Small thinly myelinated Aδ and unmyelinated C fibers are affected.

Prominent symptoms with burning, superficial, or lancinating pain often accompanied by hyperalgesia, dysesthesia, and allodynia.

Progression to numbness and hypoalgesia (Disappearance of pain may not necessarily reflect nerve recovery but rather nerve death, and progression of neuropathy must be excluded by careful examination).

Abnormal cold and warm thermal sensation.

Abnormal autonomic function with decreased sweating, dry skin, impaired vasomotion and skin blood flow with cold feet.

Intact motor strength and deep tendon reflexes.

Negative nerve conduction velocity findings.

Loss of cutaneous nerve fibers on skin biopsies.

Can be diagnosed clinically by reduced sensitivity to 1.0 g Semmes Weinstein monofilament and prickling pain perception using the Waardenberg wheel or similar instrument.

Patients at risk of foot ulceration and subsequent gangrene and amputations.

Large myelinated, rapidly conducting Aα/β fibers are affected and may involve sensory and/or motor nerves.

Prominent signs with sensory ataxia (waddling like a duck), wasting of small intrinsic muscles of feet and hands with hammertoe deformities and weakness of hands and feet.

Abnormal deep tendon reflexes.

Impaired vibration perception (often the first objective evidence), light touch, and joint position perception.

Shortening of the Achilles tendon with pes equinus.

Symptoms may be minimal: sensation of walking on cotton, floors feeling "strange", inability to turn the pages of a book, or inability to discriminate among coins. In some patients with severe distal muscle weakness, inability to stand on the toes or heels.

Abnormal nerve conduction velocity findings

Increased skin blood flow with hot feet.

Patients at higher risk of falls, fractures, and development of Charcot Neuroarthropathy

Most patients with DPN, however, have a "mixed" variety of neuropathy with both large and small nerve fiber damages.