This document provides an overview of approaches to headache by Dr. Shivaom Chaurasia. It begins by defining headache and discussing common causes, which include primary headaches that often result in disability without an underlying organic disease, and secondary headaches that have a specific underlying cause like head trauma, vascular disorders, or nonvascular intracranial disorders. The document then examines the pathophysiology of headache, important aspects to cover in a headache history, potential investigations, management strategies for different headache types including migraine, tension, and cluster headaches, and indicators for referral to a neurologist.

1. Approach To Headache
A Presentation By:
Dr. SHIVAOM CHAURASIA
MD INTERNAL MEDICINE, KUSMS
FIRST YEAR RESIDENT

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. 2. Secondary Headache:
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

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,puls
atingorthrobbing,moderatetosevereinintensity,aggravatedbyactivity,andatleas
tone 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).

13. 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

14. 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)

15. 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

16. 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.

17. 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.

18. 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.

19. 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

21. 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

22. 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).

23. 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.

25. 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.

26. 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.

27. 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)

28. 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)

29. 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.

30. 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.

31. 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

32. 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.

33. 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

34. Secondary Headache:
 Treatment of Secondary Headaches includes identifying the disease and
treating it

35. 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

36. THANK YOU!!!