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Show An Overweight Young Woman With New Headache and Normal-Appearing Optic Discs A 25-year-old overweight nulliparous woman complains of headache for the past 6 months that is worsening in the past month. She has no visual complaints. Past medical history and review of systems are unremarkable. She acknowledges a weight gain of 20 pounds in the past year. A neurologist found no abnormalities on examination 2 weeks ago. Results of brain MRI are normal. Your neuro-ophthalmologic examination is normal except for scattered high threshold points and mean deviations of -3 dB on a 24-2 Humphrey visual field protocol. The optic discs appear normal although there are no spontaneous venous pulsations. Question 1: What is your diagnosis? Dr. Digre: There are many questions that I would ask. For example, is there a family history of headache or migraine? A positive family history suggests that this is a headache-prone individual and that this headache may be migraine. What is the life history of the patient with headache? Did she have headaches when she was younger, and have they only recently worsened? Does she have chronic headache with acute attacks? What accompanies the headache? Are photophobia, phonophobia, nausea, vomiting, and worsening with activity present? Does she take herbal medicines or ointments containing vitamin A? Is there depression or menstrual irregularity? Does she have other symptoms of fatigue or daytime sleepiness? The history must also be searched for reasons to have a new chronic daily headache with ‘‘normal imaging,'' including high intracranial pressure (ICP), Chiari malformation, and chronic paranasal sinus disease. These are features easily missed on imaging or go unreported. I inquire about hypothyroidism, anemia, metabolic disorders that can be associated with chronic headache, and factors that change episodic headache into chronic headache, such as viral illness, head injury, overuse of medications, use of illicit drugs, depression, and sexual, emotional, or physical abuse (1). Obesity alone has been associated with the conversion from acute to chronic headache (2). In any overweight patient, I am especially interested in manifestations of increased ICP, such as pulse-synchronous tinnitus, visual symptoms, postural exacerbation of head-ache, worsening of headache at night, and neck or interscapular pain (3). Wang et al (4) found that the most helpful historical features in identifying increased ICP were obesity, blurred vision, seizure, and pulsatile tinnitus. I would look for subtle signs of papilledema. Is there a physiologic optic disc cup? The absence of spontaneous venous pulsations does not always mean elevated ICP (5). I also look for subtle esophoria, which can accompany increased ICP. I might attribute the visual field result, which here showed scattered high threshold spots with a 3dB mean deviation, to having a headache during the test (6). I would carefully review her ‘‘normal'' MRI scan, looking for features suggesting increased ICP that may not be reported by the radiologist, such as empty sella, dilated Kathleen B. Digre, MD Professor of Neurology and Ophthalmology University of Utah School of Medicine Salt Lake City, Utah Deborah I. Friedman, MD, MPH Professor of Ophthalmology and Neurology University of Rochester Rochester, New York Editor s note: In this section, two experts have debated a controversial issue based on case material and questions directed to them via e-mail. Neither contestant was aware of the other s responses until all of the questions were answered. The editor s comments appear at the end. Digre and Friedman: J Neuro-Ophthalmol 2010; 30: 85-90 85 Point Counter-Point optic nerve sheaths, narrowing of the transverse venous sinus, and tonsillar ectopia (7,8). The most common cause of headache in this patient would be migraine or another primary headache disorder. My diagnosis would depend on whether I can elicit features contributing to a primary headache disorder or whether I must seek an alternative explanation. Dr. Friedman: I cannot make a diagnosis without knowing more about the characteristics of the headache and other aspects of the patient's history. Is there a prior history of headaches? If so, were the previous headaches like this one? Is this a daily headache? If so, has it been daily since onset? What are the character, location, and level of disability produced by this headache? For example, does it awaken her from sleep? Is it constant or intermittent? If intermittent, what is its duration and frequency? Are there associated symptoms, such as photophobia, phonophobia, nausea, vomiting, osmopho-bia, worsening with activity, or pulsatile tinnitus? What medications is she taking, including those that are obtained over the counter? How much caffeine does she consume and with what consistency? Is there a family history of headache? Question 2: The patient's headache is of moderate grade, not particularly disabling, slightly relieved by acetaminophen, aspirin, or nonsteroidal anti-inflammatory drugs (NSAIDS).She