Chapter 11: Body Senses and Movement

Arcuate Nucleus (ARC)

A hypothalamic region containing neurons that regulates appetite and feeding.

Substance P

A neuropeptide involved in pain signaling.

Deep Brain Stimulation (DBS)

Electrical stimulation of the brain through implanted electrodes.

Spinothalamic Tract

Itch and tickle have their own receptors, pathway, and receptor proteins,

Leptin

Leptin Fat cells ARC - Inhibts NPY releases and activates POMC neurons Terminates eating (long-term)

Encapsulated receptors

More complex structures enclosed in a membrane, role is to detect touch.

POMC Neurons

Neurons in the arcuate nucleus that inhibit eating.

NPY/AgRP Neurons

Neurons in the arcuate nucleus that promote eating

Chronic Pain

Pain that persists after healing has occurred, or beyond the time in which healing would be expected to occur.

Olfactory Receptor Cells

Sensory cells in the olfactory epithelium that detect odorants.

Primary Motor Cortex (precentral gyrus)

The area on the precentral gyrus responsible for the execution of voluntary movements by organizing the activity of unspecialized cells; adds force and direction control.

Corticospinal Tract

The corticospinal tract is a major pathway in the central nervous system responsible for carrying movement-related information from the motor cortex to the spinal cord. Here's a summary of its key features and functions: Upper Motor Neurons: Neurons that travel in the corticospinal tract are known as upper motor neurons. They originate in the motor cortex and carry motor commands for voluntary movements. Connection with Lower Motor Neurons: Upper motor neurons connect with lower motor neurons in the spinal cord. Lower motor neurons directly innervate muscles, causing them to contract and generate movement. Descending Pathway: The upper motor neurons descend from the motor cortex to the brainstem, entering the midbrain through structures known as the cerebral peduncles. Formation of Pyramids: As the corticospinal tract continues into the medulla, the fibers form two bundles known as the pyramids. These pyramids create visible ridges on the exterior surface of the brainstem. Pyramidal Decussation: At the base of the pyramids, approximately 90% of the fibers in the corticospinal tract cross over to the opposite side of the brainstem in a region called the pyramidal decussation. These crossed fibers then enter the spinal cord on the opposite side of the body. Lateral and Anterior Corticospinal Tracts: There are two subdivisions of the corticospinal tract: the lateral corticospinal tract and the anterior corticospinal tract. The lateral tract contains the majority of the corticospinal fibers and controls distal muscles like those in the hands. The anterior tract controls more proximal muscles such as those in the trunk. Functional Implications: Damage to the corticospinal tract can lead to a collection of symptoms known as upper motor neuron syndrome. These symptoms include weakness or paralysis, hyperactive reflexes, decreased motor control, and altered muscle tone. Fine motor movements like writing may remain impaired even if gross motor control improves. The corticospinal tract is a crucial pathway for the voluntary control of movement, and damage to this tract can result in motor deficits. It is especially important for controlling fine, dexterous movements of the extremities. Corticospinal Tract (CST) - Voli

Substantia Nigra (midbrain)

The nucleus that sends dopamine-releasing neurons to the striatum and that deteriorates in Parkinson's disease.

Secondary Somatosensory Cortex

The part of the somatosensory cortex that receives information from the primary somatosensory cortex, from both sides of the body. Sends connections to the part of the temporal lobe that includes the hippocampus (important in learning, memory formation for somatosensory information).

Smooth Muscles

The tissues that produce rhythmic contractions of internal organs other than the heart.

Local Anesthetics

Those that are applied to or injected into the painful area-block sodium channels in the pain neurons and reduce their ability to fire.

Receptor for touch

Touch receptor --> respond to touch, vibration

Skin Senses

Touch, warmth, cold, pain, (and, possibility, itch); the senses that arise from receptors in the skin.

Stop in the thalamus for touch and pain

VPL (ventral posterolateral) thalamus

What are the major areas for movement and their functions?

Primary Motor Cortex (M1): Located in the frontal lobe, the primary motor cortex is the primary initiation point for voluntary motor movements. It contains a somatotopic map, meaning specific regions of M1 correspond to specific body parts. Stimulation of different areas in M1 can elicit movements in different body parts. Premotor Cortex: The premotor cortex, located just anterior to M1, is involved in the planning and coordination of complex movements. It helps organize motor sequences and plays a role in setting up motor plans. Supplementary Motor Area (SMA): The supplementary motor area, found in the superior frontal gyrus, is involved in the organization of sequential movements and the coordination of bilateral movements. It plays a role in the initiation of movements and is particularly important for bimanual tasks. Cerebellum: The cerebellum is located at the back of the brain and is crucial for motor coordination, balance, and error correction. It receives information about the motor plan from the primary motor cortex and ensures that movements are executed smoothly and accurately. Basal Ganglia: The basal ganglia is a group of subcortical nuclei that play a role in smoothing and refining motor movements. It is also involved in procedural memory, which relates to the learning and execution of motor skills. Disorders of the basal ganglia, such as Parkinson's disease, can lead to motor deficits. Prefrontal Cortex: While not primarily a motor area, the prefrontal cortex is involved in the higher-order aspects of motor control. It is responsible for decision-making, planning, and goal setting, all of which contribute to the organization of motor behavior. Other Motor-Related Areas: In addition to the primary areas mentioned above, other brain regions play crucial roles in various aspects of motor control. For example, the posterior parietal cortex integrates sensory information with motor planning and execution. The mirror neuron system, found in areas like the inferior parietal cortex and the premotor cortex, is involved in understanding and imitating the actions of others. It's important to note that these motor-related areas often work in coordination, with sensory input, cognitive processes, and motor

Hypovolemic Thirst

When blood volume decreases from loss of extracellular water. Ex. Sweating, urinating Pathway Baroreceptors → NST → Median Preoptic Nucleus of hypothalamus Kidney releases renin → angiotensin II → SFO → Median preoptic nucleus

What is proprioception? What sensors are used for this sense?

Proprioception is the sense that allows us to perceive and understand the position, movement, and orientation of our body parts without relying on visual or external cues. It is often described as our "body's internal GPS system" because it provides us with a continuous stream of sensory information about the state of our musculoskeletal system. This information is crucial for coordinating movements, maintaining balance, and interacting with the environment effectively. Proprioception relies on a combination of sensory receptors, neural pathways, and the brain's processing of incoming signals. The primary sensors involved in proprioception include: Muscle Spindles: These are specialized sensory receptors located within the muscle fibers (intrafusal muscle fibers). Muscle spindles detect changes in muscle length, providing information about muscle stretch, muscle tension, and the rate of muscle lengthening or shortening. This information is critical for controlling muscle contraction and maintaining posture. Golgi Tendon Organs (GTOs): Golgi tendon organs are found in the tendons where muscles attach to bones. They are sensitive to changes in muscle tension and force. GTOs help regulate muscle contractions by inhibiting muscle activity if excessive force is detected. This prevents muscle and tendon damage. Joint Receptors: These receptors are located within the capsules and ligaments surrounding the joints. They monitor the angle, direction, and speed of joint movement, providing feedback about joint position and movement. Skin Receptors: Skin contains receptors, including the Ruffini endings and Pacinian corpuscles, which contribute to proprioception. These receptors detect skin stretch, pressure, and vibration, providing additional information about limb position and movement. These proprioceptive sensors send signals to the brain through sensory nerve pathways. The information is then processed in the brain, specifically in regions of the somatosensory cortex, cerebellum, and other motor control areas. The brain integrates this sensory input and uses it to create a mental representation of the body's position and movements. The proprioceptive system is crucial for a wide range of activities, from walking an

Muscle Spindles

Receptors that detect stretching in muscles, this is then relayed to the spinal cord. Allows a muscle to respond quickly to an increased external load.

Golgi Tendon Organs

Receptors that detect tension in a muscle. They trigger a spinal reflex that inhibits the motor neurons and limits the contraction. Prevents muscles from contracting so strongly that they might be damaged.

Primary receiving area for touch and pain in the cortex

S1 (primary somatosensory cortex)

Prefrontal Cortex (PFC)

Selects the appropriate behavior and its target, using a combination of bodily and external information.

Nociceptors

Sensory receptors that respond to pain and temperature.

Organization of S1

Special organization (A1, V1, S1, not surprising). A somatotopic map - Specific areas of S1 correspond to specific body areas. Right S1 - Gets left body information Left S1 - Gets right body information Sensory homunculus - cortical magnification (fovea has more in V1), areas that have more space in S1 include mouth and hands

Inflammatory Soup

A combination of histamine, proteins (bradykinin and substance P), lipids (prostaglandins), neurotransmitters (serotonin), and cytokines that causes inflammation.

Antagonistic Muscles

Contractile tissues that produce opposite movements at a joint.

Endorphins

Function both as neurotransmitters and as hormones. Releases for pain but it does so only under certain conditions. Endorphin release inhibits the release of substance P

Cerebellum

Maintains balance, refines movements, controls compensatory eye movements. Involved in learning motor skills.

Mirror Neurons

Neurons that fire when an individual performs an action or observes someone else performing that action.

