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Author: William C Robertson, Jr, MD, Professor, Departments of Neurology, Pediatrics and Family Practice, Clinical Title Series, University of Kentucky

William C Robertson, Jr, is a member of the following medical societies: American Academy of Neurology and Child Neurology Society

Coauthor(s): Maria-Carmen B Wilson, MD, Medical Director of Pain Management, Department of Neurology, Tampa General Hospital; Associate Professor, Department of Neurology, Assistant Professor, Department of Pediatrics, University of South Florida College of Medicine; Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital

Editors: Raj D Sheth, MD, Professor, Departments of Neurology and Pediatrics, Director of Comprehensive Epilepsy Program, Department of Neurology, University of Wisconsin at Madison; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Kenneth J Mack, MD, PhD, Senior Associate Consultant, Department of Child and Adolescent Neurology, Mayo Clinic; Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital; Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants

Author and Editor Disclosure

Synonyms and related keywords: benign intracranial hypertension, hypertensive meningeal hydrops, idiopathic intracranial hypertension, otitic hydrocephalus, serous meningitis, toxic hydrocephalus, PTC, pseudotumor cerebri

Background

Pseudotumor cerebri (PTC) or idiopathic intracranial hypertension is characterized by signs and symptoms of increased intracranial pressure (ICP) without identifiable cause. PTC typically occurs among obese women of childbearing age. Although prevalence among the pediatric population is not known, the condition is not uncommon among the young. In children younger than 6 years, a specific cause for intracranial hypertension can usually be identified. These patients would therefore not be classified as having PTC. Idiopathic cases are usually seen after age 11 years.

Children with PTC usually complain of headaches and may have vomiting, blurred vision, and horizontal diplopia. The headaches are diffuse, worse at night, and often aggravated by sudden movement. Less common complaints include irritability, transitory visual loss, dizziness, and tinnitus.

As in adults, treatment is designed to decrease intracranial pressure and preserve vision.

Pathophysiology

The precise mechanism of ICP in PTC is unknown. Factors probably important in the pathogenesis include CSF production, venous sinus pressure, and CSF absorption. The importance of venous sinus pressure is seen in young children who develop thrombosis of one or more of the dural sinuses usually as a complication of otitis or mastoiditis. Evidence exists to suggest that CSF formation in PTC is probably diminished. This may be related to increased resistance to absorption at the arachnoid villi. This would be consistent with studies showing the frequent finding of elevated sagittal sinus pressure.

Evidence for each mechanism has been documented in the literature. Radioisotope cisternography has demonstrated a 3- to 5-fold decrease in CSF absorption. Although controversial, histologic evidence of vasogenic brain edema has been observed in brain biopsy specimens from a small number of patients. Increased intracranial blood volume also has been shown in several studies. Malm et al provided a long-term study of CSF dynamics in 17 patients older than 15 years using a constant pressure infusion method. The authors concluded that these patients had evidence of reduced conductance to CSF flow; however, it was insufficient to explain the increase in CSF pressure. No significant difference in rate of CSF production was noted between patients with PTC and controls. They also found that sagittal sinus pressure was elevated in over half of their patients, which was attributed to increased brain water content causing compression of venous outflow.

Hormonal influences appear to play some role in the pathogenesis of PTC. In postpuberal patients, the condition is distinctly more common among females. Obesity is a well-recognized risk factor.

Studies have suggested a relationship with nonspecific infections, minor head injury, withdrawal from cortical steroid therapy, vitamin A, acne treatment, and certain antibiotics (tetracyclines). On rare occasion, severe iron deficiency anemia, endocrinopathies, and CO2 retention have been implicated.

Frequency

United States

Epidemiologic studies in children are not available. The annual incidence among all adults in the United States appears to be 0.9 per 100,000; 3.5 per 100,000 females; and 13-19 per 100,000 obese females.

