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Drug-Induced Intracranial Hypertension

  • Background:
    • Drug-induced intracranial hypertension is a condition characterized by increased intracranial pressure presenting as an adverse drug reaction.
    • Drugs most commonly associated with intracranial hypertension include vitamin A (at doses >25,000 IU daily) and related compounds (such as isotretinoin and all-trans retinoic acid), tetracycline-class antibiotics, recombinant growth hormone, and lithium.
  • Clinical Presentation:
    • Signs of increased intracranial pressure, including persistent headache, visual disturbances, and pulse-synchronous tinnitus, after initiation of therapy with vitamin A derivatives or other suspected drugs
  • Key Diagnostic Features:
    • Prominent subarachnoid spaces around the optic nerves, flattening of the posterior sclera, intraocular protrusion of the optic nerve, optic nerve tortuosity, partially empty sella turcica, bilateral transverse sinus stenosis
  • Differential Diagnoses:
    • Idiopathic intracranial hypertension: Identical imaging appearances without exposure to predisposing therapeutics
    • Venous sinus thrombosis: Unenhanced CT demonstrates hyperdensity of the involved sinus; sinus filling defect after contrast administration
    • Hypoplastic dural venous sinuses: Usually unilateral, with consensual reduction of the size of the jugular foramen
    • Extracranial venous outflow obstruction: Demonstrated by neck CT or MRI
    • Medical conditions associated with intracranial hypertension: Identical imaging findings in the context of Addison disease and sleep apnea, among others
    • Arteriovenous fistula: Typical findings include abnormally enlarged vessels in the subarachnoid space and enlarged transosseous vessels
    • Decreased CSF absorption from prior infectious meningitis: Previous leptomeningeal enhancement and increased FLAIR signal in the CSF spaces
    • Subarachnoid hemorrhage: Associated with superficial hemosiderin deposition demonstrated by gradient-echo and SWI sequences
  • Treatment:
    • Discontinuation of the inciting drug, therapeutic lumbar puncture, and acetazolamide therapy
February 18, 2021

A 27-year-old woman with promyelocytic leukemia presenting with headache and diplopia after all-trans retinoic acid (ATRA) therapy (top row). Follow-up 20 days later after discontinuation of ATRA, lumbar puncture, and acetazolamide therapy, with complete remission of symptoms (bottom row).

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