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Biological Bases of Behavior Cheat Sheet (DRAFT) by

Biological Bases of Behavior Study Guide

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Central Nervous System

The Brain
Receives and processes sensory inform­ation, initiates responses, stores memories, and generates thoughts
Spinal Cord
Conducts signals to and from the brain, controls reflex activi­ties.

The Brain Structure

Cerebrum
The largest part of the brain, made up of the cerebral cortex and other struct­ures. The cerebrum is divided into two hemisp­heres.
Cerebellum
Coordi­nates movement by combining inform­ation from the eyes, ears, and muscles.
Brainstem
Connects the cerebrum and cerebellum to the spinal cord. The brainstem controls uncons­cious processes like sleep.

The Brain Structure Visual

Divisions of the Brain

Forebrain
Processes sensory inform­ation, helps with reasoning and proble­m-s­olving, and regulate autonomic, endocrine, and motor functions
Midbrain
Helps to regulate movement and process auditory and visual inform­ation
Hindbrain
Helps regulate automatic functions, relay sensory inform­ation, and maintain balance and equili­brium

Divisions of the Brain Visual

The Limbic System

Limbic System
(Primitive brain), regulates emotions (basic survival instin­cts), influences memori­es/­lea­rning, and motivation (basic drives).
Thalamus
Sensory relay center, receives input from all our senses except olfaction, critical in the perception of pain
Hippoc­ampus
Stores memories, consol­idation of conscious memories, stores new inform­ation and events as lasting memories
Amygdala
Processing fearful and threat­ening stimuli. Includes threat detection and activation of fear-r­elated behaviors.
Hypoth­alamus
Maintains the body's homeos­tasis, (regulates temper­ature, hunger, thirst, sleep-wake cycle). Produces hormones that stimulate or inhibit the release of hormones from the pituitary gland.
Corpus Callosum
Connects the brain's left and right hemisp­heres, allowing them to commun­icate
Basal Ganglia
Motor learning, executive functions and coordi­nation of movement, posture, inhibitory (allows us to be still)
Olfactory Bulb
is a part of the brain that processes smell
Cingulate gyrus
Involved in regulating emotions, processing pain, and regulating autonomic motor function.
Pineal gland
Helps control the circadian cycle of sleep and wakefu­lness by secreting melatonin.
Suprac­hia­smatic Nucleus (SCN)
Controls the body's circadian rhythms

The Limbic System Visual

The Cerebral Cortex Visual

The Cerebral Cortex

Cerebral Cortex
Involved in many high-level functions, such as reasoning, emotion, thought, memory, language and consci­ous­ness.
Frontal Lobe:
the largest portion of the brain (about ⅓ of the entire brain) divided into prefrontal cortex, premotor area, and motor area
Parietal Lobe:
Primary sensory areas that process somato­sensory inform­ation, sensations of touch, pain, heat, and propri­oce­ption.
Temporal Lobe:
Auditory proces­sing, memory inform­ation retrieval, and involved in emotional behavior. Connected to limbic system (hippo­campus, amygdala, etc).
Occipital Lobe:
Visual percep­tion, visual interp­ret­ation, and reading

Frontal Lobe

Left Frontal Lobe:
language, speech, and cognitive tasks. Includes broca's area
Right Frontal Lobe:
non-verbal commun­ication (facial recogn­ition) and enviro­nmental awareness
Prefrontal Cortex (PFC)
Integr­ation center for all sensory inform­ation and executive functions (decision making, planning, working memory, person­ality expres­sion, social behavior, speech and language). Person­ality center
Broca's area
Controls the muscles that produce speech and language compre­hension

Parietal Lobe

Left Parietal Lobe:
Directing attention, visual & spatial skills
Right Parietal Lobe:
Motor routines and linguistic skills (reading, writing)

Temporal Lobe

Left Temporal Lobe:
Verbal memory and language compre­hen­sion. Includes wernicke’s area.
Right Temporal Lobe:
Visual memory
Wernicke's Area
Language compre­hension = receives auditory signals from the ear and processes them to understand the meaning of spoken words

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How does the SCN interact with the Pineal Gland?
The SCN sends messages to the pineal gland, which triggers the release of melatonin at night and triggers the release of cortisol and other hormones to help you wake up in the morning.

