Neurogenic Type

🧠 Overview — What is the Neurogenic Type?

The Neurogenic Type is a pattern of emotional and behavioral disturbances that arise from direct changes in the brain — whether from injury, degeneration, inflammation, or dysfunction in the neural circuits that specifically regulate mood and personality. Most individuals who fall into this category do not start with purely psychological problems such as stress or unresolved past trauma. Instead, the sequence is: “the brain changes first, and the mind follows.”

Put simply, the brain’s rhythm goes off-beat. For example, the prefrontal–limbic circuits that control emotion and behavioral inhibition become imbalanced. As a result, the person’s mood changes in ways they themselves often can’t explain. Even when “nothing particularly terrible is happening” in their actual life, they may feel deeply sad, angry, irritable, or even suicidal without any clear external trigger.

In this group, we often find a clear history of events that have affected the brain, such as:

– Severe head trauma from accidents (TBI)

– Ischemic or hemorrhagic stroke

– Brain infections or inflammatory processes (encephalitis / autoimmune)

– Brain tumors or masses compressing the frontal or temporal lobes

– Neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Multiple Sclerosis, etc.

What stands out is that the patient’s behavior and personality often change dramatically, as if they have become “a different person” after the brain pathology occurs. For example, someone who used to be cheerful may become easily enraged and irritable; or someone who used to be socially active and engaged may turn emotionally flat, withdrawn, and uninterested in people or surroundings.

In some cases, people around them misunderstand and assume the person “changed because their character got worse” or “they’re just depressed now.” But in reality, the limbic system and prefrontal cortex — which regulate emotion and motivation — have been directly affected. The brain’s emotional control system is “no longer braking properly” or “no longer functioning the way it used to.”

Another important point is that the Neurogenic Type is not always temporary. Some individuals have symptoms that persist for many years, especially in neurodegenerative diseases where the brain gradually deteriorates over time — such as Parkinson’s disease or Alzheimer’s disease. These often begin with a persistent low mood and later progress to problems with memory and thinking.

Identifying a case as Neurogenic Type is critically important in psychiatry because it completely changes the treatment approach — from relying solely on psychotherapy to combining brain-focused rehabilitation and medical treatment. This may include antidepressants alongside medications that control neurological disease, as well as physical therapy or cognitive rehabilitation to help the brain’s networks reconnect and function more effectively.

So, to put it very simply —
The Neurogenic Type is an emotional condition in which “the brain is the true origin,” not the mind alone. The patient does not “choose” to be sad, irritable, or emotionally cold. Rather, these are the consequences of emotional circuits in the brain being damaged, degenerated, or distorted. Recovery requires rehabilitation of both the brain and the mind together.

🔍 1) Core Symptoms — Main Symptoms of the Neurogenic Type 

The core of the Neurogenic Type is that emotion / behavior / thinking change because the “brain” itself has changed.
So when we describe symptoms, we don’t frame them as “bad personality” or “overly sensitive mind,” but instead as patterns that correspond to the location and type of brain pathology.

1.1 Clear and Prominent Emotional Changes

This is the cluster of symptoms that people around the patient usually notice first.

Chronic depression after brain disease

For example, depression after stroke, Parkinson’s disease, Multiple Sclerosis, or TBI.

• The patient may feel hopeless, sad, tired of life, with weight loss or gain, and disturbed sleep.
• But if you look at their “real-life situation,” external events often do not seem bad enough to explain this level of depression.
• Thus, the abnormal mood is “not very proportional to the psychosocial context,” but is proportional to “a brain that has just been damaged.”

Mood swings, irritability, and a much lower threshold for anger

• Someone who used to be calm may now raise their voice easily, shout, lash out physically, or speak in ways that deeply hurt others.
• The slightest trigger can cause an emotional explosion, even though before the brain disease, they were not this kind of person.
• This is often linked to lesions in the frontal lobe / orbitofrontal cortex / limbic circuits, which normally play a key role in emotional inhibition.

