Seizure Disorders Study Guide PDF

Seizure Disorders Study Guide ● Define seizure as a problem with electrical impulse generation and transmission. ○ A problem with the electrical impulse generation and transmission ○ Uncontrolled electrical discharge from a group of neurons in the cerebral cortex ● Recognize that seizure activity re...

Seizure Disorders Study Guide ● Define seizure as a problem with electrical impulse generation and transmission. ○ A problem with the electrical impulse generation and transmission ○ Uncontrolled electrical discharge from a group of neurons in the cerebral cortex ● Recognize that seizure activity reflects an underlying disease. ○ Sign of underlying CNS dysfunction, acute ○ NOT a disease ○ Typically results from abnormalities in electrolyte levels within the body ● Define epilepsy. ○ Chronic neurological condition where the individual is susceptible to recurrent seizures ○ Recurring seizures without provocation ○ chronic ● Differentiate seizure activity from epilepsy. ○ A seizure is a single occurrence, whereas epilepsy is a neurological condition characterized by two or more unprovoked seizures ○ A seizure is a sign of a possible epilepsy ○ A person with epilepsy has seizure activity but not everyone who has seizure activity has epilepsy ● Identify the etiologies for epileptic seizures. ○ 70% are idiopathic ○ 30% related to conditions such as head injury or brain tumor and more ● Discuss what a seizure has in common with cardiac dysrhythmia. ○ Sign of underlying dysfunction ○ Electrolyte imbalance ○ Can be acute or chronic ○ Sign of underlying disease ○ Ischemia is an etiology ○ Diagnosis includes electrical conduction studies ○ Low magnesium could be an etiology ● Discuss seizures related to fever in children. ○ Seizure trigged by a Fever ○ Due to infection or virus ● Discuss seizures related to electrolyte imbalance. ○ Hypocalcemia ○ Hypomagnesemia ○ Hyponatremia ● Arrange the steps in order: hyponatremia to seizure activity. 1. Water intoxication 2. Hyponatremia ● ● ● ● ● ● 3. The osmolarity of the blood drops 4. Fluid is pulled from blood vessels into the brain 5. Brain cells swell 6. Blood vessels are compressed 7. Cerebral ischemia 8. seizures Discuss how low calcium or low magnesium could result in seizure activity. ○ Calcium ■ Sodium are channel gatekeeper ■ Calcium prevents unwanted entry of sodium into nerve cells of the brain → maintains normal threshold stimulus → decreases the risk for seizure ■ When sodium channels are open → easier depolarization → increases the risk of seizure ○ Magnesium ■ Hypothesis: need Mg+ for parathyroid hormone (PTH) activity and calcium absorption ■ Low Mg+ → low calcium → more sodium channels are open → fewer stimuli required to depolarize → neurons are hyperexcitable → risk for seizure Arrange the steps in order: hypocalcemia to seizure activity. 1. Hypocalcemia 2. Sodium channels open more easily 3. Lower threshold stimuli 4. seizures Explain why IICP can result in seizure activity. ○ IICP compresses arterial blood supply → reduces oxygen to the brain → results in ischemia ○ Volume and pressure increased ○ Blood vessels are compressed ○ Oxygen flow is decreased ○ Brain cells become ischemic and cell membranes can become disrupted ○ Na+ moves intracellular → rapid depolarization → seizures Explain why seizure activity can be related to brain tumors. ○ Seizure caused by tumor compressing blood supply → ischemic around the tumor → cell membrane more permeable to Na+ → rapid and erratic depolarization → Seizure activity Describe a partial seizure. ○ Disturbance occurs in just one part of the brain, affecting whatever physical or mental activity that area controls Describe a simple partial seizure. ● ● ● ● ● ● ○ Affects only ONE part of the brain ○ Without loss of consciousness Describe a complex partial seizure. ○ Affects MORE than one part of the brain ○ Begins in one area ○ Impulse spreads out to both hemispheres Describe an absence seizure. ○ Generalized, non-convulsive ○ Absent for awareness of surroundings Describe a generalized tonic-clonic seizure. ○ Involves the entire body characterized by muscle rigidity ○ Rhythmic muscle contractions ○ Loss of consciousness Discuss how to diagnose a seizure disorder. ○ Documenting seizure activity- visualization ○ EEG ○ Exclude/Rule out ■ Metabolic etiology ■ Internal problem ■ External problem Provide an overview of treatment. ○ Identify what provokes the seizure and treat it ○ Ischemic = restore perfusion ○ Correct electrolyte imbalances Recognize the treatment goal. ○ Increase the seizure threshold ○ Make it harder for nerve cells to depolarize Increased Intracranial Pressures