Battery powered BION FES network.

The Alfred Mann Foundation is completing development of a coordinated network of BION microstimulator/sensor (hereinafter implant) that has broad stimulating, sensing and communication capabilities. The network consists of a master control unit (MCU) in communication with a group of BION implants. Each implant is powered by a custom lithium-ion rechargeable 10 mW-hr battery. The charging, discharging, safety, stimulating, sensing, and communication circuits are designed to be highly efficient to minimize energy use and maximize battery life and time between charges. The stimulator can be programmed to deliver pulses in any value in the following range: 5 microA to 20 mA in 3.3% constant current steps, 7 micros to 2000 micros in 7 micros pulse width steps, and 1 to 4000 Hz in frequency. The preamp voltage sensor covers the range 10 microV to 1.0 V with bandpass filtering and several forms of data analysis. The implant also contains sensors that can read out pressure, temperature, DC magnetic field, and distance (via a low frequency magnetic field) up to 20 cm between any two BION implants. The MCU contains a microprocessor, user interface, two-way communication system, and a rechargeable battery. The MCU can command and interrogate in excess of 800 BlON implants every 10 ms, i.e., 100 times a second.

Micromodular implants to provide electrical stimulation of paralyzed muscles and limbs.

We describe the design, fabrication, and output capabilities of a microminiature electrical stimulator that can be injected in or near nerves and muscles. Each single-channel microstimulator consists of a cylindrical glass capsule with hermetically sealed electrodes in either end (2-mm diameter x 13-mm overall length). Power and digital control data can be transmitted to multiple implants (256 unique addresses) via a 2-MHz RF field created by an external AM oscillator and inductive coil. In vitro testing demonstrated accurate control of output pulsewidth (3-258 microseconds in 1-microseconds steps) and current (0-30 mA in two linear ranges of 16 steps each, up to 8.5 V available compliance voltage). Microstimulators were used successfully for chronic stimulation in hindlimb muscles of cats. Design and fabrication issues affecting yield and reliability of the packaging and electronics are discussed.

Injectable microstimulator for functional electrical stimulation.

A family of digitally controlled devices is constructed for functional electrical stimulation in which each module is an hermetically sealed glass capsule that is small enough to be injected through the lumen of a hypodermic needle. The overall design and component characteristics of microstimulators that receive power and command signals by inductive coupling from a single, externally worn coil are described. Each device stores power between stimulus pulses by charging an electrolytic capacitor formed by its two electrodes, made of sintered, anodised tantalum and electrochemically activated iridium, respectively. Externally, a highly efficient class E amplifier provides power and digitally encoded command signals to control the amplitude, duration and timing of pulses from up to 256 such microstimulators.

Cerebellar stimulation for spastic cerebral palsy: preliminary report; on-going double blind study.

To date, June 1, 1986, 33 spastic cerebral palsy (CP) patients have taken part in a double blind study testing the safety and efficacy of chronic cerebellar stimulation (CCS) for reduction of spasticity and improvement in function. Seven U.S. surgical centers involving ten neurosurgeons have implanted the Neurolith 601 cerebellar stimulator supplied by Pacesetter Systems Inc. (Sylmar, CA). A pilot study was run with three patients at Stanford University (Stanford, CA) using taped-on real (strong) and dummy (weak) magnets to control the ON-OFF status. Following the pilot study, a magnetically controllable switch was placed in line between the Neurolith stimulator and the cerebellar lead to allow more reliable switching sequences for the study. The test battery included joint angle measurements (passive and active), motor performance testing, reaction time, hand dynamometry, grooved peg board placement, hand/foot tapping, and rotary pursuit testing. Testing only was done at presurgery. Testing and ON-OFF switching was performed following recovery from surgery and at one, two, and four months. After four months, the switch was left turned ON. Of the 30 patients using the implanted switch, 11 were dropped from the study and seven are still in progress. Of the 11 dropped from the study, four were due to switch problems and three were due to double blind protocol violations, i.e., the participants discovered the stimulus status. The remaining four were removed because of a broken lead, infection, or unrelated medical problems, or refusal to participate after implant. A preliminary analysis indicated that three-quarters of the patients have a demonstrable quantitative improvement during the time the stimulation was "ON." Three patients showed no significant change.

Cardiac pathology of transvenous pacemakers in dogs.

