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Background/aims: Endonasal laser dacryocystorhinostomy (ELDCR) has many potential advantages over conventional external DCR. Although the short term results of this technique have been reported, little is yet known of the long term results, and the occurrence of late rhinostomy failure. The aim of this study was to examine the results at 3 and 12 months following ELDCR., Method: The notes of all consecutive ELDCRs performed between November 1993 and May 1995 were retrieved. Demographic information, details of surgery, and the postoperative results were noted., Results: ELDCR procedures which did not undergo lacrimal stenting showed a short term success rate of 67% at 3 months, and a further failure rate of 9% at 12 months. ELDCRs which did undergo lacrimal stenting showed a short term success rate of 82% at 3 months, and a further failure rate of 21% at 12 months. Lacrimal intubation increased the long term success rate by 8%. The success rate was lower in the presence of local risk factors for nasal mucosal scarring., Conclusions: ELDCR requires some adjunctive treatment to improve maintenance of the nasal mucosal ostia if it is to complete successfully with external DCR on grounds other than cosmesis and patient convenience.

Endoscopic holmium laser dacryocystorhinostomy can be used safely and efficiently to relieve symptoms of distal nasolacrimal duct obstruction. It has great advantages over the conventional external approach as it can be done as a day-case procedure under local anaesthesia. The excellent ablation of bone and soft tissue using this type of laser contribute to the fact that the procedure can be performed in a mean time of 20 minutes. We report on the results of our first 50 patients and review the literature on the subject.

Purpose: To review the effects on intraocular pressure control of the use of standard and heparin-coated intraocular lenses (IOLs) following combined cataract and glaucoma surgery after a minimum period of 2 years., Methods: Case note review of all patients with glaucoma who required cataract extraction combined with trabeculectomy and who were randomized to either of the two IOL types. The number of ocular hypotensive medications and the intraocular pressures were recorded pre-operatively and at 3, 6, 18 and 24 months following surgery., Results: The two groups (9 receiving standard IOLs and 10 heparin-coated IOLs) were comparable for age, sex and follow-up, as were the pre-operative intraocular pressures and number of treatments. Post-operatively, all patients achieved an intraocular pressure < 21 mmHg at the final visit, with only one patient in each group requiring topical medication, but the standard lens group had a higher intraocular pressure at 2 years (p<0.05). The magnitude of the fall from the pre-operative values was greater in the heparin-coated lens group at 2 years after surgery (p<0.02). The presence of a visible drainage bleb occurred equally frequently in the two groups., Conclusions: Use of a heparin-coated IOL does not adversely affect the intraocular pressure control following combined cataract and drainage surgery. The greater fall in intraocular pressure at 2 years in those receiving a heparin-coated IOL may have occurred by chance.

Objectives: In the past, patients with hereditary hemochromatosis have been identified predominantly from symptomatic presentation or from family studies. In the 1990s, iron studies on routine screening chemistry panels have become more commonplace. The purpose of this paper is to describe the clinical, laboratory, and presenting features of a series of patients with hereditary hemochromatosis, diagnosed from 1990 to 1995., Methods: Clinical information, serum and liver iron studies, liver histology, and phlebotomy requirements were evaluated in 40 patients with newly diagnosed hereditary hemochromatosis prospectively referred to a tertiary university-based hepatology clinic., Results: Eighty-three percent of patients came to medical attention as a result of screening blood work: 73% were asymptomatic and 78% had normal physical examinations. Only three patients had cirrhosis from hemochromatosis alone, only two were diabetic, and only two had increased skin pigmentation. These findings are in contrast to previous reports of hemochromatosis probands in which patients with symptoms and more advanced disease were identified. The hepatic iron concentration, hepatic iron index, and age at diagnosis were similar for men and women., Conclusions: With the use of screening iron studies on routine serum chemistry panels, patients with hemochromatosis can be identified and subsequently treated before they have symptoms or organ damage.