Peripheral Nervous System (PNS)

Somatic Nervous System:
Sends and receives sensory messages that control voluntary motor movement of the skeletal muscles
Automatic Nervous System:
Controls automatic or involu­ntary bodily functions of the smooth muscles and glands

Automatic Nervous System (ANS)

Primary Function:
Maintain homeos­tasis (e.g., digestion, heart rate, & breathing)
Sympat­hetic Nervous System (SNS)
The Body's mobilizing system. Prepares the body for stressful or energetic activity (e.g., fight or flight)
Parasympathetic Nervous System (PNS)
Dominates during rest state, directs mainte­nance activities (e.g., rest and rumina­tion)

Sympat­hetic & Parasy­mpa­thetic Effects

Myelin­ation of the Vagus Nerve

Vagus Nerve
A major nerve in the parasy­mpa­thetic nervous system that helps regulate heart rate, digestion, and emotional responses.
Myelination
The process of covering nerve fibers with myelin, which improves the speed and efficiency of nerve signaling.
Social Connection & Nervous System Develo­pment:
Safe Connection with Another Mammalian Nervous System:
This suggests that social intera­ctions, partic­ularly safe and supportive relati­ons­hips, help stimulate and develop the vagus nerve.
 

Neuro Disorders

Brain Locus of Neurol­ogical Disorders

Type
Disorders/ Descri­ption
Locus of the Brain
Movement disorders
tics/O­CD/­tou­rettes
Basal Ganglia
Speech deficits
 
left frontal broca’s; left temporal Wernicke’s
Sleep disorders
 
hypoth­alamus; pineal gland; SCN
Memory
 
Wernicke's aphasia
problems unders­tanding speech
left temporal lobe
Broca's aphasia
inability to express language
left frontal lobe

Brain Areas for Neurol­ogical Disorders

Delirium
Alzhei­mer's Disease (AD)
Parkin­son's Disease
Huntin­gton's Disease (Chorea)
Pseudo­dem­entia
Major Fronto­tem­poral Neuroc­ogn­itive Disorder
Major Neuroc­ogn­itive Disorder Due to HIV Infection
Neuroc­ogn­itive Disorder due to Traumatic Brain Injury

Wernicke's Enceph­alo­pathy (WE)

Most often arises in people with AUD
Symptoms:
Paralysis of the eye muscles, ataxia, confusion
Caused by thiamine deficiency (vitamin B1)
Other causes:
severe malnut­rition, prolonged vomiting, extended IV nutrition, cancer, immuno­def­ici­ency, liver disease, hypert­hyr­oidism, and severe anorexia.
Risk:
If left untreated, WE can lead to Korsakoff syndrome (KS)

Wernic­ke-­Kor­sakoff Syndrome

The disorder is associated with patients fabric­ating stories in the setting of clear consci­ous­ness. Confab­ula­tions can be sponta­neous or provoked
Cause:
Severe brain disorder caused by a deficiency of thiamine (vitamin B1)
Symptoms:
Memory distur­bances in which there are signif­icant deficits in antero­grade and retrograde memory
Immediate memory is mainta­ined, but short-term memory is diminished with intact sensorium.

