eMedicine Specialties > Neurology > Headache and Pain

Chronic Paroxysmal Hemicrania

Author: Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Coauthor(s): Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University
Contributor Information and Disclosures

Updated: Sep 3, 2009

Introduction

Background

Chronic paroxysmal hemicrania (CPH) is also known as Sjaastad syndrome. It was first described in 1974 by Sjaastad and Dale.1 In 1976, the term CPH was proposed by Sjaastad on the basis of the first 2 patients, who had daily (ie, chronic), solitary, limited attacks (ie, paroxysmal) of unilateral headache that did not shift sides (ie, hemicrania).2 CPH, which has been included in the International Headache Society (IHS) classification system since 1988, is much less common than cluster headache (CH).

The short-lasting primary headache syndromes may be divided into (1) headaches with autonomic activation and (2) headaches without autonomic activation. Headaches with autonomic activation include chronic and episodic paroxysmal hemicrania, CH, and short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT syndrome).

Pathophysiology

The mechanisms responsible for the pain in CPH remain unknown. Discussion of important features, such as unilateral intense headache, autonomic abnormalities, and effectiveness of indomethacin, may help in understanding the pathogenesis.3

The release of both trigeminal and parasympathetic neuropeptides during headache has been described.4 Activation of the ipsilateral trigeminovascular system may explain sudden unilateral headache and may lead to miosis, increased intraocular pressure (IOP), and other autonomic abnormalities.

Increased sweating and decreased salivation during attacks and inhibition of increased IOP by an alpha-blocking agent or stellate ganglion blockade suggest sympathetic involvement.

Increased tearing, nasal secretion, and miosis may be due to parasympathetic stimulation. Trigeminoparasympathetic activation during CPH attack has been suggested; increases in vasoactive intestinal peptide (ie, parasympathetic peptide) level have been reported. Levels of calcitonin gene-related peptide also are reported to be high during CPH attacks.

Pain and pressure threshold, nociceptive flexion reflex, and blink and corneal reflexes have been studied in patients with CPH. The corneal reflex thresholds have been found to be decreased bilaterally during CPH attacks. Increases in corneal temperature on the symptomatic side also have been reported; this finding may be due to increased ocular blood flow.

The effectiveness of indomethacin in CPH may be due partly to reduction of intracranial blood flow (via a nonprostaglandin mechanism) and partly to its anti-inflammatory effects.

These findings may indicate a primary central mechanism and a secondary involvement of peripheral factors, affecting both the sympathetic and parasympathetic systems.

Recent studies suggest crucial role of hypothalamus. Functional neuroimaging studies have demonstrated activation of hypothalamus in cases of trigeminal autonomic cephalgias.5,6

Frequency

United States

CPH is a rare syndrome, but the number of diagnosed cases is increasing. The prevalence of CPH is not known, but the relative frequency compared with CH is reported to be approximately 1-3%.

International

Many cases of CPH have been described throughout the world, in different races and different countries, including Australia, Czech Republic, Slovakia, Denmark, Italy, France, Mexico, Canada, Sweden, Germany, Poland, India, Spain, Brazil, South Africa, Norway, New Zealand, the United Kingdom, and the United States.

Mortality/Morbidity

Mortality rate and morbidity of CPH have not been reported, although the therapy of choice, indomethacin, is known to be associated with the risk of bleeding.

Race

CPH is not known to occur preferentially in any race. CPH has been described in Caucasians and black South Africans.

Sex

In the past, because of female preponderance, CPH was considered a disease of women. However, CPH has been reported in increasing numbers of men. A study conducted in 1979 reported a female-to-male ratio of 7:1, but a review of 84 patients in 1989 reported a female-to-male ratio of 2.3:1.

Age

CPH can occur at any age; mean age of onset is 34 years.7 The youngest patient described in the literature was aged 6 years and the oldest was aged 81 years.8,9 In one report, CPH beginning at age 3 years was described; however, it may have been related to ipsilateral occipital hemorrhagic infarction.10

Clinical

History

The pain is unilateral, always affects the same side, and is generally oculofrontotemporal in location. The literature does contain reports of a few unusual cases, for example, patients with bilateral symptoms and possible shift in the side of the headache when the CPH progresses from the nonchronic to the chronic stage.

