Physiological/Psychopharmacology + Life span development Prpjet Flashcards
What are the Hindbrain Structures: The hindbrain is located just above the spinal cord and includes the medulla, pons, and cerebellum.
- Medulla: The medulla is also known as the medulla oblongata. It’s responsible for the involuntary mouth and throat movements involved in swallowing, coughing, and sneezing, and it regulates a number of functions that are essential for survival including respiration, heart rate, and blood pressure. Brain injury and certain diseases and drugs (especially opioids) can disrupt the functioning of the medulla and result in death.
- Pons: The pons connects the two halves of the cerebellum and helps coordinate movements on the two sides of the body, and it relays messages between the cerebellum and cerebral cortex. It also plays a role in respiration and the regulation of deep sleep and rapid eye movement (REM) sleep.
- Cerebellum: The cerebellum coordinates voluntary movements and is responsible for maintaining posture and balance. Damage can cause ataxia which is characterized by symptoms associated with alcohol intoxication and include a lack of muscle control, impaired balance and coordination, slurred speech, nystagmus (jerky eye movements), and blurred or double vision. The cerebellum is important for processing and storing procedural memories (e.g., running, playing a musical instrument, driving a car) and other implicit memories (memories that operate on an unconscious, automatic level). It’s also involved in some non-motor cognitive functions including attention, linguistic processing, and visuospatial abilities.
Midbrain Structures: The midbrain connects the hindbrain to the forebrain and includes the reticular formation and substantia nigra.
- Reticular Formation: The reticular formation consists of a network of neurons that extend from the medulla into the midbrain. It’s involved in a variety of functions including regulation of muscle tone, coordination of eye movements, and control of pain. It contains the reticular activating system (RAS) which is also known as the ascending reticular activating system (ARAS). The RAS mediates consciousness and arousal, controls the sleep/wake cycle, and alerts the cerebral cortex to incoming sensory signals. Lesions in the RAS can cause a comatose state, while direct electrical stimulation or stimulation by sensory input can awaken a sleeping person and cause an awake person to become more alert.
- Substantia Nigra: The substantia nigra plays a role in reward-seeking, drug addiction, and, through its connection to the basal ganglia, motor control. Degeneration of dopamine-producing cells in the substantia nigra is a cause of the slowed movement, tremors, rigidity, and other motor symptoms associated with Parkinson’s disease.
Subcortical Forebrain Structures: These structures include the hypothalamus, thalamus, basal ganglia, amygdala, and hippocampus.
- Hypothalamus: Through its effects on the autonomic nervous system, somatic nervous system, and endocrine system, the hypothalamus helps maintain many aspects of the body’s homeostasis including body temperature, blood pressure, hunger, thirst, and sleep. In addition, it influences the development of secondary sex characteristics and sexual and reproductive behaviors by stimulating the pituitary gland to release sex hormones. The hypothalamus is also involved in aggression and emotional reactions, and electrical stimulation or damage to different areas can elicit aggressive behavior or produce crying or laughter. The hypothalamus contains the mammillary bodies, which play a role in memory, and the suprachiasmatic nucleus (SCN), which serves as the body’s biological clock and regulates the sleep-wake cycle and other circadian rhythms (physiological changes that occur during each 24-hour period).
- Thalamus: The thalamus is described as a “relay station” because it receives and then transmits sensory information to the cortex for all of the senses except smell. It also plays an important role in the coordination of sensory and motor functioning, language and speech, and declarative memory. With regard to memory, Korsakoff syndrome is caused by a thiamine deficiency that’s often the result of chronic alcoholism and that damages neurons in the thalamus and mammillary bodies. Its primary symptoms are anterograde amnesia, retrograde amnesia, and confabulation, which involves filling memory gaps (especially gaps in episodic memory) with false information that the person seems to believe is true.
- Basal Ganglia: The basal ganglia consist of the caudate nucleus, putamen, nucleus accumbens, and globus pallidus. The caudate nucleus, putamen, and nucleus accumbens are collectively referred to as the striatum and receive input from the cerebral cortex, while the globus pallidus transmits information to the thalamus. These structures are involved in the initiation and control of voluntary movements, procedural and habit learning, cognitive functioning (e.g., attention and decision-making), and emotions. Basal ganglia damage has been linked to a number of conditions including mood disorders, schizophrenia, ADHD, OCD, Tourette’s disorder, Huntington’s disease, and Parkinson’s disease.
- Limbic System: The limbic system consists of several structures that are involved in emotion. It includes the amygdala, cingulate cortex, and hippocampus.
What is in the Limbic System?
(a) Amygdala: The amygdala plays an important role in the experience of emotions, recognition of fear and other emotions in facial expressions, acquisition of conditioned fear responses, evaluation of the emotional significance of events, and attachment of emotions to memories. With regard to memory, the amygdala is involved in the formation of flashbulb memories, which are vivid and enduring memories for surprising and shocking events. The research has also found that PTSD is associated with abnormal functioning of the amygdala and ventromedial prefrontal cortex (VPC): Hyperactivity in the amygdala plays a key role in producing the distressing memories and other symptoms of PTSD, and hypoactivity of the VPC reduces its normal regulation of activity in the amygdala (Koenigs & Grafman, 2009; Koenigs et al., 2008). Finally, bilateral damage to the amygdala and temporal lobes in monkeys causes Kluver-Bucy syndrome, which is characterized by hyperphagia, hyperorality, reduced fear, hypersexuality, and visual agnosia (which is also known as psychic blindness).
(b) Cingulate Cortex: The cingulate cortex contains the cingulate gyrus and cingulate sulcus and plays a role in motivation, memory, and emotions, including emotional reactions to pain. People with damage to the cingulate cortex experience pain but are not emotionally distressed by it. Abnormalities in the cingulate cortex (and several other areas of the brain including the prefrontal cortex, orbitofrontal cortex, hippocampus, amygdala, and thalamus) have also been linked to major depressive disorder and bipolar disorder (Rajkowska, 2006).
(c) Hippocampus: The hippocampus is involved more in memory and less in emotions than the other limbic system structures are. It’s responsible for transferring declarative memories from short-term to long-term memory and plays an important role in spatial memory (memory for the spatial characteristics of the environment). The impact of damage to the hippocampus on memory is demonstrated by research linking the degeneration of cells in the hippocampus and entorhinal cortex (an area adjacent to the hippocampus) to the impairments in episodic memory and spatial navigation associated with Alzheimer’s disease. In addition, research has found that acute or chronic increases in cortisol levels in the hippocampus as the result of stress or other condition (e.g., Cushing’s syndrome, administration of cortisone) impairs the retrieval of declarative memories (Wolf, 2010). There’s also evidence that hippocampal abnormalities contribute to major depressive disorder, bipolar disorder, schizophrenia, and PTSD (Zorumski & Rubin, 2011). For example, for people with PTSD, the studies have found that the more extreme the traumatic stress and the more severe the person’s symptoms, the more likely the person would have a smaller-than-normal hippocampus. However, some studies suggest that exposure to traumatic stress causes a reduction in hippocampal volume, while others suggest that reduced hippocampal volume is a risk factor for developing PTSD after exposure to traumatic stress (e.g., Lindgren, Bergdahl, & Nyberg, 2016).