Transvenous right ventricular pacemaker catheters were implanted in 18 mongrel dogs for periods of 2 to 18 months (average 4.9 months). Heart block was produced in 15 of these dogs by injection of 37 per cent formaldehyde into the interatrial septum. In the other three dogs which served as controls, no heart block was produced and no electrical stimulation was applied to the implanted catheters. After the animals had been put to death, gross and microscopic examination of the hearts revealed four categories of morphological changes: (1) connective tissue sheath formation around the catheters, (2) endocardial papillary thickening, (3) interatrial septal changes, and (4) myocardial damage. Changes 1, 2, and 4 occurred in one or more intracardiac locations in all 18 dogs. Change 3 occurred only in the 15 dogs in which heart block was produced. The most striking histologic findings were areas of cartilagenous metaplasia in endocardium an underlying myocardium and areas of marked cellular proliferation of the endocardial cells both in the endothelium and underlying stroma. Chronic implantation of transvenous intracardiac pacemaker catheters in dogs consistently produces morphologic changes which may interfere with cardiac and pacemaker function and may hinder attempts to remove nonfunctional or unneeded catheter electrodes. The changes observed appear to be related to the presence of foreign material per se and not external electrical stimulation of the heart.

Influence of calcium, cholesterol, and unsaturation on lecithin monolayers.

Surface pressures and potentials of mixed monolayers of dicetyl phosphate-cholesterol, dipalmitoyl lecithin-cholesterol, egg lecithin-cholesterol, and phosphatidic acid-cholesterol were measured. The surface potential is shown to be a more reliable parameter for the study of interactions in monolayers than the surface pressure. Monolayers of dicetyl phosphate-cholesterol follow the additivity rule for area/molecule whereas lecithin-cholesterol monolayers deviate from it. The reverse is true for the additivity rule with regard to surface potential/molecule. Thus, the surface potential indicates that there is no interaction (or complex formation) between lecithin and cholesterol, but that there is ion-dipole interaction between dicetyl phosphate and cholesterol, as well as between phosphatidic acid and cholesterol. The apparent condensation of mixed monolayers of lecithin when cholesterol is added is explained by a consideration of molecular cavities or vacancies caused by thermal motion of the fatty acyl chains, the size of these cavities being influenced by the length and degree of saturation (especially the proportion of monounsaturation) of the fatty acyl chains and the extent of compression of the monolayer. The cholesterol molecules occupy these cavities and therefore cause no proportional increase in area/molecule in the mixed monolayers. Monolayers are liquefied by the presence of cholesterol as well as of unsaturated fatty acyl chains; in contrast, Ca(++)tends to solidify lecithin monolayers. The available evidence suggests that cholesterol can both impart fluidity to the monolayer and occupy the molecular cavities caused by the fatty acyl chains.

The ionic structure of lecithin monolayers.

Surface potentials of mixed monolayers of dicetyl phosphate and eicosanyl trimethylammonium bromide (1:1) were the same on subsolutions of 0.02 M NaCl or 0.01 M CaCl(2), which indicated that ionic phosphate does not interact with Ca(++) in the presence of a neighboring trimethylammonium group. Surface potential-pH plots of dicetyl phosphate, and of dipalmitoyl, egg, and dioleoyl lecithins showed that as the pH of the subsolution is decreased the phosphate groups in the monolayer are neutralized in the order: dicetyl phosphate > dipalmitoyl lecithin > egg lecithin > dioleoyl lecithin. The binding of cations (Na(+), Ca(++)) to the phosphate group of lecithin also showed the same order. The binding of Ca(++)) to egg phosphatidic acid monolayers, as measured by the increase in surface potential, is considerably greater than that to egg lecithin. These results suggest that there is an internal salt linkage between the phosphate and trimethylammonium groups on the same lecithin molecule. An increase in unsaturation of fatty acyl chains increases the intermolecular spacing, which reduces the ionic repulsion between polar groups, and hence strengthens the internal salt linkage. The results support the concept of a vertical rather than coplanar orientation of the phosphoryl choline group with respect to the interface. A position has been proposed for Ca(++) in the dipole lattice of lecithin from a consideration of the surface potential measurements.

Interaction of calcium ions with lecithin and sphingomyelin monolayers.

Dipalmitoyl lecithin and sphingomyelin monolayers have similar limiting areas, whereas their surface potentials are strikingly different. The double bond at the 4-5 position in sphingomyelin acts as an induced dipole in relation to the surface potentials. This was confirmed by the surface potential of hydrogenated sphingomyelin. The binding of calcium to lecithin and sphingomyelin monllayers resulted in an increase in surface potential. This increase was greater for the dipalmitoyl lecithin monolayer as compared to that for sphingomyelin. It is concluded that the binding of calcium ions to springomyelin monolayers is significantly reduced by the presence of the hydroxyl group at the 3-carbon position of the molecule.