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12 Papilledema and Idiopathic Intracranial Hypertension |
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TABLE 12–7 Associations with Idiopathic Intracranial Hypertension
1.Proven associations (meets all 4 criteria for association) Obesity, especially weight gain
2.Probable associations (meets 3 criteria but lacks case control studies) Chlordecone (Kepone) and lindane
Hypervitaminosis A Uremia
3.Possible associations (meets 2 criteria)
Steroid withdrawal in children Growth hormone—rapid brain growth Feeding in malnutrition
Hypothyroid children receiving replacement Ketoprofen and indomethacin in Bartter’s syndrome Hypoparathyroidism
Addison’s disease Uremia
Tetracycline; minocycline Nalidixic acid
Danazol
Norplant
Lithium Amiodarone Phenytoin Nitrofurantoin Ciprofloxacin Nitroglycerin
Vitamin A deficiency (infants only)
4. Unsupported (meet only 1 criterion and no data to support) Menstrual irregularity
Oral contraceptive use Iron deficiency anemia
Vitamin A deficiency (adults) Minor head trauma Hyperthyroidism
Steroid ingestion Immunization Pregnancy Menarche
Modified from Digre KB, Corbett JJ: Idiopathic intracranial hypertension (pseudotumor cerebri): A reappraisal. Neurologist 2001;7:2–67.
SECONDARY INTRACRANIAL HYPERTENSION
Pseudotumor Syndrome
Pseudotumor syndrome is a term introduced by Johnston in 1991 to denote the many conditions in which the symptoms, signs, and normal imaging resemble IIH.81 We suggest considering primary intracranial hypertension to be synonymous with IIH and using the term secondary intracranial hypertension when the cause of the increased pressure is known.
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Cerebrovenous Thrombosis
Cerebrovenous thrombosis can present exactly like IIH in 37% of cases with dural venous thrombosis, with signs including papilledema, elevated ICP, and normal CSF.82 This leads us to recommend imaging of the venous sinuses to make the correct diagnosis. Usually MRV or CT venography is sufficient to exclude venous thrombosis. Occasionally, arteriography is required. If thrombosis is found, a search for the cause is necessary (Table 12–4). Because papilledema in venous thrombosis can often be severe, aggressive evaluation and treatment may be needed to prevent blindness.83 In addition to instituting therapeutic anticoagulation, treating the papilledema-related visual loss with diuretics may be helpful. Surgical procedures such as optic nerve sheath fenestration and/or ventriculo- lumbar-peritoneal shunting may be required.
Brain Tumor
Any space-occupying lesion in the brain has the ability to increase ICP and cause papilledema. Thus, it is amazing that not all tumors in the brain cause papille-
dema. Only 50% to 60% of adults and 38% of children with documented brain tumors and increased ICP have been found to have papilledema.24,84 Hayreh
and Hayreh12 documented similar findings in the laboratory. When papilledema is present, we insist on imaging to look for space-occupying lesions. Obviously, treating the underlying tumor by surgical excision, radiation, or other methods also treats the tumor-associated papilledema, but the same principles of following and treating papilledema associated with other conditions apply in this setting.
Other Malignancies
In addition to causing space-occupying lesions, malignancies can be associated with papilledema in other ways. Carcinomatous and lymphomatous meningitis can present with signs and symptoms almost identical to those of primary intracranial hypertension.85,86 Leukemia may infiltrate the optic nerve and meninges to produce intracranial hypertension.87 Spinal tumors can also cause papilledema, although this is very difficult to diagnose unless the spinal canal is imaged. Many present identically to primary intracranial hypertension, although perhaps with slightly or greatly elevated CSF protein levels.88 Malignancy can also be associated with papilledema in gammopathies such as myeloma, or POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes).89
Hydrocephalus
Hydrocephalus especially in its acute form, behaves similarly to other spaceoccupying lesions. Hydrocephalus is generally defined as increased ICP caused by an increase of fluid within the brain. A variant is compensatory hydrocephalus, in which the fluid increase exists but there is no increased ICP. Hydrocephalus can develop by overproduction of CSF (e.g., by a choroid plexus papilloma), by aqueductal stenosis (one of the most common causes), and by decreased CSF absorption through arachnoid granulations (e.g., from subarachnoid hemorrhage
12 Papilledema and Idiopathic Intracranial Hypertension |
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or from spinal tumors that cause elevated CSF protein levels).51 Hydrocephalus can be either noncommunicating (caused by tumors or aqueductal stenosis) or communicating (where blockage is actually distal to the ventricular system, such as after subarachnoid hemorrhage). Usually, the communicating form has the slower rate of ventricular dilatation.90 In addition to papilledema, other neuro-ophthalmic and neurologic signs that can accompany hydrocephalus include sixth nerve palsy, midbrain compression by the third ventricle, gait instability, incontinence, and cognitive changes. Patients have been known to have chronic hydrocephalus without documented papilledema.51 The same general principles for following patients with papilledema pertain to hydrocephalus associated papilledema.