Talk about the FRONTAL LOBE BRO
- Frontal Lobe: The frontal lobe contains Broca’s area, the prefrontal cortex, supplementary motor cortex, premotor cortex, and primary motor cortex.
(a) Broca’s area is a major language area and is located in the dominant (usually left) frontal lobe. Damage to Broca’s area produces Broca’s aphasia, which is also known as expressive aphasia and nonfluent aphasia. People with this disorder have slow, labored speech that consists primarily of nouns and verbs. They also exhibit impaired repetition and anomia (an inability to recall the names of familiar objects), but their comprehension of written and spoken language is relatively intact.
(b) The prefrontal cortex (PFC) plays an important role in executive functions, which are also known as higher-order cognitive functions and include planning, decision-making, social judgment, and self-monitoring. It also contributes to working memory, prospective memory (memory for future events), attention, and emotion regulation. The effects of damage to the PFC depend on its location (Jones, Srinivasan, Allam, & Baker, 2012; Rosenzweig, Breedlove, & Watson, 2005): Damage to the dorsolateral PFC produces dysexecutive syndrome, which involves deficits in working memory, impaired judgment and insight, lack of planning ability, perseverative responses, and disinterest and apathy. Damage to the orbitofrontal PFC results in disinhibited syndrome, which is characterized by behavioral disinhibition, distractibility, emotional lability and inappropriate euphoria, and “acquired sociopathy.” And damage to the mediofrontal PFC produces an apathetic-akinetic syndrome, which involves decreased motor behavior and verbal output, a lack of initiative and motivation (abulia), and flat or diminished affect.
(c) The supplementary motor cortex is involved in planning and coordinating self-initiated complex movements and is active not only when people actually perform movements but also when they imagine performing them and when watching another person perform them. The supplementary motor cortex, like the premotor cortex and primary motor cortex, is somatotopically organized, which means that each part of the body is controlled by a specific cortical area.
(d) The premotor cortex is involved in planning and coordinating complex movements that are triggered by external (sensory) stimuli. Like the supplementary motor cortex, the premotor cortex is active not only when people perform movements but also when they imagine performing them or watch others perform them.
(e) In response to signals from the supplementary motor cortex and premotor cortex, the primary motor cortex executes movements by sending signals to the muscles. The effects of damage to the primary motor cortex depend on its extent and location and range from weakness to paralysis in one or more muscles in the opposite (contralateral) side of the body.
Talk about the TEMPORAL LOBE
The temporal lobe contains the auditory cortex and Wernicke’s area. The auditory cortex is involved in processing sound, and damage to this area can produce auditory agnosia, auditory hallucinations, or cortical deafness. Wernicke’s area is a major language area and is located in the dominant (usually left) hemisphere. Damage produces Wernicke’s aphasia, which is also known as receptive aphasia and fluent aphasia. People with this disorder have impaired comprehension of written and spoken language, impaired repetition, and anomia. Although their speech is fluent, it contains many word substitutions and other errors and is devoid of meaning. (Note that the arcuate fasciculus connects Wernicke’s area to Broca’s area, and damage to this structure produces conduction aphasia, which is characterized by relatively intact comprehension with fluent speech that contains many errors, impaired repetition, and anomia.)
Talk about the PARIETAL LOBE
The parietal lobe contains the somatosensory cortex, which processes sensory information related to touch, pressure, temperature, pain, and body position. Damage can cause one or more somatosensory agnosias, which include tactile agnosia (an inability to recognize objects by touch), asomatognosia (a lack of interest in or recognition of one or more parts of one’s own body), and anosognosia (denial of one’s illness). Damage to the parietal lobe can also produce hemispatial neglect, ideomotor apraxia, ideational apraxia, or Gerstmann’s syndrome: Hemispatial neglect is also known as unilateral neglect and contralateral neglect and is usually caused by damage to the right (nondominant) parietal lobe and involves neglect of the left side of the body and stimuli on the left side of the body. Ideomotor apraxia, ideational apraxia, and Gerstmann’s syndrome are usually caused by damage to the left (dominant) parietal lobe: Ideomotor apraxia involves an inability to perform a motor activity in response to a verbal command (e.g., “pretend to comb your hair”); ideational apraxia involves an inability to plan and execute a task that requires a sequence of actions (e.g., an inability to complete the steps needed to make a sandwich); and Gerstmann’s syndrome involves finger agnosia, right-left disorientation, agraphia (a loss of writing skills), and acalculia (a loss of arithmetic skills).
Talk about the Occipital lobe
The occipital lobe contains the visual cortex, which processes visual information. Damage to this area can cause visual agnosia, visual hallucinations, achromatopsia (loss of color vision), or cortical blindness. Prosopagnosia is usually caused by bilateral lesions in the occipitotemporal junction and involves an inability to recognize the faces of familiar people and, in some cases, the faces of pets and other familiar animals.
What happens with Brain Laterization?
While the right and left hemispheres participate to some degree in many functions, each hemisphere is dominant for some functions. For example, for about 95% of right-handed people and 50 to 70% of left-handed people, written and spoken language, logical and analytical thinking, and positive emotions are left hemisphere functions, while holistic thinking, intuition, understanding spatial relationships, creativity, and negative emotions are right hemisphere functions. Note that the hemisphere that’s dominant for language (the left hemisphere for the majority of people) is referred to as the dominant hemisphere, while the other hemisphere is referred to as the nondominant hemisphere.
In addition to differences in dominance, the left and right hemispheres differ with regard to their control of sensory and motor functions – i.e., for most functions, the right hemisphere controls the left side of the body and the left hemisphere controls the right side of the body. (An exception is smell: Odors that enter the left nostril are transmitted directly to the left hemisphere, and vice versa.)
Most of the initial understanding of brain lateralization was derived from research conducted by Sperry and his colleagues (e.g., Sperry, 1968) with split-brain patients whose severe epilepsy was treated by surgically severing their corpus callosums. (The corpus callosum is the main bundle of nerve fibers that allows the two hemispheres to share information with each other.) In one study, these researchers presented a picture of a spoon to the right visual fields of split-brain patients so that visual information about the spoon was transmitted only to their left (dominant) hemispheres. As a result, the patients could say that they saw a spoon and could pick out a spoon by touch with their right hands from a collection of objects that were hidden from sight, but they could not do so with their left hands. Conversely, when the researchers presented a picture of a spoon to the left visual fields of these patients so that visual information about the spoon was transmitted only to their right (nondominant) hemispheres, the patients could not say that they saw a spoon. However, they could pick out a spoon by touch with their left hands but not with their right hands.
Subsequent research using the dichotic listening task, neuroimaging, and other techniques have provided additional information on brain lateralization. For example, the dichotic listening task is used to study speech lateralization and involves presenting two different words simultaneously, with one being presented to the right ear and the other to the left ear. Results of this research has confirmed that language is lateralized to the left hemisphere for most right-handed people: When asked to repeat what they’ve just heard, the majority of right-handed people repeat the word presented to their right ear which sends signals directly to the left auditory cortex.
