Monday, July 19, 2010

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patoplasty of vascular headaches

Prof. Enrique Rojas, Prof. Joseph A. Dr. Miguel Gutierrez Ariza and Pérez-Camacho Duque *

* Revised text. And added to the original work, treatment and classification of vascular headaches by Dr. Miguel Duque Pérez-Camacho.

headaches show a rich vascular plasticity symptomatology. The most common of all migraine whose diagnosis is usually straightforward when it appears with the typical characteristics. The atypical problems of differential diagnosis with other vascular headaches, chronic vasomotor headache, the eritroposopalgia, temporal arteritis, and general mental tension headaches and depression. The diagnosis of migraine headaches should be equivalent with great caution. He has a great interest to know the replacement and alternation of symptoms around the various forms of headache. These mutations described a genuine transition substitute symptoms. INTRODUCTION

headaches patoplasty offer a rich vascular clinic, which coincides with high variability phenomena that all headaches. Possibly more than 70% of the patients we see are complaining of a headache. In each, the symptoms take different forms, as befits their different etiologies. The most common of all is the headache.
For example, in England there are over ten million migraines, according to research by Harvey-Suterland , over two hundred thousand people have to stay in bed one day a week for this reason; an estimated ten million working days are lost because of this year. Grimes , fifteen thousand patients of general practices found that about 10% complained of significant headaches. The statistics of Friedman and Lennox are higher.

of migraine should also consider other less common: vasil artery migraine, cluster headache of the Horton, called cervical headache, the headache caused by inflammation of the temporal artery is considered akin to collagen diseases and psychic headache is usually bilateral, in the pathogenesis should be considered an important vascular factor and the contraction of the muscles of the neck.


The classical descriptions of migraine rarely present diagnostic problems, provided that the development of clinical history data are properly collected. Friedman and Storch required to make the diagnosis of migraine following conditions:

1 .- What is throbbing headache, usually recurrent and

2 .- In the intercritical periods there is a full recovery in regard to headache, although it is easily recognizable personality pathology: hypersensitivity to light, noise, etc., excessive order in all its actions, people very fond of cleaning, stubborn, inflexible while shy and retiring. Perfectionist zeal. They always want to do more and better. As Marcus says Wolff : make their qualities, defect. Approach, therefore, the obsessive and enequéticos. 3 .-
neurological disorders also appear consistent visual aura in the form of photophobia, scotomata, and even hemianopsia. 4 .-
Vegetative disorders: nausea, vomiting, dizziness, diarrheal plunges, polyuria, etc.. 5 .-
have a hereditary family. 6 .-
or deleted is relieved pain in 95% of cases with ergot preparations.

Despite these general characteristics, there are many occasions when the clinical picture does not meet these conditions, leading to different varieties of vascular headache-type headache. That is, the classic problems with prodrome (in which the patient feels lethargic, weak, without strength and with some anguish in the background, and ill-shaped enclosure), aura (which in some stories do not appear, sometimes not because they do not exist, but because it has been questioning the patient, can be:

a) Hearing: tinnitus, temporary hearing loss, tinnitus, etc.;
b ) Olfactory : subjective perception of odors;
c) Buds : special flavors strangers
d) Sensitive : paresthesia as affecting half of the body opposite the headache, sometimes involving the face, hands, lower limbs, etc.

The most common type of aura is the lens: scotoma blind small at first, gradually increases. It is sometimes associated with or alternating with scintillating scotoma. There are times when this is not true, and everything is reduced to a few bright spots or moving ("floaters").

Then comes the headache crisis itself: pain in the form of oppression, frontal or fronto-temporal, which increases gradually until it becomes hemicranial. The nature of pain and accompanying clinical phenomena make the diagnosis is simple. Now there are atypical falling within the circle of depression. The relationship between migraine headaches and depression is the same as that entered the equivalent of depression and psychosomatic illnesses. What we see clinically is that there is a transition between migraine headaches and depression, with intermediate concrete cases that match the features of one or the other, making it very difficult differential diagnosis. In fact, migraineurs are predominantly psychological symptoms of depression.

Gans says that migraine and neurasthenia only differ in one symptom that has the first and the second one does not have the headache. We must also differentiate timopáticas headaches described by López Ibor, where the pain is so intense, has a larger location, appearing many times during sleep and relief throughout the day. In the same story of the patient referred to a weight on his brain that produces a clear inhibition, decrease of vitality and reducing their ability to concentrate. Locations are very common in the neck.

symptoms analysis allows us to set transitions into the distressing to the depressive or predominantly into the vessel. Some patients may even see a gradual spectrum ranging from sensory and vital feelings. It is as if the pain becomes a feeling of sadness infancy.

There are differences also those frontal headaches migraines diffuse, with a headache not as strong and which are those that usually happen in the course of endogenous depression. There is a feature of interest in these: the patient has trouble not only tell what it feels like he has, but even locate it, since it is more of a paresthesia.

