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| 1. Pharmacokinetics (PK) is both a biochemical process and a branch of pharmacology 2. PK process: The change over time of the blood levels of a drug following administration 3. PK field: Study of how the body absorbs, distributes, breaks down, and eliminate drugs 4. PK is what the body does to the drug 5. Pharmacodynamics (PD) is what the drug does to the body 6. Pharmacometric (PM): Quantitative analysis and interpretation based on PK and PD 7. Pharmacokinetics, Pharmacodynamics, and Pharmacometrics interact to study and understand a drug action, therapy, design, development, and evaluation 8. Relevance to clinical psychology: Provides the basic research data and information about creation and development of psychotropic drugs |
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| Electroencephalography (EEG) Noninvasively measures the electrical field of the brain. Provides high temporal information about brain activity in milliseconds. Clinical applications include: a. Measuring brain waves during sleep b. Monitoring anesthesia c. Contributing to the diagnosis of epilepsy. Poor spatial resolution/localization Magnetoencephalography (MEG).Noninvasively measures the magnetic field of the brain MEG has better spatial resolution than EEG.Clinical applications include: a. Contributing to the diagnosis of epilepsy. b. Pre-surgical planning Computerized tomography (CT). Uses X-rays to generate a structural brain image. Relatively low-resolution compared to newer brain imaging techniques (e.g., MRI). Clinical applications include: a. Detecting large brain tumors Positron-emission tomography (PET). Measures metabolic brain activity. Primarily used to study cognitive processes. Clinical applications include: Detecting brain lesions via the detection of abnormal functional activity Magnetic resonance imaging (MRI) Uses radio frequencies emitted by hydrogen atoms to generate high-resolution structural images of the brain.. Provides higher structural resolution than CT. Clinical utility includes detection of brain tumors and other brain abnormalities (e.g, hydroencephalus, subdural hematoma, etc.) Functional magnetic resonance imaging (fMRI) Variant of MRI. fMRI measures the hemodynamic blood oxygen level dependent (BOLD) signal a. Measures oxygen levels in the brain b. Unknown how the BOLD signal precisely maps onto neural function. fMRI provides poor temporal resolution relative to EEG measures |
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| Neuropsychological Assessment |
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| This type of test 1. Conducted after a TBI, concussion, CVA, or brain tumor 2. May be used as part of a diagnostic workup for developmental disorders such as ADHD and autism spectrum disorders 3. Measures Intelligence, Academic Achievement, Language, Visuospatial function, Memory/Attention, 4. Learning/Recall, Executive Function, and Social/Emotional Function Crystallized intelligence 1. Knowledge and skills that are acquired via learning Fluid intelligence 1. Involves the ability to reason abstractly and solve problems 2. This type of intelligence is considered independent of learning Process approach 1. Refers to an individualized approach to testing involving a custom-designed evaluation for each client Battery approach 1. Refers to a standardized approach to testing, such that each client receives the same evaluation, regardless of their presenting problem Some common evaluation measures 1. WAIS-IV/WISC-IV a. Assesses fluid and crystallized intelligence b. Measures four key domains: verbal reasoning, perceptual reasoning, working memory, and processing speed 2. Wisconsin Card Sorting Test (WCST) a. Measures the ability to use flexible problem solving strategies and shift mental sets to avoid perseveration b. Poor performance on WCST is associated with prefrontal cortical abnormalities 3. Color-Word Stroop Test a. Measures the ability to inhibit and automatic or learned response b. Poor performance on the Stroop has been associated with frontal lobe lesions, including those located in the inferior frontal gyrus and anterior cingulate cortex 4. Glascow Coma Scale (GCS) a. Most commonly used system for classifying TBI severity |
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| 1. Sit on top of the kidneys 2. Consist of adrenal cortex and adrenal medulla 3. Adrenal cortex (outer layer) synthesizes corticosteroids, including cortisol Testosterone, androgen, and aldosterone 1. Are also secreted by the adrenal cortex Responds to 1. The hypothalamic-pituitary axis (HPA), which is activated by stress Adrenal medulla (inner core) 1. Contains chromaffin cells 2. Synthesizes catecholamine hormones 3. Adrenaline (epinephrine) 4. Noradrenaline (norepinephrine) 5. Involved with the fight-or-flight response HPA axis 1. Stress is manifested through the body by activation of the HPA 2. This system is modulated by corticotropin releasing factor (CRF) 3. CRF is released by the hypothalamus 4. CRF travels to the anterior pituitary gland where it activates the production of adrenal corticotropin hormone ACTH 1. ACTH travels through the blood stream to the adrenal cortex 2. Stimulates the adrenal cortex to release cortisol Cortisol 1. Is the body's predominant hormone involved in stress 2. Produces various brain and visceral effects that manifest as neurological and physiological responses to stress 3. Increased stress is correlated with increased cortisol levels 4. Hypercortisolemia (chronically inflated cortisol levels) is associated with structural and functional brain damage as well as lower resistance to infections |
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| Action potential 1. Threshold of excitation determines whether an action potential occurs 2. When threshold is not reached, the action potential does not occur The rate law (supplements the All or None Principle) 1. Stimulus/response is stronger or weaker based on the rate at which the neuron fires, not by the strength of the action potential itself a.Higher rate of firing associated with stronger stimuli/responses b.Slower rate of firing associated with weaker stimuli/responses |
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| Brain Activity During Sleep |
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Definition
| 1. Alpha: 8-12 Hz frequency; most observable during resting (awake) with eyes closed 2. Beta: 13-30 Hz frequency; occur when an individual is alert/attentive 3. Theta: 4-7 Hz frequency; occur when an individual is transitioning from wakefulness to sleep a. Theta waves are observable during stage one sleep b. Theta waves also occur during stage two sleep; however they are interspersed with sleep spindles and K-complexes during stage two sleep c. Sleep spindles: Bursts of 12-14 Hz frequency waves d. K-complexes: Unique to stage two sleep, occur approximately once every minute 4. Delta: Less than 4 Hz; delta waves are present during the third stage of sleep which serves as the transition from light to deep sleep a. Stage three sleep is distinguished from stage four sleep based on the amount of delta activity present b. Stage three sleep contains about 20-50 percent delta activity c. Stage four sleep is comprised of more than 50 percent delta activity 5. Non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep a. NREM occurs during the first four stages of sleep b. REM begins approximately 90 minutes after sleep has begun (about 45 minutes after the onset of stage four sleep) c. After REM begins, people cycle between REM and NREM every hour and a half during the first half of the night d. There is approximately a half hour of REM sleep in each sleep cycle e. In the second half, slow-wave sleep is replaced by larger proportions of stage two sleep in each cycle, alternating with REM sleep Developmental differences in sleep cycles 1. Infants spend most sleep time in either stage two (25-30 percent) or REM (50 percent) sleep a. Infants enter REM sleep prior to entering stage two sleep 2. Delta sleep develops within the first few months a. Young children spend the largest proportions of time in delta sleep compared with other age groups 3. As age increases, the proportion of time spent in delta sleep decreases and it is instead replaced by stage two sleep a. The elderly tend to spend the least amount of time in REM and delta sleep, and predominately obtain stage two sleep |
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| Types of memories 1. Memory refers to our ability to encode, retain, and recall stored information 2. Short term memory – the encoding and storing of information for a brief duration (typically up to 30 seconds) 3. Long-term memory can be stored indefinitely 4. Categorization of memory: a. Declarative memory (also called explicit memory) refers to memories that are consciously recalled and that can be described. There are two types of declarative memory: semantic (memory for facts) and episodic (memory for specific events) b.Procedural memory: implicit memories that do not require conscious thought in order to be recalled. Procedural memory involves motor memory, such as remembering how to ride a bike or play a musical instrument Brain structure/function and memory 1. Explicit memory: located in the temporal lobe and include: hippocampus amygdala temporal cortex 2. These structures are then connected through the thalamus to the prefrontal cortex 3. Implicit memory: basal ganglia (caudate nucleus and putamen), globuspallidus, thalamus, substantianigra, and cerebellum Types of memory loss and the importance of H.M. 1. Anterograde amnesia is an inability to form new memories 2. Retrograde amnesia is an inability to retrieve memories about previous events a.In 1953, patient "H.M." underwent surgery to control seizures. Surgery included removal of: Most of his hippocampus Amygdale Entorhinal and perirhinal cortices After surgery, seizures were controlled but H.M. had severe anterograde amnesia and temporally graded retrograde amnesia after the surgery 3. Anterograde amnesia: unable to form new long-term memories for events after the surgery a.Temporally graded retrograde amnesia: H.M. had no recall of events in the 1-2 years prior to the surgery 4. Memory that was unaffected by the surgery: a.Procedural memories formed prior to surgery b. Ability to form new procedural memories c. Ability to recall long-term memories for events that occurred many years before the surgery d. Working memory. H.M.'s case has played a pivotal role in the understanding of the brain function and memory, particularly the involvement of the hippocampus in memory Role of the hippocampus 1. A convoluted tube-like structure that derives its name from the resemblance it shares with a seahorse 2. Has two regions, the Ammon's horn and the dentate gyrus, contain pyramidal and granule cells respectively 3. The cells of the Ammon's horn are more sensitive to oxygen deprivation (anoxia) than the cells of the dentate gyrus, and thus, are easily damaged during stroke 4. The hippocampus: Plays a large role in the conversion of short-term memories into long-term memories 5. Not the site of where memories are stored, as was evidenced by the fact that H.M. retained memories of his childhood despite removal of the majority of his hippocampus 6. Involved in the formation of spatial memories; memories for one's orientation in space and spatial information of the environment 7. Formation of episodic memories by the hippocampus is achieved in conjunction with the amygdale 8. The entorhinal cortex provides the primary input into the hippocampus. 9. Long-term potentiation: Intense electrical stimulation of cells in the entorhinal cortex whose axons terminate in the dentate gyrus causes a long-term increase in the magnitude of the post synaptic potential, a phenomenon that plays a role in the formation of long-term memories 10. The amygdala attaches the emotional components to the memory, while the hippocampus facilitates encoding of the factual components |
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| Neural communication refers to how cells relay information 1. Involves chemical and electrical processes 2. Conduction: An electrical process that occurs within a neuron a.During conduction, information is transmitted from the dendrite, through the axon, to the terminal buttons 3. Resting state: a.During the resting state, a neuron is negatively charged (-70 mV) with respect to the extracellular fluid 4. Action potential: a.Occurs when the neuron is stimulated by other cells, meeting its threshold of excitation b. When the threshold of excitation is reached, sodium (Na+) channels within the cellular membrane open c. Positive charged sodium ions enter the cell d. Depolarization occurs: the membrane potential increases (toward zero) e. Depolarization causes the membrane to reach +40 mV 5. Repolarization occurs: the membrane briefly becomes hyperpolarized and then returns to -70mV a. During repolarization, the sodium channels close and the potassium (K+) channels open b. Positively charged potassium ions exit the cell because the intracellular fluid is more positively charged than the extracellular fluid c. When the neuron returns to -70mV, the K+ channels close Communication between neurons occurs after the action potential is transmitted down the axon 1. The axon's terminal button release neurotransmitters into the synaptic cleft a. The synaptic cleft is the space between the terminal buttons of the presynaptic cell and receptors on the dendrites of the postsynaptic cell b. The neurotransmitters attach to binding sites on the postsynaptic receptors c. Neurotransmitter-dependent ion channels open d. Specific ions enter/leave the cell, which leads to a postsynaptic potential e. The postsynaptic potential can either be excitatory or inhibitory f. Excitatory postsynaptic potentials (EPSP) involve a depolarization of the postsynaptic membrane g. Increases the likelihood that the postsynaptic neuron will fire h. Inhibitory postsynaptic potentials (IPSP) involve a hyperpolarization of the postsynaptic membrane i. Decreases the likelihood that the postsynaptic neuron will fire |
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| Visual system Visual information enters the eye through the pupil and lens. Processed by photoreceptor cells located on the retina (the surface on the back of the eye). Rods: Located in the periphery and most active in dim light. Cones: Located in the center of the retina and used to process color and other information at normal light levels. Information sent from the eye to the brain via the optic nerve. When information leaves the eye and is sent to the contralateral (opposite) hemisphere it crosses over at the optic chiasm. The optic nerves terminate in the lateral geniculate nucleus of the thalamus. Information relayed from thalamus to the occipital lobe for visual processing. Visual fields. Each side of the eye receives visual information from the contralateral side of the visual field -- medial half of the right eye receives information from the right side of the visual field, and the lateral half of the right eye receives information from the left half of the visual field. Information from the right visual field is sent to the left hemisphere via the left optic tract. Information from the left visual field is sent to the right hemisphere via the right optic tract. Each half of the visual field is processed by one cerebral hemisphere; the left half of our visual field is processed by the right hemisphere, and the right half of our visual field is processed by the left hemisphere. Lateral inputs from both eyes are projected to the anterior portion of the occipital lobe. Medial inputs are directed to the posterior portions of the occipital lobe. Layers of the visual cortex. Primary visual cortex: Also called V1 and striate cortex . a. Largest and most important visual area. b. All visual input first comes to the V1 area, and is then projected to other occipital areas. c. Responsible for perception of sight. Area V2 also sends projections to lower visual areas a. V2 is heterogeneous with V1 in function, and performs some color, form, and movement processing, and processing spatial information V3 area: Predominantly devoted to form perception. V4 area: Function is primarily color processing, although some cells within V4 respond to both form and color. V5 area: Critical for the detection of form while in motion Theories of Color Vision 1. Trichromatic Coding: three cones to detect and perceive color; red, blue, green 2. Opponent-Process Coding: red, blue, and green cones, but also two color-sensitive ganglion cells; red-green and yellow-blue. When one is stimulated, the other is inhibited. Effect of damage to eye and optic nerve 1. Damage to the eye can result in partial or complete blindness in the eye that was damaged 2. Damage to the optic nerve can have a variety of results depending on where the damage occurs a. Hemianopia: Blindness in the part of the visual field caused by damage to either optic nerve 3. Damage to the medial optic nerves at the optic chiasm, on the other hand, results in a loss of vision in the temporal half of both eyes, a condition called bilateral hemianopia 4. Damage to the optic nerve past the optic chiasm will affect input from one half of our visual field from both eyes, thereby causing bilateral hemianopia that affects one medial and one lateral input, called homonymous hemianopia. Effect of damage to visual cortex. 1. Damage to V1: a. Most serious visual impairments b. Partial blindness in both eyes c. Blindsight: A condition associated with damage to V1 in which patients report seeing nothing, but respond to changes in the visual field such as movement, due to visual processing still occurring at lower visual areas 2. Damage to V2: global disruptions in vision, with impairments in ability to distinguish form, movement, color, and spatial orientation of patterns 3. Damage to V3: Partial loss of form perception 4. Damage to V4: a. Loss of ability to perceive color, known as cerebral achromatopsia b. Individuals with achromatopsia see the world in shades of gray c. Dyschromatopsia refers to a partial loss in color perception and is more common 5. Damage to both V3 and V4 results in complete loss of form perception 6. Damage to V5: Loss of ability to see movement. A case study of an individual with V5 damage revealed that she could see still objects, but that they disappeared when they began moving. So a person standing and talking would disappear as they walked away, or tea in a teapot would disappear as she was pouring it into a cup |