Crying easily / laughing too easily (pseudobulbar affect)

• Suddenly bursting into intense tears after hearing something only mildly sad, and being unable to stop — even though inside they’re not that sad.
• Or giggling inappropriately in situations that aren’t funny at all, such as funerals or serious meetings.
• This is not “bad manners,” but reflects a disrupted control of emotional expression.
• The patient themselves often feels uncomfortable and may say, “I can’t stop it — it just comes out on its own.”

Taken together, emotional symptoms in the Neurogenic Type give the impression that
“the mood swings or plunges deeply, even though real life is not dramatic enough to explain it.”

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1.2 Personality Changes

This part is dramatic enough that people around the patient are often shocked. It feels like:
“This is not the same person anymore.”

From calm → aggressive / impulsive

• They used to be quiet, polite, and patient.
• After a TBI or a frontal lesion, they become blunt, provocative, easily angered.
• Their emotional “brake line” becomes very short. They speak or act without thinking.
• Some start taking reckless financial risks, show changes in sexual behavior, or dare to do things they never would have done before.
  = This is classic “frontal personality change.”

From highly sociable → flat, withdrawn, emotionally detached (apathy)

• They used to enjoy conversations, meeting friends, and caring about others’ feelings.
• Suddenly, they become very indifferent, don’t want to leave the house, and lose interest in hobbies.
• When family members call to them, they respond briefly, as if nothing really matters.
• The key here is that “the patient isn’t all that distressed by their own condition — but the people around them are deeply distressed.”
• Neurogenic apathy feels more like “the lights in the head have gone out” than like pure depression (“I’m so sad I don’t want to do anything”).

Loss of motivation (amotivation) that looks more physical than purely psychological

• It’s not just laziness; it’s as if the brain can’t send a proper “start” signal to initiate action.
• Even if they know “I should get up, shower, work, do rehab,” they still feel they can’t get themselves to start.
• It resembles an engine that won’t start even though there’s still fuel in the tank.
• This is common in disorders involving the fronto-striatal circuits (e.g., basal ganglia lesions, Parkinson’s disease).

Personality change in the Neurogenic Type usually shows a clear pattern:
Before brain disease = one way, after brain disease = another way.
And this shift cannot be adequately explained by “just stress” or “just disappointment in life.”

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1.3 Disturbances in Thinking / Cognition

This part is directly tied to cognitive function.

Reduced attention and poor memory

• Forgetting appointments, misplacing things, forgetting commonly used words.
• Being unable to sustain focus on tasks that require prolonged concentration, tiring quickly, and feeling mentally fatigued.
• It can be hard to distinguish this from ADHD or pure anxiety if you don’t carefully review the brain history.
• In neurodegenerative diseases, these deficits gradually worsen in a progressive pattern.

Executive dysfunction

• Difficulty performing tasks that require multiple steps, such as cooking several dishes, managing finances, or planning complex trips.
• Decision-making becomes difficult — “I can’t choose anything” — or, on the flip side, becomes overly impulsive.
• People around them may wonder, “Why can’t they manage their own life anymore? They used to be so capable.”

Psychosis from brain disease

• Delusions (e.g., thinking someone is out to harm them, believing family members are conspiring against them).
• Hallucinations (hearing voices calling their name, seeing shadows, seeing animals, etc.).
• Often occurs in certain conditions such as Parkinson’s disease, Lewy body disease, temporal lobe epilepsy, or some forms of encephalitis.
• The key is that “psychosis occurs together with clear evidence of brain pathology,” not as an isolated phenomenon.

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1.4 Neurological and Physical Symptoms

This is where we start to suspect, “This is not just an ordinary mood disorder.”

Seizures or seizure-like episodes

• Tonic-clonic convulsions with loss of consciousness.
• Or partial seizures (brief staring spells, focal muscle jerks, etc.).
• Mood may shift abruptly after a seizure (irritability, depression, confusion).

