BioPsy Midterms - Visual Coding PDF

Module 3.1: VISION Visual Coding General Principles of Perception - The law of specific nerve energies, formulated by Johannes Müller, states that each sensory nerve produces a unique type of energy that the brain interprets in specific ways. This means that regardless of how a nerve is stimulate...

Module 3.1: VISION Visual Coding General Principles of Perception - The law of specific nerve energies, formulated by Johannes Müller, states that each sensory nerve produces a unique type of energy that the brain interprets in specific ways. This means that regardless of how a nerve is stimulated, the resulting perception—such as sound from the auditory nerve or odor from the olfactory nerve—is determined by which nerve is activated. The Eye and Its Connections to the Brain - Light enters the eye through the pupil, which is located at the center of the iris. It is focused onto the retina by the lens ( adjustable) and cornea (not adjustable), where visual receptors are located. The retina receives inverted images, with light from the left side striking the right half and vice versa, but the visual system encodes this information without duplicating the image. Route within the Retina - Light messages from visual receptors travel through several layers of cells in the retina before reaching the brain. - Receptors Receptors: Cells that detect light and initiate the visual process. - Bipolar Cells: Intermediate cells that transmit signals from receptors to ganglion cells. - Ganglion Cells: Neurons that receive input from bipolar cells and whose axons form the optic nerve. - Optic Nerve: The pathway that carries visual information from the retina to the brain. - Amacrine Cells: Cells that refine the input from bipolar cells to ganglion cells and enhance response to specific visual features. - Due to this layered structure, light must pass through the ganglion, amacrine, and bipolar cells to reach the photoreceptors, but these cells are transparent, minimizing distortion. - The area where ganglion cell axons exit the eye to form the optic nerve results in a blind spot, as there are no visual receptors at this point. Fovea and Periphery of the Retina The fovea is a specialized area of the retina for sharp vision, with minimal blood vessels and ganglion cell axons, allowing for clear detail perception due to tightly packed photoreceptors. Each foveal receptor connects to a single bipolar cell and then to a midget ganglion cell, which provides direct communication to the brain. These cells account for 70% of visual input, highlighting the significance of foveal vision. In the peripheral retina, multiple receptors converge onto fewer bipolar and ganglion cells, reducing the brain's ability to detect exact shapes but improving dim light sensitivity. Visual Receptors: Rods and Cones The vertebrate retina has two types of receptors: rods and cones. Rods, located mostly in the retina's periphery, are highly sensitive to faint light but ineffective in bright light due to bleaching. Cones, concentrated in and around the fovea, are less sensitive to dim light, function well in bright conditions, and are essential for color vision. This distribution provides sharp color vision in the fovea but limited color perception in the peripheral vision. Both rods and cones contain photopigments, chemicals that release energy when exposed to light. Components of Photopigments: - Made of 11-cis-retinal (a vitamin A derivative) attached to opsins (proteins). Opsins adjust the sensitivity of photopigments to different wavelengths of light, aiding color vision. Light Activation Process: - Light exposure converts 11-cis-retinal into all-trans-retinal, releasing energy.This energy activates second messengers within the cell, initiating visual processing.The light is absorbed in this reaction, preventing it from bouncing around the eye. Color Vision - Visible light spans wavelengths from 700 nm (red).Our perception of light is due to receptors in our eyes tuned to these wavelengths. Trichromatic (Young-Helmholtz) Theory: Suggests we perceive color by the responses of three cone types, each sensitive to different wavelength ranges (short, medium, and long). People can match any color using three wavelengths, supporting the need for only three types of cones. - Cone Sensitivity and Color Perception: Short-wavelength cones (blue), medium-wavelength cones (green), and long-wavelength cones (red) respond differently to wavelengths, allowing the brain to interpret colors based on the response ratio. Equal activation of all three cones results in white or gray perception. Variations in individual cone distribution cause minor differences in color perception among people. - Cone Distribution and Visual Limitations: Long- and medium-wavelength cones are more abundant than short-wavelength cones, making it harder to see tiny blue details compared to red, yellow, or green. In the retina’s periphery, cones are scarce, resulting in poor color vision there. The Opponent-Process Theory: The trichromatic theory doesn’t fully explain color vision, as demonstrated by the phenomenon of afterimages, where staring at a color (e.g., red) results in seeing its opposite (e.g., green) afterward. Hering proposed the opponent-process theory, suggesting we perceive colors in opposites: red-green, blue-yellow, and black-white. When one color’s perception is fatigued, the brain shifts to perceiving its opposite, explaining afterimages. The Retinex Theory: Color constancy allows recognition of colors under different lighting conditions. This is not explained by the trichromatic or opponent-process theories alone. For example, green-tinted glasses don’t prevent recognition of familiar colors (e.g., bananas as yellow). Colors can appear different depending on their context. In certain lighting, colors seem distinct (e.g., blue or yellow), but when isolated, the same colors may appear gray, illustrating the role of context in color perception.  Brightness is perceived through comparison with surrounding objects. Covering borders between different shades can reveal that perceived brightness changes are an effect of context. In Closing: Visual Receptors Color vision deficiency, often called color blindness, was one of the earliest psychological discoveries. People with this condition cannot perceive all colors others can, demonstrating that color is processed in the brain, not inherent to objects. Color deficiency arises when individuals lack a type of cone or have an abnormal one, especially impacting red-green discrimination. This is linked to the X chromosome, making red-green color deficiency more common in men (about 8% of northern European men) than in women (less than 1%). Some women have a genetic variation in the long-wavelength (red) cone, creating two slightly different receptors. This allows for finer color distinctions and more variability in color perception compared to men. How the Brain Processes Visual Information The rods and cones of the retina make synapses with horizontal cells and bipolar cells. The horizontal cells make inhibitory contact onto bipolar cells, which in turn make synapses onto amacrine cells and ganglion cells. All these cells are within the eyeball Most ganglion cell axons go to the lateral geniculate nucleus, part of the thalamus. (The term geniculate comes from the Latin root genu,meaning “knee. ” Togenuflect is to bend the knee Processing in the Retina Light striking the rods and cones decreases their spontaneous output,and the receptors make inhibitory synapses onto the bipolar cells. Therefore, light on the rods or cones decreases their inhibitory output. A decrease in inhibition means net excitation The receptor excites both the bipolar cells and the horizontal cell. The horizontal cell inhibits the same bipolar cell that was excited plus additional bipolar cells in the surround. Lateral inhibition, the reduction of activity in one neuron by activity in neighboring neurons (Hartline, 1949). Lateral inhibition heightens contrast. Further Processing The Primary Visual Cortex Receptive field, an area in visual space that excites or inhibits it. Each cell in the visual system of the brain has a receptive field. Receptors have tiny receptive fields and later cells have progressively larger receptive fields. Primate ganglion cells fall into three categories: parvocellular, magnocellular, and koniocellular The parvocellular neurons, with small cell bodies and small receptive fields, are mostly in or near the fovea. Parvocellular means “small celled,” from the Latin root parv, meaning “small." The magnocellular neurons, with larger cell bodies and receptive fields, are distributed evenly throughout the retina. (Magnocellular means “large celled,” from the Latin root magn, meaning “large." The koniocellular neurons have small cell bodies, similar to the parvocellular neurons, but they occur throughout the retina. (Koniocellular means “dust celled,” from the Greek root meaning “dust.” They got this name because of their granular appearance.) The Primary Visual Cortex Information from the lateral geniculate nucleus of the thalamus goes to the primary visual cortex in the occipital cortex,also known area 1 or the striate cortex because of its striped appearance. Some people with damage to area V1 show a surprising phenomenon called blindsight, the ability to respond in limited ways to visual information without perceiving it consciously Simple and Complex Receptive Fields A simple cell has a receptive field with fixed excitatory and inhibitory zones. The more light shines in the excitatory zone, the more the cell responds. The more light shines in the inhibitory zone, the less the cell responds. Complex cells, located in areas V1 and V2, do not respond to the exact location of a stimulus. A complex cell responds to a pattern of light in a particular orientation (e.g., a vertical bar) anywhere within its large receptive field. A cell that responds to a stimulus in only one location is a simple cell. One that responds equally throughout a large area is a complex cell.  End-stopped,or hypercomplex,cells resemble complex cells with one exception: An end-stopped cell has a strong inhibitory area at one end of its bar-shaped receptive field. The Columnar Organization of the Visual Cortex Neurons within a column of the primary visual cortex have similar properties, such as responding to lines in the same orientation Are Visual Cortex Cells Feature Detectors? Given that neurons in area V1 respond strongly to bar- or edge-shaped patterns, we might suppose that the activity of such a cell represents the perception of a bar, line, or edge. That is, such cells might be feature detectors—neurons whose responses indicate the presence of a particular feature Feature detectors, it's a neuron that detects the presence of a particular aspects of an object, such as a shape or a direction of movement. Development of the Visual Cortex In Closing: Understanding Vision by Understanding the Wiring Diagram Understanding what you see requires much more than just adding up points and lines. Vision is an active process based partly on expectations During infancy, the cells of the visual cortex have nearly normal properties. However, experience is necessary to maintain and fine-tune vision. Abnormal visual experience can change the properties of visual cells, especially if the experience occurs early in life. Cortical neurons become unresponsive to axons from an inactive eye because of competition with the active eye. If both eyes are closed, each cortical cell remains somewhat responsive to axons from one eye or the other, although that response becomes sluggish and unselective as the weeks of deprivation continue. To develop good stereoscopic depth perception, a kitten or human child must have experience seeing the same object with corresponding portions of the two eyes early in life. Otherwise, each neuron in the visual cortex becomes responsive to input from just one eye. 70 percent of all infants have astigmatism, a blurring of vision for lines in one