Question About the Physiology of Seizures

Question About the Physiology of Seizures

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Absence seizures usually occur in children between ages 4 to 14 (Hopkins Hospital). Spontaneous remission occurs in 65-70% of patients during adolescence (Medicine Central).

My question is what takes place biologically that allows you to 'grow out of them?' Is it synapse pruning in the brain or something? I have looked everywhere online but can't seem to understand the physiology of how one grows out of seizures.

Easily Learn About Human Physiology

A complete review of human physiology includes the study of tissue, organs, and the various systems that together form the human body. Physiology is a key area in the study of biology, particularly if you’re taking exams.

We present all the topics here in logical order, starting from the basics and working forward to more complex systems: animal tissues, blood, metabolism and homeostasis, nutrients and vitamins, digestion, respiration, circulation, excretion, epithelial tissue and skin, the musculoskeletal system, the nervous system, the human eye, the auditory system, the endocrine system, the immune system, gametogenesis, and reproduction.

Anyone wishing to become a life science professional needs to have a strong grasp of all the information contained here. If you’ve ever wanted to understand yourself fully, inside and out, our Q&As is where you want to be!

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What happens to food when we consume it? These absorbing Q&As explain the digestive process, what happens to food as it passes our lips and works its way through our bodies. Learn what your mouth, esophagus, stomach, duodenum, jejunum, ileum, caecum, colon, and everything in between, do with the food you eat.

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Seizures are caused by paroxysmal discharges from groups of neurons, which arise as a result of excessive excitation or loss of inhibition. The key unit of neurotransmission is the synapse, and the fundamental components of synapses are ion channels. Thus, the cause of seizures boils down to malfunction of ion channels. About one third of seizures are caused by genetic abnormalities, mostly involving ion channels. A quarter or so are caused by structural lesions. Patients with such lesions usually have additional neurological abnormalities. Some of these lesions, such as brain tumors, traumatic brain injury, infections, and perinatal brain lesions, are environmentally acquired. Others, including brain malformations, genetic tumor syndromes, and metabolic disorders are genetic or have a strong genetic component. In about half of seizure disorders, no genetic or structural abnormality is evident. Perhaps many of these cases are caused by genetic or acquired channelopathies that are not yet recognized. In addition to genes and the environment, brain (synapse) development has a strong influence on seizures. Synapses are in a state of flux during childhood and adolescence first they proliferate excessively and then they are reduced to adult levels. The dynamic state of synapses explains why most seizures begin (and often stop) for no apparent reason during childhood.

Based on the pattern of the attack, seizures are divided into generalized tonic-clonic (grand mal), partial or focal, and several special epileptic syndromes.

Structural lesions are frequently detected in focal seizures. The most common such lesions are cerebral changes resulting from perinatal brain damage, malformations, cerebral infarcts, trauma, brain tumors, and infections. These lesions involve the cerebral cortex and are characterized by neuronal loss and gliosis. Residual neurons in epileptogenic foci, show loss of dendritic spines, possibly due to loss of afferents. The sources of these afferents have been presumably destroyed by tumors, trauma, stroke, or other lesion. Even minute lesions of the cerebral cortex may destroy, out of proportion, small, inhibitory (GABAergic) interneurons, thus reducing the inhibition that controls large pyramidal cells.

In most generalized seizures, no primary lesions are detected by imaging or neuropathological examination.

The most common seizures in children and adults are partial complex seizures originating from the temporal lobe (temporal lobe epilepsy -TLE or psychomotor epilepsy). These seizures begin with a visceral sensation or other aura(breeze) and are followed by a state of impaired consciousness, automatic motor activities or convulsions. The EEG localizes the epileptogenic focus in the medial portion of the temporal lobe. Because TLE is refractory to drugs, it is often treated by resection of the temporal lobe including the hippocampus and surrounding area and the amygdala. Examination of temporal lobectomy specimens reveals pathology in most cases. The most common lesions are hippocampal sclerosis, tumors (gangliogliomas, gliomas), cortical dysplasias and hamartomas, vascular malformations, ischemic and traumatic lesions, and infectious-inflammatory lesions. In many cases, no pathology is found.

Hippocampal sclerosis (HS) or Ammon's horn sclerosis consists of loss of neurons in the dentate nucleus and the pyramidal layer of the hippocampus with variable gliosis. Four patterns of HS are recognized, the most common one involving the CA4 (end folium) and CA1 (Sommer sector) subfields of the pyramidal layer. These lesions cause shrinkage of the hippocampus that can be detected by MRI. In addition to seizures, HS is seen in a significant proportion of patients with Alzheimer's disease and other dementias.

The pathogenesis of this lesion has been the subject of a "chicken or the egg" argument for more than 100 years. Some authors propose that HS is the cause of seizures and others that it is the result of seizures. Proponents of the former view argue that the hippocampus is damaged early in life by birth injury, complicated febrile seizures, and other events, and that this damage makes it prone to seizures. Unlike the neocortex, the hippocampus continues to develop after birth and is more vulnerable to such insults. In some cases of TLE, there is a history of febrile seizures and other insults but in most cases no such history can be elicited. On the other hand, there is also strong support for the idea that HS is secondary to seizures, particularly status epilepticus. Animal experiments and observations in humans show that even a single seizure can cause neuronal damage and that this damage may occur without convulsions, is cumulative, and correlates with the duration and severity of the electrical abnormaliry. HS is also seen in patients who have seizures resulting from brain tumors, cortical dysplasias, and other brain lesions. However, some patients with seizures and status epilepticus have no HS.

The presumed mechanism of damage in HS is discharge of glutamate during the epileptic attack and the most frequent site of damage is the CA1 sector of the hippocampus. This area is also especially vulnerable to hypoxia which also initiates an excitotoxic cascade. This circular argument about HS underlines the rich connectivity and excitatory neurotransmission of certain fields of the hippocampus. However, epileptic brain damage is not limited to the hippocampus. Intractable epilepsy and status epilepticus cause also neuronal loss in the cerebral cortex, thalamus, and cerebellum (Purkinje cells). In addition, patients with epilepsy suffer brain damage from falls and have a high frequency of unexpected death.

Frequently Asked Questions About Epilepsy

Epilepsy, which is sometimes called a seizure disorder, is a disorder of the brain. A person is diagnosed with epilepsy when they have had two or more seizures.

