Nerve impulse propagation: Mechanical wave model and HH model.

The Hodgkin-Huxley model (HH model) of nerve propagation from the middle of the 20th century has not remained untouched by criticism. Complementary as well as ambivalent views of this model have been published. A real breakthrough of another model does not exist yet. Many similarities as well as contradictions between the HH model and the alternative mechanical impulse model are shown.

Demyelinating diseases as a result of cerebral edema?

Due to the elastic properties of the human organs, tissue edema causes an increased tissue pressure. This phenomenon leads to a reduction of blood circulation or ischemia, and thus leads to the hypothesis that tissue edema can be the cause of demyelinating lesions. Even though brain edema occurs in the whole brain, the authors assume that the characteristically focal appearance of demyelinated lesions, for instance of multiple sclerosis plaques, are attributable to anatomical and structural characteristics of the brain. In an experimental section, a balloon inserted into the brain and other organs removed during autopsies produces an increased tissue pressure. This model shows tissue pressure in the vicinity of the balloon up to 80mmHg. The height of the produced pressure varies in different organs and special regions of the brain. The verified pressures in the pons cerebri show that stretched myelinated fiber bundles in outer regions can induce strong pressures in enclosed edematous tissue, as seen in central pontine myelinolysis. The presented experimental results support the hypothesis that demyelinated lesions, as seen in multiple sclerosis, may be caused by increased tissue pressure, or respectively, brain edema.

Morphogenesis of the demyelinating lesions in Baló's concentric sclerosis.

In tissues with elastic properties, an edema causes a raised tissue pressure and therefore a diminished blood flow. The authors assume that an increased tissue pressure due to local and/or relapsing edema may be the cause for incomplete necrosis (e.g. demyelinated lesions) or seldom complete necrosis in the brain. Newly forming demyelinating lesions seldom show small tissue bands with normal appearing myelin sheaths in the immediate vicinity of precursor lesions (Baló type of MS). The small myelinated bands are the result of a "protected zone" on the edge of previous demyelinated lesions. The authors explain this protected zone with two arguments. Firstly, the resorptive granulation tissue of more or less older lesions is relatively rich in capillaries. These capillaries may act as an energy reservoir that can nourish not only the plaque, but also a narrow adjacent myelinated tissue band by diffusion, even if the capillary blood flow in this tissue band is limited due to the greater tissue pressure of a new developing lesion in the neighborhood. Secondly, another protective mechanism may act simultaneously: older or more sclerosed lesions and small adherent bands of myelinated tissue with them may swell less in cases of an edema than in normal tissue. The hardening of the older lesions is caused by proliferated fiber-forming astrocytes in the sense of scarring. In an area with an increased tissue pressure, the capillaries are less compressed in a sclerosed lesion than in regions of normal grey and white matter. In addition, the adherent myelinated tissue band closest to the edge of a hardened plaque is better protected against swelling and compression than the further away tissue. Theoretically, this protection zone is comparable with protected blood vessels in the Haversian canals or the medullary spaces of bones. Both theses of protecting mechanisms at the edges of demyelinated lesions support the assumption of a hypoxic causation principle of demyelinating lesions in Baló's concentric sclerosis and multiple sclerosis.

Pressure waves in neurons and their relationship to tangled neurons and plaques.

The paper based on the hypothesis that mechanical impulses cause the transmission of excitement in the peripheral and central nervous system. Possible connections between changes in the tubular neuronal network and the morphological findings of Alzheimer's disease are presented. Additionally, changes in the viscosity of the neuronal cytoplasm and changes in the walls of the neuronal fibers due to the intracellular hydrostatic pressure and pressure waves are considered possible causes of plaques, threads and tangles. The pressure causes reduced elasticity and mechanical breakdown in neuronal fiber walls. This is compared to features found in blood vessels. It is presumed that damaged membranes lead to an escape of cytoplasm from the neurons into the extracellular space. This outflow may cause the spherical structured proteinaceous plaques. On the other hand it could be that the decrease of fluid and reduced intraneuronal pressure after a membrane crack may favor the agglomeration of cytoplasm proteins in the neurons forming threads and tangles. The consolidation of the neuronal cytoplasm and the irreparable decrement of the intracellular pressure cause a loss of function and finally a dieback of the affected neurons. The reduction of blood perfusion due to an increased local tissue pressure in certain regions of the brain may promote the forming of Alzheimer deposits. An increase of preamyloid proteins and small soluble amyloid particles within the extracellular fluid can lead, along their natural drainage route, to an amyloid angiopathy.

Impulses and pressure waves cause excitement and conduction in the nervous system.

It is general accepted, that nerval excitement and conduction is caused by voltage changes. However, the influx of fluid into an elastical tube releases impulses or pressure waves. Therefore an influx of ion currents, respectively fluid motions into the elastic neuronal cells and fibres also induce impulses. This motion of charge carriers are measured by voltage devices as oscillations or action potentials, but the voltage changes may be an epiphenomenon of the (mechanical) impulses. Impulse waves can have a high speed. As stiffer or inelastic a tube wall, the greater is the speed of the impulse. Myelin sheaths cause a significant stiffening of the nerve fibre wall and myelinated fibres have a conduction velocity up to 120 m/s. The influx of fluid at the nodes of Ranvier intensifies periodically the impulse wave in the nerve fibres. The authors suggest that also the muscle end-plate acts as a conductor of axonal impulses to the inner of the muscle fibres and that the exocytosis of acetylcholine into the synaptic cleft may be an amplifier of the axonal impulse. It is discussed that intracellular actin filaments may also influence motions at the neuronal membrane. Many sensory nerve cells are excited due to exogenous or endogenous mechanical impulses. It may plausible that such impulses are conducted directly to the sensory nerve cell bodies in the dorsal root ganglia without the transformation in electric energy. Excitation conduction happens without noteworthy energy consumption because the flow of ion currents through the membranes takes place equivalent to the concentration gradient. Impulse waves cause short extensions of the lipid membranes of the cell- and fibres walls and therefore they can induce opening and closing of the included ion channels. This mechanism acts to "voltage gated" and "ligand-gated" channels likewise. The concept of neuronal impulses can be helpful to the understanding of other points of neurophysiology or neuronal diseases. This includes e.g., the brain concussion and pathohistological findings in Alzheimer dementia. To verify the concept of (mechanical) impulses in the nervous system it is necessary to carry out biophysical or mechanical investigations in very small dimensions and the authors hope to give for this a sufficient stimulus.