In this article, several classes of commonly prescribed drugs for the treatment of low back pain will be considered. For each agent or group of agents considered, mechanisms of action, efficacy and current clinical research, dosing and cost, and complications and contraindications will be discussed.

Acetaminophen (Tylenol®) is the principle member of the group of drugs classified as para-aminophenol derivatives. While acetaminophen's analgesic and antipyretic (fever reducing) effects are equal to those of aspirin, its anti-inflammatory effects are weak. Its therapeutic effects appear to be secondary to an inhibition of prostaglandin (mediators of inflammation) biosynthesis with a resultant increase in the pain threshold and modulation of the hypothalamic heat-regulating center (a part of the brain that activates part of the nervous system).

The primary mechanism of action in NSAIDs is a reduction of cyclooxygenase (enzymes that make prostaglandins) activity and a resultant decrease in prostaglandin synthesis. Prostaglandins are active mediators of the inflammatory cascade, which also serve to sensitize peripheral nociceptors (nerve endings). A reduction in their local concentration could therefore explain the combined anti-inflammatory and analgesic properties of NSAIDs.

The muscle relaxing properties of "muscle relaxants" arise not from direct activity at the muscular or neuromuscular junction level but rather from an inhibition of more central polysynaptic neuronal (nerve cells that end in synapses) events. These agents have also been shown in some studies to demonstrate superior analgesia to either acetaminophen or aspirin, and it remains uncertain if muscle spasm is a prerequisite to their effectiveness as analgesics.

Opioids occupy the second rung on the World Health Organization (WHO) analgesic ladder in the treatment of moderate to severe cancer pain and are commonly prescribed for postoperative pain, where they have been found to successfully treat both local and more generalized pain symptoms.

Colchicine has been regarded by some as the most powerful anti-inflammatory agent known to man. The beneficial effects of colchicine in the treatment of gout are apparently secondary to its ability to inhibit both the metabolic and phagocytic activity and migration of granulocytes. Colchicine's inhibition of the release of histamine containing granules from mast cells is also believed secondary to its interference with granule transportation by the microtubular system.

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