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polyradiculopathies accounted for 5 percent of all cases referred to their EMG laboratory and our experience approximates this Careful EMG testing is therefore the most useful ancillary examination in cases of complex neuropathic syndromes since the pattern of muscle denervation can be ascertained and a common root pattern can then be logically derived Of great con rmatory 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 (see page 1100) 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 neuropathy, these proximal muscles are the last to be involved Among the acute and subacute meningeal radiculopathies, neoplastic in ltration (carcinomatous and lymphomatous) is the most common Others are Lyme disease, sarcoidosis, herpes genitalis, arachnoiditis, AIDS-related cauda equina neuritis of CMV infection, or independently by EBV In the past, meningeal syphilis was a common cause Diseases of the spine, exempli ed by lumbar and cervical spondylosis, commonly impinge on nerve roots, as discussed in Chap 11 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 rarer causes of polyradiculopathy is a chronic lumbosacral syndrome associated with dural eventrations surrounding nerve roots which may complicate ankylosing spondylitis (see page 180) Finally, it should be mentioned that one is confronted not infrequently by a subacute or chronic polyradiculopathy and abnormal CSF formula, for which extensive examination fails to identify any one of the diseases enumerated above This idiopathic form of polyradiculopathy comes to our attention once or twice yearly Some will turn out to have a lymphomatous in ltration at autopsy for which reason we have on occasion asked our neurosurgeons to remove a midlumbar motor rootlet for examination Also particularly dif cult diagnostically is a polyradiculopathy that involves the motor roots exclusively or predominantly that is distinguishable from motor neuron disease except for the complete absence of widespread denervation or of progressive upper motor neuron signs and, differing from the immune motor neuropathies discussed further on, by the absence of conduction block.

FIGURE 2-1

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minute and widely dispersed, giving rise rst to pulmonary symptoms and then to multiple dermal (anterior axillary fold and elsewhere) and cerebral petechial hemorrhages Accordingly, the clinical picture is more of an encephalopathy and not strictly focal, as it is in a stroke, although in some instances it may have focal features Cerebral air embolism is a rare complication of abortion, scuba diving, or cranial, cervical, or thoracic operations involving large venous sinuses; it was formerly encountered as a complication of pneumothorax therapy Clinically, this condition may be dif cult to separate from the de cits following hypotension or hypoxia, which frequently coexist Hyperbaric treatment may be effective if instituted early Despite the large number of established sources of emboli, the point of origin cannot be determined in about 30 percent of presumed embolic infarctions In such cases, emboli may have originated from thrombi in the cardiac chambers but have left behind no residual clot and may be undetectable by even sophisticated methods such as transesophageal echocardiography and newer MR techniques Others may be due to atheromatous material arising from the aorta If extensive evaluation fails to disclose the origin, the odds still favor a source in the left heart Not infrequently the diagnosis of cerebral embolism is made at autopsy without nding a source The search for a thrombotic nidus may not have been suf ciently thorough in these cases, and small thrombi in the atrial appendage, endocardium (between the papillary muscles of the heart), the aorta and its branches, or pulmonary veins may have been overlooked Nevertheless, in some cases, even when studied carefully postmortem, no source of embolic material can be discovered Clinical Picture Of all strokes, those due to cerebral embolism develop most rapidly, like a bolt out of the blue As a rule, the full-blown picture evolves within seconds, exemplifying most strikingly the temporal pro le of a stroke With rare exceptions, there are no warning episodes The embolus strikes at any time of the day or night Getting up to go to the bathroom is a time of danger Only occasionally and for unclear reasons, the clinical picture unfolds more gradually, over many hours, with some uctuation of symptoms Possibly, in these cases, the embolus initiates a thrombotic process in the occluded vessel The neurologic picture will depend on the artery involved and the site of obstruction The syndromes related to each angioanatomic territory are the same as those outlined earlier in this chapter, under Neurovascular Syndromes A large embolus may plug the distal internal carotid artery or the stem of the middle cerebral artery, producing the full-blown syndromes that follow occlusion of these arteries More often the embolus passes into one of the branches of the middle cerebral artery, producing a strikingly focal disorder such as a motor speech disorder, a monoplegia, or a receptive type of aphasia Any fragment of the middle cerebral syndrome or the complete picture may occur; the same is true for the anterior and posterior cerebral arteries, which are affected at a lower frequency than the middle cerebral because of their lower rates of blood ow Embolic material entering the vertebrobasilar system occasionally stops in the vertebral artery just below its union with the basilar; more often it traverses the vertebral and also the basilar artery, which is larger, and is not arrested until it reaches the upper bifurcation, where it produces the abrupt onset of coma and total paralysis or one of the related top of the basilar syndromes, described earlier in the chapter Or the embolus may enter one or both.