Diabetic Lumbosacral Radiculoplexus Neuropathy

Diabetic lumbosacral radiculoplexus neuropathy is a painful condition that causes severe weakness and muscle wasting of the lower extremities. A number of clinical terms have been applied to this syndrome, including diabetic amyotrophy, femoral neuropathy of diabetes, diabetic asymmetric proximal motor neuropathy, and diabetic lumbosacral plexopathy. Differences in terminology have reflected various opinions as to the primary anatomic site of the lesion and underlying pathology. Although the syndrome was initially thought to be limited to the proximal muscles of the thigh, more recent studies have demonstrated that most cases are widespread, affecting both proximal and distal segments in bilateral lower extremities. Pathologic findings on nerve biopsy include microvasculitic changes and inflammation, suggestive of an underlying immunemediated vasculitis; however, the exact mechanism of injury is still unknown.

Clinical Manifestations. The onset of symptoms is typically focal, beginning with severe pain in the anterior thigh and hip and weakness of the thigh muscles. It is also often accompanied by weight loss. Over time, the symptoms progress to involve distal segments and eventually the contralateral limb. Less commonly, there may be additional thoracic nerve root involvement resulting in truncal pain and paresthesias. The cervical dermatomes are usually not affected, although there may be a concomitant mononeuropathy of the upper limb, such as an ulnar mononeuropathy.

Although the onset of symptoms is often fairly acute or even precipitous, the course may be insidiously progressive in some patients. Pain is the most common initial complaint. In contrast to the patient with disk disease, who can usually find a comfortable position at night, the patient with diabetic lumbosacral radiculoplexus neuropathy often has nocturnal exacerbations. The pain frequently has a dysesthetic quality evoked by touch or exacerbated by clothing, such as brassiere straps or garments fitting tightly over the thigh. When thoracic dermatomes are involved, the pain is sometimes severe enough to mimic an abdominal or cardiac crisis.

Weakness without sensory loss may be the first sign in some patients. Involvement of the quadriceps femoris and iliopsoas muscles may compromise climbing stairs or arising from a squatting position. With more distal weakness, the patient may experience gait difficulty due to a footdrop.

Diagnosis. Physical examination confirms the radicular or plexus pattern of motor loss. Deep tendon reflexes, particularly the knee jerk, are often absent. Sensory loss may be difficult to define, although the area of hyperpathia may sometimes mimic a nerve root distribution. A moderate number of patients show signs of coexisting mild symmetric distal polyneuropathy, although sensory abnormalities in the feet may also be related to distal limb involvement.

Reduced amplitudes of sensory and motor nerve conduction responses are seen on electromyogram (EMG), with needle examination findings of active denervation and neurogenic motor unit potential changes in the distribution of multiple nerve roots, including paraspinal muscles. Cerebrospinal fluid (CSF) protein is often elevated. Imaging studies of the lumbosacral spine are typically normal.

Course and Treatment. In most cases, improvement occurs spontaneously over a period of 6 to 18 months, but immune-modulating therapy may expedite recovery with regard to pain and weakness. Symptomatic management with optimal pain control and physical therapy is crucial. Relapse may occur in approximately one in five patients.

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