International

  • 1.7 per 100,000 incidence in Libya
  • 3.5 per 100,000 incidence in adult women

Mortality/Morbidity

  • Mortality rate associated with PTC is no higher than in the general population.
  • The only major morbidity is visual loss. The incidence of visual loss among children with PTC is unknown. Among all patients some degree a permanent visual loss can be seen in approximately 10% of all cases.

Sex

A strong predilection exists for women after puberty.

Age

PTC is most common among women of childbearing age. PTC has been reported in early infancy. Typically, a specific cause can be identified among young children.



History

Common signs and symptoms of PTC in the young include headache, vomiting, blurred vision, and diplopia.

  • Headaches are intermittent, diffuse, worse at night, may awaken the child, and often aggravated by sudden movement.
  • Visual disturbances include visual obscurations, blurred vision, double vision, and photophobia. Diplopia is almost always horizontal (side by side) and is secondary to paresis of the sixth cranial nerve. It has been estimated that up to 50% of children with PTC have sixth cranial nerve dysfunction.
  • Other signs of increased intracranial pressure include lethargy, irritability, and vomiting.
  • Nonspecific associated symptoms include neck stiffness, tinnitus, dizziness, clumsiness, and paresthesias.

Physical

  • The neurologic examination is typically normal with the exception of papilledema and weakness of one or both of the abducens nerves.
  • Other cranial nerve palsies have been reported on rare occasion.
  • General medical examination may reveal signs of otitis media or mastoiditis and therefore raise the possibility of venous sinus thrombosis. The presence of acne vulgaris should prompt on inquiry about the possible use of retinoic acid or tetracyclines. Physical findings of adrenal or thyroid dysfunction may also be present.
  • Papilledema: Funduscopic examination reveals optic disk nerve swelling (papilledema). Diagnosis should not be made in the absence of papilledema unless the patient has optic atrophy. Papilledema is typically bilateral but may be asymmetrical or unilateral. Visual acuity is usually preserved helping one to distinguish acute papilledema from optic neuritis.

Causes

Many conditions are associated with PTC in children, none of which are convincingly causative, with the exception of medications.

  • Following medications may be associated with PTC:
    • Retinoic acid
    • Antibiotics - Tetracycline, nitrofurantoin, fluoroquinolones
    • Hormones - Steroid use or withdrawal (even topical use), oral contraceptives, L-thyroxine
    • Vitamin A
    • Lithium
    • Immunizations - In one case report, development of PTC in a 7-month-old following DTP immunization
  • Refeeding and weight gain in nutritionally deprived children (eg, cystic fibrosis)
  • Endocrine abnormalities: These include adrenal dysfunction and Addison disease, hypothyroidism or hyperthyroidism, hypocalcemia due to vitamin D deficiency or hypoparathyroidism, and panhypopituitarism.



Arteriovenous Malformations
Aseptic Meningitis
Cavernous Sinus Syndromes
Cerebral Aneurysms
Cerebral Venous Thrombosis
Childhood Migraine Variants
Headache: Pediatric Perspective
Hydrocephalus
Medulloblastoma
Migraine Headache
Migraine Headache: Pediatric Perspective

Other Problems to be Considered

Abducens (CN VI) nerve palsy



Lab Studies

  • Diagnosis of PTC is made after exclusion of other causes of increased intracranial pressure such as mass lesions, particularly involving the midline (medulloblastoma), and causes of recurrent or chronic headache such as migraine and hydrocephalus.
  • Laboratory studies should include a workup for underlying endocrine abnormalities, if indicated by a thorough history and physical examination.

Imaging Studies

  • Brain imaging: MRI of the brain with MR venogram (MRV) is preferred. In children, CT scan of the head should be avoided when possible to minimize radiation exposure. The addition of MRV should enable one to exclude thrombosis of one of the major venous sinuses. Stenosis of the transverse sinus is a common finding in PTC but is probably the result of increased intracranial pressure. The MRI of the brain is normal but may show relatively small ventricles.
  • Brain imaging should be obtained prior to performing a diagnostic lumbar puncture. Careful measurements of opening and closing pressures should be obtained.

