I am going to attempt to condense hundreds of pages worth of neuroanatomical textbooks and other such medical gobbledegook in a manner that laymen might be able to understand. I will give explanations of complex things where I can, but I will undoubtedly miss some, so if you have a question about something I've written please feel free to ask. With that preamble out of the way:
In order to understand how ECT might treat mood disorders, one must first understand what exactly a mood disorder is and what it does to the brain.
In order to do that, one must look past simple diagnostic labels which are thrown around quite hastily and carelessly in the current academic and political climate. I have already written up a long post here:
https://sanctioned-suicide.net/thre...rder-not-a-mood-disorder.187593/#post-2969724
which goes into cursory detail about the intentional political subversion of the concept of "depression." In summary, that post explains:
>melancholia, a physical disease of the brain and nervous system, has been observed and documented since at least ancient greece
>melancholia affects the speed of bodily processes, cognition, and movement along with the internal experience of emotion and motivation
>it frequently co-occurs with mania, which can also be described in the same exact way as the previous bullet point (but rather than slowing down and a blunting of emotion, that one is a speeding up and intensity of emotion)
>there is a syndrome of stress response that normal people exhibit, which is unrelated to melancholia or mania
>that normal stress response was intentionally lumped together with melancholia under a single manufactured label of "major depression" so pharmaceutical companies could sell medications to a wider audience
>for that reason, the majority of "major depressives" do not actually have a brain disease, they instead have a normal expression of stress which has been medicalized for profit
Given all of that information, one cannot rely on mere diagnostic label annointed by current criteria – one must rely on classically defined criteria used before that enormous perversion of the medical field. And I pretty much explained it above.
Mood disorder (melancholia or mania) can be identified by the following signs:
>1. observable drastic changes in the speed of basic bodily functions, such as voluntary and involuntary movement, sleep cycle, appetite, evacuation of bowels/bladder, heart rate, temperature management, reaction time, speech, cognitive skills (things like calculating ability, ability to find words to say, planning ability, problem solving, etc), ability to feel physical pleasure, sexual activity, etc
>2. experienced emotion that is unnatural, in that it is not a regular reaction to the environment but rather an autonomous process that changes outward expression without regard to circumstance, often inappropriate and inexplicable for any given external situation
>3. an occurrence that is repetitive over the span of the patient's life, usually with the same symptoms each episode, and might be triggered by stress but is not dependent on it to come into being
Now that condensed criteria list can be applied to many states not currently recognized as "mood disorder"; to name a few:
>psychotic disorders such as the paranoid and catatonic subtypes of schizophrenia, "schizoaffective," "brief psychotic disorder" or reactive psychosis,
>some "subtypes" of depression such as postpartum, seasonal, abnormal grief states, "psychotic"
>some conditions attributed to abnormal personality such as borderline, cyclothymia, some cases of cluster A B or C "Pds"
>some forms of neurosis such as anxiety states, compulsions, excessive eating (bulimia), dissociative identity
>some cases of childhood behavioral issues such as ADHD, conduct disorders
>some cases of extreme neurological dysfunction identified as dementia or delirium
The list goes on – the main point is that
the two major forms of mood disorders (melancholia and mania) can present with basically any identifiable symptom in the realm of neurology and psychiatry, temporarily. These manifestations are limited to an episode – if that episode is treated correctly, the symptoms will go away. They are not permanent and do not reflect an underlying illness besides the mood disorder.
Now I will explain how the brain of someone with mood disorder can possibly cause the 3 criteria I listed.
Over a century of research on the function and structure of brains of mood disorder patients has revealed a few commonalities in findings. I will list them:
>the HPA axis is in overdrive. That stands for
Hypothalamic – Pituitary – Adrenal axis, which is the functional link between those 3 neurologic structures. The action of the hypothalamus (a section of the brain responsible for many bodily reflexes and mental processes such as temperature regulation and memory access) affects the pituitary gland (a section of the brain responsible for hormonal control and processes dependent on hormones such as hunger and growth) which affects the adrenal glands (located above the kidneys and responsible for the physical stress response aka fight or flight, along with extended stress responses mediated by cortisol). The three structures are interdependent so any activation of one will trigger activity in the others. In both melancholic and manic states, the HPA axis activity is much, much higher than in healthier individuals, and can be directly measured by testing the reaction of the body to injected stress hormones. In healthy individuals, after a few hours the level of stress hormones in the body will regulate themselves and return to a normal level. In mood disordered individuals in the midst of an episode, even after 24 hours the level of stress hormones will not have self regulated at all and will be much much higher than normally expected for that point in the circadian cycle.
>likewise, the
Hypothalamic-Pituitary-Thyroid axis is dysfunctional and exhibits unique and abnormal response to externally introduced thyroid hormones. Many mood disorder patients suffer from concurrent thyroid disorders that once treated prove to not be the root cause of their mood disorder.
>certain sections of the brain responsible for the regulation of movement (such as the
basal ganglia and particular areas of the
frontal lobes) are dysfunctional and directly testable with specific neurocognitive assessments that reveal impairments in the initiation of movement, the ability to inhibit movement, the ability to logically structure language, the ability to experience motivation and independently control one's own activity, etc. These areas are identically dysfunctional in either mood disorder. Interestingly enough although located in the same parts of the brain, some of these impairments are mirror opposites of eachother between melancholia and mania – experiencing a stress response can trigger either a behaviorally disinhibited, overly optimistic state or a severely behaviorally inhibited, unpleasant state, each of which are the respective backbones of mania and melancholia.
