Destructive Pulse Syndrome Part 2 © Andy D Kemp 2011
In looking at this theory in more depth, we perhaps need to consider the finer details of biological electricity, or aspect of the synapse process in greater detail, and what happens to damaged or compressed tissue cells by way of ‘thickening’ their density. While I am not a biologist, there are aspects in logical, common-sense reasoning, that may prove relative towards putting further weight behind the theory in DPS.
Using simplistic terms, the synapses or movement of energy through the nervous system will likely follow the most easiest routes through the individual cell walls in the same manner water and electricity naturally flow. However, while considering this, there is also an aspect in division or ‘doubling’ within the nerve cells; where the command synapses propel a physical motion of the cell, while at the same time relaying a response synapse back to the brain, confirming the success or failure of that command. In general terms, the aspects of breathing heart beating, etc., run on (subconscious) auto pilot, while Motor aspects in moving the body through space, require the conscious thought process; and in both cases, the feedback synapses necessitate reception and response mechanisms within the brain, via the central and peripheral nerve system.
With damaged nerve cells however, the movement and energy value in the synapse will likely be hindered. The synapse may fire between cells at different locations in the cell walls, causing the current to divert or discharge on route, or indeed sit within a cell until another incoming synapse provides sufficient power in energy to enable the continuation of the synapses along the nerve fibre. Remembering that the bi-fold nature of the synapse mechanism, means that nerve cells may allow command but withhold response, or visa versa, providing some undesired effects, that the brain will automatically try to re-address or heal to amend the situation.
With entrapped nerve fibres or groups of nerve ganglion, where the cell walls are compacted together, the tissue will become far more dense, and this will likely cause an aspect in ‘bottle necking’ where the synapses are held within the cells, and unable to continue their journey, until the external pressure releases and the cell walls expand back to their operable density. And it seems prudent to mention here, that with scared tissue, the nerve cells may never recover.
Determining the extent of nerve damage in the various parts of the anatomy at the earliest stage possible is going to be one key towards combating the knock on effects caused by insufficient synapse.
In re-describing DPS, the delay or failure of response synapses to reach the brain may cause the brain to send duplicated synapses, or choose neighbouring cells to dispatch new command synapses; rendering the first group of cells to a state in temporary idle mode. Moreover, a surge of response synapses (having gained sufficient energy for there release from a ‘bottle neck’ scenario) returning to the brain may overwhelm or destroy cells.
While occurrences in brain damage may be temporarily healed as the human body is renewing cells all the time, as we age this renewal process begins to slow down, such that, as the muscles and nerve tissues lose their elasticity of youth, the damage from 'resistance and surge' synapse patterns are most likely to physically increase; to the point where the original areas of damaged and hardened nerve fibres start to increase and give rise to adjacent or other associated areas becoming effected in a similar fashion.
In looking at this theory in identify DPS on a broader level, it may become apparent, that a common aspect in some injuries to the spinal column and central nerve may relate directly to various dispositions in disorders associated with recognised neurological diseases and malfunctions.
For instance, DPS damage predominately caused or effected by the upper areas of the spine and neck, may be attributed to a form in Motor Neuron Disease when the throat and swallowing mechanism are the significant areas initially malfunctioning, and in the later development stages if this disorder, the apparent mix-up in emotions, as the patient sheds tears when they are effectively laughing and visa versa (apparently laughing when actually being upset) are more easily understood, as the synapses are being redirected along shared pathways.
The development of DPS through the upper regions of the spine may arise or stem from a variety of causes, such as; the development of curvatures due to muscle imbalance caused by hereditary genes, posture fixations caused through lifestyle or the working environment (such as in IT or office occupations where seating and screen positions remain at a constant), to accidents such as Whiplash injuries (associated with sharp breaking of a vehicle) or contact sports like rugby and boxing.
