Large IHs can leave visible skin changes secondary to significant stretching of the skin or alteration of surface texture. When they interfere with vision, breathing, or threaten significant disfigurement (most notably facial lesions, and in particular, nose and lips), they are usually treated. Medical therapies are most effective when used during the period of most significant hemangioma growth, which corresponds to the first 5 months of life. Ulcerated hemangiomas, a subset of lesions requiring therapy, are usually treated by addressing wound care, pain, and hemangioma growth. Medication
Treatment options for IHs include medical therapies (systemic, intralesional, and topical), surgery, and laser therapy. Prior to 2008, the mainstay of therapy for problematic hemangiomas was oral corticosteroids, which are effective and remain an option for patients in whom beta-blocker therapy is contraindicated or poorly tolerated. Following the serendipitous observation that propranolol, a nonselective beta blocker, is well tolerated and effective for treatment of hemangiomas, the agent was studied in a large, randomized, controlled trial and was approved by the U.S. Food and Drug Administration for this indication in 2014. Oral propranolol is more effective than placebo, observation without intervention, or oral corticosteroids. Propranolol has subsequently become the first-line systemic medical therapy for treatment of these lesions.Since that time, topical timolol maleate in addition to oral propranalol has become a common therapy for infantile hemangiomas. According to a 2018 Cochrane review, both of these therapies have demonstrated beneficial effects in terms of clearance of hemangiomas without an increase in harms.
It is inherited in an autosomal dominant manner, such that the child of a parent with the disease has a 50% chance of inheriting the condition, if the parent is heterozygotic. However, most cases arise de novo as the result of sporadic mutations.Alexander disease belongs to leukodystrophies, a group of diseases that affect the growth or development of the myelin sheath. The destruction of white matter in the brain is accompanied by the formation of fibrous, eosinophilic deposits known as Rosenthal fibers. Rosenthal fibers appear not to be present in healthy people, but occur in specific diseases, like some forms of cancer, Alzheimer’s, Parkinson’s, Huntington’s, and ALS. The Rosenthal fibers found in Alexander disease do not share the distribution or concentration of other diseases and disorders. Pathology
Alexander disease causes the gradual loss of bodily functions and the ability to talk. It also causes an overload of long-chain fatty acids in the brain, which destroy the myelin sheath. The cause of Alexander disease is a mutation in the gene encoding GFAP.A CT scan shows:

Decreased density of white matter
Frontal lobe predominance
Dilated lateral ventricles may present

Diagnosis
Detecting the signs of Alexander disease is possible with magnetic resonance imaging (MRI), which looks for specific changes in the brain that may be tell-tale signs for the disease. It is even possible to detect adult-onset Alexander disease with MRI. Alexander disease may also be revealed by genetic testing for its known cause.