takes no other medications or supplements. There are no other pertinent symptoms. She cannot identify provocativeorameliorativefeaturesof theheadache.There isnofamily history ofheadache.Yourreview of the brainMRIconfirmsthat it is entirely normal.Whatwouldyoudo? Dr. Digre: This patient would seem to have a ‘‘new headache'' and therefore warrant further workup. However, most new headaches in patients with normal neurologic examinations and normal MRIs are ‘‘primary,'' that is, without identifi-able ‘‘structural'' cause (9). From its description as moderate in severity and attenuated by simple analgesics, her headache is probably due to tension. A headache diary may be helpful to chart provocative and ameliorating factors (10). If the patient wished, I would treat with a prophylactic medication such as low-dose nortriptyline (11) or top-iramate (12), which has weight-losing properties. I would warn about rebound headaches from medication overuse, and I would reexamine her to assess effectiveness. If the headache were to become more debilitating or the patient developed other symptoms, I would consider further workup, including a complete blood count to rule out anemia, a thyroid hormone test to rule out hyperthyroidism or hypo-thyroidism, and erythrocyte sedimentation rate to rule out autoimmune disease. If results of these are negative, I would consider performing a lumbar puncture to rule out idiopathic intracranial hypertension or viral meningitis (13,14). Dr. Friedman: My review of the ‘‘normal'' MRI assumes that there are good enough views to see subtle changes associated with increased ICP, such as empty sella, dilated optic nerve sheaths, flattening of the posterior sclera, or Chiari malformation (8). If she is taking over-the-counter analgesics frequently, there may be a component of medication overuse (‘‘analgesic rebound'') headache. I would ask about caffeine use, aspartame intake, and sleep habits/snoring that might suggest obstructive sleep apnea. I would review current medication use to be sure that she did not recently start taking something that could cause headaches. I would recommend starting a prophylactic medication for chronic tension-type headache. Because she is obese, I would discuss weight loss because obesity is a risk factor for chronic daily headache. As she has recently gained 20 pounds, my first choice would be topiramate, because it may produce weight loss. My second choice would be a tricyclic antidepressant (amitriptyline or nortriptyline), but such medication tends to cause weight gain. Perhaps a low dose would be well tolerated. Because I consider the visual field to be abnormal, I would reexamine her in 4-6 weeks and repeat the test. Question 3: The patient's neurologist begins treatment with topiramate, but at 200 mg/day; there is no reduction in headache. The patient returns to you, having read that idiopathic intracranial hypertension (pseudotumor cerebri) can be a cause of headache, especially in overweight young women. Your findings have not changed. There is no optic disc edema. She asks if a spinal tap is indicated. Is it? Dr. Digre: Because my suspicion of raised ICP is low in this patient, I would first push hard for a trial of symptomatic treatment. If it were unsuccessful, and she insisted, I would arrange for a spinal tap. Mostpatients with chronicheadaches have chronicmigraine together with exacerbating factors such as obesity, frequent medication overuse, or depression (15). Primary headache disorders, including migraine alone, do not elevate ICP (16,17). Point Counter-Point 86 Digre and Friedman:: J Neuro-Ophthalmol 2010; 30: 85-90 Chronic headache may be caused by increased ICP. However, this patient does not have any symptoms to suggest that cause. I would review the history and suggest continued treatment with topiramate to see if it will be successful later or try a different prophylactic headache medicine. Prophylactic medicines may take a long time to relieve headache (18). Women who have increased ICP (measured by lumbar puncture) as the cause of chronic headache usually have at least 1 clinical or imaging clue to the presence of elevated ICP. Marcelis and Silberstein (19) described 10 adults with increased ICP (opening pressure 230-450 mm H2O) and no papilledema as determined by an ophthalmologist. In the 7 patients who underwent fluorescein angiography, results were always normal. All 10 patients were followed for up to 30 months without the development of papilledema. The authors suggested that obese women with chronic daily headaches that are poorly responsive to medical therapy who have tinnitus and an empty sella on imaging should undergo a lumbar puncture to determine whether in-tracranial hypertension is present. Wang et al (4) reported 25 patients who had headache, no papilledema (in the 17 who underwent ophthalmoscopy), and opening pressures of 240 mm H2O or greater on at least 1 lumbar puncture. The patients with increased pressure were overweight, com-plained of blurred vision, or had seizures. Other investigators have found that headache and high ICP can exist in