Benzodiazepines are not prescribed for long-term use because of their high risk of developing dependence or addiction. If it is a result of the misuse of CNS depressants, certain medications are prescribed. In certain cases, CNS depression could also be caused by a stroke, brain trauma, an aneurysm, or a tumor. Some research shows that even conditions that don’t directly affect the brain, like diabetes or kidney and heart disease, could cause CNS depression. Sometimes these effects can be mild, but they can also be severe and potentially dangerous.
Related Conditions
- In severe cases, CNS depression can result in respiratory failure and death.
- These concentrations increase as antidepressants are administered or electroconvulsive therapy (ECT) sessions are performed.
- Awakening insomnia is a typical symptom of a major depressive episode and is accompanied by marked anxiety, especially when the pattern of the episode is with melancholy features or psychotic phenomena.
- We also notice a sensitivity of the pituitary gland in the conditions of an intact adrenal gland.
- If you or someone you know is experiencing CNS depression, seek immediate professional assistance.
- If a drug overdose is the cause of CNS depression, there are medications that can reverse these effects.
Treatment is respiratory support and, if necessary, cardiovascular support. In known-agent suicide attempts, removal of unabsorbed material by gavage or retarding absorption with charcoal is performed, but the results are of limited benefit. Usually, awaiting the metabolic removal of the agent while supporting the respirations is adequate treatment. A chronic toxicity is observed in abusers in which the predominant manifestations are irritability, trouble sleeping, and confusion. Understanding the mechanism of action of antidepressants must start from understanding the pathogenesis of depression. These include Naloxone for opioid overdoses and Flumazenil for overdoses of benzodiazepine.
Alcohol and Sedatives
Because they’re so powerful, they currently aren’t prescribed for things like anxiety and insomnia as much as they used to be. A mild slowing of the CNS may make you feel less anxious and more relaxed. That’s why CNS depressants (sedatives) are used to treat anxiety and insomnia. If you or someone you know is misusing CNS depressants, help is available. You can contact your doctor or speak with a counselor to gain support through treatment. Treatment for substance use disorder (SUD) involving CNS depressants involves drug detox and psychotherapy, such as cognitive-behavioral therapy (CBT).
Causes & Risk Factors
At least 6% of U.S. adults had a major depressive episode annually in 2020. Structural neuroplasticity is involved in the neurogenesis of adult subjects through mechanisms such as dendritic reconstruction, and functional neuroplasticity involves molecular and cellular mechanisms at the synaptic level. This phenomenon is based on the decreased firing in the dopaminergic neurons from the hippocampal system and from the basolateral amygdala. Classic tricyclic antidepressants act on a multitude of receptors, with significant correlations not only with serotonergic and noradrenergic receptors, but also with histamine and muscarinic ones. The importance of the enteric system and the disposition of the receptors at that level should not be neglected, the correspondent being the multitude of gastrointestinal symptoms in major depression. The amygdala plays a major role in expressing emotional expression, mood in situations of suffering or threat, the psychological part being involved in the previous organization of the endocrine response.
In turn, the hippocampus will exert a neurotoxic effect, which will lead to altered neuronal plasticity or directly to cellular apoptosis. MRI studies support significant changes in hippocampal volume in adults who were abused and abused in childhood, their hippocampal volume being significantly reduced compared to groups of subjects who were not exposed to stressors 14. Central nervous system depression is generally caused by the improper or excessive use of depressant drugs1 such as opioids, barbiturates, benzodiazepines, general anesthetics, anticonvulsants, and certain sleep medications.
- Some of the most common types include Luminal, Amytal, and Nembutal.
- Central nervous system depression is an important behavioural consequence of the administration of benzodiazepines, although this effect is not nearly as pronounced as with other minor tranquillisers such as meprobamate, barbiturates or even alcohol.
- Sexual and violent crime are other areas where people are known to misuse CNS depressants.
- Orbital PFC corrects the emotional or behavioral responses generated partially by the amygdala.
- Glutamate is the primary excitatory neurotransmitter in the central nervous system acting on AMPA glutamate receptors.
In the majority of cases, children in our study were able to be managed at home under the supervision of an adult. However, it is important to note that isolated cases of central nervous system depression following ingestion of an alcohol-based hand sanitiser have been described in other countries, including the US 8. This highlights central nervous system depression the importance of storing topical antiseptics, including hand sanitisers, out of reach of children. This is particularly important for younger children who are more likely to be unintentionally exposed than older children and are at greater risk of toxicity. Other measures to mitigate child exposure include keeping hand sanitisers in their original labelled containers to reduce the risk of accidental ingestion.
