Term
| What are the taste and smell sensory systems involved in? |
|
Definition
| need states; homeostasis (appetite, satiety, nutrient balance, sexual behavior) |
|
|
Term
| What type of senses are taste and smell? |
|
Definition
| chemical senses, due to nature of stimuli |
|
|
Term
| What are the 5 qualities of taste? |
|
Definition
| salty, sour, sweet, bitter, and umami |
|
|
Term
| What does each quality of taste drive us to do? |
|
Definition
| Taste recognizes nutrients and toxins; sweet stimuli are sugars and artifiicial sweeteners; bitter signals toxic compounds; salt signals electrolytes; sour stimuli are acids; umami drives intake of meats and cheeses (food containing glutamic acid) |
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|
Term
|
Definition
| olfaction/sensation of airborne stimuli and odors; so many smells that smell has a larger receptor family than taste |
|
|
Term
| What are trigeminal sensations? |
|
Definition
| common chemical sense in mouth and nose; GSA in oral and nasal mucosa that respond to burning or cooling stimuli (ex: wasabi burns nasal mucosa) |
|
|
Term
|
Definition
| taste+smell+trigeminal sensations |
|
|
Term
|
Definition
| context! The way the food looks or sounds (crunchy etc) |
|
|
Term
| What do alterations in chemosensory function signal? |
|
Definition
| disorders: obesity, diabetes, hyperT, malnutrition, Parkinson's, Alzheimer's, MS, Korsakoff's psychosis |
|
|
Term
| What happens to smell in Alzheimer's patients and how do you diagnose? |
|
Definition
| deficit in smell b/c olfactory neurons begin to degenerate early in course of disease; biopsy olfactory mucosa to diagnose |
|
|
Term
| What is Korsakoff's psychosis? |
|
Definition
| neurological disorder characterized by loss of thiamine (vit B1) in the brain |
|
|
Term
| What are common reasons that >200,000 people per year visit doctor for changes in taste/smell?/Why important? |
|
Definition
| upper respiratory infection is a common trigger- you must test patients for loss of taste and/or smell because they can be mistaken for one another; loss of smell can be a safety issue (not being able to smell smoke during a fire); serious health consequences with loss of taste/smell b/c the loss can equate to less interest in food/eating=anorexia |
|
|
Term
| where does initial taste processing take place? |
|
Definition
| receptor cells in the taste buds |
|
|
Term
| Where are the taste buds located? |
|
Definition
| Anterior tongue; posterior tongue in grooves and trenches; oral mucosa of soft palate; oral mucosa of epiglottis; filiform papillae |
|
|
Term
| What type of buds do you find on the anterior tongue and what innervates them? |
|
Definition
| fungiform papillae (epithelial structures housing ONE taste bud); innervated by chorda tympani of CN VII (facial) |
|
|
Term
| What type of buds do you find on the posterior tongue and what innervates them? |
|
Definition
| foliate and circumvallate papillae; circumvallate are much larger than fungiform and contains HUDNREDS of taste buds; innervated by CN IX (glossopharyngeal) |
|
|
Term
| What innervates the taste buds of the oral mucosa of the soft palate? |
|
Definition
| greater superficial petrosal nerve of CN VII |
|
|
Term
| What innervates the oral mucosa of epiglottis? |
|
Definition
| superior laryngeal nerve (of CN X- Vagus) |
|
|
Term
| What is unique about fungiform papillae? |
|
Definition
| just SPINES, do not actually contain taste buds |
|
|
Term
| What is the peripheral ganglion of CN VII and what is its function? Which taste buds correspond to it? |
|
Definition
| Geniculate ganglion is a primary SENSORY neuron with cell bodies for taste sensation in anterior 2/3 of tongue= fungigform and palatal taste buds |
|
|
Term
| What is the peripheral ganglion of CN IX and what is its function? Which taste buds correspond to it? |
|
Definition
| Inferior (petrosal) glossopharyngeal ganglion controls taste from posterior 1/3 of tongue= circumvallate and foliate taste buds |
|
|
Term
| What is the peripheral ganglion of CN X and what is its function? Which taste buds correspond to it? |
|
Definition
| inferior (nodose) vagal ganglion functions in sensation for taste from epiglottis= epiglottis taste buds |
|
|
Term
| How are taste buds organized? |
|
Definition
| as onion-shaped clusters of 50-100 cells on tongue and palate |
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|
Term