Other Tests

  • Assessment of the visual system
    • Visual field testing
    • Visual acuity assessment
  • Serial photographs of the fundus may be taken for follow-up.

Procedures

  • Lumbar puncture
    • Performing lumbar puncture (LP) in children can be challenging and difficult; sedation may be required. CSF pressure may be elevated falsely in the crying child. Also, no consensus exists on what constitutes the upper limit of normal for different age groups. In their review, Soler et al gave the following values:
      • 0-2 years - 75 mm H2O
      • 2-5 years - 135 mm H2O
    • Other sources cite the upper limit of normal in children as 200 mm H2O.
    • Diurnal variations in CSF pressure are seen; therefore, the pressure measured at any given time may not reflect the peaks. CSF pressure may be normal in patients with florid papilledema. If the diagnosis of PTC is suspected, then repeat LP or prolonged pressure monitoring (ie, Camino catheter or lumbar pressure catheter) should be considered.
    • The diagnosis of PTC requires that the CSF be of normal composition (ie, cell count, protein, glucose).



Medical Care

Sometimes, the symptoms of PTC resolve with the initial "diagnostic" LP. If this occurs no further medical treatment is required. Acetazolamide and steroids are the mainstays of the medical treatment of PTC.

  • Acetazolamide is administered in initial doses of 25 mg/kg/day and the dose titrated upward until clinical response is attained (maximum dose 100 mg/kg/day). Electrolytes must be monitored to evaluate for the development of hypokalemia and acidosis. If the patient remains on treatment for more than 6 months, renal ultrasound should be ordered to look for the presence of renal calculi.
  • If acetazolamide is ineffective then prednisone can be given at a dose of 2 mg/kg/day for 2 weeks followed by a 2-week taper.
  • A low-salt diet and weight reduction has been shown to be helpful in adult patients. If the child is obese, weight reduction may be beneficial.
  • The authors have had some anecdotal experience of a dramatic response with topiramate in adults with PTC. Topiramate functions as a carbonic anhydrase (CA) inhibitor and has proven to be efficacious in the treatment of headache. This medication may prove to be useful is selected children with PTC.
  • Repeat LP may help in some patients but its invasiveness and difficulty in children make it a less than ideal medical therapy. Reduction in pressures is transient.

Surgical Care

Indications for surgical intervention in the treatment of PTC are severe deterioration in vision and incapacitating headaches despite aggressive medical management. Two surgical procedures, lumboperitoneal shunting (LPS) and optic nerve sheath fenestration (ONSF), have a place in the treatment of PTC.

  • Lumboperitoneal shunting
    • LPS may relieve headache and reduce ICP in patients with PTC.
    • The long-term visual outcome of patients treated with LPS is unknown.
    • Complications of LPS include infection and shunt obstruction. Low-pressure headaches have also been reported to develop as a result of LPS.
  • Optic nerve sheath fenestration
    • ONSF has been shown to improve visual outcome.
    • ONSF has a better outcome in the patient with acutely decompensating vision and papilledema. The authors prefer optic nerve fenestration to a lumboperitoneal shunting.

Consultations

  • Neuro-ophthalmology
  • Pediatric neurology

Diet

Low-salt diet and weight loss may be beneficial. The authors' experience suggests that weight loss is difficult to achieve in the overweight adolescent.



Medications used in the treatment of PTC include acetazolamide and steroids.

Drug Category: Carbonic anhydrase inhibitors

CA is an enzyme found in many tissues of the body, including the eye. These agents catalyze a reversible reaction in which carbon dioxide becomes hydrated and CA dehydrated.