Receptor for pain

Nociceptors --> respond to pain, temperature

Phantom Pain

Pain that seems to be in a missing limb. Phantom limb is a condition where individuals who have lost a body part, not limited to limbs, continue to experience sensations, including phantom pain, from the missing body part. This phenomenon is not fully understood, but several hypotheses have been proposed to explain it: Cortical Reorganization: According to this prevailing hypothesis, when a limb is amputated, the neurons in the somatosensory cortex that used to process signals from that limb begin to respond to signals from neighboring neurons. This cross-wiring can lead to sensations felt in other parts of the body causing the stimulation of neurons originally dedicated to the missing limb, resulting in the brain perceiving sensations in the absent limb. Internal Body Representation: Another theory suggests that the brain maintains an internal representation of the body. Even after limb loss, this representation remains intact, and this persistence can lead to the feeling that the limb is still present. In cases of discordance between the intention to move the limb and the absence of sensory feedback, this neural representation could generate phantom sensations and pain. Peripheral Nervous System: The peripheral nervous system may also play a role. After limb loss, damaged nerve cells may attempt to regenerate by growing new extensions. In the absence of the limb, these extensions may form a mass of neural tissue called a neuroma. These neuromas can produce erratic signals, potentially contributing to the sensations and pain associated with phantom limbs. What is it? Perception of touch/pain in a limb that is no longer there (had before). Problem: How do we treat pain and sensation in amputations? Mirror-Box Ask them to move the intact hand and see the mirror reflection. The mirror reflection has both hands including the amputated one, visual information overrides pain. Possible Mechanism For Phantom Limb Pain Reorganization of S1 Things close by the amputated limbs place in V1 → neurons get used for more things but still have amputated limb sensations. Face areas next to hand area in S1 Touch face → perceive touch in face and hand. Confusion in perception.

Striatum

The caudate nucleus and putamen, both of the basal ganglia, and the nucleus accumbens.

Body Integrity Identity Disorder

The desire, in individuals with no apparent brain damage or mental illness, to have a healthy limb amputated. (Apotemnophilia)

Apotemnophilia

The desire, in individuals with no apparent brain damage or mental illness, to have a healthy limb amputated. (Body Integrity Identity Disorder).

Olfactory Bulb

The initial site of odor processing in the brain.

Levodopa (L-dopa)

The precursor for dopamine, it is used to treat Parkinson's disease. Dopamine will not cross the blood-brain barrier, but L-dopa will, and the brain converts it to dopamine. Has side effects (restlessness, involuntary movements).

Supplementary Motor Area (SMA)

The prefrontal area that assembles sequences of movements, such as those involved in eating or playing the piano, prior to execution by the primary motor cortex. Coordinates movements between the two sides of the body (e.g., carrying something with both hands).

Cardiac Muscles

The strong contractile tissues that make up the heart. Non-fatiguing muscles.

Skeletal Muscles

The tissues that attach to bones and move the body and limbs. Can become fatigued if overused. Also called striated muscles.

Free serve endings

processes at ends of neuronal denrites, detect warmth, cold, and pain.

Interoceptive System

provides general information about conditions within the body

What is a central pattern generator?

A Central Pattern Generator (CPG) is a neural network or circuit within the central nervous system (CNS) that is responsible for generating rhythmic, patterned motor outputs, such as walking, swimming, or flying, without the need for constant sensory input or higher-level control. In other words, CPGs are neural circuits that produce organized motor patterns or behaviors, often seen in locomotion and other repetitive activities. Key features of central pattern generators include: Autonomous Rhythmic Activity: CPGs are capable of producing rhythmic motor patterns autonomously, without the need for constant feedback from sensory inputs or higher-level control from the brain. This autonomy is particularly evident in activities like walking, where the pattern of leg movement is maintained even when sensory input is temporarily disrupted. Location in the CNS: CPGs are typically located in specific regions of the CNS, depending on the motor behavior they control. For example, in vertebrates, spinal CPGs are involved in controlling walking and other movements, while in invertebrates like crustaceans, CPGs for locomotion are often found in ganglia or nerve cord segments. Hierarchical Control: CPGs can be thought of as part of a hierarchical control system, with higher-level brain regions providing modulation and adaptation of the basic motor patterns generated by CPGs. For example, while a CPG for walking can generate the fundamental rhythmic pattern of leg movement, higher brain centers can adjust walking speed or adapt the pattern in response to changing terrain. Phylogenetic Conservation: CPGs are found in a wide range of animal species, from simple invertebrates to complex vertebrates. This conservation across species suggests the fundamental importance of these networks in generating rhythmic behaviors. Plasticity and Adaptation: CPGs can be modulated and adapted based on sensory feedback and the current context. For example, sensory input can influence the frequency or intensity of a rhythmic pattern, allowing for adjustments in response to environmental changes. Examples of CPGs include the spinal CPGs involved in walking in vertebrates and the rhythmic swimming patterns generated by CPGs in fish. Understandin

Huntington's Disease

A degenerative disorder of the motor system involving cell loss in the striatum and cortex. Starts with mild, infrequent jerky movements that result from impaired error correction. Cognitive and emotional deficits are a universal characteristic of Huntington's disease: impaired judgement, difficulty with cognitive tasks, depression, and personality changes. Degeneration of inhibitory Gaba-releasing neurons in the striatum. Mutated form of huntingtin gene. Hungtin protein. genes that silence this show promise. Tetrabenazine. Reduces excess dopamine that causes abnormal movements. Huntington's disease is a devastating neurological condition characterized by a range of symptoms that include movement problems, cognitive decline, and psychiatric issues. Here's a summary of the key points: Symptoms: Huntington's disease typically manifests in mid-life and initially presents with subtle changes in personality, cognition, and movement. Over time, symptoms progress to include chorea (involuntary, spasmodic movements), impaired coordination, muscle rigidity, and difficulties with speech and swallowing. Cognitive and psychiatric symptoms like dementia and depression also develop. Neurodegeneration: The disease is characterized by neurodegeneration, which involves the deterioration and death of neurons. The basal ganglia, a group of brain structures, are particularly affected, but other brain regions also experience degeneration. Genetic Basis: Huntington's disease is caused by a dominant genetic mutation in the huntingtin gene. This mutation involves the expansion of a trinucleotide repeat sequence (cytosine, adenine, and guanine) within the gene. More repeats are associated with a higher risk of developing the disease. Individuals with 40 or more repeats in the huntingtin gene will inevitably develop Huntington's disease. Mutated Huntingtin Protein: The mutation in the huntingtin gene results in the production of a mutated form of the huntingtin protein. These mutant proteins have a tendency to aggregate and form clusters within neurons. These clusters may contribute to the neurodegeneration seen in the disease. Movement disorder, excessive, involuntary movement Neurodegenerative disease Movement symptoms: Huntingt

Myasthenia Gravis (MG)

A disorder of muscular weakness caused by reduced numbers or sensitivity of acetylcholine receptors. The muscle weakness can be so extreme that the patient has to be maintained on a respirator.'' Drugs that inhibit the action of acetylcholinesterase (breaks down acetylcholine at synapse) give temporary relief from symptoms of MG. Drooping eyelids. Removal of the thymus (thymectomy) has now become a standard treatment for MG. Autoimmune disease

Multiple Sclerosis (MS)

A motor disorder caused by the deterioration of myelin (demyelination) and neuron loss in the central nervous system. Slowing of elimination of neural impulses. Demyelination reduces the speed and strength of movements. Desynchronized impulses because of differing loss of myelin. Unmyelinated neurons die, leaving areas of sclerosis, or harden scar tissue. Muscular weakness, tremor, pain, impaired coordination, urinary incontinence and visual problems. Autoimmune disease. A drug that blocks voltage channels, dalfampridine, helps demyelinated axons transmit signals by increasing the strength of action potentials. Harvesting stem cells is another possibility, chemotherapy. Multiple sclerosis (MS) is a complex neurological disorder characterized by various symptoms and central nervous system damage. Here's a concise overview: Onset and Symptoms: MS typically first appears between the ages of 20 and 50, and its symptoms can vary widely among individuals. Common initial symptoms include visual disturbances, abnormal sensations, and weakness. MS can affect almost any nervous system function, leading to a range of neurological problems. Cause: The exact causes of MS are not fully understood, but it is believed to result from a combination of genetic and environmental factors. One prevailing theory suggests that MS involves an autoimmune attack on the myelin sheaths that surround neurons' axons. This immune response leads to inflammation and damage in the central nervous system. Myelin Damage: A hallmark of MS is the damage to myelin, the protective covering around axons. This damage disrupts the conduction of nerve signals, contributing to the disease's symptoms. Additionally, axonal deterioration may occur as a result of myelin damage. Imaging: Brain imaging techniques can reveal lesions or plaques in the brains of MS patients. These lesions are indicative of the damage to myelin and axons within the central nervous system. Autoimmune Hypothesis: The leading hypothesis suggests that MS is an autoimmune disease, where the immune system mistakenly targets myelin as if it were foreign. This autoimmune attack results in inflammation and damage. Motor disorder from demyelination (loss of myelin) and neuron loss in

Parkinson's Disease

A movement disorder characterized by motor tremors, rigidity, loss of balance and coordination, and difficulty in moving, especially in initiating movements, caused by deterioration of the substantia nigra. The substantia nigra neurons send dopamine-releasing axons to he stratum (basal ganglia). Disease is familial, genetic foundations usually, not always. Associated with the presence of Lewy bodies. Environmental influences exist too: brain injury, being knocked unconscious (x1, x2+), toxins, pesticide exposure. Risk of Parkinson's disease is reduced as much as 80% in coffee drinkers. The risk also drops by 50% in smokers. Deep brain stimulation may be the new choice. Effective, but weight gain, increased sensitivity to pleasurable aspects of food. Other issues. Parkinson's disease is considered a neurodegenerative disease because it involves the degeneration and death of neurons. It is most frequently seen in adults over the age of 50. The most recognizable symptoms of Parkinson's initially are movement-related and generally involve a tremor that is worse when a person is at rest, bradykinesia, which is slowness of movement, rigidity, and postural impairment. Parkinson's patients also often experience non-motor symptoms like cognitive impairment or psychiatric symptoms. The causes of Parkinson's are not fully understood, but a combination of genetic and environmental factors is likely involved. Parkinson's patients have low levels of the neurotransmitter dopamine in the basal ganglia, a group of structures involved with movement (among other functions). These low dopamine levels in the basal ganglia are caused by the death of dopamine neurons in a region of the basal ganglia called the substantia nigra. The substantia nigra has high numbers of dopamine neurons, but by the end stages of Parkinson's patients have often lost more than half of the dopamine neurons in this region. The most common treatment for Parkinson's involves an attempt to restore depleted dopamine levels in the basal ganglia. Because dopamine does not cross the blood-brain barrier, dopamine cannot simply be administered to a patient. Instead, however, patients can be given a precursor to dopamine called L-DOPA. Notable for problems

Central Pattern Generator (CPG)

A neuronal network that produces a rhythmic pattern of motor activity, such as that involved in walking, swimming, flying, or breathing.