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| Amygdala, Kluver-Bucy Syndrome |
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Definition
| Characteristics of the Amygdala 1. Structure in the brain's limbic system 2. Almond-shaped structure made up of several distinct groups of nuclei 3. There is one amygdalae located deep in the medial temporal lobe of each hemisphere 4. Receives input from several brain regions including those that process sensations, such as olfactory, auditory, visual, and pain information 5. Sends projections to the hypothalamus, hippocampus, and reticular formation among others Function of the Amygdala 1. Aids in the detection of dangerous smells and contributes to the response to the "scent" of pheromones 2. Associated with emotion regulation, especially fear and anger, emotional memory formation, emotional learning (specifically classical conditioning), and motivation 3. Associated with the attachment of emotions to memories; the stronger the emotion associated with an event, the more likely the event will be remembered 4. Activates the sympathetic nervous system (through its projections to the hypothalamus and reticular formation) in threatening, fear provoking situations 5. If a neutral stimulus is repeatedly paired with a stimulus that elicits an automatic response (classical conditioning) the amygdala will eventually activate the sympathetic nervous system when only the neutral stimulus is present 6. If the emotional response is strong enough, classical conditioning may occur after one pairing of the neutral and response provoking stimulus 7.Involved in anxiety disorders 8."The High and the Low Road to the Amygdala" Effect of damage to the Amygdala 1.Animal studies of amygdalar lesions have found that lesions of the amygdala result in docility in animals 2. Stimulation of the Amygdala causes increased rage and predatory bx 3. Bilateral destruction of the Amygdala in humans leads to a disorder call Kluver-Bucy Syndrome Kluver-Bucy Syndrome 1. Bxs associated with Kluver-Bucy syndrome: decreased emotions, decreased fear or anger response, hypersexuality, psychic blindness (the inability to identify an object or person although there is no difficulty seeing the object), increased docility, mouthing of objects, and reduced motivation 2. Etiologies for Kluver-Bucy Syndrome: a.bilateral temporal lobectomy b.herpes encephalitis c.trauma d.stroke that causes amygdalar tissue to become hypoxic e.other brain diseases that cause degeneration in the medial temporal lobe |
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| Anterior Cingulate Cortex |
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Definition
| Anterior Cingulate Cortex (ACC) is located superior to the corpus callosum 1. ACC was traditionally classified as part of the limbic lobe, but it is now considered to be a distinct brain region 2. ACC is involved with processing cognitive information, emotion regulation, and autonomic control ACC is subdivided into two structurally and functionally distinct regions: dorsal ACC (dACC) and rostral ACC (rACC) 1. dACC a. dACC is located superior to the genu of the corpus callosum b. Connections with: lateral prefrontal cortex, inferior parietal cortex, and also primary motor cortex, pre-motor cortex, supplementary motor cortex, and it has projections to the spinal cord c. dACC theorized to play a role in cognitive function, including: executive function, response selection, negotiating conflict, and autonomic control; it is also sensitive to task difficulty and novelty 2. rACC a. rACC is located inferior to the genu of the corpus callosum b. Connections with: amygdala, hippocampus, hypothalamus, nucleus accumbens, ventral striatum, insula, thalamus, and orbitofrontal cortex c. rACC is associated with emotional function d. Implicated in processing emotional information and regulating emotional responses |
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| 1. Group of nuclei located in the base of the forebrain beneath the lateral ventricles 2. Nuclei consist of the caudate nucleus, the putamen, and the globuspallidus 3. Substantianigra and striatum have many connections with the Basal Ganglia and are therefore often associated with it 4. Basal Ganglia function: facilitate coordinated motor movements and contribute to the processing of thoughts and emotions 5. Activation of the Basal Ganglia is inhibitory; it is believed that the Basal Ganglia functions to inhibit actions that would interfere with smooth motor output of the intended action Basal Ganglia connections 1. The Basal Ganglia receive sensory information from many different regions of the brain 2. Putamen has rich connection to the premotor cortex, supplementary motor area, and the motor cortex 3. Caudate nucleus primarily connects to the frontal lobes where thinking, planning, and executive decision-making is conducted 4. Both the caudate and putamen send projections to the substantianigra and globuspallidus 5. The globuspallidus sends inhibitory information to the thalamus, which in turn gets relayed back to the cerebral cortex 6. The primary neurotransmitters in the Basal Ganglia are GABA and dopamine; however, they receive noradrenergic and serotonergic inputs as well Dysfunction of the Basal Ganglia 1. Damage to the Basal Ganglia causes severe disruption and is linked to the emergence of several disorders: a. Parkinson's disease – movement sxs in Parkinson's disease are caused by degeneration of neurons in the substantianigra that sends dopaminergic output to the caudate nucleus and putamen b. Huntington's disease – associated with degeneration in the caudate nucleus; because activation of the Basal Ganglia is inhibitory in nature, degeneration of these neurons is associated with loss of inhibition, leading to the involuntary movements and jerks seen frequently in patients with Huntington's chorea 2. Several other disorders are associated with disruption in Basal Ganglia functioning, including: a. Obsessive-compulsive disorder, which primarily results from disruption in caudate nucleus function.which results in disrupting control and execution of automated thoughts b. Tourette's disorder, which is more closely associated with putamen disruption, leading to difficulties in controlling automated movements, which causes tics (Carter, 1998) c. Attention deficit-hyperactivity disorder results from damage or under-development of the Basal Ganglia and reduced dopamine levels in the pathways connecting the Basal Ganglia to higher cortical areas d. Cerebral palsy develops from Basal Ganglia damage during the second or third trimester of pregnancy |
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| Development of the neural tube Prior to implantation in the uterine wall, a fertilized egg undergoes cellular division, known as cleavage. These initial cells are stem cells, and are exactly identical to one another and identical in genetic content to the fertilized egg from which they originated. Shortly after implantation, the cells begin migration: movement of cells to develop three cell layers: the ectoderm, the endoderm, and the mesoderm. The neural plate begins to develop from the ectoderm around the third week of gestation. As the neural plate develops, a crease forms, known as the neural groove, and the edges of the neural plate (neural crests) move in toward each other and fuse, forming the neural tube. The front (rostral) part of the neural tube develops into the brain, while the remainder of the tube becomes the spinal cord Development of brain from neural tube A bulge forms at the front end of the tube as the neuronal stem cells divide rapidly to form neuroblasts, a process known as neurogenesis. The neuroblasts migrate to various regions within the neural tube and three brain areas are formed: a.Prosencephalon = forebrain b. Mesencephalon = midbrain c.Rhombencephalon = hindbrain These three areas will further differentiate: a. Prosencephalon becomes the telencephalon and diencephalon b.Mesencephalon remains the mesencephalon c.Rhombencephalon becomes the metencephalon and myencephalon As neuroblasts complete migration to their final destination within the brain, they begin to differentiate into different types of adult brain cells. Differentiation is complete at birth. Typically, brain development progresses radially outwards, with the migration, differentiation and maturation of cells in the innermost brain regions occurring earlier than cells in the outermost brain regions. Therefore, the cortex is the least developed part of a newborn's brain at birth as it is the last brain structure to complete development. Following cell differentiation and maturation, neurons begin to form synapses with other neurons. Brain development at birth and in the first few years of life. At birth:. a. The brain is one-quarter to one-third its adult size b.Contains approximately 100 billion neurons After birth the neurons grow in size and develop more axons and dendrites as they increase connections with other cells. Synaptic formation: a. The number of synapses formed is slow at first and then very fast until two years of age. b. Synaptic pruning begins where there is a drastic reduction in the number of synapses in the brain by up to 50 percent c. Synaptic pruning is completed by the time the child completes puberty d. Subsequently, the number of synapses plateaus through adulthood, and then gradually declines in old age. The last phase of brain development is myelination. Myelination of axons begins soon after birth and continues up to adulthood; myelination progresses at different paces in different regions of the brain, thus allowing for the brain's capabilities to become increasingly complex Stem cells in the adult brain. Although most of the cells in the brain are a specific type of cells, designed for a specific purpose, the adult brain retains a few neural stem cells that are capable of giving rise to new brain cells. Adult stem cells in the brain line the ventricles, forming a ventricular zone, and are also found in the olfactory bulb. Stem cells divide to give rise to progenitor cells, that ultimately produce neurons and glial cells. The production of new neurons and glial cells continues into adulthood to replace old and dying neurons (Kolb &Whishaw, 2003). Gould & Gross (2002) reported that stem cells can be found in the pre-frontal, temporal, and parietal cortices; in addition, stem cells are particularly abundant in the dentate gyrus, which they believe may modulate the formation of new memories in the hippocampus |
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| Brain Hemispheres and the Corpus Callosum |
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| Description of the cerebral cortex 1. Outermost layer of the brain 2. Divided into two hemispheres: the right and the left hemisphere 3. Each hemisphere is divided into four lobes: frontal, temporal, parietal and occipital a. Frontal Lobe: prefrontal cortex (higher-order executive functions) and the motor cortex b. Temporal Lobe: auditory, speech, and memory systems c. Parietal Lobe: visual-spacial processing / sensory processing d. Occipital Lobe: vision 4. Last portion of the brain to stop growing throughout the developmental process 5. More developed in humans than any other animal Hemispheric lateralization and specialization of function 1. Left hemisphere – is dominant in 97 percent of the population a. Location of language functions b. Associated with analytical and rational thought c. Side of the brain that calculates, communicates, indulges in abstract cognition, and makes executive decisions d. Processes information that is in the right visual field e. Associated with the processing of positive emotions 2. Right hemisphere – typically the non-dominant hemisphere a.Associated with visual-spatial skills, creativity, nonverbal memory, and intuitive thought b.Allows us to perceive stimuli as a whole, facilitating our ability to read maps or draw sketches of three-dimensional objects c.In general, negative emotions, particularly fear, anger, and pessimism can be ascribed to the right hemisphere d.Processes information presented in the left visual field Implication of lateralization of functions after a stroke 1. Impact of a stroke or brain injury will be different depending on which hemisphere is affected a.Stroke in the left hemisphere will more likely affect language than a stroke in the right hemisphere b.Stroke in the right occipital lobe (the occipital lobe that is located in the right hemisphere) may result in disturbances in visual processing of information in the left visual field 2. Hemispatial neglect (also known as contralateral neglect) – a condition in which an individual is seemingly unaware of information on one side of his or her body or environment a.Occurs most commonly after a stroke to the right parietal lobe, therefore the neglect is typically for information in the left side of space. While it may include other sensory information, hemispatial neglect is most often associated with visual processing b.Individuals with hemispatial neglect may not be aware of their neglect, a condition known as anosognosia (the unawareness of one's own neurological sxs) Contralateral processing 1. Each hemisphere is responsible for processing information that is presented to the contralateral side of the body 2. Right hemisphere processes information presented in the left visual field and other sensory information presented to the left side of the body such as the tactile information from holding an object in the left hand 3. Because each hemisphere receives information from the contralateral side of the body and environment, the hemispheres must communicate with each other to integrate the information 4. Communication is done through the Corpus Callosum Corpus Callosum 1. Large bundle of axons that connect the two hemispheres and allows for this communication 2. Allows information that is processed by the right hemisphere to be sent to the left hemisphere and expressed in language 3. Example: if one is holding a ball with their left hand, the tactile information is registered in the right parietal lobe and that information is sent to the left hemisphere, where the person can say "It's a ball," when asked what they are holding Consequences of severing the Corpus Callosum 1. "Split brain" is the name used to describe the bx seen in patients whose Corpus Callosum is severed 2. Corpus Callosum may be severed in order to attempt to control epilepsy 3. When the Corpus Callosum is cut, the two hemispheres are no longer able to communicate 4. When information is presented to only one hemisphere of a split brain patient, he or she is only able to verbalize what they are seeing if it is presented in the right visual field (because information in the right visual field is processed by the left hemisphere which also houses language functions in most people) 5. A split brain patient would not be able to verbalize what is presented to the left visual field, but he or she would be able to point to what they saw 6. Roger Sperry, the pioneer in the field of split-brain research, won the Nobel Prize for his work in 1981 7. Sperry's research led to a greater understanding of lateralization of function of the brain Other means of inter-hemispheric communication 1. Anterior commissure is a bundle of fibers that connects the limbic systems in both hemispheres. This structure remains intact in split-brain patients 2. Anterior commissure allows for communication of rudimentary emotional stimuli 3. For example, if a violent film is presented to the left visual field of a split-brain patient, the patient would not be able to verbalize what they had seen, but may verbalize that they feel afraid |
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| Cell structure 1. Smallest living unit into which the body can be divided 2. Cells have primary components: Cell membrane, cytoplasm, Organelles, inclusion bodies Cell membrane 1. Semi-permeable membrane that defines the Cell's boundary 2. Separates each Cell from the extra-cellular environment 3. Cell membrane consists of a lipid bilayer and two layers of lipids Cytoplasm 1. Also called cytosol is the jellylike liquid contained within the Cell 2. Contents of Cell are suspended in the cytosol Organelles 1. Specialized structures the perform functions within the Cell 2. Several Organelles, including: a. Deoxyribonucleic acid (DNA): DNA becomes compacted into rod-shaped structures called chromosomes; adult human Cells contain 46 chromosomes Ribosomes 1. Tiny structures that serve as the Cell's site of protein synthesis 2. Ribosomes are either free-floating in the cytoplasm, or present on the outer surface of another organelle, the Endoplasmic Reticulum (ER) Endoplasmic Reticulum (ER) 1. When studded with ribosomes, called rough ER (RER) 2. Areas of ER without ribosomes, called smooth ER (SER) 3. ER surfaces are used for protein synthesis 4. Channels are used to transport newly synthesized materials Golgi apparatus 1. Responsible for processing, sorting, packaging, and delivering proteins, lipids, and other materials manufactured by RER and SER 2. Mitochondria (Cell's "power house") a. The site where adenosine triphosphate (ATP), the Cell's energy is manufactured b. The mitochondria are the only Cell Organelles that can self-replicate; they contain their own nucleic material —mitochondrial DNA |
