Multifocal Motor Neuropathy Associated with Infliximab.

BACKGROUND: The anti-tumour necrosis factor [TNF] monoclonal antibody, infliximab, is commonly prescribed in both ulcerative colitis and Crohn's disease. Neurological side effects such as optic neuritis are well recognised, although not as frequently seen as hypersensitivity and serious infections. CASE: We present a case of peripheral neuropathy in a young man on infliximab therapy for ulcerative colitis. This presented as an asymmetrical and slowly progressive weakness in his right upper limb, severely impacting on function. Investigations confirmed a diagnosis of multifocal motor neuropathy [MMN]. This has been previously described in patients receiving infliximab for rheumatological conditions. The exact mechanism is unclear, but the neuropathy responds well to intravenous immunoglobulin. In our case, infliximab was discontinued. The patient was treated with immunoglobin for 5 days and recovered rapidly. Mercaptopurine was instituted as maintanence therapy, with good effect. CONCLUSION: Gastroenterologists prescribing infliximab should be cognisant of both peripheral and central neurological complications, ensuring prompt withdrawal of the offending agent and appropriate alternative treatment.

Necrotizing skin lesion and radial nerve palsy in a patient treated with glatiramer acetate.

Glatiramer acetate (GA) is an approved and well tolerated drug for the treatment of relapsing-remitting multiple sclerosis. We report a case of a 52 year-old man with psoriasis and relapsing-remitting multiple sclerosis who developed, after 21 months of GA treatment, an injection-site cutaneous necrosis that involved both subcutaneous and muscular tissue with massive edema, followed, 3 days later, by radial nerve palsy. After few days another similar lesion appeared in another injection-site. We hypothesize that cutaneous necrosis could be due to a local dis-immune reaction and, probably, psoriasis could have played an important role in its pathogenesis.

A hypothetical mathematical construct explaining the mechanism of biological amplification in an experimental model utilizing picoTesla (PT) electromagnetic fields.

We seek to answer the conundrum: What is the fundamental mechanism by which very weak, low frequency Electromagnetic fields influence biosystems? In considering the hydrophobicity of intramembranous protein (IMP) H-bonds which cross the phospholipid bilayer of plasma membranes, and the necessity for photonic recycling in cell surface interactions after dissipation of energetic states, present models lack structure and thermodynamic properties to maintain (DeltaE) sufficient energy sources necessary for amplifications by factors of 10(12). Even though one accepts that the ligand-receptor association alters the conformation of extracellular, extruding portions of IMP's at the cell surface, and that this change can be transmitted to the cytoplasm by the transmembranous helical segments by nonlinear vibrations of proteins with generation of soliton waves, one is still unable to account for repair and balanced function. Indeed, responses of critical molecules to certain magnetic field signals may include enhanced vibrational amplitudes, increased quanta of thermal energies and order inducing interactions. We may accept that microtrabecular reticulum-receptor is associated with actin filaments and ATP molecules which contribute to the activation of the cyclase enzyme system through piezoelectricity. Magnetic fields will pass through the membrane which sharply attenuates the electric field component of an EM field, due to its high impedance. Furthermore, EM oscillations are converted to mechanical vibrations; i.e., photon-phonon transduction, to induce molecular vibrations of frequencies specifically responsible for bioamplifications of weak triggers at the membrane surface, as well as GAP junctions. The hydrogen bonds of considerable importance are those in proteins (10(12)Hz) and DNA (10(11)Hz) and may be viewed as centers of EM radiation emission in the range from the mm microwaves to the far IR. However, classical electrodynamical theory does not yield a model for biomolecular resonant responses which are integrated over time and account for the connection between the phonon field and photons. Jacobson Resonance does supply an initial physical mechanism, as equivalencies in energy to that of Zeeman Resonance (i.e., zero-order magnetic resonance) and cyclotron resonance may be derived from the DeBroglie wave particle equation. For the first time, we view the introduction of Relativity Theory to biology in the expression, mc(2)=BvLq, where m is the mass of a particle in the 'box' or 'string' (molecule in a biosystem), c is the velocity of electromagnetic field in space, independent of its inertial frame of reference, B is the magnetic flux density,v is the velocity of the carrier or 'string' (a one or two dimensional 'box') in which the particle exists, L is its dimension (length) and q represents a unit charge q=1C, by defining electromotive force as energy per unit charge. Equivalencies suggest that qvBL is one of the fundamental expressions of energy of a charged wave-particle in magnetic fields, just as Zeeman and cyclotron resonance energy expressions, gbetaB and qhB/2pim, and is applicable to all charged particles (molecules in biological systems). There may exist spontaneous, independent and incessant interactions of magnetic vector B and particles in biosystems which exert Lorentz forces. Lorentz forces may be transmitted from EM field to gravitational field as a gravity wave which return to the phonon field as microgravitational fluctuations to therein produce quantum vibrational states that increase quanta of thermal energies integrated over time. This may account for the differential of 10(12) between photonic energy of ELF waves and the Boltzman energy kT. Recent data from in vivo controlled studies are included as empirical support for the various hypotheses presented.

Nerve conduction changes in patients with mitochondrial diseases treated with dichloroacetate.

Serial measurements of nerve conduction velocities and amplitudes were performed in 27 patients with congenital lactic acidemia over 1 year of sodium dichloroacetate (DCA) administration. Patients were treated with oral thiamine (100 mg) and DCA (initial dose of 50 mg/kg) daily. Nerve conduction velocity and response amplitude were measured in the median, radial, tibial, and sural nerves at 0, 3, 6, and 12 months, and plasma DCA pharmacokinetics were measured at 3 and 12 months. Baseline electrophysiologic parameters in this population were generally below normal but as a group were within 2 standard deviations of normal means. Although symptoms of neuropathy were reported by only three patients or their families, nerve conduction declined in 12 patients with normal baseline studies, and worsening of nerve conduction occurred in the two who had abnormalities at baseline. Peripheral neuropathy appears to be a common side effect during chronic DCA treatment, even with coadministration of oral thiamine. Nerve conduction should be monitored during DCA treatment.