TAKING A HEADACHE HISTORY

Pertinent History

1.  Establish an anchor in time: when did the headaches first appear and have they changed since that time? Is there a history of head injury?

2.  Burden of headache: number of headache days/month as well as functionally incapacitating headache days. Mild headaches might otherwise not be reported, but may signal a more chronic state. Note that asking how many headaches are experienced can be deceptive as attacks can last seconds to days.

3.  If an acute headache, what was the activity at the time the headache occurred?

Triggers of attacks include sleep (too little or too much), exercise, Valsalva, cough, sex, menstruation, ovulation, stress and relaxation following stress, foods, and dehydration. These triggers in particular can trigger migraine, although headaches triggered by Valsalva should prompt an evaluation for an intracranial lesion. Cluster attacks are often triggered by sleep and alcohol.

4.  Individual attacks: first symptom, rate of progression, location of pain (in the beginning of the attack and as it progresses). Some attacks reach full intensity in an instant, and others over hours to days.

5.  Are there prodromal symptoms hours to days before the attack? These are typical of migraines.

6.  Symptoms associated with headache: photophobia or phonophobia, nausea, vomiting (when do they occur with the attacks; early nausea can alter the route of administration of an acute drug to an injection or nasal spray).

7.  Are there focal symptoms accompanying the headache? Migraine auras can involve vision, sensory, or motor symptoms and need to be distinguished from stroke or transient ischemic attack.

8.  Were the attacks positional in their onset? Low-pressure headaches generally cause orthostatic headaches at the beginning, but over time this feature may be lost. In low-pressure headache, patients are best as they awaken and the pain worsens as they arise and throughout the day with increased activity.

9.  What is the severity of an attack, how is it limiting function? It is most useful to describe the behavior and limitations in functioning that are experienced with an attack. Simply using the 1 to 10 scale often does not yield reliable information.

10.  What is the person’s behavior during an attack (bed rest, quiet, pacing, lights off)? Migraines, being worse with activity and associated with light and sound sensitivity, cause the sufferer to often seek bed rest in a quiet and dark room. Cluster headache sufferers typically rock and pace, unable to be still.

11.  What is the duration of an attack with and without treatment? Migraines typically last 4 hours to 3 days. Cluster headaches typically last 1 to 2 hours.

12.  Is there a postdrome? This is a period of time, ranging from hours to days following an attack manifested by fatigue, poor mood, and difficulty in concentration.

13.  What is currently being used to prevent attacks and to treat individual attacks? What dose, how many, for how long? How are they used? Are the acute agents used early in the attack, which increases efficacy and reduces the rate of recurrence? Are they being overused, which can lead to an increase in headaches over time? Are preventive agents being used in an adequate dose and for an adequate period of time in order to determine their efficacy? Early on in the use of preventive agents, the side effects are higher and the efficacy lower, which can lead to discontinuation.

14.  What treatments have been used in the past? What were the doses of the medications used and how long were they used? Preventive agents often take many weeks to become effective and at an adequate dose so that brief trials do not prove that the agent is ineffective.

15.  What laboratory and imaging studies have been performed in the past? Be certain to personally review these results.

16.  Is there a family history of headaches? How were their headaches described and what diagnosis was given? Be aware that the assigned diagnosis may be inaccurate.

The Primary Headaches

Primary headache disorders most commonly have onset in childhood and early adult years. Onset in the very young or very old may be worrisome. Migraine prevalence increases steadily until age 40, after which it declines, with peak prevalence from 25 to 55 years of age. Headaches are common in young children. For instance, epidemiologic studies show that by age 7, 37% to 51.5% of children report headache. In the 3-to-5-year-olds, headaches are more prevalent in boys; however, as puberty approaches the incidence and prevalence of headache increases in girls. Age, additionally, may play a role in the manifestation of a primary headache disorder. In particular, children may exhibit “migraine equivalents” such as cyclic vomiting syndrome or benign paroxysmal vertigo, which may presage the development of migraine later in life.

Migraine

Although tension-type headache is the most common variety of headache, a patient presenting to a primary care physician with episodic headache most likely has migraine. Migraine is the phenotypic expression of a large variety of conditions, often with a genetic predisposition. Many adults with migraine also have a history of carsickness, vertiginous spells, and abdominal pain in childhood.

Most attacks, if carefully investigated, begin with a prodrome, which can precede the pain by a day or more. Common prodromes include cold hands and feet, yawning, food cravings, and frequent urination. Recognizing a prodrome may lead to successful preemptive treatment.