| Where are taste receptor cells located and how are they organized? |
|
Definition
| located in taste buds (essentially at the top of bud, just beneath the taste pore, the region that pokes through the epithelium) |
|
|
Term
| How do taste receptor cells contact the environment? What is this access point called? |
|
Definition
| through opening in epithelial surface- the taste pore (the most apical processes of the taste cells are located in the taste pore region- this is at the uppermost surface of the taste bud so that the cells can interact with taste stimuli) |
|
|
Term
| How often do taste receptor cells turn over? |
|
Definition
| They turn over continously with each cell's lifespan approximately 9-10 days |
|
|
Term
| Are taste receptor cells neurons? If not, what are they and how do they fucntion? |
|
Definition
| NO! They are modified epithelial cells that possess neuronal properties. They are able to depolarize in response to stimulation and release neurotransmitters. |
|
|
Term
| In taste is there one transduction mechanism or many? |
|
Definition
| mutiple transduction mechanisms, depending on the stimuli |
|
|
Term
| How are salts and acids (sour) transduced? |
|
Definition
| depolarize taste cells by interacting directly with ion channels |
|
|
Term
| How do sweet and bitter substances and amino acids (umami) trandsuce their signals? |
|
Definition
| via G-protein coupled receptors |
|
|
Term
| What does stimulation with taste chemicals cause? |
|
Definition
| a depolarization; Ca influx; release of NT onto afferent nerve |
|
|
Term
| What activates G protein couple receptors and where are these receptors located? |
|
Definition
| the receptors located in the apical membrane of the taste pore are activated by sweeteners, umami, and bitter tastes |
|
|
Term
| Which genes encode GPCR and how do they function? |
|
Definition
| T1Rs: primarily heterodimer; T1R2 + T1R3: heterodimer responding to most sweet stimuli; T1R1 + T1R3: heterodimer that responds to most L-type amino acids; After receptor binds stimulus, you get a 2nd messenger cascade leading to cell depolarization and release of NT |
|
|
Term
| How many bitter taste genes encode GPCR (T2Rs)? How do they work? |
|
Definition
| 30 bitter taste genes; receptors are usually activated by one or just a few ligands; after binding, 2nd messenger cascades lead to an increase in intracellular Ca, either from internal stores or through cation channels |
|
|
Term
| Where is the nucleus of the solitary tract (NST) located? |
|
Definition
| brainstem, in the medulla |
|
|
Term
| What is the nucleus of the solitary tract (i.e. what does it do)? |
|
Definition
| 1st destination in CNS for taste info; key component in autonomic network; receives both gustatory and visceral (abdomen) afferent sensory info via vagus nerve; also receives from laryn and pharynx via vagus nerve |
|
|
Term
| Where does taste info synapse in NST (and through what)? |
|
Definition
| rostral part! Via Vagus, Glossopharyngeal, and Facial |
|
|
Term
| Where does taste info go from the NST? |
|
Definition
| NST-->direct projection to taste area of thalamus (VPM)-->taste areas of cortex (insula and opercular cortex) |
|
|
Term
| What is the pleasure component of taste? |
|
Definition
| sweet is rewarding b/c sweet signals nutritional content of carbs; bitter is not rewarding; pleasure/hedonism of taste reflects connection of limbic system involved in motivation (taste goes from NST to areas of brain involved in feeding and regulation: amygdala, lateral hypothalamus, mesolimbic dopamine pathway) |
|
|
Term
| Are limbic pathways (as related to taste lecture) vice versa? |
|
Definition
| yes; activity in feeding centers such as hypothalmus can modulate taste processing in brainstem (NST) |
|
|
Term
| What is ageusia? Is it common? |
|
Definition
| complete loss of taste; VERY RARE |
|
|
Term
| What is hypogeusia? What is it associated with? |
|
Definition
| reduction in or diminished taste, usually associated with URI and sometimes due to smell loss (reason you must assess smell and taste function); may also result from neurologic damage (can lead to anorexia)- neuro damage may be from radiation therapy for oral cancers (destroyed taste buds) or otolaryngological/dental procedures |
|
|
Term
| What is alcoholism associated with? |
|
Definition
| connected to sweet taste; alcoholics usually prefer sweet and ethanol can stimulate sweet taste receptors |