Drug NameAcetazolamide (Diamox, Diamox sequels)
DescriptionFirst-line drug for treatment of PTC.
Adult Dose500-4000 mg/d PO bid/tid
Pediatric Dose25-100 mg/kg/d PO; not to exceed 2 g/d
ContraindicationsDocumented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction; preexisting hypokalemia or hyponatremia; chronic noncongestive angle-closure glaucoma
InteractionsCan decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsPatients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients

Drug Category: Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Drug NamePrednisone (Deltasone, Sterapred, Orasone)
DescriptionIf acetazolamide fails to relieve symptoms of PTC, then steroids may be tried. Experience with this medication in treatment of pediatric PTC has shown that short-term use (1 month) is safe and effective.
Adult Dose60-100 mg/d PO
Pediatric Dose2 mg/kg/d PO for 2 wk; follow by 2-wk taper
ContraindicationsDocumented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease
InteractionsEstrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsAbrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur



Further Outpatient Care

  • Neuro-ophthalmology follow-up with frequent assessment of visual fields is indicated.

In/Out Patient Meds

Complications

  • As mentioned above, the most serious complication is permanent visual loss and blindness.

Prognosis

  • The natural history of PTC in childhood is poorly understood.
  • Some children respond to initial LP alone.
  • Visual loss can occur at any point in the disease and no reliable predictive factors are associated with this complication.

Patient Education

  • Patient and parental education as to the seriousness of permanent visual loss should be given. Early intervention in rapidly declining visual function is crucial to improve the long-term visual outcome.