Parkin­son's

Features:
Movement disorder with tremors, rigidity, bradyk­inesia, shuffling gait, and neurop­syc­hiatric symptoms (e.g., depres­sion, neuroc­ogn­itive disorder).
Brain Locus:
Caused by the gradual loss of dopami­nergic neurons in the Substantia Nigra (part of the Basal Ganglia, which regulates voluntary movement).
Treatment & Psycho­pha­rma­cology
Levodopa (L-Dopa) -
Dopamine precursor to improve movement
Carbidopa -
Reduces Levodopa side effects (e.g., nausea, hypote­nsion) and enhances its effect­ive­ness.
Dopamine Agonists -
Stimulate dopamine receptors
Enzyme Inhibitors -
MAO-B and COMT inhibitors slow dopamine breakdown.
Amantadine -
Helps reduce involu­ntary movements
Antich­oli­nergics -
Reduce tremors and muscle rigidity
Deep Brain Stimul­ation (DBS) -
Surgical treatment for severe cases

Alzhei­mer’s Disease (AD)

Defini­tion:
The most common major neuroc­ogn­itive disorder (NCD), accounting for up to 80% of cases.
Preval­ence:
Affects 1 in 8 people over 65, more common in women due to longer life expect­ancy.
Neurop­ath­ology:
Acetyl­choline deficiency, affecting learning and memory; Amyloid plaques & neurof­ibr­illary tangles; Damage to the hippoc­ampus and amygdala
Disease Progre­ssion:
Begins up to 20 years before symptoms appear. 1: pre-cl­inical (no symptoms), 2: MCI, 3: dementia due to AD
Symptoms
Early:
Memory loss, apathy, depression
Progre­ssive:
Disori­ent­ation, confusion, impaired judgment, behavioral changes, motor and gait issues
Late:
Loss of commun­ica­tion, failure to recognize loved ones, bedridden

Types of Dementia

Alzhei­mer's disease:
The most common type, charac­terized by the accumu­lation of amyloid plaques and tau tangles in the brain
Vascular dementia:
Caused by damage to blood vessels in the brain, which reduces blood flow and oxygen to the brain
Lewy body dementia:
Charac­terized by the presence of abnormal protein deposits called Lewy bodies in the brain.
Fronto­tem­poral dementia:
Affects the frontal and temporal lobes of the brain, leading to changes in behavior, person­ality, and language
Mixed dementia:
A combin­ation of two or more types of dementia

Dementia VS. Pseudo­-de­mentia

Pseudo­dem­entia
Cognitive impairment in older adults due to depression, mimicking a neuroc­ogn­itive disorder (NCD).
Key Differ­ences
Dementia (NCDs)
Pseudo­dem­entia
Progressive cognitive decline
Slower processing speed, difficulty with concen­tration and attention, psycho­motor retard­ation
Patients often deny memory issues
Patients acknow­ledge memory loss
Irreversible deteri­oration
Cognitive function improves once depression is treated

Sleep Patterns Over the Lifespan

REM sleep decreases with age:
Newborns: 50%; 5-year­-olds: 20–25%; Older adults: 18%
Functions of REM Sleep:
Psycho­logical restor­ation; Memory consol­idation & emotional proces­sing; Brain develo­pment; Dreaming (often bizarre and illogical)

Movement Disorders

Originates in the:
Basal Ganglia
Defini­tion:
Abnormal repetitive movements
Basal Ganglia:
also the reservoir of our over-l­earned motor patterns, like riding a bike, automatic daily habits, backing out of the driveway, etc.
Hyperk­inetic
Excess or involu­ntary movements (e.g., huntin­gton’s diseas­e/c­horea, tremors, tics/ tourette's syndrome)
Hypoki­netic
Slow or reduced movements (e.g., parkin­son's disease, dementia with lewy bodies)

Huntin­gton's Chorea

Cause:
Genetic disorder causing degene­ration of basal ganglia neurons
Symptoms:
Choreiform (jerky, involu­ntary movements); Speech outbursts; Progre­ssive cognitive decline
Onset:
Typically 40–50 years; often passed down before symptoms appear
Treatment:
No cure available

