Many cases of the poisoning of children have occurred through the ingestion of the flowers and seeds. In 1908 a case was recorded by the Board of Agriculture and Fisheries, in which two horses were alleged to have been poisoned in North Wales by laburnum seeds, a very small quantity of which was found in their stomachs after death.
Müller states that in Dalmatia goats which had eaten _Cytisus Weldeni_, though themselves uninjured, produced milk which was poisonous to man.
_Toxic Principle._ All parts contain the toxic alkaloid _Cytisine_ (C_{ 11}H_{ 14}N_{ 2}O), said by Moer and Partheil to be identical with Ulexine; it is found in the seeds to the extent of 1·5 per cent. Cornevin states that the root, wood and bark are nearly constant in toxicity, but that the leaves and pods present remarkable seasonal variations owing to the migration of the poison into the seeds. The toxic property is not destroyed by drying of the plant.
_Symptoms._ Laburnum poisoning is of the acrid, narcotic type, with, in man, nervous symptoms, abdominal pain, vomiting, purging, tetanic spasms and convulsions.
Cornevin’s observations show that the symptoms occur in three consecutive stages,—(1) excitement, (2) coma and incoordination of movement, and (3) convulsions. The order of the appearance, their duration, and the association of each with the others depend upon the susceptibility of the animal and the quantity ingested. Thus the symptoms of excitement may be present alone if only a small quantity is eaten; the duration of the symptoms in this case is never considerable, and the normal is gradually regained. In general, however, the symptoms are associated in pairs; thus when an average quantity is fed there is excitement and coma but _no_ convulsions; when large quantities are fed the first stage is suppressed or is so short as to be almost imperceptible, the coma and convulsions being present simultaneously. As regards temperature, there is, in stage (1) a rise, in stage (2) a drop, and in stage (3) a rise again near death. In stages (2) and (3) there is a slackening of respiration, the arterial tension is raised, there is an increase in the number of pulsations and a modification of the rhythm. In stage (3) near death there is a lowering of the arterial tension, and the pulsations become gradually less perceptible, but with a uniform rhythm; there is a slackening in respiration, and by the time this finally ceases the heart beats have become imperceptible.