Waking during the night is due to two things.
The physical things, such as cramps, muscle spasms, nausea etc, are down to your central nervous system. For example, when you wake up in the morning and have the shakes in your hand, that is your central nervous system acting up because it no longer has the alcohol in the system. Alcohol also inhibits the glutamate receptor--which is the cause of staggering, slurring, and general interference with muscular coordination.
The only way to deal with this, is to tough it out, or to get a benzo from your GP, such as diazepam. He'll probably tell you he can't prescribe it, but that's bull. They are told not to let anyone get hooked on it and try to keep prescriptions to only two weeks and no repeat prescriptions. One week is enough to last you through the period.
For the sake of a one week prescription and £8.40, many people have to tough it out.
The second is neural activity. The GABA receptor is enhanced by alcohol, the brain tries to overcome this calming effect by producing more adrenaline and other similar neurotransmitters. And I pinched this from a website, because I like the phrase. 'When the alcohol is completely taken away then this adrenaline and its cousins are left to run rampant in the brain.
Alcohol withdrawal syndrome is mediated by a variety of mechanisms. The brain maintains neurochemical balance through inhibitory and excitatory neurotransmitters. The main inhibitory neurotransmitter is γ-amino-butyric acid (GABA), which acts through the GABA-alpha (GABA-A) neuroreceptor. One of the major excitatory neurotransmitters is glutamate, which acts through the N-methyl-D-aspartate (NMDA) neuroreceptor.
Alcohol enhances the effect of GABA on GABA-A neuroreceptors, resulting in decreased overall brain excitability. Chronic exposure to alcohol results in a compensatory decrease of GABA-A neuroreceptor response to GABA, evidenced by increasing tolerance of the effects of alcohol.
Alcohol inhibits NMDA neuroreceptors, and chronic alcohol exposure results in up-regulation of these receptors. Abrupt cessation of alcohol exposure results in brain hyperexcitability, because receptors previously inhibited by alcohol are no longer inhibited. Brain hyperexcitability manifests clinically as anxiety, irritability, agitation, and tremors. Severe manifestations include alcohol withdrawal seizures and delirium tremens.
Translated into English. Imagine you are driving a car, with no clutch, just brake and gas pedal. You drink alcohol and the brake in your brain is applied, by the GABA on GABA-A. Glutamate on NMDA applies the gas to compensate and keep you up to speed. Long term heavy alcohol consumption inhibits the NDMA, the gas pedal doesn't seem to be working so well, so you push it right to the floor to compensate, for the brake seeming to be sticking on all the time.
Then you stop drinking/cut down by a lot. The brake has now been completely lifted off, but the gas pedal is still stuck to the floor and now you're hurtling along at 90mph. It takes a while for the brain and body to recognise this and in that period, before self rectification takes place, you have theose awful sleepless nights where your brain is doing 20 to the dozen, it just won't calm down, shut down and let you sleep.
You can of course drink and that will apply the brake, and you become stuck in a loop. It's why people try to give up, but can't. Again, a small amount of diazepam would sort this. It doesn't sort the long term problem/solution which is where nalmefene/natrexone/Campral come in.
Errors, typos and grammatical mistakes expected as I haven't proof read.