Parkin­son’s Disease

Cause:
Damage to the Substantia Nigra, caudate nucleus, and putamen, dopami­ne-rich brain areas essential for movement and mood regulation
Symptoms:
Movement diffic­ulties (tremors, rigidity, slowed initia­tion); Depres­sion, psychosis in severe cases
Possible Cause:
Bacterial infections (e.g., from foodborne pathogens) may travel via the Vagus nerve, leading to inflam­mation and degene­ration
Preval­ence:
Increasing signif­icantly (e.g., Michael J. Fox as a well-known case)
Treatment
L-Dopa (dopamine precursor)
helps tempor­arily replenish dopamine and slow symptom progre­ssion
Music Therapy
may aid movement and mood regulation

Tourette's Syndrome

Brain Area:
basal ganglia, frontal lobes and cortex
Comorb­idi­ties:
OCD; ADHD; Anxiety

Five A’s of Neurologic Symptoms

Ataxia
Impaired coordi­nation, balance, and speech
Common Cause:
Damage to the cerebellum or motor areas
Apraxia
Inability to perform skilled movements or gestures (e.g., difficulty winking)
Common Cause:
Parietal lobe damage
Aphasia
Impaired speech or language compre­hension
Types & Causes:
Receptive aphasia; Expressive aphasia; Conduction aphasia
Receptive Aphasia
Damage to Wernicke’s area (left temporal lobe); speech is not understood
Expressive Aphasia
Damage to Broca’s area (posterior frontal lobe); difficulty producing speech
Conduction Aphasia
Damage to neural pathways connecting these areas, affecting verbal repetition
Anomia
Difficulty naming objects, people, or terms
Common Cause:
Likely damage to the hippoc­ampus, thalamus, or other memory retrieval areas
Agnosia
Inability to recognize objects, people, or sensory stimuli
Common Cause:
Brain damage from strokes, injuries, dementia, or neurol­ogical disorders
Subtype of Agnosia:
Prosop­agnosia ("Face Blindn­ess­")
Prosop­agnosia
Difficulty recogn­izing faces

Brain injuries

Traumatic Brain Injuries & Concus­sions

External Trauma:
Direct blow to the head, often blood vessels are torn so blood flow is blocked, tissue dies
Internal Trauma:
stroke (either clot or brain bleed) ,aneurysm, or brain tumor (internal trauma)
Aftere­ffects of Head Trauma:
Can cause memory impair­ments (post-­tra­umatic amnesia, persistent memory deficits), executive functi­oning distur­bances, and person­ality changes
Phineas Gage Case (1848):
The most well-known case of frontal lobe dysfun­ction. His injury led to drastic person­ality changes, later associated with "­fro­nto­tem­poral dement­ia."­
Aftere­ffects of Concus­sions:
May result in a short-term loss of consci­ous­ness, antero­grade amnesia (diffi­culty forming new memories), and retrograde amnesia (loss of past memories)
Common symptoms:
Dizziness, headache, fatigue; Difficulty concen­tra­ting, memory deficits; Irrita­bility, anxiety, insomnia; Heightened sensit­ivity to noise and light; Hypoch­ond­riacal concerns

Location of Brain Trauma & it's Impact

Aphasia:
Loss of Speech or Language Compre­hension
Receptive Aphasia (Werni­cke’s Aphasia):
Damage to the left temporal lobe (Werni­cke’s area) impairs language compre­hension. The person may speak in gibberish but remain unaware of their incohe­rence. Temporal lobe damage can also affect semantic and long-term memory.
Expressive Aphasia (Broca’s Aphasia):
Damage to the posterior frontal lobe (Broca’s area) affects speech produc­tion. The person unders­tands language and knows what they want to say but struggles to verbalize it, causing frustr­ation.
Conduction Aphasia:
Damage to the neural pathways connecting Wernicke’s & Broca’s areas disrupts commun­ication between compre­hension and speech production. The person cannot effect­ively repeat verbal phrases.
Global Aphasia:
Widespread damage affecting both compre­hension and speech production, severely impairing commun­ica­tion.

