Anatomy Quiz Questions PDF

Electromyography (Clinical Ap 5-1) ​ Electromyography allows health care professionals to assess how well muscles, and the nerves that control them, are functioning. The results of an EMG scan can reveal dysfunction of the muscles or nerves, or a problem with transmission of the...

Electromyography (Clinical Ap 5-1) ​ Electromyography allows health care professionals to assess how well muscles, and the nerves that control them, are functioning. The results of an EMG scan can reveal dysfunction of the muscles or nerves, or a problem with transmission of the impulse from the neuron to the muscle call. EMGs are usually ordered for individuals showing signs of nerve or muscle disorder, including tingling, numbness, weakness in the muscle, muscle pain, or paralysis Deep Tendon (stretch) reflexes and central nervous system injury (Brain and Spinal cord) (clinical Ap 5-2) ​ Deep tendon reflexes, such as the patellar, biceps, and Achilles reflexes, can be used to assess the sensory-motor functioning of the body. ​ Most stretch reflexes involve a simple reflex arc consisting of a sensory neuron that connects directly to a motor neuron. The sensory neuron carries information from the receptor organ to the spinal cord, while the motor neuron carries information from the spinal cord to the muscle, resulting in contraction. The brain is informed of the activity, but no information from the brain is required in order to observe the reflex response. ​ Very simple stretch reflexes can be influenced by the brain. Motor neurons from the brain can either excite or inhibit the neurons in the spinal cord that control reflexes. ​ Under normal conditions, neurons from the brain inhibit the motor neurons in the spinal cord involved in deep tendon reflexes. This inhibition from the brain decreases reflexive response and prevents clonus. ​ If the spinal cord is damaged, inhibitory information from the brain cannot travel to motor neurons below the level of the spinal injury. Without the normal inhibitory effect of the brain, the reflexes below the level of injury will be hyperactive (reflexes that are significantly stronger than normal reflexes) ​ An individual with spinal cord damage loses some or all voluntary motor control and sensations below the level of spinal cord damage BUT reflexes below the level of the injury are more brisk than normal (hyperactive) due to the lack of inhibitory input from the brain. ​ The level of the injury in the spinal cord determines the degree of sensory and motor loss experience. ​ Motor information from one side of the brain controls the muscles on the opposite side of the body so if only one side of the brain is injured, the reflexes on the opposite side of the brain may be hyperactive. This is due to lack of inhibitory information form the injured side of the brain. ​ An injury of the left motor cortex in the brain will decrease inhibitory input to the right side of the body, causing hyperactive reflexes Assessment of Reflexes (Clinical Ap 5-3) \ ​ In clinical assessment, reflexes on both sides of the body should be tested and reflexive response should be symmetric. Any asymmetry may indicate damage to a specific side of the brain or spinal cord. Clinically, reflexes are graded on a somewhat quantitative basis, from 0 to 4+ in the following way: ○​ 0= no response ○​ 1+= response occurs, but slow and sluggish reflex, somewhat suppressed  ○​ 2+= a brisk, normal reflex ○​ 3+= a very brisk response ○​ 4+= hyperactive reflex with clonus present ​ Generally 2+ is normal however reflexes do vary somewhat from person to person. Some individuals may normally have more sluggish and suppressed reflexes (1+), other people may have reflexes that are normally brisker (3+). Thus reflexes of 1+,2+, 3+ may be normal, provided all reflexes have similar responses. However a complete lack of response (0) or the presence of hyperactive reflexes (4+) is almost always abnormal Deep tendon reflexes and damage to reflex arc (pathway) (clinical ap 5-4) ​ Damage to the neurons (nerves) traveling between the spinal cord and the body will result in hyperactive reflexes (reflexes that are so much weaker than normal or that are absent because these neurons cannot properly transmit impulses. ○​ EX. The viral disease poliomyelitis or polio destroys motor nerves carrying impulses from the spinal cord to the muscles. These damaged motor neurons cannot transmit any motor information to muscles, thus, individuals with polio lose motor control and lack deep tendon reflexes in affected areas. ○​ Peripheral neuropathy (nerve damage) is the most common cause of absent reflexes. Many diseases and disorders can damage the nerves, including