Heine-Medin disease

Poliomyelitis is an acute viral affection caused by any of three polioviruses (RNA/enterovirus of the picornavirus family). Poliomyelitis affects both sexes, with onset most frequently between 6 months and 15 years of age, but also older people can get it. It is spread man-to-man by coming in contact with contaminated saliva, or other bodily fluids, and enters the body through the mouth. It occurs in three types: aborted type, nonparalytic type, and paralytic type.

In some cases, asymptomatic. Polio starts as a minor illness, similar to the flu. It usually follows a prodromal phase characterized by fever, upper respiratory symptoms, or gastrointestinal symptoms; difficulty swallowing. Nausea; vomiting; diarrhoea; strypsis; abdominal pain, or influenza like symptoms (bone, muscle, and joint aches). The key symptom of Polio is paralysis without loss of sensation. 90% of the cases, mostly in children, recover within a few weeks. Polio strikes adults more severely.

The three types of poliovirus are named Brünhilde, Lansing, and Leon.

The most severe epidemics are caused by Brünhilde, a strain or type of poliovirus isolated from the spinal cord of a chimpanzee named Brünhilde. This chimpanzee was inoculated in 1939 with stool specimens from seven paralytic patients from Baltimore.

Type II of the poliovirus is the Lansing, which was recovered in 1938 from the brain and spinal cord of a young man who had succumbed to polio in Lansing, Michigan.

The third strain of poliovirus is Leon, so named because it was obtained in 1937 from the brain and spinal cord of an eleven-year-old boy named Leon, who was a victim of polio in Los Angeles.

Polio has occurred for thousands of years in all parts of the world. The bone formation of an Egyptian skeleton of the period of 3700 B.C. indicates the effects of polio, as does an Egyptian plaque from 1300 B.C. Poliomyelitis is a combination of the two Greek words: polios or grey, denoting the grey matter of the nervous system, and myelosis or marrow, denoting the myelin sheath around certain nerve fibres. There are three types: bulbar, spinal, and bulbarspinal.

Jakob Heine did the earliest report of poliomyelitis in 1840. In 1875, at the Versammlung der deutschen Naturforscher und Ärzte in Freiburg (meeting of the German Society of Natural Scientists and Physicians in Freiburg), Heine reported on paralysis in childhood that may occur following convulsions.

The German neurologist Ernst Adolf Gustav Gottfried von Strümpell (1853-1925) in 1885 described the cerebral form of poliomyelitis, which is called Strümpell’s disease II.

The Swedish physician Oskar Karl Medin (1847-1928) in 1890 was the first to carefully study an epidemic of poliomyelitis and first drew attention to the epidemic character of the disease. Dr. Ivar Wickman, a pupil of Medin, experienced the great Swedish epidemic of 1905 and was the first to express the correct conclusion that person-to-person was the manner of transmission. In 1909 the Austrian-born American immunologist and pathologist Karl Landsteiner (1868-1943), then prosector at the Royal-Imperial Wilhelminen Hospital in Vienna, and the German pathologist Erwin Popper, were able to produce signs of paralysis similar to those of poliomyelitis in a rhesus monkey, using a homogenate from the brain and spinal cord from a child who had died of the disease. This work peaked with that of Jonas Edward Salk (1914-1995) and Albert Bruce Sabin (1906-1993).

One of the most amazing things about poliomyelitis is that no epidemic of it was noted until seventy-one years ago. Large epidemics of other virus diseases, such as smallpox, yellow fever, influenza, and measles, are recorded much farther back in history.
Greer Williams, Virus Hunters (1960)

• J. von Heine:
  Beobachtungen über Lähmungszustände der untern Extremitäten und deren Behandlung.
  Stuttgart, F. H. Köhler, 1840.
  2nd edition under the title of:
  Spinale Kinderlähmung. Monograph. Stuttgart, 1860.
  In this work Heine gave the disease its present name, as he assumed that the seat of the disease was in the spinal marrow. He distinguished it clearly from cerebral infantile paralysis, hemiplegia. He points to the epidemic occurrence of spinal infantile paralysis.
• J. M. Charcot:
  Une observation de paralysie infantile s’accompagnement d’une altération des cornes antérieures de la substance grise de la moëlle.
  Written with Alex Joffroy (1844-1908).
  Comptes rendus de la Société de biologie, Paris, (1869), 1870, 5th series; 1: 312-315.
  First demonstration of the atrophy of the anterior horns of the spinal cord in infantile paralysis, confirming earlier suggestions of Jacob von Heine and the French neurologist Guillaume Benjamin Amand Duchenne de Boulogne (1806-1875).
• A. G. von Strümpell:
  Uber die akute Encephalitis der Kinder (Polioencephalitis acuta, cerebrale Kinderlähmung).
  Jahrbuch für Kinderheilkunde, 1885, 22: 173-178.
• O. Medin:
  En epidemi af infantil paralysi.
  Hygiea, Stockholm, 1890, 52: 657-668.
  German version in Verh X Int Med Kongr, 1890, 2, Abt. 6, 37-47, 1891.
  English translation in Bick, Classics of Orthopaedics, 116-123.