  • Alexandrakis G, Filatov V, Walsh T. Pseudotumor cerebri in a 12-year-old boy with Addison''s disease [letter]. Am J Ophthalmol. Nov 15 1993;116(5):650-1. [Medline].
  • Alpan G, Glick B, Peleg O. Pseudotumor cerebri and coma in vitamin D--dependent rickets. Clin Pediatr (Phila). Apr 1991;30(4):254-6. [Medline].
  • Anonymous. Benign intracranial hypertension. Br Med J. Sep 5 1970;3(722):536-7. [Medline].
  • Baker RS, Carter D, Hendrick EB. Visual loss in pseudotumor cerebri of childhood. A follow-up study. Arch Ophthalmol. Nov 1985;103(11):1681-6. [Medline].
  • Baker RS, Baumann RJ, Buncic JR. Idiopathic intracranial hypertension (pseudotumor cerebri) in pediatric patients. Pediatr Neurol. Jan-Feb 1989;5(1):5-11. [Medline].
  • Barry W, Lenney W, Hatcher G. Bulging fontanelles in infants without meningitis [letter]. Arch Dis Child. Apr 1989;64(4):635-6. [Medline].
  • Boddie HG, Banna M, Bradley WG. "Benign" intracranial hypertension. A survey of the clinical and radiological features, and long-term prognosis. Brain. Jun 1974;97(2):313-26. [Medline].
  • Burgett RA, Purvin VA, Kawasaki A. Lumboperitoneal shunting for pseudotumor cerebri. Neurology. Sep 1997;49(3):734-9. [Medline].
  • Campos SP, Olitsky S. Idiopathic intracranial hypertension after L-thyroxine therapy for acquired primary hypothyroidism. Clin Pediatr (Phila). Jun 1995;34(6):334-7. [Medline].
  • Chiu AM, Chuenkongkaew WL, Cornblath WT. Minocycline treatment and pseudotumor cerebri syndrome. Am J Ophthalmol. Jul 1998;126(1):116-21. [Medline].
  • Cinciripini GS, Donahue S, Borchert MS. Idiopathic intracranial hypertension in prepubertal pediatric patients: characteristics, treatment, and outcome. Am J Ophthalmol. Feb 1999;127(2):178-82. [Medline].
  • Cohen DN. Intracranial hypertension and papilledema associated with nalidixic acid therapy. Am J Ophthalmol. Nov 1973;76(5):680-2. [Medline].
  • Corbett JJ, Nerad JA, Tse DT. Results of optic nerve sheath fenestration for pseudotumor cerebri. The lateral orbitotomy approach. Arch Ophthalmol. Oct 1988;106(10):1391-7. [Medline].
  • Corbett JJ, Digre K. Idiopathic intracranial hypertension: an answer to, "the chicken or the egg?". Neurology. Jan 8 2002;58(1):5-6. [Medline].
  • Costigan DC, Daneman D, Harwood-Nash D. The "empty sella" in childhood. Clin Pediatr (Phila). Aug 1984;23(8):437-40. [Medline].
  • Cruz OA, Fogg SG, Roper-Hall G. Pseudotumor cerebri associated with cyclosporine use. Am J Ophthalmol. Sep 1996;122(3):436-7. [Medline].
  • Di Liberti J, O''Brien ML. Letter: Pseudotumor cerebri following patent ductus arteriosus ligation. J Pediatr. Sep 1975;87(3):489. [Medline].
  • Durcan FJ, Corbett JJ, Wall M. The incidence of pseudotumor cerebri. Population studies in Iowa and Louisiana. Arch Neurol. Aug 1988;45(8):875-7. [Medline].
  • Eggenberger ER, Miller NR, Vitale S. Lumboperitoneal shunt for the treatment of pseudotumor cerebri. Neurology. Jun 1996;46(6):1524-30. [Medline].
  • Farb RI, Vanek I, Scott JN, et al. Idiopathic intracranial hypertension. The prevalence and morphology of sinovenous stenosis. Neurology. 2002;58:26-30.
  • Giles CL, Soble AR. Intracranial hypertension and tetracycline therapy. Am J Ophthalmol. Nov 1971;72(5):981-2. [Medline].
  • Giuseffi V, Wall M, Siegel PZ. Symptoms and disease associations in idiopathic intracranial hypertension (pseudotumor cerebri): a case-control study. Neurology. Feb 1991;41(2 ( Pt 1)):239-44. [Medline].
  • Grabb PA, Albright AL, Zitelli BJ. Multiple suture synostosis, macrocephaly, and intracranial hypertension in a child with alpha-D-mannosidase deficiency. Case report. J Neurosurg. Apr 1995;82(4):647-9. [Medline].
  • Grant DN. Benign intracranial hypertension. A review of 79 cases in infancy and childhood. Arch Dis Child. Oct 1971;46(249):651-5. [Medline].
