Kernig's Sign

By A. Kozhevnikov · Neurology, Infectious Diseases

Also known as: Kernig sign

Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.

Summary

Kernig's sign, described in 1883, is the inability to fully extend the lower extremities at the knee joints when they are flexed at the hip joints. It is a key diagnostic sign of cerebrospinal meningitis and other conditions involving irritation of the brain meninges. The 1930s article discusses its clinical elicitation, historical context, and various theories of its pathogenesis, including reflex tonic muscle contraction.

Encyclopedia article (1928–1936)

KERNIG'S SIGN, established by the author in 1883, consists in the inability to fully extend the lower extremities at the knee joints when the extremities are flexed at the hip joints (see figure). It is observed in cerebrospinal meningitis due to the reflex tonic contraction of the muscles that flex the lower leg. Conversely, when the leg is extended at the knee joint, flexion at the hip joint is impossible; when an attempt is made to do this in a patient lying on their back, the leg flexes at the knee joint; whereas if the leg is flexed at the hip joint, it cannot be extended at the knee. As a result, patients with cerebrospinal meningitis cannot sit on a bed with outstretched legs; when attempting to sit up, their legs reflexively enter a semi-flexed state at the knee joints. According to some authors, Kernig's sign depends not only on the pain sensations caused by the extension of the leg, but also on

Kernig's Sign: figure 1 from the 1928–1936 encyclopedia article

Method for eliciting Kernig's sign.

reflex spasmodic contracture of the muscles flexing the lower leg, which in turn is the result of irritation of the brain membranes and an increase in cerebrospinal fluid pressure. After a lumbar puncture, the sign may disappear. Other authors, conversely, believe that neither pain sensations nor increased cerebrospinal fluid pressure can be the cause of the development of Kernig's sign and regard it as a combined, cumulative vegetative-spinal reflex; its starting point is the sensitive vegetative apparatus of the pia mater and the nerve fibers of the posterior roots. The main role in the pathogenesis of Kernig's sign and other meningeal contractures is played by changes in sarcoplastic muscle tone maintained by the vegetative nervous system. The change in tone is caused by impulses arising either in the muscle itself or in some segment of the vegetative reflex arc. Kernig's sign does not have pathognomonic significance; it is observed not only in cerebrospinal meningitis, but also in a number of other infectious diseases and intoxications accompanied by irritation of the brain membranes. Among infectious diseases, it is especially common in typhus, mainly in epidemic typhus, in encephalitis, in meningoencephalitis, etc.; it can be observed in vertebral caries, in traumatic injuries of the spinal cord, in uremia, etc. In children up to 6 months of age, examination for Kernig's sign often yields very indefinite results due to a certain rigidity of the muscles of the lower extremities.

Cite this page

“Kernig's Sign.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/kernigs-sign/