A seizure is a short change in normal brain activity.

Seizures are the main sign of epilepsy. Some seizures can look like staring spells. Other seizures cause a person to fall, shake, and lose awareness of what&rsquos going on around them.

Usually, a seizure lasts from a few seconds to a few minutes. It depends on the type of seizure.

Sometimes it is hard to tell when a person is having a seizure. A person having a seizure may seem confused or look like they are staring at something that isn&rsquot there. Other seizures can cause a person to fall, shake, and become unaware of what&rsquos going on around them.

Seizures are classified into two groups.

      1. Generalized seizures affect both sides of the brain.
      2. Focal seizures affect just one area of the brain. These seizures are also called partial seizures.

      A person with epilepsy can have more than one kind of seizure. Read more about types of seizures and what they look like.

      Not always. Seizures can also happen because of other medical problems. These problems include:

      Epilepsy can be caused by different conditions that affect a person&rsquos brain. Some known causes include:

          • .
        • Brain tumor.
        • Brain infection from parasites (malaria, neurocysticercosis), viruses (influenza, dengue, Zika), and bacteria. or head injury.
        • Loss of oxygen to the brain (for example, during birth).
        • Some genetic disorders (such as Down syndrome).
        • Other neurologic diseases (such as Alzheimer&rsquos disease).
        • For 2 in 3 people, the cause of epilepsy is unknown. This type of epilepsy is called cryptogenic or idiopathic.

          Read more about the causes of epilepsy in the National Institute of Neurological Disorders and Stroke publication: Seizures and Epilepsy: Hope Through Research external icon .

          Epilepsy is one of the most common conditions affecting the brain.

          When counting both children and adults in the United States:

              • About 5.1 million people in the United States have a history of epilepsy.
              • About 3.4 million people in the United States have active epilepsy.

              Preventing and Managing Epilepsy

              Sometimes we can prevent epilepsy. These are some of the most common ways to reduce your risk of developing epilepsy:

                  • Have a healthy pregnancy. Some problems during pregnancy and childbirth may lead to epilepsy. Follow a prenatal care plan with your health care provider to keep you and your baby healthy.
                  • Prevent brain injuries.
                  • Lower the chances of stroke and heart disease.
                  • Be up-to-date on your vaccinations.
                  • Wash your hands and prepare food safely to prevent infections such as cysticercosis.

                  A person who has a seizure for the first time should talk to a health care provider, such as a doctor or nurse practitioner. The provider will talk to the person about what happened, and look for the cause of the seizure. Many people who have seizures take tests such as brain scans for a closer look at what is going on. These tests do not hurt.

                  Learn more about how epilepsy is diagnosed external icon from the Department of Veterans Affairs.

                  There are many things a provider and person with epilepsy can do to stop or lessen seizures.

                  The most common treatments for epilepsy are:

                      • Medicine. Anti-seizure drugs are medicines that limit the spread of seizures in the brain. A health care provider will change the amount of the medicine or prescribe a new drug if needed to find the best treatment plan. Medicines work for about 2 in 3 people with epilepsy.
                      • Surgery. When seizures come from a single area of the brain (focal seizures), surgery to remove that area may stop future seizures or make them easier to control with medicine. Epilepsy surgery is mostly used when the seizure focus is located in the temporal lobe of the brain.
                      • Other treatments. When medicines do not work and surgery is not possible, other treatments can help. These include vagus nerve stimulation, where an electrical device is placed, or implanted, under the skin on the upper chest to send signals to a large nerve in the neck. Another option is the ketogenic diet, a high fat, low carbohydrate diet with limited calories.

                      Read more about the treatment options for epilepsy in the National Institute of Neurological Disorders and Stroke publication: Seizures and Epilepsy: Hope Through Research external icon .

                      Many kinds of health providers treat people with epilepsy. Primary care providers such as family physicians, pediatricians, and nurse practitioners are often the first people to see a person with epilepsy who has new seizures. These providers may make the diagnosis of epilepsy or they may talk with a neurologist or epileptologist.

                      A neurologist is a doctor who specializes in the brain and nervous system. An epileptologist is a neurologist who specializes in epilepsy. When problems occur such as seizures or side effects of medicine, the primary health provider may send the patient to a neurologist or epileptologists for specialized care.

                      People who have seizures that are difficult to control or who need advanced care for epilepsy may be referred to an epilepsy centers. Epilepsy centers are staffed by providers who specialize in epilepsy care, such as

                          • Epileptologists and neurologists.
                          • Nurses.
                          • Psychologists.
                          • Technicians.

                          Many epilepsy centers work with university hospitals and researchers.

                          There are several ways you can find a neurologist or an epileptologist near you. Your primary care or family provider can tell you about types of specialists. The American Academy of Neurology external icon and the American Epilepsy Society external icon provide a listing of its member neurologists and epilepsy specialists, including epileptologists. The National Association of Epilepsy Centers external icon also provides a list of its member centers, organized by state.

                          Self-management is what you do to take care of yourself. You can learn how to manage seizures and keep an active and full life. Begin with these tips:

                              • Take your medicine.
                              • Talk with your doctor or nurse when you have questions.
                              • Recognize seizure triggers (such as flashing or bright lights).
                              • Keep a record of your seizures.
                              • Get enough sleep.
                              • Lower stress.

                              Health and Safety Concerns

                              Women who have epilepsy face special challenges. Hormonal changes can cause some women with epilepsy to have more seizures during their period.

                              For women with epilepsy, there are also special concerns about pregnancy, because having a seizure and taking certain drugs during pregnancy may increase the risk of harm to the baby. Women can take the following steps before and during pregnancy to lessen these risks.

                                  • If you are a woman with epilepsy who plans to get pregnant, talk with your health team about how to best care for yourself and your baby.
                                  • Learn more about issues facing women with epilepsy and how to improve health on the Epilepsy Foundation&rsquos website, Women and Epilepsy external icon .

                                  Most people with epilepsy live a full life. However, the risk of early death is higher for some. We know that the best possible seizure control and living safely can reduce the risk of epilepsy-related death.

                                  Factors that increase the risk of early death include:

                                      • More serious health problems, such as a stroke or a tumor. These conditions carry an increased risk of death and may cause seizures.
                                      • Falls or other injuries that happen because of seizures. These injuries can be life-threatening.
                                      • Seizures that last over 5 minutes. This is a condition called status epilepticus. Status epilepticus can sometimes happen when a person suddenly stops taking seizure medication.

