History
Gabapentin was designed by researchers at Parke-Davis to be an analogue of the neurotransmitter GABA that could more easily cross the blood–brain barrier and was first described in 1975 by Satzinger and Hartenstein. Under the brand name Neurontin, it was first approved in May 1993, for the treatment of epilepsy in the United Kingdom. Approval by the U.S. Food and Drug Administration followed in December 1993, for use as an adjuvant (effective when added to other antiseizure drugs) medication to control partial seizures in adults; that indication was extended to children in 2000. Subsequently, gabapentin was approved in the United States for the treatment of postherpetic neuralgia in 2002. A generic version of gabapentin first became available in the United States in 2004. An extended-release formulation of gabapentin for once-daily administration, under the brand name Gralise, was approved in the United States for the treatment postherpetic neuralgia in January 2011. Society and culture
Legal status
United Kingdom
Effective April 2019, the United Kingdom reclassified the drug as a class C controlled substance. United States
Effective 1 July 2017, Kentucky classified gabapentin as a schedule V controlled substance statewide. Effective 9 January 2019, Michigan also classified gabapentin as a schedule V controlled substance. Gabapentin is scheduled V drug in other states such as West Virginia, Tennessee, Alabama. Off-label promotion
Although some small, non-controlled studies in the 1990s—mostly sponsored by gabapentins manufacturer—suggested that treatment for bipolar disorder with gabapentin may be promising, the preponderance of evidence suggests that it is not effective.
SHP-2 plays an important role in regulating expression of the Indian Hedgehog gene (IHH),  which is associated with differentiation in chondrocytes (specialized cells in cartilage tissue). Individuals affected by metachondromatosis generally demonstrate high levels of IHH expression, which is believed to be responsible for the tumor growth. Given that the mutation causes a loss of protein function and displays a dominant inheritance pattern, it is hypothesized that individuals homozygous for the disorder would display greater symptoms than heterozygous individuals, though insufficient data is available to evaluate these claims due to the rarity of the disease. Conversely, some heterozygous individuals have shown minimal effects, leading to the disorder’s designation as incompletely penetrant. The cause of this is not fully understood, but may be due to other factors influencing IHH expression. Diagnosis
Because of its rarity, metachondromatosis is often a difficult disease to recognize and diagnose. Diagnosis can be made based on clinical observations and radiographic findings as well as family history. Using radiographic methods, osteochondromas can be seen at the metaphyses of the short tubular bones, such as those in the hands and feet, pointing towards the joints. Enchondromas would also be visible along with the osteochondromas. The differential diagnosis includes hereditary multiple osteochondromas. This is a condition in which the long bones are primarily affected, and the lesions point away from the joint or growth plate. This may also result in the shortening or deformity of the affected bones. Since metachondromatosis is hereditary, genetic counseling can be offered to patients and their families.