Study Guide - 19 questions each (7 questions) ● Identify how long the brain can survive without oxygen. ○ 20% of oxygen consumption ○ The brain begins to die in 4-6 minutes ○ Irreversible loss 10 minutes ● Describe the cellular effects of prolonged ischemia. ○ Deprived blood flow is inadequate to meet the metabolic demands ○ S/S depends on the part of the brain that is blocked by oxygen ○ Permeable to sodium ○ Cells swell and the cells become reversible ● Recognize the goal of cerebrovascular disease is to save the tissue. ○ Reverse the ischemia and save the cells and tissues ● Identify cerebral ischemia as a related concern in persons with increased intracranial pressure. ○ Trigger Increase in volume (pressure in the cranium) Increased Intracranial pressure ischemic tissue ● Apply the volume and pressure concept to increased intracranial pressure. ○ Increased volume in a container that can't stretch increased pressure ● Recognize that intracranial pressure can result in cerebral ischemia. ○ The cranium stretches and the blood vessels are compressed which leads to ischemia ● Apply the concept “decrease in volume leads to decrease in pressure”. ○ Decreasing the volume will take pressure off of the cranium decreasing the pressure on the brain ● Recognize that reducing intracranial pressure can increase cerebral perfusion. ○ Decreasing IICP will increase perfusion because blood vessels will not be compressed ● Discuss how the body compensates for IICP, lowering the volume to maintain normal pressure in the cranial cavity. ○ Monroe-Kellie Hypothesis - a change in the volume of one compartment must be offset by a change in the volume of other compartments ○ Normal cranial cavity pressures are maintained by controlling the volume of blood and CFS ● Discuss the concept of autoregulation as it relates to cerebral compensation, maintaining perfusion, and oxygenation. ○ Arteries dilate when the arterial BP is low and constrict when the arterial BP is high ○ Less arterial blood flow and higher amounts of oxygen "pulled" from Hgb ● Recognize IICP as an example of compartment syndrome. ● ● ● ● ● ● ● ● ● ○ Volume of cranium rises increased pressure risk for ischemia due to compression of blood supply Review the basic concept: IICP. ○ Trigger Increase Volume (pressure in the cranium) IICP ischemic Tissues Change of level of control, abnormal movement, respiratory distress Recognize that regardless of the etiology, increased volume in the cranial cavity can increase pressure. ○ the concept of increased volume increase pressure will always lead to IICP in the cranium Summarize the process whereby IICP can result in cerebral ischemia. ○ IICP leads to the compression of blood vessels which leads to decreased blood flow and oxygen to the brain Review hyponatremia as an etiology for IICP. ○ Shifting volume into the brain increases brain volume ○ Hyponatremia particles within the cell create a pull and fluid shift into the cell ○ Swelling occurs and increases pressure which compresses blood vessels and the oxygen supply Recognize that when compensation fails ischemia can progress to irreversible cell changes. ○ Ischemia necrosis ○ Pressure above 20-25 mmHg there is a loss of compensation ○ If you don't have reperfusion then cell necrosis occurs Discuss how to diagnose IICP. ○ Changes in Level of Consciousness - behavioral (confusion ○ Medical/Physical history ○ Spinal tap to measure the level of CSF Recognize clinical signs and symptoms that suggest IICP. ○ Headache, Nausea ○ Decreased mental abilities ○ Vision issues Discuss the potential significance of papilledema. ○ The increased pressure of CSF in the subarachnoid → pressure on the optic nerve ○ This may lead to IICP Describe the etiology of papilledema. ○ Increased CSF reabsorbed into the subarachnoid space ● Recognize the Cushing Reflex as a late, often terminal sign suggesting IICP. ○ It occurs when there is pressure on the brain stem ● ● ● ● ● ● ● ○ It is adaptive and the body is trying to increase blood flow to the brain by increasing the systolic blood pressure ○ Bradycardia occurs as the body is trying to compensate for the hypertension ○ The abnormal respiratory patterns are related to pressure on the respiratory center in the medulla which is ischemic Explain the rationale for the Cushing Reflex. ○ Cerebral ischemia → sympathetic nervous system stimulation → Medulla. Vasoconstriction to raise BP to increase cerebral perfusion pressure → abnormal respiratory patterns and increase in BP which also lowers the HR. ○ This reflex consists of bradycardia, irregular respirations, and high pulse pressure, which is the body's response to increased intracranial