Acute neuropathic processes:
Botulism, degenerative  leukodystrophies, metachromatic leukodystrophy and Krabbe disease,spinal muscular atrophy, Charcot-Marie-Tooth disease (hereditary motor and sensory neuropathy type I), Dejerine-Sottas disease (hereditary motor and sensory neuropathy type III) and Refsum disease, Guillain-Barré syndrome, Chronic inflammatory demyelinating polyneuropathy, Miller-Fisher variant of Guillain-Barré syndrome

Acute neuropathic processes are uncommon in children and differ from those seen in adults. Among adults, diabetes, vascular disease, and toxins are common causes of chronic sensory or sensorimotor neuropathy with deficits in a stocking-glove distribution. Among children, acute and chronic neuropathies have variable patterns of weakness in the feet, legs, hands, or face; diminished-to-absent reflexes; or sensory loss (eg, numbness and paresthesias) distally. Childhood disorders affecting the neuromuscular junction, such as botulism, can appear in a similar fashion, although reflexes usually are normal to diminished, as described for the infant in the vignette. 

Chronic childhood neuropathies stem from degenerative disorders, hereditary disease, demyelination, or rarely toxin exposure. The degenerative leukodystrophies, such as metachromatic leukodystrophy and Krabbe disease, are associated late in their courses with neuropathy from dysmyelination, but reflexes are brisk because of overshadowing brain white matter degeneration. Infantile spinal muscular atrophy results from degeneration of the anterior horn cells and presents at birth or during the first year with hypotonia and more proximal than distal weakness, followed by bulbar weakness. Tongue fasciculations are common. Direct testing for the survival motor neuron gene has displaced muscle and nerve biopsy as the preferred initial test for making this diagnosis. Charcot-Marie-Tooth disease (hereditary motor and sensory neuropathy type I) manifests most frequently in the late second decade with progressive distal lower extremity weakness, atrophy in the intrinsic foot muscles, and pes cavus. Sensory abnormalities are  uncommon. Inheritance is autosomal dominant or X-linked. Other rare hereditary neuropathies include Dejerine-Sottas disease (hereditary motor and sensory neuropathy type III) and Refsum disease.

Chronic inflammatory demyelinating polyneuropathy is a disorder that is similar to Guillain-Barré syndrome, but fluctuating and chronic. Lead intoxication in children usually causes central nervous system dysfunction, such as neuropsychological and behavioral impairments, rather than a motor neuropathy, as in adults. Neuropathy from lead may occur in children who have sickle cell disease. Arsenic produces painful burning paresthesias as well as motor polyneuropathy. Vincristine can lead to a chronic peripheral motor neuropathy, but the drug does rarely produce striking jaw pain or fulminant weakness. (Fulminant weakness may occur in patients who have Charcot-Marie-Tooth disease).

Acute neuropathies may be demyelinating, infectious, or rarely metabolic. Guillain-Barré syndrome is a postinfectious demyelinating polyneuropathy that presents over days to weeks with ascending paralysis and areflexia. Poliomyelitis and other enteroviral illnesses can produce a motor polyneuropathy with weakness in a spotty distribution. Diphtheria can cause a toxic neuropathy similar in  appearance to Guillain-Barré syndrome, but cranial neuropathies alsomay occur. Certain tick species produce paralysis by blocking acetylcholine release at synapses and affecting large myelinated and sensory fibers. Tick paralysis typically is ascending and accompanied by areflexia. Respiratory failure and cranial neuropathies may ensue. Removal of the tick leads to a swift recovery. Acute intermittent porphyria is an extremely rare cause of acute polyneuropathy that is diagnosed by detection of urine porphobilinogen.

The weakness of foodborne and wound botulism often is mistaken for the Miller-Fisher variant of Guillain-Barré syndrome (ie, acute external ophthalmoplegia, ataxia, and areflexia, sometimes with facial weakness), diphtheric neuropathy, tick paralysis, or even poliomyelitis. Botulism is an acute flaccid paralytic illness caused by a neurotoxin produced by Clostridium botulinum. The toxin migrates via the bloodstream to peripheral cholinergic synapses, blocking acetylcholine release and impairing autonomic and neuromuscular transmission.

Infant botulism typically presents in babies younger than 6 months of age with several days of constipation, followed by difficulty in sucking, swallowing, crying, head control, or breathing, as described for the infant in the vignette. Flaccid descending paralysis then develops. The illness is more prevalent in southern Pennsylvania, California, and Utah. The disease arises from toxin produced in the gastrointestinal tract, rather than by ingestion of the toxin. Diagnosis is established by demonstrating the presence of the botulinum toxin in stool or serum.

References:
Pickett J, Berg B, Chaplin E, Brunstetter-Shafer MA. Syndrome of
botulism in infancy: clinical and electrophysiologic study. N Engl J
Med. 1976;295:770-772
Sarnat HB. Neuromuscular disorders. In: Behrman RE, Kliegman RM,
Jenson HB, eds. Nelson Textbook of Pediatrics. 16th ed. Philadelphia,
Pa: WB Saunders Co; 2000:1866-1893