Peripheral neuropathy describes a disease affecting the peripheral nervous system, the network of nerves outside the brain and spinal cord. When this damage affects multiple nerves throughout the body, it is classified as axonal sensorimotor polyneuropathy (ASMP). This progressive disorder impairs both movement and sensation, presenting a chronic challenge. Understanding ASMP provides insight into the underlying mechanisms of nerve destruction, aiding effective diagnosis and management.
Understanding the Terminology: What is Axonal Sensorimotor Polyneuropathy?
The term axonal sensorimotor polyneuropathy describes the pattern and location of nerve damage. Axonal indicates that the primary site of injury is the axon itself, the projection that transmits electrical impulses. This contrasts with demyelinating neuropathies, where the protective myelin sheath is damaged first. Axonal damage causes a loss of nerve fiber and reduces the strength of the electrical signal, known as decreased amplitude.
Sensorimotor means the disease affects two types of peripheral nerves simultaneously. Sensory nerves, which transmit information about feeling, temperature, and pain, are impacted, leading to abnormal sensations. Motor nerves, which control muscle contraction and movement, are also involved, resulting in weakness and loss of muscle function. Polyneuropathy signifies that the disease process is generalized, affecting multiple nerves throughout the body. This damage is typically symmetric, affecting both sides equally, and usually begins in the longest nerves first.
Manifestation of Symptoms (Sensory and Motor Effects)
ASMP symptoms follow a length-dependent pattern, affecting the longest nerve fibers first. This leads to the classic “stocking-and-glove” distribution, starting in the toes and feet and ascending the legs before reaching the fingers and hands. Sensory symptoms often present initially, including tingling, pins and needles (paresthesia), and burning or shooting pain. Patients may also experience numbness and a loss of proprioception (the sense of position), which can lead to balance problems and difficulty walking.
As the condition progresses, motor nerves become increasingly involved, typically affecting muscles furthest from the torso. Muscle weakness begins in the distal extremities, often causing foot drop and an altered gait. Chronic lack of nerve input eventually leads to muscle atrophy, or wasting, particularly in the small muscles of the feet and hands. The combination of sensory loss, muscle weakness, and poor balance contributes to a high risk of falls and unnoticed injuries.
Identifying the Root Causes (Etiology and Associated Conditions)
Identifying the underlying cause of ASMP is important because treatment often depends on managing the primary condition.
Metabolic Causes
Metabolic disorders represent the most frequent cause, with diabetes mellitus being the most common etiology of chronic ASMP. Chronic high blood sugar levels damage the axons, often through the glycation of nerve proteins. Metabolic syndrome and impaired glucose tolerance are also recognized risk factors for developing this type of neuropathy.
Toxic Exposure
Toxic exposure is another category where substances directly harm the nerve axons. Chronic alcohol consumption is a well-known cause, due to both direct toxicity and associated nutritional deficiencies. Chemotherapy drugs, especially platinum-based agents, are neurotoxic and can induce a painful, dose-dependent axonal polyneuropathy. Exposure to heavy metals like lead or arsenic may also result in similar nerve damage.
Nutritional and Autoimmune Factors
Nutritional imbalances can disrupt nerve health, particularly deficiencies in B vitamins such as B12, B1 (thiamin), and B6, which are necessary for proper nerve function. Conversely, excessive intake of Vitamin B6 can also cause axonal damage. Autoimmune or inflammatory conditions, such as Systemic Lupus Erythematosus (SLE) or Sjögren’s syndrome, can cause ASMP by triggering the immune system to attack the peripheral nerves.
Despite thorough diagnostic testing, a cause is never identified in a substantial number of cases. This is classified as Idiopathic Axonal Sensorimotor Polyneuropathy, a condition often seen in older adults.
Clinical Testing and Diagnosis
Diagnosis relies on a detailed neurological examination and specific electrodiagnostic tests. The physical examination confirms the pattern of sensory loss, weakness, and reduced reflexes, especially the ankle jerk reflex, which is often one of the first signs to disappear. Electrodiagnostic testing, including Nerve Conduction Studies (NCS) and Electromyography (EMG), is performed to confirm the diagnosis and classify the neuropathy as axonal.
NCS involves applying small electrical impulses to the nerves and measuring the resulting responses. In ASMP, the characteristic finding is a reduction in the amplitude of the sensory nerve action potential (SNAP) and the compound muscle action potential (CMAP). This low amplitude signifies the loss of axons, while the conduction velocity of remaining signals remains relatively normal or mildly slowed. EMG involves inserting a fine needle electrode into the muscle to assess its electrical activity, typically revealing signs of active denervation, such as fibrillation potentials.
Supporting tests, including comprehensive blood work, investigate the underlying etiology. These laboratory studies screen for metabolic conditions like diabetes, nutritional deficiencies (e.g., Vitamin B12), and markers of autoimmune disease or inflammation. When small nerve fibers are predominantly affected, a skin biopsy may be used to measure nerve fiber density, complementing the electrodiagnostic findings.
Current Management Strategies
Management of axonal sensorimotor polyneuropathy focuses on treating the underlying cause and providing symptom relief. Addressing the root condition halts the progression of nerve damage. For example, in diabetic neuropathy, maintaining strict control over blood glucose levels prevents further axonal loss. If the cause is related to toxicity or medication, cessation or modification of the exposure is the immediate priority.
Symptomatic management controls neuropathic pain. First-line pharmacological treatments include anti-seizure medications (such as gabapentinoids) or specific antidepressant classes (like duloxetine or tricyclic antidepressants) that modulate pain signals. These medications are typically started at a low dose and slowly increased to balance pain relief and side effects.
Supportive care manages functional deficits and prevents complications. Physical therapy helps patients maintain muscle strength, flexibility, and mobility, while occupational therapy assists with adapting daily activities. Due to sensory loss, meticulous foot care and protective footwear are emphasized to prevent unnoticed skin breakdown, ulcers, and infection. Assistive devices, such as canes or braces, may be required to improve balance and aid safe ambulation when muscle weakness is significant.