Have you ever wondered about how mood disorders affect your mind, neurologically? Read on to find out about the neurological destruction in mood disorders and how these conditions affect those who have it.
Neurological Impairment in Mood Disorders
A mood disorder is a common psychiatric illness representing a major cause of both disability and mortality around the world. These disorders are characterized by obvious disturbances in emotions and behaviors, for instance, extreme highs and lows. There are also other symptoms, depending on the mood disorder one has.
Mood disorders have treatments available, with a home doctor Brisbane able to provide insight and help as he monitors the progress of the patient. This is in order to maintain good health, both physically and mentally, as there are both neurological and physical symptoms patients may suffer from, including immune dysfunction. We will get into such symptoms and effects in the section below.
Within the broad descriptions of deficits are three primary domains of mood disorder symptoms, which include:
- Psychological and vegetative signs and symptoms
- Neurocognitive deficits
- Neurological abnormalities
Research shows that relationships between cognition and mood are dynamic ones, with components that are state and trait dependent. In terms of neurological function, there is a state and trait-related changed associated with mood disorders, particularly in the depressed, euthymic, and manic phases.
Due to the static nature, there are trait characteristics of neurological manifestations, which can provide insight into core brain abnormalities, which have caused mood disorders.
Etiology of the Immune Destruction in Mood Disorders
You have probably heard of reports on immune destruction in mood disorders.
Unfortunately, mood disorders, such as bipolar disorder, are strongly associated with immune dysfunction. In fact, such immune dysfunction may be most likely responsible for higher rates of inflammatory comorbidities, including autoimmune disorders, cardiovascular diseases, as well as metabolic disturbances.
While the association between immune destruction and mood disorders may be due to the metabolic effects of medications for treating such conditions, those who do not take medications may also experience impaired glucose metabolism, weight gain, and other signs of immune dysfunction. Genetics may also play a role, as there are reports of genetic alterations, which have increased immune dysfunction.
Besides this, there are other non-mutually exclusive causal factors, which are stress, pathogens, and autoimmunity.
Stress hormones may experience a stress response, which may cause low-grade inflammation. Furthermore, social isolation and loneliness are actually associated with consistent patterns of gene expressions, which increases inflammatory markers that are involved in bacterial immunity and wound healing.
Neurological Studies of Mood Disorders
1. Anterior cingulate cortex
There have been neuropathological studies of mood disorders, which were stimulated by MRI. It has been reported that there is a specific part of our anterior cingulate gyrus, which lies ventral to the genu of our corpus callosum, was 40% smaller in those who had a familial mood disorder compared to control groups.
There have also been other studies regarding this part of the brain, which plays a huge role in mood disorders. This comes from the many imaging data which remains consistent with sophisticated models of various factors, including cognition, drive, emotion, and motor control.
2. Other areas of the prefrontal cortex
There are also other parts of the brain that have been affected by the orbital and dorsolateral regions from the prefrontal cortex in those with mood disorders. Investigations have shown findings similar to those from the anterior cingulate cortex.
Key studies were performed by Rajkowska and colleagues, with their first report regarding major depression. The measurements of the dorsolateral, rostral orbital and caudal orbital prefrontal cortices have experienced decreased glial density, as well as reduced size of neurons in laminae.
3. Brainstem nuclei and subcortical regions
As for this area, there are alterations in the adrenergic and serotonergic systems, which remain the neurotransmitter theories of mood disorders like depression. There are now morphometric studies regarding the cell bodies of origin.
While reports show that there is no loss or atrophy of neurons from the locus coeruleus, a later study of bipolar disorder showed otherwise.
Inflammation-Related Histopathological Abnormalities
Research has shown histopathological changes that were observed postmortem, which may affect the circuits that involve the prefrontal cortex and brain regions. Furthermore, postmortem brain research has shown invaluable information on the cerebral cells and networks which are only in humans.
However, such research still has its limitations, and results need to be interpreted through considering various factors, as even if generated in the most optimal conditions, postmortem data is still different, especially as it went through the process of preserving the brain after death.
Symptom Criteria for Major Depressive Disorder
This is the symptom criteria for Major Depressive Disorder or Unipolar Depression. Take note that one will have to experience at least five of these symptoms within a two-week period:
- Depressed moods for most of the day
- Loss of pleasure or diminished interest
- Significant weight gain or loss
- Insomnia or hypersomnia
- Loss of energy
- Feelings of guilt or worthlessness
- Difficulty in concentrating or thinking
- Suicidal thoughts and ideations
- Psychomotor retardations or agitation
Besides these symptoms, there are other symptoms that may accompany the mood disturbances, including disruptions in normal appetite, sleep, and psychomotor functions.
Neurological Effects of Mood Disorder Treatments
Most of the test subjects who have major depression and were studied post-mortem were treated with antidepressants, with some having received other treatments, including electroconvulsive therapy, lithium, minor tranquilizers, and antipsychotics. Those with bipolar disorder have also received similar treatments, as well as other mood stabilizers including carbamazepine and sodium valproate.
Such treatments may have caused, enhances, obscured, or ameliorated any reported neuropathological alterations.
With electroconvulsive therapy, there are no demonstrable neuropathological effects, while lithium overdose causes acute neurotoxicity, but without neuropathological effects when taking therapeutic levels of it for the long term.
As for other drugs used, there aren’t any neuropathological studies of its effects yet, though small experimental literature might suggest that antidepressants can affect the neuronal morphology, promote neurogenesis, regenerate monoaminergic axons, as well as prevent loss of dendritic spines.
Wrapping It Up
I hope that this article on the neurological destruction in mood disorders helps inform you more about these conditions. If you or a loved one have a mood disorder, make sure that you continue getting yourself checked by a medical professional to monitor your health and improve your quality of life, both physically and mentally.
Do you have any questions or would like to share your knowledge and experience with mood disorders, do comment below? All of your thoughts and insights are much appreciated.
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