Headache Robert S. Kunkel Many causes of headache have been described in the medical literature. In 1988, the International Headache Society published a long, detailed classification of headache, which has proved helpful for research purposes because it has led to more reproducible and reliable studies in the field of headache. This classification was updated and revised in 2004. For practical clinical purposes, however, all headaches can be classified as one of the primary headache syndromes or as a headache that is caused by or secondary to an underlying disease process or medical condition. Because primary headaches are the most common, this discussion focuses on the diagnosis and management of those syndromes. DEFINITION The primary headache syndromes are migraine, tension-type, and cluster headaches. Migraine and cluster headaches are episodic and recurring conditions. Tension-type headache is usually episodic but like migraine, it can become chronic, occurring daily or almost daily for more than 15 days a month. None of these primary headaches is associated with demonstrable organic disease or structural neurologic abnormality. Laboratory and imaging test results are generally normal. Should an abnormality be found on testing, by definition, it most likely is not the cause of the headache. Similarly, the physical and neurologic examinations are also usually normal, but any abnormalities found are not related to the primary headache. During the headache attack however, cluster and migraine patients might have some abnormal clinical findings, and many patients with tension-type headache have demonstrable tightness in the cervical muscles, with limitation of neck motion, scalp tenderness, or both. Secondary headaches are usually of recent onset and associated with abnormalities found on clinical examination. Laboratory testing or imaging studies confirm the diagnosis. Recognizing headaches related to an underlying condition or disease is critical not only because treatment of the underlying problem usually eliminates the headache but also because the condition causing the headache may be life-threatening. PREVALENCE Primary headaches account for more than 90% of all headache complaints, and of these, episodic tension-type headache is the most common. Almost everyone has had a headache of this type. Although chronic tension-type headache occurs in only slightly more than 2% of the population, it accounts for a large number of visits to the physician’s office and missed work days. Several epidemiologic studies conducted in various areas of the world indicate that the prevalence of migraine headache ranges from 12% to 18% of the population. Migraine is three times more common in female patients. The prevalence of cluster headache is less certain. This uncommon condition probably affects less than 0.5% of the population but is underdiagnosed and is often believed to be a sinus problem by both patients and physicians. Cluster headache affects men five to eight times more frequently than women. Because the three primary headache syndromes tend to begin in persons younger than 50 years, anyone older than 50 years with a recent onset of headache should have a thorough examination and testing to look for an underlying cause. PATHOPHYSIOLOGY The pathophysiology of migraine, cluster, and tension-type headaches is not well understood. Migraine and cluster headaches are believed to initially begin in the brain as a neurologic dysfunction, with subsequent involvement of the trigeminal nerve and cranial vessels. In cluster headache, most, but not all, sufferers have overactivity of the parasympathetic nervous system. Tension-type headache can be primarily a central neurologic disturbance similar to migraine or can occur as the result of increased cervical and pericranial muscle activity, such as caused by flexion-extension injury of the neck, poor posture, or anxiety with increased clenching or grinding of the teeth. Migraine is an inherited condition in which there appears to be an episodic instability of the neurovascular system (where serotonin and other neurotransmitters play roles). Available serotonin might be diminished or neuronal receptors for serotonin and other neuroactive substances might at times become less sensitive to these agents. Periodically, the nuclei of the trigeminal nerve appear to become hyperactive and excitable. Efferent impulses over branches of this nerve go to the innervated cranial vessels, causing the release of substances that promote perivascular inflammation and vascular dilation. Dysfunction of other areas of the brainstem and hypothalamus account for the other associated symptoms of migraine, such as nausea, photophobia, phonophobia, and osmophobia. As the migraine attack progresses, the inflamed perivascular structures irritate nerve endings of the trigeminal nerve and cause afferent stimuli back into the trigeminal neurons of the brain, causing them to become sensitized, and they then continue to fire off. This process is called central sensitization. As this cyclic process continues, the scalp