                                      Rarely, people with epilepsy can experience sudden unexpected death in epilepsy (SUDEP). SUDEP is not well understood and experts don&rsquot know what causes it, but they suspect that it is sometimes due to a change in heart beats (rhythm) during a seizure. Sudden death due to heart rhythm changes also happens in people who do not have seizures.

                                      The risk of sudden death is larger for people with major uncontrolled seizures.

                                      Read more information about SUDEP.

                                      Most states and the District of Columbia will not issue a driver&rsquos license to someone with epilepsy unless that person provides documentation that he or she has not had a seizure for a specific amount of time. The seizure-free period ranges from a few months to over a year, depending on the state.

                                      Some states need a letter from your health provider to issue a license when a person has seizures that:

                                          • Don&rsquot distract the person from driving.
                                          • Happen only during sleep. These are called nocturnal seizures.
                                          • Have warning signs that alert the person that a seizure might happen. Sometimes a person feels strange before a seizure. This is called an aura.

                                          Learn state-specific information external icon about driving laws from the Epilepsy Foundation.

                                          Sometimes people with epilepsy worry that exercise or sports may worsen their seizures.

                                          Exercise is rarely a &ldquotrigger&rdquo for seizure activity. In fact, regular exercise may improve seizure control. Safely playing sports can also be great for your physical, mental, and emotional well-being.

                                          It is always important to avoid sports-related injuries that can increase the risk of seizures.

                                          Read more about safe physical activity for people with epilepsy on the Epilepsy Foundation website, Safety with Exercise and Sports external icon .

                                          Essay on the Treatment of Epilepsy | Diseases | Medical Science

                                          Here is an essay on the ‘Drugs Used for the Treatment of Epilepsy’ for class 11 and 12. Find paragraphs, long and short essays on the ‘Drugs Used for the Treatment of Epilepsy’ especially written for college and medical students.

                                          Essay # 1. Antiepileptic Drugs:

                                          Antiepileptic drugs are used in the treatment of epilepsy which includes a group of disorders of CNS characterized by partial seizures with or without secondary generalization or generalized seizures. The object of the treatment is to prevent the occurrence of seizures by maintaining an effective plasma concentration of the drug.

                                          There are several varieties of epilepsy and they vary in their response to drugs. Although, there are now a number of drugs which are useful in controlling epilepsy, it is usually best to start treatment with one drug only and use multiple drug regimens in resistant cases. Table 3.2 gives the type of epilepsy (seizures) and the choice of antiepileptic drugs.

                                          Mechanism of action:

                                          Glutamate is the excitatory neurotransmitter and γ-aminobutyric acid (GABA) is the inhibitory transmitter in the CNS. Most of the antiepileptic drugs act by inhibiting GABA transaminase, the enzyme that catabolizes GABA, thus increasing the activity of the inhibitory neurotransmitter GABA or by inhibition of the activity of glutamate. Some act by directly blocking sodium and/or calcium channels in the nerve cell membrane.

                                          I. Phenytoin (Diphenylhydantoin):

                                          Phenytoin is well absorbed orally and does not produce drowsiness or sleep. It probably acts by reducing the excitability of nerve cells by blocking sodium channels in nerve membranes and thus prevents the abnormal discharge from the epileptic foci in the brain.

                                          Phenytoin is effective in all forms of epilepsy except petit mal. It has a narrow therapeutic index and serves as an alternative to carbamazepine or sodium valproate as an antiepileptic. Monitoring of plasma concentration is necessary for optimum efficacy and avoidance of acute toxic effects.

                                          Side effects are fairly common and include drowsiness, memory impairment, ataxia, nystagmus, gum hyperplasia, hirsutism, greasy skin, macrocytic anaemia, rashes, liver damage and osteomalacia.

                                          These are common and necessitate regular measurement of plasma levels of phenytoin. Plasma phenytoin concentration is increased by NSAIDs, antibacterials, oral anticoagulants, antifungal drugs, calcium channel blockers, cimetidine and uricosuric drugs. Phenytoin accelerates the metabolism of a number of drugs such as corticosteroids, oral contraceptives, theophylline, tricyclic antidepressants and thyroxine among others.

                                          Ii. Fosphenytoin:

                                          Fosphenytoin is a pro-drug and is converted into phenytoin by the liver enzyme alkaline phosphatase. It is given by injection when phenytoin cannot be given by mouth, e.g. during status epilepticus or seizures associated with head injuries or surgery. It causes less irritation than phenytoin at the injection site.

                                          Iii. Phenobarbitone:

                                          Phenobarbitone is not the drug of choice in epilepsy because of its potential neurotoxicity. It is a long acting barbiturate which is particularly effective in grand mal, but may also be used in other types of epilepsy except petit mal. Primidone is largely converted to phenobarbitone which is responsible for its antiepileptic action. Phenobarbitone is slowly absorbed the major portion is metabolized in the liver and the rest excreted by the kidneys.

                                          Side effects are not uncommon and include drowsiness, memory impairment, ataxia, skin rash resembling measles and behavior disorders. Phenobarbitone is a powerful inducer of enzymes in the liver and increases the metabolism of a large number of drugs thereby lowering their plasma concentration and consequent reduction in their pharmacological effects.

                                          Iv. Primidone:

                                          Primidone is in many ways similar to phenobarbitone and is also effective in all forms of epilepsy except petit mal. Side effects are like phenobarbitone and include drowsiness, ataxia, nausea, visual disturbances and rashes.

                                          V. Carbamazepine (Tegretol):

                                          Carbamazepine is the drug of choice for psychomotor and grand mal epilepsy. It is also used to relieve the pain of trigeminal neuralgia and for prophylaxis of bipolar depression unresponsive to lithium. It is of no value in petit mal. The dose of carbamazepine depends more on the patient’s response than its plasma levels.

                                          Common side effects include drowsiness, dizziness, ataxia, diplopia, rashes, leucopenia, heart block, hyponatremia, occasionally jaundice and excessive salivation. Carbamazepine is contraindicated in AV conduction abnor­malities, history of bone marrow depression and porphyria.