Migraine without aura is the most common form comprising about 80% of migraines whereas migraine with aura comprised about 20%.

Migraine without Aura (ICHD-3 Criteria)

A.  At least five attacks fulfilling criteria B–D

B.  Headache attacks lasting 4 to 72 hours (untreated or unsuccessfully treated)

C.  Headache has at least two of the following four characteristics:

1.  unilateral location

2.  pulsating quality

3.  moderate or severe pain intensity

4.  aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)

D.  During headache at least one of the following:

1.  nausea and/or vomiting

2.  photophobia and phonophobia

E.  Not better accounted for by another ICHD-3 diagnosis.

Migraine with Aura (ICHD-3 Criteria)

A.  At least two attacks fulfilling criteria B and C

B.  One or more of the following fully reversible aura symptoms:

1.  visual

2.  sensory

3.  speech and/or language

4.  motor

5.  brainstem

6.  retinal

C.  At least two of the following four characteristics:

1.  At least one aura symptom spreads gradually over 5 minutes, and/or two or more symptoms occur in succession.

2.  Each individual aura symptom lasts 5 to 60 minutes.

3.  At least one aura symptom is unilateral.

4.  The aura is accompanied, or followed within 60 minutes, by headache.

D.  Not better accounted for by another ICHD-3 diagnosis and transient ischemic attack has been excluded.

In practice, the diagnosis of migraine is made more liberally as migraineurs have attacks, which vary in location, quality, and duration but are considered to be part of the “spectrum of migraine.”

How a migraine presents affects its treatment. Preventive medications are recommended when 6 or more days/month are associated with headache. A realistic expectation is to reduce the attacks by 50% and to render attacks more amenable to treatment. It remains to be determined if aggressive preventive treatment reduces the likelihood of progression.

Individual attacks need to be managed even with successful preventive treatments, as preventive agents are rarely completely successful. Most attacks can be managed with oral medications, but if attacks reach full intensity rapidly or when attacks are associated with early nausea, parenteral medications may be necessary. Auras, should they occur, generally precede the headache, but may begin during the headache period and more than one aura can occur in succession. The headache may develop gradually over several minutes to hours, but at times can reach full intensity rapidly. Attacks tend to last 4 to 72 hours, although there is a great deal of variation. Sleep may terminate attacks, particularly in children. Following the resolution of headache, there can be a postdromal period of several days during which there can be mild but persistent pain and fatigue.

Tension-type Headaches

Although tension-type headaches are the most common headache, by definition they are not disabling, and individuals self-treat and therefore rarely seek medical attention. However, headaches of similar description can occur in an individual as part of the “spectrum of migraine” and are considered to be a variation of migraine. When an individual presents with tension-type headache, it is important to query whether they also suffer other types of headaches, which may uncover the underlying migraine history. Additionally, headaches that are triggered by “tension” are not necessarily tension-type headaches. The usual symptoms are a dull, nonpulsatile headache, often described as constricting. Pericranial tenderness may be present. There is no significant nausea and no vomiting; photophobia or phonophobia, if any, is minimal; and, unlike migraine, these are not worsened with activity.

Treatment of tension-type headaches usually involves the periodic use of simple analgesics. The use of opioids is inappropriate, and the use of butalbital-containing analgesics should be sparing, if at all. Chronic tension-type headache is generally treated with amitriptyline. Small studies suggest that mirtazapine or venlafaxine may be of value. There are no significant studies supporting the use of selective serotonin reuptake inhibitors or muscle relaxants, although anecdotally, tizanidine may be helpful. Onabotulinumtoxin has not shown to be helpful. Electromyography biofeedback, cognitive behavioral therapy, and relaxation therapy may be effective.

Cluster Headaches and Other Trigeminal Autonomic Cephalalgias

A.  Cluster headache.

One of the primary headache syndromes, characterized by periods of a few weeks to a few months when one or more headaches are experienced daily, lasting 30 to 120 minutes. A great deal of variation exists. The headaches reach full intensity over minutes, but are not apoplectic in onset. The pain is always unilateral; commonly retro-orbital or temporal, but maxillary pain can exist. The quality is boring and aching often with superimposed sharp pains. Nausea, if present, is generally not prominent. The pain is associated with ipsilateral lacrimation and rhinorrhea. It is often confused with migraine although the quality, associated symptoms, and temporal profile differ. Unlike migraineurs who prefer to be still, cluster attacks are associated with relentless hyperactivity.

1.  Treatment. The treatment is only during the active cluster period and there is no evidence that continuing the treatment beyond this prevents the next cluster period.