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| 1. Paul MacLean coined the term "limbic system" in 1952 2. Consists of structures also found in other mammals 3. Related to regulation of fear and aggression 4. Associated with bxs related to motivation, such as hunger and sexual bxs 5. Related to formation and storage of memories 6. Is also called the emotion center of the brain because of its involvement in emotions such as pleasure and fear Includes several distinct but interconnected brain structures 1. Amygdala: Involved in fear response and aggression and formation of emotional memories 2. Septum: Involved in fear response and aggression 3. Hypothalamus: Associated with motivational states, such as hunger, sexual drive, sleep/wake states, body temperature 4. Hippocampus: Necessary for the formation and storage of long-term memories 5. Thalamus: A relay station, sends sensory information to the cerebral cortex 6. Olfactory cortex: Processes olfactory (smell) information Studies examining lesions of/stimulation to structure in the limbic system 1. Lesions of the amygdala result in docility in animals 2. Stimulation of the amygdala causes increased rage and predatory bx 3. Septal lesions in rats lead to "septal rage," in which the rat becomes extremely aggressive 4. Experimental bilateral temporal lobectomy (which included removal of the amygdale) in monkeys was associated with: a.mouthing of objects b.increased tameness c.hypersexuality d.visualagnosia, which is the inability to recognize objects (also called psychic blindness) 5. Kluver-Bucy Syndrome: The above constellation of bxs found in people who have damage to both anterior temporal lobes 6. Lesions in the limbic system in humans associated with decreases in motivation, ability to focus on a task, decision making, startle response, and emotional reaction to both aversive and positive emotional stimuli 7. While these individuals may be able to cognitively process stimuli, they lack the "fight or flight" response that often underlies bx 8. The Papez Circuit Theory (1937): says emotions are determined by the cingulate cortex, in particular by the cingulate gyrus projecting to the hippocampus, and the hippocampus to the hypothalamus. |
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| Areas in the Midbrain (also called mesencephalon) Midbrain is a part of the brain stem. Tectum: Roof of the Midbrain. Tegmentum: Floor of the Midbrain. Cerebral peduncles: Everything in the Midbrain except the tectum. Structures in the Midbrain Superior colliculus: Processes information related to visual stimuli and is associated with eye movements. Inferior colliculus: Receives sensory information from the ear and relays auditory stimuli. Substantianigra: Contains a large number of dopamine-producing neurons, associated with voluntary movement and motor planning. Red nucleus: Involved in movements such as arm swinging while walking and crawling in babies. Ventral tegmental area (VTA): Group of neurons in the base of the Midbrain, which are involved in the reward system of the brain. Reticular formation: Network of neurons that extends from the spinal cord, through the hindbrain and Midbrain. Plays a role in the sleep/wake cycle, arousal, attention, pain, and touch Disorders associated with the Midbrain. Parkinson's disease (PD): Degeneration of the dopaminergic neurons in the substantianigra is associated with the tremors, rigidity, and poor motor control seen in PD. Drug addiction: The pleasurable effects of drugs as well as their addictive qualities are associated with the functions of the VTA |
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| Characteristics and definition of Mirror Neurons 1. Type of visuomotor neuron that fires both when an individual produces a motor action and when the individual observes another individual perform the same motor action 2. Originally discovered in studies of the functioning of neurons in the monkey's premotor cortex 3. In humans fMRI, PET, and EEG studies provide evidence for the existence of Mirror Neurons in the motor cortex in humans Function of Mirror Neurons 1. Help plan and execute our own movement and help interpret the movements of others around us, understand facial expressions and intentions 2. Play a key role in learning because they allow for learning through observation and imitation and not trial and error 3. Contribute for learning associated with social cognition and empathy The role of Mirror Neurons in autism 1. Autism, a developmental disability that includes delays in socialization, communication, and the presence of restricted and repetitive bxs 2. Autism is also associated with deficits in imitation and social cognition, therefore, Mirror Neurons have been a recent focus of autism research Studies with Mirror Neurons 1. In children with autism activity of Mirror Neurons is suppressed during the observation of the actions of others (including observation of facial expressions) 2. Study with monkeys has revealed that some Mirror Neurons may only be active while the subject is watching an activity being performed in close proximity to itself, while others are activated in response to any activity (irrespective of how far the subject is from the activity being performed) 3. Another study found that while Mirror Neurons fire both in response to performing an action and to observing an action, the Mirror Neurons had the highest level of activity when the subjects were instructed to both observe and imitate the task |
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Term
| Pituitary Gland, Hypothalamic-Pituitary-Adrenal Axis (HPA) |
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Definition
| HPA axis - the hypothalamus, pituitary gland, and adrenal cortex 1. in long-term stress - Responsible for releasing cortisol, the "stress hormone" Anterior Pituitary lobe 1. Controls the release of various hormones from endocrine organs: a. Somatropin: Also called growth hormone (GH); promotes growth by increasing uptake of glucose and amino acids, increases protein synthesis and inhibits fat breakdown; GH levels monitored through feedback loop; stunted growth or excessive growth occurs when balance is disrupted Thyrotropin 1. Thyroid-stimulating hormones that modulate metabolism in the thyroid gland Adrenocorticotropin 1. Produced in stressful situations and stimulate release of hormones by the adrenal gland Gonadotropins 1. Regulate the gonads and the release of hormones that are necessary for sexual maturation a. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH): In females, LH and FSH stimulate ovarian development; in males, FSH is essential for spermatogenesis and LH promotes testosterone synthesis b. Premature activity of the Hypothalamic-Pituitary-Gonadotropic Axis can lead to early sexual maturation known as precocious puberty Posterior Pituitary lobe 1. Axons of neurons located in the hypothalamus terminate in the posterior Pituitary and release two hormones, which are made within the hypothalamus: a. Anti diuretic hormone (ADH, concentrates urine), and oxytocin (uterine and prostate gland contractions) b. ADH: Stimulates re-absorption of water by the kidneys c. Oxytocin: Initiates contraction of mammary glands to produce milk; initiates uterus contractions during labor; responsible for prostrate contractions in males HPA Axis 1. Includes the paraventricular nucleus of the hypothalamus a. Contains endocrine neurons that synthesize and secrete vasopressin and corticotroprin-releasing hormone (CRH) b. Regulate the anterior lobe of the Pituitary Gland c. Stimulates the secretion of adrenocorticotropin hormone (ACTH): ACTH acts on the adrenal cortices, which produce glucocorticoid hormones (e.g., cortisol); cortisol is a major stress hormone that affects brain function; the glucocorticoids in turn suppress CRH and ACTH to form a negative feedback cycle to the hypothalamus and Pituitary 2. Release of CRH from the hypothalamus is influenced by stress and the sleep/wake cycle a. Anatomical connections between brain areas such as the amygdala and hippocampus are related to HPA Axis activity b. Increased production of cortisol mediates reactions to stress, facilitating an adaptive phase of a general adaptation syndrome in which alarm reactions including the immune response are suppressed c. Atrophy of the hippocampus in humans and animals exposed to severe stress is believed to be caused by prolonged exposure to high concentrations of cortisol; hippocampus abnormalities may reduce the memory resources available to help a body formulate appropriate reactions to stress d. Abnormal HPA axis activity has been implicated in a wide range of psychological disorders, including anxiety disorder, bipolar disorder, PTSD, and MDD General Adaptation Syndrome: Hans Selye 1. Alarm Reaction: all resources allocated to fight stressor 2. Resistance Stage: resources continue to fight while adjusting functioning to continue life in the midst of stress 3. Exhaustion Stage: resources are depleted, decreased immune system Accounts for stress-related illnesses and psychiatric problems wide-spread in industrial societies. |
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Definition
| 1. Located in the dorsal half of the diencephalon 2. Relay station for all senses except olfactory 3. Most sensory input that the cortex receives arrives via the Thalamus 4. The Thalamus is considered the brain's relay system a. Divided up into multiple nuclei b. Lateral geniculate nucleus: receives input from the eyes; projects to the primary visual cortex c. Medial geniculate nucleus: receives information from the inner ear 5. The Thalamus also helps transmit information from one region of the brain to another a. The ventrolateral nucleus receives information from the cerebellum and sends information to the primary motor cortex b. When processing emotionally arousing stimuli, the Thalamus relays information to the primary visual cortex and the amygdale 6. The Thalamus is involved with focusing attention on stimuli and discriminating between sounds to distinguish language and other noises |
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| 1. Located in an area of the brain known as the metencephalon 2. Located in the back of the brain, underneath the cerebral hemispheres 3. Made up of two hemispheres and a cortex Function of the Cerebellum 1. Responsible for all coordinated body movement, precision of movement, posture, and balance 2. May be associated with other functions, as evidenced by non-movement related activation in neuroimaging studies 3. Receives input from the brain stem and spinal cord 4. Receives information from the vestibular system, located in the inner ear, which helps to maintain balance and spatial orientation Damage to Cerebellum 1. Damage to or lesions in the Cerebellum lead to difficulties with coordinated movement, balance, and posture 2. Ataxia – lack of coordinated motor movements, which can range from atypical gait and postural instability to impaired coordination of voluntary movements 3. Type of ataxia present depends on location of lesion or damage 4. Nystagmus is characterized by involuntary jerky eye movements and an inability to sustain a fixed gaze Cerebellum's role in learning and memory 1. Cerebellum contains memory cells that allow for learning new skills through trial and error 2. Procedural memory – motor memory that is created after an action is performed repetitively 3. Conditioned learning – learning that occurs due to a conditioned response, such as pulling one's hand away from a hot object or the eye-blink response, blinking in response to a tone alone after the tone has been repeatedly paired with a puff of air |
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Term
| Genetics and Genetic Disorders |
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Definition
| 1. Genetics is the study of the inherited nucleic material in our bodies 2. The cells in our bodies contain two types of nucleic materials: deoxyribonucleic acids (DNA), and ribonucleic acids (RNA) 3. DNA is considered most organisms' primary Genetic material 4. RNA is made from DNA in a process called transcription (some viruses do carry RNA as their primary Genetic material) Structure of DNA 1. Human DNA is made up of two long strands of four nucleotides: Adenine (A), Guanine (G), Cytosine (C), and Thymine (T) 2. The two strands form a double helix; the two strands that wind around each other and are connected to each other like a ladder 3. Each rung of the "ladder" is made up of two complementary nucleotides (i.e., each A or G in the first strand has a T or C respectively in its corresponding location in the complementary strand, and vice versa) 4. Each long strand of nucleic acid is tightly coiled and wrapped around proteins; these double stranded strings of DNA are called chromosomes Chromosomes 1. Humans have 23 pairs of human chromosomes (making a total of 46) 2. 23 chromosomes are inherited from the mothers and 23 from the fathers 3. The last pair of chromosomes is called the sex chromosomes, and determines a child's sex 4. If a child inherited two X chromosomes, one from the mother, and the other from the father, then she will be female; if instead, the child inherited an X chromosome from the mother and a Y chromosome from the father, then he will be male 5. Chromosomes are housed in the nucleus of cells 6. Two processes of cell divisions: a. Meiosis: used to produce gametes, which are the sex cells (i.e. sperm and ovum); gametes contain half the number of chromosomes as the parent cell (23 total) b. Mitosis: normal cell division that results in daughter cells with the same number of chromosomes as the parent cell; mitosis is used for cell reproduction during growth and repair Genetic Disorders involving chromosomal abnormalities 1. Errors occurring during meiosis result in a variety of disorders where there are abnormal numbers of chromosomes 2. Down syndrome: occurs when an individual inherits three chromosome 21 (a phenomenon called aneuploidy) 3. Other chromosomes where similar errors may occur and result in the birth of a child with a Genetic Disorder are 13, 18, X and Y 4. Other aneuploidies typically do not survive to birth, and often result in fetal miscarriages 5. Sex-linked chromosomal disorders: a. Klinefelter's syndrome occurs when an individual inherits two X, and one Y chromosome; such an individual is anatomically male, but with diminished genitalia and severely decreased fertility b. Turner’s syndrome, on the other hand, occurs when an individual fails to inherit a second sex chromosome; these individuals only have one X chromosome (denoted XO), are anatomically female, although they face similar issues as those with Klinefelter's of diminished genitalia and infertility c. A condition with YO does not exist, where an individual only inherits a Y chromosome, probably because such a fetus is unable to survive to birth 6. Chromosomal disorders also occur when a piece of a chromosome is broken off, deleted, or translocated early on in the reproductive process; such individuals may have one normal and one partial chromosome in the defective pair; the larger the defect, the more severe the disorder these individuals develop 7. William's syndrome is caused by a deletion on chromosome seven Genetic Disorders involving dysfunctional genes 1. Most Genetic Disorders occur at the level of the gene and not that of the chromosome 2. Genes are short segments of nucleic acids; several genes are located on each chromosome, interspersed by long strings of nucleic acids 3. An error in replication (the process by which DNA is copied during reproduction) may result in a slightly altered Genetic sequence; the variant gene may then produce an abnormal protein that results in a disorder 4. The DNA in genes ultimately code for proteins, therefore a mutation in a gene may result in disrupted production of the protein that is coded for by that gene 5. Two-step process of making proteins from genes: first DNA is converted to RNA, a process called transcription; then, RNA is converted to protein, a process known as translation 6. If the necessary enzymes to make RNA are not present or inhibited, DNA cannot be converted into protein (Human Genome Program, 1992) 7. Conditions such as phenylketonuria and Von Willebrand disease are caused by abnormalities to specific genes |
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Term
| Huntington's Disease, Huntington's Chorea |
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Definition
| 1. Progressive and fatal genetic neurodegenerative disorder 2. Caused by mutation of a gene called huntingtin, located on the fourth chromosome 3. Autosomal dominant genetic disorder: a. Autosomal: Located on an autosomal chromosome (non-sex chromosome) b. Dominant: Only one copy of the defective gene is necessary to inherit the disease 4. An individual with HD has a 50 percent likelihood of giving birth to a child with the defective gene 5. Age of onset is typically in the mid 30s and 40s, although in rare cases sxs can start in childhood or adolescence 6. The sxs of HD are progressive and life expectancy is typically 10-25 years after onset of sxs. Sxs of Huntington's Disease 1. Motor sxs: a. Rapid irregular jerky movements of the arms, legs, and head (also known as chorea) b. Unsteady "dancing" gait c. Facial grimacing 2. Cognitive sxs: a. Some also develop dementia associated with disorientation and confusion, personality changes, impairments in memory, and agitation. b. Sxs of depression such as anhedonia, lack of energy, and irritability are often the first psychiatric sxs associated with the disease. 3. In many cases, depression, bxal problems, and cognitive difficulties may appear prior to motor sxs 4. Misdiagnosis may occur when family history is unknown The atypical huntingtin gene 1. The gene responsible for the development of HD is called the huntingtin gene and it codes for huntingtin protein 2. The gene contains a trinucleotide repeat; a sequence of three DNA bases, cytosine-adenine-guanosine (CAG), that code for glutamine, an amino acid, which get attached to the huntingtin protein as glutamine residues 3. CAG repeats between 7 and 35 times in individuals without HD and between 36 and 120 times in individuals with HD 4. Each repeat of CAG adds additional glutamine residues to the huntingtin protein 5. Individuals with HD make an abnormal huntingtin protein with a long chain of additional glutamines. This chain distorts the protein's shape and interferes with its normal functioning. 6. The exact mechanism by which the abnormal huntingtin protein affects the brain is not well understood 7. Over time nerve cells in the brain begin to degenerate and individuals with HD begin to show sxs 8. Age of onset of sxs is associated with the number of CAG repeats; the greater the number of repeats, the younger the age of onset. 9. Primarily associated with degeneration in the basal ganglia, comprised of the caudate nucleus and putamen HD is also associated with loss of neurons in the cerebral cortex |