>areas of the brain responsible for the production and control of emotion such as the
temporal lobes, particularly the
amygdala and
hippocampus, and again areas of the
frontal lobes, are measurably dysfunctional. These areas are often assessed not quantitatively as in the previous bullet point, but qualitatively through careful comparison to descriptions of normal and abnormal emotional function. Patients with mood disorder will have difficulty in the voluntary regulation of their emotional expression and the ability to identify emotion in people besides themselves. A simple test is standing behind the patient and speaking in different tones, asking them to identify the emotion conveyed. Memory storage and retrieval are impaired, sometimes to such an extent that the patient develops state-dependent memory – that is, they cannot remember what happened while they were in a mood episode unless they again are in another of the same type of mood episode. Mood disorder patients have no control over their fight or flight response, which can be abnormally and unnaturally frequent to an extent severe enough to be labeled an anxiety disorder. They have no say in how they will feel – if they are melancholic they will not feel a smidgen of joy in response to a happy moment, and if manic they may feel even greater elation at the prospect of enduring things they would normally find horrifying. The color of their emotions are completely independent of their circumstances.
>over time mood disorders worsen. Like the river which dug the grand canyon, the effects on the brain caused by the experience of a mood disorder are self-reinforcing.
The more episodes a patient experiences, the more likely and more frequent and more severe are their episodes in the future. An illness which started with the mildest hint of melancholia will, if left untreated, steadily progress like a pendulum picking up speed and force. The effects of an unregulated bodily stress response cause frontal lobe and hippocampic degeneration that permanently worsens over time. What was initially triggered by only the most extreme and traumatic of stressful situations will over time become so sensitive as to happen after something as simple as an everyday disappointment, if there is any stressor at all. The brain, after having used the same pathways so many times, will preferentially use those same dysfunctional pathways more and more easily after each time they're used. It is quite literally a vicious cycle and it does not stop or ease on its own.
Now the reason I added that ungodly amount of background information was to hopefully more easily explain the method by which mood disorders worsen, and if that method reverses, improve. That reversal is the mechanism of ECT.
For about a hundred years parallels have been drawn between epilepsy (recurrent seizures) and mood disorder (recurrent melancholia/mania). Here are some basics of those similar points:
>they are episodic brain dysfunctions, the active symptoms of which are completely reversible by ending the episode
>although they are identified by the active periods of symptoms, there is an underlying problem of the brain which causes the episodes to occur and to recur after they're over
>with each episode the next one comes faster, harder, is more difficult to stop, is less likely to have any trigger, is longer in duration, is more physically damaging to the brain itself
>after a certain point the episodes become so damaging to the brain that new and permanent symptoms develop between episodes, reflecting the area of damage
Now it was an intersection of different observations that led to the procedure of inducing seizures electrically to treat mood disorders.
In italy it happened by accident and experimentation with different patients of different brain illnesses and different toxins which might cause seizures, that a physician discovered the psychosis of schizophrenia responded well to seizure induction. Around the same time it was noted that the psychosis or mood episodes caused by epilepsy never actually overlapped with the seizures themselves, instead each seeming to depend on the absence of the other to occur. (An interesting note, when epileptics develop psychosis in between their seizures it is treatable with ECT.) Eventually drugs which caused seizures were tested on mood disorder patients, to much success. Methods switched to electrical currents in order to better control the seizure outcome. Under anaesthesia and muscle relaxants, a single grand mal seizure is induced per session for a total of no more than 20 sessions spaced ever farther apart each time. The seizure basically "defibrillates" the neurons of the brain like an AED does to the heart during cardiac arrest. That electrical reset allows the brain to change up its accustomed dysfunctional behavior – much like the heart is "snapped out of" the abnormal rhythm which caused the arrest, the brain temporarily returns to normal healthy function and does not default to using the deeply ingrained neuronal pathways caused by the damaging recurrences of mood disorder. The effect is immediate although cumulative – the patient once awoken is so much improved they may see no further need for treatment, but if that effect is not compounded my further seizures then it will go away rather quickly. The lasting effects rely on neuroplasticity, the ability and tendency of the brain to continue to grow and prune neurons and pathways as they're used – again relying on the same mechanism that makes a mood disordered brain broken in the first place, the repeated use of the same pathway and reinforcement of it. Notably a prolonged stress response caused by HPA axis overactivity severely impairs neuroplasticity in the brain, especially the hippocampus, the area of the brain responsible for the most neurogenesis in healthy individuals. In laboratory tests, neurogenesis is greatly enhanced by the induction of seizures. Neurogenesis is helped to a lesser extent by medications such as lithium.
In conclusion, the neurotoxic process directly caused by mood disorder is halted and reversed with the induction of controlled seizures. This effect is exponentially stronger than any medication and if enough seizures are induced the positive effects are permanent, negating the risk of recurrence in the future.
Read a book some time, would you?
I will include a photograph of the books I have on hand which I referenced to jog my memory as I wrote:
im smellin bullshit
