The International Classification of Headache Disorders 2nd Edition


HEADACHE ATTRIBUTED TO A SUBSTANCE OR ITS WITHDRAWAL



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8. HEADACHE ATTRIBUTED TO A SUBSTANCE OR ITS WITHDRAWAL


8.1 Headache induced by acute substance use or exposure

8.1.1 Nitric oxide (NO) donor-induced headache

8.1.1.1 Immediate NO donor-induced headache

8.1.1.2 Delayed NO donor-headache

8.1.2 Phosphodiesterase (PDE) inhibitor-induced headache

8.1.3 Carbon monoxide-induced headache

8.1.4 Alcohol-induced headache.

8.1.4.1 Immediate alcohol-induced headache

8.1.4.2 Delayed alcohol-induced headache

8.1.5 Headache induced by food components and additives

8.1.5.1 Monosodium glutamate-induced headache

8.1.6 Cocaine-induced headache

8.1.7 Cannabis-induced headache

8.1.8 Histamine-induced headache

8.1.8.1 Immediate histamine-induced headache

8.1.8.2 Delayed histamine-induced headache

8.1.9 Calcitonin gene-related peptide (CGRP)-induced headache

8.1.9.1 Immediate CGRP-induced headache

8.1.9.2 Delayed CGRP-induced headache

8.1.10 Headache as an acute adverse event attributed to medication used for other indications

8.1.11 Headache attributed to other acute substance use or exposure

8.2 Medication-overuse headache (MOH)

8.2.1 Ergotamine-overuse headache

8.2.2 Triptan-overuse headache

8.2.3 Analgesic-overuse headache

8.2.4 Opioid-overuse headache

8.2.5 Combination medicationanalgesic-overuse headache

8.2.6 Medication-overuse headache attributed to combination of acute medications

8.2.67 Headache attributed to other medication overuse

8.2.78 Probable medication-overuse headache

8.3 Headache as an adverse event attributed to chronic medication

8.3.1 Exogenous hormone-induced headache

8.4 Headache attributed to substance withdrawal

8.4.1 Caffeine-withdrawal headache

8.4.2 Opioid-withdrawal headache

8.4.3 Oestrogen-withdrawal headache

8.4.4 Headache attributed to withdrawal from chronic use of other substances

Coded elsewhere:

7.1.2 Headache attributed to intracranial hypertension secondary to metabolic, toxic or hormonal causes, 7.3.2 Headache attributed to aseptic (non-infectious) meningitis, 10.3.6 Headache attributed to acute pressor response to an exogenous agent.

General comment

Primary or secondary headache or both?

When a new headache occurs for the first time in close temporal relation to substance exposure, it is coded as a secondary headache attributed to the substance. This is also true if the headache has the characteristics of migraine, tension-type headache or cluster headache. When a pre-existing primary headache is made worse in close temporal relation to substance exposure, there are two possibilities, and judgment is required. The patient can either be given only the diagnosis of the pre-existing primary headache or be given both this diagnosis and the diagnosis of headache attributed to the substance. Factors that support adding the latter diagnosis are: a very close temporal relation to the substance exposure, a marked worsening of the pre-existing headache, very good evidence that the substance can aggravate the primary headache and, finally, improvement or resolution of the headache after termination of effect of the substance.
Definite, probable or chronic?

A diagnosis of Headache attributed to a substance usually becomes definite only when the headache resolves or greatly improves after termination of exposure to the substance. When exposure to a substance ceases but headache does not resolve or markedly improve after 3 months, a diagnosis of A8.5 Chronic post-substance exposure headache, described in the appendix, may be considered. However, such headaches have not been documented and the criteria are proposed only for research purposes.

In the particular case of 8.2 Medication-overuse headache, a period of 2 months after cessation of overuse is stipulated in which improvement (resolution of headache, or reversion to its previous pattern) must occur if the diagnosis is to be definite. Prior to cessation, or pending improvement within 2 months after cessation, the diagnosis 8.2.7 8 Probable medication-overuse headache should be applied. If such improvement does not then occur within the 2 months, this diagnosis must be discarded.


Introduction


Migraineurs are physiologically and perhaps psychologically hyper-responsive to a variety of internal and external stimuli. Alcohol, food and food additives and chemical and drug ingestion and withdrawal have all been reported to provoke or activate migraine in susceptible individuals. The association is often based on anecdotal data and reports of adverse drug reactions.

The fact that these stimuli are associated with headache does not prove causation or eliminate the need to consider other aetiologies. Because common events happen commonly, the association between a headache and an exposure to a substance may be mere coincidence. Headache can occur just on the basis of chance. Headache can be a symptom of a systemic disease, and drugs given to treat such a condition will be associated with headache. In acute migraine drug trials, headache, as well as associated symptoms, is listed as an adverse drug reaction despite that it is a symptom of the treated disorder and not the result of treatment. Some disorders may predispose to substance related headache. Alone, neither the drug nor the condition would produce headache. A nonsteroidal anti-inflammatory drug may produce headache by inducing aseptic meningitis in susceptible individuals.