During this time, both preventive and acute medications are used. Preventive agents include verapamil, which often requires high doses, and may be combined with topiramate or divalproex. Given the severity of cluster attacks and the fact that there may be a considerable latency before preventive agents become effective, a bridge using prednisone is often advised.

Preventive agents are rarely fully effective and acute treatments need to be offered. Sumatriptan subcutaneous injections are likely to be the most effective. Unlike in migraine, 2 or 3 mg subcutaneously may suffice, and since the maximum daily dose is 12 mg, there is an opportunity to treat several attacks with these lower doses. Triptan tablets and nasal sprays are unlikely to be adequate. High-flow oxygen may also be effective; using 10 to 12 L daily with a non-rebreathing mask. This needs to be initiated early in an attack and should be continued for several minutes after the attack appears to be terminated.

Hemicrania Continua

This is a continuous, although variable in intensity, unilateral headache. Exacerbations recur throughout the day associated with ipsilateral lacrimation and rhinorrhea. A dramatic response to indomethacin is seen, which is both a treatment and a diagnostic test.

Episodic and Chronic Paroxysmal Hemicrania

These attacks are very similar to attacks of cluster headaches, except they are brief, usually a few minutes, and recurrent with multiple attacks daily. There is a less common episodic form, with remissions. When pain is severe it is accompanied by ipsilateral lacrimation and rhinorrhea. Unlike cluster, more females suffer from this condition. A dramatic and persistent response to indomethacin is characteristic although some respond to topiramate, which should be attempted given the toxicity of indomethacin.

Secondary Headaches

Headaches Due to Increased Intracranial Pressure

Headaches due to increased intracranial pressure (ICP) include mass lesions in the brain, such as tumors and abscesses.

A.  Brain tumors.

Although these have often been characterized as early morning headaches that awaken one from sleep and improve as the day advances, this is not the usual profile. In most cases of secondary headache, the headache is more prominent in those with a preexisting history of a primary headache, such as migraine. The headache experienced is then likely amplification of the preexisting headache type, often associated with more nausea, more frequent, and of longer duration. Therefore, a significant change in a preexisting headache type rather than simply a new headache should prompt a reevaluation. Only 1% of patients with brain tumors have headache as the sole manifestation. Headaches with brain tumors are commonly worse with Valsalva maneuver or exertion, which can also occur as a migraine manifestation. They may awaken the person from sleep, but this is common with cluster headache and migraine as well. Brain abscess may present as a brain tumor and fever is seen with only half of the cases.

B.  Subdural hematoma, being a mass lesion, has the same features as the headache associated with brain tumors. As they are extra-axial, the lack of focality on examination and a change in sensorium is common. A history of head trauma is not invariable, particularly in the elderly or those with alcoholism.

C.  Idiopathic intracranial hypertension is a condition of elevated CSF pressure. The most common profile is that of young, obese females with menstrual irregularities. However, thin females and males may also develop the condition. Since there is diffuse pressure elevations, no focality on examination is expected and the headache has the features of a “brain tumor headache.” Diplopia, mostly commonly secondary to sixth-nerve palsy, is common, as is pulsatile tinnitus. As the increased pressure is transmitted to root sleeves, radicular pain can accompany the headache. Papilledema is generally, but not invariably, present.

1.  Diagnosis. Magnetic resonance imaging (MRI) shows small- or normal-sized ventricles with no masses. Careful evaluation of the globes may demonstrate flattening of the posterior portion of the globe, protruding optic nerve heads, and vertical tortuosity of the optic nerves. Magnetic resonance venography (MRV) excludes a venous sinus thrombosis, although transverse sinuses may be compressed, probably secondary to the swelling, and may be falsely blamed as the cause. There is also a great deal of anatomic variability in venous sinuses. A lumbar puncture (LP) to follow is expected to show normal or low cerebrospinal fluid (CSF) protein and elevated pressure, but is otherwise normal.

2.  Etiology. Many cases are idiopathic. Many endocrinopathies, intoxications of vitamin A, tetracycline, and obesity are common triggers of the syndrome.

3.  Treatment. The course of the headache and the increased ICP may not run in parallel. Visual field testing needs to be closely monitored even if the headaches improve. Carbonic anhydrase inhibitors or loop diuretics are most commonly employed. Topiramate is a carbonic anhydrase inhibitor commonly effective in the treatment of headache, and also induces weight loss. Serial LPs are not recommended. If the vision is threatened, ventricular shunting or optic nerve fenestration is recommended, which may also improve head pain. In morbidly obese patients, bariatric surgery can be helpful.

