Psychosomatics 46:326-333, August 2005
© 2005 The Academy of Psychosomatic Medicine
Headache Attributed to Psychiatric Disorder: A Case Series
Elizabeth Loder, M.D., F.A.C.P., and
David Biondi, D.O.
Received April 28, 2004; revision received Aug. 9, 2004, accepted Sept. 13, 2004. From Harvard Medical School, Boston; and the Headache and Pain Management Programs, Spaulding Rehabilitation Hospital, Boston. Address correspondence and reprint requests to Dr. Loder, 125 Nashua St., Boston, MA 02114; eloder{at}partners.org (e-mail).
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ABSTRACT
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The association between psychiatric illness and headache is widely recognized. However, cases in which psychiatric disorders are the principal cause of headache are believed to be rare. "Headache attributed to psychiatric disorder" is a new category of secondary headache in the 2004 revision of the International Classification of Headache Disorders. The authors describe six patients in whom a psychiatric disorder is the most plausible cause of headache; most meet the new criteria or candidate criteria for headache attributed to a psychiatric disorder. The revised headache classification system appropriately recognizes headaches attributed to psychiatric disorder as a form of secondary headache.
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INTRODUCTION
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"Headache attributed to psychiatric disorder" is a new category of secondary headache introduced in the 2004 revision of the International Classification of Headache Disorders.1 Somatization disorder and psychotic disorder are specifically recognized as causes of headache. "Candidate criteria" for seven other psychiatric disorders as causes of headache are contained in the appendix "to facilitate research into the possible causal relationships between certain psychiatric disorders and headache." The classification authors comment that
Overall, there is very limited evidence supporting psychiatric causes of headache. Thus, the only diagnostic categories included in this classification are those rare cases in which a headache occurs in the context of a psychiatric condition that is known to be symptomatically manifested by headache...the vast majority of headaches that occur in association with psychiatric disorders are not causally related to them but instead represent comorbidity.1
This comment reflects the current belief that psychiatric illness can be associated with primary headache disorders and influence their course but that psychiatric disorders as the principal cause of headache are "extremely rare."2 This represents a dramatic and little-commented upon shift in medical thinking. Only a century ago, headache was viewed as largely a psychological problem. As understanding of the biological basis of primary headache, especially migraine, has increased, psychiatric explanations for headache have received less attention. Thus, the medical literature on the psychiatric causes of headache is sparse, and no reliable studies exist that clarify the frequency of these disorders.
Several studies have clarified, though, that the most common relationship between psychiatric illness and headache is bidirectional and associational rather than causative. This relationship is especially clear in the case of affective disorders and migraine. The elevated risk a patient with migraine or depression has of developing the other disorder seems attributable in most cases to shared underlying factors such as serotonergic abnormalities of the CNS. The underlying neurochemistry of many primary headache disorders, especially migraine, has much in common with the neurochemistry of various psychiatric illnesses.3,4 Even if association is the most common relationship between psychiatric illnesses and headache disorders, though, it does not preclude the possibility of a causal relationship in some circumstances. To establish causality, the authors of the headache classification emphasize that "it is crucial to establish that the headache in question occurs exclusively during the course of the psychiatric disorder. This should be interpreted to mean that the headache is manifest only during times when the symptoms of the psychiatric disorder are also manifest."1
We present a series of six case reports of headache attributed to psychiatric disorder in which there is strong evidence of a causal association between the psychiatric disorder and headache and evaluate the application of the 2004 criteria to these cases.
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CASE SERIES
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Case 1
Ms. A, a 58-year-old woman, was admitted to an inpatient pain rehabilitation program because of intractable headache. She had a history of episodic migraine without aura beginning as a teenager that responded well to treatment with simple analgesics. At age 38, within 3 days of a hysterectomy and a bilateral oophorectomy performed to treat endometriosis, she developed constant, severe, generalized head "pressure" with superimposed exacerbations of unilateral pain and associated features typical of her previous migraine. The chronic headache was believed to be an adverse effect of estrogen-replacement therapy begun after surgery, although it did not improve when estrogen-replacement therapy was discontinued. Intensive abortive and prophylactic treatment, including prolonged medication withdrawal, produced no improvement. Five years before admission, Ms. A became bed-ridden and disabled due to constant headache.
