The International Classification of Headache Disorders 2nd Edition


Headache Attributed To Disorder of Homoeostasis



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10. Headache Attributed To Disorder of Homoeostasis


10.1 Headache attributed to hypoxia and/or hypercapnia

10.1.1 High-altitude headache

10.1.2 Diving headache

10.1.3 Sleep apnoea headache

10.2 Dialysis headache

10.3 Headache attributed to arterial hypertension

10.3.1 Headache attributed to phaeochromocytoma

10.3.2 Headache attributed to hypertensive crisis without hypertensive encephalopathy

10.3.3 Headache attributed to hypertensive encephalopathy

10.3.4 Headache attributed to pre-eclampsia

10.3.5 Headache attributed to eclampsia

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 Cardiac cephalalgia

10.7 Headache attributed to other disorder of homoeostasis



Coded elsewhere:

7.1.2 Headache attributed to intracranial hypertension secondary to metabolic, toxic or hormonal causes.

General comment

Primary or secondary headache or both?

When a new headache occurs for the first time in close temporal relation to a disorder of homoeostasis, it is coded as a secondary headache attributed to that disorder. 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 a disorder of homoeostasis, 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 disorder of homoeostasis. Factors that support adding the latter diagnosis are: a very close temporal relation to the disorder of homoeostasis, a marked worsening of the pre-existing headache, very good evidence that the disorder of homoeostasis can aggravate the primary headache and, finally, improvement or resolution of the headache after relief from the disorder of homoeostasis.
Definite, probable or chronic?

A diagnosis of Headache attributed to disorder of homoeostasis usually becomes definite only when the headache resolves or greatly improves after effective treatment or spontaneous remission of the disorder. If this disorder cannot be treated effectively or does not remit spontaneously, or when there has been insufficient time for this to happen, a diagnosis of Headache probably attributed to disorder of homoeostasis is usually applied.

The alternative, when the disorder of homoeostasis is effectively treated or remits spontaneously but headache does not resolve or markedly improve after 3 months, is a diagnosis of A10.8 Chronic post-homoeostasis disorder headache. This is described only in the appendix as such headaches have been poorly documented, and research is needed to establish better criteria for causation.


Introduction


Headache disorders described here were previously referred to as Headache associated with metabolic or systemic disease. However, Headache attributed to disorder of homoeostasis was felt to capture more accurately the true nature of these headache disorders. Headaches caused by significant disturbances in arterial pressure and by myocardial ischaemia are now included in this section. In addition, disorders of homoeostatic mechanisms affecting a variety of organ systems, including altered arterial blood gases, volume disturbances as in dialysis and disorders of endocrine function, are covered here. Headache attributed to fasting is also included.

10.1 Headache attributed to hypoxia and/or hypercapnia

Comments:

Headache occurs within 24 hours after acute onset of hypoxia with PaO2 <70 mm Hg or in chronically hypoxic patients with PaO2 persistently at or below this level.

It is often difficult to separate the effects of hypoxia and hypercapnia.


10.1.1 High-altitude headache

Diagnostic criteria:

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

1. bilateral

2. frontal or frontotemporal

3. dull or pressing quality

4. mild or moderate intensity

5. aggravated by exertion, movement, straining, coughing or bending

B. Ascent to altitude above 2500 m

C. Headache develops within 24 hours after ascent

D. Headache resolves within 8 hours after descent

Comments:

Headache is a frequent complication of ascent to altitude – occurring in more than 80% of cases. 10.1.1 High-altitude headache appears to be independent of an individual’s previous history of headache, although patients with migraine may describe more severe headache that resembles their typical migraine attacks.

Acute mountain sickness (AMS) consists of at least moderate headache combined with one or more of nausea, anorexia, fatigue, dizziness and sleep disturbances. Acetazolamide (125 mg, two or three times daily) may reduce susceptibility to acute mountain sickness. Preventative strategies include allowing two days of acclimatisation prior to engaging in strenuous exercise at high altitudes, avoiding alcohol, and liberalising fluid intake. Most high-altitude headaches respond to simple analgesics such as paracetamol (acetaminophen) or ibuprofen.


