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or more often by an opportunistic CMV infection in a patient with AIDS Diagnosis This is both aided and at times confused by serologic testing (see Chap 32) The enzyme-linked immunosorbent assay (ELISA) is not altogether satisfactory because it frequently yields false-positive and, occasionally, false-negative results Western blot testing is more speci c Knowledge that the patient has lived in or visited an endemic area is useful but far more important is evidence of a tick bite followed by the characteristic rash or a wellde ned history of nonneurologic manifestations of Lyme disease (cardiac, arthritic) Indeed, one should be cautious in making this diagnosis unless a primary Lyme infectious syndrome had been present Bifacial palsy in any of these clinical contexts also favors the diagnosis Treatment Treatment of the neuropathic disease is with intravenous antibiotics, preferably ceftriaxone 2 g daily for 1 month Corticosteroids have an uncertain role in the painful radicular syndromes but we have used them in low doses and they apparently relieved the pain Sjogren-Sicca Syndrome This is a chronic, slowly progressive autoimmune disease characterized by lymphocytic in ltration of the exocrine glands, particularly the parotid and lacrimal glands resulting in keratoconjunctivitis sicca and xerostomia (dry eyes and mouth) The latter features may be combined with arthritis or with a wide range of other abnormalities, notably lymphoma, vasculitis, renal tubular defects, and quite often by a predominantly sensory polyneuropathy (see review by Kaplan et al) In the series collected by Grant and colleagues, the neuropathy was the presenting problem in 87 percent of 54 patients with the sicca complex The sicca symptoms are usually mild and often reported only upon speci c inquiry A symmetrical sensory polyneuropathy or sensory ganglionopathy is the most common pattern Sensorimotor polyneuropathy, polyradiculoneuropathy, autonomic neuropathy, or mononeuropathy (most often of the trigeminal nerve, as described by Kaltrieder and Talal) are less common We have observed yet another neuropathic syndrome taking the form of an asymmetrical sensory loss, mostly of position sense and involving the upper limbs predominantly, in association with tonic pupils and trigeminal anesthesia The sensory polyneuropathy of the Sjogren syndrome more of an in ammatory ganglionitis or sensory neuronopathy (Grif n et al) is of particular interest to neurologists, since most cases will rst be seen by them More than 90 percent of the patients are older women The sensorimotor polyneuropathic syndrome begins with paresthesias of the feet and is usually mild in degree The main clinical features are a subacute and widespread sensory loss that may include the trunk and a profoundly diminished kinesthetic sense, giving rise to sensory ataxia of the limb and of gait Loss of pain and temperature sensation is variable; tendon re exes are abolished In time, many of these patients develop autonomic abnormalities such as bowel atony, urinary retention, loss of sweating, and pupillary changes There is usually little or no pain but there have been exceptions Diagnosis Sjogren syndrome should be suspected in an older woman with sensory neuropathy or neuronopathy, particularly if sicca symptoms are present The evaluation of suspected Sjogren disease is aided by the Schirmer or Rose Bengal tests (page 461), which can demonstrate a reduction of tearing Even without this con rmatory test, we have found it advisable to perform a biopsy of the lip (at the epithelial-mucosal juncture) to detect in ammatory
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changes in the small salivary glands This is a minor of ce procedure in most instances The diagnosis of Sjogren syndrome re quires the detection of at least two collections of 50 or more lymphocytes in a 4 mm2 specimen Some patients have serologic abnormalities such as antinuclear antibodies (anti-Ro, also termed SS-A, and anti-La, or SS-B) or increased monoclonal immunoglobulins, particularly of the IgM subclass The frequency of these speci c Sjogren-speci c antibodies varies greatly between series; they may be useful as screening tests, but the lip biopsy is a far more sensitive diagnostic procedure In our series of 20 cases with salivary gland biopsies that demonstrated in ammatory changes diagnostic of the syndrome, only 6 had serologic evidence of the disease and two had positive serologic tests but a negative biopsy (Gorson and Ropper) The sedimentation rate in our patients was often slightly elevated, however, only 5 of our 20 had a value greater than 40 mm/min The main differential diagnostic entity is a paraneoplastic sensory ganglionitis Mellgren and also Leger and their colleagues have stressed the point that a proportion of unexplained polyneuropathies in middle and late life are caused by Sjogren syndrome The latter authors found typical Sjogren abnormalities in the lip biopsies of 7 of 32 patients with chronic axonal polyneuropathy that could not otherwise be classi ed Several other studies have corroborated this nding of in ammatory disruption of the minor salivary glands in obscure neuropathies, particularly in older women and in some men The diagnosis in our clinics, where lip biopsies are routinely performed in patients with nondescript sensory neuropathies, has not been nearly as frequent Nonetheless, a search for Sjogren disease may be revealing in otherwise obscure sensory neuropathies Nerve biopsies in some cases have revealed a necrotizing vasculitis, in ammatory cell in ltrates, and focal nerve ber destruction Usually, the CSF protein is normal and there is no cellular reaction The few times a dorsal root ganglion has been examined, there were in ltrates of mononuclear cells and lymphocytes and destruction of nerve cells Treatment Treatment of the sicca complex and the neuropathic manifestations is unfortunately largely symptomatic Corticosteroids, cyclophosphamide, and chlorambucil have been used when the neuropathy is severe and are indicated when there is vasculitis involving renal and pulmonary structures We have administered prednisone 60 mg daily, often in tandem with intermittent plasma exchange, with little evidence of response In a few severe cases, monthly intravenous cylcophosphamide has been added Others have recorded more encouraging results The review of the neurologic manifestations of Sjogren syn drome by La tte is recommended Idiopathic Sensory Ganglionopathies (Chronic Ataxic Neuropathy) In addition to the subacute pansensory syndrome described above and paraneoplastic, postinfectious, or toxic processes (page 1128), there is a more chronic idiopathic variety characterized by severe global sensory loss and ataxia We have encountered several such patients with sensory loss and pronounced ataxia resembling the cases described by Dalakas The numbness and sensory ndings progressed over months and spread to proximal parts of the arms and legs and then to the trunk The face and top of the scalp were nally involved Despite severe ataxia and complete are exia, muscular power remained normal Pain was not a problem There are reports of fasciculations in a few patients (but not in the ones we have seen) Within a year, most of these patients became completely disabled from the ataxia, unable to walk or even
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