becomes sore and tender to ordinary nonpainful touching. This result is called cutaneous allodynia. A few retrospective studies have suggested that closure of a patent foramen ovale is associated with a marked reduction of the frequency of migraine with aura. The foramen ovale does not close at birth in about 20% to 25% of persons. How this septal defect is associated with causing or triggering migraine with aura is unknown. Double-blind studies of catheter closure (or a sham procedure) of patent foramen ovales in migraineurs have been inconclusive. Cluster headache also is an episodic neuronal dysfunction but more likely involves areas in the hypothalamus rather than the brainstem. There is also a marked increase in blood flow through the internal carotid artery on the headache side during the attack of pain. SIGNS AND SYMPTOMS Migraine Most migraine patients do not have an aura; migraine with aura occurs in only 15% to 20% of sufferers. The aura is a well-defined visual or neurologic deficit lasting less than 1 hour and is followed by the headache within 1 hour. Most auras are visual, with photopsia (flashing lights) being most common. The aura is initially small, then enlarges or moves across the visual field. A typical migraine aura can occur without a headache. This phenomenon tends to occur later in life. Occasionally, a neurologic aura occurs, with a tingling or weakness that slowly spreads up or down an extremity. Many patients with migraine have prodromal symptoms for many hours or even a day or so before the onset of an attack. These prodromal symptoms are generally changes in mood or personality. Fatigue also is common, and occasionally hyperactivity occurs. The migraine attack lasts 6 to 72 hours. The pounding, throbbing pain of moderate to severe intensity is generally unilateral, but some patients experience bilateral pain. Pain caused by migraine worsens with physical activity. Photophobia and phonophobia are very common, and sensitivity to odors is a little less common. Migraine is a sick headache. Nausea occurs in most patients, and vomiting is very common. Dehydration can occur, which increases the pain and disability. Migraineurs want to be quiet, inactive, and in a darkened area during the attack. Approximately 60% of women experience their worst migraine attacks in conjunction with their menstrual period. Tension-Type Headache Tension-type headache is characterized by generalized pressure or a sensation of tightness in the head. The discomfort level is usually mild to moderate and does not worsen with activity. Although nausea and photophobia or phonophobia can occur, they generally are not prominent features. Tension-type headache is classified as episodic (<15 days a month) or chronic (>15 days a month). Some patients with tension-type headache exhibit evidence of increased muscle tension, with prominent scalp tenderness, muscle tenderness in the temporomandibular joint muscles, or tight, tender cervical and trapezius muscles. Poor posture is often evident, which can play a role in causing tension-type headache. If there is no evidence of increased pericranial or cervical muscle tightness (no tenderness or limitation of motion in the neck) found during clinical examination, the pain likely originates centrally or is due to psychological factors. Cluster Headache Cluster headache causes intense pain that is generally steady and boring behind one eye. The pain can spread to the temple, face, and even into the upper neck. It is so intense that most sufferers pace the floor or do vigorous exercises during the attack. The attacks are short (usually less than 3 hours in duration) and often last only 30 to 45 minutes. They occur from one to several times a day for a period of several weeks or months, then remit, leaving the patient pain free for several months or years, only to recur. During a cluster headache cycle, the attacks of pain often occur at the same time each day, most often waking the patient in the early morning hours. Eighty percent of cluster sufferers experience unilateral tearing, with conjunctival injection and ipsilateral nasal congestion. These symptoms clear as the attack leaves. Alcohol brings on an attack within a few minutes in a patient who is in a cluster headache cycle, but it does not induce an attack when the patient is in remission. Chronic Daily Headache Daily headache can occur as a chronic tension-type headache, but it is often a combination of tension-type and migraine (the type seen most often in headache clinics). This type of combination headache is not listed in the official classification, so one should diagnose both chronic tension-type headache and migraine in these patients. Most often, this type of combination or mixed headache develops in a person who initially had typical episodic migraine but in whom, over several years, a chronic daily or almost-daily headache develops. Many times, this daily headache seems to occur because of the frequent use of analgesics, especially opiate compounds and those combined with caffeine or butalbital. A daily or near-daily migraine