10.1.2 Diving headache

Coded elsewhere:

1. Migraine, 2. Tension-type headache, 4.3 Primary exertional headache, 11.2.1 Cervicogenic headache, 13.6 Supraorbital neuralgia, 13.10 External compression headache and 13.11 Cold-stimulus headache precipitated by diving are coded as those disorders.
Diagnostic criteria:

A. Headache, no typical characteristics known, fulfilling criteria C and D

B. Diving to depth below 10 m

C. Headache develops during diving and is accompanied by at least one of the following symptoms of CO2 intoxication in the absence of decompression illness:

1. light-headedness

2. mental confusion

3. dyspnoea

4. flushed feeling in the face

5. motor incoordination

D. Headache resolves within 1 hour after treatment with 100% O2

Comment:

Hypercapnia (arterial PCO2 >50 mm Hg) is known to cause relaxation of cerebrovascular smooth muscle and lead to vasodilatation and increased intracranial pressure. There is some evidence that hypercapnia in the absence of hypoxia is associated with headache. The best clinical example of headache attributed to hypercapnia occurs in divers. Carbon dioxide may accumulate in a diver who intentionally holds his or her breath intermittently (skip breathing) in a mistaken attempt to conserve air, or takes shallow breaths to minimise buoyancy variations in the narrow passages of a wreck or cave. Divers may also hypoventilate unintentionally when a tight wetsuit or buoyancy compensator jacket restricts chest wall expansion, or when ventilation is inadequate in response to physical exertion. Strenuous exercise increases the rate of CO2 production more than 10-fold, resulting in a transient elevation of PCO2 to more than 60 mm Hg. Diving headache usually intensifies during the decompression phase of the dive or upon resurfacing.

Mild non-specific headache is also common in divers with decompression illness, and may be associated with musculoskeletal pain and, in more serious cases, with focal neurological and/or respiratory symptoms, loss of consciousness and/or cognitive deficits.

Headache in divers can also occur as a result of carbon monoxide intoxication which rarely contaminates divers’ compressed-air supply if the air intake system is positioned in such a way as to gather improperly directed combustion-engine exhaust. Such headache is coded as 8.1.3 Carbon monoxide-induced headache.

Migraine, tension-type headache, primary exertional headache, cervicogenic headache, supraorbital neuralgia, external compression headache and cold-stimulus headache can occur during a dive, but diving in these instances should be considered a precipitating factor rather than the cause.


10.1.3 Sleep apnoea headache

Diagnostic criteria:

  1. Recurrent headache with at least one of the following characteristics and fulfilling criteria C and D:

1. occurs on >15 days per month

2. bilateral, pressing quality and not accompanied by nausea, photophobia or phonophobia

3. each headache resolves within 30 minutes

B. Sleep apnoea (Respiratory Disturbance Index >5) demonstrated by overnight polysomnography

C. Headache is present upon awakening

D. Headache ceases within 72 hours, and does not recur, after effective treatment of sleep apnoea



Comments:

Although morning headache is significantly more common in patients with sleep apnoea than in the general population, headache present upon awakening is a non-specific symptom which occurs in a variety of primary and secondary headache disorders, in sleep-related respiratory disorders other than sleep apnoea (eg, Pickwickian syndrome, chronic obstructive pulmonary disorder), and in other primary sleep disorders such as periodic leg movements of sleep. A definitive diagnosis of 10.1.3 Sleep apnoea headache requires overnight polysomnography.

It is unclear whether the mechanism of 10.1.3 Sleep apnoea headache is related to hypoxia, hypercapnia or disturbance in sleep.


10.2 Dialysis headache

Diagnostic criteria:

  1. At least 3 attacks of acute headache fulfilling criteria C and D

B. Patient is on haemodialysis

C. Headache develops during at least half of haemodialysis sessions

D. Headache resolves within 72 hours after each haemodialysis session and/or ceases altogether after successful transplantation

Comment:

Headache commonly occurs in association with hypotension and dialysis disequilibrium syndrome. The disequilibrium syndrome may begin as headache and then progress to obtundation and finally coma, with or without seizures. This syndrome is relatively rare and may be prevented by changing dialysis parameters.

As caffeine is rapidly removed by dialysis, 8.4.1 Caffeine-withdrawal headache should be considered in patients who consume large quantities of caffeine.