It also has a more distressing. Everything becomes clear when the patient says he fears going mad or suffering from an incurable mental illness or who fears that he may have a fit, and they mean a shift of emphasis towards depressed than anxious. The fear of losing control is to López Ibor of great significance.

The cranial tumor headaches often have a very cropped picture both as regards the pain itself as complementary examinations, the neurological examination, fundus, skull radiographs, the course of symptoms and the type and location of the pain we clarify the diagnosis.

is important to emphasize the rhythm of headaches when we have problems diagnoses. The circadian rhythm of morning worsening and improvement in the evenings we will be driven towards depressive headaches. The cyclical pattern, with a sadness masked background, we will think of an equivalent depression. The agonizing headaches are usually the pain in the twilight hours. Other times the rate of pain did not meet any particular standard, but a somewhat anarchic and capricious. In these cases we investigate symptoms aids and the presentation. Sometimes there is a kind of alternating rhythm: a few days with migraine headache, nausea, nausea and vomiting, there is some strange euphoria. Other days, when he removes the headache, feel saddened, with great fatigue and a huge concern. This is so true-soul cefalárgico sift syndrom.

migraine attacks in the vascular factor in the pathogenesis is essential, but we note also the role of psychological factors in triggering them. The cycle established by Rowbothan still relevant to the phenomena of migraine headaches circle.

Clinically there is some correlation between migraine and epilepsy. Also in seizure headache and anxiety as there are elements of the seizure aura. Follow, therefore, a similar cycle, but these coincidences are not nuclear.

Finally there is a clinical form of migraine, the headache of the lower half of the face, facial migraine, which was included in a group of neuralgias of doubtful clinical staff independently. They the precise boundaries are erased, neuralgia can be treated in the spheno-palatine ganglion, the nerve neuralgia vidian, Charlin syndrome or syndrome-Benisti Mombrun . Sometimes these patients have a history of migraines, seizures alternating with these other atypical typical. They associate the congetión of ocular and nasal mucous membranes, tearing, nasal packing, hidrorrea, etc., Being able to confuse or be very difficult differential diagnosis of cluster headache Horton. According to Mark Lanzarot and Cerdan, patients suffering from typical migraine crisis in youth and at maturity have this form of facial neuralgia.

equivalents include headache ( Liveing, Moebius ) are highlighting certain vasomotor rhinitis, dizziness (which statistically are the most common, referring either to the medication ergotamine), some trigeminal neuralgia neuralgias and certain nonspecific. Less common are paroxysmal tachycardia, precordial migraine. In children, abdominal migraine can occur without headache or go unnoticed at the box striking the abdomen. All these crises in which there is no headache or it is in the background, must be diagnosed with great caution because that may be symptoms of another illness.


Among other vascular headaches of interest in this vein, we find chronic vasomotor headache ( Heyck ) at which lacks the typical features of migraine (the presentation of the crisis, the type of pain, etc.)..
The vast majority are psychogenic. The eritroposopalgia also called cluster headache of Horton, vidian neuralgia, ciliary neuralgia and headache craniofacial independently.
Americans ( Kunkle Macropopulum Friedman, Schiller ) given their clinical characteristics have adopted the name of cluster headache can be translated as "cluster headaches or group or crowd." The pain may spread to the face, which can be confused with trigeminal neuralgia. For a long time it was thought that this was a different location neuralgia: ciliary ganglion, sphenopalatine nerve, nasociliary, etc. Today is thought to be due to a vegetative deregulation at the territory of the internal carotid artery. But it is often difficult to find an organic cause in this and other similar headaches. Thus, between 500 headaches Cohen studied, only 20% were organic, with the remaining 80% of psychological origin. The cluster headache is more common in men, not starting before forty years, with the crisis provoked by cold, heat and especially by the ingestion of alcoholic beverages. The challenge test is the safest of histamine.

temporal arteritis may be confused with any of those mentioned above. Here the throbbing pain located temporo-occipital area, adding a cutaneous hyperesthesia, local erythema and edema. The temporal artery is thickened, hard and painful, something that never occurs in migraine, there is often pain in the temporomandibular joint jaw when chewing ("intermittent claudication jaw). Today is considered (Marcos and Cerdan ) as a local symptom of a widespread disease. Thus, it is common that these patients also have intermittent claudication, gastrointestinal hemorrhage due to obstruction of the celiac trunk, etc.

The basilar artery migraine described in 1961 by Bickerstaff is a very controversial syndrome that usually presents no problems for his complete reversibility. The so-called cervical migraine described by Barre and Liéou the name of "posterior sympathetic syndrome" is usually accompanied of dizziness. The pain starts in the neck and radiating to the parietal region and retro-ocular. Differential diagnostic problem raises the headaches anxious to appear as nucalgias. The radiographic signs can clarify the problem: next to the loss of physiological cervical lordosis, Kyphotic angles, intervertebral disc injuries or spondyloarthritis. These injuries can cause a complication that is interesting to note: to narrow the foramina, can compress the vertebral artery, causing a headache of a coronary artery.