Finally, some acute or chronic substance exposures have been proven to be causally related to headache.

8.1 Headache induced by acute substance use or exposure

Coded elsewhere:

10.3.6 Headache attributed to acute pressor response to an exogenous agent.

Introduction


This group of headache disorders can be caused 1) by an unwanted effect of a toxic substance, 2) by an unwanted effect of a substance in normal therapeutic use and 3) in experimental studies.

Substances that cause headache through their toxic effects, such as carbon monoxide, cannot be studied experimentally and the causal relationship between exposure and headache has therefore to be demonstrated in clinical cases where the substance has been used accidentally or for suicide attempt.

Headache as a side effect has been recorded with many drugs, often as just a reflection of the very high prevalence of headache. Only when it occurs more often after active drug than after placebo in double-blind controlled trials can headache be regarded as a true side effect. The double blind design can also be used experimentally to study the relationship between drug effects and headache. In some cases, for example NO donors, such studies have led to a deeper understanding of the involvement of neurotransmitter mechanisms in primary headaches. A number of substances such as NO donors and histamine induce an immediate headache in normal volunteers and in migraineurs. However, it is now clear that sufferers of primary headache also develop a delayed headache one to several hours after the inducing substance has been cleared from the blood.

Knowing the potential headache-inducing effects of substances in clinical use is important in order to label these substances appropriately. In general, migraine sufferers are much more susceptible to such headaches than other individuals and the same may be true for sufferers of chronic tension-type headache, episodic tension-type headache and cluster headache during cluster periods.

Paradoxically, the headache encountered by most people after heavy alcohol use may be a positive feature because it helps avoid excessive drinking.

Combinations such as alcohol and disulfiram may cause headache when individual agents might not.


8.1.1 Nitric oxide (NO) donor-induced headache

8.1.1.1 Immediate NO donor-induced headache
Previously used terms:

Nitroglycerine headache, dynamite headache, hot dog headache
Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. Absorption of a NO donor

C. Headache develops within 10 minutes after absorption of NO donor

D. Headache resolves within 1 hour after release of NO has ended



8.1.1.2 Delayed NO donor-induced headache
Diagnostic criteria:

A. Headache, in a person who suffers from primary headache, with the characteristics of that primary headache type1 and fulfilling criteria C and D

B. Absorption of a NO donor

C. Headache develops after NO is cleared from the blood2

D. Headache resolves within 72 hours after single exposure



Notes:

1. Normal subjects rarely develop delayed NO donor-induced headache whilst migraineurs develop an attack of migraine without aura, tension-type headache sufferers develop a tension-type headache and cluster headache sufferers develop a cluster headache attack.

2. Migraine and tension-type headache develop after a mean of 5-6 hours, cluster headache typically after 1-2 hours.


Comments:

The headache is typically bilateral, pulsating and frontotemporal in location.

All NO donors (eg, amyl nitrate, erythrityl tetranitrate, glyceryl trinitrate [GTN], isosorbide mono- or dinitrate, sodium nitroprusside, mannitol hexanitrate, pentaerythrityl tetranitrate) can cause headache of this subtype particularly in persons with migraine. GTN is the best studied substance. It reliably induces headache in most normal individuals and migraine sufferers develop a more severe immediate headache than non-migraine sufferers. GTN can also cause a delayed headache in migraine sufferers which fulfils the diagnostic criteria for 1.1 Migraine without aura, even in patients whose spontaneous migraine attacks are with aura. In people with chronic tension-type headache, GTN has been shown to induce a delayed headache which has the characteristics of tension-type headache. It is not known if it has the same effect in sufferers of episodic tension-type headache. Cluster headache sufferers do not develop delayed headache outside cluster periods but, during a cluster period, GTN fairly reliably induces a cluster headache attack usually occurring 1-2 hours after intake. The delayed headache in those with migraine or tension-type headache occurs at variable times but on average 5-6 hours after exposure.

Headache is well known as a side effect of therapeutic use of nitroglycerine and other NO donors. With chronic use tolerance develops within a week, and GTN-induced headache disappears in most patients within that time. With intermittent use headache continues, and may be severe enough to compromise the use of NO donors for angina. Most heart patients are, however, male and beyond middle age, which probably explains why the problem is not of greater magnitude.

Other NO donors have been much less studied but available evidence suggests that they too may produce headache. Isosorbide mononitrate has been the subject of one formal double-blind placebo-controlled study and causes a much longer lasting headache than GTN owing to its slow release of NO.