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| 1. An autosomal recessive genetic disorder. Two recessive genes must be inherited from each parent in order to have PKU. Involves an inability to digest phenylalanine, due to lack of or severely deficient levels of phenylalanine hydroxylase, the enzyme needed to process phenylalanine. Individuals with PKU are unable to convert phenylalanine into tyrosine, resulting in high levels of phenylalanine in the blood Sxs. Mental retardation. Seizures. Microcephaly. Jerky movements of the arms and legs. Hyperactivity. Stunted growth. Unusual odor of the urine and skin. Diagnosis and Treatment. Mandatory blood testing in the United States for all newborns: heel stick shortly after birth. Managed effectively by adherence to diet extremely low in phenylalanine. Adults on phenylalanine-low diet into adulthood have better physical and mental health. Women with PKU who are pregnant or who are trying to become pregnant must adhere to the PKU diet in order to reduce risk to the fetus |
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| 1. Most common inherited bleeding disorder 2. Autosomal dominant genetic disorder a. Autosomal = non-sex chromosome b. Dominant = only one copy of the defective gene needed to inherit the disorder c. Chance of inheriting the disorder when one parent is afflicted is 50 percent d. Caused by a defect in the gene that codes for a protein called Von Willebrand factor (VWF) e. VWF promotes clotting by helping platelets stick together and attach to the walls of the blood vessel at the site of injury f. In Von Willebrand disease, there is either no VWF, it is reduced, or it is not functioning properly The disease can range from mild to severe, depending on how much vWF is present and how well it is functioning Sxs of Von Willebrand disease 1. Difficulty clotting after medical surgery or dental procedures 2. Bruising 3. Bleeding of the gums 4. Frequent nose bleeds 5. Extended bleeding time despite normal platelet counts Treatment of Von Willebrand disease 1. While mild cases may not require treatment and may go undiagnosed for many years more severe cases require routine treatment 2. Von Willebrand disease cannot be cured 3. Can typically be treated effectively through the use of: a.Medications – particularly Desmopressin (DDAVP), a synthetic hormone that promotes clotting b. Replacement therapies c. Sealants, which can be placed directly on a cut to control bleeding |
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| 1. Cluster of neurological disorders that are first observed in infancy or early childhood and persist throughout one's life. The disorder is non-infectious and non-progressive. Includes lifelong impairments in body movement and muscular coordination. Sxs Can range from mild to severe. Impairment in the ability to perform voluntary movements (ataxia). Muscle stiffness. Increased muscle tone (spasticity). Awkward gait. In severe case, may also be associated with increased drooling, learning disabilities, seizures, urinary and bowel problems, and hearing deficits. Causes. Brain damage at or after birth or (most commonly) in utero. When acquired in utero, may be due to: a. Result of infections b. Maternal health problems c. Insufficient oxygen available for the fetus When acquired after birth, may be due to: a. Viral encephalitis b. Oxygen deprivation from a seizure c.Head injury sustained in a motor vehicle accident, fall, or child abuse Contrary to the popular belief that CP results from lack of or decrease in oxygen at birth, researchers believe that this only accounts for a small percent of occurrences of CP. Prematurity, low birth weight, and multiple births increase the risk for CP. Genetics may play a role in some cases of CP Diagnosis and treatment Sxs may be present at birth, especially in severe cases. Diagnosis is typically made by age 2. In very mild cases, a diagnosis may not be made until age 4 or 5. There is no cure for CP. Treatments typically target motor skills and independent living skills. Treatment may include: a. Physical therapy b. Occupational therapy c. Assistive devices: muscle braces, walking aids, and wheelchairs d.Medicines: used to control seizures (if present), decrease muscle tone, and improve constipation |
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Definition
| 1. Prefrontal cortex a. Involved in executive function b. Planning c. Decision-making d. Attentional control e. Updating working memory 2. Damage to this regions associated with a. Personality changes b. Disturbances in planning, initiation, judgment, and goal-oriented bx 3. Motor Association cortex a. Planning movement 4. Motor cortex a. Executes movements 5. Prefrontal cortex subdivisions a. Dorsolateral prefrontal cortex (DLPFC) b. Associated with short term memory and top-down attentional control c. Damage to this region associated with difficulties with concentration/attention, and poor recall of recently learned information 6. Orbitofrontal cortex (OFC) a. Associated with judgment, self-monitoring, inhibition, and processing emotionally arousing stimuli b. Damage to this region associated with poor or heightened responses to threatening stimuli, poor decision making and judgment, and poor risk assessment c. Damage may also be associated with disinhibited bxs 7. Broca'sAreaa. Located in left inferior frontal cortex b. Involved in word retrieval c. Damage to this region may cause Broca's aphasia (an inability to retrieve words) 8. Motor Association Cortex a. Involved in planning muscle movements b. Damage to this area may cause difficulties coordinating the muscle movement required for speech 9. Primary Motor Cortex a. Responsible for carrying out muscle movements b. Damage to this region associated with difficulties with fine finger movements and a loss of speed and strength in the hands/limbs |
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Term
| Gerstmann's Syndrome, Angular Gyrus, Acalculia, Agraphia |
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Definition
| Sxs of Gerstmann's Syndrome Gerstmann's Syndrome was first described in 1924. Characterized by a combination of four specific impairments: a. Finger agnosia: Inability to identify fingers, differentiate them from one another, or orient them on command b. Right-left confusion c. Acalculia or dyscalculia: Difficulty understanding the rules of arithmetic d. Agraphia: Sxs of agraphia include frequent spelling errors, inappropriate use of upper- or lower-case letters, illegible writing, writing very slowly, and difficulty expressing thoughts in writing. Spatial difficulties, such as maintaining margins, sizing letters, etc., are also common in these patients. The writing difficulty occurs independently of a person's ability to read. Agraphia in Gerstmann's Syndrome is different from motor agraphia, which is caused by deficiencies in fine motor skills or poor muscle tone Cause of Gerstmann's Syndrome. Gerstmann's Syndrome typically occurs in adults as a result of stroke or brain injury. Gerstmann's Syndrome is thought to be caused by damage to the left parietal lobe, in the area of the angular gyrus. The angular gyrus: a. A structure located in the parietal lobe, just behind Wernicke's area.b. Located on the margin of the occipital and temporal lobes |
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Definition
| 1. It causes Acquired Immunodeficiency Syndrome (AIDS), a progressive, widespread, infectious disease 2. The majority of studies on HIV and AIDS occur in the United States, although disease is extremely widespread in developing countries in Asia and Africa 3. According to the CDC, as of 2006 a little more than 1 million individuals in the United States have HIV/AIDS 4. The majority of people with HIV are African American, homosexuals and bisexuals, and male 5. Intravenous drug users who have shared needles are also at much higher risk and represent 22 percent of the population with HIV 6. Persons who received blood transfusions prior to 1985, when HIV testing became more widespread, are also at risk 7. Mother to infant vertical transmission is the primary source of HIV infection in pediatric populations 9. Once HIV has been acquired, the disease progresses predictably in most individuals, and typically leads to death in seven to 10 years when untreated 10. Since the development of combination antiretroviral drug therapies in 1996, the life expectancy has greatly increased and may be as high as 25 years post-infection 11. HIV is a retrovirus, meaning that the virus contains Ribonucleic Acid (RNA) as its primary genetic material 12. To replicate in the host (human body), the viral RNA is converted back to DNA (a process known as reverse transcription), replicated into multiple copies, and then converted back to RNA 13. The virus attacks the CD4+T-cells of the human host's immune system 14. Progressively destroys the immune system leaving the individuals susceptible to opportunistic infections Stages of HIV infection 1. The progression from HIV infection to full-blown AIDS disease is characterized by four stages (acute, chronic [which is divided into asxatic and sxatic], and crisis or late stage) 2. The acute stage of HIV (also called primary HIV infection): a. Lasts for a few weeks after initial infection with HIV b. Characterized by the establishment of the virus in its new host c. Virus multiplies rapidly and begins to infect a large proportion of the body’s CD4+ T-cells d. Consequently, patients in the acute stage typically present with a non-specific infection (flu-like sxs) approximately three to six weeks after infection 3. Seroconversion: a. Following widespread viral infection, the body's immune system responds, and develops antibodies to fight the virus b. Since tests for HIV are designed to test for the presence of these antibodies, if seroconversion is not complete, the test may be negative although the individual is infectious c. The body fights off the infection and the sxs of acute infection subside 4. Chronic (asxatic) phase, also called stage 2: a. The body has built sufficient immunity to fight the virus; therefore, despite the virus' attacks upon the immune system, the immune system is able to contain the virus b. HIV virus continues to replicate and spread c. Typically lasts seven to 10 years, but may be lengthened considerably with medication d. In persons known as rapid-progressors, the chronic phase only lasts two to three years, while in others (non-progressors), despite a lack of treatment, this phase may last longer than 10 years e. Eventually, the proportion of infected immune cells increases and the infected individual's immune system rapidly deteriorates 5. Sxatic HIV infection (stage 3): a. Toward the end of the chronic phase, individuals become sxatic and have opportunistic infections (conditions that a healthy immune system would prevent) 6. Late stage HIV disease (crisis phase) is called AIDS a. Marked by a drastic reduction in host immunity b. AIDS is diagnosed by a combination of low count of CD4+T-cells and the presence of several severe opportunistic infections c. Opportunistic infections include neurological complications, viral and bacterial infections, and cancers d. AIDS dementia complex (ADC) is a condition that may occur at this stage that indicates central nervous system dysfunction e. Cognitive decline in ADC is similar to that in other dementias is evident, however unlike other dementias such as Alzheimer's disease, it may also have more widespread impact; affecting motor and bx in addition to cognition f. Unable to fight even the simplest of infections, these individuals eventually die from one of these complications Influence of psychosocial factors 1. Psychosocial factors such as intellectual functioning, age, and depression modified the natural course of HIV progression in infected individuals 2. HIV-infected individuals with lower intelligence quotients (IQ), older individuals, and those with somatic sxs of depression progressed more rapidly toward AIDS than individuals without these characteristics |
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Definition
| Wernicke's encephalopathy 1.A neurological disorder associated with alcoholism that may also be seen in patients with malnutrition and AIDS 2. Caused by thiamine (vitamin B-1) deficiency 3. Includes a triad of impairments: severe confusion, including inattentiveness and agitation, ataxia, and ocular (eye and vision-related) abnormalities 4. Ataxia: a. A neurological sx characterized by clumsy movements and poor coordination of muscles b. Often caused by damage to the cerebellum, which is responsible for maintaining balance and coordination c. Patients with Wernicke's disease may walk with a broad gait, or be unable to walk without losing their balance 5. Sxs can be treated with thiamine supplements (given intravenously as a fluid), which typically results in improvement but may not lead to complete recovery Korsakoff’s syndrome 1. Also a neurological disorder associated with alcoholism that may also be seen in patients with malnutrition and AIDS 2. Some researchers believe that Korsakoff'sSyndrome is simply a late-stage manifestation of Wernicke's disease 3. The term Wernicke-Korsakoff Syndrome represents the spectrum of sxs that comprise both disorders 4. Sxs of Korsakoff's syndrome: a. Severe anterograde amnesia (difficulty forming new memories) – may be linked with damage to the medial temporal lobes b. Retrograde amnesia (inability to recall old memories) – amnesia tends to span several decades in length, although it is more severe when recalling more recent time periods when compared with more remote time periods c. May result from diffuse brain damage to several cortical areas, particularly the association cortexes d. Confabulation – a process in which patients fill memory gaps with plausible stories that are untrue; they may or may not be aware that they are lying e. Poor content in conversation f. Lack of insight g. May be disinterested or distracted (apathy) 5. Treatment with B1 supplements may slow the progression of the syndrome but can not reverse it Physiological implications of thiamine deficiency 1. Thiamine deficiency interferes with the metabolism of carbohydrates 2. Carbohydrates are necessary for proper brain function 3. Leads to impaired cellular energy metabolism and brain damage in the medial temporal lobes, thalamus, mammilary bodies, cerebellum (particularly the purkinje cells), pons, and midbrain |
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Definition
| 1. Four types of blood cancer: Acute myelogenous Leukemia (AML); Chronicmyelogenous Leukemia (CML); Acute lymphocytic Leukemia (ALL); Chronic lymphocytic Leukemia (CLL) Myelogenous Leukemia (AML or CML) 1. Forms in bone marrow cells that are precursors of red blood cells, platelets, and white blood cells Lymphocytic Leukemia (ALL or CLL) 1. Forms in bone marrow cells that are designed to mature into lymphocytes Acute Leukemia (AML or ALL) 1. Fast-growing, aggressive cancers that form blast cells (myeloblasts or lymphoblasts) a. A small genetic change in one blast cell causes it to reproduce within a short time frame into almost a trillion defective and non-functional cells; they crowd the bone marrow and prevent the formation of normal red blood cells, leading to anemia and exhaustion b. Treatment typically begins with chemotherapy (with or without radiation) with the goal of killing as many cells as possible c. Treatment may also include bone marrow transplant d. Cranial irradiation is used to suppress the cancer from spreading to the brain Chronic Leukemia (CML or CLL) 1. Does not occur in blast cells, and is therefore slower growing and much less aggressive 2. The defective cell that starts the cancer begins by making blood cells (red, white, and platelets) that are almost normal (and somewhat functional) 3. The number of red blood cells made decreases, while the count of white blood cells and platelets increases 4. Over time, white blood cell and platelet count can become high, leading to sluggish blood flow and severe anemia 5. CML treatments include therapies that more effectively target cancerous cells than traditional chemotherapy, which often kills both normal and cancerous cells a. These treatments do not cure cancer, but instead keep it in remission b. The only effective cure for CML is a bone marrow transplant 6. In CLL, dysfunctional lymphocytes begin to accumulate in the bone marrow, lymph nodes, and lymphoid organs such as the spleen a. The organs then become very enlarged are detected by palpation b. The increasing crowdedness of bone marrow makes it difficult for new blood cells to form, causing anemia c. The non-functional lymphocytes also interfere with the functioning of normal lymphocytes, causing the immune system to become weakened d. CLL is treated with chemotherapy or a new class of drugs (monoclonal antibodies) which target and kill cancerous cells e. Leukapheresis may be used to filter our white blood cells to thin the blood f. Removal of enlarged lymphoid organs also helps reduce the number of white blood cells in circulation |
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| 1. Recurrent, intense, throbbing headaches often originating on one side of the head Migraine characteristics 1. Second most common type of headache 2. Affect nearly 25 million Americans 3. More frequent among women 4. Last between 4 and 72 hours 5. May occur anywhere from several times a month to once a year 6. Cause is not known, but thought to have a genetic component Two key types of Migraines (those associated with an aura, and those which are not) 1. Migraine auras 2. Neurological disturbances that occur before the start of the Migraine 3. Auras may cause an individual to see flashing lights, blind spots, numbness, or tinnitus. They are also related to euphoria, irritability, food cravings, diarrhea and thirst Four stages to a migraine 1. Prodrome 2. The aura 3. Headache 4. Resolution a. Tiredness and body aches may last for up to a day Migraine treatments 1. Antiemetics to treat nausea and vomiting during attacks 2. Anti-inflammatory medications/opiates for pain 3. Bxal therapy 4. Relaxation therapy a. Nonsteroidal anti-inflammatory drugs (NSAIDS) b. Act on serotonin receptors in smooth muscles surrounding cranial blood vessels 5. Biofeedback a. Electromyographic biofeedback (thermal biofeedback) b. Identify psychosocial triggers c. Thermal biofeedback is more effective in treating Migraines than relaxation therapy 6. Beta Blockers (commonly used to treat high blood pressure) help reduce the severity and frequency of migraines. |
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Definition
