In July 1931, notorious serial killer Peter Kürten, known as "The Vampire of Düsseldorf", was executed on the guillotine in Cologne. On 1 August 1933, in Altona, Bruno Tesch and three others were beheaded. These were the first executions in Nazi Germany. The executions concerned the Altona Bloody Sunday (Altonaer Blutsonntag) riot, an SA march on 17 July 1932 that turned violent and led to 18 people being shot dead. Marinus van der Lubbe by guillotine in 1934 after a show trial in which he was found guilty of starting the Reichstag fire. In February 1935 Benita von Falkenhayn and Renate von Natzmer were beheaded with the axe and block in Berlin for espionage for Poland. Axe beheading was the only method of execution in Berlin until 1938, when it was decreed that all civil executions would henceforth be carried out by guillotine. However, the practice was continued in rare cases such as that of Olga Bancic and Werner Seelenbinder in 1944. Beheading by guillotine survived in West Germany until 1949 and in East Germany until 1966. A group of three Catholic clergymen, Johannes Prassek, Eduard Müller and Hermann Lange, and an Evangelical Lutheran pastor, Karl Friedrich Stellbrink, were arrested following the bombing of Lübeck, tried by the Peoples Court in 1943 and sentenced to death by decapitation; all were beheaded on 10 November 1943, in the Hamburg prison at Holstenglacis.
Paraneoplastic cerebellar degeneration (PCD) is a paraneoplastic syndrome associated with a broad variety of tumors including lung cancer, ovarian cancer, breast cancer, Hodgkin’s lymphoma and others. PCD is a rare condition that occurs in less than 1% of cancer patients. As is the case with other paraneoplastic syndromes, PCD is believed to be due to an autoimmune reaction targeted against components of the central nervous system, mostly to Purkinje cells.It is thought to be triggered when tumor cells (in PCD, most commonly ovarian or breast cancer) ectopically express proteins normally expressed in the cerebellum. This is believed to trigger an anti-tumor immune response that may be clinically significant, but also an anti-neural immune response. A broad spectrum of neuronal and glial proteins has been identified as target antigens in PCD. Presentation
Neurological symptoms may include, among others, dysarthria, truncal, limb and gait ataxia and nystagmus. Symptoms often develop subacutely and progress rapidly over a period of weeks or months to a plateau period that can last for months to years and which often reflects complete loss of Purkinje cells. Pathophysiology
The anti-Purkinje cell antibodies originally described in PCD led to the hypothesis that the antibody might be pathogenic, much as earlier studies had demonstrated pathogenicity of anti-acetylcholine receptor antibodies in myasthenia gravis. However, when the antibody was used to clone the cDNA encoding the cdr2 antigen, it was found to be an intracellular protein. This led to the suggestion that there might be a cell-mediated component (T cell) in disease pathogenesis.