Aims: To assess whether timolol drops lower a raised intraocular pressure (IOP) when given sublingually. This route of administration would be useful for glaucoma patients who are unable to instil their own drops--for example, because of stroke, poor vision, arthritis, poor coordination, or blepharospasm., Methods: A placebo controlled randomised, double masked, crossover study was undertaken in the glaucoma clinic of a large teaching hospital. Twelve patients with ocular hypertension with IOPs over 21 mm Hg, normal optic discs, and full visual fields were examined by Humphrey perimetry. Single dose units of timolol maleate 0.5% drops and normal saline drops were given by instillation in one eye or sublingually. The IOP of both eyes, pulse rate, and blood pressure were all measured before and after each type of drop and route of administration., Results: Two hours after instillation of timolol in one eye, the IOP in the treated eye was reduced by a mean of 8.5 mm Hg (p = 0.0000), and by 1.66 mm Hg in the fellow eye (p = 0.03). Two hours after sublingual instillation of timolol, the IOP was reduced by 7.55 mm Hg in the study eye (p = 0.0000) and by 7.7 mm Hg in the fellow eye (p = 0.0000). There was an equal amount of reduction in pulse rate by either route, but there was no significant change in blood pressure., Conclusions: The results show that, at least after 2 hours, sublingual treatment is almost as effective as topical treatment in lowering a raised IOP.

We compared the binding of human antibodies from patients with neuropathy to the myelin-associated glycoprotein (MAG), to its cross-reactive glycolipid sulfoglucuronyl paragloboside (SGPG), and to sections of peripheral nerve. Titers were correlated with the clinical presentation and results of electrophysiological and pathological studies. Most patients had a predominantly sensory or sensorimotor demyelinating neuropathy and highly elevated antibodies to both MAG and SGPG, but 2 had highly elevated antibodies to MAG alone, and 1 to SGPG alone. Two patients had predominantly motor neuropathy and highly elevated antibodies to SGPG which reacted with MAG by Western blot but not by enzyme-linked immunosorbent assay. One patient had amyotrophic lateral sclerosis and antibodies to SGPG but not to MAG. These studies indicate that the neuropathic syndrome associated with anti-MAG or -SGPG antibodies are more heterogeneous than previously suspected, and that although most of the antibodies react with both MAG and SGPG, some may react with MAG or SGPG alone.

Cataract extraction is now routinely followed by insertion of an intraocular lens (IOL) which requires preoperative biometry to determine the most accurate implant power required. Biometry is generally performed just prior to surgery and may even require the patient to make a special hospital visit when day case surgery is contemplated. A prospective study was undertaken to determine the accuracy of axial length (AL) measurement through a dilated pupil. The AL of one eye of 64 patients admitted for cataract surgery was measured before and after dilation with a drop of tropicamide 1%. Our results show that there was no significant difference in the ALs before and after dilation (p = 0.10), and neither was there a difference in the average range of measurements (p = 0.70), with 78% of eyes having a difference of < +/- 0.3 mm between pre and post dilation ALs. We conclude that AL measurement performed on a dilated pupil can give an accurate result, and suggest that performing biometry on a dilated pupil following ocular assessment may be an efficient and time saving exercise.

We believe that a previously undocumented cause of recurrent red, watery, sore and itchy eyes in children is dysversion of the lateral eyelashes. Diagnosis requires a close examination of the lateral aspect of the eyelids where dysverted lashes are seen to be growing from normal follicles. The lateral lashes are fine, long and flexible. They curve inwards and rub on the conjunctiva and cornea, and cause the above symptoms. Secondary signs include skin changes, recurrent conjunctivitis, and corneal abrasions. Conservative treatment consisting of manual repositioning of the dysverted eyelashes is recommended so that surgery may be avoided. Recognition of the condition by the primary practitioner, and institution of the straightforward treatment described above, can obviate much morbidity. The inappropriate use of topical antibiotics and frequent return visits to the practitioner may also be thus avoided.

The early results of the first 50 primary endonasal laser dacryocystorhinostomies in 49 patients performed with the holmium:YAG laser are presented. Overall, 35 (70%) were successful in relieving symptoms of nasolacrimal obstruction after a mean follow-up period of 4 months. This improved to 79% in the subgroup of patients who underwent intubation of the naso-lacrimal system. These results were similar to the results of a retrospective study of 67 patients undergoing conventional dacryocystorhinostomy in our unit. Conventional surgery was performed under general anaesthesia in all but 1 case and all were treated as inpatients, with a mean hospital stay of 2.3 days, whereas all but 1 of the laser group had their surgery under local anaesthesia and 46 operations (94%) were performed as an outpatient procedure. Surgery was significantly quicker with the endonasal laser technique and 90% of patients questioned found this technique to be entirely acceptable.