  • The pain is usually most severe in the oculotemporal area, the forehead, and above or behind the ear. Occasionally, pain can radiate and involve the ipsilateral shoulder, arm, and neck.
  • Headache can appear at any time in patients with CPH, in contrast to CH in which the headache usually occurs at night.
  • During severe attacks, excruciating pain with throbbing, boring, pulsating, or clawlike character has been described. In contrast to patients with CH, patients with CPH usually sit quietly or may curl up in bed between attacks.
  • The attack frequency usually is 10-20 attacks per day and may range from 2-40 attacks per day. Attacks usually last 2-25 minutes, but they may last as long as 60 minutes. In one prospective study, mean attack duration was 13 minutes (range 3-46 min). In a retrospective study, the mean duration of attacks was 21 minutes (range 2-120 min).
  • CPH can be triggered by various stimuli, including neck movement, external pressure to neck, or other factors.
  • CPH attacks are accompanied by autonomic symptoms, mostly on the same side as the pain, such as red eyes, tearing, nasal congestion, and sometimes rhinorrhea. Occasionally, photophobia may be present, but gastrointestinal symptoms are very rare.
  • Recognizing the various stages and different patterns of CPH is important. For example, during severe frequent attacks, patients may describe a constant headache or persisting tenderness on the symptomatic side.
  • IHS diagnostic criteria for CPH include the following (slightly modified from the Headache Classification Committee, 198811 ):
    • At least 50 attacks fulfilling the criteria mentioned below in 2-5.
    • Attacks of severe unilateral orbital, supraorbital, and/or temporal pain always on the same side lasting 2-45 minutes
    • Attack frequency more than 5 per day for more than half of the time (periods with lower frequency may occur)
    • Pain associated with at least one of the following signs/symptoms on the symptomatic side:
      • Conjunctival injection
      • Lacrimation
      • Nasal congestion
      • Rhinorrhea
      • Ptosis
      • Eyelid edema
    • Absolute effectiveness of indomethacin (150 mg/d or less)
    • At least one of the following:
      • History, physical, and neurologic examination findings do not suggest any of several disorders that include organic headaches, headaches associated with drug withdrawal, metabolic disorders, and other conditions.
      • History and/or physical and/or neurologic examination findings do suggest such a disorder, but it is ruled out by appropriate investigations.
      • Such a disorder is present, but CPH does not occur for the first time in close relation to the disorder.
  • CPH may be present in nonchronic or chronic form, which is 4 times more common.
    • Nonchronic attacks are similar to chronic attacks but may be less severe and less frequent.
    • The term pre-CPH stage or prechronic was preferred initially on the basis of the assumption that all patients would develop chronic symptoms. However, approximately 20% of patients appear to remain in the nonchronic stage for long periods.
    • Before development of chronic symptoms, many patients (42%) pass through a nonchronic stage with attacks separated by intervals of complete remission.
    • Dividing CPH into unremitting and remitting forms may be appropriate. The unremitting form is the chronic form, which either is unremitting from the onset or evolved from the remitting form.

Physical

  • The pain is severe, and attacks are associated with autonomic features, such as lacrimation (62%), conjunctival injection (36%), ipsilateral nasal congestion (42%), rhinorrhea (36%), and eyelid edema (33%).
    • Lacrimation may occur bilaterally but is always more marked on the symptomatic side.
    • Occasionally, mild ipsilateral miosis may be observed during attacks.
  • Patients with CPH who had dissociation in pain and autonomic features also have been described.
  • No definite evidence points to a Hornerlike syndrome, such as that described in CH, but mild miosis and eyelid edema that may mimic ptosis may be observed.
  • Forehead sweating may increase on the ipsilateral side, and patients with generalized sweating have been reported.
  • The coexistence of CPH and trigeminal neuralgia is called CPH-tic syndrome; many cases of this syndrome have been reported.
  • Simultaneous occurrence of ipsilateral CH and migraine headache in patients with CPH also has been reported.
  • Perform a careful physical examination to evaluate pathological secondary headache.

Causes

No definite cause is known.

  • The past medical history in patients with CPH is usually unremarkable. History of head or neck trauma is reported in about 20% of cases, but these findings are similar to CH or migraine.
  • Occasionally, attacks may be provoked mechanically by bending or rotating the head and by applying external pressure against the transverse processes of C4-C5, C2 root, or the greater occipital nerve.
  • No familial disposition is known for CPH; families of affected individuals do not have higher incidences of CH or migraine than the general population.

More on Chronic Paroxysmal Hemicrania

Overview: Chronic Paroxysmal Hemicrania
Differential Diagnoses & Workup: Chronic Paroxysmal Hemicrania
Treatment & Medication: Chronic Paroxysmal Hemicrania
Follow-up: Chronic Paroxysmal Hemicrania
References
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Further Reading

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Keywords

Sjaastad syndrome, IHS code: 3.2 chronic paroxysmal hemicrania, ICD-9 code: 346.9 hemicrania, CPH, headache, indomethacin, chronic paroxysmal hemicrania, unilateral headache, headaches with autonomic activation, headaches without autonomic activation, chronic and episodic paroxysmal hemicrania, short-lasting unilateral neuralgiform headache with conjunctival injection and tearing, SUNCT syndrome

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Contributor Information and Disclosures

Author

Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and American Society of Regional Anesthesia and Pain Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University
Jashvant Patel, MD is a member of the following medical societies: Alberta Medical Association, American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Society of Regional Anesthesia and Pain Medicine, and Medical Society of the State of New York
Disclosure: Nothing to disclose.

Medical Editor

Jorge E Mendizabal, MD, Consulting Staff, Corpus Christi Neurology
Jorge E Mendizabal, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, National Stroke Association, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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Disclosure: eMedicine Salary Employment

Managing Editor

James H Halsey, MD, Professor, Department of Neurology, University of Alabama Medical Center
James H Halsey, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neuroimaging, Medical Association of the State of Alabama, New York Academy of Sciences, Pan American Medical Association, Sigma Xi, Society for Neuroscience, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Howard A Crystal, MD, Professor, Departments of Neurology and Pathology, State University of New York Downstate; Consulting Staff, Department of Neurology, University Hospital and Kings County Hospital Center
Howard A Crystal, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association
Disclosure: Medivations Honoraria Consulting

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