  • Gross TP, Milstien JB, Kuritsky JN. Bulging fontanelle after immunization with diphtheria-tetanus-pertussis vaccine and diphtheria-tetanus vaccine. J Pediatr. Mar 1989;114(3):423-5. [Medline].
  • Gucer G, Viernstein L. Long-term intracranial pressure recording in the management of pseudotumor cerebri. J Neurosurg. Aug 1978;49(2):256-63. [Medline].
  • Guertin SR, Levinsohn MW, Dahms BB. Small-droplet steatosis and intracranial hypertension in argininosuccinic lyase deficiency. J Pediatr. May 1983;102(5):736-40. [Medline].
  • Hosking GP, Elliston H. Benign intracranial hypertension in a child with eczema treated with topical steroids. Br Med J. Mar 4 1978;1(6112):550-1. [Medline].
  • Ireland B, Corbett JJ, Wallace RB. The search for causes of idiopathic intracranial hypertension. A preliminary case-control study. Arch Neurol. Mar 1990;47(3):315-20. [Medline].
  • Isaacman DJ. Otitic hydrocephalus: an uncommon complication of a common condition. Ann Emerg Med. Jun 1989;18(6):684-7. [Medline].
  • Jacob J, Mannino F. Increased intracranial pressure after diphtheria, tetanus, and pertussis immunization. Am J Dis Child. Feb 1979;133(2):217-8. [Medline].
  • Jay WM, Jay S. Benign intracranial hypertension with tetracycline therapy [letter]. J Pediatr. Nov 1978;93(5):901-2. [Medline].
  • Johnston I, Hawke S, Halmagyi M. The pseudotumor syndrome. Disorders of cerebrospinal fluid circulation causing intracranial hypertension without ventriculomegaly. Arch Neurol. Jul 1991;48(7):740-7. [Medline].
  • Johnston I, Paterson A. Benign intracranial hypertension. II. CSF pressure and circulation. Brain. Jun 1974;97(2):301-12. [Medline].
  • Johnston I, Paterson A. Benign intracranial hypertension. I. Diagnosis and prognosis. Brain. Jun 1974;97(2):289-300. [Medline].
  • Johnston I, Besser M, Morgan MK. Cerebrospinal fluid diversion in the treatment of benign intracranial hypertension. J Neurosurg. Aug 1988;69(2):195-202. [Medline].
  • Karahalios DG, Rekate HL, Khayata MH. Elevated intracranial venous pressure as a universal mechanism in pseudotumor cerebri of varying etiologies. Neurology. Jan 1996;46(1):198-202. [Medline].
  • Kidron D, Pomeranz S. Malignant pseudotumor cerebri. Report of two cases. J Neurosurg. Sep 1989;71(3):443-5. [Medline].
  • Kundu M, Basu J, Rakshit MM. Abnormalities in erythrocyte membrane band 3 in chronic myelogenous leukemia. Biochim Biophys Acta. Oct 2 1989;985(1):97-100. [Medline].
  • Lascari AD, Bell WE. Pseudotumor cerebri due to hypervitaminosis A. Toxic consequence of self-medication for acne in an adolescent girl. Clin Pediatr (Phila). Oct 1970;9(10):627-8. [Medline].
  • Lessell S, Rosman NP. Permanent visual impairment in childhood pseudotumor cerebri. Arch Neurol. Aug 1986;43(8):801-4. [Medline].
  • Litman N, Kanter AI, Finberg L. Galactokinase deficiency presenting as pseudotumor cerebri. J Pediatr. Mar 1975;86(3):410-2. [Medline].
  • Liu GT, Kay MD, Bienfang DC. Pseudotumor cerebri associated with corticosteroid withdrawal in inflammatory bowel disease. Am J Ophthalmol. Mar 15 1994;117(3):352-7. [Medline].
  • Liu GT, Glaser JS, Schatz NJ. High-dose methylprednisolone and acetazolamide for visual loss in pseudotumor cerebri. Am J Ophthalmol. Jul 15 1994;118(1):88-96. [Medline].
  • Malozowski S, Tanner LA, Wysowski DK. Benign intracranial hypertension in children with growth hormone deficiency treated with growth hormone. J Pediatr. Jun 1995;126(6):996-9. [Medline].
  • Mann NP, McLellan NJ, Cartlidge PH. Transient intracranial hypertension of infancy. Arch Dis Child. Aug 1988;63(8):966-8. [Medline].
  • Neville BG, Wilson J. Benign intracranial hypertension following corticosteroid withdrawal in childhood. Br Med J. Sep 5 1970;3(722):554-6. [Medline].
  • Olivier C, Rettori R, Baur O. [Orthotopic homotransplantation of the small intestine and of the right and transverse colon in man]. J Chir (Paris). Oct 1969;98(4):323-30. [Medline].