pressure. Recognize invasive monitoring as the definitive diagnostic test for IICP. ○ It is to check the pressure in the cranial cavity ○ Invasive monitoring will tell you when you are in danger of losing compensation ■ Losing compensation means you are going to move from ischemia to prolonged ischemia to risk for cell and tissue loss ○ Lowering the pressure decompresses the arteries and increases the arterial blood flow Recognize the related problem is altered [reduced] perfusion. ○ For the person with IICP, the related problem is altered or reduced perfusion Identify the goal as REPERFUSION, reverse the ischemia, and save tissues. ○ When the problem is ischemia, the goal is to reperfuse ○ To relieve ischemia, you need to. Decrease the volume in cranium → decrease the pressure → decompress the blood supply to increase oxygen and nutrient flow into the brain and allow carbon dioxide and waste products to leave the brain. Provide an overview of treatments for IICP. ○ The goal is to decrease the pressure to relieve the ischemia ○ Reducing the IICP means increasing the blood flow into and out of the brain ○ Craniectomy (bone flap) results in increasing the size of the cranial “container” ○ Draining off cerebrospinal fluid is one way to decrease the volume and decrease pressure to increase the flow to cerebral tissue. ■ Remove tumor mass or clot, chemical therapy to decrease the volume, and diuretics which may reduce the formation of CSF. ■ Controlling respiratory rate and depth Recognize that regardless of the treatment chosen the goal for IICP is the same. ○ You can reduce the volume in the cranial container or you can make the container bigger but the goal is to reperfuse and save the tissues, reverse the ischemia Recognize coma and herniation as complications of IICP. ● ● ● ● ● ● ● ● ● ● ○ Coma and herniation may be caused by the space that is occupying lesions, generalized swelling or edema of the brain, increased venous pressure, or obstruction of cerebrospinal flow (CSF). Define the Glasgow coma Scale. ○ Assess the ability of the person to open their eyes to have a normal conversation spontaneously and have a normal motor response Recognize S/S of coma related to global brain injury. ○ Diminished LOC ○ Altered respiratory response ○ change in rate or pattern causes pressure on the pons and medulla Recognize S/S of coma related to global brain injury. ○ Diminished LOC ○ Altered respiratory response ○ change in rate or pattern causes pressure on the pons and medulla Recognize Doll’s Eyes as an evaluation of pons function. ○ The eyes are fixed, straight ahead when head is rotated, the eyes don’t move Describe the process of brain herniation: A terminal complication of IICP. ○ The volume is cranial cavity is so great that the brain is pushed down towards the brain stem ○ Herniation through the tentorium that sits over the cerebellum that puts the pressure in the brain stem ○ The glasgow coma scale scores will be very low Describe the Cushing Reflex [triad] in brain herniation. ○ When it comes to the brain, it’s brain death. ○ Increased systolic BP with wide pulse pressure ■ Abnormal respiratory patterns progressing to apnea and bradycardia ■ Due to the pressure on the brain stem, the person would have doll’s eyes, fixed and dilated pupils, and an extremely low coma scale Define Brain Death. ○ Brain death is an absence of clinical brain function when the cause is identified and irreversible. Recognize mandatory criteria for diagnosing brain death in adults. ○ Fixed and dilated pupils, no motor, corneal, or cough response. No gag reflex, no response to pain, and no respiration. Identify information that can be provided by a confirmatory test. ○ They are not a mandatory test ○ Normal EEG shows a lot of electrical activity ○ Transcranial ultrasonography ~ listening for any blood flow going into the brain ○ Cerebral angiography ~ dye could compromise viability of organs for transplant Review principles of treatment for IICP. ○ You can decrease the volume or make the container bigger which will both help in decreasing the pressure ● Describe Unresponsive Wakefulness Syndrome. ○ These symptoms lasts longer than on month: ■ Normal sleep-wake cycles ■ Bowel and bladder incontinence ■ No reproducible voluntary actions ■ No response to environmental stimuli or visual tracking, and lack of language comprehension ■ Diffuse brain injury with preservation of brain stem function ● Identify the rationale for cerebral atrophy in persons with Unresponsive Wakefulness Syndrome. The Persons with unresponsive wakefulness syndrome will suffer cerebral atrophy after a period of time and the reason for that is they have no cortex. Without