Neurological side effects of glucocorticosteroids are well described and may be as serious as the diseases being treated. Neuropsychiatric disorders and myopathy are common. Most of the neurological sequelae are often related to dosage and duration of therapy and may be reversible by modification of the drug regimen. y Glucocorticosteroid use can be associated with a broad spectrum of neuropsychiatric disorders, ranging from emotional lability and anxiety to confusion, mood disorders, and psychosis. Behavioral symptoms usually begin within 5 to 14 days of starting steroids, but they may also occur during withdrawal of therapy. With the exception of multiple sclerosis, pre-existing neurological disease does not appear to increase the risk of steroid-induced mental status abnormalities. Alternate-day steroid therapy may decrease the overall incidence of behavioral changes, although it may rarely induce a cyclic behavior, with mania occurring on high-dose days and depression occurring on low-dose days.

Steroid myopathy is probably the most common drug-related disorder of muscle. There are two forms of myopathy: a common, well-known, chronic form involving type II fiber atrophy, and a rare acute form that occurs during treatment for status asthmaticus and may be associated with rhabdomyolysis. The exact incidence of the more typical chronic myopathy is uncertain, but in one series of patients with rheumatic disease, it was reported to be 7 percent. y The syndrome consists of insidious onset of painless, symmetrical proximal muscle weakness and atrophy, with the lower extremities involved first. Bulbar muscles are spared, but the diaphragm may be involved. The time of onset is variable, and the symptoms may begin from several weeks to several months after beginning treatment. The serum creatinine kinase is normal and electromyography (EMG) reveals short-duration, low-amplitude motor unit action potentials. Muscle biopsy shows type II atrophy, and electron microscopy reveals glycogen accumulation and enlarged mitochondria. Treatment consists of tapering and discontinuing the offending agent or substituting another steroid. The uncommon acute myopathy has been reported mainly in asthmatic patients who are receiving IV steroids, paralytic agents, and mechanical ventilation. The pathogenesis is unclear. y

Steroid-induced deposition of fat in the epidural space occurs in patients taking more than 40 mg of prednisone for at least 4 months. Most of these patients are already cushingoid when consequent neurological symptoms occur. The earliest and commonest feature is low back pain, and depending on the level of the lipomatosis, signs of myelopathy, cauda equina syndrome, or radiculopathy may develop. MRI can be a very useful diagnostic tool. Fat appears to be hyperintense on T1 -weighted images and less intense on T2 -weighted images, in contrast with inflammatory processes, which are brighter on T2 -weighted images. Unless it is contraindicated, laminectomy has been the treatment of choice. Further studies are needed to clarify the response to steroid tapering without surgical decompression before the onset of significant myelopathy. There have been isolated reports of corticosteroid-induced lipomatosis in the perineural spaces of peripheral nerves, leading to entrapment neuropathies.y

Increased intracranial pressure has been associated with steroid use, and the vast majority of cases involve male children. No particular dose has been implicated, but the duration of treatment is usually prolonged. Symptom onset generally occurs after discontinuation, tapering, or change in the type of steroid. Signs and symptoms are consistent with elevated intracranial pressure: headache, nausea, vomiting, papilledema, and diplopia with abducens nerve palsy. The disorder is usually self-limited. Patients have improved after changing the type or dose of steroids (using lower or higher dose) or lumbar puncture. y

Glucocorticosteroids have been reported to enhance physiological tremor. Propranolol can be useful in controlling this movement disorder if steroid withdrawal is not possible. Intrathecal administration of glucocorticosteroids can be associated with sterile meningitis, arachnoiditis, and pachymeningitis. Epidural steroids can have the same complications because the epidural and subarachnoid spaces are not totally separate but communicate via arachnoid villi and epidural veins. Additionally, inadvertent sub-arachnoid injections occur during about 2.5 percent of epidural attempts. y

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