  • Pasquariello PS Jr, Schut L, Borns P. Benign increased intracranial hypertension due to chronic vitamin A overdosage in a 26-month-old child. The increased intracranial pressure subsided promptly with steroid therapy and cessation of vitamin A. Clin Pediatr (Phila). Apr 1977;16(4):379-82. [Medline].
  • Portnoy HD, Croissant PD. Megalencephaly in infants and children. The possible role of increased dural sinus pressure. Arch Neurol. May 1978;35(5):306-16. [Medline].
  • Radhakrishnan K, Ahlskog JE, Cross SA. Idiopathic intracranial hypertension (pseudotumor cerebri). Descriptive epidemiology in Rochester, Minn, 1976 to 1990. Arch Neurol. Jan 1993;50(1):78-80. [Medline].
  • Radhakrishnan K, Ahlskog JE, Garrity JA. Idiopathic intracranial hypertension. Mayo Clin Proc. Feb 1994;69(2):169-80. [Medline].
  • Raghavan S, DiMartino-Nardi J, Saenger P. Pseudotumor cerebri in an infant after L-thyroxine therapy for transient neonatal hypothyroidism. J Pediatr. Mar 1997;130(3):478-80. [Medline].
  • Roach ES, Sinal SH. Initial treatment of cystic fibrosis. Frequency of transient bulging fontanel. Clin Pediatr (Phila). Aug 1989;28(8):371-3. [Medline].
  • Rothner AD, Brust JC. Pseudotumor cerebri. Report of a familial occurrence. Arch Neurol. Jan 1974;30(1):110-1. [Medline].
  • Roussounis SH. Benign intracranial hypertension after withdrawal of topical steriods in an infant. Br Med J. Sep 4 1976;2(6035):564. [Medline].
  • Scott IU, Siatkowski RM, Eneyni M. Idiopathic intracranial hypertension in children and adolescents. ALYSIS. Aug 1997;124(2):253-5. [Medline].
  • Sergott RC, Savino PJ, Bosley TM. Modified optic nerve sheath decompression provides long-term visual improvement for pseudotumor cerebri. Arch Ophthalmol. Oct 1988;106(10):1384-90. [Medline].
  • Sharma DB, James A. Letter: Benign intracranial hypertension associated with nitrofurantoin therapy. Br Med J. Dec 28 1974;4(5947):771. [Medline].
  • Sklar FH, Beyer CW Jr, Clark WK. Physiological features of the pressure-volume function of brain elasticity in man. J Neurosurg. Aug 1980;53(2):166-72. [Medline].
  • Soelberg Sorensen P, Gjerris F, Svenstrup B. Endocrine studies in patients with pseudotumor cerebri. Estrogen levels in blood and cerebrospinal fluid. Arch Neurol. Sep 1986;43(9):902-6. [Medline].
  • Soler D, Cox T, Bullock P. Diagnosis and management of benign intracranial hypertension. Arch Dis Child. Jan 1998;78(1):89-94. [Medline].
  • Speer C, Pearlman J, Phillips PH. Fourth cranial nerve palsy in pediatric patients with pseudotumor cerebri. Am J Ophthalmol. Feb 1999;127(2):236-7. [Medline].
  • Spoor TC, McHenry JG. Long-term effectiveness of optic nerve sheath decompression for pseudotumor cerebri. Arch Ophthalmol. May 1993;111(5):632-5. [Medline].
  • Spoor TC, Ramocki JM, Madion MP. Treatment of pseudotumor cerebri by primary and secondary optic nerve sheath decompression. Am J Ophthalmol. Aug 15 1991;112(2):177-85. [Medline].
  • Stuart BH, Litt IF. Tetracycline-associated intracranial hypertension in an adolescent: a complication of systemic acne therapy. J Pediatr. Apr 1978;92(4):679-80. [Medline].
  • Sugerman HJ, Felton WL 3rd, Sismanis A. Gastric surgery for pseudotumor cerebri associated with severe obesity. Ann Surg. May 1999;229(5):634-40; discussion 640-2. [Medline].
  • Wall M. Idiopathic intracranial hypertension. Neurol Clin. Feb 1991;9(1):73-95. [Medline].
  • Winrow AP, Supramaniam G. Benign intracranial hypertension after ciprofloxacin administration. Arch Dis Child. Oct 1990;65(10):1165-6. [Medline].
  • Ziai M, Abassioum K. Intracranial hypertension, papilledema, and normal neurologic investigations. Clin Pediatr (Phila). Nov 1973;12(11):30A-31A. [Medline].
  • ePocrates. '. 1999-2000;Editor-in-Chief Thomas H. Lee, MD:[Full Text].

Pseudotumor Cerebri: Pediatric Perspective excerpt

Article Last Updated: Jul 19, 2006