10.3 Headache attributed to arterial hypertension

Comment:

Mild (140-159/90-99 mm Hg) or moderate (160-179/100-109 mm Hg) chronic arterial hypertension does not appear to cause headache. Whether moderate hypertension predisposes to headache at all remains controversial, but there is little evidence that it does. Ambulatory blood pressure monitoring in patients with mild and moderate hypertension has shown no convincing relationship between blood pressure fluctuations over a 24-hour period and presence or absence of headache.

10.3.1 Headache attributed to phaeochromocytoma

Diagnostic criteria:

A. Intermittent discrete attacks of headache accompanied by at least one of the following and fulfilling criteria C and D:

1. sweating

2. palpitations

3. anxiety

4. pallor

B. Phaeochromocytoma demonstrated by biochemical investigations, imaging and/or surgery

C. Headache develops concomitantly with abrupt rise in blood pressure

D. Headache resolves or markedly improves within 1 hour of normalisation of blood pressure



Comments:

Paroxysmal headache occurs in 51-80% of patients with phaeochromocytoma. It is often severe, frontal or occipital and is generally described as either pulsating or steady in quality. An important feature of the headache is its short duration: <15 minutes in 50% and <1 hour in 70% of patients. Other features include apprehension and/or anxiety, often with a sense of impending death, tremor, visual disturbances, abdominal or chest pain, nausea, vomiting and occasionally paraesthesia. The face can blanch or flush during the attack.

The diagnosis is established by the demonstration of increased excretion of catecholamines or catecholamine metabolites, and can usually be secured by analysis of a single 24-hour urine sample collected when the patient is hypertensive or symptomatic.

When hypertensive encephalopathy is present, headache is coded as 10.3.3 Headache attributed to hypertensive encephalopathy. When the diagnosis of phaeochromocytoma has not yet been made, and hypertensive encephalopathy is not present, patients may meet the diagnostic criteria for 10.3.2 Headache attributed to hypertensive crisis without hypertensive encephalopathy.

10.3.2 Headache attributed to hypertensive crisis without hypertensive encephalopathy

Diagnostic criteria:

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

1. bilateral

2. pulsating quality

3. precipitated by physical activity

B. Hypertensive crisis defined as a paroxysmal rise in systolic (to >160 mm Hg) and/or diastolic (to >120 mm Hg) blood pressure but no clinical features of hypertensive encephalopathy

C. Headache develops during hypertensive crisis

D. Headache resolves within 1 hour after normalisation of blood pressure

E. Appropriate investigations have ruled out vasopressor toxins or medications as causative factors



Comment:

Paroxysmal hypertension may occur in association with failure of baroreceptor reflexes (after carotid endarterectomy or subsequent to irradiation of the neck) or in patients with enterochromaffin cell tumours.

10.3.3 Headache attributed to hypertensive encephalopathy

Diagnostic criteria:

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

1. diffuse pain

2. pulsating quality

3. aggravated by physical activity

B. Persistent blood pressure elevation to >160/100 mm Hg with at least two of the following:


  1. confusion

  2. reduced level of consciousness

  3. visual disturbances (other than those of typical migraine aura) including blindness

  4. seizures

C. Headache develops in close temporal relation to blood pressure elevation

D. Headache resolves within 3 months after effective treatment and control of hypertension

E. Other causes of the neurological symptoms have been excluded

Comments:

Hypertensive encephalopathy is thought to occur when compensatory cerebrovascular vasoconstriction can no longer prevent cerebral hyperperfusion as blood pressure rises. As normal cerebral autoregulation of blood flow is overwhelmed, endothelial permeability increases and cerebral oedema occurs. On MRI, this is often most prominent in the parieto-occipital white matter.

Although hypertensive encephalopathy in patients with chronic arterial hypertension is usually accompanied by a diastolic blood pressure of >120 mm Hg, and by grade 3 or 4 hypertensive retinopathy (Keith-Wagner classification), previously normotensive individuals may develop signs of encephalopathy with blood pressures as low as 160/100. Hypertensive retinopathy may not be present at the time of clinical presentation.

Any cause of hypertension, including phaeochromocytoma and ingestion of vasopressor toxins, can lead to hypertensive encephalopathy.