the cortex they have no need for the association tracks that make up the white matter. It’s sort of a disuse syndrome they don’t use the white matter the white matter atrophies Unresponsive wakefulness syndrome diagnosis when the condition last longer than month. The person has normal sleep wake cycles, bowel and bladder incontinence, no reproducible voluntary actions they have no cerebral cortex ● Recognize cardiac arrest as an etiology for Unresponsive Wakefulness Syndrome. Cardiac arrest is also an etiology for unresponsive wakefulness syndrome the pump is not pumping. Oxygen isn’t being delivered to the cortex and the cortex dies they have cortical anoxia that’s why with cpr we do compression first get the oxygen backup to the brain Respiratory stress for etiology for URWS street drug overdose respiratory arrest. The heart beating but lungs aren’t delivering any oxygen into the blood. The cortex becomes ischemic and becomes anoxic and you can lose the cortex that why there’s such a push to have naloxone available for person in the event of a narcotic overdose. ● Explain how traumatic brain injury can result in IICP. Because of the degree of tissue injury and inflammation. The swelling the increased volume and increased pressure. Traumatic brain injury can result in increased intracranial pressure TRIGGERS could be fall most common, assault, stuck by/against, motor vehicle unknown/other. ● Discuss how blast injury can result in IICP. Blast injury is what happened at the Boston marathon for example. They use improvised explosive device that caused blast injury ● Explain coup contrecoup. Traumatic brain injury can be the result of coup counter coup injury where the head move forward and back inside the cranial cavity ● Describe a concussion. Concussion is a jarring of the brain or shaking of the brain ● Describe the potential effects of a concussion. The potential effects of a concussion or a jarring of the brain can be short or long term. The potential effect could result in loss of consciousness ● 1. 2. 3. 4. ● Arrange the steps in order: concussion. Something crashes into the skull Brain moves within the skull Brain elongates Axons stretched or twisted Describe a contusion. Contusion is cerebral bruise and it will show in mri or ct scan ● Describe chronic traumatic encephalopathy. It is brain degeneration likely cause by repeated head traumas diagnosis only made at autopsy. It’s a rare condition among the general population but it is more common in contact sports such as football and in soldiers. There are difficulties with cognition thinking, physical problem, emotional and other behaviors issues. ● Discuss why hematomas are etiologies for IICP. The concept is that hematomas occupy space that increase volume and increases pressure within the cranial cavity. Hematomas is a trigger or an etiology increased volume increased pressure ischemic tissues changes in level of consciousness abnormal movement respiratory and cardiovascular patterns the concept for increased intracranial pressure is the same the trigger is different ● Identify the types of hematomas. Subdural hematoma: between the brain and the dura. It’s a venous bleed Epidural hematoma: is above the dura that the arterial bleed and there is a hematoma within tissue itself an intracerebral hematoma ● Describe a Subdural Hematoma: SDH. Subdural hematoma is a collection of blood beneath the dura its a venous bleed and notice the bridging veins if the brain is pushed back and forth inside the skull in essence is flopping back and forth inside the skull those bridging veins can be torn and when they tear the bleed into the Subdural space. A Subdural hematoma increase volume increase pressure. ● Explain the etiology for presenting signs and symptoms. Timing. Weakness in the right arm and leg is evidence potential evidence of the ischemia int he area of the motor cortex that tumor of blood caused the area of local ischemia and sign and symptoms depend on the issue that’s ischemic ● Explain the role of CT Scans and MRI in making the diagnosis of hematomas. Ct scan result identifies a Subdural hematoma and notice that right ventricle the right lateral ventricle is being compress and the midline that line right down the center of the brain that midline is starting to move or be pushed to the opposite side that would be called shifting of the midline ● Identify the goal for a person with SDH. The goal is to reperfuse in order to achieve that goal it require that the pressure in the brain be decreased that collection of blood be removed ● Provide an overview of treatment for a person with SDH. Decrease volume to decrease pressure in order to