In recent years there has been a lot about the fact that many neuralgia are due to chronic states of anxiety and unresolved conflict situations. In our experience this is not always so, as the clinical examination reveals a muscular contracture that often does not exceed the normal limits. Sometimes the headaches trying Tenson differences of vascular headaches is not possible, even in some patients is associated both mechanisms: vascular muscle, giving way to a combined headaches. Their frequency has increased dramatically today. It is not uncommon in some cases alternate migraine with this form. Usually bilateral, frontal or occipital and is accompanied by great anxiety, occurring between Y40 20 years. This headache can land in a traffic headache clinical depressive with a pretty clean, so that antidepressant treatments caused a clear improvement, although being a secondary depressive symptoms, total remission I require a thorough investigation of conflicts originating and their ability to digest such circumstances. In this regard the substitution and the alternating cephalalgic syndromes presents a very broad plasticity, so that some symptoms are clinically followed each other. This dynamic development of symptoms and even their confluence, it is not only enrich the knowledge and natural history of disease. Hence we should talk about a diagnosis metablética born of these mutations and symptomatic changes. Lopez-Ibor Dressing, have spoken on occasions "changes in syndromes" to refer to these issues. Spiegelberg of syndromalternation. Groen et al. displacement syndromes. Sometimes the same treatment as their excessive power or simply because of their habitual action that originates Landolt has called "the phenomenon of forced normalization", ie that the treatment modifies the clinical picture by removing a symptom and leaving clear path to another or moving geographically headache from one place to another, with the consequent change in symptoms added.

Thus, certain cephalic paresthesias become digestive symptoms, for example, then head back pain, but with a different nature. In many paintings of this type there is a phasic rhythm, we may speak of depressive equivalent. In others there this year, but in the background of the clinical picture there is a vital sadness perceptible phenomenologically, we speak of masked depression.

One last question, can you talk a teleological movement syndromes? This is not always given in a particular way, or even with an objective external causes. The transition takes symptom substitution, sometimes unsuspected directions, but sometimes this is not so and costs catamnésica predict the evolution of the patient. Within the area of \u200b\u200btension headaches is something we should not forget: to remove the headache without resolving the conflict that caused it can happen that will break the existing balance and thus originating new symptoms with a function also rehabilitation. SUMMARY

The demostrate a rich vascular Headaches sintomatologic platicity. The most frequent-of the migraine, Whose simple diagnosis Tends to Be When It applas with the typical characteristics. The atypical forms present differents diagnostic problems with other vascular headache-the chronic headache vasomotora , the headache histaminic of Horton, the arithis of the temporal- in general with the headaches due to psyquic tension and depression. The diagnosis of the equivalent of migraine should be done with great caution. Et is of great interest to know the supplency and alternation of symptoms with regards around of headaches. These mutacions describe an authentic substitution syntomatologic transition.


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• Friedman, A., Von Storch, T., Merritt, H. - Neurology, 4.773
• Friedman, Background not migraine. Cochrane.
• Heyck, H. - Headaches. Ed Marin. Barcelona.
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• Lennox WG, Lennox, MA - Epilepsy and related disorders. Little Brown. Boston
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• López Ibor, JJ blues. Paz Montalvo. Madrid-Influence of new drugs in psychiatric nosology. International Congress of Neuro-pharmacology. Munich.
• López Ibor, JJ and Lopez Alina-Ibor, JJ organischen Krankheiten bei Depression. Valdener Symposium.
• Alina Lopez-Ibor, JJ Los depressive equivalents. Paz Montalvo. Madrid. • Lazarot
Marcos, M. Jaquecas. Rev. Clin. Esp. 56, 302
Lazarot • Mark M. and Cerdan Vallejo A. The migraine Sandoz, Barcelona. •
Marcasen, R, M, Wolf JAMA Migraine HS, 139.198. •
Moebius, E. Die Migraine. Vienna •
Rowbotham, GF Migraine and the sympathetic nervous pathways. Brit. Med. H., 4470, 319. •
Spiegelberg, U. - Zur Psychosomatic December Shift Syndrome (Feldwechsel). Hamburger Gespräche.


