Determining Direction of Axonal Flow in the Equine Ramus Communicans by Ultrastructural Examination of the Plantar Nerves 2 Months after Transecting the Ramus

The ramus communicans, neural connection between medial and lateral plantar nerves of the horse, was transected to determine the degree to which medial and lateral plantar nerves contribute to the plantar ramus. After 2 months, sections of plantar nerves immediately proximal and distal to the communicating branch were collected and processed for electron microscopy. All examined nerves had undergone Wallerian degeneration and contained regenerating and mature fibers. Layers of the myelin sheath were separated by spaces and vacuoles, indicating demyelination of medial and lateral plantar nerves. Shrunken axons varied in diameter and were surrounded by an irregular axolemma. Shrunken axoplasm of both myelinated and non-myelinated fibers contained ruptured mitochondria and cristae, disintegrating cytoskeleton, and vacuoles of various sizes. The cytoplasm of neurolemmocytes contained various-sized vesicles, ruptured mitochondria within a fragile basal lamina and myelin whorls of multilayered structures indicative of Wallerian degeneration. These ultrastructural changes, found proximal and distal to the ramus in medial and lateral plantar nerves, suggest that axonal flow is bi-directional through the ramus communicans of the pelvic limbs of horses, a previously unreported finding. As well, maturity of nerves proximal and distal to the ramus indicates that all nerve fibers do not pass through the ramus.

Muscle Atrophy and Hypertrophy

Muscle atrophy is usually caused by interruption of axonal flow (axonal neuropathies, motor neuron diseases, etc.). If weakness is out of proportion to atrophy, conduction block due to demyelinating neuropathy should be suspected. Chronic myopathies and immobility may also cause atrophy, but no EMG evidence of denervation or myopathy is respectively found. The pattern of atrophy is often helpful to localize the lesion. Atrophy of the interossi and preservation of the bulk of the thenar muscles suggest ulnar neuropathy, but atrophy of both would suggest a C8 or plexus pathology. Muscle enlargement may be due to tissue replacement (fatt, amyloid), which can be confirmed by EMG and MRI, or may be due to real muscle hypertrophy from excessive discharges (neuromyotonia).