Exertional Headaches

The headaches of mass lesions can be triggered by exertion, but other etiologies share this feature. Benign cough headaches are most common in middle-aged males, and headaches have an abrupt onset with cough or sneezing or stooping triggering this pain. The disorder is generally self-limiting and indomethacin can be of value. Other exertional headaches exist, including a pain of abrupt onset with orgasm, and also can be prevented with indomethacin. All of these cases should be evaluated to exclude structural causes. Some cases of benign exertional headaches respond to propranolol or nadolol.

Headaches of Abrupt Onset

Thunderclap headache refers to headache, which reaches it full intensity over seconds. The most worrisome is the headache of subarachnoid hemorrhage. Although “the worst headache of my life” in the emergency room is likely to be a severe migraine, this history should always prompt an evaluation to exclude a subarachnoid hemorrhage with, at the minimum, a noncontrast computed tomography (CT) scan. It is not rare for a subarachnoid hemorrhage to have a more gradual onset. The mortality with each subarachnoid hemorrhage approaches 50% so it is essential to make a rapid diagnosis. Low-volume bleeds, often referred to as “sentinel headaches,” commonly precede a catastrophic subarachnoid hemorrhage, and intervention at this point is often life saving. A short-lived headache or a good response to a medication does not exclude a low-volume hemorrhage.

Recurring thunderclap headaches are less likely to be due to recurring subarachnoid hemorrhages, but reversible cerebral vasoconstriction syndrome (RCVS) commonly presents in the way. RCVS is a heterogeneous group of conditions leading to a multifocal narrowing of intracerebral arteries. Magnetic resonance angiography (MRA), computed tomography angiography (CTA), or catheter angiography is used to make this diagnosis, which can be elusive. Each headache tends to resolve over minutes to hours and RCVS tends to be self-limited over a few weeks.

Headache with Stroke

More than a quarter of strokes cause headaches early in the attack, and the number might even be higher with large strokes and those strokes within the posterior circulation. Nausea and vomiting are common in this setting, which may be difficult to distinguish from migraine. Migraineurs, particularly those with aura, are at higher risk of stroke, although migrainous strokes more likely occur interictally than at the time of a migraine.

Venous sinus thrombosis generally has headache of abrupt onset with a subsequent increase in ICP.

Cervical artery dissections arise from an intimal tear with the subsequent development of an intramural hemorrhage. Headache is the presenting feature in about 75% of cases. In a carotid dissection, the pain occurs along the ipsilateral face and neck and head. Almost half have an ipsilateral Horner’s syndrome. With a vertebral artery dissection the pain is in the neck and occiput and pulsatile and continuous in quality. Stroke can occur up to 2 weeks later. A history of neck trauma is common, but not invariable.

Headaches Associated with Infection

Headaches can occur with infections of the central nervous system in those with systemic infections, or as a postinfectious headache. Postinfectious headache is suspected when the headache persists 3 months after presumed resolution of an acute intracranial infection. Although unproven, it is suspected that these headaches are due to an inflammatory, immune-mediated source.

Sinusitis is a common diagnosis for headaches, but acute sinusitis is more likely to be the etiology if there is purulent drainage and objective imaging evidence. Chronic sinusitis is an uncommon cause of headache. A study by Schreiber found that in those with self- or physician-diagnosed “sinus headache” migraine was overwhelmingly the cause of their symptoms. The trigeminoautonomic reflex, seen in migraine and other types of head pain, triggers lacrimation and rhinorrhea, often accounting for the confusion.

Orthostatic Headaches

A.  Low CSF pressure.

Headache that is worse upon standing is most commonly due to a low CSF pressure, either following an LP, or from a leak in another location. Acute CSF oligemia occasionally presents as a thunderclap headache. This occurs after 30% of LPs, and may be best prevented with the use of atraumatic needles, but prolonged bed rest after an LP is of little value. The treatment involves direct repair of the site of the leak although epidural blood patches or prolonged epidural saline infusions may prove to be effective. Overshunting in one with a ventricular shunt can cause a similar headache and those with a shunt treated with topiramate can become overshunted. Pachymeningeal enhancement on MRI and downward displacement of the cerebellar tonsils strongly suggests a low CSF pressure.

The site of a CSF leak leading to a spontaneous intracranial hypotension is often indeterminate. This can include leaks from meningeal diverticula, erosion of dura from an adjacent lesion, excessive coughing, head trauma, or dural root sleeve tears.