EXPLAIN the Nervous system dude:
Nervous System: The nervous system is divided into the central and peripheral nervous systems. The central nervous system (CNS) includes the brain and spinal cord. The peripheral nervous system (PNS) transmits signals between the CNS and the rest of the body and includes the somatic and autonomic nervous systems: The somatic nervous system (SNS) transmits information from the body’s sensory receptors to the CNS and from the CNS to the skeletal muscles. It’s responsible for actions that are usually considered voluntary. The autonomic nervous system (ANS) transmits information from the body’s smooth muscles and organs to the CNS, and vice versa. It’s responsible for activities that are usually considered involuntary, although some of these activities can be brought under voluntary control using biofeedback and other techniques.
The ANS is further divided into the sympathetic and parasympathetic nervous systems. The sympathetic nervous system is responsible for preparing the body for action. For instance, during the body’s fight-or-flight response to an emergency, the sympathetic nervous system causes pupil dilation, sweating, and increased heart and respiration rates and inhibits digestion and sexual activity. In contrast, the parasympathetic nervous system is responsible for activities that govern rest and relaxation, and it causes the body to return to its pre-emergency state after a fight-or-flight response. Although the sympathetic and parasympathetic nervous systems exert opposite effects on the body, they’re both active to some degree most of the time and work together cooperatively for some functions. For example, both play a role in the male sexual response: The parasympathetic nervous system is necessary for erection, while the sympathetic nervous system is responsible for ejaculation.
Talk about Neurons for me.
- Structure of the Neuron: Neurons vary in size and shape, but all have one or more dendrites, a soma (cell body), and an axon. The dendrites receive information from other cells; the soma contains the nucleus, mitochondria, ribosomes, and other elements essential for the survival of the cell; and the axon transmits information to other cells. Some axons are insulated with myelin, which is produced by glia and speeds up the conduction of information through the axon.
- Conduction Within Neurons: The communication of information in the nervous system involves two processes – conduction within neurons and transmission between neurons. Conduction of information within neurons is an electrochemical process that begins when a neuron’s dendrites receive sufficient stimulation from other neurons. Prior to stimulation, a neuron is in a resting state, which means the fluid inside the cell is negatively charged relative to fluid outside the cell. However, when a neuron is sufficiently stimulated, channels in the cell membrane open, allowing positively charged sodium ions to enter the cell, which causes it to become depolarized (less negative). When stimulation reaches a minimum threshold, complete depolarization occurs and this triggers an electrical impulse known as an action potential. After an action potential occurs, the neuron returns to its resting state.
Note that action potentials are all-or-none responses, which means they either occur or don’t occur and, when they occur, they have the same intensity. Consequently, stimulus intensity is not encoded by the intensity of an action potential but, instead, by the frequency of the action potentials generated by a neuron and/or by the number of neurons that generate action potentials.
What happens in the transmissions of neurons?
Transmission Between Neurons: The transmission of information between neurons is referred to as synaptic transmission and is usually chemical. It begins when an action potential reaches the axon terminal (the end of the axon). This causes the release of a neurotransmitter into the synaptic cleft, which is the space between the axon terminal of the presynaptic neuron and the dendrite of an adjacent postsynaptic neuron. Neurotransmitters can have either an excitatory or inhibitory effect, which means they can either increase or decrease the likelihood that an action potential will occur in a postsynaptic neuron. Once a neurotransmitter has had its effect on a postsynaptic neuron, it’s inactivated by, for example, being absorbed by the presynaptic neuron or being broken down by an enzyme.
What is DOPAMINE?
Dopamine serves both excitatory and inhibitory functions. It contributes to movement, personality, mood, and sleep and has been identified as a contributor to several disorders. For example, a low level of dopamine in the substantia nigra has been linked to Parkinson’s disease, while an excessive level in the caudate nucleus has been linked to Tourette’s disorder. And, according to the dopamine hypothesis, schizophrenia is due to high levels of dopamine or hyperactivity of dopamine receptors.
There are several dopaminergic pathways that transmit dopamine from one area of the brain to another: The mesolimbic dopaminergic pathway begins in the ventral tegmental area and ends in the ventral striatum (nucleus accumbens). It’s an essential part of the brain’s “reward circuit” and plays a role in the reinforcing effects of cocaine, amphetamines, nicotine, alcohol, opiates, and other substances of abuse (Adinoff, 2004). There’s evidence that the dorsolateral prefrontal cortex initiates the motivation to obtain a reward by sending signals to the ventral tegmental area and the nucleus accumbens (Ballard et al., 2011). The mesocortical dopaminergic pathway begins in the ventral tegmental area and ends in the prefrontal cortex. It’s involved in emotion, motivation, and executive cognitive functions. The tuberoinfundibular dopaminergic pathway begins in hypothalamus and ends in the pituitary gland and plays a role in hormone regulation, especially the inhibition of prolactin release. Finally, the nigrostriatal dopaminergic pathway begins in the substantia nigra and ends in the dorsal striatum (caudate nucleus and putamen). It plays a key role in the production of purposeful movement.
What is Acetocholyine (ACH) ?
Acetylcholine (ACh): ACh is both excitatory and inhibitory and is involved in movement, arousal, attention, and memory. With regard to movement, ACh causes muscles to contract, and myasthenia gravis is an autoimmune disorder that causes muscle weakness by destroying ACh receptors at neuromuscular junctions. With regard to memory, low levels of ACh in the entorhinal cortex and hippocampus have been linked to the early memory loss associated with Alzheimer’s disease.
What is Glutamate?
Glutamate: Glutamate is an excitatory neurotransmitter and contributes to movement, emotions, learning, and memory. Excessive glutamate can cause cell damage and death, which is referred to as “glutamate-induced excitotoxicity” and is believed to contribute to a number of conditions including stroke, seizure disorders, and several neurodegenerative diseases including Huntington’s disease and Alzheimer’s disease.
What is Norepinephrine?
Norepinephrine: Norepinephrine is an excitatory neurotransmitter and is involved in arousal, attention, learning, memory, stress, and mood. According to the catecholamine hypothesis, some forms of depression are caused by a deficiency of norepinephrine while mania is due to excessive norepinephrine.
What is Serotonin?
Serotonin: Serotonin is also known by its chemical name, 5-hydroxytryptamine (or 5-HT). It has an inhibitory effect and plays a role in many functions including arousal, sleep, sexual activity, mood, appetite, and pain. Low levels of serotonin in certain areas of the brain have been linked to depression, increased risk for suicide, bulimia nervosa, obsessive-compulsive disorder, and migraine headaches. There’s also evidence that people with anorexia nervosa have higher-than-normal brain levels of serotonin that cause anxiety and obsessive thinking and that food restriction lowers serotonin levels which alleviates these symptoms (e.g., Kaye, Fudge, & Paulus, 2009). Finally, higher-than-normal blood levels of serotonin have been found in individuals with autism spectrum disorder and individuals with chronic schizophrenia who also have enlarged cerebral ventricles and/or cerebral atrophy.
What is GABA?
Gamma-Aminobutyric Acid (GABA): GABA is a primary inhibitory neurotransmitter and is involved in memory, mood, arousal, sleep, and motor control. Low levels of GABA have been linked to insomnia, seizures, and anxiety, and benzodiazepines reduce anxiety and induce sleep by amplifying the effects of GABA. Degeneration of GABA and ACh cells in the basal ganglia contributes to the motor symptoms of Huntington’s disease.