                                          Carbamazepine, like phenytoin and phenobarbitone, causes induction of hepatic enzymes which may reduce the efficacy of oral contraceptives. Erythromycin increases the serum concen­trations of carbamazepine. Oxcarbazepine is a pro-drug that is converted into an active metabolite. Its actions are similar to carbamazepine and are used in patients allergic to carbamazepine.

                                          Vi. Sodium Valproate:

                                          Valproate acts by inhibiting GABA metabolism in the brain. It has a much broader range of anticonvulsant action and is effective in all forms of epilepsy including petit mal.

                                          An attractive feature of valproate is its relative freedom from sedative cognitive (mental activity), and behavioural effects as compared with phenytoin, phenobarbitone, and the benzo­diazepines. Drowsiness, thinning of the hair and weight gain is common. Platelet count and fibrinogen concentration may be reduced but serious hemorrhagic complications are rare. Rare idiosyncratic metabolic reactions that produce fatal hepatotoxicity are the most serious complications. Valproate is contraindicated in active liver disease, family history of severe hepatic dysfunction and porphyria.

                                          Aspirin, erythromycin and cimetidine increase plasma valproate concentration. Antidepressants, antimalarials, antipsychotics antagonise the anticonvulsant effects of valproate.

                                          Vii. Vigabatrin:

                                          Vigabatrin irreversibly inhibits GABA transaminase, resulting in an increase in synaptic GABA. Vigabatrin is particularly effective in psychomotor seizures—a condition where carbamazepine, valproate and phenytoin fail to offer complete control of the seizures in 40% of patients. Antiepileptic effects do not correlate with serum concentrations, and plasma monitoring is therefore not necessary.

                                          These are reported to be mild, reversible and similar to those for other anti-epileptics such as sedation, confusion, amnesia and visual field defects. Vigabatrin is relatively free of adverse cognitive effects. The most important adverse effect is the production or exacerbation of psychosis. Vigabatrin is contraindicated in visual field defects.

                                          Viii. Lamotrigine:

                                          Lamotrigine is a novel antiepileptic drug, which reduces the release of the excitatory neurotransmitter, glutamate. It is indicated in psychomotor and grand mal epilepsy and better tolerated than carbamazepine.

                                          Ataxia, drowsiness, diplopia and nausea occur in a small proportion of patients. Rashes, which may be dangerous, occur particularly in children. It should not be used in patients with hepatic or renal impairment.

                                          Ix. Clonazepam:

                                          Clonazepam is a benzodiazepine and is useful in all forms of epilepsy, but its sedative effects may be prominent. It is con­traindicated in respiratory disease, hepatic and renal impairment.

                                          X. Clobazam:

                                          Clobazam is also a benzodiazepine and is used as an adjunct in epilepsy. Its side effects are similar to that of diazepam.

                                          Xi. Felbamate:

                                          Felbamate is effective over a wide range of epileptic conditions. Because of its dangerous adverse effects such as hepatitis and aplastic anemia, the use of felbamate is restricted to only one particular childhood epilepsy called the Lennox-Gastaut syndrome, which does not responds to other drugs.

                                          Xii. Ethosuximide:

                                          Ethosuximide is the drug of choice for petit mal. It may aggravate grand mal and may, if necessary be, combined with a drug which controls grand mal epilepsy.

                                          Gastrointestinal disturbances, weight loss, drowsiness, ataxia, photophobia, headache and depression are common. Rarely psychotic states, rashes, hepatic and renal changes and blood disorders may occur.

                                          Essay # 2. Other Drugs:

                                          Acetazolamide, a carbonic anhydrase inhibitor, is a second-line drug for psychomotor and grand mal. Piracetam, gabapentin, topiramate and tiagabine are used as adjunctive treatment for psychomotor epilepsy.

                                          I. Status Epilepticus:

                                          Diazepam is the most effective and is given intravenously in a dose of 10 mg. In young children rectal diazepam is quite effective and useful particularly if intravenous injection is difficult. There is high risk of venous thrombophlebitis with diazepam, which is minimized by giving diazepam emulsion (as Diazemuls). Other benzodiazepines, clonazepam and lorazepam are also used lorazepam has the advantage of a long duration of action.

                                          Although diazepam will usually stop the fits, relapse quite commonly occurs within the next hour. To prevent relapses phenytoin or more usually fosphenytoin is given intravenously with ECG monitoring, since it is a cardiac depressant.

                                          Alternatively, phenobarbitone sodium can be given by intravenous injection. If the fits still persist chlomethiazole should be given intravenously. It should not be given in acute pulmonary insufficiency. Finally, if all therapies fail, thiopentone can be given by intravenous injection, using artificial ventilation, if necessary.

                                          Paraldehyde is an oily liquid with pungent smell. It is a CNS depressant which controls status epilepticus. It is given rectally or by deep intramuscular injection. It is not the first line treatment for status epilepticus, but has the advantage of relatively freedom from severe respiratory depression seen with other drugs and does not require close monitoring and respiratory support.

                                          Ii. Anti-Epileptics and Pregnancy:

                                          Antiepileptic drugs given during pregnancy are associated with an increased risk of fetal malformations. Carbamazepine, phenytoin and valproate carry the risk of neural tube and other defects. To counteract the risk of congenital defects, women should receive folic acid (5 mg) daily before and throughout pregnancy.

                                          In view of the risk of neonatal bleeding associated with carbamazepine, phenobarbitone and phenytoin, prophylactic vitamin K is recommended before the delivery. Antiepileptic drugs induce liver enzymes and thus increase the rate of breakdown of oral contraceptives, which requires necessary changes in the patient’s method of contraception.

                                          Human Physiology - Locomotion & Movement Questions

                                          HOME THEORY MEDIA quiz. MISSION The muscle you can see on the microscope screen was stained for myosin ATPase and a darker stain indicates a higher capacity to use ATP. This means muscles can contract more quickly and can be considered fast twitch. Which of the three cells on the microscope screen can be considered fast twitch? a) 1 and 2 b) 1, 2, and 3 c) 2 and 3 d) 1 VIEW THEORY VIEW IMAGE

                                          Human Physiology - Locomotion & Movement

                                          A mutation occurs in the tail domain of a myosin I protein. Which of the following is MOST likely to occur as a result of this mutation? O Myosin filaments may not be formed by myosin I. O The actin binding ability of this myosin I protein may be inhibited. The myosin I protein may no longer be able to carry cargo. O The myosin I protein may no longer be able to hydrolyze ATP.