10.3.4 Headache attributed to pre-eclampsia

Diagnostic criteria:

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

1. bilateral

2. pulsating quality

3. aggravated by physical activity

B. Pregnancy or puerperium (up to 4 weeks post-partum), and pre-eclampsia defined by both of the following:

1. hypertension (>140/90 mm Hg) documented on two blood pressure readings at least 4 hours apart

2. urinary protein excretion >0.3 g per 24 hours

C. Headache develops during periods of high blood pressure

D. Headache resolves within 7 days after effective treatment of hypertension

E. Appropriate investigations have ruled out vasopressor toxins, medications or phaeochromocytoma as causative factors



Comment:

A placenta appears essential for the development of pre-eclampsia. Pre-eclampsia is a multi-system disorder with various forms. In addition to hypertension and proteinuria, tissue oedema, thrombocytopenia and abnormalities in liver function can occur. Pre-eclampsia appears to involve a strong maternal inflammatory response, with broad immunological systemic activity.

10.3.5 Headache attributed to eclampsia

Diagnostic criteria:

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

1. bilateral

2. pulsating quality

3. aggravated by physical activity

B. Pregnancy or puerperium (up to 4 weeks post-partum), and eclampsia defined by all of the following:

1. hypertension (>140/90 mm Hg) documented on two blood pressure readings at least 4 hours apart

2. urinary protein excretion >0.3 g per 24 hours

3. a seizure has occurred

C. Headache develops during periods of high blood pressure

D. Headache resolves within 7 days after effective treatment of hypertension

E. Appropriate investigations have ruled out vasopressor toxins, medications or phaeochromocytoma as causative factors

F. Stroke has been excluded



Comment:

Case reports indicate that eclampsia can occur in the puerperium as well as during pregnancy.

10.3.6 Headache attributed to acute pressor response to an exogenous agent

Coded elsewhere:

8.1.6 Cocaine-induced headache.
Diagnostic criteria:

  1. Headache, no typical characteristics known, fulfilling criteria C and D

  2. An appropriate agent or toxin has been administered or ingested and an acute rise in blood pressure has occurred

  3. Headache develops in close temporal relation to the acute rise in blood pressure

  4. Headache resolves within 24 hours after normalisation of blood pressure

  5. No other mechanism for the headache is apparent



Comments:

Apart from cocaine, agents that can produce acute elevations of blood pressure include sympathomimetics and amphetamines, and monoamine oxidase inhibitors when interactions with tyramine-containing foods occur.

There is insufficient evidence to set criteria for how large an elevation in blood pressure is required to produce headache, and this may vary from person to person. Criterion D is arbitrary, but included to increase the specificity of the diagnostic criteria.


10.4 Headache attributed to hypothyroidism

Diagnostic criteria:

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

1. bilateral

2. non-pulsatile

3. continuous


  1. Hypothyroidism is demonstrated by appropriate investigations

  2. Headache develops within 2 months after other symptoms of hypothyroidism become evident

  3. Headache resolves within 2 months after effective treatment of hypothyroidism



Comment:

It has been estimated that approximately 30% of patients with hypothyroidism suffer from headache. Its mechanism is unclear. There is a female preponderance and often a history of migraine in childhood. Headache attributed to hypothyroidism is not associated with nausea or vomiting.

10.5 Headache attributed to fasting

Coded elsewhere:

Hypoglycaemia-induced migraine is coded according to subtype under 1. Migraine, with hypoglycaemia considered as a precipitating factor.
Diagnostic criteria:

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

1. frontal location

2. diffuse pain

3. non-pulsating quality

4. mild or moderate intensity

B. The patient has fasted for >16 hours

C. Headache develops during fasting

D. Headache resolves within 72 hours after resumption of food intake



Comments:

Headache with fasting is significantly more common in individuals with a prior history of headache. In those individuals with a prior history of migraine, the headache may resemble 1.1 Migraine without aura.

The likelihood of headache developing as a result of a fast increases with the duration of the fast.

The headache associated with fasting does not appear to be related to duration of sleep, to caffeine withdrawal or to hypoglycaemia. Although headache may occur under conditions of hypoglycaemia-induced brain dysfunction, there is no conclusive evidence to support a causal association. Fasting headache can occur in the absence of hypoglycaemia, insulin-induced hypoglycaemia does not precipitate headache in migraine sufferers, and headache is not a complaint of patients presenting to the emergency department with symptomatic hypoglycaemia. Well-controlled studies are needed to demonstrate a causal relationship, if one exists.