headache can occur from the frequent use of ergotamine tartrate or any of the triptan drugs. This headache pattern has been called rebound headache or medication overuse headache. Secondary Headache Secondary headache may be caused by many different diseases. However, neurologic symptoms and signs are almost always present before there is significant headache in patients who have a mass lesion in the brain. Temporal arteritis generally occurs in persons older than 50 years and may be associated with any type of headache. The pain of temporal arteritis is typically not throbbing and, although it is usually situated in the temples, can be nonlocalized. Fatigue and a low-grade fever are often present. The erythrocyte sedimentation rate is high, usually greater than 60 mm/hour. Diagnosis is confirmed by a temporal artery biopsy, which shows giant cell inflammation. Treatment should begin with 60 to 80 mg of prednisone per day as soon as the diagnosis is suspected, even before the confirmation by biopsy. One study suggested that methotrexate may be effective in allowing treatment with a lower dose of steroids, whereas another study did not show any benefit of adding this drug. If not treated, 20% to 30% of patients with this disease develop permanent partial or complete visual loss in the affected eye. Therefore, prompt treatment is essential. Aneurysms do not cause chronic recurring headache unless they compress a cranial nerve. They manifest with a severe pain at the time of rupture. Occasionally, an arteriovenous malformation mimics migraine, particularly if it is located in the occipital lobe, but these lesions are more apt to cause seizures or to bleed. Headaches with a postural component need to be evaluated to exclude a lesion in the posterior fossa or a condition with low CSF pressure. Pericranial inflammation such as a sinus infection, an ear infection, or dental disease should be evident on examination and is usually of a more recent, acute onset. Sleep apnea may be a factor in waking headaches. Systemic conditions such as endocrine disorders, anemia, sepsis, and hypertension can be associated with a non localized headache, but more often such conditions exacerbate an underlying migraine or tension-type headache. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window)Like this:Like Loading... Related Related posts: Anaphylaxis Chronic Nonmalignant Pain Polymyalgia Rheumatica and Giant Cell Arteritis Systemic Scleroderma Stay updated, free articles. 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Headache Robert S. Kunkel Many causes of headache have been described in the medical literature. In 1988, the International Headache Society published a long, detailed classification of headache, which has proved helpful for research purposes because it has led to more reproducible and reliable studies in the field of headache. This classification was updated and revised in 2004. For practical clinical purposes, however, all headaches can be classified as one of the primary headache syndromes or as a headache that is caused by or secondary to an underlying disease process or medical condition. Because primary headaches are the most common, this discussion focuses on the diagnosis and management of those syndromes. DEFINITION The primary headache syndromes are migraine, tension-type, and cluster headaches. Migraine and cluster headaches are episodic and recurring conditions. Tension-type headache is usually episodic but like migraine, it can become chronic, occurring daily or almost daily for more than 15 days a month. None of these primary headaches is associated with demonstrable organic disease or structural neurologic abnormality. Laboratory and imaging test results are generally normal. Should an abnormality be found on testing, by definition, it most likely is not the cause of the headache. Similarly, the physical and neurologic examinations are also usually normal, but any abnormalities found are not related to the primary headache. During the headache attack however, cluster and migraine patients might have some abnormal clinical findings, and many patients with tension-type headache have demonstrable tightness in the cervical muscles, with limitation of neck motion, scalp tenderness, or both. Secondary headaches are usually of recent onset and associated with abnormalities found on clinical examination. Laboratory testing or imaging studies confirm the diagnosis. Recognizing headaches related to an underlying condition or disease is critical not only because treatment of the underlying problem usually eliminates the headache but also because the condition causing the headache may be life-threatening. PREVALENCE Primary headaches account for more than 90% of all headache complaints, and of these, episodic tension-type headache is the most common. Almost everyone has had a headache of this type. Although chronic tension-type headache occurs in only slightly more than 2% of the population, it accounts for a large number of visits to the physician’s office and missed work days. Several epidemiologic studies