.

33. Preventive Management Of Headache:
 Prophylactic medications should be considered if a patient at
least three disabling migraine per month. It is important to
review patient use of all medication and comorbidities.
 Lifestyle modification:
 Patient should keep a headache calendar to identify possible
triggers.
 Patient should reduce alcohol, caffeine and other triggers that
might increase the risk of migraine.

34. 1. Migraine Headache:
1. Abortive Therapy:
• Moderate : NSAIDs, Sumitriptans, Dopamine Antagonists
• Severe: Naratriptan, Sumitriptan (s.c./ n.s.)
• Extreme: Opiods
• Intravenous Metoclopromide is recognized as effective therapy
for acute migraine.
• I.V. Ketorolac an effective alternative in ED
• 2. Prophylaxis:
• High efficacy: Beta blockers, TCAs, Antiepileptics like Valproic
• Low efficacy: Verapamil, Flunarizine

35. Status Migrainosus
• Migraine lasting greater than 72 hours in duration
• Refractory to conventional treatment
• Steroid burst – oral methylprednisolone, prednisone
• “Headache cocktail”:
• Ketorolac 60mg IM
• Diphenhydramine 50mg IM
• Prochlorperazine 10mg IM
• Patient must have a driver

36. 2. Tension-Type Headache:
• The pain of TTH can generally be managed with simple analgesics
such as acetaminophen, aspirin, or NSAIDs.
• Behavioral approaches including relaxation can also be effective.
• TRIPTANS in pure TTH are NOT HELPFUL, although triptans are
effective in TTH when the patient also has migraine.
• For chronic TTH , AMITRIPTYLINE is the only proven treatment
Other TCA, SSRI and the benzodiazepines have not been shown to
be effective.

37. 3. Cluster Headache:
• Abortive agents:
• Oxygen (8L/min for 10 mins or 100% by mask)
• Triptans (sumitriptan)
• Prophylactic:
• CCBs – MOST effective for CH prophylaxis. Most used Verapamil others: Nimodipine and
diltiazem
• Corticosteroids to terminate the CH cyle and in preventing immediate recurrence
• High dose prednisolone is first prescribed and gradually tapered
• Beta blockers are not used as it may precipitate bradycardia occuring during CH

38. Secondary Headache:
• Treatment of Secondary Headaches includes identifying the
disease and treating it

39. References:
• Harrison’s_Principles_of_Internal_Medicine,_Twentieth_Edition_(Vol
.1_&_Vol.2
• Davidson’s Principles and Practice of the Medicine- 23rd
Edition.
• The Washington Manual Of Medical Therapeutics- 34th
Edition

40. THANK YOU!!!