Benzodiazepines are tranquillisers. Their neurotoxic chemical nature randomly impairs parts of the CNS to a point of depression (suppressed neurotransmission) followed by microscopic inflammation, possible autoimmunity, juxtacortical hyper-intensities and eventual fibrotic lesions that are seldom repairable with regenerative therapy.

Medical terminology for destructive chemicals is often denoted by the terms ’suppressants’ or ‘depressants’. This is the reason why benzodiazepines are also known as ‘CNS depressants’.

CNS depression; GABA induced neuronal hyperpolarization alter brain electrochemistry thereby causing a level of dependence (addiction). This dependence is what leads to further, more permanent damage as the subject ages. At one point it renders a subjective neurological diagnosis, the moment, damage is large enough to appear on an MRI.

In a natural state of neurological degeneration, the brain consciously inhibits neurotransmission or degenerates less essential parts due to the lack of resources (oxygen or nutrition). It selectively slows motor activity first, before impairing any cognitive functions. While an artificial impact such as from benzodiazepines results in random, simultaneous, phased CNS damage. Until a certain age, this damage is easier countered by the body. As a result of constant exposure, the CNS electrical load is redistributed over to the remaining unaffected part of the CNS. This is the characteristic excitotoxicity often referred to in Benzodiazapin damage. The impact of this alteration in neuroelectrophysiology is easier understood by following the example below:

Imagine a 100 ampere motor drawing electricity from single gauge wires when it runs. If the single gauge wiring was replaced with 10 gauge (1/10 thinner), the motor would eventually burn out the new wiring when turned on. A simple electrical overload. Same is the case with the overloaded (healthier, but degenerating) part of a partial CNS depressed brain. The stress of additional neurotransmission in the remainder of the CNS, causes neuro-protective GABA production to inhibit overall neurotransmission in the CNS. Note that GABA is released all over, whereby it affects two opposite states of the CNS in opposite ways. (1) It inhibits the already depressed CNS while (2) trying to counter excitotoxicity in the healthier, degrading part of the CNS. The state of excitotoxicity releases inflammatory cytokines that invite immune action towards degenerating neuronal tissue.

Therapeutic strategy with the aim of reversing benzodiazepine induced excitotoxicity therefore requires a plan to reestablish balance, not abrupt spilling and differentiation of cells in the name of therapy. Starting with investigation in order to determine vasculature, autoimmunity, peripheral, motor, sensory and CNS degeneration by clear differentiation between cause(s), effects and symptoms. If this is not paid attention to during therapeutic planning, a multitude of imbalances will render further complications, as in the case for many patients so far, who’ve received abrupt cell administrations. Even though a single cell administration can aid one reconstructive approach, a thoroughly planned combination of procedures, personalised for the patient, to improve the brain’s environment along with specific cell biologics, with objectives to disrupt all contributing cycles can establish long term healing and reversal. Just like a polluted aquarium will continue killing new fish, it is essential to fix the polluted water before adding new fish.