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(See also page 586) Although capable of producing diverse clinical presentations, most often the remote effect of cancer takes the form of a predominantly distal, symmetrical sensory, or sensorimotor polyneuropathy occurring as a remote effect of carcinoma or lymphoma Weakness and atrophy, ataxia, and sensory loss of the limbs may advance over several weeks or months to the point where the patient is con ned to a wheelchair or bed; usually the CSF protein concentration is mildly elevated All these symptoms may occur months or even a year or longer before a malignant tumor is found, although usually the tumor is apparent and is most often lung cancer In most series, a mixed sensorimotor polyneuropathy is four to ve times more frequent than a purely sensory one The latter is the more distinctive syndrome (described originally by DennyBrown); it is characterized by a loss of all modalities of sensation spreading from the distal to the proximal segments of the limbs and eventually to the trunk and face There is severe ataxia and loss of tendon re exes, but motor power is retained More recently, it has been appreciated that the sensory loss in the beginning may have a multifocal distribution The illness reaches its peak in a few weeks or months, and in a very few instances as mentioned the development has been as rapid as that of GBS The pathologic changes are those of an in ammatory and destructive sensory neuronopathy (ganglionitis) and are sometimes part of a more widespread disorder of the nervous system related to the anti-Hu antibody (also termed antinuclear neuronal antibody); see page 585 This has proven to be most typical of small-cell cancer of the lung In a large series of 71 patients with sensory neuronopathy reported by Dalmau and colleagues, more than half were associated with symptomatic in ammatory lesions in the temporal lobes (limbic encephalitis, page 586), the brainstem, and rarely the anterior horn neurons of the spinal cord Other distinctive paraneoplastic syndromes such as cerebellar degeneration and Lambert-Eaton myasthenic syndrome were combined with polyneuropathy in isolated cases, and there were signs of dysautonomia in 28 percent Our experience has been otherwise, with most cases of the myasthenic syndrome occurring in isolation The CSF protein is moderately elevated but acellular and shows high titers of the anti-Hu antibody Sensory potentials are usually absent in all nerves after a few weeks but may be spared early on The localization of anti-Hu antibody to the several affected regions of the nervous system and to the tumor itself has led to speculation that the lung tumors are typically small or inevident because the antibody suppresses tumor growth Almost all cases of paraneoplastic sensory neuropathy and a proportion of the more nondescript sensory predominant or sensorimotor paraneoplastic polyneuropathies also demonstrate anti-Hu antibodies, making, serum anti-Hu testing useful in distinguishing paraneoplastic varieties of sensory neuropathy and neuronopathy from those due to postinfectious or immune disorders such as Sjogren syndrome and HIV infection The nding of high antibody titers should lead to.

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detailed radiologic and, in appropriate cases, bronchoscopic or PET examinations to detect an underlying cancer A rare vasculitic mononeuritis multiplex that occurs with cancer is discussed further on An unusual assortment of polyneuropathies have been associated with non-Hodgkin lymphomas of both T- and B-cell types and with several related conditions such as Castleman disease (angiofollicular lymphoid hyperplasia), intravascular T-cell lymphoma (and the related lymphomatoid granulomatosis, page 565), hypersensitivity lymph node hyperplasia (angioimmunoblastic or immunoblastic lymphadenopathy), and Kimura disease (lymphoid hyperplasia with eosinophilia mainly involving skin) In most of these neuropathies, particularly the one associated with Castleman disease, there is a paraproteinemia, often polyclonal, thereby relating this group to the paraproteinemic neuropathies and to osteosclerotic myeloma, discussed later In several of our cases, the neuropathic manifestations have appeared simultaneously with lymph node enlargement in the groin, axilla, or thorax Clinically, the illness takes the form of GBS, chronic demyelinating polyneuropathy, subacute motor polyneuropathy or anterior horn cell disease, lumbar and brachial plexopathy, or a polyradiculopathy each occurring as a paralymphomatous condition clearly separable from cases of meningeal and neural in ltration by tumor Corticosteroids have been helpful in some of our patients with the lymphoid diseases; in others, the neuropathy resolves spontaneously or with radiation of the lymph nodes but otherwise progresses for months Vallat and colleagues have summarized their experience with the more conventional types of neuropathy accompanying non-Hodgkin lymphoma Intravascular lymphoma, a widespread neoplastic and vascular disease described on page 565, may involve the peripheral nerves in a multiple mononeuropathy pattern The various forms of paraneoplastic polyneuropathy are manifest clinically in 2 to 5 percent of patients with malignant disease The gures are higher if one includes the neuropathies accounted for by malnutrition and pressure palsies that occur in the later stages of cancer, and those identi ed by EMG in asymptomatic patients (Henson and Urich) As alluded to earlier, carcinoma of the lung accounts for about 50 percent of the cases of paraneoplastic sensorimotor polyneuropathy and for 75 percent of those with pure sensory neuropathy (Croft and Wilkinson); nevertheless, these neuropathies may be associated with neoplasms of all types Although anti-Hu binds to the peripheral nerve, the pathology of the paraneoplastic polyneuropathies has not been completely de ned In the purely sensory type, there is not only a loss of nerve cells in the dorsal root ganglia but also an in ammatory reaction (Horwich et al) much the same changes as occur with the sensory neuronopathy of Sjogren syndrome In the mixed sensorimotor polyneuropathy, the degeneration is greater in the distal than it is in the proximal segments of the peripheral nerves, but it extends into the roots in advanced cases Dorsal root ganglion cells may be reduced in number If the histologic examination is performed early in the course of the neuropathy, sparse in ltrates of lymphocytes are observed, distributed in foci around blood vessels Their relation to both segmental demyelination and axonal degeneration of myelinated bers is unclear No tumor cells are seen in the nerves or spinal ganglia, unlike the rare instances of carcinomatous and lymphomatous mononeuropathy multiplex, in which tumor cells actually in ltrate nerves Degeneration of the dorsal columns and chromatolysis of anterior horn cells are secondary to changes in the peripheral nerves and roots The overall prognosis of the paraneoplastic neuropathies is poor Even though the polyneuropathy may stabilize and not pro-.