Current Neuro-­Imaging Options

PET Scan:
Quick, cost-e­ffe­ctive images of basic struct­ures, very useful as first-line assessment in emerge­ncies to identify brain issues that need emergent care (brain bleeds, etc). Uses radio
MRI:
More expensive, detailed images possible with enhanced soft-t­issue resolution to pick up more subtle structural issues. Uses magnetic resonance
CT Scan:
Detailed metabolic picture of brain function. Can give info about low (Alzhe­imer's, stroke­/blood vessel damaging affecting function) or high (brain tumor or other inflam­matory or cancer­-re­lated process). Uses radioa­ctive dye

Memory­/Types of Amnesia

Retrograde Amnesia:
Occurs after head trauma, such as a blow to the head. The person cannot recall events leading up to the injury, sometimes spanning weeks or months before the event. However, the ability to form new memories remains intact.
Antero­grade Amnesia
Seen in conditions like Alzhei­mer’s disease, where working memory fails, preventing the formation of new memories. The person struggles to learn new inform­ation, making daily functi­oning difficult. Remote (long-­term) memory, partic­ularly music memory, is often preserved. Linked to damage in memory­-re­lated brain struct­ures, such as the hippoc­ampus.
Psycho­genic Amnesia
Caused by psycho­logical factors rather than physical brain damage. Follows different patterns from neurol­ogical disorders. Short-term memory and the ability to form new memories remain intact. Long-term autobi­ogr­aphical memory is affected, leading to loss of personal details (e.g., name, birthd­ate). Unlike neurol­ogical amnesia, where long-term memory tends to be retained.
Psycho­genic Amnesia /(Psych) = Only one that long-term is affected

Differ­entiate Types of Seizures

Types of Seizures:
Genera­lized & Focal Seizures
Genera­lized Seizures (Gran & Petit Mal):
Affect both hemisp­heres of the brain from the start and often cause loss of consci­ous­ness. (grand mal & petit mal)
Gran Mal:
Sudden loss of consci­ousness and stiffening (tonic activity), followed by clonic activity (rhythmic jerking). Most well-known type.
Petit Mal:
Brief episodes of staring, often mistaken for daydre­aming. Occur most frequently in children. Last 0-30 sec
Focal Seizures (Partial Seizures):
Originate in a specific area of one hemisphere of the brain. They may or may not cause loss of awareness. (simple partial & complex partial)
Simple Partial:
Person remains conscious and aware. Charac­terized by abnormal movements that begin in one group of muscles and progress to adjacent groups of muscles in a slow wave of seizure activity per location in the back of the frontal lobe motor area.
Complex Partial:
Person has impaired consci­ousness or awareness. May involve staring, repetitive movements (lip-s­mac­king, hand rubbing), or confusion. The person may not remember the seizure after it ends. Often a manife­station of temporal lobe epilepsy
Next Two Are Focal Seizures
Jacksonian Seizure:
A type of focal seizure that originates in the primary motor cortex of the brain (part of the frontal lobe) and progresses in a charac­ter­istic pattern. Begins with localized muscle twitching (jerking movements) in a small part of the body, such as a finger, toe, or corner of the mouth. Spreads gradually to larger areas of the body (e.g., from hand → arm → face).
Temporal Lobe Epilepsy (TLE)
A type of focal seizure. Originate in the temporal lobes of the brain. Common Symptoms Before: Déjà vu. Can turn into tonic-­clonic (grand mal) seizure.

