This document summarizes information about different types of headaches, including their causes, characteristics, and treatment. It discusses primary headaches like tension-type headaches and migraines as well as secondary headaches caused by other medical issues. Diagnostic criteria, pathophysiology, and management strategies are provided for several common headache types. The document also covers complications, atypical facial pain, and rebound headaches that can arise from medication overuse.

1. Headaches and facial pain
The I.M. Sechenov First Moscow State Medical University
Chair of nervous diseases

2. Primary and secondary headaches (HA)
Primary HA - independent disease
Secondary HA - a symptom of another neurological, physical or mental
illness
Prevalence of HA in the population 25-40%
8%

3. • Tissue covering the skull (skin, muscles, tendons,
mucous membranes)
• Meningeal artery
• Large intra-and extracranial arteries
• Venous sinuses
• Dura base of the brain
• Cranial nerves: trigeminal, glossopharyngeal, vagus, I
and II cervical roots
Possible sources of pain impulses in headache
Parenchyma of the brain has no pain receptors

4. Examination of the patient with headache
• Careful questioning (complaints, history)
• Clinical (somatic, neurological) examination
• In indications- additional methods:
 CT or MRI of the head
 Lumbar puncture (for suspected neuroinfection or
subarachnoid hemorrhage)

5. • Tension-type headache (45-84%)
• Migraine (5-15%)
• Cluster headache (0.1-0.4%)
• Chronic paroxysmal hemicrania
• Others
The most common primary headaches

6. Diagnostic criteria:
•Existence of disease, that can cause HA
•Temporary association or other evidence (clinical,
neurovisualization) of their causation
•Increase or disappearance of HA after successful
treatment or spontaneous remission of the disease that
cause HA
Secondary HA

7. Mechanisms of secondary headache
• Tension
• Offset
• Inflammation
• Compression of tissues
and anatomical structures
• Increase of intracranial
pressure
• “Volume” process
• Difficulty of venous outflow
• Brain edema
• Stimulation of nociceptors
(streamed with blood, its decay
products, inflammation)
• Increased pulsation of cerebral
arteries

8. Causes of secondary HA
• Injuries to the head and neck
• Non-vascular intracranial processes
• The pathology of intra-and extracranial vessels
• Medications and other substances or abrupt
withdrawal
• Violations of homeostasis
• Infections
• Pathology of the skull, neck, eyes, ears, nose, sinuses,
teeth, etc.
• Mental illness

9. Headache characteristics, requiring immediate inspection
of patient
• The "new" HA
First emerged HA
HA with changed characteristics (appearance of new symptoms)
• Acute development of a strong HA
• Subacute onset with an increase in the intensity of pain
• HA, accompanied by:
Fever
Ultra high BP levels (above 220 mm)​​
Neurological manifestations: stiff neck muscles, swelling of the
optic nerve, focal symptoms, altered consciousness, seizures

10. Headache characteristics, requiring additional instrumental and
laboratory examination of the patient
• Hypertensive characteristics of HA:
 Bursting character of HA
 Morning HA
 HA, accompanied by nausea, vomiting, not bringing relief
 Forced position of the head
• Increasing HA after "light gap" in patients after traumatic brain
injury
• Resistant to standard treatment
• Always clearly sided HA
• HA, the first occurred after 60-65 years
• The presence of cancer
• The presence of neuroendocrine disorders (acromegaly, diabetes,
amenorrhea, etc.)

11. • Migraine without aura
• Migraine with aura
• Complications of migraine
 Migraine status
 Migrainous stroke
Сlassification of migraine
Migraine - a chronic disease of the nervous system, which
appears stereotyped attacks of unilateral pulsating headache
accompanied by symptoms of nausea, vomiting, photo-and
phonophobia.

12. Headache lasts 4-72 hours
• Severe headaches
• Unilateral localization
(typically) or bilateral (in some
cases)
• Pulsating / vibrating character
• Aggravated by physical activity
Intolerance to light
(photophobia)
Pale skin face
Nausea and vomiting
Intolerance to noise
(phonophobia)
Aura symptoms observed in
20% of migraine attacks
•visual aura
•sensory aura
•motor aura
•psychic aura
Clinical characteristics of migraine

13. Visual aura in migraine

14. Visual and sensory aura

15. •Management of attacks
Nonspecific
Specific
•Prevention of attacks
Principles of migraine treatment

16. Pathophysiology of pain in migraine
Neuropeptides
Neurokinin А
Substance Р
CGRP
Realisation of neuropeptides
- vasodilatation
- Neurogenic inflamation
V nerve
ganglion
5-HT1D receptors
5-HT1B
receptors
Vasodilatation
Transduction of pain
signal
Central pain
transmission
PAIN

17. Management of migraine attacks
• Non-narcotic analgesics: aspirin, paracetamol and
other NSAIDs, citramon, sedalgin etc.
• Ergotamine derivatives: ergotamine gidrotartrat
(kofetamin, kafergot, kaffetin) dihydroergotamine
(digidergot).
• Triptans - 5-HT1 serotonin receptors agonists:
sumatriptan (imigran), naratriptan (naramig),
zolmitriptan (zomig)
• Antiemetics: metoclopramide, domperidone

18. Prevention of migraine attacks
• β-blockers: propranolol (Inderal), atenolol
• Antidepressants: amitriptyline, SSRIs (fluoxetine,
paroxetine, sertraline) SIOZSN (venlafaxine,
milnacipran, duloxetine)
• Calcium channel blockers: flunarizin, verapamil
• antiepileptic drugs: valproic acid, topiramate
• Vasoactive drug vazobral