| MS affects the central nervous system (CNS) Lesions in brain and spinal cord related to demyelization. Cause is unknown. Onset is usually in young adults, disproportionately affects females MS sxs may include: Numbness or weakness in muscles. Loss of vision (partial or complete) associated with pain during eye movement. Blurry/double vision. Tingling or sensations of pain in various parts of the body. Tremors. Lack of coordination. Unsteady gait (ataxia). Poor balance. Fatigue. Dizziness. Slurred speech. Forgetfulness and poor concentration. Muscles spasticity. Bowel/bladder/sexual dysfunction Four primary subtypes, based on pattern of disease progression Relapse-remitting(85-90 percent of individuals with MS): characterized by relapses followed by months to years of remission, with no new signs of disease activity. Secondary progressive: 65 percent of those with relapse-remitting type then begin to have progressive neurologic decline between acute attacks without any definite periods of remission. Primary-progressive: Approximately 10-15 percent of individuals who never have remission after their initial MS sxs. Characterized by progression of disability from onset, with no, or only occasional and minor, remissions and improvements. Progressive-relapsing: Steady neurologic decline after onset of the disorder but also suffer clear superimposed attacks. This is the least common of all subtypes |
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| 1. Also called convulsions. Related to abnormal electrical activity in the brain. Associated with changes in consciousness and/or bx. Between 1 and 5 percent of people will have at least one seizure in their lifetime. Prevalence of multiple seizures is much lower, occurring only in one in 200 individuals. Presence of a seizure does not indicate that the person has epilepsy. Seizures related to epilepsy are recurrent and not due to temporary causes. Causes of Seizures. Seizures can be idiopathic (due to unknown cause). Changes in brain tissue due to traumatic brain injury, brain tumor, disease, or stroke. Temporary causes of seizures include: drug use or withdrawal, disease, or fever. Genetic factors are also thought to contribute to epilepsy by predisposing an individual to seizures. Environmental factors largely influence whether or not an epileptic disorder will develop in a particular individual who is pre-disposed. Sxs and types of Seizures. Sxs of a seizure depend on whether the seizure involves focal disruption of brain activity (partial seizures) or global disruption (generalized seizures). Partial seizures a. Simplepartial:Do not involve loss of consciousness; may be associated with changes in sensory perception (i.e. change in how things look, sound, or smell), other sensory sxs, including dizziness or tingling, and involuntary jerking of a part of the body b.Complexpartial:Do involve an altered level of consciousness and a decreased ability to interact with the environment; are associated with staring or non-purposeful repetitive movements, such as walking in circles or smacking lips. Also associated with changes in mood and uncontrollable laughing or fear Generalized seizures: Due to atypical brain activity involving the entire brain a.Absence seizures (otherwise known as petit mal): Staring (with lack of awareness) and can also sometimes involve subtle body movements. b.Myoclonicseizures:Involve jerking or twitching of the limbs. Usually involve both sides of the body. c.Atonic seizures: Associated with loss of muscle tone and result in sudden collapse d.Grand mal(also known as tonic clonic) seizures:Loss of consciousness, stiffening, shaking, and/or convulsing of the entire body, and sometimes loss of bladder control. May be followed by confusion, fatigue, and headache Prior to onset of seizure, some individuals experience an aura. The aura can include specific sensory experiences (a smell, noise, or feeling) that consistently precede seizures that warn them of the upcoming seizure Diagnosis of Seizures Most frequently diagnosed using electroencephalograms (EEGs). Individuals with epilepsy often have atypical brain wave patterns even when they are not having a seizure. Other tests, such as blood tests, MRI, and computerized tomography (CT) scan may also be used to help determine potential causes of the seizure Treatment of Seizures Epilepsy is treated with anticonvulsant (i.e. antiepileptic) medications such as phenobarbital and Depakote. It is very important that anticonvulsant medication be taken as prescribed a. Depakote: requires regular blood tests to monitor liver functioning b. Phenobarbital: requires gradually tapering the medication when stopping it to avoid serious side effects, including seizures, hallucinations, hypertension, and insomnia In many cases, medications effectively control the seizures, so that the individual is seizure free. Others continue to have seizures, despite taking medications, but the severity and frequency of the seizures is reduced. Individuals with epilepsy also often reduce their risk of seizure through bxal changes. For example, use of alcohol, sleep deprivation, emotional stress, and other environmental factors can increase the likelihood that a seizure will occur among those with epilepsy. If the seizures are severe enough and do not respond to medications, surgery may be indicated to remove the focus of abnormality. This is most likely to be done when the origin of the seizure is limited to a specific, well-defined area of the brain that is not involved in vital functions |
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| Primary Sleep Disorders 1. Class of disorders that involved disrupted sleep 2. Sleep problems are not due to another mental disorders, medical condition, or a substance Dyssomnias 1. Abnormalities in amount, quality of time of sleep 2. Include: Primary Insomnia, Primary Hypersomnia, Narcolepsy, Breathing-Related Sleep Disorder, Circadian Rhythm Sleep Disorder Parasomnias 1. Abnormal bxal or physiological events during sleep 2. Include: Nightmare Disorder, Sleep Terror Disorder, and Sleepwalking Disorder Dyssomnias 1. Primary Insomnia: Ongoing difficulties falling asleep or staying asleep 2. Primary Hypersomnia: Excessive sleepiness that is evidenced by excessive nighttime or daytime sleep episodes 3. Narcolepsy: Sudden "sleep attack" that occurs without warning 4. Cataplexy: An attack that occurs during wakefulness which causes temporary muscle paralysis 5. Sleep Apnea (example of breathing-related sleep disorder): Characterized by pauses in breathing that occur during sleep 6. Circadian Rhythm Sleep Disorder: Results from a mismatch between the sleep-wake schedule required by an individual's environment and his/her own circadian sleep-wake schedule Parasomnias 1. Nightmare Disorder: Frequent, recurrent nightmares mostly during REM sleep 2. Sleep Terror Disorder: Abrupt awakenings that usually involve a panicky scream or cry; occur within the first third of the night, during sleep stage; when awoken, the individual typically has no memory of the dreams 3. Sleepwalking Disorder: Occurs when an individual is observed to engage in various activities while asleep; sleepwalking occurs during sleep stages 3 or 4 Non-DSM-IV-TR Sleep Disorders 1. REM Sleep Bx Disorder: Refers to the experience of atypical incomplete paralysis during REM sleep 2. Fatal Familial Insomnia (FFI): Genetically inherited disorder of insomnia that eventually leads to death due to lack of REM sleep |
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| Spinal cord consists of nerve fibers that extends from the brain 1. The central nervous system (CNS) consists of the brain and spinal cord 2. Spinal cord nerve fibers include: a. Efferent nerve fibers (carry information to organs) b. Afferent nerve fibers (carry information from organs) Spinal cord injuries (SCI) occur due to damage to the spinal cord 1. 11,000 SCIs happen per year 2. Young adults are at greater risk (particularly males) 3. SCIs can co-occur with traumatic brain injuries (TBI) 4. The spinal column can be divided into five segments, each containing a different number of vertebrae: a.7 Cervical (neck & arms) vertebrae (C1 to C7) b. 12 Thoracic (chest & arms) vertebrae (T1 to T12) c. 5 lumbar (legs) vertebrae (L1 to L5) d. 5 sacral vertebrae (S1 to S5, fused) 5. Categorization of SCIs a. "Complete" SCI - no voluntary motor or sensory function below the injury site b. "Incomplete" SCI - some voluntary and/or sensory function below the injury site is preserved American Spinal Injury Association (ASIA) classification system 1. ASIA A: No motor or sensory function preserved in S4-S5 (complete) 2. ASIA B: Preserved sensory but not motor function below the injury level and includes S4-S5 (incomplete) 3. ASIA C: Motor function is preserved below the level of the injury and more than half of the key muscles are less than grade 3 4. ASIA D: Motor function is preserved below the level of the injury and more than half of the key muscles are greater than grade 3 5. ASIA E: Normal neurological function despite the presence of an SCI; implies that an individual can have an SCI without having any neurological deficits that are detectable upon examination Quadriplegia 1.Injury of the spinal cord in the cervical column 2. Movement and sensation below the neck is lost indefinitely 3. Breathing problems may occur if the diaphragm is affected causing individuals to require a ventilator 4. Bladder, bowel, and sexual dysfunction problems often occur Paraplegia 1. Injury of spinal cord is severed below the first thoracic spinal nerve in the lumbar area 2. Retains upper body movement and sensation (including hands and arms) 3. Refers to loss of control and feeling below nipple line and down to the legs 4. Bladder, bowel, and sexual dysfunction often occur Hemiplegia 1. Paralysis in one half of the body 2. Most common in victims of stroke Paresis 1. Weakening in part of the body 2. Less severe than overall paralysis Hemiparesis 1. Half of the body is weakened Psychological sequelae of SCI 1. Adjustment to injury 2. Depression and/or anxiety 3. SES and social support |
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| Hemorrhagic Strokes 1. Caused by bleeding within the brain (intra-axial hemorrhage) or within the skull but outside of the brain (extra-axial hemorrhage) 2. May occur as a result of a weakened or malformed blood vessel or a traumatic brain injury 3. Causes brain damage by: loss of blood supply, distortion of brain tissue or toxicity of the blood in brain tissue 4. Most common type of strokes among people ages 18-45 5. Survival rate after a hemorrhagic stroke is approximately 20 percent. Ischemic Strokes 1. Disruption of blood flow due to a blockage in one of the blood vessels 2. Brain cells die due to lack of oxygen 3. May be caused by a blood clot (thrombosis) or a foreign object such as an air bubble, tumor, or plaque that becomes detached from the arterial wall (embolism) 4. Overall, ischemic Strokes are the most common type of Stroke and make up approximately 80 percent of all Strokes Types of ischemic Strokes 1. Middle cerebral artery (MCA) blockage is the most common type of ischemic Stroke Mortality rate of MCA stroke: 15 and 30 percent within one month following the event 2. Posterior cerebral artery (PCA) Strokes are less common and less severe than MCA Strokes 3. Death is rare following PCA Stroke 4. Sxs of PCA Stroke include: a. Severe visual deficits b. Visual agnosia – an inability to recognize or name objects despite seeing them c. Apperceptiveagnosia – difficulty drawing objects from memory d. Sensory loss Sxs of a Stroke 1. Sxs vary, depending on which artery is involved and which brain area is affected. Often include paralysis on one side of the body (hemiplegia), slurred speech, dizziness, and confusion 2. Aphasia – Impairments of language production or comprehension. Some form of aphasia occurs in approximately 35-40 percent of Stroke victims 3. Broca's aphasia – impairment of expressive language, characterized by: a. Slow, halting, labored speech b. Sentences that include disjointed words and lack function words c. Impaired intonation 4. Wernicke's aphasia – on the other hand, is a receptive language aphasia a. Language comprehension is impaired b. Fluent speech production c. Content of their speech is limited due to the misuse of words with similar sounds or meanings 5. Conduction aphasia – condition that results when the area that connects Broca's area and Wernicke's area is damaged. Ability to produce and comprehend language is retained but anomia is present 6. Motor skills – Frequently affected by a Stroke a. Ideomotor apraxia – inability to execute simple motor functions on command. Limb-kinetic apraxia – clumsy movements b. Oral-buccal-lingual apraxia – inability to perform movements of the face and jaw when instructed Risk factors of Stroke 1. Increased age 2. Atherosclerosis (build-up of cholesterol in the artery) 3. Hypertension (high blood pressure) 4. Sex – middle cerebral artery stroke is more common in males, with a ratio of males to females of 3:1 |
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| Temporal and Parietal Lobe Damage |
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Definition
| Temporal Lobe Damage 1. Involved with auditory, speech, and memory systems 2. Left Temporal Lobe damage can lead to impairments such as: Difficulties recognizing/producing language (Wernicke's aphasia) 3. Right Temporal Lobe damage can lead to impairments such as: Difficulties perceiving pitch, rhythm, and emotional tone of speech and difficulties perceiving music 4. Hippocampus damage can lead to impairments with storing and recalling information from long-term memory Parietal Lobe Damage 1. When the somatosensory cortex is damaged, loss of sensation in specific regions of the body may occur 2. Somatosensory cortex is mapped precisely to different organs, the area of injury predicts quite accurately the area of numbness 3. Injury to the posterior Parietal Lobes leads to impairment in visual guidance of hand and limb movements 4. Difficulties with proprioception 4. Damage to the left posterior parietal lobe can lead to apraxia, acalculia, and left-right confusion (i.e., Gerstmann's syndrome) 5. Damage to the right posterior Parietal Lobe can cause contralateral neglect and impairments in spatial cognition (i.e., difficulties with facial recognition) |
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| 1. Due to sudden trauma 2. Automobile accidents are the leading cause of TBI TBI classification system 1. Mild, Moderate, Severe 2. Glascow Coma Scale (GCS) a. Measures neurological response at time of injury b. GCS > 13 = mild TBI c. GCS 9 -12 = moderate TBI d. GCS < 8 = severe e. GCS has limited ability to predict outcome f. Other factors such as loss of consciousness (LOC) at time of injury and post-traumatic amnesia (PTA) should be taken into consideration Two predominant types of TBI: closed and open 1. Closed head injuries (also called non-penetrating/blunt/ "coup" injuries) a. Most common type of TBI b. A contusion occurs at the location of the blow c. Coup countercoup injuries occur when there is an injury at the site of the blow, but also a second injury due to the brain ricocheting inside the scalp d. Duration of LOC following a closed head injury is related to the severity of the resulting impairment 2. Open head injuries a. Occur when the skull is cracked or penetrated b. Sequalae is varied, but the sxs are often highly specific to the location of focal brain damage Secondary damage to brain due to TBI includes 1. Axon shearing 2. Diffuse lesions 3. Shearing fiber tracts (e.g., corpus callosum, anterior commissures) 4. Hemorrhage and brain clots that increase intracranial pressure (ICP) 5. Edema 6. Diffuse brain damage can lead to: a. Impaired cognitive abilities b. Executive function deficits c. Slow speed of processing d. Poor attention/concentration 7. Fatigue 8. Changes in physical ability 9. Changes in personality Recovery from brain damage 1. Bulk of recovery occurs during the first six to nine months following the event 2. 80-95 percent of recovery occurs within 12-18 months 3. Maximum recovery happens 2-3 years following injury 4. Reduced quality of life is typically expected 5. Risk for subsequent TBI is higher than those who have never sustained a TBI Post-concussion syndrome (PCS) is considered a mild form of TBI 1. Sxs may include a. Memory and attention/concentration impairments b. Fatigue c. Insomnia d. Headaches e. Vertigo f. Dizziness g. Irritability h. Aggressiveness i. Anxiety/depression j. Sensory (visual/hearing/smell) impairments |
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| Different neurotransmitters are implicated in various psychological disorders 1. Some disorders are caused by excessive levels of certain neurotransmitters, while others may result from deficits 2. Psychotropic medications exert their effects at the synaptic cleft between neurons (the point of neurotransmitter release by one cell, and receipt by the adjacent) Agonists 1. Medications that enhance synaptic transmission and increase post-synaptic effects Antagonists 1. Medications that inhibit synaptic transmission and decrease post-synaptic effects Competitive Agonists and Antagonists 1. Molecules that share structural similarities with a particular neurotransmitter 2. Mimics the neurotransmitter and bind to the same site on receptors that the neurotransmitter typically binds to 3. Competitive Agonist increases post-synaptic effects by mimicking the neurotransmitter's effects 4. Competitive Antagonist occupies the binding site and prevents the neurotransmitter from binding, which results in reduced transmission and activity Noncompetitive Agonists and Antagonists 1. Typically do not share structural similarities with a neurotransmitter because they bind to sites on the receptor that are different from where the neurotransmitter binds 2. When bound to a receptor site, they alter its shape 3. This changes the receptor's affinity for the neurotransmitter 4. Affinity can be described as the force of attraction between the neurotransmitter and the receptor, and refers to how potently a neurotransmitter binds to a receptor site; higher affinity results in more potent binding and vice versa 5. Noncompetitive Agonists work to increase the receptor's affinity for the neurotransmitter, resulting in increased binding and higher post-synaptic effects 6. Noncompetitive Antagonists decrease the receptor's affinity for the neurotransmitter, causing decreased binding and post-synaptic effects Direct Agonists/Antagonists 1. Medications that exert their effects by mimicking the neurotransmitter and binding to its receptors Indirect Agonists/Antagonists 1. Medications that exert their effects by indirectly altering neurotransmitter release, uptake, or binding Inverse Agonists 1. Have the opposite pharmacological effect than the effect produced by a neurotransmitter Partial Agonists 1. Have a lesser effect than those produced by a neurotransmitter Medical application of Agonists/Antagonists 1. Older generation drugs (e.g., MAOIs) have lower specificities are associated with more side effects a. Highly specific drugs (e.g., SSRIs) are designed to minimize these problems 2. Drugs can be designed to be specific to a particular receptor (e.g., target D2, but not other dopamine receptors) |