What are ENDORPHINS?
Endorphins: The endorphins are inhibitory, and their effects are similar to those of opioid drugs – e.g., they contribute to feelings of pleasure and well-being and have analgesic effects. It’s believed that acupuncture may relieve pain by stimulating the release of endorphins.
What are the basic effects of drugs on neurotransmitters?
Neurotransmitters and Drug Effects: Psychoactive drugs vary from weak to strong in terms of their binding affinity (tendency to bind to receptor sites on postsynaptic cells) and receptor efficacy (tendency to activate receptors). They can also be classified on the basis of their effects on neurotransmitters. (a) Agonists mimic or increase the effects of a neurotransmitter. (b) Partial agonists produce effects that are similar to (but weaker than) the effects of a neurotransmitter. (c) Inverse agonists produce effects that are the opposite of the effects of a neurotransmitter or agonist. (d) Antagonists do not produce any effects on their own but block or reduce the effects of a neurotransmitter or agonist.
What does the HIPPOCAMPUS do?
Hippocampus: The importance of the hippocampus for memory was demonstrated by the consequences of surgery performed on a patient known as H.M. as treatment for his severe seizures. The surgery involved bilateral removal of his hippocampus, amygdala, and medial temporal lobe. Following surgery, H.M.’s short-term memory and procedural memory were intact; however, he exhibited some deficits in remote long-term episodic memory and was unable to transfer any new declarative information from short-term to long-term memory. Subsequent studies using brain imaging techniques confirmed that the hippocampus plays an important role in the consolidation of long-term declarative memories – i.e., the transfer of declarative memories from short-term (working) memory to long-term memory. The studies have also found that the hippocampus is involved in spatial working memory.
What areas of the brain are for movements?
Basal Ganglia, Cerebellum, and Supplementary Motor Area: These areas are essential for procedural memories and other implicit memories (memories that operate on an unconscious, automatic level). Patients with damage to these areas have trouble learning new skills and performing previously learned skills.
What does the prefrontal cortex do?
Prefrontal Cortex: The prefrontal cortex is essential for the working memory aspect of short-term memory. It’s also important for prospective memory, with lesions adversely affecting event-based prospective memory more than time-based prospective memory. (Event-based prospective memory involves remembering to perform an intended action when the memory is triggered by an external cue – e.g., remembering to give your co-worker a message when you see her. Time-based prospective memory involves remembering to perform an intended action at a certain time without an external cue – e.g., remembering to take a cake out of the oven in 30 minutes.)
What happens when damage to Thalamus and Mammilary bodies?
Thalamus and Mammillary Bodies: Damage to these areas can cause anterograde and retrograde amnesia.
Talk about Long term potentiation and which part of the brain it is responsible in
Neural Mechanisms: Initial information on the neural mechanisms responsible for learning and memory was provided by research conducted by Kandel and his colleagues (e.g., Kandel, 1976). Their subjects were sea slugs (Aplysia), which were ideal subjects because of the small number and large size of their neurons. The results of their studies indicated that classical conditioning of reflexes had two effects: The short-term storage of information involved an increase in the release of the neurotransmitter serotonin, while long-term storage involved the development of new synapses and changes in the structure of existing neurons.
Researchers subsequently identified a similar phenomenon in other animals and humans and referred to it as long-term potentiation (LTP). LTP was first observed in glutamate receptors in the hippocampus but was subsequently observed in other areas of the brain including the amygdala and entorhinal cortex. It occurs in a neuron as the result of rapid and/or high-frequency stimulation and is believed to play an essential role in learning and memory formation. Researchers also found that changes in synapses associated with the formation of long-term memories depends on the synthesis of RNA, which is necessary for protein synthesis. For example, studies have found that administering a drug that inhibits RNA synthesis around the time of training prevents the formation of long-term (but not short-term) memories.
Talk about different stages of sleep
Stages of Sleep: Sleep is divided into five stages, with each stage having a different electroencephalogram (EEG) pattern:
(a) Stage 1 is a transitional stage between wakefulness and sleep. During this stage, low frequency, high amplitude alpha waves (which are characteristic of a drowsy state) are replaced by low frequency, low amplitude theta waves.
(b) Theta waves continue during Stage 2 but are interrupted by sleep spindles (sudden bursts of moderately fast waves) and K-complexes (large slow waves).
(c) Stage 3 begins after a person has been asleep for about 20 minutes and is characterized by low frequency, high amplitude delta waves.
(d) Delta waves continue during Stage 4 but are of higher amplitude. Stages 3 and 4 are also referred to as slow-wave sleep and deep sleep.
(e) Rapid eye movement (REM) sleep begins after a person has been asleep for 80 to 90 minutes, and its EEG pattern is similar to the Stage 1 pattern. REM sleep is also referred to as paradoxical sleep because it’s characterized by an active brain and physiological arousal while the body’s major muscle groups are nearly paralyzed and the person is very difficult to arouse. Most dreams occur during REM sleep and are more vivid, bizarre, and detailed than those that occur during non-REM sleep.
Following about 10 minutes of REM sleep, a person cycles through the non-REM and REM sleep stages again and this continues throughout the sleep period. However, as the night progresses, the duration of REM sleep increases and the duration of Stage 3 and Stage 4 sleep decreases.
Lifespan change in sleep
Lifespan Changes in Sleep: Sleep patterns change in a predictable way with increasing age. Newborn infants sleep longer than older children and adults do, spend more time in active (REM) sleep, and begin the sleep period with active sleep that is followed by quiet (non-REM) sleep. This sequence reverses at about three months of age, and the four stages of non-REM sleep are evident by about six months. In addition, total sleep time decreases from 14 to 16 hours a day in infancy to about eight hours in adulthood. Although older adults do not require less sleep than younger adults, they have more trouble falling asleep, spend less time in deep sleep (especially Stage 4 sleep), experience more evenly distributed REM sleep throughout the night, wake up more often during the night, and experience an advanced sleep phase, which is also known as circadian phase advance and involves going to sleep earlier in the evening and waking up earlier.
What is the James Lange Theory?
James-Lange Theory: This theory proposes that exposure to an emotionally salient stimulus causes a physiological reaction which, in turn, is perceived as an emotion – e.g., when a person is faced with a growling bear while hiking in the woods, her heart begins to beat faster and she starts breathing more deeply, and she then feels afraid. In other words, the experience of an emotion follows (rather than precedes) physiological arousal. A related and more recent explanation for emotion is provided by the facial feedback hypothesis, which predicts that facial expressions associated with specific emotions initiate physiological changes that are consistent with those emotions. Research supporting the facial feedback hypothesis has found that mimicking a facial expression that’s associated with a specific emotion causes us to experience that emotion – e.g., smiling makes us feel happy.
What is the Cannon-Bard Theory
(Think Bird and a Cannon flying together) and then informing the ThaLAMUS that both is happening (prefrontal cortex and sympathetic nervous system)
Cannon-Bard Theory: Cannon-Bard theory proposes that the experience of an emotion and physiological arousal occur together when an environmental stimulus causes the thalamus (which receives input from the senses) to simultaneously send signals to the cerebral cortex and the sympathetic nervous system. Unlike James-Lange theory, this theory views all emotions as involving similar physiological arousal and contends that, for this reason, differences in emotional reactions cannot be attributed to differences in the nature of physiological arousal.