Purpose: To compare measurements of the vertical diameter of the optic disk using the Heidelberg Retinal Tomograph (HRT) and planimetric methods., Methods: On the HRT, three measurements of the vertical disk diameter were made on 32 eyes from a composite image using the circle draw facility and were compared with three measurements of the central image of the 32 tomographic cuts. These were repeated by a second observer. Measurements were compared with those obtained from photographs using the three corrections described by Bengtsson and Krakau., Results: For the HRT, there was minimal intraobserver variation, coefficient of variation (1.515% to 1.882% for the two observers). Interobserver variation was also small (CoV 1.969%). The authors found the closest agreement with the HRT measurements using regression analysis was obtained using correction 3 (r = 0.8258). HRT measurements were significantly smaller (P < 0.0001) by a constant amount of 0.13 mm across the range of optic disk size. There was a significant difference between the HRT measurement of the composite image and the central cut (P = 0.0003 for observer 1)., Conclusions: HRT measurements are significantly smaller than those from photographs and, therefore, are not interchangeable.

In a study to determine the prevalence of monoclonal gammopathy (MG) among patients with motor neuron disease (MND), 6 out of 56 (10.7%) were found to have a monoclonal paraprotein. Of these 6 patients, 4 had an IgG and 2 had an IgA paraprotein. The clinical syndromes consisted of amyotrophic lateral sclerosis in 2 patients, lower motor neuron syndrome with preserved reflexes in at least one limb in 3 patients, and motor neuropathy with multifocal conduction block in 1 patient. The presence of gammopathy appears to correlate with the absence of marked upper motor neuron involvement and with elevated CSF protein concentration. An underlying malignant disorder was ruled out in all 6 patients, and they were considered to have MG of undetermined significance (MGUS). In a control group of 121 age-matched patients with other neuroimmunological disorders, 5 patients (4.13%) had MG. Four of these had gammopathy associated with malignant myeloma, and 1 had MGUS. These results support previous reports of increased prevalence of MGUS in patients with MND and suggest that an autoimmune mechanism may play a role in the disease.

There has been recent interest in the progression of diabetic retinopathy following extracapsular cataract extraction (ECCE) especially with vitreous loss. It is well known that diabetic retinopathy progresses after intracapsular cataract extraction (ICCE) but was thought to be less common after ECCE. We present 7 patients with symmetrical non-proliferative diabetic retinopathy who underwent ECCE with intraocular lens (IOL) implantation. These patients ranged in age from 56 to 69 years; 2 were insulin-dependent diabetics (IDDM) and 5 non-IDDMs. Rubeosis iridis developed quickly between post-operative outpatient visits despite good diabetic control and a static retinal picture in the fellow eye. Visual loss following the onset of rubeosis was severe, with 3 patients needing cyclocryotherapy and eventually having no perception of light. The rapid onset of rubeosis between post-operative outpatient visits leads us to suggest much shorter periods between reviews than is current practice and the consideration of routine panretinal photocoagulation in the immediate post-operative period in diabetics with worsening retinopathy after ECCE and IOL. Possible causes of the increase in neovascularisation and rubeosis are discussed. The most important message highlighted by these case histories is that the surgery and follow-up of diabetic patients undergoing surgery should be undertaken by an ophthalmologist with an interest in diabetes. Where there is no recognised diabetic retinal specialist in a unit, then early referral to such an ophthalmologist is recommended when complications arise.

We reviewed the clinical and electrophysiologic features of 36 patients with increased titers of IgM anti-GM1 antibodies. Mildly elevated titers of up to 3,200 were not associated with any particular clinical syndrome or disease. Clinically, 14 of 16 patients with highly elevated titers of 6,400 or higher had progressive weakness with lower motor neuron signs; six had active tendon reflexes and eight had absent reflexes, but none had definite upper motor neuron signs. Electrophysiologic studies showed spontaneous activity in all 14 patients, one or more motor conduction blocks in nine, slowed motor conductions in one, and normal conductions in four patients. None had abnormal sensory conductions. These patients presented with a syndrome that has features of, but is distinct from, both motor neuron disease and demyelinating neuropathy.

A subset of human anti-GM1 ganglioside antibodies cross-reacts with Gal(beta 1-3)GalNAc bearing glycoproteins in peripheral nerve and spinal cord. The same oligosaccharide determinant is recognized by the lectin peanut agglutinin (PNA) which binds at the nodes of Ranvier in intact peripheral nerve. The Gal(beta 1-3)GalNAc bearing glycoproteins were isolated using PNA lectin affinity chromatography followed by separation on Western blot, and the proteins were subjected to partial amino acid sequence analysis. Two major PNA binding glycoproteins were identified in peripheral nerve and spinal cord; one had an approximate molecular weight of 120 kD and had sequence homology to the oligodendrocyte-myelin glycoprotein (OMgp). The other migrated between 70 and 80 kD and had sequence homology to the hyaluronate binding domain of versican, which has been reported to share sequence homology with the 70 kD proteins hyaluronectin and the glial hyaluronic acid binding protein (GHAP). By immunocytochemistry, OMgp was localized to the paranodal region of myelin, and the protein homologous to the hyaluronate binding domain of versican was localized to the nodal gap in peripheral nerve. These PNA binding glycoproteins might be target antigens for autoantibodies in peripheral nerve.