Hedonic Hunger

A neuropeptide that activates NPY/AgRP neurons and inhibits POMC neurons, influencing eating behavior.

Orexin

A neuropeptide that activates NPY/AgRP neurons and inhibits POMC neurons, influencing eating behavior.

Out-Of-Body Experience

A phenomenon, usually resulting from brain damage or epilepsy, in which the person hallucinates seeing his or her detached body from another location, such as from a position above the body.

What is a receptive field for touch? Where on the body do we see small receptive fields?

A receptive field in the context of touch, or somatosensation, refers to the specific area of the body's surface that, when stimulated, leads to a response in a particular sensory neuron. These sensory neurons, located in the skin and underlying tissues, are responsible for detecting tactile sensations and transmitting them to the brain. Receptive fields for touch can vary in size, and they are generally smaller in areas where tactile discrimination and precision are essential. The smaller the receptive field, the better the spatial resolution, meaning the ability to discern finer details of a stimulus. Small receptive fields are commonly found in areas of the body where fine tactile discrimination is crucial. Here are some examples of body areas with small receptive fields: Fingertips: The fingertips are highly sensitive and have very small receptive fields, allowing for precise tactile discrimination. This is particularly important for activities like braille reading, sewing, and playing musical instruments. Lips: The lips have small receptive fields, enabling precise control over movements and the ability to detect subtle variations in texture, temperature, and pressure. Tongue: The tongue, especially the tip, has small receptive fields that contribute to the ability to taste and distinguish different flavors and textures in food. Palms: While larger than the fingertips, the palms of the hands still have relatively small receptive fields compared to areas like the back. Toes: The toes, similar to the fingertips, have small receptive fields that are important for balance, grip, and detecting tactile information when walking or wearing shoes. In contrast, body areas with larger receptive fields typically have reduced spatial resolution. For example, the back or upper arm has larger receptive fields, making them less precise for fine tactile discrimination but more suitable for detecting broader patterns of touch and pressure. The distribution of receptive field sizes across the body is closely related to the functional demands of each body part. Small receptive fields in areas like the fingertips, lips, and tongue enable humans to perform tasks that require high tactile acuity and precision.

Dermatome

A segment of the body served by a spinal nerve. Each dermatome overlaps the next by one third to one half. Body sense information enters the spinal cord (via spinal nerves) or the brain (via medulla, and travels to the thalamus. To the projection area, somatosensory cortex. Most not all cross from one side of the body to the other side of the brain.

Familial

A term referring to a characteristic that occurs more frequently among relatives of a person with the characteristic than it does in the population.

Lewy Bodies

Abnormal clumps of protein that form within neurons, found in some patients with Parkinson's disease and Alzheimer's disease.

Premotor Cortex

An area anterior to the primary motor cortex that combines information from the prefrontal cortex and posterior parietal cortex and begins the programming of a movement. Such as the target being reached for and its location, which arm to use, and the arm's location.

Posterior Parietal Cortex

An association area that brings together the body senses, vision, and audition. It determine the body's orientation in space, the location of the limbs, and the location in space of objects detected by touch, sight, and sound. The region of the brain responsible for integrating sensory information, spatial perception, and motor planning. It does not itself produce movements but passes its information on to frontal areas that do. The right posterior parietal cortex can produce neglect (foreign limb syndrome, xenomelia). Out of body experience. Incorporates entire body into an illusion.

Piriform Cortex (PC)

Brain area involved in odor discrimination and perception.

Gustatory Cortex

Brain region in the insula responsible for processing taste information.

What are dermatomes?

Dermatomes are specific areas of skin that are primarily supplied by a single spinal nerve. Each spinal nerve carries sensory information from a particular region of the body's surface to the spinal cord and, ultimately, to the brain. Dermatomes help map the sensory innervation of the body. There are a total of 31 pairs of spinal nerves in the human body, and each one is associated with a specific dermatome. These dermatomes are arranged in a segmented pattern, with each one covering a distinct area of the skin. Understanding dermatomes is essential for clinical purposes, such as diagnosing sensory impairments, nerve injuries, and conditions that affect specific regions of the body. Dermatomes are commonly depicted as a diagram with the body divided into different sections, each associated with a particular spinal nerve. While there is some degree of anatomical variation among individuals, dermatomes serve as a general guide for understanding sensory innervation. It's important to note that dermatomal patterns do not perfectly align with simple anatomical boundaries but are more indicative of the nerve roots from which they originate. In medical practice, dermatomes are used to assess sensory function, especially in cases of nerve damage, spinal cord injuries, or neurological disorders. By evaluating the sensation in specific dermatomes, healthcare professionals can pinpoint the location and severity of sensory abnormalities and make informed clinical decisions. Understanding dermatomes is particularly useful for diagnosing and managing conditions that affect sensory functions, as it helps healthcare providers identify the precise nerve root or spinal segment that may be affected.

What signals are important for detecting pain?

Detecting pain involves specialized receptors called nociceptors. Nociceptors are sensory neurons that are designed to respond to potentially harmful or noxious stimuli. These receptors play a crucial role in alerting the body to potential threats and injuries, as pain is a protective mechanism that helps prevent further harm. The primary signals important for detecting pain include: Mechanical Damage: Nociceptors respond to mechanical stimuli that can cause tissue damage, such as intense pressure, pinching, or cutting. When these mechanical forces exceed a certain threshold, nociceptors generate pain signals. Thermal Damage: Nociceptors can detect extremes of temperature, both heat and cold. Extremely high temperatures (heat) and extremely low temperatures (cold) can trigger pain responses. Temperature-related pain is often referred to as thermal pain. Chemical Irritation: Chemicals released during tissue damage or inflammation can activate nociceptors. Substances such as prostaglandins, bradykinin, histamine, and certain neurotransmitters contribute to the sensation of pain. These chemicals can sensitize nociceptors, making them more responsive to other pain-inducing stimuli. Ischemia: Lack of blood flow (ischemia) can deprive tissues of oxygen and nutrients, leading to the activation of nociceptors. The buildup of waste products, such as lactic acid, in ischemic tissues can also contribute to pain. Polymodal Nociceptors: Some nociceptors are polymodal, meaning they can respond to multiple types of noxious stimuli. For example, they may be sensitive to both mechanical pressure and temperature extremes, allowing them to signal pain in response to various forms of injury. Inflammatory Pain: Inflammatory processes, such as those associated with tissue injury or infection, can lead to the release of inflammatory mediators. These mediators can sensitize nociceptors, making them more responsive to painful stimuli, even at lower intensity levels. Pain perception is a complex process that involves the transmission of pain signals from nociceptors to the spinal cord and then to the brain. Once pain signals reach the brain, they are further processed, leading to the perception of pain, which can vary in intensity an

What is Parkinson's Disease (PD) and its neurobiological basis?

Dopamine Depletion: In Parkinson's disease, there is a significant loss of dopaminergic neurons in the substantia nigra. These neurons project to a region of the brain called the striatum, which is a critical component of the basal ganglia. The depletion of dopamine in the striatum disrupts the balance between two pathways within the basal ganglia: the direct and indirect pathways. This imbalance leads to motor dysfunction. Basal Ganglia Dysfunction: The basal ganglia is a group of subcortical structures involved in motor control and procedural memory. It helps coordinate and refine motor movements. In Parkinson's disease, the loss of dopamine disrupts the normal functioning of the basal ganglia, resulting in the characteristic motor symptoms of the disease. Motor Symptoms: The most common motor symptoms of Parkinson's disease include resting tremors, bradykinesia (slowed movement), muscle rigidity, impaired posture and balance, and an impaired gait (often referred to as the "Parkinson's shuffle"). These symptoms are collectively known as parkinsonian motor symptoms. Non-Motor Symptoms: While Parkinson's disease is primarily associated with motor symptoms, it also manifests with various non-motor symptoms. These can include depression, anxiety, cognitive impairment, and sleep disturbances. Genetics and Environmental Factors: The exact causes of Parkinson's disease are not fully understood. While many cases are sporadic, a small percentage are linked to specific genetic mutations. Additionally, there is evidence that environmental factors, such as exposure to certain toxins, may contribute to the development of the disease. The current standard of care for Parkinson's disease is primarily focused on managing symptoms and increasing dopamine levels in the brain. Medications such as Levodopa (L-Dopa) are commonly used to replace dopamine. Deep brain stimulation (DBS), a surgical procedure that involves implanting electrodes in the brain, can also provide relief from motor symptoms, especially in cases where medications are less effective. Despite these treatments, there is currently no cure for Parkinson's disease, and the condition tends to progress over time. Ongoing research is focused on understanding the un

Ghrelin

Ghrelin Stomach ARC - Activates AgRP neurons to release NPY Initiate Eating

What is Huntington's disease (HD) and its neurobiological basis?