conducted in various areas of the world indicate that the prevalence of migraine headache ranges from 12% to 18% of the population. Migraine is three times more common in female patients. The prevalence of cluster headache is less certain. This uncommon condition probably affects less than 0.5% of the population but is underdiagnosed and is often believed to be a sinus problem by both patients and physicians. Cluster headache affects men five to eight times more frequently than women. Because the three primary headache syndromes tend to begin in persons younger than 50 years, anyone older than 50 years with a recent onset of headache should have a thorough examination and testing to look for an underlying cause. PATHOPHYSIOLOGY The pathophysiology of migraine, cluster, and tension-type headaches is not well understood. Migraine and cluster headaches are believed to initially begin in the brain as a neurologic dysfunction, with subsequent involvement of the trigeminal nerve and cranial vessels. In cluster headache, most, but not all, sufferers have overactivity of the parasympathetic nervous system. Tension-type headache can be primarily a central neurologic disturbance similar to migraine or can occur as the result of increased cervical and pericranial muscle activity, such as caused by flexion-extension injury of the neck, poor posture, or anxiety with increased clenching or grinding of the teeth. Migraine is an inherited condition in which there appears to be an episodic instability of the neurovascular system (where serotonin and other neurotransmitters play roles). Available serotonin might be diminished or neuronal receptors for serotonin and other neuroactive substances might at times become less sensitive to these agents. Periodically, the nuclei of the trigeminal nerve appear to become hyperactive and excitable. Efferent impulses over branches of this nerve go to the innervated cranial vessels, causing the release of substances that promote perivascular inflammation and vascular dilation. Dysfunction of other areas of the brainstem and hypothalamus account for the other associated symptoms of migraine, such as nausea, photophobia, phonophobia, and osmophobia. As the migraine attack progresses, the inflamed perivascular structures irritate nerve endings of the trigeminal nerve and cause afferent stimuli back into the trigeminal neurons of the brain, causing them to become sensitized, and they then continue to fire off. This process is called central sensitization. As this cyclic process continues, the scalp becomes sore and tender to ordinary nonpainful touching. This result is called cutaneous allodynia. A few retrospective studies have suggested that closure of a patent foramen ovale is associated with a marked reduction of the frequency of migraine with aura. The foramen ovale does not close at birth in about 20% to 25% of persons. How this septal defect is associated with causing or triggering migraine with aura is unknown. Double-blind studies of catheter closure (or a sham procedure) of patent foramen ovales in migraineurs have been inconclusive. Cluster headache also is an episodic neuronal dysfunction but more likely involves areas in the hypothalamus rather than the brainstem. There is also a marked increase in blood flow through the internal carotid artery on the headache side during the attack of pain. SIGNS AND SYMPTOMS Migraine Most migraine patients do not have an aura; migraine with aura occurs in only 15% to 20% of sufferers. The aura is a well-defined visual or neurologic deficit lasting less than 1 hour and is followed by the headache within 1 hour. Most auras are visual, with photopsia (flashing lights) being most common. The aura is initially small, then enlarges or moves across the visual field. A typical migraine aura can occur without a headache. This phenomenon tends to occur later in life. Occasionally, a neurologic aura occurs, with a tingling or weakness that slowly spreads up or down an extremity. Many patients with migraine have prodromal symptoms for many hours or even a day or so before the onset of an attack. These prodromal symptoms are generally changes in mood or personality. Fatigue also is common, and occasionally hyperactivity occurs. The migraine attack lasts 6 to 72 hours. The pounding, throbbing pain of moderate to severe intensity is generally unilateral, but some patients experience bilateral pain. Pain caused by migraine worsens with physical activity. Photophobia and phonophobia are very common, and sensitivity to odors is a little less common. Migraine is a sick headache. Nausea occurs in most patients, and vomiting is very common. Dehydration can occur, which increases the pain and disability. Migraineurs want to be quiet, inactive, and in a darkened area during the attack. Approximately 60% of women experience their worst migraine attacks in conjunction with their menstrual period. Tension-Type Headache Tension-type headache is characterized by generalized pressure or a sensation of tightness in the head. The discomfort level is usually mild to moderate and does not