direction (e.g., horizontal, vertical, or one of the diagonals), caused by an asymmetric curvature of the eyes. Parallel Processing in the Visual Cortex The primary visual cortex (V1) sends information to the secondary visual cortex(area V2), which processes the information further and transmits it to additional areas. Researchers distinguish between the ventral visual stream, responsible for perceiving objects, and the dorsal stream, responsible for visual guidance of movements They call the ventral stream through the temporal cortex the perception pathway or the “what" pathway, because of its importance for identifying and recognizing objects The dorsal stream through the parietal cortex is the action pathway or the “how” pathway, because of its importance for visually guided movements The Inferior Temporal Cortex The inferior temporal cortex detects objects and recognizes them despite changes in position, size, and so forth. In the inferior temporal cortex, cells that respond strongly to the original respond about the same to the contrast reversal and mirror image but not to the figure–ground reversal. Visual agnosia (meaning “visual lack of knowledge”) is an inability to recognize objects despite otherwise satisfactory vision. It is a common result from damage in the temporal cortex Part of the fusiform gyrus of the inferior temporal cortex, especially in the right hemisphere, responds more strongly to faces than to anything else. Recognizing Faces A circuit including the fusiform gyrus of the temporal cortex is specialized for recognizing faces. People with impairments in this circuit experience prosopagnosia, a difficulty in recognizing faces despite nearly normal vision in other regards. The Middle Temporal Cortex Two areas especially important for motion perception are area MT (formiddle temporalcortex), also known asareaV5, and an adjacent region, areaMST(medial superior temporal cortex). These areas receive input mostly from the magnocellular path, which detects overall patterns, including movement over large areas of the visual field.  Given that the magnocellular path is color insensitive, MT is also color insensitive. Motion Blindness The middle temporal cortex (including areas MT and MST) is specialized for detecting the direction and speed of a moving object. People with damage in this area experience motion blindness, an impairment in their ability to perceive movement. You do not see your own eyes move because area MT and parts of the parietal cortex decrease their activity during voluntary eye movements, known as saccades. Even people with an intact brain experience a brief period of motion blindness beginning about 75 ms before a voluntary eye movement and continuing during the eye movement Module 3.2: CHAPTER 6 (OTHER SENSORY SYSTEMS) Other Sensory Senses Each species responds to the most useful kinds of information. Humans, too, have important sensory specializations. Our sense of taste alerts us to the bitterness of poisons but does not respond to substances such as cellulose that neither help nor harm us. Our olfactory systems are unresponsive to gases that we don’t need to detect (e.g., nitrogen) but highly responsive to the smell of rotting meat. Audition Evolution has been described as “thrifty.” After it has solved one problem, it modifies that solution for other problems instead of starting from scratch. Sound and the Ear Human hearing is sensitive to sounds that vibrate the eardrum by less than one-tenth the diameter of an atom, and we can detect a difference between two sounds as little as 1/30 the interval between two piano notes Physics and Psychology of Sound Sound waves- are periodic compressions of air, water, or other media. amplitude of a sound wave is its intensity frequency of a sound is the number of compressions per second, measured in hertz (Hz, cycles per second) Pitch- the related aspect of perception. Sounds higher in frequency are higher in pitch The height of each wave corresponds to amplitude, and the number of waves per second corresponds to frequency Most adult humans hear sounds starting at about 15 to 20 Hz and ranging up to almost 20,000 Hz Timbre- tone quality or tone complexity prosody - conveying emotional information by tone of voice Anatomists distinguish the outer ear, the middle ear, and the inner ear Pinna- the familiar structure of flesh and cartilage attached to each side of the head - helps us locate the source of a sound middle ear- a structure that had to evolve when ancient fish evolved into land animals tympanic membrane- or eardrum, vibrates when sound waves reach the middle ear oval window- a membrane of the inner ear. English (hammer, anvil, and stirrup)/ Latin (malleus, incus, and stapes)- three tiny bones that transmit the vibrations to the oval window. These bones, the smallest bones in the body Cochlea- the snail-shaped structure of the inner ear hair cells- known as auditory receptors, lie between the basilar membrane of the cochlea on one side and the tectorial membrane on the other Pitch Perception place theory- states that the basilar membrane resembles the strings of a piano, with each area along the membrane tuned to a specific frequency. - According to this theory, each frequency activates the hair cells at only one place along the basilar membrane, and the nervous system distinguishes among frequencies based on which neurons respond frequency theory- according to this theory, the entire basilar membrane vibrates in synchrony with a sound, causing auditory nerve axons to produce action potentials at the same frequency volley principle of pitch discrimination, the auditory nerve as a whole produces volleys of impulses for sounds up to about 4000 per second, even though no individual axon approaches that frequency The Auditory Cortex As information from the auditory system passes through subcortical areas, axons cross over in the midbrain to enable each hemisphere of the forebrain to get most of its input from the opposite ear.. The information ultimately reaches the primary auditory cortex (area A1) in the superior temporal cortex The organization of the auditory cortex parallels that of the visual cortex The auditory system has a pathway in the anterior temporal cortex specialized for identifying sounds, and a pathway in the posterior temporal cortex and the parietal cortex specialized for locating sounds motion deaf- patients with damage in parts of the superior temporal cortex, they hear sounds, but they do not detect that a source of a sound is moving area A1 -responds to imagined sounds as well as real ones damage to the primary auditory cortex does not produce deafness tonotopic map- expresses gradients in the representation (maps) of sound properties Sound Localization Sound localization is less accurate than visual localization Determining the direction and distance of a sound requires comparing the responses of the two ears. One method is the difference in time of arrival at the two ears Time of arrival - is useful for localizing sounds with a sudden onset Another cue for location is the difference in intensity between the ears. sound shadow - makes the sound louder for the closer ear A third cue is the phase difference between the ears. Every sound wave has phases with peaks 360 degrees apart. sounds travel faster in water than in air Individual Differences Amusia- commonly called “tone deafness, they have trouble recognizing tunes, cannot tell whether someone is singing off-key, and do not detect a “wrong” note in a melody - results from either an impairment of the prefrontal cortex, or input to it from the auditory cortex. Absolute pitch- or “perfect pitch”, is the ability to hear a note and identify it two categories of hearing loss: · conductive deafness- or “middle-ear deafness”, when diseases, infections, or tumorous bone growth prevent the middle ear from transmitting sound waves properly to the cochlea. · nerve deafness- or “inner-ear deafness”, results from damage to the cochlea, the hair cells, or the auditory nerve Tinnitus- frequent or constant ringing in the ears The Mechanical Senses mechanical senses-respond to pressure, bending, or other distortions of a receptor vestibular sensation- which detects the position and movement of the head Audition is also a mechanical sense because the hair cells are modified touch receptors Sensations from the vestibular organ detect the direction of tilt and the amount of acceleration of the head The vestibular organ consists of the saccule, utricle, and three semicircular canals otoliths - Calcium carbonate particles lie next to the hair cells - push against different sets of hair cells and excite them - tell the brain which direction you are moving, and they also record which direction the head tilts when you are at rest. three semicircular canals- oriented in perpendicular planes, are filled with a fluid and lined with hair cells. - record only the amount of acceleration, not the position of the head at rest somatosensory system- the sensation of the body and its movements Pacinian corpuscle- detects vibrations or sudden displacements on the skin neuron membrane- the onion-like outer structure provides mechanical support that resists gradual or constant pressure Merkel disks- respond to light touch, such as when you feel an object On average, women can detect grooves about 1.4 mm apart, whereas men need the grooves to be about 1.6 mm apart.. It reflects the fact that on the average, women have smaller fingers. Apparently women have the same number of Merkel disks as men, but compacted into a smaller area. The systems for cooling and heating show an interesting asymmetry: Cold-sensitive neurons in the spinal cord respond to a drop in temperature. a cell that responds to a drop from 39° C to 33° C would also respond to a drop from 33° C to 27° C Cold-sensitive neurons adapt quickly, and show little response to a constant low temperature. In contrast, heat-sensitive neurons in the spinal cord respond to the absolute temperature, and they do not adapt. Capsaicin- a chemical found in hot peppers such as jalapeños, stimulates the receptors for painful heat Somatosensation in the Central Nervous System Information from touch receptors in the head enters the central nervous system (CNS) through the cranial nerves. Information from receptors below the head enters the spinal cord and passes toward the brain through any of the 31 spinal nerves including 8 cervical nerves, 12 thoracic nerves, 5 lumbar nerves, 5 sacral nerves, and 1 coccygeal nerve. Each spinal nerve has a sensory component and a motor component. Dermatome- a limited area of the body where each spinal nerve innervates (connects to) Insular cortex- respond only to the pleasantness of the sensation, not the sensation itself primary somatosensory cortex- essential for touch experiences - Damage to the somatosensory cortex impairs body perceptions. Many sensations sometimes evoke strong emotions, but pain is unique among senses because it always evokes an emotion, an unpleasant one. Pain sensation begins with the least specialized of all receptors, a bare nerve ending Mild pain releases the neurotransmitter glutamate, whereas stronger pain releases glutamate but also certain neuropeptides including substance P and CGRP (calcitonin gene-related peptide). pain-sensitive cells- cells in the spinal cord that relay information to several sites in the brain The spinal paths for pain and touch are parallel, but with one important difference: The pain pathway crosses immediately from receptors on one side of the body to a tract ascending the contralateral side of the spinal cord. Touch information travels up the ipsilateral side of the spinal cord to the medulla, and then crosses to the contralateral side. Hurt feelings resemble physical pain in several regards. cingulate cortex- an area responsive to the emotional aspects of pain Hurt feelings are like real pain in another way: You can relieve hurt feelings with pain-relieving drugs such as acetaminophen (Tylenol®) opioid mechanisms systems that respond to opiate drugs and similar chemical. the