A male aged 54 years presented with a pathological fracture of the right femur at the subtrochanteric level. The fracture site showed a lytic lesion with expansion of the bone, considered to be a metastasis. On histology, however, the area turned out to be malakoplakia of bone. The patient responded well to antibiotics and sulphonamides along with skeletal traction. This appears to be the fourth reported case of malakoplakia of bone.

Using immunofluorescence microscopy we found that gp120 binds to the surface of rat dorsal root ganglia neurons and human neuroblastoma cells but not to rat fibroblasts or glial cells. The binding of gp120 to neurons was eliminated by pretreatment with trypsin, which removes cell-surface proteins, but not with chloroform: methanol, which removes glycolipids. As control, neuronal staining by antisulfatide antibodies was eliminated by pretreatment with chloroform: methanol but not with trypsin. The gp120 binding to neurons was also inhibited by the mouse monoclonal antibody 01, which binds to galactocerebroside and cross-reactive glycoproteins. These studies suggest that the receptor for gp120 on the surface of the dorsal root ganglia neurons is a glycoprotein. This interaction may mediate the effects of human immunodeficiency virus type 1 in sensory neuropathy.

We investigated the binding of the gp120 glycoprotein of the human immunodeficiency virus (HIV-1) to neural glycolipids and glycoproteins by ELISA. The gp120 protein bound to sulfatide (GalS), a sulfated glycolipid autoantigen implicated in sensory neuritis, and to the myelin associated glycoprotein (MAG), an autoantigen in demyelinating neuropathy. Binding of gp120 to MAG was inhibited by the HNK-1 antibody, which recognizes a sulfated glucuronic acid epitope, suggesting that the interaction involves carbohydrate determinants. Sulfatide and MAG are potential receptors for gp120 in peripheral nerve and may have a role in the neuropathy associated with HIV-1 infection.

Increased titers of anti-sulfatide antibodies were detected by ELISA in 5 of 200 patients and control subjects. All 5 patients had sensory impairment; 4 had neuropathy, and one had multiple sclerosis. Of the patients with neuropathy, 2 had a clinical syndrome of small fiber sensory neuropathy with normal electrophysiological or nerve biopsy studies, 1 had a sensorimotor axonal neuropathy associated with IgM monoclonal gammopathy, and 1 had sensorimotor neuropathy with multifocal motor conduction block and anti-GM1 antibodies. The anti-sulfatide antibodies bound to the surface of unfixed rat dorsal root ganglia neurons and human neuroblastoma cells, and to fixed sections of central and peripheral myelin. No binding was detected following intraneural injection into rat sciatic nerves. Pre-absorption with sulfatide but not with galactocerebroside eliminated the tissue binding activity. These findings indicate that increased titers of anti-sulfatide antibodies are found in patients with sensory impairment but are not restricted to a particular neurological syndrome or type of neuropathy. The significance of anti-sulfatide antibodies is uncertain although sulfatide on dorsal root ganglia neurons may be a target antigen.

Immune mechanisms are thought to be important in a subpopulation of patients with schizophrenia. We examined the specificity of neural antibodies in patients with schizophrenia to identify a possible antigen. Serum antibodies from patients with schizophrenia and control subjects were tested for binding to protein extracts of human neuroblastoma cells by western blot. Protein antigens were characterised by aminoterminal and internal aminoacid sequence analysis. 14 of 32 (44%) otherwise healthy patients with schizophrenia had antibodies to a neuroblastoma protein of molecular weight 60 kDa. By partial sequence analysis, this protein was identified as the 60 kDa human heat-shock protein (hsp) that is the P1 mitochondrial protein, and which is 50% homologous to the mycobacterial 65 kDa hsp. Antigens that crossreact with hsp65 have been implicated in the pathogenesis of adjuvant-induced arthritis in rats and autoimmune diabetes in mice. Of 100 normal subjects or disease controls, antibodies to hsp60 were found in only 8 patients, all of whom had active infectious or inflammatory disease. Our results support the presence of abnormal immune reactivity involving hsp60 in a subset of patients with schizophrenia. The immune response may be related to the pathogenesis of the disease.

