Post on 15-Apr-2017
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