Upon admission, she reported continuous, generalized headache rated 10 on a pain scale of 0–10. She was taking 15 tablets per day of a barbiturate-containing combination medication, 90 mg/day of continuous-release morphine sulfate, 10 mg/day of diazepam, and 25 mg/day of amitriptyline. A physical examination showed a flat affect and poor eye contact; no evidence of a thought disorder was apparent. Ms. A was cachectic, with pronounced muscle wasting. Her examination was otherwise without abnormalities. A magnetic resonance imaging (MRI) scan of her head performed 2 months before her admission was normal. Laboratory results, including thyroid studies and a measure of her erythrocyte sedimentation rate, were normal.
Diagnoses of transformed migraine and probable analgesic-induced rebound headache were made. Diazepam, barbiturates, and opioids were tapered and discontinued. One mg of subcutaneous dihydroergotamine was administered every 8 hours for 3 days. Ms. A participated in a functional restoration program of physical and occupational therapy and group and individual psychotherapy. No improvement in her headaches occurred over the subsequent 2 weeks. A further history obtained from her daughters revealed that at the time of her headache onset, coincident with her hysterectomy/oophorectomy and institution of estrogen-replacement therapy, she had developed psychotic depression. Estrogen-replacement therapy was discontinued, and Ms. A underwent ECT, which improved her ability to function but had no effect on the headaches. Over the years, Ms. A, her family, and physicians noted continued signs and symptoms of depression but attributed them to her unrelenting headache.
Based on this information, a diagnosis of headache due to depression was made, and headache-specific medications, such as dihydroergotamine, were discontinued. Fluoxetine, 20 mg/day, was begun and increased gradually to 80 mg/day. Ms. A continued the functional restoration program. At discharge 2 weeks later, she reported some improvement in her headaches and an improved ability to cope with her pain. Discharge recommendations included a psychiatric follow-up and continuation of fluoxetine.
Ms. A returned 4 months later and reported that her headaches had completely resolved. An examination showed a smiling and cheerful patient who had gained weight. She had taken a part-time job and was redecorating a vacation home. She has now been followed for 4 years. Two years after discharge, she discontinued taking fluoxetine because of significant weight gain; a constant, unremitting headache unresponsive to symptomatic treatment recurred. Treatment with venlafaxine was begun, and her headaches again disappeared. Since then, Ms. A has discontinued antidepressants several times because of side effects; each time the headaches have recurred.
This patient’s headaches met the candidate criteria listed in Appendix 2 for a diagnosis of headache attributed to major depressive disorder. Although she had a prior history of migraines without aura, her disabling headaches began in close temporal association to an episode of major depression with psychotic features and were unresponsive to previously effective therapy and to other treatments for migraine. The headaches disappeared with treatment of depression, recurred when therapy was discontinued, and resolved with reinstitution of treatment for depression. The time course of her improvement and its association with improved mood was most consistent with the antidepressant effect of fluoxetine. Although a prophylactic effect of fluoxetine on migraine has been suggested,5 evidence from clinical trials does not support its usefulness as a migraine prophylactic agent; it also seems unlikely that a patient who had no response of any kind to more effective and better-validated migraine therapies would respond to a drug of lower efficacy.
Case 2
Mr. B, a 40-year-old man, had only mild, intermittent, and nondisabling headaches until age 37. Two weeks after the unexpected neonatal death of his first child, he developed a constant, generalized headache of fluctuating intensity with no associated features. A full medical and neurological evaluation, including an MRI scan of his head, was unrevealing, and intensive treatment, including the use of triptans, ergots, beta-blockers, tricyclic antidepressants, tizanidine, baclofen, anesthetic injections, and sinus surgery produced no improvement in his headaches. Three years after the onset of his headaches, Mr. B was unable to work and reported an average headache intensity of 8 on a scale of 10 despite treatment with 20 mg/day of paroxetine, 40 mg/day of sustained-release oxycodone, and four tablets per day of oxycodone. He was admitted to an inpatient pain rehabilitation unit. Aggressive treatment, including the use of parenteral dihydroergotamine, steroids, triptans, and opioids, had no effect on his headaches.
A consulting psychologist obtained a history of depressed mood, a low energy level and fatigue, insomnia, and a 40-lb weight gain in 2 years. Mr. A had a score of 30 on the Beck Depression Inventory, indicating severe depression. These symptoms had been attributed to bereavement, but the psychologist believed that a diagnosis of major depression was more likely. Treatment with a high dose of venlafaxine was begun, and Mr. B participated in group and individual psychotherapy. Headache medications were discontinued, and paroxetine and opioids were tapered and discontinued. At the time of discharge, Mr. B had intermittent headaches rated an average of 3 on a scale of 0–10, and his depressive symptoms had improved. Three months after discharge, Mr. B contacted the treatment team to inform them that his headaches were mild and infrequent; he had returned to work and reported few symptoms consistent with depression.