                                          Human Physiology - Locomotion & Movement

                                          c X Which of the following statements concerning gap junctions is CORRECT? O A gap junction made up of a total of 2 connexons will have a total of 6 connexins. Gap junctions close to protect cells adjacent to a damaged cell. Gap junctions allow the passage of ions and metabolites (less than 1000 Daltons) both to and from the extracellular fluid. O Gap junctions allow the sharing of organellar membranes, such as in the case of the smooth endoplasmic reticulum (SER).

                                          Human Physiology - Locomotion & Movement

                                          PROGR DAY 1 08:09 SCORE: 0/120 Click to answer the quiz q MEDIA MISSION THEORY HOME Which symptom is NOT common in Parkinson's disease? a) Tremor b) Recurrent bleedings c) Stiffness d) Uncontrolled movements VIEW THEORY MacBook Air Dll F8 F7 OOO F6 F5 F4 F3 * & @ % $ # 8 7 6 4 5 3 U Y T E R G H J C

                                          Human Physiology - Locomotion & Movement

                                          Question 24 1 pts Dr. Nair has inherited a rare genetic disorder where his sarcoplasmic reticulum in his skeletal muscles are "leaky". This means there are small openings in the sarcoplasmic reticulum that allow calcium ions to pass through. What will be common symptoms for Dr. Nair? NOTE: Select all correct answer choices. Fatigue (due to low energy) Paralysis (lack of muscle contractions) Cramps (involuntary contractions)

                                          Human Physiology - Locomotion & Movement

                                          Question 23 1 pts When ATP is present in the cytoplasm but not calcium ions, myosin heads will be: o unbound in a high energy state O bound to actin subunits in a high energy state O bound to actin subunits in a low energy state O unbound in a low energy state 1 pts Question 24

                                          Human Physiology - Locomotion & Movement

                                          Question 25 1 pts You are helping Eldon Tyrell create replicants to work in off-world colonies. You want to design muscle cells that can produce the most tension. At the very least, these muscle cells will have an abundant amount of: O Myofibril O Moments that will be lost in time, like tears in rain. O Mitochondria O Sarcolemma

                                          Human Physiology - Locomotion & Movement

                                          Question 28 1 pts In a typical single twitch of a muscle, when exactly does cross-bridge cycling begin? O When calcium is released from the sarcoplasmic reticulum O When the action potential travels down the T-tubule O When calcium binds to troponin O When tropomyosin shifts and reveals the actin filament 1 pts Question 29

                                          Human Physiology - Locomotion & Movement

                                          Question 38 1 pts If there were no calcium-ATPases in the sarcoplasmic reticulum, what would happen to cross-bridge cycling during a single switch? It would only occur for a very short duration It would not occur. It would occur continuously until ATP runs out.

                                          Human Physiology - Locomotion & Movement

                                          Question 32 1 pts When calcium ions are present in the cytoplasm but not ATP, myosin heads will be: O bound to actin subunits in a high energy state O unbound in a high energy state O unbound in a low energy state O bound to actin subunits in a low energy state 1 pts Question 33

                                          Human Physiology - Locomotion & Movement

                                          D Question 39 1 pts Chickens use their breast muscles to do powerful, quick motions like flying or fighting. What type of muscle fiber is chicken breast muscle is probably mostly comprised of? O Fast, glycolytic muscle fibers O Fast, oxidative muscle fibers O Slow, glycolytic muscle fibers O Slow, oxidative muscle fibers

                                          Human Physiology - Locomotion & Movement

                                          Question 29 1 pts If a muscle cell had very short T-tubules couldn't reach all of the myofibrils, how much tension would the muscle fiber create, relative to a normal muscle fiber? Assume sarcoplasmic reticulum can still react to activity at the neuromuscular junction. O No tension would be created. O No difference in tension creation. O Less tension would be created. O More tension would be created. Question 30 1 pts

                                          Topic 6: Human Physiology

                                          This topic has 12% of occurance in the papers 1 and 2.
                                          Below you can find the subtopics of Topic 6 and the percentage of how many times they appear on the exams from the past years.

                                          6.1 Digestion and absorption
                                          Very Common Subtopic

                                          Focus more on these understandings, applications and skills:

                                          • Villi increase the surface area of epithelium over which absorption is carried out
                                          • Villi absorb monomers formed by digestion as well as mineral ions and vitamins
                                          • Different methods of membrane transport are required to absorb different nutrients
                                          • Processes occurring in the small intestine that result in the digestion of starch and transport of the products of digestion to the liver
                                          • Identification of tissue layers in transverse sections of the small intestine viewed with a microscope or in a micrograph

                                          Questions related to these are:

                                          • Describe the villi and microvilli function and structure in the small intestine.
                                          • Be able to identify the structure of small intestine in a micrograph
                                          • Outline the way in which nutrients are absorbed in the body.

                                          6.2 The Blood System
                                          Common Subtopic

                                          Focus more on these understandings, applications and skills:

                                          • Arteries convey blood at high pressure from the ventricles to the tissues of the body
                                          • Arteries have muscle cells and elastic fibres in their walls
                                          • The muscle and elastic fibres assist in maintaining blood pressure between pump cycles
                                          • Capillaries have permeable walls that allow exchange of material between cells in the tissue and the blood in the capillary
                                          • Veins collect blood at low pressure from the tissues of the body and return it to the atria of the heart
                                          • The heart beat is initiated by a group of specialised muscle cells in the right atrium called the sinoatrial node
                                          • The sinoatrial node acts as a pacemaker
                                          • The sinoatrial node sends out an electrical signal that stimulates contraction as it is propagated through the walls of the atria and then the walls of the ventricles
                                          • Identification of blood vessels as arteries, capillaries or veins from the structure of their walls
                                          • Recognition of the chambers and valves of the heart and the blood vessels connected to it in dissected hearts or in diagrams of heart structure

                                          Questions related to these are:

                                          • Identify and label the heart structure, as well as blood vessels
                                          • Outline the differences between arteries,veins and capillaries.
                                          • Describe the cardiac cycle.
                                          • Outline the role of pacemaker.