Neurot­ran­smitter Functions & Effects

Neurot­ran­smitter
Behaviors or Diseases Related
Acetyl­choline (ACh)
Learning and memory; Alzhei­mer's Disease's muscle movement in the peripheral nervous system. + ACh = spasms. - ACh = paralysis
Dopamine (DA)
Reward circuits; Motor circuits involved in Parkin­son's disease; Schizo­phrenia
Norepi­nep­hrine (NE)
Arousal; Depression
Serotonin (5HT)
Depres­sion, Aggres­sion; Schizo­phrenia behavior.
GABA
Anxiety disorders, Epilepsy; Major inhibitory neurot­ran­smitter in the brain
Glutamate
Learning; Major excitatory neurot­ran­smitter in the brain
Endogenous Opioids
Pain; Analgesia (inability to feel pain); Reward
KEY TERMS:
Mania: arousal, aggression
ADHD: learning, memory
Addiction: reward

Specific Disorders & Neurot­ran­smi­tters

Alzhei­mer's disease
Acetyl­cho­line, due to it's role in the develo­pment of memory of the hippoc­ampus
(Repet­itive) Movement disorders
dopamine, due to it's role in movement
Depression
Low serotonin and low norepi­nep­hrine
Mania
Low serotonin and high norepi­nep­hrine
Anxiety
Too little GABA.
Schizo­phrenia
Excess dopamine; GABA & Glutamate imbalance
Autism
Too much serotonin; GABA & Glutamate imbalance
Substance use disorder
(Repet­itive) Movement disorders: Parkin­sons, tics, OCD

Glutamate and GABA

Maintain a homeos­tatic balance
Glutamate & GABA have a seesaw relati­onship
When glutamate is high, GABA is low
Children with autism and related disorders tend to lean towards excess glutamate and low GABA
Balance must be maintained for their bodies and nervous system to function properly
Excessive Levels of Glutamate: Can lead to excito­tox­icity (overs­tim­ulation of neurons), contri­buting to neurod­ege­ner­ative diseases (e.g., Alzhei­mer’s, epilepsy, anxiety, stroke).
Deficiency in GABA: Can lead to excessive excita­bility, associated with anxiety, seizures, and insomnia.
Excessive Levels of GABA: Sedation, cognitive slowing, motor impair­ments.
Disorders Related to this Imbalance: Epilepsy (excess excita­tion, insuff­icient inhibi­tion). Schizo­phrenia (dysfu­nction in both systems). Anxiety disorders (GABA defici­ency).

Glutamate and GABA

Maintain a homeos­tatic balance
Glutamate & GABA have a seesaw relati­onship
When glutamate is high, GABA is low
Children with autism and related disorders tend to lean towards excess glutamate and low GABA
Balance must be maintained for their bodies and nervous system to function properly
Excessive Levels of Glutamate: Can lead to excito­tox­icity (overs­tim­ulation of neurons), contri­buting to neurod­ege­ner­ative diseases (e.g., Alzhei­mer’s, epilepsy, anxiety, stroke).
Deficiency in GABA: Can lead to excessive excita­bility, associated with anxiety, seizures, and insomnia.
Excessive Levels of GABA: Sedation, cognitive slowing, motor impair­ments.
Disorders Related to this Imbalance: Epilepsy (excess excita­tion, insuff­icient inhibi­tion). Schizo­phrenia (dysfu­nction in both systems). Anxiety disorders (GABA defici­ency).
 

Disorders

Depression

Impact on the Brain:
Can lead to brain shrinkage
Neurot­ran­smitter Imbala­nces:
Serotonin, dopamine, and norepi­nep­hrine. All of which are interc­onn­ected
Glutamate:
Profoundly out of balance
Treatment: Mild to Moderate Depression
Regular exercise can be as effective as antide­pre­ssants; Psycho­therapy (CBT) to help address negative thought patterns
Treatment: Moderate to Severe Depression
Antide­pre­ssant medica­tions may be necessary, though it can take time to find the right one. Side effects (e.g., sexual dysfun­ction, weight gain, emotional blunting) can be a challenge
Treatment: Electr­oco­nvu­lsive Therapy (ECT):
Used for severe or treatm­ent­-re­sistant depres­sion, partic­ularly when rapid symptom relief is needed (e.g., in cases of suicid­ality or catato­nia).
Emerging & Altern­ative Options
Ketamine therapy:
Research suggests it may rapidly reduce depressive symptoms, partic­ularly in treatm­ent­-re­sistant cases
Transc­ranial Magnetic Stimul­ation (TMS):
A non-in­vasive treatment using magnetic pulses, effective for depres­sion, OCD, and other condit­ions.