Talk about Schacters two factor theory!
Schachter and Singer’s Two-Factor Theory: This theory is also known as cognitive arousal theory and describes the experience of emotion as the result of physiological arousal followed by an attribution (“cognitive label”) for that arousal. Like Cannon-Bard theory, it assumes that physiological arousal is similar for all emotions but also proposes that differences in the experience of emotion are due to differences in the attributions for the arousal, which depend on external cues. Evidence for this theory was provided by Schachter and Singer’s (1962) “epinephrine studies” in which subjects experiencing unexplained arousal looked to the environment (the behavior of a confederate) to determine what emotions they were experiencing. Schachter and Singer’s studies generated a great deal of research on the misattribution of arousal, which is the tendency to mislabel arousal when its cause is unknown or ambiguous.
Studies on two-factor theory also led to Zillman’s (1971) excitation transfer theory, which is often erroneously described as being synonymous with misattribution of arousal. Although excitation transfer theory incorporates the concept of misattribution of arousal, Zillman described it as an explanation of how physical arousal elicited by one event can be transferred to and intensify arousal elicited by a later unrelated event. It’s based on three assumptions: (a) Physical arousal associated with emotions (e.g., elevated heart rate and blood pressure) decays slowly and can continue for some time following the event that elicited the arousal. (b) Residual arousal caused by one event can intensify arousal caused by a subsequent unrelated event. (c) People often have limited insight into the causes of their physical arousal and, consequently, can misattribute their intense arousal solely to the subsequent unrelated event. For example, the arousal induced by watching a violent film can linger and make people who are subsequently provoked by a confederate respond with greater anger toward the confederate than do people who watched a nonviolent film (Cantor, 2003). The research has found that excitation transfer applies to a variety of emotional reactions. For instance, residual arousal from sexual excitation has been found to intensify subsequent anger, sadness, and altruism, and residual excitation from fear has been found to intensify subsequent sexual attraction and joy.
What is Lazarus’ Cognitive Appraisal Theory?
Lazarus’s Cognitive Appraisal Theory: Lazarus’s (1991) cognitive appraisal theory proposes that differences in emotional reactions to events are due to different appraisals of those events. In other words, two people can experience the same event but respond with different emotions because they appraise the situation differently. It also assumes, in contrast to other theories, that physiological arousal follows cognitive appraisal.
Cognitive appraisal theory distinguishes between three types of appraisal: (a) Primary appraisal involves evaluating the event to determine if it’s irrelevant, benign-positive, or stressful. When the person decides the event is stressful, he/she then determines if it involves a threat, a challenge, or harm/loss. According to Lazarus, primary appraisal is affected by several factors including the person’s beliefs, values, motivation, and expectations. (b) Secondary appraisal occurs when the person determines that the event is stressful and involves identifying his/her coping options and the likelihood that the options will adequately deal with the event. (c) Reappraisal occurs when the person monitors the situation and, as appropriate, changes his/her primary and/or secondary appraisal.
Cerebral Cortex and Emotion
Cerebral Cortex: The two hemispheres of the cerebral cortex play different roles in the mediation of emotion. Areas in the left (dominant) hemisphere mediate happiness and other positive emotions, and damage to these areas produces a “catastrophic reaction” that involves depression, anxiety, fear, and paranoia. In contrast, areas in the right (nondominant) hemisphere mediate sadness and other negative emotions, and damage to these areas produces an “indifference reaction” that involves inappropriate indifference and/or euphoria.
Amygdala and emotions/memories
Amygdala: The amygdala is part of the limbic system and is involved in several aspects of emotion: It’s responsible for recognizing fear in facial expressions, attaching emotions to memories, and evaluating incoming information to determine its emotional significance and then mediating the emotional reaction to it. Electrical stimulation of the amygdala can produce a fear or rage response, and bilateral lesions can cause a loss of the fear response without a loss of other emotional responses.
Hypothalamus and emotion
Hypothalamus: The hypothalamus regulates the physical signs of emotion through its communication with the autonomic nervous system and pituitary gland. The role of the hypothalamus in emotion has been confirmed by studies finding that bilateral lesions in certain areas can produce rage and that electrical stimulation of certain areas can cause other emotions such as pleasure or fear.
Stress and EMotion?
Stress: An influential model of the body’s reaction to stress is provided by Selye’s (1976) general adaptation syndrome, which proposes that the body’s response to all types of stress is the same and involves three stages: During the initial alarm reaction stage, increased activity of the sympathetic nervous system provides the body with the energy it needs to respond to the stressor with a fight-or-flight reaction. If the stressor persists, the resistance stage begins. During this stage, some physiological functions return to normal while cortisol (a stress hormone) continues to circulate at an elevated level to help the body maintain a high energy level and cope with the stressor. Then, if the stress or its effects are not resolved, the exhaustion stage begins. In this stage, physiological processes begin to break down. (Additional information on Selye’s general adaptation syndrome is provided in the organizational psychology content summary covering satisfaction, commitment, and stress.)
Selye’s model has been challenged by research finding that physiological, psychological, and behavioral responses to stress are not always the same but, instead, are affected by the type of stress and a person’s genetic make-up and previous experiences. One reconceptualization of the stress response is provided by McEwen’s allostatic load model, which is based on the assumption that “the brain is the key organ of stress … because it determines what is threatening and therefore stressful, and also determines the physiological and behavioral responses [to stress]” (2006, p. 367). McEwen identifies the amygdala, hippocampus, and prefrontal cortex as the primary mediators of these functions. He also uses the following terms to describe the body’s response to stress: Allostasis refers to processes that allow the body to achieve stability by adapting to change. For example, elevated blood pressure and cortisol level may be necessary to adapt to a stressful event. These processes result in an allostatic state that can be maintained for a limited period of time without having adverse consequences. However, an extended allostatic state due to chronic stress or repeated episodes of acute stress can produce wear-and-tear on the body and brain, which is referred to as an allostatic load. Then, if the allostatic load continues for days, weeks, or longer, it can become an allostatic overload, which has adverse effects on the person’s physical and psychological health. For example, it can cause dysregulation of the immune system, which increases a person’s vulnerability to disease, and/or can result in PTSD, major depressive disorder, a substance use disorder, or other stress-related psychiatric disorder. According to McEwen, the nature of allostasis and consequences of allostatic load vary from person to person due to several factors, including differences in genetic makeup, resilience, and perceptions about the controllability of the stressor.
Cerebrovascular Accident
Cerebrovascular Accident: A cerebrovascular accident (CVA) is also known as a stroke and is caused by a sudden interruption of blood flow to the brain. The leading risk factor is hypertension; others include heart disease, diabetes, cigarette smoking, alcoholism, older age, male gender, African American race, and family history of stroke. Symptoms depend on which artery is involved: (a) The middle cerebral artery is the artery that’s most often involved in a stroke. Symptoms of a stroke involving this artery include contralateral sensory loss and weakness (especially in the arm and face), contralateral visual field loss, and aphasia when the dominant hemisphere is affected or apraxia and contralateral neglect when the nondominant hemisphere is affected. (b) Symptoms of a stroke involving the posterior cerebral artery include unilateral cortical blindness and other visual impairments, impaired language, and memory loss. (c) Symptoms of a stroke involving the anterior cerebral artery include contralateral weakness (especially in the leg), impaired insight and judgment, mutism, apathy, and confusion.