8.1.2 Phosphodiesterase (PDE) inhibitor-induced headache

Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. A single dose of a phosphodiesterase inhibitor has been given

C. Headache develops within 5 hours of PDE inhibitor intake

D. Headache resolves within 72 hours



Comment:

PDEs are a large family of enzymes that break down cyclic nucleotides cGMP and cAMP. When PDEs are inhibited, the levels of cGMP and/or cAMP therefore increase. PDE-5 inhibitors sildenafil and dipyridamole are the only formally studied compounds in this group. The headache, unlike GTN-induced headache, is monophasic. In normal volunteers it has the characteristics of tension-type headache but in migraine sufferers it has the characteristics of migraine without aura. Headache has been noted as a side effect of sildenafil in clinical trials but only recent experimental studies have shown that, in young persons – especially females – the side effect occurs in a majority of subjects and in migraine patients sildenafil usually induces a migraine attack. Migraine sufferers should be warned of this side effect.

8.1.3 Carbon monoxide-induced headache

Previously used terms:

Warehouse workers’ headache
Diagnostic criteria:

A. Bilateral and/or continuous headache, with quality and intensity that may be related to the severity of carbon monoxide intoxication1, fulfilling criteria C and D

B. Exposure to carbon monoxide (CO)

C. Headache develops within 12 hours of exposure

D. Headache resolves within 72 hours after elimination of carbon monoxide



Note:

1. Typically: mild headache without gastrointestinal or neurological symptoms with carboxyhaemoglobin levels in the range 10-20%; moderate pulsating headache and irritability with levels of 20-30%; severe headache with nausea, vomiting and blurred vision with levels of 30-40%.
Comments:

With higher carboxyhaemoglobin levels (>40%) headache is not usually a complaint because of changes in consciousness.

There are no good studies of the long-term effects of CO intoxication on headache. Casuistic evidence suggests the possibility of chronic post-intoxication headache.


8.1.4 Alcohol-induced headache

8.1.4.1 Immediate alcohol-induced headache
Previously used terms:

Cocktail headache
Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. Ingestion of beverage containing alcohol1

C. Headache develops within 3 hours after ingestion of alcoholic beverage

D. Headache resolves within 72 hours



Note:

1. The effective dose has not been determined.
Comment:

A few subjects develop headache due to a direct effect of alcohol or alcoholic beverages. This is much rarer than delayed alcohol-induced headache.
8.1.4.2 Delayed alcohol-induced headache
Previously used terms:

Hangover headache
Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. Ingestion of a modest amount of alcoholic beverage by a migraine sufferer or an intoxicating amount by a non-migraine sufferer

C. Headache develops after blood alcohol level declines or reduces to zero

D. Headache resolves within 72 hours



Comment:

This is one of the commonest types of headache. It remains unclear whether, in addition to alcohol, other components of alcoholic beverages play a role. It also remains uncertain whether the mechanism is a delayed response to toxic effects or whether mechanisms similar to those responsible for delayed NO donor-induced headache may be involved.

The susceptibility to hangover headache of well-diagnosed headache patients compared with non-headache sufferers has not been determined. In migraine sufferers a migraine attack can be induced the next day after modest intake of alcoholic beverages, while non-migraineurs usually need a high intake of alcoholic beverages in order to develop 8.1.4.2 Delayed alcohol-induced headache.


8.1.5 Headache induced by food components and additives

Previously used terms:

Dietary headache
Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. Ingestion of a minimum dose of food component or additive1

C. Headache develops within 12 hours after substance intake

D. Headache resolves within 72 hours after single intake



Note:

1. Phenylethylamine, tyramine and aspartame have been incriminated but their headache-inducing potential is not sufficiently validated.
8.1.5.1 Monosodium glutamate-induced headache
Previously used terms:

Chinese restaurant syndrome
Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. aggravated by physical activity

B. Ingestion of monosodium glutamate (MSG)

C. Headache develops within 1 hour after MSG ingestion

D. Headache resolves within 72 hours after single intake

Comment:

MSG-induced headache is typically dull or burning and non-pulsating, but may be pulsating in migraine sufferers. It is commonly associated with other symptoms of this syndrome including pressure in the chest, pressure and/or tightness in the face, burning sensations in the chest, neck or shoulders, flushing of face, dizziness and abdominal discomfort.

8.1.6 Cocaine-induced headache

Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. Use of cocaine

C. Headache develops within 1 hour after cocaine use

D. Headache resolves within 72 hours after single use



Comment:

Headache is a reported side effect of cocaine use. It is frequent, develops immediately or within one hour after use and is not associated with other symptoms unless there is concomitant stroke or TIA.