ADHD

 

Bipolar Disorder: Tx & Consid­era­tions

Mood Stabil­izers:
Used to manage mood swings in bipolar disorder, preventing both manic and depressive episodes
Common Meds:
Lithium; antico­nvu­lsants (e.g., valproate & lamotr­igine); atypical antips­ych­otics
Electr­oco­nvu­lsive Therapy (ECT)
Typically used for severe cases of bipolar disorder or treatm­ent­-re­sistant depres­sion; Involves brief electrical stimul­ation of the brain while the patient is under anesth­esia. Effective for acute mood episodes but usually considered after medication and therapy have failed.

Psychotic Disorders

Medica­tions that block dopamine can help reduce psychotic symptoms, partic­ularly halluc­ina­tions and disorg­anized thinking, known as "­pos­iti­ve" symptoms of psychotic disorders
However, "­neg­ati­ve" symptoms (e.g., apathy, low motiva­tion, and reduced activity) may be less responsive to treatment
Due to side effects, medication adherence is often a challenge for indivi­duals with psychotic disorders

Panic Disorder

 

ECT Treatment

ECT involves a brief electrical stimul­ation of the brain while the patient is under anesthesia
Used in patients with severe major depression or bipolar disorder that has not responded to other treatments
Side effects:
Memory loss (retro­grade amnesia) is a signif­icant concern; Patients may experience gaps in memory from weeks to months before treatment; If ECT is repeated over time, cumulative memory loss can become disruptive
retrograde amnesia - an individual is unable to recall events that occurred before the onset of brain injury/ trauma, but ability to form new memories is intact.

Psycho­pha­rma­cology

Antide­pre­ssants Classes

Drug Class
Function
SSRIs
Blocks reuptake of serotonin from space between neurons
SNRI
Block serotonin & norepi­nep­hrine reuptake
NDRI
Block reuptake of norepi­nep­hrine & dopamine
TCAs
Tricyclic antide­pre­ssants affects serotonin & norepi­nep­hrine
MAOIs
Block recycling of serotonin, norepi­nep­hrine, & dopamine
Others
Affect serotonin/ norepi­nep­hrine in other ways

SSRI Danger Warnings

Increased Youth Suicide Risk
Serotonin Syndrom
Neurol­eptic Malignant Syndrome

Risk with Antich­oli­nergic Agents

Seniors:
Antich­oli­nergic agents interact with many common medica­tions taken by older people
Risk of dementia:
Increased risk of dementia in people who used them for longer than a few months

Antips­ych­otics

 

Moveme­nt/­Memory Medica­tions

 

Sleep/Mood Medica­tions

 

Neurol­eptic Medica­tions Side Effects

 

Tardive Dyskinesia

 

Serotonin Syndrome

Mild
Moderate
Life Threat­ening
Mydriasis (dilated pupils)
Altered Mental Status (e.g., agitation, disori­ent­ation, excite­ment)
Delirium
Shiver­ing­/Sw­eating
Autonomic Hypera­ctivity (e.g., rigidity, tachyc­ardia, hypert­hermia)
Hypert­ension/ Hypert­hermia
Tachyc­ardia (mild)
Neurom­uscular Abnorm­alities (e.g., tremor, clonus, hyperr­efl­exia)
Muscle rigidity/ Tachyc­ardia
Management Stages:
Observe for at least 6 hrs
Admit to hospital; Cardiac monitoring
Intensive Care Unit; cooling meaures
Benzod­iaz­epines
Cyproh­ept­adine
Sedation; SkM paralysis; ventil­ation