CNS Depression: Understanding causes, symptoms, diagnosis, and treatment
The hippocampus is also the area where neurogenesis continues in the mature brain, being the area with high neuroplasticity. Opposition disorder in childhood causes decreased hippocampus, impaired neurogenesis, impaired glial cells, synaptic impairment, all of which ultimately lead to HPA axis dysfunction. MRI studies support low hippocampal volume in adults known as former abused children.
The overuse of depressants can lead to symptoms of CNS depression, including slowed reflexes, lightheadedness, fatigue, and difficulty breathing. Depressants affect GABA, an inhibitory neurotransmitter that slows down activity in the brain. When severe, CNS depression caused by substances such as opioids, alcohol, barbiturates, benzodiazepines, and sleeping medications can be fatal. PFC has a significant inhibitory regulatory effect on limbic structures.
Therefore, for depressed patients, exposed to early psychotrauma, serotonin receptor 3A genotype (HTR3A-42C.T) has been linked to a loss of gray matter in the hippocampus and PFC 21. The regulatory model of the system on the HPA axis in depression includes atypical responses to Dexamethasone, increased basal cortisol levels and hyperreactivity to stressors at psychological level. This leads to abnormalities in the negative feedback system of the HPA axis, as well as abnormalities in the production of hormones in the range of corticotrophins (CRH). We also notice a sensitivity of the pituitary gland in the conditions of an intact adrenal gland.
The central nervous system is made up of the brain and spinal cord, which control most bodily functions, including breathing and the heart. CNS depression occurs when a person’s central nervous system has slowed down, causing a slower heart rate and slower breathing. Benzodiazepines, also known as Benzos, are also used to treat anxiety and sleep disorders, although they are considered less addictive than barbiturates. Xanax, Valium, and Prosom are some of the most common types of Benzodiazepines. You might experience mild CNS depression from the prescribed use of CNS depressants or severe CNS depression from the misuse of CNS depressants, traumatic brain injury, or certain other conditions.
There is a hyperactivity of the amygdala when the depressed patient is exposed to negative stimuli but also a hypoactivity at this level when the person in question benefits from positive stimuli. Post-mortem studies performed on patients with MDD have shown both a low number of glial cells and an alteration of their morphology, which is mainly found in PFC compared to other regions of the brain. The results suggest that glial function is deficient or even compromised in PFC and represents the anatomical substrate of depressive symptoms. We are talking here about a junctional intercellular communication that involves a gap between sections, a noticeable gap in astrocytes and which in turn leads to changes in neural function in PFC 18. Barbiturates are powerful medications, and over time medical professionals have shifted from using them to treat anxiety and sleep disorders to being used as anticonvulsants (anti-seizure medications). The autonomic nervous system and the HPA axis are directly related to the concept of stress.
A chemical imbalance of neurotransmitters in the brain, like serotonin, can play a role in depression, but the causes of the condition are often more complex. You may even lose your appetite entirely or fail to eat the right amount of nutritious food. A sudden loss of interest in eating in older adults can lead to a condition called geriatric anorexia.
It may also be difficult for them to understand as symptoms can manifest and cause physical reactions. Frequent episodes of crying may be a symptom of depression, although not everyone cries if they’re depressed. The adaptation of the homologous zone supposes the assumption of the respective cognitive process will be taking over by the opposite hemisphere through a homologous region. Cross-reassignment appears when structures previously devoted to the processing of a particular type of sensory input now accept the receipt of that input through a new sensory mode. The extension of the brain map involves the enlargement of a functional region of the brain from close to close, by accumulating new performances of areas that previously did not deal with that function or mental process.
In such clinical situations, the anatomical substrate is represented by the basal ganglia and the frontal cortex, especially the lesions that affect the striatal area or the left PFC lead to major depressions of organic cause. MRI studies of focal hyperactivity showed a more prevalent white matter lesions in territories linked to the frontal cortex and basal ganglia. Also, specific volumetric abnormalities involving the frontal cortex are noted in primary depression 22. MDD implies a decrease in the ability to react to the reward and the left prefrontal hypoactivity observed in depression supports the behavioral deficit in approaching the reward-punishment system. Neural neuroplasticity involves the ability of the nervous system to modify its activity based on an intrinsic and extrinsic stimulus, to reorganize itself from structural, functional point of view and its connections. A fundamental property of neurons is their ability to alter their power in terms of the efficiency of synaptic transmission through a diverse number of mechanisms.
ECT is perhaps the most effective antidepressant therapy, with the most profound effects on the mechanisms of brain neuroplasticity. Unfortunately, the short-term retrograde amnesia that occurs after each ECT session makes it difficult to examine cognitive improvement in depressed patients treated with ECT. There are also studies that support the improvement of memory and other cognitive functions in depressed patients after drug treatment. Studies have shown that for MDD patients, treated with Fluoxetine, the verbal memory improved.
