Home >> Diseases Of Children >> Intestinal Bacteria to Neoplasms And Parasites Of >> Landrys Paralysis Acute Ascending

Landrys Paralysis Acute Ascending Paralysis

disease, spinal, bulbar, findings, time, intoxication and observed

LANDRY'S PARALYSIS (ACUTE ASCENDING PARALYSIS) In 1859 Landry described a clinical picture which consists in flaccid paralysis of the skeletal muscles, beginning in the lower extremities and rapidly ascending, and terminates fatally in a short time through involve ment of the bulbar nerves and the respiratory centre. The pathologic findings in Landry's cases were negative.

Since his time the disease has been studied by many clinicians and pathologists, among whom Westphal, Flernhardt, Kahler, Pick, Wappen schmidt, etc., have contributed greatly to our knowledge of it. It is observed in individuals of every period of life. Cases occurring in children have been described among others by Liegard (2,1 years old), Kahler, Pick, Heubner, Soltmann, Gru, Rumpf, etc. On the whole, however, the disease is distinctly rare.

The first symptom is paralysis of the toes and feet, sometimes accompanied by dragging pains and parmsthesia. Within a few hours the entire leg becomes paralyzed. By the end of several more hours, or at most a day, paralysis is complete in both legs. After a short interval the muscles of the trunk, back and thorax are attacked in turn, and with in a short time the arms also are paralyzed, the paralysis beginning in the shoulders and fingers. But the dreadful clisease continues to spread; alarming interference with deglutition, speech and respiration develops, and the unfortunate patient is finally robbed of all power of movement except the movements of the face and eyes. Death occurs from asphyxia, and consciousness is retained to the end. Aside froni pariesthesia and sensations in the extremities before the appearance of the paralysis, pain is usually- absent. The cutaneous and tendon reflexes are absent, electric irritability disappears or the reactions of degeneration are present, feeble stimuli being often sufficient to produce severe contractions. The sphincters escape, and there are no trophic disturbances. If the disease begins with bulbar symptoms, death occurs before the paralysis becomes universal. Fever is not present, ftS a rule, but has been described in children (Soltmann).

The average duration of the disease is from I to weeks. Most of

the cases end fatally, although arrest of the disease has been observed at every stage, even that of bulbar involvement.

Our knowledge of the pathology, anatomy and pathogenesis of this disease is still incomplete. In the cases which have been examined so far the findings were either negative or those of acute inflammation of the spinal cord (poliomyelitis acutissima) and of the medulla oblongata, neuritis of the roots of the spinal nerves, or, finally, acute polyneuritis. With the newer methods of examination negative findings are becoming more and more rare. On the strength of these pathologic findings and the corresponding clinical symptoms we distinguish a medullary, bulbar, and neuritic form of Landry's paralysis (Leyden-Goldscheider). But the identity of all the forms of this disease is now no longer questioned, and the theory of an acute intoxication is generally acceptetl, the differ ences in the clinical pictiire being explained by the point of attack, the severity of the intoxication, and the duration of the clisease (Oppenhei Remak). It is difficult to determine whether the disease is localized in the spinal cord or in the peripheral nerves, and Ilaymond's designation cellulo-neurite aigve anterieure therefore has much to recommend it.

The nature of the intoxication that is responsible for Landry's paralysis is unknown. The disease has been observed after anthrax, diphtheria, influenza, typhoid fever and gonorrInea, and the corresponding microorganisms have been demonstrated in the pathologic preparations.

The only conditions with which the disease could be confounded are some spinal affections (spinal infantile muscular atrophy and poliomye litis) and polynetnitis, and the diagnosis is speedily settled by the rapid course of the disease. The prognosis is unfavorable. Mercury and ergotin have been recommended. Counterirritation with the actual cautery has also been recommended, but whether such an heroic measure is justifiable in the case of a patient's suffering from such a pitiable disease must be left to the physician's OWII feelings.