TBI
Traumatic Brain Injury: A traumatic brain injury (TBI) can be open or closed: The consequences of open head injuries depend on the injury’s location and severity, but closed head injuries share several characteristics: They cause more widespread damage than an open head injury and may produce a loss of consciousness. Also, when the person regains consciousness, he/she is likely to experience a combination of emotional, cognitive, behavioral, and physical symptoms. Cognitive symptoms often include some degree of anterograde and retrograde amnesia. Anterograde amnesia is also known as post-traumatic amnesia when it’s due to TBI, and its duration is a good predictor of recovery from other symptoms. When retrograde amnesia occurs, recent long-term memories are affected more than remote memories; and, when lost memories begin to return, those from the most distant past are recovered first. With regard to prognosis, most people experience the most recovery during the first three months with substantial additional improvement during the first year (e.g., Carroll et al., 2004; Lawhorne & Philpott, 2010). Many people continue to have some symptoms indefinitely, however, especially those with a moderate to severe injury.
DISCUSS HUNTINGTON’S DIESEASE (MOTOR disorder)
Huntington’s Disease: Huntington’s disease is a neurodegenerative disorder that involves affective, cognitive, and motor symptoms. It’s caused by an autosomal dominant gene, and offspring of a person with this gene have a 50% chance of inheriting the disorder. Huntington’s disease has been linked to abnormalities in the basal ganglia and abnormal levels of several neurotransmitters including GABA and glutamate. The onset of symptoms is typically when the person is between 30 and 50 years old. The progression of the disorder varies but affective symptoms (e.g., depression and mood swings) often precede cognitive and motor symptoms, which suggests these symptoms are not just a reaction to the disease but, instead, a manifestation of underlying pathological changes. Cognitive symptoms include short-term memory loss and impaired concentration and judgment, and motor symptoms include clumsiness, fidgeting, involuntary movements, and facial grimacing. As the disease progresses, affective, cognitive, and motor symptoms worsen, with athetosis and chorea beginning several years after the disorder’s onset: Athetosis involves nonrhythmic, slow, writhing movements, while chorea is characterized by involuntary rapid, jerky movements in the arms, legs, and trunk. In the later stages, movement disorders are severe, and the person has trouble speaking and swallowing and may meet the criteria for mild or major neurocognitive disorder.
DISCUSS PARKINSON’S DISEASE (MOTOR disorder)
Parkinson’s disease is a neurodegenerative disorder that produces prominent motor symptoms. It is believed to be due to an interaction between genetic factors and environmental risk factors, and it has been linked to a loss of dopamine-producing cells in the substantia nigra and basal ganglia, which causes the disorder’s motor symptoms. There’s also evidence that excessive glutamate activity in the basal ganglia is implicated in the progression of Parkinson’s disease (Gasparini, Di Paolo, & Gomez-Mancilla, 2013) and that degeneration of norepinephrine neurons in the locus coeruleus is responsible for non-motor symptoms, including depression, cognitive deficits, and sleep disturbances (Paredes-Rodriguez et al., 2020). Finally, research has linked variants of the ApoE gene to an increased risk for neurocognitive disorder due to Parkinson’s disease as well as other neurocognitive disorders including neurocognitive disorder due to Alzheimer’s disease, neurocognitive disorder with Lewy bodies, and vascular neurocognitive disorder (Verghese, Castellano, & Holtzman, 2011).
There’s no cure for Parkinson’s, but symptoms are temporarily alleviated in the early stages with L-dopa, which increases dopamine levels. The main symptoms of Parkinson’s disease represent four categories: tremor that begins in the hands and includes “pill rolling,” impaired balance and equilibrium, muscle rigidity, and slowed voluntary movement (bradykinesia). Up to 50% of people have depression at some time during the disorder, with depressive symptoms preceding motor symptoms in about 20% of cases (Capp-Ahlgren & Dehlin, 2001; Lieberman, 2003). Some people eventually develop mild or major neurocognitive disorder.
Talk about SEIZURE DISORDERS
Seizure Disorders: Seizure disorders are caused by abnormal electrical activity in the brain.
- Focal Onset Seizures: Focal onset seizures begin in a localized area in one cerebral hemisphere and affect one side of the body, although they may spread and become generalized. Focal onset aware seizures (also known as simple partial seizures) don’t affect consciousness, while focal onset impaired awareness seizures (also known as complex partial seizures) cause a change in consciousness and may begin with an aura. The symptoms of both types depend on the origin of the seizure and may include abnormal sensations, hallucinations, a sense of déjà vu, and/or automatisms (e.g., lip smacking, repetitive finger tapping, walking in circles).
- Generalized Onset Seizures: Generalized onset seizures affect both hemispheres and include generalized onset motor seizures and generalized onset non-motor seizures. Generalized onset motor seizures are also known as tonic-clonic seizures and grand mal seizures. They cause a change in consciousness and include a tonic phase that involves a stiffening of muscles in the face and limbs that’s followed by a clonic phase that involves jerky rhythmic movements in the arms and legs. When the person regains consciousness, he/she may be depressed, confused, or fatigued and have no memory for the events that occurred during the seizure. Generalized onset non-motor seizures are also known as absence seizures and petit mal seizures. They involve a very brief loss of consciousness with a blank or absent stare and, for some people, their eyes turn upwards and eyelids flutter.
Discuss the Migraine Headaches
Migraine Headaches: Migraine headaches involve an intense, throbbing pain that’s usually on one side of the head and may be accompanied by nausea or vomiting and sensitivity to light or other sensory stimuli. There are two types: Migraine headaches with aura are also known as classic migraines and migraine headaches without aura are also known as common migraines. Migraines can be triggered by emotional stress or relaxation after stress, abrupt weather changes, alcohol, certain foods, missing a meal, or other factors, and their intensity may be worsened by bending forward and by walking or other routine physical activity. The cause of migraine headaches is not totally understood, but they have been linked to a low level of serotonin. Treatments include nonsteroidal anti-inflammatory drugs, ergot alkaloids, SSRIs, SSRI agonists, beta blockers, and a combination of thermal biofeedback and autogenic training.
Whats up with Hypertension?
Hypertension: There are two types of hypertension: Primary hypertension is also known as essential hypertension and is diagnosed when the physiological cause of the high blood pressure is unknown, while secondary hypertension is diagnosed when high blood pressure is due to a known disease. Primary hypertension accounts for up to 90% of all cases and is referred to as the “silent killer” because it’s often asymptomatic. Factors that increase the risk for primary hypertension include obesity, tobacco use, excessive salt intake, stress, male gender, older age, African American race, and a family history of hypertension. Treatment emphasizes lifestyle changes and may also include a diuretic, beta blocker, ACE inhibitor, or other blood pressure medication and biofeedback or relaxation training.