A patient with sensorimotor mononeuritis multiplex had a type II cryoglobulin with an IgM kappa M-protein that appeared to contain monoclonal anti-MAG antibodies of the same isotype. A sural nerve biopsy demonstrated necrotizing arteritis and features of both axonal degeneration and demyelination. IgM kappa and C3 deposits were present on the myelin sheath of some residual nerve fibers. The findings suggest that the anti-MAG antibodies contributed to the myelin damage, while cryoprecipitates may have caused the vasculitis and axonal degeneration.

Anti-GM1 antibodies were measured in 22 patients with the Guillain-Barré syndrome (GBS) and compared with anti-GM1 antibody activity in patients with other neurological or immunological diseases and in normal subjects. Four out of 22 patients with GBS had raised IgM, IgG, or IgA anti-GM1 antibody activities. All four patients were tetraparetic with only minimal or no sensory deficit. Three of the patients had highly raised antibody activity and showed severe residual deficits, while of the remaining patients with GBS, only one remained severely affected. One patient had anti-GM1 antibodies specific for GM1, whereas the other three patients showed antibody activity with asialo-GM1 or GD1b. The presence of anti-GM1 antibodies may define a subgroup of patients with GBS who have a poor prognosis.

Increased titres of anti-neurofilament antibodies have been reported in neurodegenerative disorders, and it has been suggested that such antibodies might be pathogenic. We investigated the specificity of an IgA monoclonal antibody (MAb) from a patient with amyotrophic lateral sclerosis which reacted with neurofilaments and bound to the surface of neuroblastoma cells. In Western blots, the immunoaffinity-purified IgA bound to the 220-kD, high-molecular-weight neurofilament protein (NFH) and cross-reacted with several closely migrating protein bands with apparent mobility of 62-68 kD in neuroblastoma cells and extracts of normal human spinal cord. Following crosslinking to the surface of radiolabeled neuroblastoma cells, the IgA MAb immunoprecipitated a 65-kD protein, indicating that the protein was present on the cell surface and available to the antibodies for binding. Several other MAbs to NFH did not immunostain the surface of neuroblastoma cells or bind to the 65-kD protein, indicating that the protein was not a fragment of NFH. Thus, antibody binding to the 65-kD protein, possibly by cross-reacting with NFH, may have contributed to the neuronal degeneration.

Antibodies to GM1 or Gal(beta 1-3)GalNAc are associated with motor or sensorimotor neuropathy and with motor neuron disease. To investigate the role of these antibodies in the neurological disorder, rabbits were immunized with GM1 or with Gal(beta 1-3)GalNAc-BSA, and studied serologically, electrophysiologically and pathologically. Development of antibodies to the immunizing antigens was associated with a fall in the ratio of the amplitudes of the compound muscle action potential evoked by proximal versus distal stimulation of the sciatic nerve. Pathological studies revealed mild axonal degeneration and immunoglobulin deposits at the nodes of Ranvier in peripheral nerve, resembling those reported in a patient with motor neuropathy, motor conduction block and anti-GM1 antibodies. These studies provide evidence that anti-GM1 or anti-Gal(beta 1-3)GalNAc antibodies cause conduction abnormalities and indicate that the antibodies may exert their effect, in part, by binding at the nodes of Ranvier in peripheral nerve.

A 75-year-old woman had breast carcinoma, an IgA paraprotein and autopsy-proven amyotrophic lateral sclerosis. Autopsy tissues showed immune-reactive IgA within surviving motor neurons and deposits of IgA and C3 within renal glomeruli. By indirect immunofluorescence, the patient's serum contained high-titer IgA that bound to axons and to the perikarya of nerve cells in central and peripheral nervous system. The IgA paraprotein reacted with the 200 kDa, high molecular weight subunit of neurofilament protein (NFH) in Western blots of purified neurofilaments. It also reacted with dephosphorylated NFH and with NFH expressed as a fusion protein in E. coli, suggesting that the autoantibody recognized a peptide epitope. The IgA crossreacted with a surface antigen of cultured human neuroblastoma cells but mouse monoclonal antibodies to NFH did not. Absorption of the patient's serum with neurofilaments eliminated IgA binding to neuroblastoma cells, indicating that the same antibodies bound to both determinants. The IgA paraprotein seems to be an autoantibody with specificity for neurofilament protein and a cell surface component of neuronal cells; the antibody may have been important in the pathogenesis of neuronal degeneration.