Huntington's disease (HD) is a devastating neurodegenerative disorder that primarily affects motor control but also leads to cognitive decline and psychiatric symptoms. The condition is caused by a genetic mutation and is inherited in an autosomal dominant manner, meaning that if a person inherits one mutated gene from either parent, they will develop the disease. Neurobiological Basis: The neurobiological basis of Huntington's disease is primarily associated with a genetic mutation and the impact it has on the brain's structure and function: Genetic Mutation: The underlying genetic mutation responsible for HD is a trinucleotide repeat expansion within the HTT gene. This gene encodes a protein called huntingtin. In people with HD, there is an abnormal repetition of the CAG trinucleotide sequence within the HTT gene. This genetic mutation leads to the production of an altered huntingtin protein (mutant huntingtin) with an expanded polyglutamine tract. The length of this repeated CAG sequence is inversely correlated with the age of disease onset and directly related to disease severity. Accumulation of Mutant Huntingtin: Mutant huntingtin has a propensity to aggregate and form insoluble clumps or inclusions in neurons. These clumps are toxic to neurons and interfere with their normal functions. Selective Neuronal Degeneration: HD primarily affects the basal ganglia, a group of structures deep within the brain responsible for motor control and coordination. Neurons within the striatum (composed of the caudate nucleus and putamen) are particularly vulnerable. Over time, the progressive loss of neurons in these areas leads to the characteristic motor symptoms associated with HD, including chorea (involuntary, jerky movements) and dystonia (muscle rigidity). Impact on Cortical Regions: As HD advances, it affects other regions of the brain, including the cerebral cortex. This leads to cognitive deficits, psychiatric symptoms (such as depression, irritability, and psychosis), and changes in personality. Glutamate Excitotoxicity: One of the mechanisms underlying neuronal damage in HD is excitotoxicity. The mutant huntingtin protein interferes with glutamate signaling in the brain. Excessive glutamate signaling can lea

What are the changes in the basal ganglia functions in HD?

Huntington's disease (HD) is a neurodegenerative disorder that significantly affects the functions of the basal ganglia, leading to various motor, cognitive, and psychiatric symptoms. The changes in basal ganglia function in HD are primarily due to the progressive degeneration of specific structures within the basal ganglia, particularly the striatum. Here are some of the key changes in basal ganglia functions in HD: Loss of Striatal Neurons: HD is characterized by the selective and progressive degeneration of medium spiny neurons in the striatum, particularly in the caudate nucleus and putamen. These neurons are primarily inhibitory and are responsible for modulating motor activity. As these neurons degenerate, the inhibitory output from the striatum is reduced. Dopamine Dysregulation: The substantia nigra, a structure within the basal ganglia that produces dopamine, also degenerates in HD. This leads to an imbalance in dopamine levels within the basal ganglia. Dopamine plays a crucial role in regulating movement and mood, and its dysregulation contributes to motor symptoms and psychiatric disturbances in HD. Direct and Indirect Pathways: The basal ganglia consist of two main pathways: the direct pathway, which promotes movement, and the indirect pathway, which inhibits movement. In HD, the imbalance between these pathways results in difficulties initiating and coordinating movements, leading to motor symptoms like chorea (involuntary, jerky movements) and dystonia (sustained muscle contractions). Cognitive Impairments: The basal ganglia also play a role in cognitive functions, including decision-making, executive function, and procedural memory. Degeneration in these areas can lead to cognitive impairments, such as difficulties in planning, organizing, and multitasking. Psychiatric Symptoms: The basal ganglia have connections with brain regions involved in mood regulation, and their dysfunction can lead to psychiatric symptoms in HD. These symptoms may include depression, anxiety, irritability, and other mood disturbances. Dysregulation of Glutamate: Changes in glutamate signaling within the basal ganglia are also observed in HD. Glutamate is the primary excitatory neurotransmitter in the brain, and its dys

What is the relative role of genetics and environment in risk of HD?

Huntington's disease (HD) is primarily caused by a genetic mutation, and genetics play a dominant role in determining a person's risk of developing the condition. However, the interplay between genetics and environmental factors can also influence the risk and age of onset of HD to some extent. Genetics: The main underlying cause of HD is a mutation in the HTT gene, located on chromosome 4. Specifically, HD is associated with the expansion of a CAG trinucleotide repeat within the HTT gene. This repeat expansion leads to the production of an abnormal form of the huntingtin protein. HD is inherited in an autosomal dominant manner. This means that if a person inherits a single copy of the mutated gene from one parent, they are at risk of developing the disease. Each child of an affected parent has a 50% chance of inheriting the mutated gene. The length of the CAG repeat in the mutated HTT gene is inversely correlated with the age of onset of HD. Individuals with longer CAG repeats tend to develop symptoms at an earlier age and often experience more severe disease. Environmental Factors: While genetics plays a predominant role in HD, some environmental factors may influence the age of onset and progression of the disease. These factors are less well-understood than the genetic basis of HD and may not apply to every individual with the condition. Some potential environmental factors include: Lifestyle and Diet: Some studies suggest that a healthy diet and regular exercise might help delay the onset of HD symptoms or slow the disease's progression. Stress: High levels of stress may exacerbate HD symptoms, so managing stress could be beneficial. Medications: Some medications may have interactions with HD symptoms or treatment. Consultation with a healthcare professional is important when considering medications. It's important to note that while environmental factors may influence the age of onset and course of HD, they are secondary to the genetic mutation as the primary cause of the disease. As a result, individuals who carry the mutated HTT gene are at a high risk of developing HD, regardless of environmental factors. Additionally, genetic testing and counseling can provide valuable information to individuals who

Meissner's Corpuscles and Merkel Disks

Merkel's Discs (Slowly-Adapting): Merkel's discs are slowly-adapting receptors with very small receptive fields. They provide high spatial resolution and are particularly dense in the fingertips. Merkel's discs are well-suited for processing information related to shape and texture, making them important for fine tactile discrimination. Meissner's Corpuscles (Rapidly-Adapting): Meissner's corpuscles are rapidly-adapting receptors with relatively small receptive fields. While their spatial resolution is lower than that of Merkel's discs, they excel at transmitting information about movement between the skin and external surfaces. These receptors are essential for sensing texture and detecting objects sliding against the skin, which is crucial for maintaining grip.

What is multiple sclerosis (MS) and its neurobiological basis?

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). It primarily involves the brain and spinal cord. MS is characterized by the progressive destruction of myelin, a fatty substance that surrounds and insulates nerve fibers (axons) in the CNS. The loss of myelin disrupts the normal conduction of nerve impulses, leading to a wide range of neurological symptoms. The neurobiological basis of MS is complex and involves an autoimmune response, inflammation, demyelination, and axonal damage. Here are the key features of MS: Autoimmune Response: MS is considered an autoimmune disease because the immune system mistakenly identifies components of the CNS, particularly myelin, as foreign invaders. T cells and B cells of the immune system are activated and attack myelin and other CNS components. The exact trigger for this autoimmune response is not fully understood but is thought to involve a combination of genetic and environmental factors. Inflammation: The autoimmune response leads to inflammation within the CNS. Immune cells infiltrate the brain and spinal cord, causing damage to myelin and neural tissue. This inflammatory process is associated with the formation of lesions or plaques in the CNS, which can be visualized using imaging techniques. Demyelination: In MS, the immune system's attack on myelin results in the loss of myelin from axons. Demyelination disrupts the normal saltatory conduction of nerve impulses, slowing or blocking the transmission of signals along affected nerve fibers. It is a hallmark feature of the disease. Axonal Damage: In addition to demyelination, MS can also lead to axonal damage and degeneration. This occurs when axons are directly targeted by the immune system or when they are affected by the loss of myelin. Axonal damage contributes to the neurological symptoms and disability associated with MS. Lesions and Scarring: MS is often associated with the formation of characteristic lesions in the white matter of the CNS. These lesions are areas of demyelination and inflammation. Over time, the CNS attempts to repair itself by forming scar tissue (sclerosis) in and around the lesions. These scars may impede neural signaling and further cont

What is the role of muscle spindles or golgi tendon organs?