Weakness on one side of the body (hemiparesis)

• Difficulty lifting one arm, dragging one leg.
• Indicates a lesion in motor pathways (such as stroke), often linked to subsequent mood changes.

Movement abnormalities

• Tremor, muscle rigidity, slowed movements (bradykinesia).
• Classic in Parkinson’s disease and certain neurodegenerative disorders.
• Frequently co-occurs with depression and apathy → creating a picture of “both mood and body slowing down together.”

Unsteady gait / poor balance / frequent falls

• Suggests involvement of the cerebellum, brainstem, or balance-related pathways.
• When these appear together with abnormal mood → it strongly points toward a neurogenic, rather than purely psychological, origin.

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1.5 Marked Impairment in Function and Relationships

Performance crashing dramatically after a brain event

• A person who used to manage large projects suddenly struggles with simple tasks.
• Supervisors or colleagues might interpret this as “they’re not trying,” when in reality the brain simply can’t keep up.

Family / romantic / workplace relationships breaking down due to emotional changes

• Constant irritability toward family members, harsh words, emotional abuse — even though the person was previously gentle and polite.
• Partners feel as though they’re living with “a different person,” even though the face is the same.
• When no one explains the concept of the Neurogenic Type, both the patient and their loved ones become trapped in cycles of anger, guilt, and confusion.

Summary of Core Symptoms:
It is a mix of emotion, personality, cognition, and movement changing together in a pattern that is tied more closely to “the brain” than to “life drama.”

📋 2) Diagnostic Criteria — Conceptual Diagnostic Framework 

Once again, “Neurogenic Type” is a descriptive conceptual label, not an official diagnostic term.
So when we write criteria, they are conceptual criteria designed to help readers distinguish neurogenic cases from conditions that are purely psychological.

2.1 Clear Evidence of Brain Disease / Brain Abnormality

This is the strictest — and most crucial — criterion.

There must be at least one of the following:

• CT / MRI / EEG / PET or other imaging clearly indicating a lesion.
• A history of severe TBI (loss of consciousness, intracranial bleeding, etc.).
• A formal medical diagnosis of stroke, epilepsy, neurodegenerative disease, brain tumor, encephalitis, etc., by a physician.

If there is no evidence of brain disease at all, but the person has emotional problems → we classify it first under standard mood/anxiety/personality disorders.

The purpose of this criterion is to “prevent us from throwing the term Neurogenic Type at every emotionally distressed case.”

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2.2 Emotional / Behavioral Changes Begin “After” Brain Abnormality, Within a Plausible Time Window

The temporal order should roughly be:

1. Brain problem occurs →
2. Within a few weeks to several months →
3. Mood/behavior begins to change.

Examples:

• A stroke patient becomes severely depressed within 3 months after their stroke.
• After surgical removal of a frontal lobe tumor, the family immediately notices: “Their personality is totally different now.”
• Shortly after developing temporal lobe epilepsy, the person starts to have strange mood swings, irritability, and episodes of intense fear.

If the person has had longstanding emotional problems for many years and later happens to have a stroke → interpretation becomes more complex. It may be a pre-existing mood disorder plus stroke, rather than a “pure” Neurogenic Type.

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2.3 Prior to Brain Issues, Personality/Mood Were “Relatively Normal,” or It’s Clearly Visible That “After the Brain Changed, Everything Changed Again”

We look for two main patterns:

• People with no prior major psychiatric history, whose mood/behavior collapses for the first time after a brain disease.
• People with some pre-existing difficulties, but whose symptoms change in quality after the brain event — e.g., from mild anxiety previously to full-blown irritability + apathy + neurogenic cognitive decline.

This helps distinguish:

• Someone with a long-standing personality disorder, bipolar disorder, or severe MDD who later has a stroke or TBI → this is best viewed as “brain disease layered on top of existing psychiatric illness,” not a pure Neurogenic Type.

