Axonal neuropathy vs Demyelinating neuropathy

Central nervous system disorders are crippling, as they affect our movements as well as the sensory functions of the body. Nerve cells are called neurons. Each neuron has a main body and radiating fibrils of short and long lengths. The short fibrils are called dendrons while the long ones are called axons. Both the dendrons and axons are responsible for transmission of information in the form of chemical and electrical impulses to other neurons and other parts of the body like muscles.

A neuropathy is the medical term for any condition involving the neurons. Axonal neuropathy is a neurological disorder that involves degeneration and loss of axons, whereas demyelinating neuropathy causes degeneration of myelin (fatty layer of insulating substance) surrounding axons of neurons. It is confirmed that if demyelinating diseases are not treated in time, then they will eventually damage the axons too.

The leading cause of axonal damage is any auto-immune condition where auto-antibodies attack the coating of motor nerves without causing inflammation or loss of myelin. Usually, the sensory nerves are spared but the motor nerves are affected. Motor nerves are the ones that conduct commands from the brain to the body, for example, movements, etc. In the case of acute diseases, axonal neuropathy is seen in a variant of Guillian Barre Syndrome. In the case of chronic disorders, it is seen in conditions like diabetes, leprosy, etc. where both motor and sensory nerves are damaged as the disease progresses.

Demyelinating disorders are generally seen due to genetic causes, infectious agents and autoimmune reactions. In these, the myelin which surrounds the axons of neurons is gradually destroyed by antibodies. This myelin coating is needed for faster transmission of impulses and hence, once myelin is lost, impulse transmission is either very slow or completely lost. In demyelinating neuropathy, both sensory and motor nerves are affected. This is a very characteristic difference between the two neuropathies.

Clinically, in an axonal neuropathy, movements of muscles are affected. There is tingling, numbness and a prickling sensation noted. Sensitivity to temperature may be lost in the affected area. There is loss of reflexes without sensory loss. There is a paralytic feeling of limbs in axonal neuropathy, whereas in demyelinating neuropathy there is a progressive weakness and fatigue of muscles. Also, there is blurred vision, double vision, movement difficulties, incoordination of muscles. Hence, walking and balancing become difficult. There is incontinence of urine and stools. Loss of reflexes in muscles that are not particularly weak or wasted is a classic feature of demyelination. On the other hand, selective loss of the ankle jerk reflex in the presence of wasting and weakness of the foot is more typical of an axonal damage.

In patients with axonal neuropathies, the impulse conduction velocity recorded from distant muscles like foot and ankle is less but relatively normal near proximal sites like arms. In the case of demyelinating neuropathy, patients show slowing of conduction of impulses at both proximal and distal sites on electromyogram.
Treatment for both the conditions depends on modifications of lifestyle, reduction in alcohol intake and prevention of brain injury. Autoimmune processes cannot be completely stopped but the trigger factors can be controlled and the destruction kept under control. Axonal neuropathy can be controlled by immunoglobins given intravenously or by plasmapheresis. Treatment majorly is based on the injury and the symptoms experienced. Steroids are employed extensively in controlling both neuropathies.

Summary: Axonal neuropathy is very similar to demyelianting neuropathy. The main difference lies in the affection of sensory nerves that conduct sensations from the senses to the brain.

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