brakes on prolonged pain endorphins- a contraction of endogenous morphines, he transmitters that attach to the same receptors as morphine gate theory - was an attempt to explain why some people withstand pain better than others and why the same injury hurts worse at some times than others - states that spinal cord neurons that receive messages from pain receptors also receive input from touch receptors and from axons descending from the brain. These other inputs can close the “gates” for the pain messages—and they do so at least partly by releasing endorphins morphine- block messages from thinner axons that convey slower, duller pain Cannabinoids—chemicals derived from or similar to marijuana—block certain kinds of pain Capsaicin- a chemical in jalapeños and similar peppers that stimulates receptors for heat. Placebo- a drug or other procedure with no pharmacological effects. - increases activity in parts of the prefrontal cortex, suggesting that a placebo exerts its effects by top-down control of sensations and emotions Damaged or inflamed tissue, such as sunburned skin, releases histamine, nerve growth factor, and other chemicals that help repair the damage but also magnify the responses of nearby heat and pain receptors Nonsteroidal anti-inflammatory drugs, such as ibuprofen, relieve pain by reducing the release of chemicals from damaged tissues itch -is a separate sensation. Researchers have identified special receptors for itch You have two kinds of itch that feel about the same, although their causes are different; - Frst, when you have mild tissue damage, such as when your skin is healing after a cut, your skin releases histamines that dilate blood vessels and produce an itching sensation. - Second, contact with certain plants, especially cowhage (a tropical plant with barbed hairs), also produces itch. The itch receptors are slow to respond, and when they do, their axons transmit impulses at the unusually slow velocity of only half a meter per second - Itch is useful because it directs you to scratch the itchy area and remove whatever is irritating your skin. -Vigorous scratching produces mild pain, and pain inhibits itch Opiates- decrease pain, increase itch The Chemical Senses Theorists believe that the first sensory system of the earliest animals was a chemical sensitivity chemical sense- enables a small animal to find food, avoid certain kinds of danger, and even locate mates. Taste- is useful for just one function, telling us whether to swallow something or spit it out. Taste results from stimulation of the taste buds. Taste buds- the receptors on the tongue Flavor- is a combination of taste and smell endopiriform cortex- taste and smell axons converge onto many of the same cells in this area The receptors for taste are not true neurons but modified skin cells. papillae – where mammalian taste receptors are located, can be found on the surface of the tongue - A given papilla may contain up to 10 or more taste buds and each taste bud contains about 50 receptor cells. In adult humans, taste buds lie mainly along the edge of the tongue Western society has described tastes in terms of sweet, sour, salty, and bitter. However, some tastes defy categorization in terms of these four labels miracle berry- (native to West Africa) gives little taste itself but temporarily changes sweet receptors, contains miraculin miraculin—that modifies sweet receptors, enabling acids to stimulate them sodium lauryl sulfate- a chemical that intensifies bitter tastes and weakens sweet ones, Gymnema sylvestre- Salty, sour, and bitter substances taste the same as usual, but sugar becomes tasteless Adaptation- reflects the fatigue of receptors sensitive to sour tastes cross-adaptation—reduced response to one taste after exposure to another glutamate- monosodium glutamate (MSG), tastes somewhat like unsalted chicken broth. English language had no word for this taste, so English-speaking researchers adopted the Japanese word umami. Oleogustus- the taste of fats Mechanisms of Taste Receptors · saltiness receptor- detects the presence of sodium, simply permits sodium ions on the tongue to cross its membrane · Sour receptors- detect the presence of acids · Sweetness, bitterness, and umami receptors -resemble the metabotropic synapses · Bitter taste used to be a puzzle because bitter substances include a long list of dissimilar chemicals. - we have not one bitter receptor but a family of 30 or more. Each responds to a few related compounds taste “phantoms,”- you might experience taste even when nothing was on your tongue nucleus of the tractus solitarius (NTS)- a structure in the medulla where the taste nerves project insula- is the primary taste cortex supertasters- people with more taste buds nontasters- people with the fewest taste buds OLFACTION Olfaction- the sense of smell, is the response to chemicals that contact the membranes inside the nose - Olfaction is especially important for our food selection. - Olfaction also plays an important role in social behavior. Researchers estimate that people can distinguish among more than a trillion olfactory stimuli. olfactory cells- the neurons responsible for smell, line the olfactory epithelium in the rear of the nasal air passages cilia -(threadlike dendrites) that extend from the cell body into the mucous surface of the nasal passage olfactory bulb - sends axons to the olfactory area of the cerebral cortex Individual Differences 1.Genetic Differences: People differ significantly in their sense of smell due to variations in olfactory receptor genes. On average, two random individuals differ in about 30% of these genes. 2. Age-Related Changes: Odor sensitivity declines with age, but the decline varies by odor. Mushroom: Sensitivity stays constant. Onion: Moderate decline. Rose: Significant decline. Reduced smell sensitivity can be an early sign of Alzheimer’s or Parkinson’s disease. 3. Gender Differences: Women generally have a better sense of smell than men across all ages and cultures. Young women become increasingly sensitive to faint odors they focus on, detecting them at much lower concentrations. This heightened sensitivity may be influenced by female hormones. Pheromones vomeronasal organ (VNO)- is a set of receptors located near, but separate from, the olfactory receptors pheromones- chemicals released by an animal that affect the behavior of other members of the same species Olfactory receptors respond to a new odor but not to a continuing one.VNO receptors, however, continue responding even after prolonged stimulation Synesthesia- is the experience some people have in which stimulation of one sense evokes a perception of that sense and another one also When people misperceive a stimulus—as in an illusion—the synesthetic experience corresponds to what the person thought the stimulus was, not what it actually was Module 4.2: CHAPTER 10 (NEUROCOGNITIVE DISORDERS) BRAIN TUMORS Tumor, or neoplasm (literally, “new growth”), is a mass of cells that grows independently of the rest of the body. Meningiomas—tumors that grow between the meninges, the three membranes that cover the central nervous system. About 20 percent of tumors found in the human brain All meningiomas are Encapsulated tumors—tumors that grow within their own membrane. As a result, they are particularly easy to identify on a CT scan, they can influence the function of the brain only by the pressure they exert on surrounding tissue, and they are almost always benign tumors—tumors that are surgically removable with little risk of further growth in the body. Encapsulation is the exception rather than the rule when it comes to brain tumors. Infiltrating tumors- are those that grow diffusely through surrounding tissue. As a result, they are usually malignant tumors; that is, it is difficult to remove or destroy them completely, and any cancerous tissue that remains after surgery usually continues to grow. Gliomas (brain tumors that develop from glial cells) are infiltrating, rapidly growing, and unfortunately the most common form of malignant brain tumors. About 10 percent of brain tumors do not originate in the brain. Metastatic tumors (metastasis refers to the transmission of disease from one organ to another). They grow from infiltrating cells that are carried to the brain by the bloodstream from some other part of the body.Many metastatic brain tumors originates as cancers of the lungs. Acoustic Neuromas (neuromas are tumors that grow on nerves or tracts), Encapsulated tumors that grow on cranial nerves VIII. STROKES Strokes are sudden-onset cerebrovascular disorders that cause brain damage. In the United States, stroke is the fifth leading cause of death, the major cause of neurological dysfunction, and a leading cause of adult disability. The symptoms of a stroke depend on the area of the brain affected, but common consequences of stroke are amnesia, aphasia (language difficulties), psychiatric disorders, dementia, paralysis, and coma. Infarct- The area of dead or dying tissue produced by a stroke. Surrounding the infarct is a dysfunctional area called the penumbra. The tissue in the penumbra may recover or die in the ensuing days, depending on a variety of factors. Accordingly, the primary goal of treatment following stroke is to save the penumbra. Cerebral hemorrhage (bleeding in the brain) occurs when a cerebral blood vessel ruptures and blood seeps into the surrounding neural tissue and damages it. Bursting aneurysms are a common cause of intracerebral hemorrhage. An aneurysm is a pathological balloonlike dilation that forms in the wall of an artery at a point where the elasticity of the artery wall is defective. Aneurysms can occur in any part of the body. Can be congenital (present at birth) or can result from exposure to vascular poisons or infection. Individuals at risk of aneurysms should make every effort to avoid cigarette smoking, alcohol consumption, and hypertension. Cerebral Ischemia- disruption of the blood supply to an area of the brain. 3 main causes of cerebral ischemia -thrombosis -embolism -arteriosclerosis Thrombosis- a plug called thrombus is formed and blocks blood flow at the site of its formation. May be composed of a blood clot, fat, oil, an air bubble, tumor cells, or any combination thereof. Embolism- the plug, called an embolus, is carried by the blood from a larger vessel, where it was formed to a smaller one, where it becomes lodged; in essence, an embolus is just a thrombus that has taken a trip. Arteriosclerosis- the walls of blood vessels thicken and the channels narrow, usually as the result of fat deposits; this narrowing can eventually lead to complete blockage of the blood vessels. Ischemia-induced brain damage has two important properties. -First, it takes a while to develop. Soon after a temporary cerebral ischemic episode, there usually is little or no evidence of brain damage; however, substantial neuron loss can often be detected a day or two later. -Second, ischemia-induced brain damage does not occur equally in all parts of the brain—particularly susceptible are neurons in certain areas of the hippocampus. Glutamate- the brain’s most prevalent excitatory neurotransmitter, plays a major role in ischemia-induced brain damage. -After a blood vessel becomes blocked, many of the blood-deprived neurons become overactive and release excessive quantities of glutamate. The glutamate in turn overactivates glutamate receptors in the membranes of postsynaptic neurons. NMDA (N-methyl-D-aspartate) receptors- glutamate receptors most involved in this reaction. -NMDA-receptor antagonists are effective following acute ischemic stroke. However, to be effective they need to be administered almost immediately after the stroke. The excessive internal concentrations of Na+ and Ca2+ ions in postsynaptic neurons affect them in two ways: -They trigger the release of excessive amounts of glutamate from the neurons, thus spreading the toxic cascade to yet other neurons; and they trigger a sequence of internal reactions that ultimately kill the postsynaptic neurons. tissue plasminogen activator (a drug