reperfuse ○ Anti-inflammatory medications, burr holes, when possible herniation is suspected craniectomy may be done make the container bigger to relieve pressure and ischemic brain is an irritated brain so a person with cerebral ischemia may be at risk for seizures and anti-convulsant would be given if needed ● Describe an Epidural Bleed …Hematoma. ○ Epidural bleed is arterial bleed the middle meningeal artery is commonly affected when this artery torn usually as a result of fall there is arterial bleeding into the epidural space above the dura ● Explain the etiology for rapid onset of S/S in persons with epidural hematoma. ○ Arterial bleed increases volume and increases pressure the brain is. being pushed to the opposite side the midline of the brain is shifting to the opposite side . Headache was probably the earliest manifestation suggesting the bleed. ● Provide an overview of treatment for epidural hematoma. ○ Surgery to remove clot ■ Relieve pressure ■ Reduce IICP ■ Improve cerebral perfusion pressure ● Explain how brain injury could result in diabetes insipidus [DI]. ○ Concussion, contusion, brain surgery for hematomas can result in diabetes insipidus ○ Deficient antidiuretic hormone (DI) ○ Trauma to hypothalamus causes DI ○ How would it show up?= polyuria ○ Treatment ?= Vasopressin and replace lost fluids until DI resolves itself. ● Explain how subarachnoid hemorrhage results in increased intracranial pressure. ○ SAH increases volume in cranium and increases pressure ● Discuss the possible etiologies for intracranial aneurysms. ○ Cerebral aneurysms can burst inside or outside of the brain ○ When aneurysms burst outside of the brain they bleed into the Subarachnoid space resulting in subarachnoid hemorrhage ○ Which increases volume in the cranium and increases the pressure ○ Congenital for some ○ Hypertension ○ Often not possible to determine etiology for an individual aneurysm ○ Autosomal dominant polycystic kidney disease .= have 5-40 % risk for intracranial aneurysm. ● Explain the etiology for S/S of SAH. ○ Subarachnoid hemorrhage is usually result of aneurysms rupture on the surface of the brain ○ Trauma could also result in subarachnoid hemorrhage ○ Many aneurysm of brain arise from circle of willis ○ S/S is based on the cerebral tissue being compressed ○ Such as headache related to leak prior to rupture ● Describe how to diagnose SAH. ○ CT scan or MRI ○ Lumbar puncture pull blood ● Provide an overview of treatment for a subarachnoid hemorrhage. ○ Measures to reduce IICP ○ Prevent vasospasm ○ Prevent seizures ○ Clipping and coiling ● Arrange the steps in order: SAH. ○ Rupture of middle cerebral artery aneurysm ○ Bleeding into the subarachnoid space ○ Headache, stiff neck, photophobia ○ IICP and ischemia ○ Changes in LOC ● Discuss hemorrhagic stroke prevention. ○ Intracranial aneurysm is most common problem treated in an attempt to prevent hemorrhagic stroke ○ Controlling blood pressure ○ Hypo coagulation can led to HBA ○ Bleeding into tumors ○ AV malformation ● Provides an overview of meningitis. ○ Inflammation of the meninges( covering of the brain) ● Identify etiologies for meningitis. ○ Haemophilus influenzae ; Hib vaccine ■ First dose at 2 months ○ Pneumococcal meningitis; pneumococcal conjugate ■ At 2 months ○ Neisseria meningitidis ○ Meningococcal meningitis ; vaccine for older children ○ The first dose should be given at 11-12 years old and booster dose at 16 years old. ● Recognize IICP as a related concern in persons with meningitis. ● ● ● ● ○ Inflammation increases capillary permeability which results in swelling inside the container that cannot stretch. Explain the rationale for presenting S/S. ○ Fever and chills = because it’s a infection ○ N/V = impact on medulla ○ Photophobia= optic nerve passes through the subarachnoid space and passes through the meninges and when it’s irritated that influences optic nerves and can result in photophobia ○ Mental status changes= increased intracranial pressure ○ Kernig’s sign= when leg is raised ○ Brudzinski sign= when neck is flexed Identify the definitive diagnostic test for meningitis. ○ Lumbar puncture ○ CT scan ○ Need to check cerebral spinal fluid with spinal tap Arrange the steps in order: meningitis to hydrocephalus. ○ Exposure to Haemophilus influenzae ○ Meninges are inflamed ○ Meninges becomes swollen ○ Hydrocephalus on x-ray ○ Less CSF enters the subarachnoid space ○ CSF backs up to the lateral ventricles Provide an overview of prevention and treatment. ○ Prevention ■ Vaccination- infants - pneumococcal meningitis ■ Adults living in close quarters; meningococcal ○ Treatment ■ Antibiotic for bacterial meningitis ■ Reduce brain