Headaches and facial pain

The I.M. Sechenov First Moscow State Medical UniversityChair of nervous diseases

Primary and secondary headaches (HA)

Primary HA - independent diseaseSecondary HA - a symptom of another neurological, physical or mental illness

Prevalence of HA in the population 25-40%

8%

• 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

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)

• Tension-type headache (45-84%)• Migraine (5-15%)• Cluster headache (0.1-0.4%)• Chronic paroxysmal hemicrania• Others

The most common primary headaches

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

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

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

Headache characteristics, requiring immediate inspection of patient• The "new" HAFirst emerged HAHA 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:FeverUltra high BP levels (above 220 mm)Neurological manifestations: stiff neck muscles, swelling of the

optic nerve, focal symptoms, altered consciousness, seizures

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.)

• 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.

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

Visual aura in migraine

Visual and sensory aura

•Management of attacks

Nonspecific

Specific

•Prevention of attacks

Principles of migraine treatment

Pathophysiology of pain in migraine

NeuropeptidesNeurokinin АSubstance РCGRP

Realisation of neuropeptides- vasodilatation - Neurogenic inflamation

V nerve ganglion

5-HT1D receptors

5-HT1B receptors

Vasodilatation

Transduction of pain signal

Central pain transmission

PAIN

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

Prevention of migraine attacks

• -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

• Chronic migraine

• Migraine status

• Migrainous infarction

Complications of migraine

• 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)

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

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

Treatment of TTH

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

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

Treatment of cluster headache

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

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

• 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

headacheCauses 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

• NeurogenicTrigeminal neuralgiaGlossopharyngeal nerve

neuralgia • MyogenicMyofascial syndrome of

facial muscles

• SymptomaticEye diseaseORL diseaseDental diseasePathology of the

temporomandibular joint• Psychogenic

Classification of facial pain

• 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

Pathogenesis of trigeminal neuralgia

1 – trigeminal nerve root2 – artery, compressed the root

Trigeminal nerve

artery

• Carbamazepine (finlepsin) at 600-1200 mg per day or

anothe antiepileptic drugs (oxcarbazepine, pregabalin,

levetiracetam)

• Surgical treatment

Treatment of trigeminal neuralgia

Surgical treatment of trigeminal neuralgia

1 – trigeminal nerve2 – artery3 – patient's own muscle tissue, fixing the new interposition artery and nerve

Trigeminal nerve

separator

artery

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