10.6 Cardiac cephalalgia

Diagnostic criteria:

A. Headache, which may be severe, aggravated by exertion and accompanied by nausea and fulfilling criteria C and D

B. Acute myocardial ischaemia has occurred

C. Headache develops concomitantly with acute myocardial ischaemia

B. Headache resolves and does not recur after effective medical therapy for myocardial ischaemia or coronary revascularisation

Comment:

Diagnosis must include careful documentation of headache and simultaneous cardiac ischaemia during treadmill or nuclear cardiac stress testing. Failure to recognise and correctly diagnose 10.6 Cardiac cephalalgia can have grave consequences. Therefore, distinguishing this disorder from 1.1 Migraine without aura is of crucial importance, particularly since vasoconstrictor medications (eg, triptans, ergots) are indicated in the treatment of migraine but contraindicated in patients with ischaemic heart disease. Both disorders can produce severe head pain accompanied by nausea and both disorders can be triggered by exertion. Migraine-like headache may be triggered by angina treatment such as nitroglycerine.

10.7 Headache attributed to other disorder of homoeostasis

Diagnostic criteria:

A. Headache fulfilling criteria C and D

B. Evidence of a disorder of homoeostasis other than those described above

C. Headache develops within 2 months after onset of the disorder, and other evidence exists that the disorder can cause headache

D. Headache resolves within 3 months after relief from the disorder of homoeostasis



Bibliography

10.1.1 High-altitude headache; 10.1.3 Sleep apnoea headache

Aldrich MS, Chauncey JB. Are morning headaches part of obstructive sleep apnea syndrome? Arch Intern Med 1990;150:1265-1267.

Appenzeller O. Altitude Headache. Headache 1972;12:126-129.

Ginsberg MD. Carbon monoxide intoxication: clinical features, neuropathology and mechanisms of injury. J Toxicol Clin Toxicol 1985;23:281-288.

Heckerling PS, Leikiin JB, Maturen A, Perkins JT. Predictors of occult carbon monoxide poisoning in patients with headache and dizziness. Ann Intern Med 1987;107:174-176.

Jozefowicz, RF. Neurologic manifestations of pulmonary disease. Neurologic Clinics 1989;7: 605-16.

Lipton RB, Mazer C, Newman LC, Solomon S. Sumatriptan relieves migraine-like headaches associated with carbon monoxide exposure. Headache 1997;37:392-395.

Loh, NK; Dinner, DS; Foldvary, DO; Skobieranda, F; Yew, WW. Do patients with obstructive sleep apnea wake up with headaches? Arch Intern Med 1999;159:1765-1768.

Poceta JS, Dalessio DJ. Identification and treatment of sleep apnea in patients with chronic headache. Headache 1995;35:586-589.

Porcelli J, Gugelchuk G. A trek to the top: A review of acute mountain sickness. J Amer Osteopath Assoc 1995;95:718-720.

Silber E, Sonnenberg P, Collier DJ, Pollard A, Murdoch DR, Goadsby PJ. Clinical features of headache at altitude: a prospective study. Neurology 2003;60:1167-71.



10.1.2 Diving headache

Cheshire WP, Ott MC Jr. Headache in divers. Headache 2001;41:235-247.

Edmonds RC, Greene ER, Schoene RB, et al. Diving and subaquative medicine. 3rd Ed. Oxford: Butterworth-Heinemann;1992:404-406.

Sliwka U, Kransney JA, Simon SG, et al. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. Aviat Space Environ Med 1998;69:299-306.

10.2 Dialysis headache

Antoniazzi AL, Bigal ME, Bordini CA, Speciali JG. Headache associated with dialysis. The IHS criteria revisited. Cephalalgia 2003;23:146-9.

Jameson, MD, Wiegmann, TB. Principles, uses, and complications of hemodialysis. Medical Clinics of North America 1990;74:945-60.



10.3 Headache attributed to arterial hypertension

Dodick DW. Recurrent short-lasting headache associated with paroxysmal hypertension: a clonidine-responsive syndrome. Cephalalgia 2000;20:509-514.

Gus M, Fuchs FD, Pimentel M, Rosa D, Melo AG, Moreira LB. Behavior of ambulatory blood pressure surrounding episodes of headache in mildly hypertensive patients. Arch Intern Med 2001;161:252-255.