Muscle spindles and Golgi tendon organs are specialized sensory receptors found in muscles and tendons. They play distinct roles in providing the nervous system with information about muscle length and tension, helping to regulate muscle function and prevent injury. Muscle Spindles: Location: Muscle spindles are small, spindle-shaped structures located within the muscle tissue, typically in parallel with the muscle fibers. Function: Muscle spindles are proprioceptors, which means they provide information about muscle length and changes in muscle length. They are particularly sensitive to rapid changes in muscle length. When a muscle is stretched or lengthened, the muscle spindles are activated, and they send sensory information to the central nervous system. Role in Muscle Contraction: Muscle spindles play a crucial role in the regulation of muscle contraction. When a muscle is stretched, such as during the initial phase of a movement, muscle spindle activation triggers a reflex called the "stretch reflex." The stretch reflex causes the muscle to contract to resist overstretching, helping to maintain muscle tone and stability. Fine Motor Control: Muscle spindles also contribute to fine motor control by providing feedback to the nervous system about the position and movement of various body parts. Golgi Tendon Organs (GTOs): Location: Golgi tendon organs are found at the junction between muscles and tendons. Function: Golgi tendon organs are proprioceptors that provide information about muscle tension or force. They are highly sensitive to changes in muscle tension. When a muscle contracts, it generates force and tension in the attached tendon. The Golgi tendon organs detect this increased tension and send sensory signals to the central nervous system. Role in Muscle Control: Golgi tendon organs serve as a protective mechanism. When muscle force and tension reach a certain threshold, the Golgi tendon organs are activated, and they can trigger an inhibitory reflex. This reflex causes the muscle to relax, reducing tension and preventing excessive force. It serves as a safeguard against muscle or tendon damage during overly forceful contractions. Contributions to Muscle Control: Golgi tendon organs help prevent o

What is myasthenia gravis (MG) and its neurobiological basis?

Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by muscle weakness and fatigue, particularly in the skeletal muscles responsible for voluntary movements. The neurobiological basis of MG involves an immune system malfunction that affects neuromuscular communication. Here are the key components of MG's neurobiological basis: Autoimmune Disorder: MG is considered an autoimmune disorder because the immune system mistakenly attacks components of the neuromuscular junction. In the normal neuromuscular junction, motor neurons release the neurotransmitter acetylcholine, which binds to acetylcholine receptors (AChRs) on the muscle cell membrane. This binding triggers muscle contractions. Antibodies Against AChR: In MG, the immune system produces antibodies that target and bind to acetylcholine receptors on the muscle cell membrane. This antibody response is primarily directed against the nicotinic AChRs. These antibodies interfere with the normal functioning of AChRs, leading to muscle weakness. Complement Activation: The binding of antibodies to AChRs in the neuromuscular junction can activate the complement system, which is part of the immune response. Complement activation leads to the destruction of AChRs and disruption of neuromuscular transmission. Reduced AChR Density: Over time, the presence of antibodies and complement activation can lead to a decrease in the density of AChRs on the muscle cell membrane. This reduction in AChR density further impairs neuromuscular communication, resulting in muscle weakness. Thymus Involvement: In some cases of MG, abnormalities in the thymus gland are observed. The thymus plays a role in the development of immune cells. In individuals with MG, the thymus may contain clusters of immune cells, such as B lymphocytes, which are involved in the production of the AChR antibodies. Thymic abnormalities are more common in MG with early onset. Muscle Fatigue: The impaired neuromuscular transmission in MG results in muscle fatigue and weakness, particularly during sustained or repetitive muscle contractions. Symptoms may vary in severity, and individuals with MG may experience intermittent weakness or weakness that worsens throughout the day. The primary ne

Pacinian corpuscles and Ruffini Endings

Pacinian Corpuscles (Rapidly-Adapting): Pacinian corpuscles are also rapidly-adapting receptors, but they have very large receptive fields. They are thought to be most effective at transmitting information about vibrations generated when objects are contacted or grasped by the hand. This information is valuable, especially when using tools. Ruffini's Endings (Slowly-Adapting): Ruffini's endings are slowly-adapting receptors with large receptive fields. Although their exact function is not fully understood, they appear to respond to skin stretching, such as what occurs during finger and hand movements. This information may play a role in generating awareness of finger and hand positions. These different types of touch receptors contribute to our ability to perceive and interact with the physical world by providing information about the position, shape, texture, pressure, and movement of objects we come into contact with.

Anterolateral System

Pain begins at nociceptors, cutaneous receptors that are specialized to detect noxious stimuli like extreme pressure, very hot or cold temperatures, or tissue damage. When activated, nociceptors send a signal to the spinal cord; the signal will be sent to the brain on pathways that make up what is known as the anterolateral system. The anterolateral system consists of three major pathways: the spinothalamic, spinoreticular, and spinomesencephalic tracts. 3 tracts, need to know 2 of them Spinothalamic Tract (STT) - Pain and temperature (START IN THE SPINE) Nociceptor → 1st synapse in spinal cord → **(crosses the midline, in spinal cord)** → VPL thalamus → S1 Spinoencephatic Tract → Pain inhibition (START IN THE SPINE) Nociceptor → 1st synapse in spinal cord → **(crosses the midline, in the spinal cord)** → PAG (periaqueductal gray area) in the midbrain (brainstem/) → VPL thalamus → S1

What are pharmacological and internal mechanisms of pain relief?

Pain relief can be achieved through various mechanisms, including pharmacological (medications) and internal mechanisms that involve the body's own pain-modulation systems. Here's an overview of both approaches: Pharmacological Pain Relief: Pharmacological methods involve the use of medications to alleviate pain. These medications work through different mechanisms and are often categorized based on their modes of action: Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): NSAIDs, such as ibuprofen and naproxen, reduce pain by decreasing inflammation and blocking the action of enzymes that produce pain-inducing chemicals (prostaglandins). They are effective for pain caused by inflammation, such as arthritis or injury. Opioids: Opioid medications, like morphine, oxycodone, and hydrocodone, are powerful pain relievers. They work by binding to opioid receptors in the brain and spinal cord, reducing the perception of pain. Opioids are typically used for severe pain, such as post-surgery pain or cancer-related pain. Acetaminophen: Acetaminophen (paracetamol) is often used to relieve pain and reduce fever. It is not considered an NSAID and works by affecting the brain's perception of pain. It is commonly used for mild to moderate pain and has a lower risk of causing stomach irritation than NSAIDs. Antidepressants: Some types of antidepressant medications, such as tricyclic antidepressants and selective serotonin and norepinephrine reuptake inhibitors (SNRIs), can be effective in managing certain types of chronic pain, including neuropathic pain. Anticonvulsants: Certain anticonvulsant drugs, such as gabapentin and pregabalin, are used to treat neuropathic pain conditions. They work by modulating abnormal electrical activity in nerves. Local Anesthetics: Local anesthetics, like lidocaine, can be administered to block pain signals by numbing specific areas of the body. They are often used for regional pain relief during medical procedures or for certain types of localized pain. Topical Analgesics: Creams, gels, or patches containing analgesic medications can be applied directly to the skin to provide localized pain relief. Internal Mechanisms of Pain Relief: The body has built-in mechanisms to modulate pain perception and

What are the changes in the basal ganglia functions in PD?

Parkinson's disease (PD) is characterized by significant changes in the function of the basal ganglia, a group of subcortical structures in the brain that play a key role in motor control. These changes lead to the characteristic motor symptoms associated with PD. Here are some of the key changes in basal ganglia function in PD: Dopamine Depletion: The most prominent change in the basal ganglia in PD is the loss of dopaminergic neurons in the substantia nigra pars compacta (SNc). Dopamine is a crucial neurotransmitter that modulates the activity of the basal ganglia. In PD, the loss of dopaminergic neurons results in a significant reduction in dopamine levels in the striatum, a part of the basal ganglia that receives dopaminergic input. This disruption of the dopamine system is a central feature of PD. Imbalance in Direct and Indirect Pathways: The basal ganglia control movement by regulating the balance between the direct and indirect pathways. In PD, the loss of dopamine leads to an imbalance between these pathways. The indirect pathway, which inhibits movement, becomes overactive, while the direct pathway, which promotes movement, is underactive. This imbalance results in difficulty initiating and coordinating movements, leading to symptoms like bradykinesia (slowness of movement), rigidity, and resting tremors. Inhibition of Thalamocortical Circuitry: The thalamus is a critical relay station in the brain that transmits motor signals from the basal ganglia to the motor cortex. In PD, due to the increased inhibitory influence of the indirect pathway and the decreased excitatory influence of the direct pathway, there is a reduced thalamic output to the motor cortex. This leads to a decreased ability to initiate and control voluntary movements. Loss of Procedural Memory: The basal ganglia also play a role in procedural memory, which is the ability to learn and execute motor skills. In PD, the dysfunction of the basal ganglia can lead to difficulties in learning and performing motor tasks. This is why people with PD often have difficulty with activities that require motor skills, such as handwriting. Non-Motor Symptoms: While the basal ganglia's primary role is in motor control, they also have non-motor functi

What is phantom limb pain? How can mirror therapy be used to treat this type of pain?

Phantom limb pain is a complex and often debilitating condition in which individuals who have had a limb amputated continue to perceive pain or other sensations originating from the missing limb. It is a well-recognized phenomenon and a common complication following limb amputation. Phantom limb pain can take various forms, including pain, itching, burning, tingling, and the sensation that the missing limb is in an uncomfortable or unnatural position. The exact mechanisms behind phantom limb pain are not entirely understood, but several theories have been proposed. One leading theory is cortical reorganization, which suggests that the brain areas responsible for processing sensory and motor information related to the amputated limb undergo changes. In this reorganization, the regions of the brain that previously represented the amputated limb may become hyperactive and produce sensations or pain. Mirror therapy is a non-invasive treatment approach that aims to alleviate phantom limb pain and other phantom limb sensations by providing visual feedback to the brain. It was first developed by neuroscientist Vilayanur S. Ramachandran. The therapy involves the use of a simple apparatus: a mirror is placed vertically in such a way that it creates the illusion of the missing limb's reflection when the intact limb is viewed in the mirror. The steps involved in mirror therapy are as follows: Mirror Placement: The mirror is set up vertically, dividing the individual's field of view, with the intact limb visible on one side and the mirrored reflection on the other side. This creates the illusion that the amputated limb is still present and moving. Visual Feedback: The individual is instructed to focus on the mirror and the reflected image of the intact limb. Mirror Movements: While watching the mirror, the individual is guided to perform symmetrical movements with both the intact limb and the phantom limb. This means that if the intact hand is moved, the individual should imagine that the amputated hand is making identical movements in the mirror. The goal of mirror therapy is to provide the brain with visual input that suggests the missing limb is still present and functioning normally. This visual feedback can help red

What is the mechanism for how pharmacological medications and DBS can be used to treat symptoms of PD?