                                          6.3 Defence against infectious disease
                                          Very Common Subtopic

                                          Focus more on these understandings, applications and skills:

                                          • Some strains of bacteria have evolved with genes that confer resistance to antibiotics and some strains of bacteria have multiple resistance
                                          • Florey and Chain’s experiments to test penicillin on bacterial infections in mice

                                          Questions related to these are:

                                          • Explain antibiotic resistance in bacteria strains
                                          • Describe Florey and Chain’s experiments, leading to discovery of penicillin.
                                          • Explain the antibody production.

                                          6.4 Gas exchange
                                          Least common subtopic

                                          Focus more on these understandings, applications and skills:

                                          • Ventilation maintains concentration gradients of oxygen and carbon dioxide between air in alveoli and blood flowing in adjacent capillaries
                                          • Air is carried to the lungs in the trachea and bronchi and then to the alveoli in bronchioles
                                          • Type I pneumocytes are extremely thin alveolar cells that are adapted to carry out gas exchange
                                          • Type II pneumocytes secrete a solution containing surfactant that creates a moist surface inside the alveoli to prevent the sides of the alveolus adhering to each other by reducing surface tension
                                          • Muscle contractions cause the pressure changes inside the thorax that force air in and out of the lungs to ventilate them
                                          • Different muscles are required for inspiration and expiration because muscles only do work when they contract
                                          • Monitoring of ventilation in humans at rest and after mild and vigorous exercise

                                          Questions related to these are:

                                          • Explain the ventilation mechanism.
                                          • Outline the effect of exercise on ventilation.
                                          • Identify the role of Type I and II pneumocytes.

                                          6.5 Neurons and synapses
                                          Least common subtopic

                                          Focus more on these understandings, applications and skills:

                                          • Neurons transmit electrical impulses
                                          • Neurons pump sodium and potassium ions across their membranes to generate a resting potential
                                          • An action potential consists of depolarization and repolarization of the neuron
                                          • Nerve impulses are action potentials propagated along the axons of neurons
                                          • Propagation of nerve impulses is the result of local currents that cause each successive part of the axon to reach the threshold potential
                                          • Synapses are junctions between neurons and between neurons and receptor or effector cells
                                          • When presynaptic neurons are depolarized they release a neurotransmitter into the synapse
                                          • A nerve impulse is only initiated if the threshold potential is reached
                                          • Secretion and reabsorption of acetylcholine by neurons at synapses
                                          • Blocking of synaptic transmission at cholinergic synapses in insects by binding of neonicotinoid pesticides to acetylcholine receptors

                                          Questions related to these are:

                                          • Explain how nerve impulse passes along the neuron.
                                          • Explain the synapse transmission.
                                          • Describe how pesticide neonicotinoid kills insects.

                                          6.6 Hormones, homeostasis and reproduction
                                          Very Common Subtopic

                                          Focus more on these understandings, applications and skills:

                                          • Thyroxin is secreted by the thyroid gland to regulate the metabolic rate and help control body temperature
                                          • Leptin is secreted by cells in adipose tissue and act on the hypothalamus of the brain to inhibit appetite
                                          • Melatonin is secreted by the pineal gland to control circadian rhythms
                                          • A gene on the Y chromosome causes embryonic gonads to develop as testes and secrete testosterone
                                          • Testosterone causes pre-natal development of male genitalia and both sperm production and development of male secondary sexual characteristics during puberty
                                          • Estrogen and progesterone cause pre-natal development of female reproductive organs and female secondary sexual characteristics during puberty
                                          • The menstrual cycle is controlled by negative and positive feedback mechanisms involving ovarian and pituitary hormones
                                          • Testing of leptin on patients with clinical obesity and reasons for the failure to control the disease
                                          • Causes of jet lag and use of melatonin to alleviate it
                                          • Annotate diagrams of the male and female reproductive system to show names of structures and their functions

                                          Questions related to these are:

                                          • Explain jet lab and how melatonin which is produced in the pineal gland influences it.
                                          • Explain leptin role on obesity.
                                          • Explain how temperature is regulated by the body.
                                          • Outline the menstrual cycle and its hormones roles on it.
                                          • Identify the male reproductive system

                                          If you’re in SL, this is the end of the exam tips and tricks. If you’re HL, then continue on to the next topic.

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                                          Changes in your thoughts and feelings:

                                          • Being slow to respond, or not being able to respond right away, when someone talks to you
                                          • Forgetting things (memory loss)
                                          • Having a hard time talking or writing
                                          • Feeling “fuzzy”
                                          • Feeling depressed, sad, or upset
                                          • Feeling scared, confused, or anxious
                                          • Feeling frustrated, embarrassed, or ashamed

                                          Changes in your body:

                                          • Feeling dizzy or lightheaded
                                          • Headache or other types of pain
                                          • Nausea or upset stomach
                                          • Feeling thirsty
                                          • Feeling weak (maybe only in one part or side of your body)
                                          • Feeling like you need to go to the bathroom, or losing control of your bowels or bladder
                                          • Wanting to sleep or feeling tired
                                          • If you fell during your seizure, you may have injuries, like bruises, cuts, broken bones or a head injury. If you were injured, see your doctor or to the emergency room.

                                          BioGeoChemical Cycles

                                          • What is all the biomass created from?
                                          • What three things do all organisms need in order to live?
                                          • Why are the biogeochemical cycles important?

                                          Why do we say that Ecology is a strict natural science?

                                          What are "emergent properties" and why are they important?

                                          In the early stages of life on Earth, Photosynthesis greatly outweighed Respiration. What was the result of this phenomenon?

                                          What is the relationship between organisms and their environment?

                                          Why is it fair to say that many processes operate in similar way at all scales?

                                          Why is it legitimate to view the biosphere as a network of genes?

                                          Most organisms in the world are __________.

                                          Why does metabolic diversity exist?

                                          What type of organisms are responsible for most of that diversity?

                                          Why is it important to look at the interaction of organisms in the environment, rather than just at each organism separately?

                                          What do food webs represent in terms of biogeochemical cycles? Why?

                                          Why are the various efficiencies defined for the food web diagrams important?

                                          How is it possible that, collectively, terrestrial and aquatic ecosystems have approximately equal contributions to total global photosynthesis, despite great differences in the biomass of their primary producers?

                                          What factors determine variability in terrestrial ecosystem productivity?

                                          What factors determine variability in aquatic ecosystem productivity?

                                          How does the mode of regeneration of nutrients in the soil determine the character of the ecosystem?

