Besides the clinical pattern of the neurological deficit, a major difference exists between the common length-dependent diabetic polyneuropathy (LDDP) and focal or multifocal neuropathies that occur in diabetic patients. The LDDP does not show any trend to improve and either progresses relentlessly or remains relatively stable over years. Conversely, the focal diabetic neuropathies may relapse, but their course remains self-limited. In this article, the author reviews the clinical and pathological aspects of diabetic neuropathies associated with inflammatory phenomena.

Focal and Multifocal Diabetic Neuropathy

PDN of the Lower Limbs

Diabetic patients, usually over the age of 50, may present with PDN of the lower limbs characterised by a variable degree of pain and sensory loss associated with proximal muscle weakness and atrophy. This syndrome, originally described by Bruns and then by Garland,^2,3 has also been reported under different names.^4–11 The neurological picture is usually unilateral. Clinically, the patterns and the course of PDN strikingly differ from those of LDDP. In the University Hospital of Bicêtre’s study on PDN that included 27 patients, 24 with NIDDM and three with IDDM, the mean age at diagnosis was 62 years (range 46–71 years) and the male to female ratio was 16:11.⁸

Clinical Features of PDN

The onset of neuropathy can be acute or subacute. The patients complain of numbness or pains of the anterior aspect of the thigh, often of the burning type, worse at night and by contact. Difficulty in walking and climbing stairs is common due to weakness of the quadriceps and iliopsoas muscles. In fatter patients, early muscle wasting is often easier to palpate than to see. The patellar reflex is decreased or more often abolished. In most cases, the syndrome progresses over weeks or months, then stabilises and spontaneous pains decrease, sometimes rapidly. Approximately one-third of the patients experience a definite sensory loss over the anterior aspect of the thigh and the others a painful contact dysaesthesia in the distribution of the cutaneous branches of the femoral nerve, without definite sensory loss. Another cause, such as mechanical or malignant, must always be excluded before concluding that the neuropathy is related to diabetes.

In most cases, the patient’s condition improves after months, but sequelae – including disabling weakness and amyotrophy, sensory loss and patellar areflexia – are common. In a survey of long-term follow-up of up to 14 years, recovery began after a median interval of three months (range one to 12 months). The first improvement was decreased pain, resolution beginning within a few weeks and being almost complete by 12 months. Residual discomfort in the patients may take up to three years to subside.⁹ On the other hand, relapses are common, sometimes in spite of good diabetic control. In one-fifth of the patients that the University Hospital of Bicêtre investigated for this syndrome, relapses occurred within a few months. Thus, the clinical features of PDN, with frequent motor involvement, asymmetry of the deficit and gradual, yet often incomplete, spontaneous recovery, differ markedly from those of LDDP in which the sensory deficit is associated with motor signs only in extreme cases and in which symptoms virtually never improve spontaneously.

Figure 1: Inflammatory Infiltrate in the Superficial Peroneal Nerve of a Patient with Multifocal Diabetic Neuropathy (Hematoxylin and Eosion Staining)