diabetes, alcoholism, pernicious anemia, toxins such as lead, guillain-barre syndrome, and vitamin B deficiencies, leading to decreased or absent reflexes. Effect of exercise programs on reaction times cognition (clinical ap 5-5) ​ Exercise can improve: reaction times, balance, coordination, response time in daily events like walking or driving ​ Studies shoe that regular exercise can improve cognitive performance as well as improve mood, mental alertness, and contribute to an overall sense of well-being. ​ Aerobic physical exercise has been shown to improve blood flow to the brain, which may improve brain function and may also help to protect the neurons from damage caused by free radicals ​ Studies show that changes that occur in the brain as a result of sustained exercise may be due to “neuroplasticity” of the brain ○​ Neuroplasticity is basically the ability of the brain to change its activity in response to experiences or stimuli by reorganizing itself –its structure, neuron connections, or even its function Exercise 5: ​ Impulses (action potentials) are like tiny little electrical currents carried throughout the body by neurons (specifically the axons of neurons). Some of these impulses causes muscle contraction, some relay sensory information to the brain, some are involved with cognitive process and problem solving Resting Membrane Potential: ​ There are three factors that contribute to creating the resting membrane potential: 1. Unequal pumping of sodium and potassium by the sodium-potassium pump 2. Unequal diffusion of sodium and potassium across plasma membrane 3. The presence of large, negatively charged proteins inside the cell (maintaining a membrane potential is critical for the initiation and conduction of nerve impulses) Action Potentials ​ An action potential is initiated by the neuron when the electrical charge difference across the plasma membrane is changed, allowing the inside of the plasma membrane to become more positively charged than resting membrane potential. This occurs due to the movement of additional positively charged ions into the cells. ​ In order for these additional sodium ions to enter the cell, there must be some kind of stimulus that creates a change in permeability of the plasma membrane to sodium ions. Most of the time, the stimulus is a chemical (usually a neurotransmitter) that binds to specific receptors in the plasma membrane. ​ If the charge inside the plasma membrane becomes positive enough to reach threshold, an action potential is initiated. ​ Reaching threshold triggers a series of events that occur in the action potential ○​ First, this stimulates the opening of voltage gated sodium and potassium ion channels. Voltage gated sodium ions open first, allowing sodium to rush into the cell ○​ The inside of the plasma membrane becomes more and more positive and reaches 30+ mV. This influx of sodium, driving the charge difference across the plasma membrane from threshold to 30+mV is known as Depolarization phase of the action potential ○​ Once a charge of 30+ mV is reached, the clow-to-open voltage gated potassium channels open and, since the inside of the cell has a much higher concentration of potassium than the extracellular fluid, the potassium will rush out of the cell. As the positively charged potassium ions leave the cell, the inside of the plasma membrane becomes more and more negative again, until the charge is returned to the resting membrane potential. This return to the resting membrane potential as potassium leaves the cell is known as the repolarization phase of the action potential. ○​ Potassium channels close slowly, allowing more potassium to leave the cell than is necessary to simply return to resting membrane potential. As additional potassium leaves, the inside of the plasma membrane becomes more negative than resting membrane potential, creating a small hyperpolarization ○​ Last, the sodium-potassium pump will return sodium and potassium to their original locations and RMP is restored. Synaptic Transmission of Impulses ​ Impulses are transmitted from one cell to another at synapse. Most synapses use a chemical called a neurotransmitter to transmit an impulse from cell to cell ​ As the impulse reaches the end of an axon, voltage gated channels in the axon terminals open and calcium enters the axon terminal, this calcium triggers the synaptic vesicles to move and fuse with the pre-synaptic membrane. ​ The neurotransmitter is released into the synaptic cleft and diffuses across the cleft, where it binds to ligand gated neurotransmitter receptors on the post-synaptic membrane. Binding opens ion specific channels and allows ions to enter or leave the cell.  ○​ If positively charged ions enter, the inside of the plasma membrane becomes more positive and is depolarized. This is considered an excitatory transmission as the cell is closer to threshold. If threshold is reached, action potential will be generated. ○​ If negatively charged ions enter (like chloride) or positively charged ions leave, the inside of the plasma membrane becomes more negative (hyperpolarization); the cell is further from threshold, therefore this is considered an inhibitory transmission. The transmission of the impulse at the synapse is the slowest ○​ Speed of Impulse Conduction ​ How fast an impulse can travel is dependant on two factors: ○​ The amount of myelin around the axon ○​ The diameter of the axon ​ An increase in either of the two of these factors will increase the speed at which the impulse is conducted along the axon. An increase in diameter allows from faster impulse conduction as there is less resistance to ion movement in the axon ​ Myelin serves to insulate and protect axons, as well as increase the speed of impulse conduction. In myelinated axons, all ion channels are concentrated in the areas without myelin and the events of the action potential occur only at the nodes. ​ The impulse appears to jump from node to node in what is known as saltatory conduction ​ Unmyelinated axons have continuous conduction. In continuous conduction, voltage gated ion channels are located along the entire length of the axon and the events of the action potential occur along the entire length of the axon. Consequently, saltatory conduction, where the action potential events occur only at the nodes, allow for much faster impulse conduction than continuous conduction. ​ Nerve fibers (axons) are classified as type A fibers, type B fibers, type C fibers ○​ Type A: have most myelin and largest diameter, conduct impulses at 15-130 meters/second) ○​ Type B: have some myelin and are medium in diameter so they conduct slower generally 3-15 meters/second ○​ Type C: lack myelin and have smallest diameter thus conduct impulses the slowest usually >3 meters/second Deep Tendon or Stretch Reflex ​ The deep tendon or stretch reflex involves only one synapse between sensory and motor neurons. No association neurons are involved; thus, it is known as a monosynaptic reflex (one synapse) ​ Function of the stretch reflex is to resist and prevent excessive stretching of the muscle that could possibly damage the muscle fibers… resisting over-stretching ​ Receptor in the stretch reflex are a special muscle fiber apparatus called muscle spindle apparatus located in all skeletal muscles. Each muscle spindle contains 3-10 thin non contractile muscle cells called intrafusal fibers that are enclosed in connective tissue. The central regions of these fibers are susceptible to stretching and are innervated by sensory neurons  ​ In the spinal cord, the sensory neurons synapse directly with the motor neurons. These motor neurons then transmit an impulse to the muscle (effector organ). The muscles are stimulated to contract, thus preventing over-stretching and possible tissue damage. While the spinal reflex is occuring, impulses are also sent to the cerebrum, so that the individual is made consciously aware of muscle stretch and reflex contraction. Information is also passed to the cerebellum to assist in coordination and maintaining balance. ​ The most commonly observed stretch reflex is the knee-jerk or patellar reflex ​ There is a very short period of time after the stimulus is applied when there is no apparent response at all. This period is called the latent period because this period is so short, it is not visible with the naked eye but can be observed recorded on the computer ​ During the latent period the nerve impulses must travel from the receptor to the spinal cord via sensory neurons, across the synapse to the association neurons and to motor neurons. The impulse then travels down the motor neuron, where it must cross the neuromuscular junction to the muscle cell. More time is required for depolarization of the muscle cell membrane and all of the events that lead to muscle contraction ​ Despite the fact that the latent period is very short – a fraction of a second – there is a great deal of activity that occurs during this time. Only after myosin heads bing to actin can the myosin heads flex and cause shortening of the muscle fiber Electromyography ​ Electromyography measures the electrical activity in the muscles that stimulate contraction (the recording is done on a EMG, electromyogram) ​ There are 2 ways in which this electrical activity can be recorded ○​ By inserting electrodes into the muscle ○​ Placing the electrodes on the surface of the skin