Peripheral neuropathies caused by exogenous toxins or dysmetabolic states are relatively common. Most present as motor–sensory polyneuropathy, usually axonal in type. The underlying pathophysiology of such polyneuropathies is discussed in the previous chapter (Chapter 65).
First noticeable symptoms tend to be sensory and consist of tingling, prickling, burning, or band-like dysesthesias in the balls of the feet, in the tips of the toes, or generally over the soles. Symmetry of symptoms and findings in a distal graded fashion is the rule, but occasionally dysesthesias appear in the sole of one foot a brief time before the other one, or perhaps are more pronounced in one foot at first. Care must be used to avoid confusion with a mononeurothapy multiplex, in which initial sensory symptoms tend to appear in the distributions of individual digital nerves, usually asymmetrically, and in either a hand or a foot.
As a polyneuropathy worsens, both weakness and usually pansensory deficit and loss of tendon jerks spread more or less concurrently in a centripetal and symmetrical fashion, and if severe enough, involve even the torso and the axial parts of the body as well as the limbs. Numbness and imbalance are the main sensory features and are usually accompanied by positive symptoms, dysesthesias and pain. As a rule, pain in polyneuropathy is dysesthetic in character and is most prominent distally, but there is often an accompanying nerve trunk component. The character of this is deep aching pain and is generally experienced more proximally than the dysesthetic pain (Asbury, 1990; Asbury & Fields, 1984).
When sensory disturbance is severe and ascends to midthigh in the legs and to the elbows, a tent-shaped area of hypesthesia on the lower abdomen may be demonstrated. This grows broader and the apex extends rosterally toward the sternum or higher as the neuropathy worsens. This tent-shaped sensory disturbance on the anterior torso is nerve-length dependent and in this case involves dying back of the segmental truncal nerves. It can be mistaken for sensory deficit of spinal cord origin if care is not taken to check for a sensory level posteriorly on the back and to outline with care the precise area of deficit.