Analgesics and anti-inflammatory estoroídicos

Aspirin and paracetamol are considered as first choice, being effective mainly in pictures moderate, especially if taken at the beginning of the attack. Used at doses of 500 - 1000 mg and have a very similar efficiency. It is preferable to use liquid forms of analgesics to achieve more rapid effects (lysine acetylsalicylate, or effervescent tablets).
more intense in the tables can also be used aintiinflamatorios drugs (NSAIDs) that have a rapid onset of action. Examples are ibuprofen (400-800 mg), naproxen (750mg), naproxen sodium (825 mg = 3 tablets of 275 mg once), ketoprofen (75 mg), ácidomefenámico (500 mg) or flufenamic acid.
may also be interesting given metoclopramide (10 mg) 10 to 30 minutes before the analgesic. Avoid gastric stasis that can impede the absorption of the analgesic, relieves nausea and vomiting and may have antimigraine action itself. This is especially important in patients where vomiting is an important element in the migraine attack.

respecting contraindications, ergotamine is effective in a number of severe cases not responding to painkillers. The effectiveness can be the order of 50%. Caffeine enhances the effect, but other combinations are worth much more dubious. The main drawback is the toxicity (ergotism). Do not exceed 10-12 mg per week or repeated treatments with an interval less than three days.
oral absorption is quite irregular. The rectal suppositories much better and can give results in cases not responding to oral treatment. The sublingual route, the parenteral or inhalation are also very effective but there is no ready market in our country.
The previous administration of metoclopramide (see above) may improve oral absorption and contributes to alleviating the vomiting that sometimes occur as a side effect. Are due to central chemoreceptor stimulation and therefore also occur with rectal ergotamine preparations. Dihydroergotamine

is less potent than ergotamine, which means it is less effective but also has fewer side effects. Other countries have enough acceptance by injection or intranasal, but Spain is only available orally, relatively little use.

Almotriptan, Eleptriptán, Naratriptan, frovatriptan, rizatriptan, sumatriptan and zolmitriptan .

Ergotamine most likely acts by stimulating serotonin receptors. Sumatriptan is a stimulant of 5-HT 1B / D, more effective than ergotamine and with fewer side effects. The combination of very high efficiency (almost 90%), low rate of adverse effects and relieve indecently fast attack phase where it has been converted to the SC injection of sumatriptan in a favorite in the emergency treatment. However it should not be administered to patients receiving ergotamine or dihydroergotamine for the additive toxic effects. It is therefore appropriate to ask about the medication prior to the emergency. Orally the action is somewhat slower and the response rate is lower, but is the highest in the migraine (50-75%). Its main drawback is that in 40% of cases the attack is played at 24-48 hours (although it responds to a second dose).

-called "second-generation triptans" , have better oral pharmacokinetic conditions that sumatriptan. Its bioavailability is higher (45-75%) and therapeutic plasma levels are reached more rapidly (30-60 min). Half-lives are also higher. The basic pharmacological profiles are similar to that of sumatriptan, except that show greater activity on the 5-HT 1B / D and a higher lipophilicity and brain penetration. Thus, in addition to peripheral vasoconstriction and inhibition of perivascular trigeminal terminals, these new "triptans" act directly attenuate the excitability of cells within the trigeminal nucleus. As regards its power to enter into the coronary arteries is similar to that of sumatriptan. Naratriptan has earlier onset of effect than sumatriptan, although with slightly lower responses, but sample produces a lower recurrence of migraine attacks and is better tolerated. Zolmitriptan , almoptriptán, eletriptan, frovatriptan and rizatriptan are also well tolerated and at least as effective, or even something else that sumatriptan. In a meta-analysis of 53 clinical trials controlados1 including more than 24,000 migraine patients concluded that all employees triptans are effective and reasonably well tolerated, although eleptriptán (80 mg), rizatriptan (10 mg) and almotriptan (12 , 5 mg) 1 appear to show greater consistency in the response.


are quite effective in cases of urgency or refractory tables although the mechanism of action is unknown. The most useful is the injection of 10 mg of metoclopramide to intravenously. Effective, but less comfortable are three IV dose of chlorpromazine ( 0.1 mg / kg) spaced 15 minutes.

Opioid Analgesics

Use in emergency cases where the above treatment is ineffective. is often used morphine or methadone, sometimes associated with promethazine which acts as a sedative and antiemetic.


Dexamethasone oral or depot injection may be useful in tables exceeding 24 hours. There is desirable to repeat the treatment before three weeks. Preventive Treatment

The goal of treatment is reduced to less than half the frequency of attacks. Consider preventive treatment applied to patients suffering three or more attacks per month. Try on therapeutic possibilities in case of failure before. Beta blockers

often effective in 60% -70% of cases and the rate of side effects is quite low if contraindications are respected. Keep in mind that not all beta blockers are effective in migraine. Choose from propranolol, atenolol, metoprolol, and nadolol . Are totally ineffective oxpenolol, acebutolol and prenolol and moderately effective (and therefore less desirable) pinolol and timolol. The dose must be adjusted individually and sometimes much higher than necessary to complete adrenergic blockade (eg, propanolol begins with 40-80 mg / day but sometimes you need 320 mg / day). Reaching high-dose beta-blockers before leaving as ineffective. One option that works in many cases refractory is to associate the beta-blocker with amitriptyline (individually adjust the latter) but perhaps should be tested before the second and third chances.

