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Prednisone is a man-made “corticosteroid” drug that suppresses the adrenal glands. The adrenal glands are located on top of the kidneys and produce hormones that affect many bodily functions. Their major role is to release hormones in response to stress, and these include corticosteroids (cortisol-also called hydro-cortisone) and catecholamines (epinephrine or adrenaline and norepinephrine). The adrenals also produce male hormones called androgens and affect kidney function by releasing a hormone called aldosterone.
Prednisone is also particularly effective at suppressing the function of the immune system, and because of this is used to treat certain inflammatory diseases such as allergic reactions, inflammatory bowel diseases, some types of arthritis, multiple sclerosis, some types of childhood seizures and autoimmune diseases. It is also important as a supplemental therapy for treating chronic lung disease, some types of kidney disease and cancer. Although it has many uses in treating these conditions, prednisone has significant adverse effects from both short-term and long-term use.
Short-term side-effects from prednisone include high blood sugar (glucose) levels, fluid retention, headaches, acne, weight gain and increased blood pressure. Patients can experience insomnia, euphoria and, rarely, mania. The drug can also cause depressive symptoms and anxiety in some individuals.
Side-effects from long-term use include Cushing's syndrome, osteoporosis, glaucoma, cataracts, type II diabetes mellitus and GI bleeding. When prednisone is taken for longer than seven days, this signals the body that it does not need the adrenals to produce any more cortisol, and the ability to manufacture natural corticosteroids is lost. For this reason, prednisone is not abruptly stopped, but the dosage is gradually reduced to give the adrenal glands time to recover.
When prescribed in higher doses or for extended periods of time, prednisone suppresses the body's immune system as well as inflammation. However, because prednisone suppresses the immune system, it leaves patients more susceptible to infections.
Relationship to autism spectrum disorders (ASD):
Prednisone started to be used to treat some childhood epilepsies (seizures) in the 1970s (Jan et al, 1972; Snead et al, 1983), as it helped to reduce seizure frequency and normalize EEGs. In the 1980s, prednisone began to be used for treatment of seizures and abnormal EEGs in Landau-Kleffner Syndrome and Lennox-Gastaut syndrome, where its effects on speech recovery were noted (Lerman et al, 1991; Sinclair DB, 2003). Due to hope for reversal of language regression, some neurologists began using prednisone to treat autism spectrum disorders in the 1990s, even when no seizures or EEG abnormalities were noted. This, numerous hypotheses on the relationship of the immune system to the etiology of autism, and the finding of neuroinflammation in postmortem autism brain (Vargas et al, 2005) has continued to fuel the expectation that prednisone will develop into a treatment for autism. Currently there are no published or on-going randomized placebo-controlled trials of prednisone use in autism. This may be due to the many risks involved compared to unknown benefits.
To complicate matters, some practitioners have proposed the use of prednisone in ASD solely to decrease the immune activation noted in the Vargas et al study. Unfortunately the type of immune reaction noted in autism brain (innate immune system activation) is not affected by prednisone and other immuno-therapies, which generally target adaptive immune activation. For more information, the reader is referred to: Neuroimmunopathology Laboratory
For now, treatment of individuals with ASD with prednisone should be considered only as part of a randomized placebo-controlled trial.
1. Jan JE, Hill RH, Low MD. 1972 Cerebral complications in juvenile rheumatoid arthritis Can Med Assoc J 107: 623-625.
2. Snead OC 3rd, Benton JW, Myers GJ. 1983 ACTH and prednisone in childhood seizure disorders Neurology 33: 966-970.
3. Lerman P, Lerman-Sagie T, Kivity S. 1991 Effect of early corticosteroid therapy for Landau-Kleffner syndrome Dev Med Child Neurol 33: 257-260.
4. Sinclair DB. 2003 Prednisone therapy in pediatric epilepsy Pediatr Neurol 28: 194-198.
5. Vargas DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo CA. 2005 Neuroglial activation and neuroinflammation in the brain of patients with autism Ann Neurol 57: 67-81.
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