that breaks down blood clots) or an endovascular therapy (the surgical removal of a thrombus or embolus from an artery). Administration of these treatments within a few hours after the onset of ischemic stroke can lead to better recovery. TRAUMATIC BRAIN INJURIES About 50–60 million people experience some form of traumatic brain injury (TBI) each year; and about 50 percent of us will experience a TBI at least once in our lives. Closed-head TBIs- brain injuries produced by blows that do not penetrate the skull. Types of closed-head TBIs Contusions- are closed-head TBIs that involve damage to the cerebral circulatory system. -Such damage produces internal hemorrhaging, which in turn produces a localized collection of blood in the brain—in other words, a bruised brain. -Occurs when the brain slams against the inside of the skull. -Skull is the major factor for the development of contusions. -contussions frequently occur on the side of the brain opposite the side struck by a blow. Subdural space—the space between the dura mater and arachnoid membrane, and severely distort the surrounding neural tissue. Subdural hematoma- “puddle” of blood. Contrecoup injuries- is that the blow causes the brain to strike the inside of the skull on the other side of the head. Mild TBI (mTBI)- when there is a disturbance of consciousness following a blow to the head and there is no evidence of a contusion or other structural damage. -most TBIs are mTBIs. -once called concussions. The term “concussion” is no longer deemed appropriate because it was associated with the mistaken assumption that its effects involved no long-term damage. Chronic traumatic encephalopathy (CTE) is the dementia (general intellectual deterioration) and cerebral scarring often observed in boxers, rugby players, American football players, and other individuals who have experienced repeated mTBIs. INFECTIONS OF THE BRAIN Invasion of the brain by microorganisms is a brain infection, and the resulting inflammation is called encephalitis. 2 common types of brain infections: bacterial infections and viral infections. *Bacterial infections- when bacteria infect the brain, they often lead to the formation of cerebral abscesses—pockets of pus in the brain. Bacteria are also the major cause of meningitis (inflammation of the meninges). Penicillin and other antibiotics sometimes eliminate bacterial infections of the brain, but they cannot reverse brain damage that has already been produced. Syphilis- are passed from infected to noninfected individuals through contact with genital sores. The infecting bacteria then go into a dormant stage for several years before they become virulent and attack many parts of the body, including the brain. General paresis- the syndrome of mental illness and dementia that results from a syphilitic infection. *Viral Infections There are two types of viral infections of the nervous system: those that have a particular affinity for neural tissue and those that attack neural tissue but have no greater affinity for it than for other tissues. Rabies, which is usually transmitted through the bite of a rabid animal, is a well-known example of a virus that has a particular affinity for the nervous system. The fits of rage caused by the virus’s effects on the brain increase the probability that rabid animals that normally attack by biting will spread the disorder. -It does not usually attack the brain for at least a month after it has been contracted, thus allowing time for preventive vaccination. The mumps and herpes viruses are common examples of viruses that can attack the nervous system but have no special affinity for it. Although these viruses sometimes spread into the brain, they typically attack other tissues of the body. Viruses involvement in the etiology (cause) of disorders is often difficult to recognize because they can lie dormant for many years before producing symptoms. NEUROTOXINS The nervous system can be damaged by exposure to anyone of a variety of toxic chemicals—chemicals that can enter general circulation from the gastrointestinal tract, from the lungs, or through the skin. Toxic psychosis- chronic mental illness produced by a neurotoxin. Tardive dyskinesia (TD)— Its primary symptoms are involuntary smacking and sucking movements of the lips, thrusting and rolling of the tongue, lateral jaw movements, and puffing of the cheeks. Some neurotoxins are endogenous (produced by the patient’s own body). Stress hormones, such as cortisol, are also believed to produce neurotoxic effects. GENETIC FACTORS Some neuropsychological diseases of genetic origin are caused by abnormal recessive genes that are passed from parent to offspring. Individuals who inherit one abnormal recessive gene do not develop the disorder, and the gene is passed on to future generations. Down syndrome- occurs in the mother during ovulation, when an extra chromosome 21 is created in the egg. Thus, when the egg is fertilized, there are three chromosome 21s, rather than two, in the zygote. -The consequences tend to be characteristic disfigurement, intellectual disability, early-onset Alzheimer’s disease (a type of dementia), and other troublesome medical complications. Inherited factors play major roles in virtually all neuropsychological disorders, and it seemed that the offending genes would soon be identified and effective treatments developed to target them. First, numerous loci on human chromosomes have been associated with each disorder—not just one or two. Second, about 90 percent of the chromosomal loci involved in neuropsychological disorders did not involve protein-coding genes; rather, the loci were in poorly understood sections of the DNA. PROGRAMMED CELL DEATH Apoptosis- a process of neurons and other cells that have genetic programs for destroying themselves. -plays a critical role in early development by eliminating extra neurons. It also plays a role in brain damage. Necrosis- passive cell death resulting from injury. It now seems that if cells are not damaged too severely, they will attempt to marshal enough resources to destroy themselves via apoptosis. Apoptosis is clearly more adaptive than necrosis. In necrosis, the damaged neuron swells and breaks apart, beginning in the axons and dendrites and ending in the cell body. This fragmentation leads to inflammation, which can damage other cells in the vicinity. Necrotic cell death is quick—it is typically complete in a few hours. In contrast, apoptotic cell death is slow, typically requiring a day or two. Apoptosis of a neuron proceeds gradually, starting with shrinkage of the cell body. Then, as parts of the neuron die, the resulting debris is packaged in vesicles—a process known as blebbing (one of my (SB) favorite words). As a result, there is no inflammation, and damage to nearby cells is kept to a minimum. NEUROLOGICAL DISEASES EPILEPSY Epileptic seizure- primary symptom of epilepsy, but not all persons who suffer seizures are considered to have epilepsy. -such a one-time seizure could be triggered by exposure to a convulsive toxin or by a high fever. The diagnosis of epilepsy is applied to only those patients whose seizures are repeatedly generated by their own chronic brain dysfunction. Convulsions (motor seizures)- these often involve tremors (clonus), rigidity (tonus), and loss of both balance and consciousness. Most seizures involve subtle changes of thought, mood, or behavior that are not easily distinguishable from normal ongoing activity. Many cases of epilepsy are associated with faults at inhibitory synapses, synapses that are normally responsible for preventing excessive excitatory activity in the brain. Dysfunctional activity in the astrocytes is also implicated in the development of seizures. The diagnosis of epilepsy rests heavily on evidence from electoencephalography(EEG). Epileptic auras- some individuals with epilepsy experience peculiar psychological changes just before the seizure. Epileptic auras are important for two reasons; First, the nature of the auras provides clues concerning the location of the epileptic focus. Second, epileptic auras can warn the patient of an impending convulsions. Focal seizures/generalize seizures- a seizure that does not involve the entire brain. The synchronous activity does not spread to the entire brain. They are not often accompanied by a total loss of consciousness or equilibrium. -The specific behavioral symptoms depend on where the disruptive discharges begin and into what structures they spread. Simple seizures- are focal seizures whose symptoms are primarily sensory or motor or both; they are sometimes called Jacksonian seizures after the famous 19th-century neurologist Hughlings Jackson. Simple seizures involve only one sort of sensory or motor symptom, and they are rarely accompanied by a loss of consciousness. Complex seizures- often begin in the temporal lobes and usually do not spread out of them. Accordingly, those who experience them are often said to have temporal lobe epilepsy. About half of all cases of epilepsy in adults are of the complex variety. During a complex seizure, the patient engages in compulsive, repetitive, simple behaviors commonly referred to as automatisms and in more complex behaviors that appear almost “normal.” International League Against Epilepsy (ILEA)—the group responsible for defining the diagnostic criteria for seizures and epilepsy. Recommends that focal seizures be classified in terms of the level of disruption of consciousness during the seizure, ranging from no disruption of consciousness (as is true for many simple seizures) to disrupted consciousness (as is true for many complex seizures). Generalized seizures- involve the entire brain. Some begin as focal discharges that gradually spread through the entire brain. Such sudden-onset generalized seizures may result from diffuse pathology or may begin focally in a structure, such as the thalamus, that projects to many parts of the brain. Tonic-clonic seizure- the primary symptoms are loss of consciousness, loss of equilibrium, and a violent tonic-clonic convulsion (that is, a convulsion involving both tonus and clonus). Tongue biting, urinary incontinence, and cyanosis (turning blue from a lack of oxygen during a convulsion) are common manifestations of tonic-clonic convulsions. Hypoxia- a shortage of oxygen supply to a tissue, such as brain tissue, that accompanies a tonic-clonic seizure can itself cause brain damage. Absence seizures- second type of generalized seizure. Are not associated with convulsions; their primary behavioral symptom is a loss of consciousness associated with a cessation of ongoing behavior, a vacant look, and sometimes fluttering eyelids. -most common in children, and they frequently cease at puberty The EEG of an absence seizure is different from that of other seizures; it is a bilaterally symmetrical 3-per-second spike-and-wave discharge. Although there is no cure for epilepsy, the frequency and severity of seizures can often be reduced by anticonvulsant medication. Other treatment options include stimulation of the vagus nerve, transcranial magnetic stimulation, and the ketogenic diet (a diet consisting of high levels of fat, moderate levels of protein, and low levels of carbohydrates). Brain surgery is sometimes used. PARKINSON’S DISEASE Parkinson’s disease is a movement disorder of middle and old age that affects 1–2 percent of the population over the age of 65. The initial symptoms of Parkinson’s disease are mild—perhaps no more than a slight stiffness or tremor of the fingers—but they inevitably increase in severity with advancing years. The most common symptoms of the full-blown disorder are a tremor that is pronounced during inactivity but not during voluntary movement or sleep, muscular rigidity, difficulty initiating movement, slowness of movement, and a masklike face. There is a more rapid cognitive decline with age in Parkinson’s patients than in the general population. A majority of Parkinson’s patients will display symptoms of dementia if they live for more than 10 years after their initial diagnosis. In the majority of