Figure 1.
Brigadier-General William A. Hammond, Surgeon-General of the Federal Army during the U.S. Civil War.
Brady National Photographic Art Gallery, Washington, D.C. Courtesy of the U.S. Library of Congress.
Figure 2.
Hammond as a Civilian Neurologist . 1877.
c. 1877. Hammond described athetosis in 1871. Etching by E.B. Hall. Courtesy of the U.S. National Library of Medicine.
Figure 3.
Woodcuts of Athetosis.
The woodcuts were made from photographs, and were included as illustrations in the first edition of William Hammond’s Text-book of Nervous Diseases in 1871.2 The top figure was of Hammond’s own case, and the lower was from a case of J.C. Hubbard.
Figure 4.
Philadelphia Neurologist Silas Weir Mitchell in 1881.
Mitchell described post-paralytic chorea in 1874.23 Courtesy of the U.S. National Library of Medicine.
Figure 5.
British Neurologist Sir William Gowers.
Gowers felt there was considerable overlap between Hammond’s athetosis and “post-hemiplegic disorders of movement.” 21, 22 Courtesy of the U.S. National Library of Medicine.
Figure 6.
Post-paralytic Choreoathetosis.
Post-paralytic choreoathetosis was recognized by many eminent late 19th-century neurologists, including Charcot, Gowers, and Mitchell. Athetosis was often considered as just a form of post-hemiplegic chorea, even though Hammond’s original case and some others never experienced a hemiparesis. The left-most column of illustrations from Gowers’ textbook (1888)21 show “continuous mobile spasm (athetosis) after slight hemiparesis” in a 24-year-old syphilitic patient who developed left hemiparesis at age 23 and abnormal involuntary movements 4 months later. The center column of illustrations, also from Gowers’ textbook (1888),21 are some of the postures of the left hand of a 23-year-old male with “post-hemiplegic mobile spasm”; the abnormal movements began one year after onset at the time of some improvement in volitional movement. The right-most column of illustrations were derived from those of German neurologist Adolph von Strümpell as shown in the late nineteenth-century multi-authored American textbook of neurology edited by Francis Dercum (1895).37
Figure 7.
Left-sided Post-hemiplegic Choreoathetosis.
Illustrations are from Gehirnpathologie (1905) by Russian-Swiss neuropathologist Constantin von Monakow (1853–1930).38
Figure 8.
French Neurologist Jean-Martin Charcot in 1893.
Charcot dismissed athetosis as “simply choreiform movements” or as “only a variety of post-hemiplegic hemichorea.”20 From the American Journal of Insanity [1893; 50 (October): Frontispiece].
Figure 9.
New York Neurologist Landon Carter Gray.
Like many American neurologists, and particularly those from New York, Gray was supportive of Hammond’s concept of athetosis.44 Courtesy of the U.S. National Library of Medicine.
Figure 10.
Generalized Dystonia Diagnosed as Athetosis.
In 1908, Philadelphia neurologist William Spiller described a 12-year-old boy as having progressive spasticity and generalized “athetosis,” but provided clinical data that contradicted both of these findings.53 This was likely a generalized dystonia, and probably a case of dystonia musculorum deformans or torsion dystonia (three years before the disorder was described by German neurologist Hermann Oppenheim).
Figure 11.
British Physician Sir Thomas Watson, . 1873.
c. 1873. Watson applied the concept of “insanity of the muscles” in regard to chorea as early as 1841. This concept was later applied to athetosis. Photograph by Barraud & Jerard, Photographers, London. Courtesy of the U.S. National Library of Medicine.
Figure 12.
Cognitive Impairment and Athetosis.
Patient with cognitive impairment and athetosis reported by British physician Thomas Claye Shaw in 1873. Occasional cases of hemi-athetosis were reported in association with either cognitive impairment or insanity, with non-progressive cognitive impairment most commonly noted in congenital cases of double athetosis. Unlike the situation with Huntington’s disease, adult-onset hemi-athetosis was not associated with either progressive dementia or psychiatric dysfunction.
Figure 13.
Pathology of Hammonds Original Case of Athetosis.
’s Original Case of Athetosis. Drawings by New York neurologist Edward Spitzka (1852–1914). In 1871, Hammond had proposed that the responsible lesion in athetosis would be found in the basal ganglia. The corresponding pathology of Hammond’s original case, as reported by his son Graeme Hammond in 1890, confirmed Hammond’s prediction. Furthermore, “the direct motor tract in the internal capsule was not involved to any extent.” Hammond’s prediction and the subsequent confirmation are often regarded as a landmark in the clinicopathologic correlation of movement disorders, and specifically in the linkage of abnormal movements to pathology of the basal ganglia.
Figure 14.
Austrian Neuropsychiatrist Gabriel Anton, . 1890.
c. 1890. Anton found bilateral putaminal lesions with patches of “hypermyelinated” nerve fibers in congenital cases of double athetosis. Public domain. Courtesy of Wikimedia Commons.
Figure 15.
Gross Neuropathology in Double Athetosis.
Gross neuropathology in a patient with double athetosis as reported by Philadelphia neurologist William Spiller in 1920.82 Top figure shows a section through the left basal ganglia of a control patient without athetosis, while the lower figure shows a section at about the same level from a case of double athetosis. According to Spiller’s report: “The degeneration affects the putamen and the tissue consists of loose neuroglia. There is no large cavity in the putamen.” In cases of double athetosis, the findings were similar on both sides.