1 Ferrari, Roon KI, Lipton RB, Goadsby PJ. Oral triptans (serotonin 5-HT (1B/1D) agonists in acute migraine treatment: a meta-analysis of 53 trials. Lancet 2001, 358 (9294): 1668-75.


pizotifen is effective in a large number of patients (40-60% according to some authors, 70% according to others). Produce drowsiness (minimized by giving it in single dose at bedtime) and stimulation of appetite, which is a slight disadvantage compared with beta-blockers . Cyproheptadine is very similar and especially effective in children. Adults often complain of excessive sleepiness.

Calcium antagonist

have similar effectiveness to that of pizotifen (around 50%) and may take 6-8 weeks to take effect. Decreases the frequency of the attacks, but not the intensity. Cerebral vasodilatdora action can sometimes cause headaches resembling migraine. It is used for exercising flunarizine antimigraine action without producing peripheral vasodilation.

Valproic Acid

The mechanism of action is poorly understood but the antimigraine efficacy has been demonstrated by several clinical trials. As above, further decreased the frequency of attacks the intensity or duration and the response rate is around 50%. It usually starts with 250 mg twice daily and adjusted gradually to 500 mg, 2 times a day. Especially useful is the prophylaxis of tables with prolonged aura or basilar migraine. Topiramate

antiepileptic drug that has received its approval for use in the prophylaxis of migraine. The recommended total daily dose of migraine prophylaxis is 100 mg / day in two divided doses (50 mg every 12 hours). You should start with 25 mg daily, administered at night, during the first week. Subsequently increase dose, at weekly intervals in 25 mg / day to reach the optimal dose of 100 mg. Antidepressants

Tricyclic antidepressants (amitriptyline is the most studied) has a preventive action of migraine, regardless of whether or not the patient is depressed. The mechanism of action is unknown but possibly antiserotonin action, and the dose must be adjusted individually (for amitriptyline is 25 to 300 mg a day, a night shot). The efficacy is similar to propranolol. Especially useful in mixed syndromes (migraine combined with tension headaches) or in patients who abuse painkillers or ergotamine.

MAOIs are also effective, but because of the possibility of side effects should be considered drugs of last resort. Analgesics

NSAIDs have shown efficacy in migraine prophylaxis. Can be tested for example 250 mg of naproxen twice or three times a day, but can also be used idnometacina, ketoprofen and mefenamic acid. The best application of NSAIDs is the prevention of menstrual migraine. Treatment (with ketoprofen or mefenamic acid) should begin 3 days before menstruation and continuing throughout the lifetime of the battery.

N02CA: Antimigraine: Ergot alkaloids

Action and mechanism:

migraine treatments, semisynthetic ergot alkaloids (ergot). At therapeutic doses, produces peripheral vasoconstriction by stimulating alpha-adrenergic receptors. At the level of abnormally dilated carotid artery bed, vasoconstriction of that is useful for eliminating the attack associated migraine.

Paradoxically, at higher doses of dihydroergotamine has competitive blocking activity of alpha-adrenergic receptors.

Pharmacokinetics: Oral: Its bioavailability is very low values \u200b\u200bhave been 0.1-1.5%. Is absorbed in an irregular and incomplete (Tmax = 45 min - 2 h). The degree of protein binding is 90%. It is extensively metabolized, probably in the liver. It is mainly eliminated via bile in the feces. Its half-life is 21 h. Intranasal

: Dihydroergotamine is rapidly absorbed after intranasal administration (Tmax = approx. 45 min.) Bioavailability absolute intranasal dihydroergotamine is approx. A 43 + - 24%. Between 70 and 80% of the plasma is related to the unchanged drug, indicating a lower metabolism of unchanged drug that obtained after oral administration. It binds 93% to plasma proteins. The apparent volume of distribution at steady state is about 800 l. The total body clarification is approx. 1.5 l / min, reflecting primarily the liver clarification. The main route of excretion is biliary tract with the feces. Following intranasal administration, the urinary excretion of unchanged drug and its metabolites amounted to 2%.

To optimize the nasal absorption and prevent loss of drug, we recommend a 15-minute interval between two consecutive doses.

International Classification of Headache,
The International Classification of Headache Disorders, 2nd Edition. Headache Classification Subcommittee of the International Headache Society.