Medications
Although no medication has unequivocally caused intracranial hypertension, there are many instances in which taking a medication was associated with intracranial hypertension and discontinuing it stopped the high pressure. Although some medications such as tetracycline and minocycline have often been associated with IIH,91 others have rarely if ever been reported, and the reporting may have preceded the era of modern imaging.
In evaluating any medication for possible association with intracranial hypertension, one should consider whether the medication was associated with the condition and if stopping the medication brought remission. In addition, one should determine whether restarting the medication brought about signs of intracranial hypertension, and if a controlled trial demonstrates evidence of an association. Table 12–8 has a review of medications and proposed mechanisms for ICP.
Increased Venous Pressures and Cardiopulmonary Disease
Increased venous pressures have long been known to cause intracranial hypertension. In 1934 Friedfeld and Fishberg92 reported a linear relationship between venous and CSF pressure. The cause-and-effect relationship between increased venous pressures and intracranial hypertension can manifest itself in
development of papilledema associated with acute and chronic and respiratory failure, as well as with congestive heart failure.93,94 When the underlying dis-
ease is treated successfully, the venous pressures subside and the papilledema resolves.
Growth Disorders
Achondroplasia is an example of a growth disorder associated with papilledema. This autosomal dominant condition results in short stature and an abnormally large head. Hydrocephalus, venous stenosis, and associated narrowed spinal cord and canal have been postulated as mechanisms for increased pressure.95 Treatment of growth disturbances with growth hormone has also resulted in intracranial hypertension.96
Nutritional Disorders
Many cases of increased ICP in conjunction with papilledema have been reported as a consequence of hypervitaminosis A. Within 6 months of stopping
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TABLE 12–8 |
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Medications Reported to Cause Intracranial Hypertension |
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Strength of |
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Medication |
Type of Association |
Proposed Mechanism |
Association* |
Reference |
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Vitamin A and its |
Elevated serum vitamin A and |
Alteration of egress through |
þþþ |
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derivatives |
CSF related to increased ICP |
granulations |
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Antibiotics |
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þþþ |
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The “cyclines” |
Use of the cyclines associated |
Alteration of absorption |
91, 97–99 |
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Tetracycline |
with increased ICP |
mechanism by affecting |
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Minocycline |
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cyclic adenosine |
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Doxycycline |
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monophosphate at the |
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arachnoid granulation |
þþþ |
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Nalidixic acid |
Use of drug associated with |
Unknown mechanism |
99 |
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increased ICP, mainly in |
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children |
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þþ |
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Fluoroquinolones |
Use of drug associated with ICP |
Drug is similar to nalidixic acid |
100 |
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(e.g., |
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ciprofloxacin) |
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þ |
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Sulfamethoxazole |
Drug associated with ICP |
Unknown mechanism |
101 |
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Nitrofurantoin |
Use of the drug associated with |
Unknown mechanism |
þþ |
102 |
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ICP |
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Psychiatric drugs |
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þþþ |
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Lithium |
Use associated with ICP |
Adverse affect on Na-K pump |
103 |
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creating intracellular edema |
þ |
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Chlorpromazine, |
Use associated with ICP |
Unknown |
104 |
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imipramine, |
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thioridazine, |
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phenothiazine |
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Steroids |
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þþ |
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Corticosteroids |
Withdrawal associated with |
Unknown effect, may have to |
105 |
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ICP; rare reports of steroids |
do with fluid balance |
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themselves associate with |
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ICP |
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þþþ |
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Growth hormone |
Use associated with ICP; |
Associated with fluid retention; |
106 |