8.1.7 Cannabis-induced headache

Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. stabbing or pulsating quality

3. feeling of pressure in the head

B. Use of cannabis

C. Headache develops within 12 hours after cannabis use

D. Headache resolves within 72 hours after single use

Comment:

Cannabis use is reported to cause headache associated with dryness of the mouth, paraesthesias, feelings of warmth and suffusion of the conjunctivae.

8.1.8 Histamine-induced headache

Comment:

Histamine has been shown to cause an immediate headache in non-headache sufferers and an immediate as well as a delayed headache in migraine sufferers. The latter fulfils criteria for 1.1 Migraine without aura. The headache-inducing property of histamine has been studied after intravenous administration, after cutaneous administration and after inhalation: all routes of administration have the same effect. The mechanism is primarily mediated via the H1 receptor because it is almost completely blocked by mepyramine.
8.1.8.1 Immediate histamine-induced headache
Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. Absorption of histamine

C. Headache develops within 10 minutes after absorption of histamine

D. Headache resolves within 1 hour after absorption of histamine has ceased



8.1.8.2 Delayed histamine-induced headache
Diagnostic criteria:

A. Headache, in a person who suffers from primary headache, with the characteristics of that primary headache type1 and fulfilling criteria C and D

B. Absorption of histamine

C. Headache develops after histamine is cleared from the blood2

D. Headache resolves within 72 hours after single exposure



Notes:

1. Normal subjects rarely develop delayed histamine-induced headache whilst migraineurs develop an attack of migraine without aura, tension-type headache sufferers develop a tension-type headache and cluster headache sufferers develop a cluster headache attack.

2. Migraine and tension-type headache develop typically after 5-6 hours, cluster headache typically after 1-2 hours.


8.1.9 Calcitonin gene-related peptide (CGRP)-induced headache

Comment:

The headache-inducing property of CGRP has been studied only in one double-blind controlled trial. There is, however, no doubt that CGRP causes an immediate headache. Delayed migraine attacks were induced in 3 out of 10 subjects. Recently, it has been shown that a CGRP antagonist is effective in the acute treatment of migraine.
8.1.9.1 Immediate CGRP-induced headache
Diagnostic criteria:

A. Headache with at least one of the following characteristics and fulfilling criteria C and D:

1. bilateral

2. frontotemporal location

3. pulsating quality

4. aggravated by physical activity

B. Absorption of CGRP

C. Headache develops within 10 minutes after absorption of CGRP

D. Headache resolves within 1 hour after absorption of CGRP has ceased



8.1.9.2 Delayed CGRP-induced headache
Diagnostic criteria:

A. Headache, in a person who suffers from primary headache, with the characteristics of that primary headache type1 and fulfilling criteria C and D

B. Absorption of CGRP

C. Headache develops after CGRP is cleared from the blood2

D. Headache resolves within 72 hours after infusion of CGRP



Notes:

1. Normal subjects rarely develop delayed CGRP-induced headache whilst migraineurs develop an attack of migraine without aura, tension-type headache sufferers develop a tension-type headache and cluster headache sufferers develop a cluster headache attack.

2. Migraine and tension-type headache develop typically after 5-6 hours, cluster headache typically after 1-2 hours.


8.1.10 Headache as an acute adverse event attributed to medication used for other indications

Diagnostic criteria:

A. Headache fulfilling criteria C and D

B. Use of a medication for a therapeutic indication other than headache

C. Headache develops within minutes to hours after use

D. Headache resolves within 72 hours after cessation of use



Comments:

Headache has been reported after use of a number of drugs. The following are the most commonly incriminated: atropine, digitalis, disulfiram, hydralazine, imipramine, nicotine, nifedipine, nimodipine. A longer list can be found in the appendix (table 1).

The headache characteristics are not very well defined in the literature but most are dull, continuous, diffuse and moderate to severe.


8.1.11 Headache attributed to other acute substance use or exposure

Diagnostic criteria:

A. Headache fulfilling criteria C and D

B. Acute use of or other acute exposure to a substance other than those described above

C. Headache develops within 12 hours of use or exposure

D. Headache resolves within 72 hours after single use or exposure



Comments:

Headache has been reported after exposure to a number of organic and inorganic substances. The following are the most commonly incriminated substances:

Inorganic compounds: arsenic, borate, bromate, chlorate, copper, iodine, lead, lithium, mercury, tolazoline hydrochloride.

Organic compounds: alcohols (long-chain), aniline, balsam, camphor, carbon disulfide, carbon tetrachloride, clordecone, EDTA, heptachlor, hydrogen sulfide, kerosene, methyl alcohol, methyl bromide, methyl chloride, methyl iodine, naphthalene, organophosphorous compounds (parathion, pyrethrum).

The headache characteristics are not very well defined in the literature but most are dull, diffuse, continuous and moderate to severe.





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