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| 1. Often utilized in psychological treatment to control sxs and allow psychotherapy 2. Various classification systems include: chemical structure, clinical effect, and pharmacologic mechanism 3. Clinical effect classification useful to clinicians: Groups the drugs under the effects they appear to exert on the sxs of certain disorders Antidepressants 1. SSRIs: Prevent the reuptake of serotonin from the synapses, prolonging its availability and effects in the brain a. Popular SSRIs: Prozac (fluoxetine), Paxil (paroxetine), Zoloft (sertraline), Celexa (citalopram), Lexapro (escitralopram), and Luvox (fluvoxamine) b. Prescribed for depression, anxiety, OCD, eating disorders, and also aggressive bx, irritable-bowel syndrome, and fibromyalgia 2. SNRI Serotonin-norepinephrine reuptake inhibitors: Increase both serotonergic and noradrenergic activity a. Effexor (venlafaxine) and Cymbalta (duloxetine) b. SNRIs treat anxiety disorders, attention deficit-hyperactivity disorder (ADHD), and neuropathic pain 3. TCA Tricyclic Antidepressants: Exert a general inhibitory effect on the reuptake of all monoamine neurotransmitters, including norepinephrine, dopamine, and serotonin. Many side effects and dietary restrictions; typically prescribed only if SSRIs ineffective a. Tofranil (imipramine) and Anafranil (clomipramine) b. TCAs treat depression, anxiety, and obsessive-compulsive disorder, and neuropathic pain 4. MAOI Monoamine Oxidase Inhibitors (MAOI): Inhibit the activity of monoamine oxidase, which breaks down monoamines and thereby increases serotonin, dopamine, and norepinephrine levels in the brain. They are particularly effective in the treatment of atypical depression and have been found to help people quit smoking. In general, however, because they cause more side effects and have more drug and dietary interactions than SSRIs and TCAs, they are typically reserved as last-option antidepressants a. MAOIs brand-names include: Nardil (phenelzine), Parnate (tranylcypromine) and Emsam (selegiline, the newly developed patch)Anti-obsessional 1. This is a useful sub-category of the main antidepressant list, emphasized because of their effects on obsessive thoughts (via serotonergic action) 2. It is mostly comprised of SSRIs and includes Prozac, Zoloft, Paxil, Luvox, Celexa, Lexapro and also the TCA Anafrenil (clomipramine) Mood stabilizers and anti-convulsants 1. This is a class of drugs commonly used to treat bipolar disorder 2. The anti-convulsants were traditionally manufactured for the treatment of epileptic seizures, but subsequently found useful also as mood stabilizers 3. Examples include: Eskalith and Lithonate (lithium carbonate), Symbiax (a synthesis of olanzapine and fluoxetine), Tegretol (carbamazepine), Trileptal (oxcarbazepine), Depakote (divalproex), Lamictal (lamotrigine), Topomax (topiramate) and Gabirtril (tiagabine) Psychostimulants 1. Widely used in the treatment of attention deficit disorders 2. Includes "blockbusters" Ritalin and Concerta (methylphenidate), Dexedrine (dextroamphetamine) and Adderall (d- and l- amphetamine) Antipsychotics 1. These medications are mainly used to treat psychotic illness; they can also be used as adjuncts for depressive disorders when appropriate 2. This class can be further divided in low and high potency, as well as typical (traditional) and atypical (newer) a. Low Potency only means that a higher dosage is needed for the desired effect, and does not have to do with side effects and sedative power. Low Potency antipsychotics are known to have significant side effects and sedative power. b. Low Potency medications include: Thorazine (chlorpromazine), Mellaril (thioridazine), Clozaril (Clozapine) and Seroquil (quietapine) c. High Potency medications include: Loxitane (loxapine), Stelazine (trifluoperazine), Prolixin (fluphenazine), Navane (thiothixene), Haldol (Haloperidol), Risperdal (risperidone), Zyprexa (olanzapine) and Abilify (aripiprazole), among others Anti-anxiety 1. Can be further divide into Benzodiazepines and Other Anti-Anxiety Agents 2. They are widely used to treat both anxiety and mood disorders, and can be adjuncts in antipsychotic regimes 3. Benzodiazepines include: Valium (diazepam), Librium (chlordiazepoxide), Klonopin (clonazepam), and Ativan (lorazepan) 4. Other anti-anxiety agents include: BuSpar (buspirone), Neurontin (gabapentin), and the beta-blocker Inderol (propanolol) Hypnotics 1. This class includes mostly "sleepers," such as Dalmane (flurazepam), Doral (quazepam), Restoril (temazepan); the newer Ambien (zolpidem), Sonata (zaleplan) and Lunesta (eszoplclone), as well as the antihistaminic Benadryl (diphenhydramine) for its sedative side effects Over the counter compounds and natural/herbal medications 1. These products have been shown to treat psychological conditions in clinical trials 2. They include: St. John's Wort (an herbal product shown to treat depression and anxiety), SAM-e (shown effective for depression), and Omega-3 (shown effective for depression and bipolar disorder) 3. Use judgment when using them |
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| Selective serotonin reuptake inhibitors (SSRIs) 1. Serotonin agonists – prevent the reuptake of serotonin from synapses, thereby prolonging the effects of serotonin 2. Indication: a. Most popular treatment for serotonergic imbalances b. Primarily used to treat disorders such as depression c. Some anxiety disorders d. Obsessive-compulsive disorder (OCD) e. Aggressive bx f. Irritable-bowel syndrome g. Fibromyalgia g. Eating disorders (e.g., bulimia nervosa, which is associated with low levels of serotonin) 3. Examples of SSRIs: Prozac (fluoxetine) is one of the most common SSRIs used to treat depression, Paxil (paroxetine), Zoloft (sertraline), Celexa (citalopram), Lexapro (escitralopram), and Luvox (fluvoxamine) 4. SSRIs produce fewer side effects than MAOIs and Tricyclic Antidepressants, making them a more popular option 5. Side effects: Dry mouth, vivid dreams, constipation, sexual dysfunction, nausea, drowsiness, dizziness, changes in appetite, weight loss or gain, suicidality, and liver or kidney impairment. a. Side effects typically diminish within the first few weeks of taking the medication b. SSRI regimens are usually started at a low dose and gradually increased to reduce the risk of side effects c. Abrupt early discontinuation of the medication is not advisable Serotonin-norepinephrine reuptake inhibitors (SNRI) 1. Work to increase both serotonergic and noradrenergic activity 2. SNRIs include Effexor (venlafaxine), Cymbalta (duloxetine) and Wellbutrin (bupropion), among others 3. SNRIs are used to treat anxiety disorders, attention deficit-hyperactivity disorder (ADHD), and neuropathic pain 4. Side effects of SNRIs are similar to those of SSRIs Tricyclic Antidepressants (TCA) 1. Class of Antidepressant medications used since the 1950s 2. Exert general effect on the reuptake of all monoamine neurotransmitters, including norepinephrine, dopamine, and serotonin 3. TCAs also have affinity for muscarinic receptors 4. Produce fewer side effects than MAOIs 5. Not as effective as SSRIs 6. Used in the treatment of: depression, anxiety, obsessive-compulsive disorder, and neuropathic pain 7. Commonly used TCAs include imipramine (Tofranil) and clomipramine (Anafranil) 8. Side effects of TCAs: a. Generally more severe than that of SSRIs b. Include dry mouth, blurred vision, constipation, difficulty with urination, and hyperthermia c. Other side effects include anxiety, drowsiness (somnolence), confusion, increased appetite, decreased sexual ability, and some cardiovascular effects d. Similar to SSRIs, side effects typically disappear in a few weeks and are better tolerated when the medication is slowly increased e. TCA toxicity can lead to severe cardiovascular and neurologic effects and is often fatal Monoamine oxidase inhibitors (MAOI) 1. First class of Antidepressants to be developed 2. MAOIs inhibit the activity of monoamine oxidase, which breaks down monoamines and thereby increases serotonin, dopamine, and norephinephrine levels in the brain 3. Cause more side effects and have more drug and dietary interactions than SSRIs and TCAs, therefore they are typically reserved as a last-option Antidepressant 4. The recently developed MAOI skin patch (transdermal patch) reduces these risks 5. Interactions between MAOIs chemicals (e.g., tyramine) in certain foods and other drugs may result in hypertensive crises; thus, individuals taking MAOIs should avoid consuming foods that contain high levels of tyramine, such as aged cheese, aged wines, liver, beer, and soy products 6. MAOIs are particularly effective in the treatment of atypical depression and have been found to help people quit smoking 7. Some common MAOIs include isocarboxazid (Marplan), iproniazad (Iprozid), and phenelzine (Nardil) Serotonin syndrome 1. Both SSNIs and MAOIs can cause serotonin syndrome if taken in combination with SSRIs, tryptophan, illicit substances, or other over-the-counter medications such as Saint John's Wort (itself thought to be a MAOI), which are known to increase serotonin levels 2. Serotonin syndrome is a severe and potentially fatal condition, which includes agitation, restlessness, rapid heart rate, dilated pupils, loss of muscle coordination, and cognitive sxs (e.g., hallucinations, confusion) Use of Antidepressants in other populations 1. Both panic disorder and chronic pain problems are commonly treated prophylactically with Antidepressants 2. There is little concern in prescribing Antidepressants to someone who has schizophrenia and is depressed 3. Pregnant women – neonates born to mothers who were taking SSRIs during pregnancy may suffer from SSRI withdrawal and may be at a greater risk for certain perinatal conditions 4. Studies have shown that Prozac, Zoloft, and Paxil may cause increased agitation, aggression, psychosis, and suicidality in some individuals, particularly adolescents 5. Although the risk of cardiovascular accidents is lower in SSRIs, there still remains some risk; therefore use of SSRIs for individuals with coronary artery disease is contraindicated 6. Most significant concern in prescribing Antidepressants is for someone who has bipolar disorder, as administration of an antidepressant may trigger a manic episode |
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| Antipsychotic Medications and Side Effects |
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| Psychosis definition 1. A sudden or gradual loss of contact with reality 2. Characterized by the development of delusions, hallucinations, and disorganized bx 3. Psychosis can be affiliated with a wide range of disorders, including: bipolar disorder, major depressive disorder, brain tumors, seizure disorder, schizophrenia, dementia, and stroke Antipsychotic Medications 1. Block D2 dopamine receptors Treatment of psychotic sxs with "typical" Antipsychotic Medications 1. Focused on sx management 2. Antipsychotic side effects can be severe: a. Patients discontinue medications due to side effects b. Akathisia is the most common side effect: Involves feeling dysphoric, restless, tapping of feet, rocking and shifting Early ("typical") Antipsychotic Medications 1. Neuroleptic medications such as Thorazine and Haloperidol 2. Effective in controlling positive sxs, such as hallucinations and delusions 3. Often ineffective in treating negative sxs, including anhedonia and dulled emotionality 4. Typical Antipsychotics are thought to block dopamine receptors, along with others, leading to a range of unintended side effects: a. Anticholinergic side effects include: Dry mouth, difficulty urinating, constipation, blurry vision b. Adrenergic side effects include: Postural hypotension and sexual dysfunction c. Histaminergic side effects include: Increased sedation and gradual weight gain d. Extrapyramidal Side Effects (EPS): Due to interference with the dopamine system; Parkinsonian-like sxs; tremor, body rigidity e. Dystonia: An acute side effect that occurs within a few days of treatment onset; involuntary muscle contractions that lead to postural abnormalities; difficulty swallowing (dysphagia); uncontrollable eye movements; blank stares (oculogyric crisis)f. Akathisia: Refers to a sense of distress and restlessness; rocking back and forth, shuffling, pacing, or other repetitive movements g. Tardive Dyskinesia (TD): Results from chronic antipsychotic use; sxs include involuntary, uncontrollable, restless movements (facial grimaces, tongue protusions, eye blinking, and limb movements) h. Neuroleptic malignant syndrome (NMS): Potentially fatal syndrome associated; sxs include severe muscle rigidity and hyperthermia, diaphoresis, dysphagia, tremor, incontinence, changes in consciousness, mutism, tachycardia, elevated/labile blood pressure, leucytosis, and muscle injury; onset of NMS usually occurs within four weeks of beginning a neuroleptic medication Treatment with new class of Antipsychotics "atypical Antipsychotics" 1. Atypical Antipsychotics serve as serotonin and dopamine antagonists 2. Include clozapine, risperidone, quetipaine, olanzapine, and ziprasidone 3. Treat negative sxs 4. Increased effectiveness in treatment-resistant patients 5. Produce fewer EPS effects 6. Clozapine is associated with a risk of agranulocytosis, and requires careful monitoring of blood levels; Agranulocytosis has not been associated with other atypical Antipsychotics |
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| 1. Work on gamma-aminobutyric acid (GABA) receptors in the brain 2. Benzodiazepines are indirect GABA agonists 3. They cause a structural change in the GABA receptor that increases its affinity for GABA 4. Increased GABA activity results in CNS depression 5. Used to treat anxiety disorders (especially panic disorder), agitation, seizures, and muscle spasms Typical side effects include 1. Sleepiness, confusion, impaired judgment, unsteadiness, and anterograde amnesia 2. Impair the ability to safely operate vehicles or machinery 3. Paradoxical affects, such as increased anxiety or suicidal ideation may occur Commonly used Benzodiazepines include 1. Xanax, Valium, Ativan, Klonopin, and Restoril 2. Short acting: Ativan and Xanax a. Act quickly, have short half-lives, and are eliminated quickly from the body b. Lower addiction property, used when immediate and temporary relief is critical c. Are associated with more amnesic effects 3. Long acting: Valium and Klonopin a. Have lengthy elimination times and accumulate in the body b. Greater potential for addiction c. Used to treat insomnia or generalized anxiety disorder 4. Long-term use precautions: a. Results in tolerance and dependence as well as cross-tolerance b. If stopped abruptly, can produce serious withdrawal sxs, including insomnia, vivid dreams, increased anxiety, tachycardia, tremors, perspiration, tinnitus, and depression. Abrupt cessation from very long-term use may result in catatonia, delusions, psychosis, delirium, and even death c. Patients must be weaned of Benzodiazepines gradually and carefully Research findings 1. Amygdala is a primary site of Benzodiazepine action 2. Anxiety disorders are thought to be related to the reduction in the number of GABA receptors or to the effects of a neuromodulator that blocks the benzodiazepine binding site and produces an antagonistic effect |
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| Definition and effects of opiates Class of drugs that contain opium. Includes the narcotics morphine, oxycodone, and methadone. Codeine and heroin are also opiates and are synthesized from morphine. Primarily used medically to treat severe pain and maintenance treatment for addiction. Provide a euphoric sensation, sometimes referred to as a "rush." Also have an analgesic, or pain reducing, effect. Other effects include cough suppression, constipation, sedation and depression of respiration. Administration: orally, subcutaneously (under the skin), through intravenous (IV) injections (directly into the veins), or smoked. Continuous use of opiates produces tolerance -- the opiate user must continually increase the dosage of the drug in order to achieve the same "high" a. Tolerance is a result of the desensitization of the opiate receptors, which can last for hours to days after last use b.An opiate overdose may result in a coma with respiratory distress or failure, cardiac arrest, and death Opiates can be lethal when used in combination with other CNS depressants, as the combination can exacerbate respiratory depression. According to Inaba and Cohen, opiate overdose (by itself or in combination with depressants) is responsible for 4,000-5,000 deaths per year Opiates' effect on the brain Easily cross the blood-brain barrier because of their similarity to the brain's endogenous opioids, including endorphins and enkephalins -- the brain's natural pain relievers. Opiates bind to receptors throughout the brain. Pleasurable effects of opiates are primarily related to their effect in the ventral tegmental area, where opiates function to increase the amount of dopamine available, by blocking the release of GABA. Opiates function to decrease pain by blocking the effects of Substance P, a neuropeptide that is associated with pain perception. Addiction to opiates is easy to develop. Approximately 4.6 million Americans use an illicit opiate prescription every month. Neurological changes are often seen in individuals who chronically use opiates and include alterations to the opiate receptors in the hippocampus, the cerebral cortex, and the amygdale. Opiate withdrawal. Opiate withdrawal occurs after prolonged use (usually several weeks). Generally begins within 12 hours of the last administration. Often leads the user to continue use in order to avoid full-blown withdrawal sxs. Sxs include dysphoria, anxiety, watering eyes, runny nose, yawning, sweating, restlessness, irritability, tremor, nausea, vomiting, diarrhea, increased blood pressure and heart rate, chills, cramps, and muscle aches. Sxs can last anywhere from a week to ten days after last use and are not usually lethal |