swelling= steroids ■ Other symptomatic treatment ■ Treatment for headache ■ Darkened room for photophobia Discuss meningococcal septicemia. ● ● ● Utilize independent study materials to review content related to Encephalitis. ● ● Utilize independent study materials to review content related to intracranial neoplasms. Neurodegenerative Disorders Study Guide - 8 each Parkinson’s Disease (6 Questions) ● Identify the neurotransmitter deficiency in persons with Parkinson’s Disease. ○ Deficiency in the neurotransmitter dopamine ● Explain the relationship between dopamine and movement. ○ ● Explain how dopamine deficiency affects movement. ○ Dopamine allows the motor cortex to receive coordinated messages ○ Allow for smooth coordinated movement ● Discuss the incidence of Parkinson’s Disease. ○ after the age of 50 ○ The second most common degenerative nervous system disorder ○ It affects both men and women ● Explain the etiology of Parkinson’s Disease. ○ Unknown ○ Multifactorial genetics + environment = cell death ○ Maybe viral exposure to autoimmunity cell death ● Describe the presentation of Parkinson’s Disease. ○ Tremors and rigidity ○ Stooped posture ○ Short, shuffling steps ● Discuss how Parkinson’s Disease is diagnosed. ○ Physical exam ■ 80% loss of dopamine ■ Rigidity movement or tremors ■ Bradykinesia ● Tremors occur that occur at rest and stop with activity ● Recognize the cardinal clinical manifestation: Tremor. ○ Character - rhythmic movements of muscles while at rest ○ Location - hands, feet, neck, face ○ Aggravating factors - activity relieves tremors, resting and postural tremors ● Recognize bradykinesia as a cardinal movement abnormality in persons with PD. ○ Slow movement - cardinal movement abnormality ○ Tremors that occur at rest and stop with activity ● Describe the clinical manifestation: Rigidity. ○ Jerky cogwheel movements ○ Unilateral → bilateral ○ Most evident during the Passive Range of Motion ● Identify autonomic nervous system issues. ○ Parkinson disease can also impact the autonomic ganglion. ■ There are less sympathetic nervous system effects so the person may develop orthostatic hypotension ○ There are risks for injury, falling related to orthostatic hypotension as well as loss of postural reflexes. ○ The parasympathetic nervous system may also have difficulty getting the word out or sending out messages which can result in constipation or urinary retention. ● Explain the etiology of altered thought processes. ○ 50-80% of persons with Parkinson disease may develop cognitive dysfunction late in the disease. ○ The cognitive dysfunction or altered thought processes may affect.. ■ Memory ■ Paying attention ■ Making judgment ● Provide an overview of treatment. ○ The treatment for Parkinson is directed towards reducing the rigidity, improving mobility, and improving QOL. ○ Medications are given to replace lost dopamine ( Levodopa/ Carbidopa) ■ The goal is to restore the balance between dopamine and acetylcholine Multiple Sclerosis (4 Questions ) ● Recognize multiple sclerosis as an autoimmune disease. ○ Multiple sclerosis is an immune mediated disorder that occurs in genetically susceptible people (genetic susceptibility + environmental trigger) ■ The incidences are higher in 1st degree relatives or in monozygotic twins ● Identify the cells and tissues attacked in persons with MS. ○ The Oligodendrocyte are targeted the cells that produce myelin and the myelin sheath itself ■ The insulating portion of the nerve ● Explain the impact of Multiple Sclerosis on nerve conduction. ○ There is myelin breakdown (Demyelination) ○ Demyelination results in nerve transmission that is weak and erratic (erratic meaning not even or regular in pattern) ● Discuss how to diagnose MS. ○ It is made based on.. ■ The history ~ the damaged nerves may result in paresthesia and visual impairments (blurred, double, temp blindness) ■ the physical ■ diagnostic test results ● Explain why optic neuritis is a possible presenting sign. ○ The initial signs in many persons.. Temp diplopia, eye pain, burning, and temp blindness ○ The optic nerve is myelinated and would be affected by the autoimmune attack on the myelin ● Recognize [skeletal muscle and autonomic] motor signs and symptoms suggestive of MS. ○ Motor sign and symptoms- weakness, dragging a foot(foot drops)- inability to raise the foot up at the ankle, impaired physical mobility and risk for injury: falls ○ Involuntary contraction which is an imbalance in electrical activity resulting in some hyperactive stretch reflexes chord reflexes are hyperactive because they are not being mediated by impulses coming from higher up. ● Explain the rationale behind impaired