Pharmacological Medications and Deep Brain Stimulation (DBS) are two common approaches used to treat the symptoms of Parkinson's disease (PD). They act through different mechanisms to alleviate the motor symptoms associated with PD. Here's how each of these treatments works: Pharmacological Medications: Dopamine Replacement: The primary mechanism of action for many PD medications is to supplement or enhance the brain's dopamine levels. Since PD is characterized by a loss of dopaminergic neurons in the substantia nigra, leading to decreased dopamine levels in the striatum, these medications aim to restore dopamine function. Levodopa (L-Dopa): Levodopa is a precursor to dopamine. It is converted into dopamine in the brain. L-Dopa can cross the blood-brain barrier, making it an effective treatment for PD. Once in the brain, it's converted into dopamine and helps increase dopamine levels in the striatum. This alleviates motor symptoms, particularly bradykinesia (slowness of movement) and rigidity. Dopamine Agonists: These medications mimic the action of dopamine in the brain. They bind to dopamine receptors and activate them, thus directly increasing dopaminergic activity. Dopamine agonists include drugs like pramipexole and ropinirole. COMT Inhibitors and MAO-B Inhibitors: These medications work by prolonging the effects of dopamine in the brain. Catechol-O-methyltransferase (COMT) inhibitors, such as entacapone, prevent the breakdown of dopamine, while monoamine oxidase-B (MAO-B) inhibitors, like selegiline, reduce the breakdown of dopamine. This enhances dopamine levels and extends its action. Deep Brain Stimulation (DBS): Surgical Intervention: DBS is a surgical procedure that involves implanting electrodes into specific regions of the brain. The most common target for DBS in PD is the subthalamic nucleus (STN) or the globus pallidus internus (GPi). The choice of target depends on the patient's individual characteristics and symptoms. Electrical Stimulation: Once the electrodes are implanted, they are connected to a neurostimulator device, similar to a pacemaker, which is usually placed under the skin near the collarbone. This device sends electrical impulses to the targeted brain region. Modulation of Abnorm

How does gate control theory explain pain?

The Gate Control Theory of pain, proposed by Ronald Melzack and Patrick Wall in 1965, offers a psychological explanation for how we experience and perceive pain. This theory suggests that pain perception is not solely determined by the physical injury or noxious stimulus itself but is also influenced by cognitive and emotional factors. The theory introduces the concept of a "gate" in the spinal cord that can open or close, modulating the transmission of pain signals to the brain. Here's how the Gate Control Theory explains pain: The "Gate" in the Spinal Cord: The spinal cord acts as a gatekeeper for pain signals traveling from the body to the brain. In this theory, there is a hypothetical "gate" in the dorsal horn of the spinal cord, where sensory nerve fibers from the body synapse with second-order neurons. When the gate is open, pain signals are allowed to pass through and reach the brain, leading to the perception of pain. Factors Influencing the Gate: Noxious (painful) stimuli, such as tissue damage or injury, activate small-diameter nerve fibers known as C-fibers and A-delta fibers. Non-noxious sensory input, such as touch or pressure, activates large-diameter nerve fibers. Cognitive and emotional factors, like attention, anxiety, or anticipation of pain, can influence whether the gate is open or closed. The "Closing" Mechanism: When non-noxious sensory input (e.g., gentle touch or rubbing) activates large-diameter nerve fibers, it stimulates inhibitory interneurons in the spinal cord. These inhibitory interneurons release neurotransmitters that inhibit the transmission of pain signals from the C-fibers and A-delta fibers. As a result, the gate closes, preventing the pain signals from reaching the brain. Perception of Pain: The gate control mechanism suggests that when the gate is closed, pain perception is reduced, and the individual feels less pain. Conversely, when the gate is open, pain signals are transmitted to the brain, and the person experiences more intense pain. Individual Differences: The Gate Control Theory helps explain why individuals may experience pain differently in the same situation. Factors like distraction, relaxation, or a person's mental state can influence whether the gate is ope

Somatosensory Cortex

The area in the parietal lobes that processes the skin senses and the senses that inform us about body position and movement, or proprioception, the primary somatosensory cortex is on the postcentral gyrus.

What are the main structures of the basal ganglia? How are they connected in the direct and indirect pathways of the basal ganglia?

The basal ganglia is a group of interconnected subcortical nuclei in the brain that play a crucial role in motor control, as well as in various non-motor functions. The main structures of the basal ganglia include the following: Striatum: The striatum is the primary input nucleus of the basal ganglia and consists of two major components: the caudate nucleus and the putamen. It receives excitatory inputs from various cortical regions, including the motor cortex. Globus Pallidus: The globus pallidus is divided into two segments: Globus Pallidus Internus (GPi): This structure is involved in the direct pathway and plays a role in facilitating movement. Globus Pallidus Externus (GPe): This structure is involved in the indirect pathway and is associated with inhibiting movement. Subthalamic Nucleus (STN): The subthalamic nucleus is a small nucleus located beneath the thalamus. It plays a role in facilitating movement and is part of the indirect pathway. Substantia Nigra: The substantia nigra is divided into two parts: Substantia Nigra Pars Compacta (SNc): This region contains dopaminergic neurons that project to the striatum and are important for motor control. Degeneration of these neurons is associated with Parkinson's disease. Substantia Nigra Pars Reticulata (SNr): This region is part of the indirect pathway and is involved in inhibiting movement. The basal ganglia is known for its role in modulating motor activity, and it does so through two primary pathways: the direct pathway and the indirect pathway. These pathways work in tandem to regulate motor output and maintain the balance of excitatory and inhibitory signals that influence movement. Here's how they are connected: Direct Pathway: The direct pathway promotes movement. It begins with excitatory inputs from the cortex to the striatum (caudate and putamen). The striatum sends inhibitory signals to the internal segment of the globus pallidus (GPi) and substantia nigra pars reticulata (SNr). With the GPi and SNr less active (inhibited), they no longer inhibit the thalamus. The thalamus is then free to send excitatory signals to the motor cortex, promoting motor activity. Indirect Pathway: The indirect pathway acts to inhibit movement. It also begins with ex

Basal Ganglia

The caudate nucleus, putamen, and globus pallidus, located subcortically in the frontal lobes; they participate in motor activity by integrating and smoothing movements using information from the primary and secondary motor areas and the somatosensory cortex. Uses information from primary and secondary motor areas and the somatosensory cortex to integrate and smooth movements; apparently involved in learning movement sequences. Basal ganglia - structure with many parts Substania nigra - Has dopaminergic neurons Pathways (Direct/Indirect) Direct pathway - Allows movement Indirect pathway - Inhibits movement Dopamine role from substantia nigra - facilitate movement In the direct pathway - Allows movement In the indirect pathway - Prevents the indirect pathway from inhibiting movement. (when dopamine is present, the net result is movement). Non-motor loops with basal ganglia and cortex (motor loop) how it connects to other parts of the brain. Non-motor functions of basal ganglia include: Emotion Response Inhibition

Somatotopic Map

The form of topographic organization in the motor cortex and somatosensory cortex, such that adjacent body parts are represented in adjacent areas of the cortex.

Gate Control Theory

The hypothesis that pressure signals arriving in the brain trigger an inhibitory message that travels back down the spinal cord, where it closes a neural "gate" in the pain pathway.

Indirect Pathway of the Basal Ganglia

The indirect pathway is a neural circuit within the basal ganglia that plays a role in the inhibition of movement. It operates in conjunction with the direct pathway to help regulate and fine-tune motor control. Understanding the indirect pathway is essential for comprehending the overall functioning of the basal ganglia. Here's how the indirect pathway works: Corticostriatal Input: Like the direct pathway, the process begins with signals from the cerebral cortex, particularly the motor regions, indicating the intention to make a movement. These signals are transmitted via glutamate neurons. Inhibition of Globus Pallidus External (GPe): Unlike the direct pathway, in the indirect pathway, the signals first activate GABAergic neurons in the striatum. These striatal neurons project to the globus pallidus external (GPe). The activation of GPe neurons inhibits their typical inhibitory effect on the subthalamic nucleus (STN). Activation of Subthalamic Nucleus (STN): The STN neurons, now relieved from GPe inhibition, become activated by excitatory projections from the cortex. The STN neurons, in turn, stimulate GABAergic neurons in the globus pallidus internal (GPi) and substantia nigra pars reticulata (SNr). Inhibition of Thalamic Neurons: The GABA neurons from GPi and SNr project to the thalamus. Their inhibitory action suppresses the thalamic neurons that typically transmit signals to motor regions of the cerebral cortex, which regulate movement. Inhibition of Movement: As a result of the inhibition of thalamic neurons, the indirect pathway effectively suppresses or inhibits movement. It acts as a check against unwanted or inappropriate movements. Role of Dopaminergic Modulation (SNc): Neurons from the substantia nigra pars compacta (SNc) project to the striatum through the nigrostriatal pathway. Dopamine released in the striatum has an excitatory effect, but it primarily impacts the direct pathway, enhancing its activity. In contrast, the indirect pathway is relatively less influenced by dopamine. The inhibition of the indirect pathway helps facilitate movement, and dopamine depletion in conditions like Parkinson's disease can lead to difficulties initiating movements due to the indirect pathway's reduced inhibi