1. Migraine.
• 1.1 Migraine without aura.
• 1.2 Migraine with aura. Or 1.2.1
typical migraine aura. Aura 1.2.2
typical or non-migraine headache.
or without headache 1.2.3 Typical aura.
familial hemiplegic migraine or 1.2.4.
sporadic hemiplegic migraine or 1.2.5. 1.2.6
or basilar type migraine.
• 1.3 Childhood periodic syndromes that are commonly precursors of migraine. Cyclic Vomiting
or 1.3.1. 1.3.2
or abdominal migraine.
or 1.3.3 Benign paroxysmal vertigo of childhood.
• 1.4 Retinal migraine.
or 1.5 Complications of migraine.
chronic migraine or 1.5.1. 1.5.2 State
or bad migraine.
or persistent Aura without infarction 1.5.3. 1.5.4
or migrainous infarction. 1.5.5
or triggered seizure migraine.
• 1.6 probable migraine. 1.6.1
or probable migraine without aura. 1.6.2
or probable migraine with aura.
probable chronic migraine or 1.6.5.
2. Tension-type headache (CT).
• 2. Tension-type headache (CT).
or 2.1 Infrequent episodic CT. 
CT 2.1.1 Infrequent episodic pain associated with pericranial tenderness. 
CT 2.1.2 Infrequent episodic pain not associated with pericranial tenderness.
frequent episodic or 2.2 CT. 
CT 2.2.1 Frequent episodic pain associated with pericranial tenderness. 
2.2.2 Frequent episodic CT not associated with hypersensitivity pericranial painful.
chronic or 2.3 CT.  2.3.1 CT
chronic pain associated with pericranial tenderness.  2.3.2 CT
chronic pain associated with pericranial tenderness. CT or 2.4
likely. 
probable infrequent episodic CT 2.4.1. 
probable frequent episodic CT 2.4.2.  2.4.3
chronic CT probable.
3. Cluster headache and other trigeminal-autonomic headaches.
• 3.1 Cluster headache.
or 3.1.1 Episodic cluster headache.
or 3.1.2 Chronic cluster headache. Paroxysmal Hemicrania
• 3.2. 3.2.1
or episodic paroxysmal hemicrania.
or 3.2.2 Chronic paroxysmal hemicrania.
• 3.3 SUNCT (Short-lasting unilateral headache Neuralgiform Attacks with Conjunctival injection and Tearing). • 3.4 Headache
trigeminal autonomic likely. 3.4.1
or probable cluster headache. 3.4.2 Paroxysmal Hemicrania
or probable. 3.4.3
or probable SUNCT.
4. Other primary headaches.
• 4.1 primary stabbing headache.
• 4.2 Primary cough headache. • 4.3 Headache
primary exercise.
• 4.4 Headache associated with primary sexual activity. Preorgasmic
or 4.4.1 Headache. 4.4.2
or orgasmic headache. • 4.5 Hypnic
• 4.6 Bursting headache (thunderclap) primary. • 4.7 Hemicrania
continuous. • 4.8
chronic headache from the start.
5. Headache attributed to cranial trauma, cervical, or both.
• 5.1 Acute post-traumatic headache. 5.1.1
or acute post-traumatic headache attributed to moderate or severe head injury. 5.1.2
or acute post-traumatic headache attributed to mild head injury.
• 5.2 post-traumatic chronic headache.
or 5.2.1 Chronic post-traumatic headache attributed to moderate or severe head injury.
or 5.2.2 Chronic post-traumatic headache attributed to mild head injury.
• 5.3 Headache attributed to acute WAD. • 5.4
chronic headache attributed to whiplash.
• 5.5 Headache attributed to traumatic intracranial hematoma.
or 5.5.1 Headache attributed to epidural hematoma.
or 5.5.2 Headache attributed to subdural hematoma.
• 5.6 Headache attributed to other head injury, cervical, or both.
or 5.6.1 Headache attributed to acute head injury, cervical, or both.
or 5.6.2 Headache attributed to chronic head injury, cervical, or both.
• 5.7 post-craniotomy headache.
5.7.1 Headache or Acute post-craniotomy.
or post-craniotomy headache 5.7.2 Chronic.
6. Headache attributed to cranial or cervical vascular disorder. • Headache
6.1 attributed to ischemic stroke or transient ischemic attack.
or 6.1.1 Headache attributed to ischemic stroke (stroke).
or 6.1.2 Headache attributed to transient ischemic attack (TIA).
• 6.2 Headache attributed to traumatic intracranial hemorrhage.
or 6.2.1 Headache attributed to intracerebral hemorrhage.
or 6.2.2 Headache attributed to subarachnoid hemorrhage.
• 6.3 Headache attributed to vascular malformation does not rotate.
or 6.3.1 Headache attributed to saccular aneurysms.
or 6.3.2 Headache attributed to arteriovenous malformation.
or 6.3.3 Headache attributed to dural arteriovenous fistula.
or 6.3.4 Headache attributed to cavernous angioma.
or 6.3.5 Headache attributed to encephalotrigeminal or leptomeningeal angiomatosis (Sturge Weber syndrome).
• 6.4 Headache attributed to arteritis.
or 6.4.1 Headache attributed to giant cell arteritis.
or 6.4.2 Headache attributed to primary angiitis of the central nervous system.