cases, there is no obvious cause, and no family history of the disorder. Most cases of Parkinson’s disease are likely the result of interactions between multiple genetic and environmental factors. Substantia nigra—the midbrain nucleus whose neurons project via the nigrostriatal pathway to the striatum of the basal ganglia. Dopamineis normally the major neurotransmitter released by most neurons of the substantia nigra, there is little dopamine in the substantia nigra and striatum of long-term Parkinson’s patients. Autopsy often reveals clumps of a protein called alpha-synuclein in the surviving dopaminergic neurons of the substantia nigra—these clumps are known as Lewy bodies. The symptoms of Parkinson’s disease can be alleviated by injections of L-dopa—the chemical from which the body synthesizes dopamine. However, l-dopa is not a permanent solution; it typically becomes less and less effective with continued use, until its side effects outweigh its benefits. Deep brain stimulation- is a treatment option when medication is not effective in the treatment of Parkinson’s disease. ). Unfortunately, it can cause side effects such as cognitive, speech, and gait problems, and it does not slow the progression of Parkinson’s disease. Subthalamic nucleus- a nucleus that lies just beneath the thalamus and is richly connected to the basal ganglia. HUNTINGTON’S DISEASE Huntington’s disease is a progressive motor disorder, it is rare (1 in 7,500), it has a simple genetic basis, and it is always associated with severe dementia. The first clinical sign of Huntington’s disease is often increased fidgetiness. As the disorder develops, rapid, complex, jerky movements of entire limbs (rather than individual muscles) begin to predominate. Also prominent are psychiatric symptoms and cognitive deficits. Eventually, motor and cognitive deterioration become so severe that sufferers are incapable of feeding themselves, controlling their bowels, or recognizing their friends and relatives. There is no cure; death typically occurs about 20 years after the appearance of the first symptoms. Huntington’s disease is passed from generation to generation by a single mutated dominant gene, called huntingtin. The protein it codes for is known as the huntingtin protein. Because the gene is dominant, all individuals carrying the gene develop the disorder, as do about half their offspring. The huntingtin gene has remained in the gene pool because, once inherited, the first symptoms of the disease do not appear until after the peak reproductive years (at about age 40). The cell death in the striatum destroys the connections between the striatum and the cortex, and it is this disconnection which is believed to result in the early symptoms of Huntington’s disease. MULTIPLE SCLEROSIS Multiple sclerosis (MS)-is a progressive disease that attacks the myelin of axons in the CNS. The first symptoms typically appear in early adulthood. Autoimmune disorder—a disorder in which the body’s immune system attacks part of the body as if it were a foreign substance. In MS, the myelin sheath on axons is the focus of the faulty immune reaction. Experimental autoimmune encephalomyelitis- an animal model of MS, can be induced by injecting laboratory animals with myelin and a preparation that stimulates the immune system. The progression of MS is driven by an interaction between immune-system reactivity and neural degeneration. Remyelination -refers to the generation of new myelin sheaths on axons—a job taken care of by oligodendroglia in the CNS. Diagnosing MS is typically done with MRI, and it focuses on identifying the time course of development of white-matter lesions. MRI-based diagnosis is typically complex because the nature and severity of MS lesions depends on a variety of factors, including their number, size, and location. Common symptoms of advanced MS are visual disturbances, muscular weakness, numbness, tremor, and ataxia (loss of motor coordination). In addition, cognitive deficits and emotional changes occur in some patients. Epidemiology- is the study of the various factors such as diet, geographic location, and age that influence the distribution of a disease in the general population. Immunomodulatory drugs- were approved for the treatment of MS, and a large number of them are now available for MS treatment. Although these drugs are still widely prescribed for MS, their benefits are only marginal, and they help only some MS patients. ALZHEIMER’S DISEASE Alzheimer’s disease is the most common cause of dementia in the elderly; it currently affects about 50 million people worldwide. -terminal illness 3 stages Preclinical stage- involves pathological changes in the brain without any behavioral or cognitive symptoms. Prodromal stage- involves mild cognitive impairment. The cognitive impairment observed during this stage is not nearly as severe as that seen in full-blown Alzheimer’s disease but it is an indicator that the symptoms of Alzheimer’s disease are progressing. Dementia stage- there is initially a progressive decline in memory, deficits in attention, and personality changes; this is eventually followed by marked confusion, irritability, anxiety, and deterioration of speech. Eventually the patient deteriorates to the point that even simple responses such as swallowing and bladder control are difficult. 3 defining neuropathological characteristics Neurofibrillary tangles- are threadlike tangles of tau protein in the neural cytoplasm. Tau protein normally plays a role in maintaining the overall structure of neurons. Amyloid plaques- are clumps of scar tissue composed of degenerating neurons and aggregates of another protein called beta-amyloid which is present in healthy brains in only small amounts. Neurofibrillary tangles are particularly prevalent in medial temporal lobe structures such as the entorhinal cortex, amygdala, and hippocampus—all structures involved in various aspects of memory. Mutations to four different genes have been shown to contribute to the early-onset, familial form; however, these four gene mutations seem to contribute little (only about 1 percent) to the more common, late-onset form. Attention has focused on one particular gene, the gene on chromosome 19 that codes for the protein apolipoprotein E (APOE). APOE binds to beta-amyloid, and that such binding reduces beta-amyloid clearance from the brain, and it increases beta-amyloid clumping, leading to the development of amyloid plaques. There is currently no cure for Alzheimer’s disease. amyloid plaques are the primary symptom of the disorder; that is, the plaques cause all the other symptoms. High-plaque normals- many people without observable dementia carry significant loads of amyloid plaques. However, these high-plaque normals also lacked the inflammation associated with Alzheimer’s disease. It is widely believed that in order to be effective against Alzheimer’s disease, treatments must be administered during the preclinical or prodromal stages. The problem is that when patients first seek help for Alzheimer’s symptoms, they typically are already in the dementia stage and have extensive brain pathology. 15 percent of the neurons in the brains of Alzheimer’s patients without Down syndrome contain an extra copy of chromosome 21. Pathogenic spread hypothesis- proposes that many common neurodegenerative diseases (e.g., Alzheimer’s disease, Parkinson’s disease) result from the presence of misfolded proteins that initiate a chain reaction causing other proteins to misfold. 3.3 MOVEMENT The Control of Movement Three categories of Vertebrate Muscles smooth muscles control the digestive system and other organs, skeletal or striated muscles control movement of the body in relation to the environment Cardiac Muscles controls the heart Muscles and Their Movements Eachmuscleiscomposedofmanyfibers, Although Each Muscle Fiber Receives Information from only one axon, a given axon may innervate more than one muscle fiber. An axon branching to innervate several muscle fibers. A neuromuscular junction is a synapse between a motor neuron axon and a muscle fiber. In skeletal muscles, every axon releases acetylcholine at the neuromuscular junction, and acetylcholine always excites the muscle to contract. A deficit of acetylcholine or its receptors impairs movement. Each muscle makes just one movement, a contraction. There is nomessagetocauserelaxation;the muscle relaxes when it receives no message to contract. There is also no message to move a muscle in the opposite direction. Biceps contracts Triceps relaxes Biceps relaxes extensor muscle -straightensthearm flexor muscle- brings your hand toward your shoulder Antagonistic Muscles-Movingalegor arm back and forth requires opposing sets of muscles,Triceps contracts FastandSlow Muscles fast-twitch fibers -withfastcontractions and rapid fatigue. Prolonged use of fast-twitch fibers results in fatigue because the process is anaerobic usingreactionsthatdonotrequire oxygen at the time but need oxygen for recovery. slow-twitch fibers-with less vigorous contractions and no fatigue, Slow-twitch fibers do not fatigue because they are aerobic—they use oxygen during their movements. Muscle Control by Proprioceptors Proprioceptors - Muscle proprioceptors detect the stretch and tension of a muscle and send messages that enable the spinal cord to adjust its signals. When a muscle is stretched, the spinal cord sends a signal to contract it reflexively. Muscle spindle- Wheneverthe muscle is stretched more than the antagonistic muscle,the muscle spindle sends a message to a motorneuroninthespinalcord, which in turn sends a message back to the muscle, causing a contraction. Golgitendonorgans- They act as a brake against an excessively vigorous contraction. Golgi Tendon organs detect the tension that results during a muscle contraction. Avigorous muscle contraction inhibits further contraction by activating the Golgi tendon organs. Voluntary and Involuntary Movements Reflexes are consistent automatic responses to stimuli. We generally think of reflexes as involuntary because they are insensitive. Movements Varying in Sensitivity to Feedback Aballistic movement,- such as a reflex,is executed as a whole: Once initiated, it cannot be altered. Sequences of Behaviors Central pattern generators, - neural mechanisms in the spinal cord that generate rhythmic patterns of motor output. The stimulus that activates a central pattern generator does not control the frequency of the alternating movements. A fixed sequence of movements is called a motor program.Once Begun,thesequence is fixed from beginning to end. Brain Mechanism of Movement The Cerebral Cortex also called “gray matter” the outermost layer of nerve cell tissue. It plays the key role in memory, thinking, learning, reasoning , problem solving, emotions, consciousness and function related to our senses. Primary Motor Cortex the pre central gyrus of the frontal cortex just anterior to the central sulcus to elicit movements. It provides most of the output to medulla and spinal cord The primary motor cortex is also active when you imagine movements, remember movements, or understand verbs related to movements (Tomasino & Gremese, 2016). Primary Somatosensory Cortex feels which part of the body, and which areas of the motor cortex control muscles in which parts of the body. Primary Motor Cortex Movement Planning Execution of Movements Control of Muscle Groups Motor Learning Primary Somatosensory Cortex Spatial Awareness Tactile Discrimination Integration of Sensory Inputs Body Image and Schema Response to Pain THROWING A BALL How do they work together? Sensory Input Processing: The somatosensory cortex receives and interprets sensory information from the body, such as touch, position, and pain. Feedback Loop: As movements are initiated, the somatosensory cortex continuously monitors sensory feedback, providing real-time data about body position and movement. Motor Planning: Based on the sensory input, the primary motor cortex plans and initiates movements, selecting the appropriate motor commands for precise execution. Coordination: The two areas communicate to ensure smooth coordination. The somatosensory cortex informs the primary motor cortex about adjustments needed based on ongoing sensory feedback. Learning and Adaptation: Together, they contribute to motor learning, allowing for adaptation and refinement of movements through practice and experience. Response to Errors: If discrepancies between intended and actual movement occur (e.g., if an object is missed), the somatosensory cortex helps detect this, enabling the primary motor cortex to adjust future movements accordingly. Antisaccade Task The antisaccade task is a cognitive psychology test used to study eye movement control and executive functions. In this task, participants are asked to look in the opposite direction of a visual stimulus that suddenly appears. For example, if a target appears on the right side, participants must look to the left. Overall, the antisaccade task is a valuable tool in both clinical and experimental settings for exploring the intricacies of cognitive control and eye movement. Mirror Neurons are active both during preparation for a movement and while watching someone else perform the same or similar movement are activated not only by seeing an action, but also any reminder of actions. Certain cells respond to hearing an action as well as seeing or doing it. CONNECTIONS FROM THE BRAIN TO THE SPINAL CORD Corticospinal Tracts - paths from cerebral cortex to the spinal cord Lateral Corticospinal Tract - is a pathway of axons from the primary motor cortex Red Nucleus - a midbrain area that controls certain aspects of movements Pyramids - bulges of the medulla; lateral tract crosses to the contralateral (opposite) side of the spinal cord. It controls movements in peripheral areas, especially the hands and feet. Medial Corticospinal Tract - includes axons from many parts of the cerebral cortex, not just the primary motor cortex and its surrounding. Vestibular Nucleus - brain areas that receive input from the vestibular system. Medial Tracts - controls mainly the muscles of the neck, shoulders and trunk and therefore bilateral movements as walking, turning, bending and standing up, and sitting down. Lateral Tract - controls muscles in the lateral parts of the body, such as hands and feet. Medial Tract - controls muscles in the medial parts of the body including trunk and neck. Finger to Nose Test The finger-to-nose test is a simple neurological exam used to assess coordination, balance, and fine motor skills. During the test, a person is asked to touch their own nose with their finger, often while their eyes are closed, and then touch the examiner's finger or a target placed at a distance. Cerebellum Latin for “little brain” It function as balance and coordination It contains more neurons than the rest of the brain combined and a huge number of synapses. Cellular Organization are axons parallel to one another and perpendicular to the planes of the Purkinje cells. are flat (two dimensional) cells in sequential planes, parallel to one another Basal Ganglia The Basal Ganglia controls the vigor of movements It has more influence on self-initiated movements which are generally slower The Basal Ganglia are essential for learning motor habits that are difficult to describe in words. Libet’s Study of Conscious Decision and Movement Measurements Readiness Potential (RP): An electrical activity in the brain (specifically the motor cortex) that occurs before voluntary movement. Conscious Awareness: Participants noted the exact moment they became consciously aware of their decision to move. Movement Disorders Movement Disorder refers to abnormal conditions affecting motor systems, characterized by disruptions in normal neural networks leading to various forms of abnormal motor behavior. They could be increased movement (like spasms, jerking or shaking). Parkinson’s Disease Strikes 1 to 2 percent of people over age 65, results from the gradual loss of dopamine- releasing axons from the substantia nigra to the striatum. Causes & Treatment Combination of Genetic and Environmental Factors Genetic Researchers have identified at least 28 gene variants that increase the risk of Parkin son’s disease. None of those genes by itself has a major effect, but having several of them produces a cumulative effect. Still, no one can examine your chromosomes and predict with much accuracy whether or not you will develop the disease Environmental Factors In Northern California 1982, several young adults developed symptoms of Parkinson’s disease after using a drug similar to heroin. Many other users had developed symptoms ranging from mild to fatal. The substance responsible for the symptoms was MPTP, a chemical that the body converts to MPP+, which accumulates in, and then destroys, neurons that release dopamine, partly by impairing the transport of mitochondria from the cell body to the synapse. L-Dopa Treatment Because Parkinson’s disease results from a dopamine deficiency, a logical goal is to restore the missing dopamine. A dopamine pill would be ineffective because dopamine does not cross the blood–brain barrier, and since Levodopa or L- dopa is a precursor to dopamine that does cross the barrier, it might be a good treatment. However, L-dopa treatment increases dopamine release in all axons, including those that had deteriorated and those that were still functioning normally. Even if it adequately replaces lost dopamine, it does not replace other transmitters that are also depleted. It does not slow the continuing loss of neurons. Huntington’s Disease Huntington’s disease (also known as Huntington’s chorea) is an incurable neurological disorder that is mostly inherited.  Huntington’s disease can occur at any age, but most often between the ages of 30 and 50. Once the symptoms emerge, both the psychological and motor symptoms grow progressively worse and culminate in death (Chorea comes from the same root as choreography. The rhythmic writhing of chorea resembles dancing.) Gradually, the tremors interfere more and more with walking, speech, and other voluntary movements. People lose the ability to develop motor skills. Symptoms Motor symptoms usually begin with arm jerks and facial twitches. Then tremors spread to other parts of the body and develop into writhing People with Huntington’s disease also suffer psychological disorders including apathy, depression, sleeplessness, memory impairment, anxiety, hallucinations and delusions, poor judgment, alcoholism, drug abuse, and sexual disorders ranging from complete unresponsiveness to indiscriminate promiscuity. Symptoms & Causes Heredity and Presymptomatic Testing In 1993, researchers located the gene for Huntington’s disease on chromosome number 4, a spectacular accomplishment for the technology available at the time.. Now an examination of your chromosomes can reveal with almost perfect accuracy whether or not you will get Huntington’s disease. The critical area of the gene includes a sequence of bases C-A-G (cytosine, adenine, guanine), which is repeated 11 to 24 times in most people. That repetition produces a string of 11 to 24 glutamines in the resulting protein. Up to 35 C-A-G are considered safe from Huntington’s. 36 to 38, possibly even 39 or 40, might not get the disease, and if they do, it probably will not manifest until old age. People with more repetitions are nearly certain to get the disease, unless they die of other causes earlier. Similarity and Difference Parkinson’s Disease and Huntington’s Disease, Both Parkinson’s disease and Huntington’s disease are progressive neurodegenerative disorders that affect the central nervous system. In Parkinson's disease, people may experience rigidity and slowed movements, while in Huntington's disease, people may experience cognitive and psychological symptoms. Conclusion Emphasize the point that control of movement is closely related to cognition. People with either condition are likely to suffer apathy, cognitive deficits, and a lack of pleasure and motivation. The psychological problems often develop before any noticeable motor problems. In short, the mechanisms of movement are also the mechanisms of thought. MODULE 4.3: PLASTICITY AFTER BRAIN DAMAGE Almost all survivors of brain damage show behavioral recovery to some degree. Some of the mechanisms rely on the growth of new branches of axons and dendrites, similar to the mechanisms of brain development. Possible causes of brain damage include tumors, infections, exposure to radiation or toxic substances, and degenerative conditions such as Parkinson’s disease and Alzheimer’s disease. Closed head injury - a sharp blow to the head that does not puncture the brain. - most common in young people - The effects of closed head injury depend on severity and frequency. One cause of damage after closed head injury is the rotational forces that drive brain tissue against the inside of the skull. Another cause is blood clots that interrupt blood flow to the brain. A common cause of brain damage, especially in older people, is temporary interruption of normal blood flow to a brain area during a stroke. Stroke- known as a cerebrovascular accident. Ischemia - A common type of stroke - It is the result of a blood clot or other obstruction in an artery. - In ischemia, the neurons deprived of blood lose much of their oxygen and glucose supplies Hemorrhage - less common stroke - result of a ruptured artery. - In hemorrhage, the neurons are flooded with blood and excess oxygen, calcium, and other chemicals Edema- (the accumulation of fluid), which increases pressure on the brain and the probability of additional strokes. Both ischemia and hemorrhage also impair the sodium– potassium pump, leading to an accumulation of sodium inside neurons. The combination of edema and excess sodium provokes excess release of the transmitter glutamate, which over-stimulates neurons, damaging both neurons and synapses. Immediate Treatments Tissue plasminogen activator (tPA)- breaks up blood clots. To get a benefit, a patient should receive tPA quickly, at least within 4.5 hours after a stroke. It is difficult to determine whether a stroke was ischemic or hemorrhagic. An MRI scan distinguishes between the two kinds of stroke, but MRIs take time, and time is limited. Treatments might be effective shortly after a stroke: strokes kill neurons by overstimulation, one approach has been to decrease stimulation by blocking glutamate synapses or blocking calcium entry. Other approaches include cooling the brain, antioxidants, antibiotics, albumin, and treatments affecting the immune system Exposure to cannabinoids (the chemicals found in marijuana) minimizes the damage caused by strokes in laboratory animals. One theoretical rationale was that cannabinoids decrease the release of glutamate. Cannabinoids are helpful only if administered within the first hours after a stroke. In fact, the research on laboratory animals indicates that cannabinoids are most effective if taken shortly before the stroke. One study did find that stroke patients with cannabinoids in their bloodstream, indicating marijuana use before the stroke, had on average less severe damage from the stroke. What are the two kinds of stroke, and what causes each kind? - The more common form, ischemia, is the result of occlusion of an artery. The other form, hemorrhage, is the result of a ruptured artery. Why is tPA not helpful in cases of hemorrhage? - The drug tPA up blood clots, and hemorrhage results from a blood vessel, not a blood clot. Later Mechanisms of Recovery After the first days following brain damage, many of the surviving brain areas increase or reorganize their activity. In most cases the recovery depends mostly on increased activity by the spared cells surrounding the area of damage. Increased Brain Stimulation A behavioral deficit after brain damage reflects more than just the cells that died. After damage to any brain area, other areas that have lost part of their normal input become less active. For example, shortly after damage in one brain hemisphere, its input to the other hemisphere declines, and therefore