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2.4 Emotional / Behavioral Symptoms Cannot Be Fully Explained by Psychological or Social Factors Alone

For example:

• A person with a warm family life, stable finances, and no new psychosocial stressors suddenly becomes severely depressed after a stroke → the weight of evidence leans toward neurogenic.

• Or someone in early Parkinson’s disease feels profoundly sad or suicidal even though they have not yet lost many functional roles → this suggests brain chemistry and dopamine/serotonin circuits are major drivers.

This criterion does not say that “psychological factors don’t matter.”
It says:
If we compare causes and brain pathology is clearly more compelling than life stress, we classify the case as Neurogenic Type.

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2.5 Evidence Linking Symptoms to Specific Neural Circuits

This criterion is used when detailed imaging or neuro exams are available:

For example:

• Lesion / atrophy in the frontal lobe → aggression, disinhibition, poor decision-making.
• Basal ganglia / thalamus lesions → depression, psychomotor slowing, apathy after stroke.
• Temporal lobe involvement → mood swings + fear + déjà vu + psychotic-like symptoms (in some epilepsy cases).

This criterion serves to “upgrade our confidence” that the symptoms are not random but map onto specific neurocircuits.

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2.6 Formal Diagnostic Categories in DSM/ICD That Correspond to the Neurogenic Type

In real clinical practice, doctors do not write “Neurogenic Type” on the chart.
Instead, they use diagnoses such as:

• Depressive disorder due to another medical condition
• e.g., depression due to stroke / Parkinson’s / MS.

• Personality change due to another medical condition
• Used in cases where personality changes dramatically after a lesion.

• Major or Mild Neurocognitive Disorder with mood/behavior disturbance
• e.g., Alzheimer’s disease with behavioral disturbance.
• Frontotemporal neurocognitive disorder with disinhibition.

When writing content on your website, we can frame it like this:

Clinically, Neurogenic Type conditions are often classified under official diagnoses such as
“Depressive disorder due to another medical condition” or
“Personality change due to another medical condition,”
depending on whether the main feature is severe depression or a marked personality change following brain damage.

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2.7 Why Is It So Important to Distinguish the Neurogenic Type?

Because if we “pick the wrong genre,” the entire treatment plan will be wrong.

If we assume:

“They’re burned out from work, stressed, and life is rough, that’s why they’re depressed.”

→ We might focus only on psychotherapy / life coaching / self-help.

But if, in reality:

“They’ve just had a stroke / they have Parkinson’s / they have temporal lobe epilepsy,”

→ We must address the brain disease, adjust neurological medications, provide neurorehab, and offer family psychoeducation.

Labeling a case as Neurogenic Type (in a content/educational sense):
= helps loved ones stop blaming themselves and stop blaming the patient with thoughts like
“Why can’t they just be stronger?” or
“Their personality changed because they’re not trying hard enough.”

🧩 Subtypes or Specifiers — Subgroups of the Neurogenic Type

We can divide subtypes based on the underlying brain disease plus the leading emotional pattern, such as:

1. Post-Stroke Neurogenic Type

• Focuses on “post-stroke depression” or emotional instability after ischemic/hemorrhagic stroke.
• Very common among stroke patients and significantly influences recovery, physical rehabilitation, and overall quality of life.

2. Epilepsy-Linked Neurogenic Type

• Occurs in patients with epilepsy, especially temporal lobe epilepsy.
• Features may include depression, anxiety, mood swings, irritability, and psychotic-like symptoms in some cases.
• Sometimes mood changes appear before/after seizures (peri-ictal mood changes).

3. Neurodegenerative-Linked Neurogenic Type

• Found in conditions such as Alzheimer’s disease, Frontotemporal dementia (FTD), Parkinson’s disease, Lewy body disease.
• Hallmarks include apathy, irritability, depression, emotional blunting, and personality change.

4. TBI-Related Neurogenic Type

• After the brain is injured by accidents (car crashes, falls, etc.).
• Common patterns: irritability, poor emotional control, impulsivity, harsher or more aggressive speech, or clearly increased depressive symptoms.

