Abstract
The thalidomide molecule is a remarkable molecule that exists in a racemic mixture of optical isomers. In the 1950s, due to its teratogenicity, the levorotatory isomer led to its dramatic downfall. However, the molecule with its panoramic mechanisms of action and its uncanny ability to intercalate within the geometry of deoxyribonucleic acid (DNA), led to its remarkable renaissance; thalidomide being United States Food and Drug Administration (FDA)-approved for at least 13 different indications ranging from multiple myeloma to leprosy to glioblastoma. Thalidomide-induced polyneuropathy is usually reversible and is the rate-limiting step in its long-term use. The development of a polyneuropathy is invariably associated with a cumulative dose exceeding 20 grams. However, the polyneuropathy is almost always a sensory neuropathy. Asymmetry, bona fide weakness such as difficulty standing on the heels, a poly-ganglioneuropathy pattern with widespread or patchy numbness and sensory ataxia should raise a red flag and an alternative diagnosis should be considered. We present a typical case of a thalidomide-induced sensory neuropathy in order to highlight the resurgence of thalidomide use in clinical practice. We review the literature and outline the molecular biology of the thalidomide molecule.