the other hemisphere shows deficits also. Diaschisis - from a Greek term meaning “to shock throughout” - refers to the decreased activity of surviving neurons after damage to other neurons. - If diaschisis contributes to behavioral deficits following brain damage, then increased stimulation should help. Injecting amphetamine significantly enhanced both behaviors, and animals that practiced the behaviors under the influence of amphetamine showed long lasting benefits. Injecting a drug to block dopamine synapses impaired behavioral recovery. After someone has had a stroke, would it be best (if possible) to direct stimulant drugs to the cells that were damaged or somewhere else? - is best to direct a stimulant drug to the cells that have been receiving input from the damaged cells. Presumably, the loss of input has produced diaschisis. Regrowth of Axons Damage to the brain or spinal cord damages many axons of neurons that survived the damage. Damaged axons in the peripheral nervous system do grow back at a rate of about 1 mm per day, following its myelin sheath to the original target. Damaged axons also grow back in the spinal cord of a fish, under the control of a gene that is active in glia cells However, axons do not grow back in the mammalian brain or spinal cord, at least not enough to produce any benefit  A cut in the nervous system causes astrocytes to form scar tissue, thicker in mammals than in fish The astrocytes release chemicals that keep nearby neurons alive, and procedures that remove the scar lead to tissue degeneration A damaged axon does not automatically start growing back. If the damaged axons were sensory rather than motor, then extensive sensory experience is necessary for the axons to restore function Ordinarily, the surface of dendrites and cell bodies is covered with synapses, and a vacant spot doesn’t stay vacant for long. After a cell loses input from an axon, it secretes neurotrophins that induce other axons to form new branches, or collateral sprouts, that take over the vacant synapses. In the area near the damage, new synapses form at a high rate, especially for the first two weeks. Collateral sprouting in the cortex contributes to behavioral recovery in some cases. However, the result depends on whether the sprouting axons convey information similar to those that they replace. For example, the hippocampus receives much input from an area called the entorhinal cortex. If the entorhinal cortex is damaged in one hemisphere, then axons from the entorhinal cortex of the other hemisphere sprout, take over the vacant synapses, and largely restore behavior. However, if the entorhinal cortex is damaged in both hemispheres, then axons from other locations sprout into the vacant synapses, conveying different information. Under those conditions, the sprouting interferes with behavior and prevents recovery. Denervation Supersensitivity Neurons make adjustments to maintain a nearly constant level of arousal. After learning strengthens one set of synapses, other synapses weaken. Conversely, if a certain set of synapses becomes inactive—perhaps because of damage elsewhere in the brain—the remaining synapses become more responsive, more easily stimulated. This process of enhanced response, known as Denervation supersensitivity or receptor supersensitivity. Denervation supersensitivity or receptor supersensitivity- has been demonstrated mostly with dopamine synapses. Denervation supersensitivity helps compensate for decreased input. However, when either collateral sprouting or denervation supersensitivity occurs, it can strengthen not only the desirable connections, but also undesirable ones, such as those responsible for pain. Is collateral sprouting a change in axons or dendritic receptors? - Axon Is denervation supersensitivity a change in axons or dendritic receptors - Dendritic receptors Reorganized Sensory Representations and the Phantom Limb If a brain area loses some of its incoming axons, we can expect denervation supersensitivity, collateral sprouting, or both. The result is either increased response to a synapse that previously produced little effect, or response to an axon that previously did not attach at all What happens if an entire arm is amputated? - They found that the stretch of cortex previously responsive to that limb was now responsive to the face. After loss of sensory input from the forelimb, the axons representing the forelimb degenerated, leaving vacant synaptic sites at several levels of the CNS. Evidently, axons representing the face sprouted into those sites in the spinal cord, brainstem, and thalamus. Or perhaps axons from the face were already present but became stronger through denervation supersensitivity. Phantom limb - a continuing sensation of an amputated body part. - That experience can range from tingling to intense pain, either occasionally or constantly. - The phantom sensation might last days, weeks, or a lifetime. Modern methods show that phantom limbs develop when the relevant portion of the somatosensory cortex reorganizes and becomes responsive to alternative inputs. For some people, seeing someone else being touched can also elicit a sensation in the phantom limb. For example, suppose axons representing the face come to activate the cortical area previously devoted to an amputated hand. A touch on the face now produces a facial sensation but it also produces a sensation in the phantom hand. The part of the cortex responsive to the feet is adjacent to the part responsive to the genitals. Two patients with foot amputations felt a phantom foot during sexual arousal! One reported feeling orgasm in the phantom foot as well as the genitals—and enjoyed it intensely. The representation of the genitals had spread into the cortical area responsible for foot sensation. Is there any way to relieve a painful phantom sensation? - In some cases, yes. Many amputees who learn to use an artificial arm report that their phantom sensations gradually disappear. As they start attributing sensations to the artificial arm, they displace the abnormal connections that caused phantom sensations. What is responsible for the phantom limb experience? - Synapses that used to receive input from the now amputated part become vacant. Axons representing another part of the body take over those synapses. Now stimulation of this other part activates the synapses associated with the amputated area, but that stimulation is like the amputated area. Someone with brain damage may have lost some ability totally or may be able to find it with enough effort. Much recovery from brain damage depends on learning to make better use of the abilities that were spared. For example, if you lose your peripheral vision, you learn to move your head from side to side to compensate. Deafferented- lost of afferent (sensory) input. A person with brain damage who appears to be functioning normally is working harder than usual. The recovered behavior deteriorates markedly after drinking alcohol, physical exhaustion, or other kinds of stress that would minimally affect most other people. It also deteriorates in old age. A monkey that loses sensation from one arm stops using it, but a monkey that loses sensation from both arms does use them. Why? - A monkey that lost sensation in one arm is capable of moving it, but finds it easier to walk with the three intact limbs. When both arms lose their sensations, the monkey is forced to rely on them. Module 4.1 Genetics and Evolution of Behavior Everything you do depends on both your genes and your environment. Consider facial expressions. A contribution of the environment is obvious: You smile more when the world is treating you well and frown when things are going badly. Does heredity influence your facial expressions? Researchers examined facial expressions of people who were born blind and therefore could not have learned to imitate facial expressions. Controversies arise when we move beyond the generalization that both heredity and environment are important. For example, do differences in human intelligence depend mostly on genetic differences, mostly on environmental influences, or both equally? Similar questions arise for sexual orientation, alcoholism, weight gain, mental illness, and much else that interests psychologists and the general public. This module should help you understand these issues, even when the answer remains uncertain. We begin with a review of genetics, a field that has become more and more complicated as research has progressed. Mendelian Genetics Historical Belief: Before Gregor Mendel’s studies, inheritance was thought to blend traits like colors mixing. Mendel’s Discoveries: Mendel demonstrated that inheritance happens through genes, distinct units that preserve their structure across generations. Genes typically exist in pairs on chromosomes, though male mammals have a unique unpaired X and Y chromosome arrangement. Gene Structure: Genes are found on DNA, but their arrangement isn’t always fixed. Some genes overlap, and parts of chromosomes can affect gene expression without producing proteins. Protein Synthesis: DNA sequences direct RNA synthesis, with messenger RNA (mRNA) guiding the creation of proteins. Proteins are assembled from 20 amino acids based on DNA and RNA codes. They form bodily structures or act as enzymes to regulate chemical reactions. Not all RNA produces proteins; some have regulatory functions. Genetic Variation: Homozygous: Both chromosomes have identical genes.  Heterozygous: Chromosomes carry different genes, allowing for varied traits (e.g., one gene for blue eyes, another for brown). Mendelian genetics laid the foundation for understanding heredity and genetic complexity, essential to biology and modern genetics. Gene Types: Dominant Genes: Show effects in both homozygous and heterozygous states (e.g., brown eye gene). Recessive Genes: Only show effects when homozygous (e.g., blue eye gene). PTC Taste Sensitivity Example: Dominant gene for high PTC sensitivity (T) results in tasting PTC; recessive gene (t) means low sensitivity. Heterozygous parents have a 25% chance of homozygous dominant (TT), 50% chance of heterozygous (Tt), and 25% chance of homozygous recessive (tt) offspring. Genetic Complexity: Traits like eye color involve multiple genes (10+), and height involves over 180. Genes interact, affecting multiple characteristics, with expression influenced by environmental factors and limited to certain cells. Sex-Linked and Sex-Limited Genes -Linked Genes: Found on sex chromosomes (X and Y), while other chromosomes carry autosomal genes. Females have two X chromosomes; males have one X and one Y. Males determine offspring sex by contributing an X (female) or Y (male) chromosome. X-Linked Traits: X-linked genes include traits like red-green color vision deficiency. Males with a recessive gene on the X chromosome are color deficient (no second X to counterbalance). Females require two copies of the recessive gene to exhibit color deficiency. Y Chromosome: Small but influences other genes. X-Linked Color Vision Deficiency: Color vision deficiency is X-linked, affecting about 8% of men (who have one X chromosome) but less than 1% of women (who have two X chromosomes). Sex-Limited Genes: Present in both sexes but active primarily in one, influenced by sex hormones. Examples: genes for chest hair in men, breast size in women, and reproductive traits in animals. Effects of sex-limited genes typically emerge at puberty due to hormonal changes. These genes contribute to traits influenced by biological sex differences. Genetic Changes Mutation: A heritable DNA change, often altering a single base. Mutations rarely benefit organisms but can have impactful exceptions, like two mutations in the human FOXP2 gene that support language development. Duplication and Deletion: A segment of a chromosome may appear twice (duplication) or be missing (deletion). Small duplications/deletions (microduplications/microdeletions) often contribute to neurological or psychological disorders, such as certain forms of schizophrenia. Genetic changes, though