This patient’s headaches met the candidate criteria for headache attributed to major depressive disorder. Onset in close proximity to a severely stressful life event that triggered the depressive disorder, improvement in headache with treatment of depression, and lack of response to traditional headache therapy all support a diagnosis of headache caused by depression. In this case, the patient’s depressive symptoms were attributed to bereavement, and recognition of their significance was delayed. The dose of tricyclic antidepressant used to treat his headache was likely too low to produce a full antidepressant effect. As in case 1, this patient required high doses of nontricyclic antidepressants for a full resolution of his headaches.
Case 3
Ms. C, a 52-year-old woman, was seen for complaints of headaches since age 22. She reported headaches occurring on average 20 days a month that were low grade and nondescript, with superimposed exacerbations that met criteria for migraine. She reported a history of overuse of barbiturate-containing medications and had recently been hospitalized for barbiturate withdrawal. Since then, she had used sumatriptan daily. Trials of sumatriptan withdrawal, gabapentin, amitriptyline, and sodium valproate were ineffective. Acupuncture, physical therapy, and massage aggravated her headache. Ms. C was wealthy and traveled extensively to consult well-known physicians. Extensive treatments, both traditional and nontraditional, for headache and her other complaints had proved ineffective or produced unusual, dramatic, or paradoxical effects.
Ms. C reported significant distress from headaches but had a score of 1 (minimal disability) on the Migraine Disability Assessment Scale. Her past medical history was significant for depression, anxiety, Raynaud’s phenomenon, and fibromyalgia. Upon a review of systems, she endorsed numerous disabling somatic complaints, including weight loss, fatigue, frequent sore throats, sinus infections, palpitations, abdominal pain, menstrual pain and irregularities, alternating diarrhea and constipation, paresthesias, and dizziness. She reported no history of previous physical or sexual trauma. Her physical and neurological examinations were normal; previous neuroimaging studies were without abnormality.
This patient met the criteria for a diagnosis of "Headache Attributed to Somatization Disorder" (Appendix 2). That her current headaches were attributable to this diagnosis and did not represent a separate primary headache disorder were indicated by their failure to respond to migraine-specific treatment and their worsening and improvement in conjunction with other somatic symptoms. Despite bitter complaints of distress related to headache, this patient suffered no functional impairment from them. Recognition that the patient’s headache complaints were attributable to somatization disorder is important to avoid potential harm from aggressive, unnecessary medical indications. Although curative treatment for somatization disorder does not exist, that may change in the future; in the meantime, psychiatric consultation may help with management. This case illustrates the complex natural history of headache in a single individual. This patient began with a primary headache disorder (migraine) that may have been aggravated by medication overuse and then perpetuated, chronified, or amplified by psychiatric disease.
Case 4
Diane, a 17-year-old girl with no personal or family history of headache, developed a constant, generalized headache without associated features at age 14 that prevented regular school attendance. The headaches remitted during summer vacation but recurred when school started the next fall and again became incapacitating. Her physical and neurological examinations were normal. An MRI scan of her head showed a small area of increased T2 signal in the left frontal lobe but was otherwise normal. Diane did not overuse symptomatic treatment for headache. Headache treatment with propranolol, prochlorperazine, ergotamine, divalproex sodium, carbamazepine, paroxetine, cyproheptadine, nonsteroidal anti-inflammatory drugs, barbiturate-containing medications, biofeedback, nortriptyline, prochlorperazine, ergotamine, and dietary manipulations produced no improvement, and Diane was admitted to an inpatient pain rehabilitation program.
Intensive medical and nonpharmacological therapy of the headaches, including parenteral dihydroergotamine, divalproex sodium, steroids, and physical therapy did not improve them. A psychiatric consultant did not believe that psychiatric factors played an important role in Diane’s condition but did recommend the use of lorazepam, 0.5 mg b.i.d., to treat anxiety. She reported modest improvement in her headaches and at discharge planned to finish high school and attend college.