5. Tumor / Structural Lesion-Linked Type

• Brain tumors or masses (such as frontal meningioma) can cause extremely dramatic personality changes.
• The person may look as if they have a “personality disorder syndrome,” but in reality, it is the result of a mass compressing the frontal lobe.

6. Inflammation / Autoimmune Neurogenic Type

• For example, autoimmune encephalitis, lupus cerebritis, paraneoplastic syndromes.
• These can cause mood symptoms, psychosis, and personality changes alongside other neurological signs.

🧬 Brain & Neurobiology — Brain and Neurobiology of the Neurogenic Type

The Neurogenic Type is a pattern of mood disturbance in which “the origin does not lie in the psyche but begins with changes in the brain itself.”
What differentiates it from typical mood disorders is that the brain exhibits objectively detectable abnormalities — whether lesions, tissue degeneration, inflammation, or neurotransmitter imbalance at the level of entire networks.

From a neuroscience perspective, “emotion” is not located in a single spot in the brain. It is the outcome of coordinated activity across multiple systems — such as the frontal cortex, limbic system, basal ganglia, thalamus, and brainstem nuclei. These communicate using four major neurotransmitter groups: serotonin, dopamine, norepinephrine, and the GABA–glutamate balance.

When these structures become imbalanced → emotional circuits collapse in a cascade.
This leads to what we call “Neurogenic Emotional Dysregulation” — unstable mood, slowed thinking, and impaired inhibition of behavior.

🔹 1. Frontal Lobe / Prefrontal Cortex

This is the center of “Executive Control” — the part of the brain that functions like the CEO of the nervous system.

• The dorsolateral prefrontal cortex (DLPFC) manages analytical thinking, planning, impulse control, and sequencing of thought.
• The orbitofrontal cortex (OFC) is involved in behavioral inhibition and evaluating the emotional value of stimuli.
• The ventromedial prefrontal cortex (vmPFC) is linked with empathy, guilt, and self-awareness.

If this region is damaged (e.g., TBI, frontal tumor, stroke) → a person may show:

• Poor emotional control (disinhibition).
• Impulsive behavior and rash decision-making.
• Harsh / aggressive / inappropriate speech.
• Loss of social awareness or tact (social inappropriateness).
• Or, in the opposite direction, some become extremely apathetic, with a shutdown-like state (abulia).

This frontal dysfunction is often associated with “frontal-type depression,” where patients feel more like their emotional energy is extinguished rather than “sad with a clear reason.”

🔹 2. Limbic System (Amygdala, Hippocampus, Cingulate Gyrus)

This is the “heart of emotion and emotionally-tagged memories.”

• The amygdala generates fear, anger, and rapid emotional reactions.
• The hippocampus encodes emotional memories and experiences.
• The cingulate cortex (especially the anterior cingulate cortex – ACC) bridges emotion and cognition, and plays a role in assessing distress (pain perception, guilt, empathy).

In the Neurogenic Type, connectivity between the amygdala and prefrontal cortex is often disrupted.

• If the amygdala is hyperactive and the prefrontal cortex cannot “brake” it → irritability, anxiety, and mood swings emerge.
• If the amygdala is hypoactive → emotional flatness, indifference, lack of engagement with surroundings.

fMRI studies show that post-stroke depression and Parkinson’s depression often involve hypometabolism in the ACC and ventral striatum, indicating real damage to limbic-frontal communication.

🔹 3. Basal Ganglia / Thalamus

These two structures function like a “gearbox” that coordinates both movement and motivation.
The key circuit is the fronto-striatal-thalamic loop, connecting prefrontal cortex → basal ganglia → thalamus → back to prefrontal cortex.

• When this circuit functions well → people feel motivated, mentally sharp, and physically agile.
• When it fails → there is psychomotor retardation (slowed thinking and movement) and apathy.