cognition. ○ Impaired cognition is often common in individuals with multiple sclerosis more than half of all persons with MS will develop problems with cognition it depends on the amount of central nervous system damage and the locations of the lesions in the brain. ● Describe how to confirm the diagnosis of multiple sclerosis. ○ The history and physical exam might be suggestive for MS Main diagnostics test for MS is the MRI ● Recognize the implications of plaques and scar tissue seen on an MRI. ○ MRI will show the plaques and the scar tissue which showed tup as a white spot on an MRI as you can see on the picture. High number of lesions would represent more sign and symptoms ● Identify visual evoked potential results consistent with MS. ○ Visual evoked potentials can also be used to assist in the diagnosis of multiple sclerosis. VEP patient sits before a screen on which an alternating checkerboard patterns is displayed. You are checking for sped of nerve conduction how quickly does the impulse get from the eyes to the occipital cortex. ● Identify spinal tap results consistent with the diagnosis of MS. ○ When the myelin breakdown because of that autoimmune attack it releases a protein myelin basic protein that protein is found in the cerebral spinal fluid . Spinal tap also can check for the evidence of inflammation . Oligoclonal bands present suggesting inflammation in the cerebral spinal fluid and we know that all autoimmune disease have an overriding inflammatory component ● Provide an overview of goals and treatment. ○ Goal=Preserving the ability of nerve conduction impulse to reduce the number of flare-ups and to maintain quality of life as the person defined it ○ Treatment= its important to modify the course of the disease to slow down the progression of the disease . With disease modifying medications Amyotrophic Lateral Sclerosis (4 Questions) ● Provide an overview of Amyotrophic Lateral Sclerosis, an upper and lower motor neuron disease. ○ It primarily involves the degeneration and eventual death of these motor neurons, leading to a loss of voluntary muscle control. ALS can manifest in various ways, affecting different regions of the central nervous system. ○ There is no cure for ALS ● Describe the effect neuron cell degeneration has on motor function, including respiratory function. ○ Motor Function: The degeneration of upper motor neurons (UMNs) in the brain and lower motor neurons (LMNs) in the spinal cord leads to a breakdown in communication between the nervous system and voluntary muscles. This results in muscle weakness, atrophy, and eventually paralysis. ○ Respiratory Function: ALS can affect the muscles involved in breathing, as respiratory muscles are controlled by both upper and lower motor neurons. ● Identify how to diagnose ALS. ○ ALS diagnosis is primarily clinical, involving a thorough neurological examination evidence of progressive muscle weakness and the absence of alternative explanations for the symptoms. ○ Electromyography (EMG) and nerve conduction studies can help confirm the presence of both upper and lower motor neuron dysfunction. ● Explain the concept of impaired physical mobility in persons with ALS. ○ As the disease progresses, individuals experience increasing difficulty with walking, moving, and performing daily activities. ● Identify the cause of death. ○ Respiratory musculature (group of muscles involved in breathing) Huntington’s Disease (2 Questions) ● Describe the inheritance pattern. ○ an autosomal dominant inheritance pattern. ○ This means that an affected individual has a 50% chance of passing the mutated gene on to each of their offspring. ● Identify the chromosomal abnormality. ○ expansion of a specific sequence of DNA within the HTT gene located on chromosome 4. ○ In individuals with Huntington's disease, there is an abnormal and expanded repetition of CAG within the gene (cytosine, adenine, guanine). ● Explain how the disease progresses. ○ Huntington's disease is a progressive neurodegenerative disorder that affects both the body and mind. ○ The disease typically manifests in adulthood, usually between the ages of 30 and 50. ● Explain the rationale behind cognitive impairment. ○ primarily due to the progressive degeneration of neurons in specific regions of the brain, particularly the basal ganglia and cortex. ○ The basal ganglia is involved in motor control, while the cortex is crucial for cognitive functions. ○ The mutant HTT gene leads to the production of a toxic protein called mutant huntingtin. ○ This abnormal protein interferes with various cellular processes, disrupts neuronal function, and causes cell death. Which leads to cognitive impairment