overweight women without an obvious clinical clue. In a large headache clinic population, Mathew et al (20) found that 12 patients (15%) with chronic daily refractory headache had opening pressures of up to 450 mm H2O. Vieira et al (21) reported that 6 (10%) patients with chronic migraine had documented increased ICP. All had a body mass index (BMI) of 25 kg/m2. Among patients with tension headache or chronic migraine, Bono et al (22,23) found that if magnetic resonance venography (MRV) showed dural venous sinus stenosis, increased ICP was likely. Torbey et al (24) reported that ICP monitoring of 10 patients with intractable headaches disclosed B-waves and that 9 of 10 patients had plateau waves indicating increased ICP. I am concerned that measurements of opening pressure in these reports may have overestimated its level, particularly if the patient was not relaxed, the legs were not outstretched, or the pressure was taken with the patient sitting up. A slight Valsalva maneuver can elevate opening pressure (25). Dr. Friedman: I agree with the performance of a lumbar puncture in this patient and I will explain why. I acknowledge that idiopathic intracranial hypertension (IIH) without papilledema is very rare although the diagnostic criteria allow for this ‘‘variant'' of IIH. Digre et al (26) found that only 20 (5.7%) of patients with IIH in their practice lacked papilledema. But it happens. IIH should be considered as a secondary cause of headache in anyone with new daily persistent headache, chronic daily headache, or frequent headaches that are treatment resistant or worsening headaches in a patient with a previously stable episodic headache disorder (13). Nonetheless, having performed ophthalmoscopy on every new patient that I have evaluated for headache over the past 20 years, I have never found papilledema in any of them. The concept of IIH without papilledema in patients with refractory headaches was first reported by headache specialists. Among 85 patients with refractory transformed migraine at the Houston Headache Clinic who had a lumbar puncture to exclude chronic meningitis or increased ICP, elevated opening pressures (270-450 mm H2O) were found in 12 (14%) (20). Acetazolamide or furosemide was added to the antimigraine therapy, leading to ‘‘a reduction in the number of days with severe headache, reduced consumption of abortive agents, and overall improvement of quality of life'' (20). Opening pressures on lumbar punctures performed 3-20 months later ranged from 210 to 360 mm H2O. Statistical analysis was not performed. A larger case-control study compared clinical features in patients with IIH with and without elevated opening pressures (4). IIH without papilledema was diagnosed in 25 headache patients based on an opening pressure of at least 200 mm H2O on 2 occasions. Sixty control subjects consisted of those with intractable chronic daily headache and a normal opening pressure. Statistical predictors of high ICP were obesity, history of seizure, blurred vision, and pulsatile tinnitus (highest predictive factor). Those with high opening pressure were considerably more overweight than those without it. The headache profiles were similar in both groups. Analgesic overuse was common (80%) in both groups. In that study, the patients in both groups were treated with serial lumbar punctures. A 56% improvement in headache occurred in these patients, but the response in the control group was not reported. There was a similar response in both groups to dihydroergotamine and diuretics. Five patients with elevated opening pressures underwent shunt surgery (2 had 1 operation, 2 had 3 operations, and 1 had 4 operations). Three of the 5 shunted patients consistently reported improvement in headache. Diuretics and corticosteroids conferred no additional benefit in shunted patients. Another study compared clinical features in headache patients with and without papilledema (26). BMI and age at onset were not significantly different between the 2 groups. Obesity (mean BMI 34.5 kg/m2) was present in 18 (90%) of the patients without papilledema. Patients with papilledema presented within 1 year of symptom onset, whereas patients without papilledema presented an average of 5 years after symptom onset. Patients without papilledema had headaches with migrainous features, and these patients were less likely than patients with papilledema to experience transient visual obscurations, pulsatile Point Counter-Point Digre and Friedman: J Neuro-Ophthalmol 2010; 30: 85-90 87 tinnitus, diplopia, or visual loss. If visual field loss was present, it was usually nonorganic. Headache response to therapy was no different in the 2 groups, although 3 of 4 patients without papilledema had improvement in their headaches with shunting.Most patients without papilledema had spontaneous optic disc venous pulsations, consistent with the fact that their cerebrospinal fluid (CSF) opening pressures were lower (mean 312 mm H2O) than those in patients with papilledema (mean 330 mm H2O, P , 0.01). Headache treatment in both groups consisted of diuretics (usually