We compared anti-GM1 IgM antibody titers in patients with various neurologic diseases and in normal subjects. We found increased titers in patients with lower motor neuron disease, sensorimotor neuropathy, or motor neuropathy with or without multifocal conduction block. In patients with other diseases, titers are similar to those in normal individuals, suggesting that anti-GM1 antibody levels are not increased nonspecifically after neural injury or inflammatory diseases. Anti-GM1 antibodies in many of the patients occur as monoclonal gammopathies, predominantly of lambda light-chain type, but the antibodies are sometimes polyclonal with normal or increased serum IgM concentrations. Most of the anti-GM1 antibodies appear to react with the Gal(beta 1-3)GalNAc epitope which is shared with asialo-GM1 and GD1b, but in some patients the antibodies are more specific for GM1 and associated with motor neuropathy. Patients with motor or sensorimotor peripheral neuropathy or lower motor neuron disease should be tested for anti-GM1 antibodies or anti-Gal(beta 1-3)GalNAc antibodies, as therapeutic reduction in antibody concentrations was reported to result in clinical improvement in some patients.

An IgM monoclonal autoantibody (M-protein) with anti-Gal(beta 1-3)GalNAc activity from a patient with lower motor neuron disease bound to the surface of motoneurons isolated from bovine spinal cord. The Gal(beta 1-3)GalNAc epitope is shared by the gangliosides GM1 and GD1b and by several glycoproteins in the nervous system, and binding was abolished by preabsorbing the patient's serum with GM1. Antibodies specific for GM1, however, which do not bind to GaL(beta 1-3)GalNAc, did not bind to the motoneurons. This suggests that Gal(beta 1-3)GalNAc bearing glycoproteins or glycolipids other than GM1 are expressed on the surface of motoneurons, while GM1 may be absent or shielded, and that antibody binding to the cell surface might contribute to the development of the motor neuron disease.

The HNK-1 carbohydrate epitope, which is shared by several members of the immunoglobulin gene super-family, is also the target epitope for IgM anti-MAG autoantibodies in patients with demyelinating neuropathy. By Western blot analysis, there are 7 HNK-1 immunoreactive glycoproteins in human peripheral nerve myelin, two of which have previously been identified as the myelin associated glycoprotein (MAG) and the P0 glycoprotein. In this study, the remaining HNK-1 bearing glycoprotein bands were characterized by immunoblot and NH2-terminal sequence analysis, and were all identified as degradation products or aggregates of the Po glycoprotein. MAG and P0 are therefore the only HNK-1 bearing glycoproteins in human peripheral nerve myelin.

A patient with atypical manifestations of Epstein-Barr Virus (EBV) encephalomyelitis is presented. The patient had unusual spinal fluid immunoglobulin abnormalities, the syndrome of inappropriate anti-diuretic hormone secretion, autonomic dysfunction and spinal arachnoiditis. The cisternal CSF, with a very high IgG level (34.3 mg/dl; normal less than 6.1) but a normal albumin content, displayed evidence of massive intrathecal immunoglobulin production. This was further confirmed by the presence of oligoclonal bands. These clinical manifestations have not previously been reported in encephalomyelitis associated with EBV infection.

Neuroblastoma cells are frequently used as targets in studies of autoimmune diseases of the nervous system. We examined the human neuroblastoma cell line, LAN-5, for the presence of autoantigens that react with naturally occurring autoantibodies in human sera. Antibodies to the HNK-1 and Gal(beta 1-3)GalNAc epitopes, which have been implicated in human autoimmune neuropathy and motor neuron disease, respectively, immunostained the surface of the neuroblastoma cells, and antibodies to the 200 kDa high molecular weight neurofilament protein (NFH) immunostained the cytoplasm and cell processes. The NHK-1 and Gal(beta 1-3)GalNAc epitopes were associated with several glycoprotein bands in Western blots of the neuroblastoma cells, and the HNK-1 epitope was also shared by a glycolipid which co-migrated with 3-sulfoglucuronyl paragloboside (SGPG) from peripheral nerve, indicating that SGPG is synthesized in neuronal cells. Northern blot analysis revealed a single RNA band of 4800 bp for NFH in normal brain but two RNA species of 4800 and 3800 bp in both neuroblastoma and adrenal cells, confirming their common origin. The neuroblastoma cells appear to contain antigens that bind to naturally occurring autoantibodies in human serum and might therefore be useful for detecting and investigating the effects of anti-neuronal antibodies. The antibody populations being investigated, however, should be distinguished from other autoantibodies which might be present in the patients' serum.