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Definition
| 1. Inability to perceive/identify a stimulus secondary to brain damage Can be visual, tactile, or auditory 1. Subcategories include a. Prosopagnosia: Difficulties identifying faces b. Auditory Agnosia: Difficulties recognizing sounds c. Tactile Agnosia: Difficulties recognizing common objects through touch d. Autotopagnosia: Difficulties naming body parts e. Finger Agnosia (subcategory of autotopagnosia): Difficulties distinguishing between various fingers f. Simultanagnosia: The ability to only recognize one object in the visual field at a time g. Form Agnosia: The ability to see details, but not the whole h. Anosognosia: A condition where individuals are unaware of their own agnosia impairments 2. ApperceptiveAgnosia a. Caused by damage to brain regions that are involved with early processing of stimuli (e.g, causes incoming stimulus to not be perceived correctly) b. Individual's ability to identify a perceived object may be intact, but the stimuli sent downstream for identification is jumbled 3. Associative Agnosia a. Results from brain damage that affects later stages of the identification process b. Objects may be perceived correctly, but individuals with associative agnosia will have difficulty identifying the object c. Individuals might be able to identify the function or copy an image of the object, but they are unable to accurately identify/name it |
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| Anterograde and Retrograde Amnesia |
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Definition
| 1. Amnesia is a general term that refers to impairments in or loss of memory. There are organic and psychogenic causes of amnesia Organic causes Amnesia can occur as a result of brain damage due to surgery, stroke, trauma, substance abuse, electro-convulsive therapy, brain infections or other factors. Heavy drinking can result in blackouts, a type of Anterograde Amnesia. Chronic consumption of alcohol can produce a syndrome called Korsakoff's syndrome, which causes severe Anterograde and some Retrograde Amnesia due to permanent brain damage. Benzodiazepines can also cause Anterograde Amnesia. The "date-rape" drug is comprised of benzodiazepines and other chemical substances that also produce Anterograde Amnesia. Anterograde Amnesia can also be caused by brain damage, due to a concussion, stroke, or neurosurgical removal of certain brain regions The CA1 region of the hippocampus, which is particularly sensitive to lack of oxygen, is often damaged during stroke. The case of H.M.:. a. Most famous case study of human memory. b. Underwent bilateral, medial temporal lobectomy to relieve him of severe epilepsy. c. Following surgery, H.M. had severe and total Anterograde Amnesia. d. Had partial Retrograde Amnesia, and more specifically "temporally graded Retrograde Amnesia," able to recall events in his early childhood; however, lost memories of events that occurred closer to his surgery. Psychogenic causes. Of psychological origins: intense stress due to traumatic event, such as witnessing or being the subject of crime, war combat, etc., and other traumatic events. Amnesia may be temporary or permanent. Permanent amnesia is most often related to organic factors. Temporary Amnesia is mostly related to psychological reasons, but may also result from milder traumatic brain injury. As the memory returns, it does so in a temporal fashion, with the memories furthest away from the trauma returning before those closer to the traumatic event. Amnesia does not affect an individual's awareness, attention span, personality, or identity. Sxs of Anterograde Amnesia. Ability to recall memories that were formed prior to the onset of amnesia, but inability to recall events that occur after the onset. Although often referred to as short-term memory loss, it appears that the deficit occurs in long-term coding of events. Specifically associated with inability to encode declarative (or explicit) memories, which includes memories that are available for conscious recall such as memories of events (episodic memory) or facts (semantic memory). Non-declarative, also known as implicit or procedural, memory is unaffected. This includes: perceptual, stimulus-response, and motor activities that are learned unconsciously. Patients with Anterograde Amnesia are unable to talk about events that have occurred since the traumatic episode, but they are able to learn procedural tasks. Patients with Anterograde Amnesia have intact short-term memory, so they are able to enjoy a television episode or card game from start to finish, but are unable to recall the show or game the next day. Anterograde Amnesia is often accompanied by some amount of Retrograde Amnesia. Two other types of Amnesia. Transient/Global amnesia occurs when a person forgets everything. There is no recall of anything. Dissociative memory occurs when personality/identity recall is impaired. |
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| Sxs and causes of Tachycardia and Bradycardia Tachycardia: rapid heart rate of more than 100 beats per minute. Causes of Tachycardia: a.Normal response to physiological stress b. Damage to the heart from heart disease or a previous heart attack c. Congenital heart defect d. Anxiety and stress e. Stimulant drug use f. Side effect of some psychotropic medications, such as lithium, carbamazepine (Tegretol), olanzepine (Zyprexa), and valproate Bradycardia: heart rate of less than 60 beats per minute. Causes of Bradycardia: a.Variety of heart defects b. Sinus node that is functioning improperly c. Hypothyroidism d. Medications e. Certain illegal drugs Treatment of Bradycardia Depends on the cause of the Bradycardia. If due to side effect of medication or hypothyroidism treatment will target those conditions. Uncontrollable Bradycardia that causes fainting or disabling fatigue may be treated with surgical implantation of a pacemaker Treatment of Tachycardia Some forms of Tachycardia are not harmful and do not require treatment.. Other forms can be treated through a.Medications b. Surgical interventions c. Lifestyle changes Most common medical treatment is beta blockers, which work by blocking beta-adrenergic receptors and, thereby, blocking the activity of catecholamines such as epinephrine (adrenaline) and norepinephrine. As a result, they suppress the body's fight-or-flight response, decrease anxiety, reduce tremor, and restore heart rate to normal. Characteristics of Beta Blockers Beta blockers are relatively non-specific, meaning that they bind and block all three types of beta-adrenergic receptors. Inhibit the function of epinephrine and norepinephrine on the sympathetic nervous system (i.e. inhibit the body’s fight or flight response). Beta blockers are used to treat other conditions such as anxiety because of their effect on the fight or flight response. Can be used to enhance performance in persons with stage fright. Most common side effects of beta blockers are low blood pressure (hypotension), Bradycardia, impairments in circulation, insomnia and difficulty sleeping, depression (as a result of decreased norepinephrine activity in the CNS), and exhaustion. The first beta blocker to be developed was propranolol (Tefera& Perry, 2007). |
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| Sxs of Delirium Sudden change in cognitive functioning. Memory impairments: a.Inability to recall events that took place since the onset of the delirium (anterograde amnesia) b.Inability to recall events that took place prior to the delirium (retrograde amnesia) Disruptions in language: a. Incoherent speech b. Inability to stop speech patterns Disorientation and confusion to time and place. Reduced alertness. Increased distractibility. Perceptual disturbances such as hallucinations. Changes in mood and personality Causes of Delirium Occurs due to a variety of mental and physical conditions, including: a. Substance intoxication b. High fever c. Head trauma d. Acute mania e. Severe dehydration f. Heart disease g. Liver failure h. Kidney failure i. Severe anemia j. Hypoglycemia k. Shock (such as following a surgery) l. A variety of metabolic conditions Delirium is a serious condition that requires immediate medical attention, as it is typically associated with a serious underlying disease or condition. Treatment of Delirium Typically temporary and shows improvement once the underlying condition has been treated. No medications specifically treat delirium. Medications may help with the agitation or aggression associated with delirium. Frequent orientation to time and place and the presence of familiar people and objects may be helpful in reducing confusion. Providing a calm, comfortable environment also reduces agitation and irritability. If the underlying cause is treated effectively, the delirium typically resolves within a week, although it may take longer for cognitive processes to completely return to baseline |
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| Causes 1. Among individuals with diabetes a. Results from too much insulin in the body b. Skipping meal and not adjusting insulin dose. 2. Individuals without diabetes a. May be associated with genetic metabolic conditions b. Over-production of insulin by the pancreas c. Insufficient carbohydrates intake among people who are very physically active d. Medications: large doses of aspirin and some prescription medications used to treat conditions such as pneumonia and malaria Sxs 1. Hunger 2. Nervousness or anxiety 3. Excessive sweating 4. Dizziness or fainting 5. Fatigue 6. Shakiness 7. Confusion 8. Difficulty speaking 9. Rapid heart rate 10. Severe sxs: seizures, brain damage, or death Treatment 1. Eating foods high in sugar content quickly restores blood sugar levels 2. If loss of consciousness occurs, an intravenous drip containing sugars and carbohydrates can be used |
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Definition
| 1. Difficulty focusing on objects that are close (such as when reading) 2. Due to less elasticity of the eye lens 3. Changes the "near point" – the distance where objects come into one's visual focus, which is approximately four inches in young adults and between 40-80 inches in 60-year-old adults 4. Natural part of the aging process 5. Sxs first become evident around the age of 45 Treatment 1. Treated with reading glasses for individuals who do not otherwise need to correct their vision 2. Bifocals can be used to treat Presbyopia in individuals who already wear glasses 3. Individuals who use contact lenses can wear one lens to see objects far away and one to see objects that are close, although this interferes with depth perception 4. Newer contacts are being developed that allow individuals to use one contact lens to correct for both myopia and Presbyopia |
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Definition
| Presentation 1. Sxs similar to dementia: memory loss, difficulty concentrating, word-finding difficulty and bxal changes 2. Associated with psychiatric disorder, typically major depressive disorder 3. Most common in the elderly 4. Improves with the effective treatment of the underlying psychiatric condition Differences from organic dementia 1. Dementia is progressive, while Pseudodementia can improve with treatment of the underlying psychiatric condition 2. Dementia has a gradual worsening of sxs, while Pseudodementia has a more sudden onset 3. Dementia thought to be caused by brain degeneration in specific regions; Pseudodementia is related to changes in serotonergic and noradrenergic activity |
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| Definition Stimulation of a sensory modality leads to the secondary unintended stimulation of a different sensory pathway Synesthesia demographics . Occurs in one in 25,000 individuals. Runs in families a. Likely has a genetic component Etiological theories Synesthesia is a by-product that occurs when signals that activate one sensory domain also excite neurons located in a nearby sensory domain.. Incomplete pruning process: As the cortex develops, inappropriate connections fail to be pruned Individual differences Exist in the development of sensory cortices, making each individual's perception of the world unique. Synesthesia is an example of individual differences in sensory perception |
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| 1. A neurotransmitter in the central nervous system (CNS) and peripheral nervous system (PNS) CNS 1. Is comprised of the brain and spinal cord PNS 1. Comprised of the nerves that carry information from the sensory organs to and from the CNS. It can be subdivided into the SNS and ANS 2. Somatic nervous system (SNS) a. Receives sensory input and controls the skeletal muscles and voluntary movement 3. Autonomic nervous system (ANS) a. Controls activity that is primarily involuntary, but can also be voluntary (e.g., breathing) 4. Sympathetic nervous system a. Responsible for "fight or flight" response 5. Parasympathetic nervous system a. "rest and digest" – deactivates sympathetic responses Neural mechanisms involved with Ach 1. In CNS a. Released by neurons in the dorsolateral pons, basal forebrain, and medial septum b. Low levels of ACh are found in individuals with Alzheimer’s disease and are associated with confusion/memory loss ACh agonists may facilitate increased attention, concentration, and memory by promoting the release of more Ach 2. In PNS a. ACh is found in ganglia and at neuromuscular junction of all parasympathetic and some sympathetic neurons 3. It has inhibitory effects in PNS a. Relaxed muscle tone b. Decreased heart rate c. Normal digestion ACh receptors 1. Nicotinic (ionotropic receptor) a. Binds to nicotinic receptors and promotes alertness and memory 2. Muscarinic (metabotropic receptor) a. Binds to metabotropic receptors Excitatory effects of Ach 1. Muscle contraction 2. If ACh is blocked, or the production is inhibited, paralysis may occur (e.g., Botox) ACh-related disease: Parkinson's disease 1. Associated with relative increase in ACh levels and a decrease in dopamine 2. Treatments aim to restore ACh-dopamine balance via dopamine agonists and ACh antagonists |
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Definition
| 1. Dopamine is an important brain neurotransmitter. Produced from tyrosine, an amino acid that is abundantly present in foods we eat. Tyrosine is metabolized to L-dopa through an enzymatic process. Dopamine exerts its effects in the brain through binding to one of six brain receptors. Dopamine has been implicated in motor bx, cognition, and pleasure and reward systems Role of Dopamine in Parkinson's disease Parkinson's disease associated with severe depletion of dopaminergic neurons, primarily in the substantianigra, which leads to motor rigidity, tremors, and difficulty initiating movement. Dopamine as a supplement is unable to cross the blood-brain barrier, however its precursor L-dopa can, therefore Parkinson's disease is treated with L-dopa supplements in order to increase the level of Dopamine in the brain. L-dopa is considered a Dopamine agonist, as it causes a net increase in dopaminergic activity in the brain Role of Dopamine in drug addiction Dopamine plays an integral role in the brain's reward system. At extremely high concentrations, dopamine can trigger hallucinations, delusions, and psychosis. Amphetamines, cocaine, and nicotine are Dopamine agonists, meaning they increase the amount of DA in the synaptic cleft by increasing the amount of Dopamine released and blocking the neurotransmitter's re-uptake of DA. Cocaine has similar effects upon the brain, whereupon Dopamine levels are elevated Role of Dopamine in schizophrenia The Dopamine hypothesis of schizophrenia proposes that schizophrenia is related to excessive Dopamine activity. Support for the Dopamine hypothesis of schizophrenia: a. Schizophrenia-like side effects from amphetamine abuse b. Ability of antipsychotics to reduce sxs of schizophrenia Detractors to the Dopamine hypothesis: a. Studies with schizophrenics have produced inconsistent results b. Not all studies have shown differences in Dopamine, Dopamine-receptor, or Dopamine-reuptake levels in the brain of individuals with schizophrenia when compared to control subjects c.To date, the role of Dopamine (if any) in the occurrence of schizophrenia remains widely debated Impact of long-term use of antipsychotic medication that are Dopamine antagonists Antipsychotics used to treat schizophrenia block the Dopamine receptor D-2 and thereby reduce Dopamine's activity in the brain. Long-term use of antipsychotics can lead to tardive dyskinesia, a neurological movement disorder characterized by involuntary facial movements, tongue thrusting, jaw swinging, and repetitive chewing |
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| An eating disorder characterized by: a. Body weight that is less than 85 percent of ideal; refusal to maintain normal weight b. Fear of becoming fat c. Distorted body image d. Amenorrhea in post-menarchal females Individuals with Anorexia Nervosa display disturbance in their perception of their body's shape and size and refuse to maintain a normal weight. Although by definition their body weight is less than 85 percent of the ideal one for age and height, they still view themselves as too fat. Intense fear of becoming overweight leading to restrictive diets and often over-exercise. Although the cause of Anorexia is the subject of much debate, it has been suggested that Anorexia is due to a combination of factors including genetics, social influences, and personality traits Brain involvement in Anorexia Past research has demonstrated that the hypothalamus (mediates serotonin in action) may be impaired in anorexics, such that the neural connections between appetite sensors and those that precipitate the feeling of hunger are ineffective. However, more recent research demonstrated that anorexics do, in fact, show normal or even elevated responses to food. For example, when exposed to carbohydrate-rich foods, elevations in levels of insulin in the blood of anorexics occur to a larger extent than in normal controls. In general, Anorexia is associated with abnormalities in several neurotransmitter levels, including serotonin, which plays a part in appetite regulation. Furthermore, the anorexic brain shows a lower serotonin/dopamine ratio (Aguilera, Selgas, Codoceo&Bajo, 2000) Physiological and psychological sequelae Physiological sequelae: a. Bradycardia (slow heart rate) b. Leukopenia (decrease in white blood cells) c. Anemia d. Abnormal electrolyte levels Psychological sequelae: a. Sxs that are consistent with depression b. Social withdrawal c. Depressed mood d. Irritability e. Insomnia f. Diminished interest in sex While the psychological sxs may indicate a comorbid depressive disorder, they may be secondary to the eating disorder Treatment for Anorexia Pharmacological treatment has proved to be ineffective for Anorexia. Treatment generally involves medical interventions (i.e., restoring an individual's nutritional levels), nutritional education, establishing an eating program, and working with the anorexic person in individual cognitive bxal psychotherapy and family therapy |