worsen with activity. Although nausea and photophobia or phonophobia can occur, they generally are not prominent features. Tension-type headache is classified as episodic (<15 days a month) or chronic (>15 days a month). Some patients with tension-type headache exhibit evidence of increased muscle tension, with prominent scalp tenderness, muscle tenderness in the temporomandibular joint muscles, or tight, tender cervical and trapezius muscles. Poor posture is often evident, which can play a role in causing tension-type headache. If there is no evidence of increased pericranial or cervical muscle tightness (no tenderness or limitation of motion in the neck) found during clinical examination, the pain likely originates centrally or is due to psychological factors. Cluster Headache Cluster headache causes intense pain that is generally steady and boring behind one eye. The pain can spread to the temple, face, and even into the upper neck. It is so intense that most sufferers pace the floor or do vigorous exercises during the attack. The attacks are short (usually less than 3 hours in duration) and often last only 30 to 45 minutes. They occur from one to several times a day for a period of several weeks or months, then remit, leaving the patient pain free for several months or years, only to recur. During a cluster headache cycle, the attacks of pain often occur at the same time each day, most often waking the patient in the early morning hours. Eighty percent of cluster sufferers experience unilateral tearing, with conjunctival injection and ipsilateral nasal congestion. These symptoms clear as the attack leaves. Alcohol brings on an attack within a few minutes in a patient who is in a cluster headache cycle, but it does not induce an attack when the patient is in remission. Chronic Daily Headache Daily headache can occur as a chronic tension-type headache, but it is often a combination of tension-type and migraine (the type seen most often in headache clinics). This type of combination headache is not listed in the official classification, so one should diagnose both chronic tension-type headache and migraine in these patients. Most often, this type of combination or mixed headache develops in a person who initially had typical episodic migraine but in whom, over several years, a chronic daily or almost-daily headache develops. Many times, this daily headache seems to occur because of the frequent use of analgesics, especially opiate compounds and those combined with caffeine or butalbital. A daily or near-daily migraine headache can occur from the frequent use of ergotamine tartrate or any of the triptan drugs. This headache pattern has been called rebound headache or medication overuse headache. Secondary Headache Secondary headache may be caused by many different diseases. However, neurologic symptoms and signs are almost always present before there is significant headache in patients who have a mass lesion in the brain. Temporal arteritis generally occurs in persons older than 50 years and may be associated with any type of headache. The pain of temporal arteritis is typically not throbbing and, although it is usually situated in the temples, can be nonlocalized. Fatigue and a low-grade fever are often present. The erythrocyte sedimentation rate is high, usually greater than 60 mm/hour. Diagnosis is confirmed by a temporal artery biopsy, which shows giant cell inflammation. Treatment should begin with 60 to 80 mg of prednisone per day as soon as the diagnosis is suspected, even before the confirmation by biopsy. One study suggested that methotrexate may be effective in allowing treatment with a lower dose of steroids, whereas another study did not show any benefit of adding this drug. If not treated, 20% to 30% of patients with this disease develop permanent partial or complete visual loss in the affected eye. Therefore, prompt treatment is essential. Aneurysms do not cause chronic recurring headache unless they compress a cranial nerve. They manifest with a severe pain at the time of rupture. Occasionally, an arteriovenous malformation mimics migraine, particularly if it is located in the occipital lobe, but these lesions are more apt to cause seizures or to bleed. Headaches with a postural component need to be evaluated to exclude a lesion in the posterior fossa or a condition with low CSF pressure. Pericranial inflammation such as a sinus infection, an ear infection, or dental disease should be evident on examination and is usually of a more recent, acute onset. Sleep apnea may be a factor in waking headaches. Systemic conditions such as endocrine disorders, anemia, sepsis, and hypertension can be associated with a non localized headache, but more often such conditions exacerbate an underlying migraine or tension-type headache. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window)Like this:Like Loading... Related Related posts: Anaphylaxis Chronic Nonmalignant Pain Polymyalgia Rheumatica and Giant Cell Arteritis Systemic Scleroderma Stay updated, free articles. 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