or 6.4.3 Headache attributed to secondary angiitis of the central nervous system. • 6.5
carotid or vertebral artery pain.
or 6.5.1 Headache or facial pain attributed to cervical arterial dissection. 6.5.2
or post-endarterectomy headache. 6.5.3 Headache
or carotid angioplasty.
or 6.5.4 Headache attributed to intracranial endovascular procedures. 6.5.5 Headache
or angiography.
• 6.6 Headache attributed to cerebral venous thrombosis.
• 6.7 Headache attributed to other intracranial vascular disorder. 6.7.1
or cerebral autosomal dominant arteriopathy subcortical conInfartos and leukoencephalopathy (CADASIL).
or 6.7.2 Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes (MELAS).
or 6.7.3 Headache attributed to benign angiopathy of the central nervous system.
or 6.7.4 Headache attributed to pituitary apoplexy.
7. Headache attributed to nonvascular intracranial disorder.
• 7.1 Headache attributed to increased cerebrospinal fluid pressure.
or 7.1.1 Headache attributed to idiopathic intracranial hypertension.
or 7.1.2 Headache attributed to intracranial hypertension secondary to metabolic causes, toxic or hormonal.
or 7.1.3 Headache attributed to intracranial hypertension secondary to hydrocephalus.
• 7.2 Headache attributed to decreased cerebrospinal fluid pressure. 7.2.1
or post-lumbar puncture headache. 7.2.2 Headache
or cerebrospinal fluid fistula.
or 7.2.3 Headache attributed to decrease in idiopathic cerebrospinal fluid pressure (or spontaneous).
• 7.3 Headache attributed to noninfectious inflammatory disease.
or 7.3.1 Headache attributed to neurosarcoidosis.
or 7.3.2 Headache attributed to meningitis aseptic (non-infectious).
or 7.3.3 Headache attributed to other non-infectious inflammatory disease.
or 7.3.4 Headache attributed to lymphocytic hypophysitis.
• 7.4 Headache attributed to intracranial neoplasm.
or 7.4.1 Headache attributed to increased intracranial pressure or hydrocephalus caused by neoplasm.
or 7.4.2 Headache attributed directly to the tumor.
or 7.4.3 Headache attributed to carcinomatous meningitis.
or 7.4.4 Headache attributed to hypersecretion or hyposecretion hypothalamic or pituitary.
• 7.5 Headache attributed to intrathecal injection.
• 7.6 Headache attributed to epileptic seizure. 7.6.1 Hemicrania
or epileptic. 7.6.2 Headache
or post-critical.
• 7.7 Headache attributed to type I Chiari malformation
• 7.8. Syndrome of transient Headache and Neurological Deficits with cerebrospinal fluid Lymphocytosis (handle).
• 7.9 Headache attributed to other intracranial vascular disorder.
8. Headache attributed to a chemical or deletion.
• 8.1 Headache induced by acute exposure to use or unasustancia.
or 8.1.1 Headache induced by nitric oxide donors. 
Headache induced by nitric oxide donors immediately. 
Headache induced by nitric oxide donors deferred.
or 8.1.2 Headache induced by phosphodiesterase inhibitors.
or 8.1.3 Headache induced by carbon monoxide. 8.1.4
or alcohol-induced headache. 
alcohol-induced immediate headache.
 Delayed alcohol-induced headache.
or 8.1.5 Headache induced by food components and additives. 
MSG-induced headache.
or 8.1.6 Headache induced by cocaine.
or 8.1.7 Headache induced by cannabis. 8.1.8
or histamine-induced headache.
 Immediate histamine-induced headache.
 Delayed histamine-induced headache.
or 8.1.9 Headache induced gene-related peptide of calcitonin (CGRP). 
Headache CGRP-induced immediate.
 Delayed CGRP-induced headache. 01.08.1910
or acute headache as an adverse event attributed to medication-induced headache 01/08/1911
or other use or acute exposure to a substance. • 8.2
medication overuse headache. 8.2.1
or ergotamine overuse headache. 8.2.2
or triptan overuse headache. 8.2.3
or analgesic overuse headache.
or 8.2.4 Headache attributed to opioid abuse. 8.2.5 Headache
or abuse of various medications.
or 8.2.6 Headache attributed to abuse of other medications. 8.2.7
or medication overuse headache probable.
• 8.3 Headache as an adverse event attributed to medication chronic.
or 8.3.1 Headache induced by exogenous hormones.
• 8.4 Headache attributed to the removal of substances.
or 8.4.1 Headache attributed to caffeine withdrawal. 8.4.2 Headache
or opiate withdrawal. 8.4.3 Headache
or estrogen withdrawal.
or 8.4.4 Headache attributed to withdrawal after chronic use of other substances
9. Headache attributed to infection.
• 9.1 Headache attributed to intracranial infection.
or 9.1.1 Headache attributed to bacterial meningitis.
