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).

Clinical features

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.

In the 10 years since the second edition of Diseases of the Nervous System appeared, extraordinary change has taken place in the field of neurosciences, both basic and clinical. In accordance with what is happening in the neurosciences, major changes have occurred with this third edition. Organization of subject matter and ordering of topics has changed substantially, in some cases dramatically. Of the contributors, a number of the authors for the previous two editions have written again in their special fields of expertise, but overall, more than three-quarters of the contributors are new to these pages. Two new editors have been added, Peter J. Goadsby and Justin C. McArthur; Cambridge University Press is the new publisher; and a new subtitle, Clinical Neuroscience and Therapeutic Principles has supplanted the previous one.

Despite these changes, the purpose of these reference volumes remains the same, namely to summarize what the scientific method, as applied to problems of neurological dysfunction, has taught us about the pathophysiology of neurological disorders. To say it differently, our purpose is not to focus on incidence, natural history, phenomenology and semeiology of neurological disorders, although these aspects are touched upon, but rather to focus on the mechanisms of neurological disease and the principles that form the basis for management and therapeutics. In addition to the emphasis on pathophysiology and principles of therapy, three other axioms guided the planning of this edition, just as they did for the previous editions. First, contributors were chosen who brought clinical expertise to bear as well as scientific authoritativeness. Second, we tried to assure that the depth with which each topic covered was relatively uniform from one chapter to the next. There is a corollary to this principle of uniformity. Given that these volumes are a general reference covering the entire field of neurological disorders, each chapter is, by necessity, a relatively brief summary of where matters stand in that particular disorder or area of interest. This level of detail will be insufficient for some readers. When this is the case, readers are urged to consult the primary literature listed in the references.