Periaqueductal Gray (PAG)

The part of the nervous system made up of the cranial nerves and spinal nerves. The periaqueductal gray (PAG) is a region of gray matter located in the midbrain surrounding the cerebral aqueduct. It serves various functions, including: Autonomic Regulation: The PAG is involved in regulating heart rate, blood pressure, bladder control, and other autonomic processes. Vocalizations: It plays a role in the production of vocalizations. Fear and Defensive Reactions: The PAG is associated with the generation of fearful and defensive responses. However, the PAG is most well-known for its role in analgesia, which is the reduction of pain. Stimulation of the PAG has been observed to inhibit pain in both animals and humans. While the exact mechanisms are not fully understood, the primary pathway involves PAG neurons projecting to the raphe nuclei in the medulla oblongata. These activated raphe nuclei neurons, in turn, project to the dorsal horn of the spinal cord, where they inhibit pain-signaling neurons. This process prevents pain signals from reaching the brain. The PAG's natural ability to inhibit pain may come into play during extreme stress or situations where individuals experience top-down control of pain, such as the placebo effect. Additionally, the PAG contains a significant number of opioid receptors, suggesting its involvement in the analgesic effects of opioid drugs. The primary area for controlling the descending pain pathway Gate-Control Theory → Relies on the role of PAG PAG → Raphs nuclei → Dorsal here in the spinal cord (inhibits). Prevents pain signals to keep them from entering the brain

What is the role of the posterior parietal cortex in the senses?

The posterior parietal cortex (PPC) plays a critical role in sensory integration and various aspects of perception, particularly in the visual and somatosensory domains. It is located in the parietal lobe of the brain and is divided into two main regions: the superior parietal lobule (SPL) and the inferior parietal lobule (IPL), each with distinct functions. Here are some of the key roles of the posterior parietal cortex in the senses: Multisensory Integration: The PPC is known for its role in integrating sensory information from different modalities, such as vision, touch, proprioception, and audition. It helps create a unified perception of the surrounding environment by combining information from these senses. For example, it plays a role in spatial perception and object recognition by integrating visual and somatosensory inputs. Spatial Processing: The PPC is crucial for processing spatial information, including the perception of object locations, distances, and orientations in the external world. It's involved in functions like reaching and grasping, where accurate spatial processing is essential. Sensory-Motor Integration: The PPC is a key area for sensorimotor integration, linking sensory information to motor responses. It plays a role in planning and executing movements based on sensory input, such as reaching for an object in the environment. Body Schema: The PPC contributes to the development and maintenance of the body schema, which is the brain's representation of the body's spatial and functional characteristics. This helps us be aware of our body's position and orientation in space. Attention and Awareness: The PPC is involved in directing attention and maintaining awareness of sensory stimuli. It helps in shifting attention between different sensory modalities and objects of interest in the environment. Cognitive Functions: In addition to sensory processing, the PPC is implicated in higher-order cognitive functions, including decision-making, memory, and language. It plays a role in tasks that require executive control and strategic planning. Sensory Processing Abnormalities: Dysfunctions in the posterior parietal cortex can lead to sensory processing disorders or conditions like neglect syndro

What is the relative role of genetics and environment in risk of PD?

The risk of Parkinson's disease (PD) is influenced by both genetic and environmental factors, but the relative contributions of these factors can vary among individuals. Here's an overview of the role of genetics and the environment in the risk of developing PD: Genetics: Familial PD: While most cases of PD are considered sporadic, meaning they occur without a clear family history of the disease, a small percentage of cases are familial, meaning they have a genetic component. Mutations in specific genes have been linked to familial PD. The most well-known genes associated with familial PD are SNCA, LRRK2, and PARK2, among others. Idiopathic PD: The majority of PD cases are idiopathic, meaning there is no known genetic mutation that directly causes the disease. However, even in idiopathic cases, genetics may play a role. Certain genetic variations, including polymorphisms in several genes (e.g., GBA, MAPT), are associated with an increased risk of developing PD. These genetic variations may contribute to the disease in combination with environmental factors. Environmental Factors: Toxins: Exposure to certain environmental toxins has been linked to an increased risk of PD. One well-known example is exposure to pesticides and herbicides, including the herbicide paraquat. Other potential toxins include industrial chemicals like trichloroethylene and heavy metals like lead. Head Trauma: Some studies suggest that a history of head trauma, such as concussions, may be associated with an increased risk of PD. Infection and Inflammation: Chronic inflammation and certain infections have also been investigated as potential environmental risk factors for PD. Interaction Between Genetics and Environment: PD likely results from a complex interplay between genetic susceptibility and environmental exposures. For individuals with genetic predispositions (e.g., specific gene variants associated with PD), environmental factors may act as triggers or modifiers. These factors can include exposure to toxins, traumatic brain injuries, infections, and other environmental stressors. It's important to note that having a genetic risk factor for PD does not guarantee that an individual will develop the disease. Similarly, exposure to env

Vestibular Sense

The sense that helps us maintain balance and that provides information about head position and movement. The receptors are located in the vestibular organs. Vestibular organ contains three semicircular canals, utricle and saccule. Three loops arranged in different planes of orientation makes them especially responsive to movement of the head in three directions. The system responds only to acceleration and stops responding when speed stabilizes. The utricle and saccule monitor head position relative to gravity. (where up is). Cell receptors in the utricle are arranged in a horizontal patch, whereas the saccule's receptors are on its vertical wall; together, the two organs can detect tilt in any direction. The brain combines information about the object's spatial location with inputs from the vestibular sense and from proprioception to tell us what arm and hand movements are required. Can trigger reflexive eye movements.

Proprioception

The sense that informs us about the position and movement of the parts of the body. Report tension and length in muscles and angle of limbs at the joints. PIEZO2 receptor.

How is the somatotopic map in the cortex organized?

The somatotopic map in the cortex is organized in a specific manner that reflects the arrangement of body parts and their representation in the brain. This map is found in the primary somatosensory cortex, often referred to as S1, which is located in the postcentral gyrus of the parietal lobe. The organization of this map is somatotopic, meaning it's arranged based on a "body map." Here's how it's organized: Homunculus: The somatotopic map is often illustrated as a distorted figure called a "sensory homunculus." In this representation, the size of each body part corresponds to the relative amount of cortical space devoted to processing sensory information from that body part. Body parts with greater sensory sensitivity or motor control, like the hands and face, have larger representations. Contralateral Representation: One of the key features of the somatotopic map is that it follows a contralateral representation. This means that the left hemisphere of the somatosensory cortex processes sensory input from the right side of the body, and the right hemisphere processes sensory input from the left side of the body. This contralateral arrangement is also seen in the motor cortex. Distal to Proximal Organization: In the sensory homunculus, body parts are arranged based on a "distal to proximal" organization. This means that body parts with more distal locations, such as the fingers and toes, are represented in the lateral parts of the somatosensory cortex, while more proximal body parts, like the trunk and face, are represented in the medial parts. Fine Discrimination: Body regions that require fine sensory discrimination, such as the hands and fingers, have more extensive representations, reflecting the high density of touch receptors in these areas. This allows for greater sensitivity and precision in perceiving tactile information. Multiple Representations: The somatotopic map actually comprises multiple representations. For instance, there are separate representations for touch, proprioception (awareness of body position), and pain. These different representations may overlap or have distinct locations in the somatosensory cortex. Overall, the somatotopic map in the cortex is a crucial organizational structur

What is the treatment for MG?

The treatment for myasthenia gravis (MG) aims to alleviate symptoms, improve neuromuscular transmission, and suppress the autoimmune response. It typically involves a combination of approaches, including medications, thymectomy (removal of the thymus gland), and supportive therapies. The choice of treatment depends on the severity of the condition, the specific symptoms, and individual factors. Here are the main treatment options for MG: Acetylcholinesterase Inhibitors: These medications, such as pyridostigmine and neostigmine, increase the levels of acetylcholine at the neuromuscular junction. They help improve neuromuscular transmission and alleviate muscle weakness. These drugs are commonly used to manage MG symptoms. Immunosuppressive Medications: To reduce the autoimmune response and prevent the production of antibodies against acetylcholine receptors, various immunosuppressive drugs may be prescribed. Examples include corticosteroids (e.g., prednisone), azathioprine, mycophenolate mofetil, and cyclosporine. These medications help stabilize the disease and reduce symptom severity. Monoclonal Antibodies: Rituximab, a monoclonal antibody, targets and depletes B cells responsible for producing antibodies against acetylcholine receptors. It can be used when other treatments are not effective or are poorly tolerated. Thymectomy: In cases where there are thymic abnormalities or thymomas (tumors), surgical removal of the thymus gland (thymectomy) may be considered. Thymectomy can lead to a significant improvement in MG symptoms, particularly in individuals with early-onset MG. Plasma Exchange (Plasmapheresis): Plasma exchange is a procedure in which the patient's blood is filtered to remove harmful antibodies and immune proteins. This can provide temporary relief from severe MG symptoms but is not a long-term solution. Intravenous Immunoglobulin (IVIG): IVIG therapy involves infusions of immunoglobulin (antibodies) from healthy donors. It can temporarily boost the immune system and reduce MG symptoms. IVIG is often used in acute exacerbations or as a bridge to other treatments. Medications to Manage Side Effects: Medications to manage side effects or complications of MG may also be prescribed. For example, medi

What is the vestibular sense? What sensors are used for this sense?

