Peripheral Polyneuropathy

Peripheral neuropathy is a relatively common disorder with a prevalence that may reach up to 10% of the general population. Peripheral neuropathy is often a manifestation of a systemic disease such as diabetes, alcohol abuse, or leprosy. However, about 20% of neuropathies remain idiopathic; a significant number of these cases are likely inherited in nature.

The myriad of etiologies of peripheral neuropathy pose a daunting task for the clinician. Investigating peripheral neuropathy has included several approaches. First, is the pattern recognition approach where a diagnosis of a polyneuropathy is based on highly specific associated findings such as the Mee line in arsenic or thallium poisoning, red tongue in vitamin B12 deficiency, or predilection of the sensory loss to cool areas of the body (such as earlobes, nipples, and buttock) in leprosy. Unfortunately, this approach applies to a minority of patients usually with advanced disease, requires a vast clinical experience and is mostly accomplished by senior neurologists. The second approach frequently used by many physicians (including some neurologists) is a “shotgun” approach by ordering a battery of tests on every patient with a neuropathy. This irrational approach is costly and may result in incorrect diagnosis secondary to incidental abnormalities, such as elevated blood glucose in a patient with CIDP. The third recommended approach is a systematic approach that utilizes mainly the clinical findings and EDX studies to generate a more limited differential diagnosis and help guide the laboratory investigations necessary for establishing a final diagnosis (Table C26-1). Additional studies that are useful in the accurate diagnosis of peripheral neuropathy include autonomic testing, quantitative sensory testing, antibody testing, and skin or cutaneous nerve biopsy.

Table C26-1 Essential Steps in the Classification and Etiologic Diagnosis of Peripheral Polyneuropathy

The Temporal Profile of the Polyneuropathy Is the polyneuropathy subacute or chronic? If chronic, is the disorder progressive, relapsing and remitting, or stepwise? Subacute – consider Guillain-Barré syndrome, porphyria, diphtheria, critical illness, and drugs/toxins Chronic relapsing and remitting – consider CIDP and drugs/toxins Chromic progressive – consider CIDP, metabolic disorder*, nutritional deficiency, and toxins

The Anatomic Pattern of the Polyneuropathy Is the polyneuropathy distal, proximal, or both? Are there any foot or spine deformities (pes cavus or kyphoscoliosis)? Is the polyneuropathy symmetric or asymmetric? If asymmetric, do the findings follow specific peripheral nerve distribution? Distal – consider metabolic disturbance*, vitamin deficiency, toxins, drugs, critical illness, hereditary Distal and proximal – consider Guillain-Barré syndrome, CIDP, porphyria Asymmetric – consider vasculitis, CIDP, HNPP Mononeuropathy multiplex – consider multifocal motor neuropathy, Lewis-Sumner syndrome, HNPP, vasculitis, leprosy Pes cavus or kyphoscoliosis – consider CMT, HNPP

The Type(s) of Nerve Fiber Involvement Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Case 7 Case 11 Case 23 Case 20 Stay updated, free articles. Join our Telegram channel Join Tags: Electromyography in Clinical Practice A Case Study Approach Aug 12, 2016 | Posted by admin in CARDIOLOGY | Comments Off on Case 26 Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access