Exposure of neural tissue to excessive amounts of benzyl alcohol has been associated with toxicity and in rare events has resulted in death. Adverse reactions
Adverse reactions may overshadow the therapeutic effects of methylprednisolone. Central nervous system
There is minimal clinical diagnostic criteria to define the psychic adverse effects (PAE) associated with methylprednisolone use in patients with systemic lupus erythematosus (SLE). The  prevalence varies from 1.3 to 62% of adult treated patients. The type and severity of neuropsychiatric symptoms also varies significantly between patients, with 33% of patients reporting mild to moderate PAE and 5-10% reporting severe PAE. Methylprednisolone dose and duration have been implicated in PAE development. 20 mg/day of prednisone (16 mg/day of methylprednisolone) is the threshold dosage for PAE development agreed upon by many studies. Short-term pulse IV therapy at high doses is associated with rapid onset of manic and hypomanic symptoms, whereas long term therapy gives rise to depressive symptoms (suicide attempts infrequent). PAE are reversible with treatment reduction or discontinuation. Metabolic and endocrine
Iatrogenic Cushings Syndrome is a direct complication of glucocorticoid therapy, and the most common cause of exogenous Cushings Syndrome. Clinical features of Cushings Syndrome is inclusive of many adverse effects in glucocorticoid therapy. Traditional symptoms include weight gain, myopathy, osteoporosis, increased risk of infection, hypertension and psychological effect. Fat deposition is centralized on the trunk, in between shoulders ("buffalo hump"), and on the face ("moon face"). Patient education and provider monitoring is the first step in recognizing and diagnosing Iatrogenic Cushings Syndrome.
This association changes physiochemical properties of the membrane; activating membrane proteins, altering cellular functions and ultimately influencing cation transport through the plasma membrane and stimulating the proton leak across the inner mitochondrial membrane. Hindered oxidative phosphorylation compromises ATP production, a major energy source for cellular energy metabolism and immune function. In vivo studies of Con-A stimulated thymocytes (in rats) and human immune cells that were administered high doses of methylprednisolone has been shown to inhibit respiration in a dose-dependent manner, inhibit plasma calcium and sodium uptake, and increase cytoplasmic calcium concentration. The summative process is as follows: Methylprednisolone intercalates in the plasma membrane, causes physiochemical changes, activates membrane proteins that inhibit plasma calcium and sodium uptake (mimicking an energy deficit state). ATP consumption drops (resembled by inhibited respiration), resulting in protein permeability at the inner mitochondrial membrane and uncoupling of oxidative phosphorylation. Of notable importance, DNA/RNA synthesis was not hindered. The dependency of house keeping cells and immune cells on ATP, results in immunosuppression during ATP deficit. Specific immune functions effected by this process are cytokinesis, migration, phagocytosis, antigen processing and presenting, antibody synthesis, cytotoxicity and regulation. The HPA axis
The activation of the hypothalamic-pituitary axis (HPA axis) stimulates the production of endogenous glucocorticoids within the adrenal cortex. The HPA axis interprets stimuli (stress, inflammation and circadian cues) and transduces a corresponding physiochemical response. Glucocorticoids released in the blood, serve as a messenger by binding to glucocorticoid receptors in a wide distribution across the body, including the HPA axis itself.