A special pattern of polyradiculopathy occurs wherein all the sensory roots are involved, simulating tabes dorsalis. The clinical state is similar to that of a sensory ganglionopathy described earlier. Largeand small-fiber sensory loss is combined with ataxia while power is normal and there is no atrophy. A prominent feature is shooting and burning pain. We have occasionally found sensory loss over the anterior abdomen and thorax in these cases, a finding more typical of chronic dying-back axonal polyneuropathy.
Some of the diseases that affect nerve roots predominantly already have been discussed. They can be grouped into three broad categories: (1) diseases of the spinal column that compress adjacent roots; (2) infiltrative diseases of the meninges that secondarily involve the roots as they course through the subarachnoid space, mainly neoplastic of granulomatous infiltrations such as sarcoid; and (3) intrinsic neuropathies, inflammatory, infectious, or diabetic, that have a predilection for the radicular portion of the nerves. An elevated CSF protein and a pleocytosis usually accompany neoplastic or inflammatory meningeal diseases; the others show variable formulas in the spinal fluid.
Often what appears to be a polyneuropathy on clinical grounds will be found to have an electrophysiologic pattern of root disease at multiple spinal levels. McGonagle and colleagues estimated that polyradiculopathies accounted for 5 percent of all cases referred to their EMG laboratory and our experience approximates this. Consequently, careful EMG and nerve conductions testing is the most useful ancillary examination in cases of complex neuropathic syndromes because the pattern of muscle denervation can be ascertained with greater certainty than by clinical means and a common root pattern can then be logically derived. Of great confirmatory value is the preservation of sensory potentials in nerves that innervate regions of sensory loss and supply weak and denervated muscles. This proves that the lesion is located proximal to the dorsal root ganglion and spares the peripheral sensory axons. Loss of the F and H late responses is also typical of polyradiculopathies. The proximal location of the lesion can be further corroborated by early evidence of weakness and denervation in the paraspinal, gluteal, or rhomboid muscles, which are supplied by nerves that arise very proximally from the roots. In axonal cases of neuropathy, these proximal muscles are the last to be involved.
Among the acute and subacute meningeal radiculopathies, neoplastic infiltration (carcinomatous and lymphomatous) is the most common. Others are Lyme disease, sarcoidosis, herpes virus, arachnoiditis, AIDS-related cauda equina neuritis of CMV infection, or independently, EBV meningoradiculitis. In the past, meningeal syphilis, of course, was a common cause (tabes dorsalis).
Diseases of the spine, exemplified by lumbar and cervical spondylosis, commonly impinge on nerve roots, as discussed in Chap. 10. Metastatic carcinoma of the vertebral bodies may compress one or several adjacent roots by encroaching on posterolateral recesses of the canal and proximal neural foramina. Among rare causes of polyradiculopathy is a chronic lumbosacral syndrome associated with dural eventrations surrounding nerve roots, which may complicate ankylosing spondylitis.