                                          Why is there a need for a number of mechanisms of nutrient transport from the deep ocean to the sunlit surface waters in the oceans?

                                          Is it possible that in the same environment two different things would be limiting for two different organisms? Why or why not?

                                          Why is it important that the nutrients cycle through the biosphere?

                                          The flux of CO2 to the atmosphere due to human activities is only a small fraction of the flux due to global respiration. Why, then, is it causing a significant increase in the reservoir of CO2 in the atmosphere?

                                          Hee Jung Chung

                                          Epilepsy is a common chronic brain disorder that is caused by excessive brain activity clinically characterized as seizures. About 40% of epilepsy is associated with genetic mutations. The cause for the rest of epilepsy is unclear. Since ion channels are critical regulators of neuronal activity, the goals of my research program at the University of Illinois at Urbana Champaign (UIUC) have been to (1) understand how epilepsy mutations affect ion channel function and lead to hyperexcitability in inherited or de novo epilepsy, and (2) identify molecular mechanisms that alter ion channels to cause hyperexcitability in acquired epilepsy.

                                          To investigate these two areas, my lab uses interdisciplinary approaches including primary neuronal culture, live and fixed microscopy, biochemistry, electrophysiology, and mouse genetics.

                                          (1) What are the mechanisms underlying polarized localization of KCNQ channels?

                                          My lab has a keen interest in specific neuronal location of ion channels and their roles in intrinsic excitability and epilepsy. We study KCNQ/Kv7 potassium channels that prevent repetitive and burst firing of action potentials, and are mutated in humans who have benign familial neonatal epilepsy (BFNE), severe symptomatic drug-resistant epileptic encephalopathy, intellectual disability, and autism.

                                          We are actively investigating how mutations of Kv7 channels associated with BFNE and epileptic encephalopathy disrupt their functions and neuronal distribution, ultimately leading to neuronal hyperexcitability and epilepsy. Since the fundamental function of a neuron depends critically on precise localization and density of these channels, we also study the mechanisms by which polarized distribution of Kv7 channels in axons is established, maintained, and regulated. My laboratory has made significant contributions to the mechanistic understanding of epilepsy mutations and axonal targeting of Kv7 channels (Cavaretta et al., 2014 Kim et al., submitted Zhang et al, in preparation).

                                          Understanding these fundamental physiologic and pathologic mechanisms involving Kv7 channel trafficking will help us develop therapeutic strategy to reverse the effects of epilepsy mutations.

                                          (2) What are the molecular mechanisms underlying homeostatic plasticity?

                                          To identify mechanisms underlying plasticity of intrinsic membrane properties, we focus on homeostatic plasticity, which is an ability of neurons to adapt their electrical activity within a physiologic range in response to neuronal activity or sensory experience. The fundamental question is: “when and how do neurons exploit homeostatic plasticity to stabilize their network as a normal adaptive response, or to cause persistent hyperexcitability as a pathological manifestation in epilepsy?” To answer this, we must first understand how homeostatic plasticity is induced in the normal brain. When I started my own laboratory, no molecular players and signaling pathways were identified for homeostatic plasticity of intrinsic excitability.

                                          My laboratory has identified the signaling pathways underlying homeostatic control of intrinsic excitability in cultured hippocampal neurons, which are distinct from homeostatic synaptic scaling (Lee and Chung, 2014 Lee et al., 2015). Using unbiased gene expression profiling, we have identified genes that are regulated during induction of homeostatic plasticity. They encode multiple regulators of excitability (such as potassium channels) and synaptic transmission (such as STEP61). Our follow-up studies discovered that reduced Kv7 current and Kv7.3 level are associated with homeostatic scaling of hippocampal excitability (Lee et al., 2015), whereas striatal-enriched protein tyrosine phosphatase (STEP61) mediates homeostatic plasticity of excitatory synaptic strength by modulating tyrosine phosphorylation of AMPA and NMDA receptors (Jang et al., 2015 Jang et al., 2016). We also identified that prolonged seizures are associated with caspase-dependent cleavage and down-regulation of GIRK potassium channels (Baculis et al., 2017).

                                          Current research interests in plasticity include (1) the function and regulation of axonal Kv7 channels in homeostatic plasticity of hippocampal circuits, and (2) the role of STEP61 in homeostatic plasticity during pathogenesis of epilepsy and Alzheimer's disease, and (3) development of novel transgenic mice to study homeostatic plasticity in vivo.


                                          Cornell University-HHMI Undergraduate Research Fellowship (1994)
                                          Paul Ehrlich Young Investigator Award, Johns Hopkins University (2002)
                                          Ruth L. Kirschstein National Research Service Award (2004-2007)
                                          Basil O'Connor Starter Scholar Research Award, March of Dimes Foundation (2011-2013)
                                          Carver Young Investigator Competition Award, Roy J. Carver Charitable Trust (2011-2014)
                                          Targeted Research Initiative for Severe Symptomatic Epilepsies Grant Award, Epilepsy Foundation (2013-2014)
                                          James E. Heath Award for excellence in teaching in Physiology, University of Illinois (2014)

                                          Representative Publications

                                          Baculis BC*, Weiss AC*, Pang W*, Jeong HG, Lee JH, Liu DC, Tsai NP, and Chung HJ (2017). Prolonged seizure activity causes caspase dependent cleavage and dysfunction of G-protein activated inwardly rectifying potassium channels. Scientific Reports, 2017 Sep 267(1):12313. PMID: 28951616

                                          Liu DC, Seimetz J, Lee KY, Kalsotra A, Chung HJ, Lu H, and Tsai NP (2017). Mdm2 mediates FMRP- and Gp1 mGluR-dependent protein translation and neural network activity. Human Molecular Genetics, ddx276,

                                          Jang SS, Jeong H, Chung HJ (2017). Electroconvulsive seizures in rats and fractionation of their hippocampi to examine seizure-induced changes in postsynaptic density proteins. Journal of Visualized Experiments, 2017 Aug 15(126). doi: 10.3791/56016. PMID:28829421

                                          Zhu J, Lee KY, Jewett KA, Man H, Chung HJ, Tsai N-P- (2017). Epilepsy-associated gene Nedd4-2 mediates neuronal network activity and seizure susceptibility through AMPA receptors.PLOS Genetics, 2017 Feb 1713(2):e1006634, PMID:28212375

                                          Vega L JC, Lee MK, Qin EC, Lee KY, Chung HJ, Leckband DE, Kong H (2016). Three dimensional conjugation of recombinant N-Cadherin to a hydrogel for in vitro anisotropic neural growth. Journal of Materials Chemistry B Materials for Biology and Medicine, 4(42):6803-6811. PMCID: PMC5423733

                                          Jang SS*, Royston SE*, Lee G#, Wang S#, and Chung HJ (2016). Seizure-induced regulations of amyloid-beta, STEP61, and STEP61 substrates involved in hippocampal synaptic plasticity. Neural Plasticity, 2016:2123748. PMCID: PMC4835651.

