Diagnosis of polyneuropathy

Important in the diagnosis of polyneuropathy is the anamnesis (questioning of the patient) and the examination of the patient. During the anamnesis, family nervous disorders, alcohol, drug and medicine addiction and possible contact with toxic agents at work (exposure) are asked. Mostly pain and symmetrical sensory disturbances of the feet and hands, including sensitive irritation symptoms such as the “burning feet“, i.e. burning soles of the feet, as well as swaying dizziness and nocturnal muscle cramps are stated.

and Burning Feet Syndrome. The examination begins with a test of sensitivity, which can be impaired in all qualities, e.g. sense of touch or vibration. The self-reflexes are usually reduced or even extinguished in the lower extremities.

The Achilles tendon reflex, also a self-reflex, is already absent before sensitivity disorders are detectable. Thus, the detection of glove- or stocking-shaped sensitivity disorders with a reduced sense of vibration on the lower legs and missing reflexes almost always leads to the diagnosis of polyneuropathy. Coordination is also examined.

Pronounced ataxia is observed in cases of mercury poisoning and in diabetic and alcoholic polyneuropathy (“Pseudotabes diabetica or alcoholica”). Asymmetrical distribution patterns of the multiplex type are frequent in diabetes mellitus, lead polyneuropathy as well as polyneuropathies after tick bite (borreliosis), syphilis and leprosy infection. Also common in diabetes mellitus are mononeuropathy and involvement of cranial nerves.

Psychological susceptibilities are observed especially in alcoholism, porphyria and thallium poisoning. The medical history and the clinical examination are supplemented by laboratory chemical tests to clarify the cause of the polyneuropathy. The following tests are performed: in the blood.

  • The blood count
  • The electrolyte
  • Blood sugar-
  • Liver and kidney values
  • Vitamin B12and
  • Folic acid

A distinction is made between polyneuropathies with predominant damage to the myelin sheath of the nerve fiber (demyelination), which entails a significantly reduced nerve conduction velocity with normal strength of impulse, and polyneuropathies with predominant damage to the nerve process (axon degeneration), which entails normal NLG with lower strength of impulse. Electroneurography (ENG) measures the nerve conduction velocity, which can be normal, moderate or greatly reduced, depending on the cause of the polyneuropathy. In electromyography (EMG), spontaneous impulses can be measured in cases of predominant axon degeneration, which do not occur in this way in a healthy nerve.

In addition to ENG and EMG, a suralis biopsy can be performed to clarify an axonal or demyelinating form. In this procedure, tissue from the sural nerve, a nerve that lies superficially under the skin of the lower leg, is removed and examined. In addition, an increase in the protein concentration in the cerebrospinal fluid of the brain and spinal cord (cerebrospinal fluid) can be detected in many polyneuropathies, such as diabetic polyneuropathy. Sensory disorders and pain in polyneuropathies are often confused with arterial circulatory disorders.