A case of transorbital intracranial damage underlying a seemingly innocuous injury.
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Child↗
Biomedical subjects
S A Sadiq
Publications and source records attributed to S A Sadiq.
Progression of diabetic retinopathy and rubeotic glaucoma following cataract surgery.
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.
Aged↗
Motor neuron disease and monoclonal gammopathy.
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.
Adolescent↗
Vertical optic disk diameter: discrepancy between planimetric and SLO measurements.
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.
Glaucoma↗
Identification of Gal(beta 1-3)GalNAc bearing glycoproteins at the nodes of Ranvier in peripheral nerve.
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.
Amino Acid Sequence↗
Malakoplakia of bone presenting as a pathological fracture.
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.
Bone Diseases↗
Clinical and electrophysiologic correlates of elevated anti-GM1 antibody titers.
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.
Adult↗
The gp120 glycoprotein of human immunodeficiency virus type 1 binds to sensory ganglion neurons.
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.
Animals↗
Antibodies to the human 60 kDa heat-shock protein in patients with schizophrenia.
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.
Antibodies↗
The gp120 glycoprotein of HIV-1 binds to sulfatide and to the myelin associated glycoprotein.
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.
Animals↗
Vasculitic neuropathy in a patient with cryoglobulinemia and anti-MAG IGM monoclonal gammopathy.
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.
Aged↗
Anti-sulfatide antibodies in neurological disease: binding to rat dorsal root ganglia neurons.
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.
Aged↗
Anti-GM1 antibodies in patients with Guillain-Barré syndrome.
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.
Adolescent↗
Human monoclonal antineurofilament antibody cross-reacts with a neuronal surface protein.
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, Monoclonal↗
Experimental autoimmune neuropathy with anti-GM1 antibodies and immunoglobulin deposits at the nodes of Ranvier.
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.
Animals↗
Monoclonal gammopathy and motor neuron disease.
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Amyotrophic Lateral Sclerosis↗
Characterization of HNK-1 bearing glycoproteins in human peripheral nerve myelin.
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.
Antibodies, Monoclonal↗