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also insulin-like |
perhaps more frequent in |
possible insulin-like growth |
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growth factor |
children with renal disease |
factor affect on increasing |
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production in the choroid |
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plexus |
þ |
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Oral |
Use associated with increased |
Possibly related to increased |
107 |
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contraceptives |
ICP |
weight gain |
þ |
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Levonorgestrel |
Use associated with ICP |
Weight gain |
10 |
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Danazol |
Use associated with ICP; both |
Weight gain; change in |
þ |
10 |
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IIH and venous thrombosis |
coagulation? |
þ |
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Leuprorelin |
Associated with ICP |
Unknown |
108 |
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(Lupron) |
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þ |
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Stanazol and |
Associated with ICP |
Unknown—weight gain? |
10 |
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anabolic steroids |
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Other drugs |
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þ |
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Oxytocin |
Associated with ICP |
Unknown |
109 |
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Amiodarone |
Associated with ICP but also |
Unknown |
þ |
110 |
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AION |
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þ |
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Perhexiline |
Associated with ICP; used for |
Unknown |
111 |
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maleate |
angina |
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þ |
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Phenytoin |
Associated with ICP |
Unknown |
112 |
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Nitroglycerin |
Associated with ICP |
Increased blood volume |
þ |
113 |
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þ |
114 |
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Table continued on following page
305 Hypertension Intracranial Idiopathic and Papilledema 12
TABLE 12–8 Medications Reported to Cause Intracranial Hypertension (Continued)
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Strength of |
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Medication |
Type of Association |
Proposed Mechanism |
Association* |
Reference |
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Ketoprofen, |
Associated with ICP in Bartter’s |
Alteration in Na-K |
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indomethacin |
syndrome |
ATPase pump |
þ |
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Cyclosporine |
Associated with ICP |
Unknown |
115 |
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Cytosine |
Associated with ICP |
Unknown |
þ |
116 |
arabinoside |
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Toxins |
þþ |
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Chlordecone and |
Toxins associated with ICP |
Inhibition of the Na-K |
117, 118 |
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lindane |
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ATPase pump action |
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AION, anterior ischemic optic neuropathy; CSF, cerebrospinal fluid; ICP, intracranial pressure; IIH, idiopathic intracranial hypertension. *Strength: Medication associated with ICP (þ); withdrawing medication improves (þþ); restarting worsens (þþþ); clinical trial shows
association (þþþþ).
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excess vitamin A ingestion, the papilledema resolves. Intracranial hypertension in association with papilledema has also been reported as a complication of parenteral hyperalimentation and during implementation of catch-up nutritional interventions instituted after diagnosis of nonorganic failure to thrive. Increased ICP and papilledema have been observed in patients with the eating disorder bulimia; nutritional deprivation could have been a contributing factor.10
Endocrine Disease
Associations of endocrinologic factors with increased ICP have been studied, but they have not been as well characterized as have other, more conclusively documented associations. Increased ICP with concurrent papilledema has been observed in patients with hypoparathyroidism, although thus far, no mechanisms have been suggested for this observation. No studies have shown that hypothyroidism or hyperthyroidism causes increased ICP. Papilledema in association with both Addison’s disease and Cushing’s disease has been reported; but further evaluation is necessary to understand the possible links between these endocrine disorders and increased ICP.10
Infections
Table 12–4 lists infections associated with ICP and papilledema. The mechanism by which these cause intracranial hypertension has been postulated to be meningitis; alternatively, infections can be associated with venous thrombosis and inflammation. Successful treatment of the infection is the key to papilledema resolution. However, many other causes of visual loss associated with infection will not respond to traditional therapy for papilledema. For example, inflammation around the nerve can lead to infarction or optic neuritis and visual loss. Treatment of such cases requires careful consideration.
Acknowledgment
I acknowledge the assistance of Susan Schulman with the preparation of this chapter.
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