19. • Chronic migraine
• Migraine status
• Migrainous infarction
Complications of migraine

20. • Headaches last from 30
minutes to 7 days
• In chronic forms headache lasts
all day, every day
Mild photophobia or
phonophobia when expressed
attacks
• Dull pain, persistent, but
changes in intensity throughout
the day
• The pain is described as a
squeezing or pressure
• Two-sided localization in the
form of "hard hat" or "Slam" /
"bandage" around the head
• Headache does not increase
during physical activity or
taking alcohol
Episodic tension-type headache -
less than 15-days a month
Chronic tension-type headache -
more than 15 days a month
Clinical characteristics of tension-type headache (TTH)

21. Pathophysiology of pain in TTH
• Personality traits
• Chronic stress
• Anxiety and depressive
disorders
Features of the
functioning of
nociceptive and
antinociceptive systems
Hypertone of pericranial
muscles
TENSION-TYPE
HEADACHE

22. Drug therapy
• Non-narcotic analgesics
• Antidepressants
 Amitriptyline
 SSRIs (fluoxetine, fluvoxamine)
 SSNRIs (venlafaxine, milnacipran, duloxetine)
• Atypical benzodiazepines: alprazolam
• Muscle relaxants: sirdalud
Drug-free treatment
• Massage
• Physiotherapy
• Autotraining
• Biofeedback
• Botulinum toxin
Treatment of TTH

23. The attack triggered by alcohol,
cold, wind or heat, bursting in
the face, vasodilators, arousal
and sleep
Unilateral or bilateral sweating
Redness of the face on pain side
Rhinorrhea
Headache lasts 15-90 minutes• Excruciating pain, localized
behind or around one eye
• The pain may radiate to the top
of the head, jaw, nose, chin
and teeth.
• Ptosis
• Lacrimation and conjunctival
changes on pain side
• Miosis
Cluster headache

24. Management of attacks
• Inhalation of oxygen through the mask
• Triptans
• Dihydroergotamine i/v, i/m, intranasal
• 4% solution of lidocaine intranasally
• Sol. Diazepami i/v
Prevention of attacks
• Lithium carbonate
• Prednisolone
• Calcium channel blockers (verapamil)
• Antiepileptic drugs
Treatment of cluster headache

25. Chronic paroxysmal hemicrania
• The headache lasts an average
of 1-3 minutes
• The average number of attacks
per day 14
• None cluster
100% response to indomethacin
In severe attacks marked nausea,
vomiting
Seizures can be triggered by
mechanical movements of the
head
• Severe or excruciating pain,
localized in the eyes, forehead
or crown
• The pain may radiate to the
ear, neck and shoulder
Rhinorrhea with same side, nasal
discharge, mild ptosis, swelling
century, conjunctival redness and
tearing

26. Rebound headache (HA due to excessive intake of
drugs)
Diagnostic criteria:
•Headache develops within 3 months of daily
medication
•Exist minimal dose of drug
•Headache is chronic (at least 15 days per
month)
•Headache increase after stop the medication
•Headache reduction in 1 month after
cancellation of the drug

27. • Complete removal of the drug abuse
• Detoxification (prednisolone 60 mg daily for the first 2 days and
40 mg per day of the next two days, and 20 mg per day for the
next 2 days of dexamethasone orally or i/v)
• Anticonvulsants (topiramate 100 mg per day) and / or
antidepressants (amitriptyline 50-75 mg daily)
• Transfer to another medication (not from the group of drugs of
abuse)
• Psychotherapy
• Initial development of a program of treatment of primary
headache
Causes of an unsuccessful rebound Ha treatment
• Undiagnosed form of one of the secondary HA
• The combination of two or more different types of HA
(migraine, tension-type headache, etc.)
Treatment of rebound HA

28. • Neurogenic
Trigeminal neuralgia
Glossopharyngeal nerve
neuralgia
• Myogenic
Myofascial syndrome of
facial muscles
• Symptomatic
Eye disease
ORL disease
Dental disease
Pathology of the
temporomandibular joint
• Psychogenic
Classification of facial pain

29. • Intensive paroxysmal pain in the area of innervation of the
second or third branches of the trigeminal nerve, lasting from
seconds to minutes
• Characterized by the presence of trigger (start) zones, which
occurs during stimulation of a typical attack of pain
Trigeminal neuralgia
• Attack of neuralgia often occurs
when eating, talking, and
mechanical stimulation
(washing, cleaning)
• Lack of sensation disorders on
the face, head

30. Pathogenesis of trigeminal neuralgia
1 – trigeminal nerve root
2 – artery, compressed the root
Trigeminal
nerve
artery

31. • Carbamazepine (finlepsin) at 600-1200 mg per day or
anothe antiepileptic drugs (oxcarbazepine, pregabalin,
levetiracetam)
• Surgical treatment
Treatment of trigeminal neuralgia

32. Surgical treatment of trigeminal neuralgia
1 – trigeminal nerve
2 – artery
3 – patient's own muscle tissue, fixing the new
interposition artery and nerve
Trigeminal nerve
separator
artery

33. Pathology of the temporomandibular joint
Two of the following symptoms of a diagnosis:
•The pain is worse in the movements of the
lower jaw and / or compression of the teeth
•Marked limitation of jaw movement
•Notes sound phenomenon in time of joint
movement
•Revealed sensitivity of the joint capsule to its
palpation, combined with radiographic evidence
of changes in the joint
Moderate pain, distributed in temporal, parotid, occipital, and,
sometimes, in the neck and shoulder areas