                                          Jang SS*, Royston SE*, Xu J, Cavaretta JP, Vest MO, Lee KY, Lee S, Jeong H, Lombroso PJ, and Chung HJ(2015). Regulation of STEP61 and tyrosine-phosphorylation of NMDA and AMPA receptors during homeostatic synaptic plasticity. Molecular Brain, 8(1):55. PMCID: PMC4578242.

                                          Lee K*, Royston SE*, Vest MO, Ley DJ, Lee S, Bolton EC, and Chung H (2015). (*These authors contributed equally). N-methyl-D-aspartate Receptors mediate Activity-dependent Down-Regulation of Potassium Channel Genes during the Expression of Homeostatic Intrinsic Plasticity. Molecular Brain. 8(1):4.

                                          Wang Y, Cai E, Rosenkranz T, Ge P, Teng KW, Lim SJ, Smith A, Chung HJ, Sachs F, Sachs F, Green W, Gottlieb P, and Selvin PR (2014). Small Quantum Dots Conjugated to Nanobodies as Immunofluorescence Probes for Nanometric Microscopy. Bioconjugate Chemistry. 25(12):2205-11.

                                          Wang Y, Cai E, Rosenkranz T, Ge P, Teng KW, Chung HJ, Sachs F, Gottlieb P, and Selvin PR (2014). Stable small quantum dots for synaptic receptor tracking on live neurons. Angewandte Chemie, 53(46):12484-8.

                                          Lee KY and Chung HJ (2014). NMDA receptors and L-type voltage-gated Ca2+ channels mediate the expression of bidirectional homeostatic intrinsic plasticity in cultured hippocampal neurons. Neuroscience, (277):610-23.

                                          Cavaretta JP*, Sherer KS*, Lee KY, Issema RS, Kim EH, and Chung HJ (2014). (*These authors contributed equally). Polarized Axonal Surface Expression of Neuronal KCNQ Potassium Channels is Regulated by Calmodulin Interaction with KCNQ2 Subunit. PLos One, 9(7):e103655. DOI:10.1371/journal.pone.0103655.

                                          Chung HJ (2014). Role of calmodulin in neuronal Kv7/KCNQ potassium channels and epilepsy. Frontiers in Biology. 9(3):205-15.

                                          Vega L JC, Lee MK, Jeong JH, Smith CE, Lee KY, Chung HJ, Leckband DE, Kong H. (2014). Recapitulating cell-cell adhesion using N-Cadherin biologically tethered to substrates. Biomacromolecules 15(6):2172-9.

                                          Hearing M, Kotecki L, Marron Fernandez de Velasco E, Fajardo-Serrano A, Chung HJ, Luján R, Wickman K. (2013). Repeated Cocaine Weakens GABAB-Girk Signaling in Layer 5/6 Pyramidal Neurons in the Prelimbic Cortex. Neuron 80(1):159-70

                                          Chung HJ*, Lee HK* (2009). Constructing a road map from synapses to behaviour. Meeting on Synapses: From Molecules to Circuits & Behavior. (*These authors contributed equally to this work). EMBO Rep.,10(9):958-62. PubMed Central [PMCID2750071]

                                          Chung HJ*, Woo-ping Ge*, Xiang Qian, Ofer Wiser, Jan YN, and Jan LY (2009). G-protein activated inwardly rectifying potassium channels mediate depotentiation of long-term potentitation. (*These authors contributed equally to this work). Proc Natl Acad Sci U S A, 106(2): 635-40.

                                          Chung HJ, Xiang Qian, Melissa Ehlers, Jan YN, and Jan LY (2009). Neuronal activity regulates phosphorylation-dependent surface delivery of G-protein activated inwardly rectifying potassium channels. Proc Natl Acad Sci U S A, 106(2): 629-34.

                                          Chung HJ, Jan YN, and Jan LY (2006). Impaired polarized surface expression of neuronal KCNQ channels as a mechanism for benign familial neonatal convulsion. Proc Natl Acad Sci U S A, 103 (23): 8870-5

                                          Chung HJ, Lau LF, Huang YH and Huganir RL (2004). Regulation of NMDA Receptor complex and trafficking by activity-dependent phosphorylation of NR2B subunit PDZ ligand. J Neurosci, 24(45):10248-59.

                                          Heynen AJ, Yoon BJ, Liu CH, Chung HJ, Huganir RL and Bear MF (2003). Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation. Nat Neurosci. 6(8):854-62.

                                          Chung HJ*, Steinberg JP*, Huganir RL, Linden DJ (2003). Requirement of AMPA receptor GluR2 phosphorylation for cerebellar long-term depression. (*These authors contributed equally to this work). Science, 300(5626):1751-5.

                                          McDonald BJ, Chung HJ, and Huganir RL (2001). Identification of Protein Kinase C phosphorylation sites within the AMPA receptor GluR2 subunit. Neuropharmacology, 41(6):672-679

                                          Kim CH*, Chung HJ*, Lee H-K-, and Huganir RL (2001). Interaction of the AMPA receptor subunit GluR2/3 with PDZ domains regulates hippocampal long term-depression. (*These authors contributed equally to this work). Proc Natl Acad Sci U S A, 98(20):11725-30

                                          Xia J, Chung HJ, Wihler C, Huganir RL, and Linden DJ (2000). Cerebellar long-term depression requires PKC-regulated interactions between GluR2/3 and PDZ domain-containing proteins. Neuron, 28(2):499-510.

                                          Chung HJ, Xia J, Scannevin RH, Zhang X, and Huganir RL (2000). Phosphorylation of the AMPA receptor subunit GluR2 differentially regulates its interaction with PDZ domain-containing proteins. J Neurosci, 20(19):7258-67.

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