stronger pupillary constriction occurs with very frequent stimulations
because of the additive effect of acetylcholine at the postsynaptic region.
This additive effect occurs when the interval between the release of acetylcholine
is significantly less than the time it takes for acetylcholine to be destroyed
in the cleft. Progressively weaker pupillary constriction occurs with
infrequent stimulation because repetitive stimulation at a slow rate does
not have this additive effect.
Seizures may occur in neonates
with botulism and are often due to hyponatremia (which results from inappropriate
secretion of antidiuretic hormone) or asphyxia. Classic electrodiagnostic
findings are an incremental response in muscle action potential produced
by very frequent repetitive nerve stimulation (20 to 50 Hz) and abundant
brief and small polyphasic motor unit and fibrillation potentials. These
findings are not present in all cases, therefore, their absence does not
exclude infantile botulism. The diagnosis of botulism rests on finding
C botulinum in the stools. Treatment with human botulism immune
globulin is effective. Supportive treatment is needed. Infantile botulism
is a self-limiting disease that lasts from 2 to 8 weeks.
produces hypotonia, weakness, abdominal distention, absent bowel sounds,
and constipation. It usually occurs in newborns after the mother has received
a large amount of intravenous magnesium sulfate. It is a presynaptic defect.
The diagnosis is confirmed by a serum magnesium level above 4.5 mEq/L.
Treatment is supportive. Exchange transfusion may help in very severe
produce weakness, hypotonia, dilated pupils, atonic bladder, and paralytic
ileus. Treatment consists of elimination of antibiotics and support. Hypotonia
due to aminoglycoside therapy occurs more frequently in neonates with
other disorders that affect the myoneural junction; therefore, the use
of aminoglycosides in a neonate with a disorder of myoneural junction
involvement should be avoided.