Likewise, the development of DPS through lower regions of the spine may cause similar symptoms attributed to Secondary or Idiopathic Parkinson’s where the synapses are hindered, disorientated and again routed along shared pathways; typically and often effecting one side of the body first, corresponding to the root of the injury. In cases associated with repetitive strain injuries, this may be more apparent in regard to the natural right or left handed aspect of the patient. Although, in spinal injuries, where dehydrated or disc hernias are present, it should be noted that injury, and or swelling on one side of the spine may cause ‘bottle necking’ scenarios on the opposite side, where the extending nerve branches are squeezed against the vertebrae bone structures around their corresponding areas of exit.
Another cause of DPS may emanate through the compacting of the spine at the base of the back, where dehydrated discs allow pressure to bear upon the sciatic nerves as they exit the spinal column. Noting that physical damage and scarring to the sciatic nerves may also occur through a process of being constantly bruised by shocks associated with sports such as horse riding, prolonged periods in a static sitting posture taking the full weight of the body and or with insufficient cushioning for the absorption of any mechanical vibration when operating machines.
While it may be considered that DPS may also develop through physical limb injuries (including those occurring in childhood) where a major nerve has been damaged for life, and as a result, there is a continual measure in ‘bottle necking’ to cause the characteristic resistance and surge aspect of this disorder (with increasing effect, to greater manifestation as the body ages and nerve tissues lose elasticity). To a certain degree some of the nerve synapses may well be re routed as the body compensates for the damaged nerve cells and the extent of such injuries may not become fully apparent until such time; as to when the central nerve is directly effected or the condition of the spinal column compounds the synapse imbalance with additional imbalances.
Typical symptoms may include, pins and needle's sensations, tingling and warmth feelings, current rushes and muscle twitching in a limb and a longer time period for a limb to achieve a relaxed state (in comparison to the other limbs).
Further symptoms towards diagnosis include noticeable aspects in occurrence as the body relaxes for sleep. These include, impromptu limb jerks, rushing of synapse charges up the central nerve resulting in momentary dizziness, drying and tingling in the wet areas of the mouth, echo in the ear chamber, buzzes and popping sensations in the brain. It should be noted that such symptoms may only occur spasmodically during time of stress, and at times when the spinal discs are dehydrated sufficiently to magnify the resistance and surge aspect in synapse to these noticeable measures. Akin to this, any disorientation in a response synapse, reflecting the prior conditioning of the returning response synapses, occurring within the area of the brain, may result in a mirrored misdirection; producing feelings of anxiety, and other mental aspects to occasional illusion and hallucination as the brain readapts to these fluctuations.
In my experience, physiotherapy and exercises to gently stretch the spine to alleviate the restricted compressed nerve ways with an increase in fluid intake to assist disc dehydration drastically reduces the aspect in ‘bottle necking’ to allow unhindered flow in synapses through the blood brain barrier; while supplements like Borage oil will assist in maximising the natural dopamine production in the Adrenal glands.
Alleviating physical pressure and locally treating damaged areas of nerve tissue where appropriate, upon all the nerve branches and central nerve returning the response synapses will obviously reduce the destruction of cells in the brain. With the central nerve and branches running very close to the surface of the back; it should be possible to correlate and measure synapse power levels with adaptation of modern technology, identifying the unwanted drops in the synapses charge in energy, towards pin pointing where localised treatments (that may include stimulating nerve fibres using Tens to improve muscle tone and realign nerve cells ‘clearing pathways so to speak’ to actively direct the route of the synapses) to eradicate hardened ganglions and the subsequent ‘bottle necks.’ In short there is in fact more treatments readily available to reducing neurological disorders than the topping up of depleted dopamine levels.
It may also be worth considering for a moment, that while the hardening of the nerve tissue at ‘the blood brain barrier,’ may restrict the flow of naturally produced dopamine's (that assist to channel or carry the synapses) it appears that to a certain extent, the consumption of Synthetic dopamine's (as found in prescribed levadopa medicines) borne within their various chemical compound carriers, may enable gateways to operate through the thickened walls, and accordingly the aspect in physiotherapy may reduce the need or necessitate a change in prescribed doses in synthetic levadopa.