The vestibular sense, also known as the vestibular system, is the sensory system responsible for providing the brain with information about spatial orientation, balance, and movement of the head and body in relation to gravity. It plays a crucial role in maintaining our equilibrium and stability. The primary sensors used for the vestibular sense are located in the inner ear, specifically in the vestibular apparatus. The vestibular apparatus includes three semicircular canals and two otolithic organs: Semicircular Canals: These are three fluid-filled tubes that are oriented at right angles to each other. They are responsible for detecting angular or rotational movements of the head. Each canal has sensory hair cells located at its base that are sensitive to the movement of the fluid inside the canal when the head rotates. The information from these canals allows us to perceive changes in the speed and direction of head movement, such as when we turn our heads or spin around. Otolithic Organs: Utricle: The utricle contains sensory hair cells and is responsible for detecting linear acceleration and changes in horizontal head position, such as moving forward and backward or tilting the head from side to side. Saccule: The saccule is also equipped with sensory hair cells and detects linear acceleration and changes in vertical head position, such as moving up and down. These sensors provide the brain with information about changes in head position and movement in three-dimensional space. The vestibular system is closely interconnected with the visual and proprioceptive systems, allowing us to maintain balance and orientation by coordinating information from different sensory modalities. When there is a mismatch between the sensory input from the vestibular system and the input from other systems, it can lead to sensations of dizziness, vertigo, and spatial disorientation. The information from the vestibular sense is processed in the brainstem and cerebellum and contributes to our sense of spatial awareness, postural control, and the coordination of movements. It is essential for activities like maintaining an upright posture, walking, and adjusting our gaze when we move our heads.

Dorsal Columns-Medial Lemniscus Pathway

This is the primary pathway that carries information about touch to the brain. It also conveys information about proprioception, which relates to the body's position in space and comes from proprioceptors in muscles and joints. Pathway Flow: Cutaneous receptors or proprioceptors send signals via dorsal roots into the spinal cord. In the spinal cord, these signals travel upwards through one of two fiber bundles within the dorsal columns: The fasciculus gracilis: Carries information from the lower half of the body. The fasciculus cuneatus: Carries information from the upper limbs and torso. In the medulla, the fasciculus gracilis and fasciculus cuneatus synapse at specific areas known as the nucleus gracilis and the nucleus cuneatus, respectively. The next part of the pathway involves a fiber bundle called the medial lemniscus. The medial lemniscus crosses over to the other side of the brain (decussates) before ascending to the thalamus. In the thalamus, it synapses in the ventral posterolateral nucleus (VPL). Somatosensory Cortex: A third part of the pathway arises from the thalamus and travels up to the somatosensory cortex, specifically to an area known as the postcentral gyrus. This cortex contains the primary sensory area for touch in the brain, known as the somatosensory cortex. Somatotopic Organization: The somatosensory cortex is somatotopically organized, meaning that specific parts of the cortex receive signals from distinct areas of the body. This organization allows for the integration of information about the nature and location of sensations. It's in the somatosensory cortex that the conscious perception of these sensations begins. The dorsal columns-medial lemniscus pathway is a fundamental neural circuit responsible for processing fine touch, proprioception, and vibration sensations. TOUCH INFORMATION (excluding head) → fine touch, vibration, conscious proprioception (knowing where our body is in space). PATHWAY: Touch Receptor → Ipsilateral (same side) Medulla (brainstem) → ** (crosses midline after the medulla/traveling along medial lemniscus) ** → VPL Thalamus (stop in the thalamus) → S1 (postcentral gyrus/parietal)

What are the receptors for skin senses (touch, temperature, texture, and pain)?

Touch (Pressure and Tactile Sensation): Merkel Cells (Merkel Discs): Found in the upper layers of the skin, particularly in the fingertips and other sensitive areas. They are involved in detecting fine details and shapes. Meissner's Corpuscles: Located in the dermal papillae of hairless skin, especially in the fingertips and lips. They are sensitive to light touch, low-frequency vibrations, and changes in texture. Pacinian Corpuscles: Situated in the deeper layers of the skin. They are sensitive to deep pressure and high-frequency vibrations. Ruffini Endings: Found in the dermis and subcutaneous tissue. These receptors respond to skin stretching and are involved in proprioception (awareness of body position). Temperature Sensation: Thermoreceptors: These receptors are sensitive to changes in temperature. They are located in the skin and mucous membranes throughout the body. There are two types: Cold Receptors: Respond to decreases in temperature, such as cooling of the skin. Warm Receptors: Respond to increases in temperature, such as warming of the skin. Texture Sensation: The perception of texture is primarily a result of the combined action of various types of touch receptors, including Meissner's corpuscles and Merkel cells. These receptors sense fine details and variations in surface texture. Pain Sensation: Nociceptors: Nociceptors are specialized pain receptors widely distributed throughout the skin, internal organs, and other tissues. They respond to noxious stimuli, including tissue damage, extreme temperatures, and chemical irritants. Nociceptors transmit signals indicating pain and potential harm to the central nervous system.

Parieto-insular vestibular cortex (PIVC)

Why excessive eye movements, from reading in a moving car, can cause dizziness and nausea. The PIV receives information from smell and taste receptors as well, which is why nausea and disgust are linked. If you easily get motion or seasickness, chances are you have a more sensitive PIV cortex. Taking an antihistamine drug (such as Dramamine) can decrease PIV activation and therefore reduce nausea.

Congenital Analgesia

a disorder in which an individual is born incapable of experiencing pain

Direct Pathway of the Basal Ganglia

caudate, putamen (together known as the striatum), globus pallidus, subthalamic nucleus, and substantia nigra. The basal ganglia play a significant role in various functions, with the direct pathway being one of the well-known circuits that influence motor control. Direct Pathway: Corticostriatal Input: The process begins when the cerebral cortex, particularly motor regions, sends signals related to the intention to make a movement. These signals are transmitted through glutamate neurons. Striatum Activation: Glutamate neurons stimulate neurons in the striatum, specifically the caudate and putamen. The activated striatal neurons release GABA (a neurotransmitter) in the globus pallidus internal and substantia nigra pars reticulata. Inhibition Release: GABA released in the globus pallidus internal and substantia nigra pars reticulata acts to inhibit their activity. This inhibition prevents the suppression of thalamic neurons involved in initiating movement. Facilitation of Movement: With the release of GABA and the decreased inhibition, a "gate" for movement is opened. This facilitates the initiation of the intended movement. Substantia Nigra Pars Compacta (SNc): The substantia nigra is divided into two parts, with the pars compacta playing a significant role in the direct pathway. Dopaminergic Modulation: Neurons in the substantia nigra pars compacta send dopamine projections to the striatum through the nigrostriatal pathway. Enhancement of Direct Pathway: Dopamine has an excitatory effect on the direct pathway. It enhances the activity of the striatum, making it more responsive to the corticostriatal input. This results in increased facilitation of movement. In summary, the direct pathway is a neural circuit within the basal ganglia responsible for facilitating movement. When the cortex signals the intention to move, it triggers a series of events involving the striatum, globus pallidus, substantia nigra, and thalamus. The substantia nigra pars compacta plays a key role in enhancing the activity of the direct pathway through the release of dopamine, which further promotes movement initiation

What is unique about chronic pain compared to acute pain?

dividuals. Here are some key differences between chronic pain and acute pain: Duration: Acute Pain: Acute pain is a temporary and short-lived sensation that typically results from an injury or specific trauma. It serves as a warning signal to alert the body to potential harm or damage. Acute pain usually resolves as the underlying issue or injury heals, typically within a few days to a few weeks. Chronic Pain: Chronic pain persists for an extended period, typically lasting for three months or longer. It may continue well after the initial injury or condition has healed. Chronic pain often becomes a long-term health issue and may be considered a disease in itself. It can last for months or even years. Underlying Causes: Acute Pain: Acute pain typically has a clear and identifiable cause, such as an injury, surgery, illness, or inflammation. It is a direct response to tissue damage or noxious stimuli. Chronic Pain: Chronic pain may not have an obvious or easily identifiable cause. It can result from various conditions, including degenerative diseases, nerve damage, autoimmune disorders, or persistent inflammation. Chronic pain can also develop without any initial injury or disease and may be influenced by complex factors, including genetics, psychological, and environmental factors. Adaptive vs. Maladaptive: Acute Pain: Acute pain serves an adaptive function by alerting the body to potential harm. It encourages protective behaviors, such as avoiding harmful situations and promoting the healing process. Once the underlying issue is resolved, acute pain diminishes. Chronic Pain: Chronic pain is often considered maladaptive. It does not serve a clear protective or healing function and can be disruptive to daily life. In many cases, chronic pain persists long after any potential protective or healing role has been fulfilled. Treatment Approach: Acute Pain: Acute pain is typically managed by addressing the underlying cause. Treatment may involve pain relievers, rest, physical therapy, or interventions to promote healing. Once the underlying issue is resolved, acute pain diminishes. Chronic Pain: Chronic pain management often focuses on improving an individual's quality of life and functionality because it may not be