A few patients with severe atherosclerotic ischemic disease of the iliac or leg arteries will be found to have localized sensory changes or diminished reflexes. Usually, the other effects of ischemia—claudication and pain at rest, absence of distal pulses and trophic skin changes—are so prominent that the neurologic changes are minor by comparison. In experimental studies, combined occlusion of the aorta and multiple limb vessels are required to produce neural ischemia because of the profusely ramifying vasculature. In our experience of 12 patients with a critically ischemic leg, there was a neuropathy with a pronounced distal predominance; sensory loss in the feet was worse than the symptoms might suggest and there was mild weakness of the toes and depression or loss of the ankle reflex (Weinberg et al). Although paresthesias, numbness, and deep aching pain at rest were characteristic, the patients were more limited by symptoms of their vascular claudication than by the neuropathic ones. Restoration of circulation to the limb by surgical or other means resulted in some improvement of the regional neuropathy. Reviews of the literature on this subject can be found in the writings of Eames and Lange.
A poorly understood but presumably localized ischemic neuropathy occurs in the region of arteriovenous shunts (fistulas) that have been placed for the purpose of hemodialysis. Complaints of transient diffuse tingling of the hand are not uncommon soon after creation of the shunt but only a few patients develop persistent forearm weakness, numbness and burning in the fingers, reflecting variable degrees of ulnar, radial, and median nerve, and possibly also muscle, ischemia. The role of an underlying uremic polyneuropathy in facilitating this neuropathy has not been studied.
A progressive, symmetrical polyneuropathy as a result of systemic cholesterol embolism has been described by Bendixen and colleagues. An inflammatory and necrotizing arteritis surrounds embolic cholesterol material within small vessels and appears to account for the progression of symptoms. This neuropathic process is more often discovered at autopsy than it is in the clinic, being eclipsed during life by the cerebral manifestations of cholesterol embolism. The peripheral part of the illness simulates the polyneuropathy of a small-vessel polyarteritis.
The generalized granulomatous disease of sarcoidosis infrequently produces subacute or chronic polyneuropathy, polyradiculopathy, or mononeuropathies. A painful, small-fiber sensory neuropathy has also been described by Hoitsma and colleagues. Any of the neuropathies may be associated with granulomatous lesions in muscles (polymyositis) or with signs of CNS involvement, most often of the stalk of the pituitary with diabetes insipidus or a myelopathy (see Chap. 31).
Involvement of a single nerve with sarcoid most often implicates the facial nerve (facial palsy), but sometimes multiple cranial nerves are affected in succession (see Chaps. 35 and 44). Next in frequency is weakness and reflex and sensory loss, appearing sequentially (polyradiculopathy), in the distribution of several spinal nerves or roots. The occurrence of large, irregular zones of sensory loss over the trunk is said to distinguish the neuropathy of sarcoidosis from other forms of mononeuropathy multiplex. This pattern particularly when accompanied by pain, resembles diabetic radiculopathy (see earlier in “Diabetic Multiple Mononeuropathies and Radiculoplexus Neuropathy”).