Basal ganglia lesions or small vessel disease often leave patients feeling as if “the internal lights are out,”
even though their body is still capable of movement, their drive to act or think almost vanishes.

The thalamus also acts as a “central station” for emotional processing.
When an infarct or hemorrhage occurs here (thalamic stroke), patients can develop dramatic mood changes — including both depression and euphoria.

🔹 4. Neurotransmitters — The Brain Chemicals That Ignite Symptoms

Emotion is the cumulative effect of balanced neurochemical signaling across synapses.

Serotonin (5-HT):

• Plays a central role in mood stabilization.
• Drops significantly in post-stroke depression and Parkinson’s disease → causing sadness, low mood, and recurrent negative thoughts.

Dopamine:

• Linked with “reward from accomplishing something” and “motivation to act.”
• In Parkinson’s disease (where dopamine is depleted in the basal ganglia) → patients often feel apathy and anhedonia (loss of pleasure in previously enjoyed activities).

Norepinephrine:

• Involved in energy, attention, and arousal.
• This system often fails in strokes affecting the brainstem → causing lethargy, easy fatigue, and lack of focus.

GABA / Glutamate:

• These two act as opposing forces that maintain the excitation-inhibition balance in the brain.
• GABA = inhibitory, reduces neural excitability.
• Glutamate = excitatory, drives electrical signaling.
• In epilepsy or excitotoxic states → glutamate overload can overstimulate neurons, causing damage and leading to intense emotionality or aggression.

🔹 5. Neuroinflammation & Neurodegeneration

In many brain disorders, we see micro-level inflammation (microglial activation), leading to the release of cytokines such as IL-1β, TNF-α, and IL-6. These disrupt the synthesis of serotonin and dopamine, contributing to depressive mood.
This is known as “inflammatory depression.”

At the same time, neuronal degeneration (neurodegeneration) in conditions like Alzheimer’s, Lewy body disease, and FTD gradually disrupts synaptic networks between frontal and limbic regions → increasing negative affect and weakening emotional inhibition.

In some cases, chronic systemic inflammation (e.g., from diabetes, lupus, COVID-related neuroinflammation) may also push the brain into a neurogenic mood disorder state.

🔹 6. Network-Level View: “Brain Circuits No Longer Talking the Same Way”

Modern neuroimaging (e.g., fMRI, DTI) has shown that in the Neurogenic Type, the problem is not just “one damaged brain spot,” but disrupted communication between multiple regions.

Examples of impaired networks:

• Default Mode Network (DMN): involved in self-reflection — often overactive in neurogenic depression.
• Salience Network (SN): selects emotionally relevant stimuli — its activity becomes dysregulated in Parkinson’s and post-stroke states.
• Central Executive Network (CEN): governs attention and decision-making — often hypoactive in patients with frontal lesions.

In short, the brain is “no longer coordinating properly” between the emotional brain and the rational brain → emotions become misaligned with external reality.

⚠️ Causes & Risk Factors — Causes and Risk Factors 

The Neurogenic Type usually arises from physical and biological factors that damage or disrupt brain circuits directly, unlike typical mood disorders that are more often rooted in psychological trauma or stress.

🔸 1. Medical / Neurological Factors

Stroke / TIA

• The leading cause of neurogenic depression.
• Lesions in the basal ganglia, left frontal lobe, or anterior cingulate → carry a 30–50% risk of depression.
• Right-hemisphere lesions → more often associated with mood lability and reduced empathy.

Traumatic Brain Injury (TBI)

• Strong impacts cause brain contusions or diffuse axonal injury.
• Patients may experience immediate personality shifts — becoming aggressive, irritable, disinhibited, or profoundly depressed.
• The more the frontal or temporal lobes are involved, the more prominent the emotional disturbances.

Neurodegenerative Disorders

• Alzheimer’s Disease: starts with memory loss → later apathy, irritability, and depression.
• Frontotemporal Dementia (FTD): dramatic personality changes (disinhibition, hypersexuality, lack of empathy).
• Parkinson’s Disease: dopamine loss in the basal ganglia → depression, apathy, anxiety.
• Lewy Body Disease: psychosis occurs alongside mood disturbances.