acetazolamide) with or without other migraine medications. A Swedish study (27) compared opening pressure and other parameters in 10 patients with IIH with papilledema and 10 consecutive patients with chronic tension-type headache. Nine patients in each group were women. As in the study by Digre et al (26), the mean BMI was the same (31 kg/m2) in both groups. All patients with IIH had opening pressures greater than 350 mm H2O. The patients with chronic tension-type headache had opening pressures between 180 and 250 mm H2O and 50% were between 200 and 250 mm H2O. I have identified at most 3 patients (all women) whom I believe to have had IIH without papilledema or any imaging abnormalities. Two were slim with no risk fac-tors for IIH, and 1 had only intermittent symptoms at intervals of weeks to months between ‘‘bouts'' of severe headaches that only responded to lumbar puncture. Although this patient lacks papilledema, the change in her baseline headache pattern is a ‘‘red flag'' for a secondary cause of headache. Although uncommon, IIH without papilledema is a diagnostic consideration and I would perform a spinal tap. There are many factors to consider in regard to lumbar puncture technique. I generally perform a tap in an obese patient in the sitting position and move the patient to the lateral decubitus position to measure opening pressure, using an anxiolytic drug if needed. If the patient is morbidly obese, I would have a member of the interventional radiology staff perform the puncture under fluoroscopic guidance. A possible confounder is the use of sedatives during the procedure. Lumbar punctures are performed in our radiology department, often under conscious sedation. The potential hypercapnia from hypoventilation during sedation may cause artificially high opening pressure measurements. However, a very anxious patient may cry or perform a Valsalva maneuver and raise CSF pressure. Neville and Egan (25) found that patients could easily increase their opening pressure during a lumbar puncture by 150 mm H2O or more with a Valsalva maneuver. It is hard to convince patients to have another spinal tap if they have a bad experience the first time. Question 4: A lumbar puncture is performed under fluoroscopy without sedation. You are told that the opening pressure, measured in the lateral decubitus position with the patient relaxed, is 240 mm H2O. The cerebrospinal fluid constituents are normal. After the lumbar puncture, the patient experiences a new, more severe headache than she had had before the spinal tap, but it is postural and disappears after 10 days, leaving her with the previous chronic headache. Is this opening pressure high enough to warrant a diagnosis of idiopathic intracranial hypertension? If not, how high must the opening pressure be to warrant that diagnosis? How would you manage this patient? Dr. Digre: This patient has no symptoms of high ICP, no signs of high ICP, and no relief when her pressure is lowered. She does not have IIH. What is normal opening pressure? Although the normal range is often said to be between 100 and 180- 200 mm H2O, studies (28,29) show that there is an even wider variation of ‘‘normal.'' Continuous pressure measurements show that normal individuals may have pressures that fluctuate up to 250 mm H2O (30,31). In a series of 242 adults (55% women) undergoing lumbar pressure, Whiteley et al (32) demonstrated a mean opening pressure of 170 mm H2O with a range from 80 to 280 mm H2O. They calculated the 95% range to be 100 to 250 mm H2O. Although the opening pressure increased with BMI, the increase was not clinically significant. They cautioned that the diagnosis of increased ICP or IIH would have to be made cautiously if the opening pressure were not elevated well above these values. On the other hand, opening pressures between 200 and 250 mm H2O have been found in patients with IIH and papilledema (7, 30). I have diagnosed IIH in patients without papilledema and published the results in 20 such cases, comparing them with 20 patients with IIH and papilledema (26). We found that the symptoms and signs were similar in the 2 groups except that papilledema and sixth cranial nerve palsy were more frequent in the patients with IIH. IIH without papilledema constitutes about 5% of our patients with IIH. Others (20,33) have found that IIH without papilledema constitutes up to 20% of patients with chronic daily headache and that such patients benefit from treatment with acetazolamide and an antimigraine drug (4). Even modest weight loss can be helpful (34,35). Point Counter-Point 88 Digre and Friedman:: J Neuro-Ophthalmol 2010; 30: 85-90 This patient has a new daily headache, which could be of the chronic tension or ‘‘new daily persistent headache'' type (36). Treatment of either of these headache types is challenging. New daily persistent headache is often associated with a previous viral infection. Treatment has been difficult and often resistant to all efforts (37). I suggest that the patient keep a diary of exacerbating factors, and I would treat with a tricyclic antidepressant (amitriptyline or