In cases where there is suspected CSF rhinorrhea leading to headache, assaying this fluid for glucose and β₂ transferrin can document that it is indeed CSF and a CT of the paranasal sinuses should be performed.

B.  Postural orthostatic tachycardia syndrome (POTS) can also lead to orthostatic headaches, particularly in young thin females. Typically, nonpositional headaches also occur. Coexisting fatigue, exercise intolerance, and attacks that are similar to panic attacks occur. The diagnosis is best made with a tilt table examination and may be treated with hydration, exercise, and increased salt intake, with β blockers, fludrocortisone, or midodrine added.

Giant Cell Arteritis

This condition is rare under the age of 60 and generally causes a diffuse scalp pain, which can be confused with tension-type headache or the scalp allodynia seen in an advanced migraine attack or chronic migraine. This condition can affect any artery before it pierces the dura, so that myocardial infarctions, bowel infarctions, and other ischemic complications can occur aside from blindness. Jaw claudication is commonly seen and queried by asking whether the jaw hurts with sustained chewing, in contrast with acute jaw pain that can occur with temporomandibular joint dysfunction with chewing or jawing.

Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are generally found and a superficial temporal artery biopsy is done to confirm the diagnosis. The treatment is with high dose and prolonged course of corticosteroids. After a prolonged treatment course the condition generally resolves, but recurrences are common and with recurrences the ESR and CRP can be normal.

Hypertension and Headache

Modest hypertension does not cause headache and may actually be protective for head pain. Approximately 20% of patients with hypertensive crises have headaches, and therefore, head pain may accompany severe levels of hypertension.

The Examination of a Headache Patient

1.  Vital signs: Are there significant abnormalities in blood pressure, or fever? Fever strongly suggests an infection.

2.  Is there evidence of head injury? (Battle’s sign, Raccoon’s eyes, hemotympanum, CSF rhinorrhea, or otorrhea) Is dentition poor, which might be a local site of infection, which can lead to the development of a cerebral abscess or cerebritis?

3.  Is there a disturbance of consciousness? This nearly always suggests a secondary headache.

4.  Provocative tests for facet joint pathology, occipital groove, and supraorbital nerve tenderness, is there limitation of neck movement, is there carotid artery tenderness? Anteroposterior neck stiffness suggests a meningeal process.

Cervical facets may be locally tender or may cause pain radiation locally or into the shoulders or upper back, and rarely radiate in the front or down an arm or into the fingers.

5.  Is there purulent drainage from the sinuses? Nasal congestion or clear nasal discharge is commonly seen with migraine and cluster and does not suggest sinusitis.

6. Neurologic examination is clearly important. Elevated ICP can generally be recognized on the funduscopic evaluation with papilledema and lack of spontaneous venous pulsations. Hemiparesis, hemisensory loss, and aphasia strongly suggest a secondary headache even though this can be seen with migraine with aura.

Laboratory tests to be considered:

1.  Complete blood count, complete blood chemistries, thyroid panel, ESR, CRP, drug screen.

2.  CT scans of sinuses and nasal septum. Chronic sinusitis, rather than acute, is often irrelevant to headache production but can worsen a preexisting primary headache syndrome. Sphenoid sinusitis is an unusual cause of chronic headache and may not be excluded with MRI of the brain and better evaluated on a CT of the paranasal sinuses.

3.  CT scan of the brain is the preferred test to exclude acute brain hemorrhage.

4.  MRI brain, in general, is the imaging test of choice in headache. In the posterior fossa there may be relevant pathology, and this region may be poorly imaged with CT scanning. Chronic subdural hematomas are better evaluated with MRI compared to CT.

5.  MRA or CTA can be used to screen for vascular disease. It is also often used as a screen for cerebral aneurysms. However, small aneurysms can be missed and in cases of known aneurysmal bleed, conventional catheter angiography is still required.

6.  MRV is often used to exclude a venous sinus thrombosis as a cause of headache. Negative studies are useful, but these studies frequently demonstrate asymmetries or possible occlusions, which may or may not be relevant.

7.  In cases where meningitis needs to be excluded, an LP is mandatory and in critically ill patients should not be delayed for imaging studies.

8.  In cases of orthostatic headache, where a CSF leak needs to be excluded, CT myelography is a preferred test although a negative test does not exclude this diagnosis. Although the resolution of the study is high, low-volume leaks are often undetected. In such cases, radionuclide cisternography may prove helpful, scanning for evidence of indium outside of the dura. Nasal pledgets, which are placed during the test, are then scanned for radioactivity, which if found would suggest a CSF leak though the cribriform plate that can occur from a head injury.

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