What’s up with Endocrine Disorders?
Endocrine Disorders: Disorders of the thyroid gland are among the most common endocrine disorders. Hyperthyroidism is caused by hypersecretion of thyroid hormones, and its symptoms include an increased rate of metabolism, elevated body temperature, heat intolerance, increased appetite with weight loss, accelerated heart rate, insomnia, emotional lability, and reduced attention span. Hypothyroidism is caused by hyposecretion of hormones and involves a decreased rate of metabolism, reduced appetite with weight gain, slowed heart rate, lowered body temperature, cold intolerance, depression, lethargy, decreased libido, confusion, and impaired concentration and memory.
The pituitary gland is responsible for the release of several hormones including antidiuretic hormone (ADH), which is also known as vasopressin and is responsible for the amount of water excreted in the urine. A low level of ADH due to a tumor, infection, stroke, pituitary surgery, or other factor can cause central diabetes insipidus. Its symptoms include frequent and excessive urination, extreme thirst, dehydration, constipation, weight loss, and low blood pressure. (When diabetes insipidus is caused by a failure of the kidneys to respond to ADH, it’s referred to as nephrogenic diabetes insipidus.)
What is the thing about first generation antispsychotics?
First-Generation Antipsychotics: The first-generation antipsychotics (FGAs) are also known as traditional and conventional antipsychotics and include chlorpromazine (Thorazine), haloperidol (Haldol), thioridazine (Mellaril), and fluphenizine (Prolixin). These drugs are used to treat schizophrenia and other disorders with psychotic symptoms and are more effective for treating positive symptoms than negative symptoms. The FGAs exert their therapeutic effects primarily by blocking dopamine (especially D2) receptors.
The major side effects of the FGAs fall into three categories: (a) Anticholinergic side effects are most likely with low potency FGAs (e.g., chlorpromazine and thioridazine) and include dry mouth, blurred vision, urinary retention, constipation, and tachycardia. (b) Extrapyramidal side effects are most likely with high-potency FGAs (e.g., haloperidol and fluphenizine) and include parkinsonism (resting tremor, muscle rigidity, slowed movement), dystonia (uncontrollable muscle contractions), akathisia (a sense of inner restlessness), and tardive dyskinesia. Tardive dyskinesia is potentially life threatening, begins after long-term drug use, and is more common in women and older adults. It starts with involuntary, rhythmic movements of the tongue, face, and jaw and, over time, may also affect the limbs and trunk. Tardive dyskinesia is irreversible for some patients and is treated by gradually withdrawing the drug, administering a benzodiazepine, or switching to a second-generation antipsychotic. (c) Neuroleptic malignant syndrome (NMS) is a rare life-threatening side effect. Its symptoms include muscle rigidity, a high fever, autonomic dysfunction (e.g., unstable blood pressure, tachycardia, excessive sweating), and an altered mental state (e.g., confusion, combativeness). Treatment involves having the person stop taking the drug at the first sign of symptoms and providing him/her with supportive therapy (e.g., hydration, cooling).
What is up with the SEcond Generation Antipsychotics?
Second-Generation Antipsychotics: The second-generation antipsychotics (SGAs) are also known as atypical antipsychotics and include clozapine (Clozaril), risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel), and aripiprazole (Abilify). Like the FGAs, they’re used to treat schizophrenia and other disorders with psychotic symptoms, and some are FDA-approved as an adjunctive treatment for major depressive disorder. There’s evidence that the SGAs are as effective as or more effective than the FGAs for treating the positive symptoms of schizophrenia and more effective than the FGAs for treating the negative symptoms, although this may be true for only some SGAs (e.g., Leucht et al., 2009). In addition, an SGA (especially clozapine) may be effective when FGAs have been ineffective. These drugs alleviate positive symptoms primarily by blocking dopamine (especially D3 and D4) receptors and alleviate negative and cognitive symptoms primarily by blocking serotonin receptors (e.g., Stepnicki, Kondej, & Kaczor, 2018).
The SGAs are less likely than the FGAs to cause extrapyramidal side effects; however, they can cause anticholinergic effects, neuroleptic malignant syndrome, and metabolic syndrome. Metabolic syndrome involves substantial weight gain, high blood pressure, insulin resistance, hyperglycemia, and increased risk for diabetes mellitus and heart disease. In addition, clozapine and, to a lesser extent, other SGAs can cause agranulocytosis, which is a potentially life-threatening condition that involves a dangerously low white blood cell count and requires regular white blood cell monitoring.
Talk about SSRIS
Antidepressants: The major antidepressants include the selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), norepinephrine dopamine reuptake inhibitors (NDRIs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs).
- SSRIs: The SSRIs include fluoxetine (Prozac, Sarafem), fluvoxamine (Luvox), paroxetine (Paxil), sertraline (Zoloft), and citalopram (Celexa). The SSRIs are the most frequently prescribed antidepressants and are generally considered to be the first-line pharmacological treatment for major depressive disorder and persistent depressive disorder. Some are also used to treat other disorders including premenstrual dysphoric disorder, OCD, panic disorder, generalized anxiety disorder, PTSD, bulimia nervosa, and premature ejaculation. The SSRIs exert their therapeutic effects primarily by blocking the reuptake of serotonin at nerve synapses. In addition, there’s evidence that fluoxetine also increases levels of norepinephrine and dopamine (Bymaster et al., 2002).
The SSRIs are comparable to the TCAs in terms of efficacy and have several advantages: The SSRIs have fewer side effects, are safer in overdose (e.g., are less cardiotoxic), and are safer for older adults. Side effects include mild anticholinergic effects, gastrointestinal disturbances, insomnia, anxiety, and sexual dysfunction, and abrupt cessation of an SSRI can cause discontinuation syndrome, which involves headaches, dizziness, mood lability, impaired concentration, sleep disturbances, and flu-like symptoms. Also, combining an SSRI with an MAOI, lithium, or other serotonergic drug can cause serotonin syndrome, which is potentially fatal and involves extreme agitation, confusion, autonomic instability, hyperthermia, tremor, seizures, and delirium. Treatment for serotonin syndrome requires immediate withdrawal of the serotonergic drugs and providing appropriate medical interventions for its symptoms. Like other antidepressants, the SSRIs have a delayed onset of therapeutic effects on depressive symptoms of about two to four weeks (Antidepressant Medication, 2017).
Talk about SNRI
SNRIs: The SNRIs include venlafaxine (Effexor), duloxetine (Cymbalta), and desvenlafaxine (Pristiq). They’re used to treat major depressive disorder, social anxiety disorder, and neuropathic pain and other pain disorders. The SNRIs are similar to the SSRIs in terms of efficacy, although there’s some evidence they may be more effective for severe depression (e.g., Thronson & Pagalilauan, 2014). Their therapeutic effects are due to inhibition of the reuptake of serotonin and norepinephrine at synapses.
The side effects of the SNRIs are similar to those of the SSRIs and, like the SSRIs, they can cause discontinuation syndrome when abruptly stopped and serotonin syndrome when combined with other serotonergic drugs. Because of their effects on norepinephrine, they can elevate blood pressure and may be contraindicated for patients with hypertension or heart problems.