nortriptyline), a calcium channel blocker (verapamil), or an anticonvulsant (topiramate and valproate are Food and Drug Administration-approved for headache therapy; levetiracetam, gabapentin, and pregabalin would be off-label uses). Tizanidine and botulinum toxin therapy are also considerations for treatment of her headaches (38,39). I would also look for (and possibly treat) a sleep distur-bance, depression, or anxiety. Weight loss would also be help-ful (39). I would continue to follow her for other findings. Dr. Friedman: The opening pressure in this patient falls into the ‘‘gray zone,'' not clearly meeting the criteria for IIH but above the level that is considered unequivocally normal (30). Although the response to lumbar puncture is not diagnostic of IIH, improvement in her headache after the lumbar puncture might lend some credence to that diagnosis. The development of a postlumbar puncture headache might cloud the clinical picture but should resolve within a week. At this point, I am still not convinced that the patient has IIH and would proceed with a sleep study to make sure that she does not have obstructive sleep apnea. A higher dose of topiramate may be required or she may respond to a different prophylactic medication. Repeating the lumbar puncture is also an option. Acetazolamide or furosemide treatment may benefit this patient. The experiences of Mathew et al (20) and Digre et al (26) have indicated that some patients without papilledema improve after shunting, but I try to avoid shunting whenever possible because of the high failure rate and the ‘‘downward spiral'' that repeated shunting creates for patient and physician. Editor's Comments This patient is meant to represent an overweight young woman with new chronic headache, a normal ophthalmic examination showing no papilledema, and a normal brain MRI, in whom the consideration of ‘‘idiopathic intracranial hypertension without papilledema'' (IIHWOP) would come up. It did come up for our 2 experts, board-certified neuro-logists with considerable experience in the care of patients with headache and IIH. They both consider IIHWOP a real but rare entity on the basis of several publications (4,19- 24,26), including one co-authored by Dr. Digre (26). Those reports have described obese patients with chronic head-ache- often described as ‘‘transformed migraine''-who have undergone lumbar puncture that has shown an opening pressure greater than 200 mm H2O (usually greater than 250 mm H2O). In some of those patients, headache has improved after the lumbar puncture, in others after treatment with carbonic anhydrase inhibitors or other diuretics, and in a small minority after cerebrospinal diversion procedures. In this Point Counter Point, both debaters dismissed the diagnosis of IIHWOP because the opening pressure of 240 mmH2O was too low and there were no other corroborative features (pulsatile tinnitus and empty sella). Yet in the publication coauthored by Dr. Digre (26), the cutoff pressure between control subjects and those labeled as having IIH with or without papilledema was an opening pressure of 260 mm H2O, not so much higher than the 240 mm H2O of our patient! Would an opening pressure of 260 have changed their minds? Although Drs. Digre and Friedman agree that IIHWOP is rare, other authors have asserted that IIHWOP could account for 10% (21) or 15% (20) of patients with chronic daily headache. No one doubts that ICP can be chronically elevated without causing papilledema. But in the absence of papilledema, there are no reliable indicators to mark IIH. Basing a diagnosis of IIHWOP on sustained relief of headache after a trial of an ICP-lowering agent is risky. Headache is much too subjective a complaint and can arise from too many other causes. Besides, many patients with chronically elevated ICP do not report headache, probably because intracranial nociceptive receptors rapidly adapt under those circumstances. As the debaters both admit, there are many technical errors in doing a lumbar puncture that can lead to a falsely elevated opening pressure. Thus, I am uneasy about making the diagnosis of IIHWOP unless the opening pressure is greater than 300 mm H2O on at least 2 lumbar punctures done with optimal technique or on ICP monitoring. Even if those conditions are met, I would hesitate to prescribe ICP-lowering agents such as acetazolamide, which can cause kidney stones and induce life-threatening allergic reactions. Nor would I expose the patient to the compli-cations of a CSF shunt. After all, visual function is not at risk in IIHWOP, and relief of headache is the only objective of treatment. I have yet to make a diagnosis of IIHWOP. Am I missing something? Point Counter-Point Digre and Friedman: J Neuro-Ophthalmol 2010; 30: 85-90 89 REFERENCES 1. Tietjen GE, Brandes JL, Digre KB, et al. History of childhood maltreatment is associated with comorbid depression in women with migraine. Neurology 2007;69: 959-68. 2. Lipton RB. Tracing transformation: chronic migraine classification, progression, and epidemiology. 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