Diane was followed for the next 2 years with little change in her situation. During her first year of college, she developed episodic bilateral leg weakness and stumbling. These episodes became more frequent over the next 3 months, and she began to fall, although she never suffered injury. Coincident with her gait disturbance, Diane developed more intense headaches and complaints of double vision, visual blurring, and an inability to read. Evaluation at another medical facility revealed a normal computerized tomography (CT) scan of her head, a normal lumbar puncture, and normal physical and laboratory examinations. A neurological consultant noted a nonphysiological gait disturbance but no other abnormalities. Diane was readmitted to the inpatient pain rehabilitation program.
Upon admission, she reported a generalized, constant headache without associated symptoms that were rated 8 on a scale of 0–10. Her examination on admission was notable for a bizarre ataxic gait with some stereotactic movements. A neurological consultant agreed that the gait disturbance was nonphysiological. An ophthalmological consultant found only mild myopia. A psychiatric consultant believed that a diagnosis of somatization disorder was most likely in view of the evolution of symptoms over time. A history of previous milder neurological symptoms occurring at times of transition (such as the loss of a boyfriend) was obtained. Diane and her family were told that no serious dangerous explanation for her symptoms had been found and were reassured that she would gradually improve with physical and occupational therapy. Over the course of the next 3 weeks, Diane’s gait disturbance and visual symptoms disappeared, and the headaches returned to their previous constant and manageable level.
Diane has been followed for 7 years. Her headaches have waxed and waned, disappearing for up to 5 months at a time and then recurred, each time unresponsive to traditional medical therapy. Other medically unexplained symptoms, including abdominal pain, double vision, ringing in the ears, fatigue, nausea, dizziness, blurred vision, insomnia, fainting, urinary disturbances, and pelvic pain have appeared and fluctuated in intensity and severity.
This patient’s headaches met the criteria for a diagnosis of "Headache Attributed to Somatization Disorder" (Appendix 1). The likely presence of somatization disorder in this case was not recognized at the initial presentation, in large part because headache was the first to appear of the multiple, chronic complaints of unexplained physical symptoms required for diagnosis. Multiple, sometimes confusing neurological symptoms can occur in conjunction with various primary headache disorders or other headache syndromes. Somatization disorder is distinguished from them by the variety and number of symptoms, many of which do not occur with headache disorders. Curative treatment for somatization disorder does not exist; symptoms generally wax and wane over a patient’s lifetime.6 In this case, the patient’s headache complaints have improved and worsened in parallel with other problems, such as the nonphysiological gait disturbance, that were clearly somatoform in nature, allowing a definitive diagnosis to be made. It is worth noting that for patients whose somatoform disorder does not remit or respond to treatment, the new headache classification scheme will allow only a diagnosis of "headache probably attributed to somatization disorder" to be made, even when the number and variety of other symptoms and lack of response to headache-specific treatments make the diagnosis certain in the minds of treating clinicians. This same high standard of proof is not required for attribution of other symptoms to somatization disorder.
Case 5
Mr. E, a 27-year-old man, was admitted to an inpatient pain rehabilitation program with a 2-year history of headaches refractory to medical therapy. He reported an onset of headaches at age 17, occurring three to four times a day. The headaches lasted around 20 minutes and were invariably located behind the left eye. Mr. E reported associated puffiness, redness, and stuffiness in the left eye, with ipsilateral nasal pain and congestion. He said that during the headaches he cried and paced the floor; at times he "passed out." He received public assistance because the headaches made it "impossible" for him to finish high school or hold a job as a telemarketer. There was a history of nicotine dependence and past cocaine abuse.
Outpatient evaluation had been extensive. MRI and CT scans of his head, an EEG, and ultrasound examinations were normal. Sumatriptan injections and oxygen were initially helpful but then lost effectiveness. Sodium valproate and biofeedback were not useful. Meperidine and other opioids were said to be the only medications that "really worked." Methysergide and steroids were said to have helped, but concern about side effects limited their use.
After admission to the inpatient pain program, lithium and verapamil were begun for a presumed diagnosis of cluster headaches. On daily medical rounds, Mr. E reported that the medications were ineffective; he said that he continued to have three to four headaches daily, now occurring only at night. He requested opioid treatment for headache from the night nursing staff, who recorded that Mr. E did not seem to be in pain; they did not observe ptosis, lacrimation, or conjunctival injection. The nursing staff was asked to photograph Mr. E when he next came in with a headache in an attempt to document the autonomic signs that he described. He cheerfully agreed to this plan, but no further episodes of headache occurred.