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| 1. Anxiety disorder include generalized Anxiety disorder (GAD), social phobia, panic disorder, and post-traumatic stress disorder (PTSD) 2. Treatment includes medication and bxal therapy; are treated using similar medication regimens 3. The combined effect of these two treatments is the most effective Brain regions associated with Anxiety disorders 1. Several brain regions have been implicated: amygdala, medial prefrontal cortex, and posterior cingulated cortex. The hypothalamic-pituitary-adrenal (HPA) axis, is also implicated in Anxiety, due to the part it plays during the body stress response, and stress hormones secretion 2. Panic disorder has been associated with abnormalities in the hippocampus and midbrain 3. PTSD has been associated with changes in the emotion-learning activity of the amygdale Neurotransmitters and hormones associated with Anxiety disorders 1. Increased levels of Anxiety are associated with increased noradrenergic function 2. Anxiety disorders may be associated with a decreased number of GABA receptors in the brain and/or the presence of a neuromodulator that blocks these receptor sites 3. Persons with Anxiety have chronically elevated levels of circulating stress hormone, cortisol, and a corresponding desensitization of cortisol receptors in the brain; this system is modulated by the hypothalamic-pituitary-adrenal axis Medication treatment of Anxiety disorders 1. Serotonin reuptake inhibitors (SSRIs), such as fluvoxamine, a serotonin agonist, have proved to effectively treat Anxiety disorders, suggesting that serotonin may play a role in Anxiety disorders 2. Effexor (venlafaxine), which is a serotonin and norepinephrine reuptake inhibitor (SNRI), has shown extremely good efficacy in treating Anxiety and is quickly replacing SSRIs as the most popular treatment choice for this family of disorders 3. Beta-adrenergic blocking drugs such as propranolol may be used in treating acute Anxiety associated with specific stressful events (e.g., public speaking, stage fright) 4. Beta-adrenergic blocking drugs affect peripheral manifestations of Anxiety, including palpitations, tachycardia, tremors, and sweating 5. Propranolol may produce side effects such as bradycardia, fatigue, malaise, and decreased sexual ability 6. Benzodiazepines (such as Xanax and clonazepam) address this decrease in GABA by binding to sites on the GABA receptor 7. Because of their addictive potential, and the risk of rebound sxs, the use of benzodiazepines in Anxiety treatment is usually temporary, and limited 8. The effectiveness of GABAergic, noradrenergic, and serotonergic drugs in treating Anxiety suggests the role of the respective neurotransmitters they target in the biological basis of Anxiety (Barlow & Durand, 2005) |
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Term
| Attention Deficit-Hyperactivity Disorder |
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Definition
| 1. ADHD is characterized by two sx clusters: inattention and hyperactivity/impulsivity 2. Sxs of Inattention: Difficulty sustaining attention in tasks or play activities, making careless mistakes due to lack of attention, not finishing tasks, difficulty organizing tasks, being distracted by extraneous stimuli, frequently losing things 3. Sxs of Hyperactivity: Fidgetiness, excessive talking, typically the child seems to be "on the go," difficulty sitting quietly 4. Impulsivity is characterized by frequent interrupting, blurting out answers, and difficulty waiting his or her turn 5. In order to meet criteria for ADHD, the child must have six or more bxs in either the inattention or hyperactive/impulsive domains 6. These bxs must have been present for at least six months 7. Approximately 9.5% of all children ages 4-17 are diagnosed with ADHD 8. Gender ratio ranges from 4:1-9:1 (males to females) depending on the setting 9. Sxs of ADHD must be present prior to the age of 7 10. Children with ADHD are often rejected by peers and are subjected to punishment and other negative sequelae by teachers and parents 11. As a result, they often develop comorbidities such as aggression, conduct disorder, learning disabilities, depression, anxiety, and low self-esteem 12. There are higher rates of antisocial personality disorder and substance abuse disorders among adults with ADHD (Carlson, 2005) Brain abnormalities associated with ADHD based on brain imaging studies 1. Decreased brain activity has been observed in many right hemispheric regions of children with ADHD, including: The right anterior cingulate cortex, whose role is to focus attention on a particular stimulus, the right prefrontal cortex, which is important for impulse control, decision-making, and planning 2. Abnormalities in the dopamine: D4 and D5 receptor structures and the dopamine transport gene have been associated with an increased risk for developing ADHD, sxs of inattention in ADHD are associated with reduced number of dopamine receptors in the nucleus accumbens and midbrain Treatment of ADHD 1. ADHD is treated using both bxal techniques and medication 2. Stimulant medication use began in the 1930s and continues to show effectiveness in treating ADHD today 3. Medications such as methylphenidate (Ritalin, Metadate, Concerta), D-amphetamine (Dexedrine, Dextrostat), and pemoline (Cylert) are also helpful in the majority of cases 4. Ritalin inhibits the reuptake of dopamine Amphetamines are dopamine agonists 5. They have been shown to temporarily increase concentration and reduce hyperactivity and impulsivity 6. Although a seemingly paradoxical effect, it is thought that amphetamines increase the levels of excitatory neurotransmitters in the cortex 7. Increased cortical activity, in turn, inhibits limbic activity and increases focus, attention, and executive decision-making abilities (Carlson, 2005) 8. Downside of stimulant medication a. Side effects of Ritalin may include short-term growth suppression and appetite loss b. Drug holidays are recommended (during summer or after school hours) to allow children to compensate for any growth issues c. Stimulants fail to maintain their benefits long term, and their use has not been positively associated with academic improvement d. Associated with a high potential for abuse and can cause several unwanted side effects such as insomnia, drowsiness, and irritability 9. More recently, a non-addictive selective norepinephrine reuptake inhibitor, called Strattera (atomoxetine), has been developed to treat ADHD 10. Other antidepressants such as Wellbutrin (bupropion), imipramine, and a drug used to treat high blood pressure (clonidine) have also shown some success in treating ADHD (Barlow & Durand, 2005) |
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| Diagnostic features 1. Impaired social interactions a.Marked impairment in nonverbal communication bxs b. Failure to develop peer relationships c. Lack of social/emotional reciprocity 2. Communication/language deficits a.Delay of spoken language b. Impaired ability to sustain reciprocal conversation with others 3.Echolalia a.Echoing words that are said by another person 4.Palilalia a. Repeating words that have been self-generated or said by oneself 5.Concrete interpretation of verbal information a. Abstract thinking is impaired (e.g., understanding humor may be difficult) Repetitive/stereotyped bx 1. Limited interests a.Restricted range of interests (e.g., only Pokemon cartoon characters, a specific fascination with computers, etc.) 2.Sxs are observable prior to age 3 a.DSM-IV-TR criteria requires that sxs are present prior to the age of 3 Differential Diagnoses 1. To differentiate from Asperger's disorder a. Asperger's disorder is ruled out if early language delays are present 2. To differentiate Rett's disorder a.Rett's disorder: a neurodevelopmental disorder that affects girls almost exclusively; males who do survive to term usually die shortly after birth b. Diagnosed after a period of normal development that is followed by a slowing of development, loss of purposeful use of hands, problems with walking, slowed brain development and decline in head growth between 5 to 48 months of age 3. To differentiate Childhood Disintegrative Disorder a. CDD involves a regression multiple areas of function after a period of at least 2 years of normal development 4. To differentiate from Social phobia a. Social Phobia may co-occur and it is hallmarked by a fear of social situations Neural correlates of social impairments 1. Abnormal activity in the fusiform gyrus a. Located in the ventral temporal lobe b. Related to face recognition 2. Abnormal activity in the amygdala a. Subcortical bilateral brain region b. Related to detecting emotional salience of stimuli |
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| Catecholamine Hypothesis of Depression |
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Definition
| Catecholamines play a primary role in the development of depression 1. Reduced levels of norepinephrine cause depression 2. Higher levels of norepinephrine cause elation 3. Supported by studies showing MAOIs and TCAs are efficacious in treating depression through their effects on norepinephrine |
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Term
| Chronic Pain & Gate Control Theory |
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Definition
| The Gate Control Theory of Chronic Pain 1. Proposed by Melzack and Wall in 1965 2. Sought to explain how thoughts and emotions can affect the perception of pain, as opposed to pain perception being based entirely on the physical stimulus 3. The theory proposed that there are two types of fibers that send information to the brain: Thick fibers transmit non-nociceptive sensory information, such as touch and vibration; smaller fibers transmit nociceptive (pain) information to the thalamus 4. These fibers meet up in the dorsal horn of the spinal cord, where their activation either "opens" the gate, sending pain information to the thalamus via projection neurons, or "closes" the gate via inhibitory neurons, stopping the pain from being perceived or greatly diminishing its intensity 5. Whether or not the gate is open or closed depends on the relative activity in the large and small fibers: a. If the large fibers are relatively more active than the small fibers (i.e., more tactile information is being transmitted than pain information) then the gate will be closed b. This explains why rubbing or lightly tickling an injured area reduces the pain in that area; it stimulates the large fibers to close the "gate" c. Similarly, when a person receives good news while in pain, the non-pain signal will work to inhibit the person's pain 6. This suggests first, that pain perception is the result of a combination of factors that are processed in the brain, and second, that the brain can be trained to perceive pain differently using this principle (Melzack, 1993) Definition and cause of Chronic Pain 1. Defined as pain lasting longer than three to six months or pain that persists beyond the usual amount of time for the tissue to heal 2. According to the Gate Control Theory of Pain, chronic pain is the result of the "gate" being left open, or in other words, the dorsal horn remaining sensitized Psychological and psychosocial influences of pain 1. Interaction between pain and depression: a. Several recent studies have shown that depression and anxiety can increase sensitivity to pain and decrease the threshold for pain b. Conversely, pain can aggravate depression c. Pain and depression share biochemical pathways 2. This may explain why tricyclic antidepressants (TCAs) have an analgesic effect 3. Other psychological factors: a. Studies have also shown that individuals who use passive coping strategies are more likely to develop chronic pain, while those who use active coping strategies are not (Mercado, 2005) 4. Several psychosocial factors exacerbate pain: a. Females, persons who are single, persons with poor general health, and those with a poor perception of their health-status are at an increased likelihood of experiencing chronic pain Interventions for Chronic Pain 1. Given the psychological factors associated with pain perception, management of Chronic Pain often targets more than the physiological aspect of pain 2. Therapy can be used to target: a. A patient's anxiety and depression b. Beliefs about pain c. Coping strategies d. Family dynamics around the pain e. Negative reinforcement of the pain 3. Pharmacological treatment of pain: a. Narcotics (e.g. morphine) are only used in the management of acute pain as chronic use increases the likelihood of tolerance and dependence in the patient b. Selective Serotonin Reuptake Inhibitors (SSRIs), which have fewer side effects than TCAs, can be effective in the management of chronic pain c. Medications that inhibit reuptake of both serotonin and norepinephrine are demonstrably more effective than SSRIs d. Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) such as venlafaxine (Effexor) now hold the greatest promise in alleviating chronic pain while minimizing troublesome, interfering side effects |
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| Mental health care differences among Asian Americans and Caucasians 1. Historically lower rates of hospitalization for mental illness a. Not due to lower rates of severity or mental illness, but higher thresholds for seeking services b. Time delay from onset of illness to treatment is significantly longer in Asian Americans than other ethnic groups c. Some Asian Americans are less likely to raise mental health concerns; rather, they focus on physical ailments d. Some Asian Americans are more likely to seek non-allopathic remedies and ascribe non-medical explanations for their mental health sxs e. Ethnic Differences in mental health treatment are likely influenced by acculturation level f. Other factors such as age, sexual orientation, marital status, and ability may contribute to clinical presentation 2. Ethnic Differences in medical treatment a. Asian Americans and Caucasians respond different to psychotropic medications: Some Asian Americans respond to significantly lower doses of medications when compared to Caucasians; differences are due to differences in metabolism rates b. Ethnic differences among other ethnic groups: Hispanic/Latinos and African Americans may be more sensitive to certain drugs such as lithium, traditional neuroleptics, and tricyclic antidepressants |
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| James-Lange theory of emotion Proposed independently in 1880s by William James and Carl Lange. Identification of an emotion follows a physiological event Cannon-Bard theory of emotion Proposed in the 1920s by Walter Cannon and Philip Bard. This theory argued against the James-Lange theory. Physiological response follows the experience of an emotion. Cortical processing is involved in eliciting a physiological response to a stimulus Lazarus theory of emotion Cognitive assessment of one's circumstance precedes the physiological response and the emotion. People who make the same cognitive appraisal will experience the same emotion, regardless of whether their environmental experience was the same. Two people in the same environment will experience different emotions if their cognitive appraisals of the event differ. Three distinct forms of cognitive appraisal: a. Primary appraisal refers to the evaluation of the salience of an event b. Secondary appraisal refers to the evaluation of an individual’s ability to cope with an event c. Re-appraisal occurs when an individual monitors a situation as necessary and then modifies their primary and secondary appraisals |
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Definition
| Weber's law 1. Was initially proposed by Ernst Weber and later elaborated on by Gustav Fechner in the 1860s 2. Weber’s research was an attempt to quantify the relationship between the actual physical magnitude of a stimulus and the perceived sensation of the stimulus 3. The law is concerned with the minimal magnitude necessary before a stimulus can be perceived a. For example, Weber's Law might predict the minimum brightness necessary for a light (or a star in the sky) to be seen 4. Also predicts the minimum change in intensity that is required before the change can be perceived" a. For example, if we are holding a weight in our hands, Weber's Law would predict how much weight must be added before we perceive the difference 5. The difference threshold is called the just noticeable difference (JND) 6. Can be applied to various sensory perceptions such as vision, sound, and touch (pressure). Relationship between a stimulus (or the change in the stimulus) and its perception is not directly proportional, but rather logarithmic a. For example, the difference in your perception of pressure when you add a second book onto the one you are already carrying is smaller than the difference in perception you might feel if you added the same book to the already heavy stack of five books you are carrying 7. Works best in the middle range of any sensation 8. Not as good at predicting the JND when the intensity of the stimulus is either very low or very high 9. Also not good at predicting pain threshold or predicting our perception of any stimulus beyond the pain threshold 10. Steven's Power Law: The strength of a particular sensation is linked to the intensity of a stimulus raised to an exponential power a. if exponent is greater than number one, the line will curve up b. if the line is one, the result is a straight line c. if the exponent is less than one, the result is a slope downward d. Steven's Power Law superseded the Weber-Fechner Law |
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