Epilepsy (Especially Temporal Lobe Epilepsy)

• Recurrent seizures cause chronic changes in brain chemistry.
• Patients have 2–3 times higher risk of depression and anxiety than the general population.
• Some experience “pre-ictal depression” (mood drops before a seizure) and “post-ictal euphoria.”

Brain Tumors / Structural Lesions

• Masses in the frontal or temporal lobes can abruptly and dramatically alter personality.
• Even benign tumors such as meningiomas can cause severe emotional dyscontrol.
• Often accompanied by headaches, visual disturbances, and cognitive decline.

Infectious / Autoimmune Encephalitis

• Brain inflammation from viruses (HSV, Japanese encephalitis) or autoimmune processes (e.g., anti-NMDA receptor).
• Often begins with mood changes, irritability, depression, or psychosis before progressing to overt neurological symptoms.

🔸 2. Biological Factors

• Age: The older a person is, the higher the risk of vascular lesions and neurodegeneration.
• Genetics: Certain genes such as APOE4 (Alzheimer’s) and PARK genes (Parkinson’s) increase vulnerability.
• Sex: Women have a higher risk of post-stroke depression, partly due to greater sensitivity of serotonin systems.
• Metabolic / Vascular factors: Diabetes, hypertension, hyperlipidemia, and smoking cause chronic cerebral small vessel disease.
• Hormones: Declines in estrogen/testosterone with aging affect serotonin and dopamine pathways.

🔸 3. Psychological and Social Factors (That Exacerbate Symptoms)

Even though the root cause is in the brain, psychosocial factors can significantly worsen symptom severity.

Loss of functional capacity in daily life (loss of function)

• Stroke or Parkinson’s patients who can no longer perform simple tasks, such as walking or writing, often feel a deep loss of self-worth.

Loss of social or family roles

• Going from being the family provider to being “the patient” leads to the feeling of “being a burden.”
• This feeling itself directly fuels depression in brain-injured patients.

Lack of social support

• If the family doesn’t understand that behavior changes stem from brain damage → they tend to blame the patient for “acting badly.”
• This leads to greater stress and emotional isolation.

Insufficient care from the healthcare system

• Patients who lack access to rehabilitation or specialized neuropsychiatric treatment often deteriorate more quickly because their symptoms are never addressed in a comprehensive way.

🔸 4. Summary of Causal Relationships

Level	Mechanism	Emotional Effect
Brain structure (Structure)	lesion, degeneration, tumor	Personality change, poor emotional control
Neural circuits (Circuit)	frontal–limbic disconnect	mood swing, irritability, apathy
Neurochemistry (Neurochemical)	serotonin/dopamine depletion	depression, loss of motivation
Inflammation (Inflammation)	elevated cytokines	fatigue, depressed mood
Psychosocial (Psychosocial)	lack of support	depression, withdrawal

All of these together form what we call the “Neurogenic Cascade” —
Starting from brain → chemistry → emotion → behavior → broken relationships → feeding back into the brain again.
If this cycle is not interrupted by integrated treatment, it will repeat and gradually lead to further structural brain deterioration.

🩺 Treatment & Management — Management of the Neurogenic Type

The goal is not only to “improve mood,”
but to treat the underlying brain disease + restore daily functioning at the same time.

1. Treating the Neurological Cause

• Optimize management of the brain disorder (e.g., control seizures, treat tumors, rehabilitate stroke, manage vascular disease, etc.).
• The more the lesion activity is reduced and the more stable the brain becomes, the more mood symptoms tend to improve.

2. Pharmacological Treatment

• Antidepressants (SSRIs, SNRIs, etc.).
• Mood stabilizers in cases with severe mood swings or irritability.
• Antipsychotics when psychotic symptoms or severe agitation are present.
• Must carefully monitor interactions with neurological drugs (e.g., antiepileptics) and cognitive side effects.