Talk about NDRI, TCA, and MAOISs
NDRIs: The NDRIs include bupropion (Wellbutrin, Zyban), which is used to treat major depressive disorder and assist with smoking cessation and exerts its therapeutic effects by inhibiting the reuptake of norepinephrine and dopamine at synapses. Side effects include skin rash, decreased appetite and weight loss, agitation, insomnia, dizziness, and seizures. Advantages of bupropion are that it causes few anticholinergic effects, does not cause sexual dysfunction, and is not cardiotoxic. Note that bupropion and other antidepressants that increase levels of norepinephrine and dopamine have an energizing effect, which means they’re useful for patients who have low energy and motivation but not for those who have insomnia or are very anxious.
- TCAs: The TCAs include amitriptyline (Elavil), imipramine (Tofranil), clomipramine (Anafranil), nortriptyline (Pamelor), desipramine (Norpramin), and doxepin (Sinequan). These drugs are used to treat major depressive disorder, panic disorder, obsessive-compulsive disorder (especially clomipramine), and neuropathic pain (especially nortriptyline and amitriptyline). They exert their therapeutic effects by inhibiting the reuptake of norepinephrine, serotonin, and dopamine at synapses.
The side effects of the TCAs include cardiovascular effects (e.g., hypertension, tachycardia, orthostatic hypotension), anticholinergic effects, sedation, weight gain, and sexual dysfunction. Because they’re cardiotoxic and lethal in overdose, the TCAs must be prescribed with caution for patients who have heart disease or are suicidal.
- MAOIs: The MAOIs include phenelzine (Nardil), isocarboxazid (Marplan), and tranylcypromine (Parnate). These drugs are useful for patients with treatment-resistant depression or atypical depression, which involves reversed vegetative symptoms such as hypersomnia, increased appetite, and reactive dysphoria. The enzyme monoamine oxidase deactivates norepinephrine, serotonin, and dopamine, and the MAOIs increase the levels of these neurotransmitters by inhibiting the activity of this enzyme.
Side effects include anticholinergic effects, orthostatic hypotension, sedation, and sexual dysfunction. They may also produce a hypertensive crisis when taken in conjunction with certain drugs (e.g., amphetamines, antihistamines) or food containing tyramine (e.g., aged cheese and meat, soy products, beer, red wine, sauerkraut, fava beans, ripe bananas). Symptoms of a hypertensive crisis include a severe throbbing headache, neck pain or stiffness, rapid heart rate, nausea and vomiting, sweating, sensitivity to light, confusion, and delirium.
Talk about sedatives
Sedatives, Hypnotics, and Anxiolytics: The sedatives, hypnotics, and anxiolytics include the benzodiazepines, barbiturates, and azapirones.
- Benzodiazepines: The benzodiazepines include diazepam (Valium), alprazolam (Xanax), and lorazepam (Ativan). These drugs increase GABA activity and are used to treat anxiety, insomnia, seizures, and alcohol withdrawal. The most common side effects are drowsiness and sedation; others include weakness, unsteadiness, impaired memory and concentration, anticholinergic effects, sexual dysfunction, and, in older adults, disorientation and confusion. These drugs can have a paradoxical effect and cause excitability and anxiety, and chronic use can result in tolerance, dependence, and withdrawal symptoms, which may cause rebound anxiety and depression, anorexia, delirium, and seizures. Combining a benzodiazepine with alcohol can have a synergistic depressant effect that can be lethal.
- Barbiturates: The barbiturates include thiopental (Pentothal), amobarbital (Amytal), and secobarbital (Seconal). These drugs enhance GABA activity and are used as a general anesthetic and as a treatment for anxiety, insomnia, and seizures. Side effects include drowsiness, dizziness, confusion, ataxia, cognitive impairment, and paradoxical excitement. Chronic use can lead to tolerance, dependence, and withdrawal symptoms, and sudden withdrawal can cause seizures, delirium, and death. Like the benzodiazepines, taking a barbiturate in conjunction with alcohol can be lethal.
- Azapirones: These drugs include buspirone (BuSpar), which is used to treat generalized anxiety disorder and other anxiety disorders. Side effects include dizziness, dry mouth, sweating, nausea, and headache. An advantages of buspirone is that it does not cause sedation, dependence, or tolerance.
Talk about Narcotics
Narcotic-Analgesics (Opioids): The narcotic-analgesics mimic the effects of the body’s natural analgesics (endorphins and enkephalins) and include the natural opioids (opium, morphine, heroin, codeine) and synthetic and semi-synthetic opioids (methadone, oxycodone, hydrocodone, fentanyl). Narcotic-analgesics are used as a pre-surgery anesthetic and to treat pain, and methadone is used for heroin detoxification. Methadone doesn’t produce the pleasurable effects of heroin, but it does reduce the craving for heroin and withdrawal symptoms. Side effects of the narcotic-analgesics include dry mouth, nausea, pupil constriction, postural hypotension, drowsiness, dizziness, constipation, and respiratory depression, and an overdose can cause convulsions, coma, and death. Chronic use leads to dependence, tolerance, and withdrawal symptoms. Initial withdrawal symptoms are similar to the flu (e.g., runny nose, watery eyes, nausea, muscle aches, fever, and yawning); these are followed by insomnia, abdominal cramps, vomiting, diarrhea, rapid heartbeat, and elevated blood pressure. Note that drug overdose is the leading cause of accidental deaths in the United States, with opioids being the most frequent cause of these deaths (Schiller, Goyal, Cao, & Mechanic, 2020).
Talk about Bet-blockers
Beta-Blockers: Beta-blockers inhibit the activity of the sympathetic nervous system and are used to treat hypertension, cardiac arrhythmias, migraine headache, and essential tremor. These drugs include propranolol (Inderal) which is also used to treat anxiety, with research suggesting that it’s more effective for alleviating the somatic symptoms of anxiety than its psychological symptoms (e.g., apprehension, worry, dread). The side effects of propranolol include hypotension, decreased sex drive, insomnia, nausea and vomiting, dry eyes, dizziness, and depression. Abrupt discontinuation is contraindicated because it can cause rebound hypertension, tremors, headaches, confusion, and cardiac arrhythmia.
Mood stabilizers
Mood Stabilizers: The mood stabilizers are used to treat bipolar disorder and include lithium and anticonvulsant medications.
- Lithium: Lithium (Eskalith, Lithobid) is the first-line drug for acute mania and classic bipolar disorder (euphoric mania without rapid cycling). Common side effects include nausea, vomiting, diarrhea, a metallic taste, increased thirst, weight gain, hand tremor, fatigue, and impaired memory and concentration. Lithium levels must be regularly checked to avoid lithium toxicity, which can cause seizures, coma, and death.
Anticonvulsant Drugs: These drugs are used to treat acute mania and bipolar disorder with mixed episodes and include carbamazepine (Tegretol) and valproic acid (Depakene). Side effects include nausea, dizziness, sleepiness, lethargy, ataxia, tremor, visual disturbances, and impaired concentration. Blood levels must be monitored to avoid liver failure when taking valproic acid or carbamazepine and to avoid agranulocytosis (low white blood cell count) and aplastic anemia when taking carbamazepine.
