Withdrawal | Valium®

Withdrawal

Benzodiazepines are a very effective drug, especially for the treatment of acute anxiety or agitation. The disadvantage of this group of drugs, however, is their high potential for dependence. Dependency can develop after a short time and even at normal doses.

Many patients therefore suffer from benzodiazepine dependence, often even without being aware of it. The dependence is psychological and physical in nature. Withdrawal therefore causes physical and psychological withdrawal symptoms.

Because of the high risk of developing dependency, the use of Valium® and co should normally always be limited to a few weeks. In practice, however, this is often not the case. If there has been a development of dependency, it must be discussed with the person concerned how to continue.

As a rule, withdrawal should be sought if the underlying disease permits. The principle here is not to stop taking the drug completely overnight, but to gradually reduce the dose. Depending on the dose level, the dose can be reduced relatively quickly at the beginning.

For example, the dose can be reduced at weekly intervals. Especially towards the end of the treatment, however, some patients show pronounced withdrawal symptoms, so that the reduction should be very slow. The aim is to stop the drug permanently and completely. The symptoms that occur during withdrawal include anxiety, restlessness, mood swings, nightmares, sleep disturbances, sweating, lack of appetite, nausea, visual disturbances such as flickering eyes or blurred vision, changes in the sense of smell and taste, hypersensitivity to light and sounds, tinnitus, tremor (shaking of the hands), palpitations and an increase in blood pressure. Severe withdrawal symptoms include hallucinations, fear or belief of being persecuted, seizures and delirium.

Side effects

Common side effects of Valium® include severe daytime fatigue, prolonged reaction time (dangerous in traffic! ), dizziness, gait problems, muscle weakness, concentration problems, headaches, confusion and temporary memory loss. More rare side effects are gastrointestinal complaints (nausea, diarrhea, constipation, vomiting), lack of urine excretion (urinary retention), chest pain, low blood pressure and pulse, depressive moods, loss of libido (decrease in sexual desire), cycle disorders in women, increase in appetite, dry mouth, allergic skin reactions (redness, itching), visual disturbances, depressive mood and hallucinations.

Especially in older people, a so-called paradoxical reaction can occur when taking Valium®. Patients do not become calmer because of the medication, but are very restless, agitated and anxious. If taken in too high doses, Valium® can lead to impaired breathing, especially in combination with alcohol, sleeping pills or other depressants.

Laboratory use of diazepam can lead to an increase in liver values, which should be observed. If the liver values rise sharply, the drug may have to be discontinued. Valium® (diazepam) acts at a receptor in the brain.

This receptor is located on nerve cells and regulates the influx of chloride ions into the cell by coupling it to a channel. Such channels are necessary because otherwise the cell is quite impermeable to ions of any kind. Only through the presence of pumps, channels and receptors (which are often coupled to channels) can ions thus pass from the inside of the cell to the outside or from the outside to the inside of the cell.

If this would not be the case and the ions could follow their gradient freely (i.e. from the location of the higher to the location of the lower concentration), the cell would shrink or burst by the following osmotic (balancing) water flow and thus become inoperative. The receptor to which Valium® (diazepam) binds is called the GABA receptor. GABA (gamma-aminobutyric acid) is a neurotransmitter.

It is the ligand for this receptor.This means that when GABA binds, the receptor undergoes a conformational change and the channel belonging to the receptor complex becomes permeable to chloride ions for a few milliseconds. Since the chloride concentration outside the cell is much higher than inside, chloride ions flow into the cell interior during this short phase of the open channel. Chloride ions are simply negatively charged.

So the cell gets a more negative potential through its inflow. If you dive a bit deeper into the cell physiology, you can see as a law that a cell becomes more active when its potential becomes more positive. The normal resting potential of a cell is in the range between -60 and -80 mV (millivolts).

When negative ions flow out or positive ions flow in, the potential of the cell approaches 0 (depolarization). Once it has reached a certain threshold, an action potential is created and the cell becomes excited, i.e. active. The opposite is true for the influx of negative charge, as in the case of the GABA receptor.

Chloride ions flow in, so the potential of the cell becomes even more negative. The cell becomes hyperpolarized. This makes it even less excitable, so it would take much more “effort” to put it into an active state.

So what is the effect of Valium®? It binds to the GABA receptor and alters its conformation so that it becomes even more receptive to the binding of its GABA ligand. Thus, a hyperpolarizing chloride influx occurs more quickly and easily and the cell becomes more excitable.