often disadvantageous, play critical roles in evolution and disease. Epigenetics Epigenetics and Gene Expression Overview Epigenetics explores gene expression changes that don’t alter the DNA sequence but impact gene function, often influenced by environment, behavior, or life events. Cell and Gene Activity: Every cell in the body shares the same DNA, yet different genes are active in different cell types and at various life stages, like puberty or fetal development. Inheritance of Epigenetic Changes: Experiences such as stress, nutrition, and trauma can trigger changes in gene expression that may carry over to future generations. Studies have shown that children of stressed or malnourished parents can inherit gene expression changes that affect their health and behavior. Histones and DNA Methylation: Gene expression changes occur through mechanisms like histone modification and DNA methylation. Histones, which bind DNA, may loosen or tighten to control gene activity, while methylation adds or removes methyl groups to turn genes on or off. Experiences Alter Genes: Events like trauma, learning, and environmental changes can switch genes on or off, impacting long-term behavior, mental health, and physical traits. This blurs the line between genetic inheritance and environmental influence, as experiences directly shape gene expression. Heredity and Environment of Genetics and Environment: Traits are shaped by both heredity and environment. Genetic heritability measures how much variation in traits can be attributed to genetics in a given population and time. Environmental effects can often interact with genetic predispositions, making this complex. Twin and Adoption Studies: By comparing identical and fraternal twins, or adopted children to both biological and adoptive parents, researchers assess genetic influence. Twin studies, for instance, show that traits like loneliness, cognitive performance, and even television watching often have substantial heritability. Role of Genetic Studies: Specific gene studies use candidate gene or genome-wide association approaches. The candidate approach focuses on individual genes thought to influence specific traits, while genome-wide studies search for patterns across the genome. However, such studies face challenges, including the difficulty of identifying genes with strong behavioral impacts, as most gene effects are small. Epigenetics and Gene Expression: Environmental influences also operate through epigenetic changes, which alter gene expression without changing DNA sequences. These changes can influence behaviors across generations. Stress, learning, and diet, for example, can lead to epigenetic modifications that influence traits like stress responses or memory. Implications and Limitations: Although genetics plays a major role in psychological traits, identifying the exact genetic underpinnings is challenging. Behavior is influenced by multiple genes with small individual effects, as well as complex interactions with environmental factors. Environmental Modification Genetic traits, even those with high heritability, can be significantly influenced by environmental interventions. A prime example is phenylketonuria (PKU), a genetic disorder resulting from a recessive gene that impairs the metabolism of the amino acid phenylalanine. If untreated, toxic levels can lead to intellectual disabilities, behavioral problems, and developmental delays. Approximately 1% of Europeans carry the recessive gene for PKU, but its prevalence is lower among other populations. Early newborn screening allows for the identification of elevated phenylalanine levels, prompting immediate dietary interventions. The prescribed low-phenylalanine diet is critical in preventing brain damage, yet it is difficult to maintain due to strict restrictions on high-protein foods like meats, eggs, and dairy products. Additionally, individuals must avoid artificial sweeteners such as aspartame, which contains phenylalanine. Initially, it was believed that children could discontinue the diet after several years. However, research has shown that elevated phenylalanine levels can still harm the mature brain, emphasizing the necessity of lifelong dietary management. For women with PKU, maintaining a strict diet during pregnancy and breastfeeding is crucial, as high phenylalanine levels can adversely affect fetal development. Overall, PKU illustrates how environmental factors, particularly diet, can modify genetic traits and their expression, highlighting the importance of early intervention and ongoing management to mitigate the impact of genetic disorders. How Genes Influence Behavior No gene produces its effects by itself. A gene produces a protein that interacts with the rest of body chemistry and with the environment. Exactly how a gene might influence behavior is a complex issue, with many answers in different cases. A gene could influence your behavior even without being expressed in your brain. Suppose your genes make you unusually attractive. As a result, strangers smile at you and many people want to get to know you. If their reactions to your appearance influence your personality, then the genes alter your behavior by altering your environment! For another example, imagine a child born with genes promoting greater than average height and running speed. Because of these factors, the child shows early success at basketball, and soon spends more and more time playing basketball. As a result, the child spends less time than average on other pursuits—watching television, playing chess, or anything else. This is a hypothetical example, but it illustrates the point: Genes can influence behavior in roundabout ways. We should not be amazed by reports that nearly every human behavior has some heritability The Evolution of Behavior Charles Darwin, known as the founder of evolutionary theory, didn’t like the term evolution. He preferred descent with modification, emphasizing the idea of changes without necessarily implying improvement. Evolution is a changeover generations in the frequencies of various genes in a population. We distinguish two questions about evolution: How did some species evolve, and how do species evolve? To ask how a species did evolve is to ask what evolved from what. For example, because humans are more similar to chimpanzees than to other species, biologists infer a common ancestor. Fossils also help to illuminate changes over time. As new evidence becomes available, biologists sometimes change their opinions about the evolutionary relationship between one species and another. In contrast, the question of how species evolve is a question of how the process works, and that process is a necessary outcome from what we know about reproduction. The reasoning goes as follows: Because of genetic influences, offspring generally resemble their parents. That is, “like begets like.” Mutations, recombinations, and microduplications of genes introduce new heritable variations that help or harm an individual’s chance of surviving and reproducing. Certain individuals reproduce more than others do,thus passing on their genes to the next generation. Any gene that is associated with greater reproductive success will become more prevalent in later generations. Therefore, the current generation of any species resembles the individuals who reproduced in the past. If a change in the environment causes a different gene to increase the probability of survival and reproduction, then that gene will spread in the population. Because plant and animal breeders have long understood this idea, they choose individuals with a desired trait and make them the parents of the next generation through a process called artificial selection. Over many generations, breeders have produced exceptional racehorses, chickens that lay huge numbers of eggs, hundreds of kinds of dogs, and so forth. Darwin’s (1859) insight was that nature also selects. If certain individuals are more successful than others in finding food, escaping enemies, resisting illness, attracting mates, or protecting their offspring, then their genes will become more prevalent in later generations. Given a huge amount of time, this process can produce the wide variety of life that we in fact observe. Common Misunderstandings about Evolution. 1. Inheritance of Acquired Characteristics: Many believe that structures or behaviors can evolve through use or disuse, a concept attributed to Lamarck. For instance, they might think that because little toes are used less, they are shrinking in future generations. In reality, evolutionary change requires genetic variation; traits persist through reproduction, not usage. 2. Human Evolution and Survival: Some argue that modern medicine halts human evolution, claiming “survival of the fittest” is obsolete. However, evolution hinges on reproduction—if certain traits lead to higher reproductive success, those genes will thrive regardless of survival alone. 3. Evolution Equals Improvement: Evolution does not inherently mean improvement. It defines fitness as the success of gene propagation. A trait that’s beneficial today may become disadvantageous as environmental conditions shift. For instance, a peacock’s bright feathers attract mates but may also increase predation risks. 4. Benefits to Genes, Not Individuals or Species: Evolution favors genes that enhance their replication, not individuals or species. A gene that encourages self-sacrifice for offspring may spread if it results in more surviving descendants. Claims of species-level benefits, like lemmings jumping off cliffs, misinterpret natural selection, as such behaviors would eliminate the very genes promoting them. 1.Does the use or disuse of some structure or behavior cause an evolutionary increase or decrease in that feature? This misconception stems from Lamarckian evolution, which suggests that traits can evolve through use or disuse. In reality, traits are inherited based on genetic variations, not usage. 2. Have humans stopped evolving? Some argue that modern medicine prevents evolution, but evolution is based on reproduction, not just survival. Genes that confer reproductive advantages will continue to spread. 3. Does “evolution” mean “improvement”? Evolution refers to the success of gene propagation, not necessarily improvement. Traits beneficial in one environment may not be advantageous in another. 4. Does evolution benefit the individual or the species? Evolution favors genes that enhance replication. It does not support self-sacrificing behaviors that harm individuals, as those genes would not survive. Evolutionary Psychology Evolutionary psychology explores how behaviors evolved, emphasizing the evolutionary and functional explanations behind human actions. It posits that behaviors characteristic of a species emerged through natural selection, providing advantages in ancestral environments. Examples: Different species evolved distinct types of vision suited to their lifestyles. Animals that face danger while sleeping tend to sleep less than safer species. Dietary habits vary among species based on survival needs, such as bears storing fat versus small birds eating minimally. One significant behavior is the infant grasp reflex, which historically benefited our ancestors, allowing infants to cling to their mothers as they climbed trees or escaped predators. Controversial Explanations Some evolutionary explanations are debated: Sexual Behavior: More men than women show interest in casual sex. This might stem from reproductive advantages, as men can pass on their genes by impregnating multiple women, while women’s reproductive potential is limited. Aging: Humans typically live around 70-80 years, but genetic variations affect aging. Some researchers speculate that aging may have evolved to reduce competition with offspring, although some species continue to reproduce throughout their lives. Altruism Altruistic behavior, which benefits others at a cost to oneself, raises questions about its evolutionary advantages. Altruism exists in humans—through charitable acts and personal