The density of the
axoplasmic neurofilaments was normal.
In Section 4, the united model of signal propagation is described including the interacting electrical signal (action potential), the mechanical wave in the surrounding biomembrane, and the wave in the
axoplasmic fluid inside the nerve fibre.
Further, infarction of the nerve fiber layer forms cotton wool spots, with stasis in
axoplasmic flow association [20].
In addition, magnetic field treatment can affect angiogenesis, neuronal protein synthesis, synaptic neurotransmitters, and
axoplasmic transport, resulting in positive outcomes in patients with diabetic neuropathy (11, 12).
Mercury damages the nerves in several ways: it interferes with membrane and receptor functions, and neurotransmitter transport and metabolism; it interrupts cytoskeletal proteins, and interferes with
axoplasmic flow and signal transduction; it interferes with cell respiration, energy metabolism and others.[3] Among the 16 patients, six patients presented with proteinuria, but without edema.
These pathophysiological changes are associated with ischemia, which develops as a result of direct mechanical damage to the peripheral nerves, cessation of the
axoplasmic flow or compression of vascular structures feeding peripheral nerves due to compression (2).
Vibration-induced disruption of retrograde
axoplasmic transport in peripheral nerve.
Studies have demonstrated that mechanical stress could cause physical alterations in the ONH, such as misalignment of the fenestrate in lamina cribrosa, which may lead to
axoplasmic flow obstruction due to its back bowing.
Pathogenesis includes increased Cerebro Spinal Fluid (CSF) production, decreased drainage, intracranial space occupying lesions, traumatic cerebral contusion, venous outflow obstruction, dural sinus thrombosis and idiopathic intracranial hypertension (IIH).1 IIH is a separate entity, mainly a diagnosis of exclusion, characterized by papilledema without identifiable neurological pathology, and is common in obese women of child bearing age.2 Since the optic nerve sheath can be traced as continuation of the subarachnoid space, transmission of effects of raised ICP to the optic nerve causes disruption of the
axoplasmic flow, swelling of axons, leakage of water and proteins with resultant optic disc swelling, or papilledema.3,4
It is thought that obstruction of
axoplasmic flow causes axons to swell acutely, giving rise to microvesicular changes.
Activation of innate immune response initiates a cascade of inflammatory signaling pathways and subsequent biochemical responses [3], which eventually leads to a variety of cellular disturbances such as microtubules dissolution,
axoplasmic perturbation, glial response, and even cell death.