It was learned that hospitalization had enabled Mr. E to avoid a drug-related court appearance. The possibility of malingering was considered, and verapamil and lithium were discontinued. The headaches did not recur. Four sublingual doses of 0.4 mg of nitroglycerin were administered 10 minutes apart in an unsuccessful attempt to provoke cluster headaches. A diagnosis of malingering was made and discussed with Mr. E. He denied feigning headache but did not become angry. At discharge later that day, he requested that the physician fill out a form to enable him to continue receiving disability benefits. Four years after discharge, he died unexpectedly; an autopsy and testing confirmed that the cause of death was a heroin overdose.
This patient met the criteria for a diagnosis of malingering,7 a condition in which symptoms are feigned in order to obtain financial or other gain. Disability payments, access to opioid medications, and avoidance of legal consequences of illicit drug use were all achieved through the patient’s headache complaints. That the headache was feigned seems highly likely. It had reportedly been present daily for 10 years before admission, resistant to a wide variety of treatments, but disappeared promptly upon hospitalization and close scrutiny. Typical headaches were not provoked with discontinuation of lithium and verapamil or administration of sublingual nitroglycerin, a maneuver reported to be "100% effective" in inducing cluster headache when given in sufficient doses during an active cluster period.8 It is not clear how the patient learned so well the description of cluster headache necessary to convince physicians of its presence. One possibility is that he read about or observed the disorder in someone else; a more likely possibility is that he had true cluster headache at times but feigned it at others. The latter situation is similar to patients with pseudoseizures, many of whom have true epileptic seizures as well.9 Some headache patients with drug addiction or dependence may well have begun with an episodic primary headache disorder and then developed drug addiction that leads to malingering. Referral for psychiatric or addiction treatment is indicated.
The revised International Classification of Headache Disorders does not recognize malingering as a cause of headache, nor does it contain candidate criteria for headache caused by this disorder. This case suggests that such a category should be added. The patient’s headaches were present when needed to obtain external rewards but disappeared under circumstances where that was not possible or detection was likely. Finally, this patient’s death from a drug overdose highlights the importance of making a diagnosis of headache due to malingering. In this case, it removed at least one means of access to the opioid drugs that ultimately led to his death.
Case 6
Mr. F, a 34-year-old man, was admitted to an inpatient pain rehabilitation program with complaints of chronic headache requiring the use of large amounts of butorphanol nasal spray. He reported onset of headache at age 8 or 9, initially intermittent but constant, with intermittent exacerbations for the 3 years before admission. Headache exacerbations as described met criteria for migraine without aura. His MRI studies and a lumbar puncture were normal. Extensive trials of traditional headache medications were minimally helpful.
Mr. F reported a history of atrial fibrillation, cardiomyopathy, left hemiparesis related to a previous cerebrovascular accident, herniated lumbar disk with residual foot drop, hypertension, hyperemesis, schizoaffective disorder, tobacco abuse, chronic sinusitis, and sinus surgery. Genetic testing for MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis, and stroke) was pending. Mr. F had been frequently hospitalized and undergone numerous invasive procedures related to these diagnoses.
Mr. F displayed volatile and inconsistent behavior during his hospitalization. He made numerous demands for opioid medications to treat headache and requested extensive testing to evaluate the causes of headache. An episode of left-sided weakness and confusion prompted transfer to an acute care hospital for evaluation of possible stroke; no evidence of abnormality was found. Intermittent gait disturbance, falls, and complaints of acute muscle weakness were accompanied by variable and nonphysiological findings upon examination. A psychiatric consultant noted how much he appeared to enjoy his illness and the attendant diagnostic and treatment procedures. A diagnosis of factitious disorder was suspected. Twenty-four-hour Holter monitoring showed no evidence of atrial fibrillation. An ECG showed no evidence of cardiomyopathy. A call to the genetics laboratory revealed that testing for MELAS syndrome had been negative.
Previous medical records were obtained and revealed a recent hospitalization for complaints of left-sided weakness. An embolic cerebrovascular accident related to atrial fibrillation had been suspected; tissue plasminogen activator was administered. Fluctuating, embellished, and inconsistent results noted upon physical examination during that hospitalization, along with a 48-hour Holter monitor showing no evidence of atrial fibrillation, led to a diagnosis of probable factitious disorder. The review of previous medical records also turned up a thorough workup by a previous physician, who had independently concluded that the patient had factitious disorder.