Kruszewski P, Bieniaszewski L, Neubauer J, Krupa-Wojciechowska B. Headache in patients with mild to moderate hypertension is generally not associated with simultaneous blood pressure elevation. J Hypertension 2000;18:437-444.

Lance JW, Hinterberger H. Symptom of pheochromocytoma with particular reference to headache, correlated with catecholamine production. Arch Neurol 1976;33:281-288.

Land SH, Donovan T. Pre-eclampsia and eclampsia headache: classification recommendation [letter]. Cephalalgia 1999;19:67-9.

Loh KC, Shlossberg AH, Abbott EC, Salisbury SR, Tan MH. Phaeochromocytoma: a ten-year survey. Quart J Med 1997;90:51-60.

Mannelli M, Ianni L, Cilotti A, Conti A. Pheochromocytoma in Italy: A multicentric retrospective study. Eur J Endocrinol 1999;141:619-624.

Thomas JE, Rooke ED, Kvale WF. The neurologists experience with pheochromocytoma. JAMA 1966;197:754-758.

Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000;356:411-417.

Walker JJ. Pre-eclampsia. Lancet 2000;56:1260-65.

Weiss NS. Relation of high blood pressure to headache, epistaxis, and selected other symptoms. The United States Health Examination Survey of Adults. N Engl J Med. 1972;287:631-3.

Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension 1996;27:144-147.



10.4 Headache attributed to hypothyroidism

Airaghi L, Catania A. Endocrine headache. In: Seminars in headache management. Neuroendocrinological aspects of headache, vol 4, number 4. B.C.Decker Inc, 1999: 1-15.

Amy JR. Tests of thyroid function in chronic headache patients. Headache 1987;27:351-3.

Arafah BM, Prunty D, Ybarra J, Hlavin ML, Selman WR. The dominant role of increased intrasellar pressure in the pathogenesis hypopituitarism, hyperprolactinemia, and headache in patients with pituitary adenomas. J Clin Endocrinol Metab 2000; 85: 1789-93.

Fenichel NM. Chronic headache due to masked hypothyroidism. Ann Intern Med 1948;29:456-60.

Moreau T. Headache in hypothyroidism. Prevalence and outcome under thyroid hormone therapy. Cephalalgia 1988; 18: 687-689.

10.5 Headache attributed to fasting

Dalton K. Food intake prior to migraine attacks. Study of 2,313 spontaneous attacks. Headache 1975;15:188-193.

Dexter JD, Roberts J, Byer JA. The five hour glucose tolerance test and effect of low sucrose diet in migraine. Headache 1978;18:91-94.

Malouf R, Brust JCM. Hypoglycemia: causes, neurological manifestations, and outcome. Ann Neurol 1985;17:421-430.

Mosek, AC, Korczyn, A.D. Yom Kippur Headache. Neurology 1995;45: 1953-1955.

Pearce J. Insulin induced hypoglycaemia in migraine. J Neurol Neurosurg Psychiat 1971;34:154-156.

Service FJ. Hypoglycemic disorders. In: Wyngaarden JB, Smith LH, Bennett JC, eds. Cecil’s textbook of medicine, 18th ed. Philadelphia: WB Saunders, 1992:1310-1317.



10.6 Cardiac cephalalgia

Blacky RA, Rittlemeyer JT, Wallace MR. Headache angina. Am J Cardiol 1987;60:730.

Bowen J, Oppenheimer G. Headache as a presentation of angina: reproduction of symptoms during angioplasty. Headache 1993;33:238-239.

Fleetcroft R, Maddocks JL. Headache due to ischaemic heart disease. J R Soc Med 1985;78:676.

Grace A, Horgan J, Breathnach K, Staunton H. Anginal headache and its basis. Cephalalgia 1997;17:195-6.

Lefkowitz D, Biller J. Bregmatic headache as a manifestation of myocardial ischemia. Arch Neurol 1982;39:130.

Lipton RB, Lowenkopf T, Bajwa ZH, Leckie RS, Ribeiro S, Newman LC, Greenberg MA. Cardiac cephalgia: a treatable form of exertional headache. Neurology 1997;49:813-816.

Vernay D, Deffond D, Fraysse P, Dordain G. Walk headache: an unusual manifestation of ischemic heart disease. Headache 1989;29:350-351.




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