or 9.1.2 Headache attributed to lymphocytic meningitis.
or 9.1.3 Headache attributed to encephalitis.
or 9.1.4 Headache attributed to brain abscess.
or 9.1.5 Headache attributed to subdural empyema.
• 9.2 Headache attributed to systemic infection.
or 9.2.1 Headache attributed to systemic bacterial infection.
or 9.2.2 Headache attributed to systemic viral infection.
or 9.2.3 Headache attributed to other systemic infection.
• 9.3 Headache attributed to HIV / AIDS.
• 9.4 post-infectious chronic headache. 9.4.1
or chronic headache after bacterial meningitis.
10. Headache attributed to disorder of homeostasis.
• 10.1 Headache attributed to hypoxia, hypercapnia or both. 10.1.1 Headache
or high altitudes. 10.1.2 Headache
or diving. 10.1.3 Headache
or sleep apnea.
• 10.2 Dialysis headache.
• 10.3 Headache attributed to arterial hypertension.
or 10.3.1 Headache attributed to phaeochromocytoma.
or 10.3.2 Headache attributed to hypertensive crisis without hypertensive encephalopathy.
or 10.3.3 Headache attributed to hypertensive encephalopathy.
or 10.3.4 Headache attributed to pre-eclampsia.
or 10.3.5 Headache attributed to eclampsia.
or 10.3.6 Headache attributed to acute pressor response to an exogenous agent.
• 10.4 Headache attributed to hypothyroidism.
• 10.5 Headache attributed to fasting. • 10.6 Headache
• 10.7 Headache attributed to other disorder of homeostasis.
11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures ...
• 11.1 Headache attributed to disorder of cranial bone.
• 11.2 Headache attributed to disorder of the neck.
or 11.2.1 Cervicogenic headache.
or 11.2.2 Headache attributed to retropharyngeal tendonitis.
or 11.2.3 Headache attributed to craniocervical dystonia.
• 11.3 Headache attributed to ocular disorder.
or 11.3.1 Headache attributed to acute glaucoma.
or 11.3.2 Headache attributed to refractive errors.
or 11.3.3 Headache attributed to heterophoria or heterotropia.
or 11.3.4 Headache attributed to ocular inflammatory disorder.
• 11.4 Headache attributed to disorder ears.
• 11.5 Headache attributed to rhinosinusitis.
• 11.6 Headache attributed to disorder of teeth, jaws or related structures.
• 11.7 Headache or facial pain attributed to disorder of the temporomandibular joint.
• 11.8 Headache attributed to other disorder of the skull, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures.
12. Headache attributed to psychiatric disorder.
• 12.1 Headache attributed to somatization disorder.
• 12.2 Headache attributed to psychotic disorder.
13. Cranial neuralgias and central causes of facial pain.
• Neuralgia 13.1 trigeminal.
or 13.1.1 Classical trigeminal neuralgia. 13.1.2
or symptomatic trigeminal neuralgia.
• Glossopharyngeal neuralgia 13.2.
or 13.2.1 Classical glossopharyngeal neuralgia.
or 13.2.2 Symptomatic glossopharyngeal neuralgia.
• intermediate nerve neuralgia 13.3.
• 13.4 superior laryngeal neuralgia. • 13.5 nasociliary
• 13.6 Supraorbital neuralgia.
• 13.7 Other terminal branch neuralgias.
• occipital neuralgia 13.8. • 13.9
neck-tongue syndrome.
• External compression headache 13.10. • Headache
stimuli 13.11 cold. 13.11.1Cefalea
or attributed to external application of a cold stimulus
. 13.11.2Cefalea
or attributed to ingestion or inhalation of a cold stimulus
• 13.12 Constant pain caused by compression, irritation or distortion
cranial nerves or upper cervical roots by structural lesions
. • Optic neuritis
ocular diabetic neuropathy • 13.14. 13.15
• Headache or facial pain attributed to herpes zoster. 13.15.1
or headache or facial pain attributed to acute herpes zoster. 13.15.2
or post-herpetic neuralgia.
• 13.16 Tolosa-Hunt syndrome.
• 13.17 "Migraine" ophthalmoplegic.
• 13.18 Central causes facial pain. 13.18.1Anestesia
or painful. 13.18.2Dolor
or central post-stroke. 13.18.3Dolor
facial or attributed to multiple sclerosis. 13.18.4Dolor
or persistent idiopathic facial. 13.18.5Síndrome
or burning of the mouth.
• 13.19 Other cranial neuralgia or other centrally mediated facial pain.
14. Other types of headache, cranial neuralgia, central or primary facial pain.
• 14.1 Headache not elsewhere classified.
• 14.2 Headache unspecified.
REFERENCES 1 .- Catalog Medicines.
Prepared by the technical department of the General Council of Official Colleges of Pharmacists. 2 .- Memorix
, particularly Neurology. Peter Berlit. Grass editions
Dr. Miguel Perez-Camacho Duque
Director of


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