3. Brain and Functional Rehabilitation (Neurorehab)

• Cognitive rehabilitation / occupational therapy.
• Physical therapy.
• Re-training of activities of daily living.

4. Psychotherapy / Psychoeducation

• Use formats adapted to the patient’s cognitive level.
• CBT, supportive therapy, and family therapy help others understand that

“this is the brain changing, not just the person getting worse because of their ‘character.’”

5. Family and Caregiver Support

• Teach the typical pattern of neurogenic symptoms: mood lability, apathy, irritability.
• Provide management tools: setting routines, reducing overstimulation, communicating directly but without emotional escalation.

6. Long-Term Care

• Monitor brain and mood symptoms as a single integrated unit.
• Adjust medications and rehabilitation plans periodically.
• Watch closely for suicidality in patients with co-existing depression, especially in post-stroke, Parkinson’s, and epilepsy.

📝 Notes — Key Points to Emphasize in the Article

• The Neurogenic Type is not an official diagnostic label, but a conceptual tool that helps readers see that

• sometimes mood and personality change because the brain itself has truly changed.

• It is crucial not to blame oneself or the patient with ideas like “bad character” or “lack of self-control” while ignoring underlying brain disease.

• Using the term Neurogenic Type helps distinguish these cases from those driven primarily by psychological trauma or longstanding personality traits.

• This concept is particularly suitable for a neuroscience / psychoeducation site like NeuroNerdSociety, because it:

• Bridges the world of “psychiatry” with “neurology.”
• Helps readers understand that, in some cases, mental health = brain health in a very literal sense.
• It pairs well with other subtypes such as “Psychogenic Type,” “Personality-Linked Type,” “Trauma-Linked Type” to create a clear, structured framework for your site.

📚 References

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Kanner AM. “Mood and Anxiety Disorders in Epilepsy.” Neurologic Clinics. 2011;29(1):69-85.

Starkstein SE, Robinson RG. Depression in Neurologic Disease. Oxford University Press; 2015.

Fuster JM. The Prefrontal Cortex. 5th ed. Academic Press; 2015.

Tekin S, Cummings JL. “Frontal-Subcortical Neuronal Circuits and Clinical Neuropsychiatry: An Update.” Journal of Psychosomatic Research. 2002;53(2):647-654.

Cummings JL, Mega MS. Neuropsychiatry and Behavioral Neuroscience. Oxford University Press; 2003.

Mayberg HS. “Limbic-Cortical Dysregulation: A Proposed Model of Depression.” Journal of Neuropsychiatry and Clinical Neurosciences. 1997;9(3):471-481.

Krishnan KRR. “Neuroanatomic and Neurochemical Correlates of Neurogenic Depression.” Biological Psychiatry. 2002;52(7):512-528.

Chagas MHN, Tumas V, et al. “Depression in Parkinson’s Disease: Clinical, Biological, and Pathophysiological Features.” Frontiers in Psychiatry. 2013;4:25.

Sadock BJ, Sadock VA, Ruiz P. Kaplan & Sadock’s Synopsis of Psychiatry. 12th ed. Wolters Kluwer; 2023.

Sachdev PS, et al. “Neuropsychiatric Consequences of Traumatic Brain Injury.” Psychiatric Clinics of North America. 2001;24(4):769-788.

Feinstein A, et al. “Depressive Disorders in Multiple Sclerosis.” Lancet Neurology. 2014;13(7):700-709.

Drevets WC, Price JL, Furey ML. “Brain Structural and Functional Abnormalities in Mood Disorders: Implications for Neurocircuitry Models of Depression.” Brain Structure and Function. 2008;213(1-2):93-118.

Liu CH, et al. “Neuroinflammation in Major Depressive Disorder: A Review of PET Imaging Studies.” Frontiers in Psychiatry. 2021;12:705904.

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