Based on this information, anticoagulation with warfarin was discontinued. The treatment team discussed the diagnosis of factitious disorder with Mr. F and recommended that his treatment in the hospital focus solely on functional improvement with no further testing or medication. He became angry, threatened legal action against the staff and hospital, and several days later signed out against medical advice. No complaints of headache occurred before his leaving the hospital.
This patient met criteria for a diagnosis of factitious disorder (Appendix 3) with combined physical and psychological symptoms in which patients intentionally feign physical or mental signs or symptoms with the apparent goal of occupying the sick role.7 Complaints of headache disappeared once the patient was aware that the medical team viewed the symptom as part of a psychiatric disorder and was not prepared to perform further investigation or treatment. The sheer number and variety of other symptoms, along with the invasive and potentially dangerous treatments to which he submitted, suggest that the patient’s primary motivation was to occupy the patient role. This patient may also have been malingering in an effort to obtain opioid medication. As with the previous case, this patient may have begun with a primary headache disorder and developed other behaviors over time. Headache attributed to factitious disorder is not included in the main International Classification of Headache Disorders or the appendix, but this case suggests that it should be.
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CONCLUSION
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This case series provides evidence in support of the view that psychiatric disorders can cause headache. The revised international headache diagnostic and classification system appropriately recognizes headache attributed to psychiatric disorder as a form of secondary headache; in addition to psychotic and somatization disorders, future revisions of the criteria should explicitly recognize depression, undifferentiated somatoform disorder, and malingering and factitious disorders as psychiatric disorders that can cause headache. The mechanisms through which psychiatric disorders give rise to headache are not clear. Further work in this area is important because it is difficult to prove causality by comparing two clinically diagnosed conditions.
This series further suggests that headaches of psychiatric origin, especially in patients with refractory headache, may not be rare, just rarely diagnosed. Many patients with similar presentations are seen in specialty headache programs; this series consists of cases in which the psychiatric nature of the headache disorder is particularly clear. All but one of the case patients resided in a specialized inpatient pain unit for a period of several weeks, giving the staff of experienced pain psychologists, psychiatrists, and headache experts ample opportunity to observe demeanor, behavior, treatment response, and social interactions. It is important to emphasize that a diagnosis of headache secondary to psychiatric disease can only be made when a careful history and evaluation, including testing where indicated, has excluded other potential secondary causes of headache.
Recognition that headache can be a somatic manifestation of psychiatric disease (a somatic preoccupation, a somatic delusion, or intentionally feigned) is not incompatible with a view that psychiatric problems are only associated or influencing elements in the majority of recurrent, benign headache syndromes. Physicians may be reluctant to make a diagnosis of headache attributed to psychiatric disorder because of fear that the passage of time will reveal a medical explanation for the headaches, because curative treatment for the psychiatric disorder does not exist, or because patients are unwilling to accept such a diagnosis. As these cases illustrate, though, delay in diagnosis may result in delay in effective treatment and harm from unnecessary treatments. In addition, as treatment of psychiatric disorders improves, accurate diagnosis will increasingly have important clinical implications.
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REFERENCES
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- The International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004; 44:1–160
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- Breslau N, David GC, Andreski P: Migraine, psychiatric disorders, and suicide attempts: an epidemiologic study of young adults. Psych Res 1991; 37:11–23
- Breslau N, Schultz LR, Stewart WF, Lipton RB, Lucia VC, Welch KM: Headache and major depression: is the association specific to migraine? Neurol 2000; 54:308–313[Abstract/Free Full Text]
- Saper JS, Silberstein SD, Lake AE, Winters ME: Double-blind trial of fluoxetine: chronic daily headache and migraine headache. Headache 1994; 34:497–502[CrossRef][Medline]
- Barsky AJ, Borus JF, Functional somatic syndromes. Ann Int Med 1999; 130:910–921[Abstract/Free Full Text]
- American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, Text Revision. Washington, DC, American Psychiatric Publishing, 2000
- Ekbom K: Nitroglycerin as a provocative agent in cluster headache. Arch Neurol 1968; 19:487–493[Abstract/Free Full Text]
- Chabolla DR, Krahn LE, So EL, Rummans TA: Psychogenic nonepileptic seizures. Mayo Clin Proc 1996; 71:493–500[Abstract]
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ABSTRACT
INTRODUCTION