|
|
Term
| Where are olfactory receptor neurons and cell bodies found (yes, these are actually neurons, unlike taste buds)? |
|
Definition
| upper nasal epithelium: mucosa on septum and lateral wall, superior to turbinates |
|
|
Term
| Where do axons of smell receptor neurons pass? |
|
Definition
| through performations of cribiform plate on route to olfactory bulbs |
|
|
Term
| Where does smell signal go once it reaches the olfactory bulb? |
|
Definition
| from bulb to olfactory tracts- the tracts carry higher order axons on way to forebrain targets |
|
|
Term
|
Definition
| the olfactory nerve- tiny individual axons of olfactory receptor neurons projecting to olfactory bulb (axons of olfactory receptor neurons form CN I) |
|
|
Term
| How might axons of olfactory receptor neurons be injured? |
|
Definition
| damaged or sheared during head injury |
|
|
Term
| Where do olfactory receptor neurons (ORNs) reside? |
|
Definition
| cell bodies embedded in epithelium; cell bodies send apical processes to terminate in mucous layer and apical tips contain large cilia that spread out into olfactory mucosa; ORNs are surrouned by supporting cells |
|
|
Term
| How often do olfactory receptor neurons turn over? |
|
Definition
| continuously, like taste cells; derived from basal cells |
|
|
Term
| What type of receptors are the olfactory receptors? |
|
Definition
| 7 transmembrane domain proteins located on olfactory cilia |
|
|
Term
| How many olfactory receptor genes are there? Do they all work? Why do we have that many/that few? Do receptors bind one stimulus or many? |
|
Definition
| 630 olfactory receptor genes to deal with >400,000 odorant stimuli; 50% of genes are non-functional pseudogenes; receptors can bind more than one stimulus b/c stimulus molecules have epitopes |
|
|
Term
| What are epitopes? What do they do? |
|
Definition
| different chemical side groups that interact with particualr residues within binding pocket on a receptor molecule |
|
|
Term
| Do receptors recognize the entire molecule/odorant? How is this an advantage? |
|
Definition
| no, they recognize only the epitope- this way, a single receptor can recognize multiple sitmuli as long as each stimuli has a common epitope; a stimulus with multiple epitopes may recognize multiple receptors |
|
|
Term
| How does smell information reach CNS? |
|
Definition
| via receptor neurons to olfactory bulb to to glomeruli (the processing units) |
|
|
Term
| What happens once odorants bind the receptors? |
|
Definition
| 2nd messenger pathway is activated, leading to recepto cell depolarization and propagation of an AP down the axon all the way to the olfactory bulb, where transmitter is released onto dendrites of high-order neurons in the bulb |
|
|
Term
| Describe the 2 types of 2nd messenger pathways in smell? |
|
Definition
| Some odorants activate a cAMP pathway to block a non-specific cation channel; other odorants activate an IP3 pathway to open a Ca channel which opens a Cl conductance channel |
|
|
Term
|
Definition
| processing unit/cluster of cells where input neuron (ORNs) synapse with 2nd order cells- cluster of cells might include: axon terminals from ORNs, dendrites from mitral cells, tufted cells, and other cell types |
|
|
Term
| Are ORNs specific in their convergence or can they converge on any receptor? |
|
Definition
| a particular type of ORN conveges onto a single glomerulus in the bulb (each ORN expresses a SINGLE receptor type) |
|
|
Term
| How is an individual odor represented in olfactory system? |
|
Definition
| a distinct pattern of receptors! each odor activates a particular subset of glomeruli (only one receptor is expressed per ORN and ORNs target individual glomeruli)- different odorants produce unique spatial maps of activity across olfactory bulb; different odors may overlap in what they activate but each odor has a UNIQUE PATTERN |
|
|
Term
| Where do synaptic interactions of smell occur? |
|
Definition
| within the glomerlui in the olfactory bulb |
|
|
Term
| What are mitral and tufted cells? |
|
Definition
| output neurons of the bulb; they send axons to olfactory cortex and other structures in limbic system (such as amygdala); hippocampus (memory- smell has a strong relationship to memory) |
|
|
Term
| How are mitral and tufted cells related to glomeruli? |
|
Definition
| their dendrites are in the glomeruli, and this is how they are activated |
|
|
Term
|
Definition
| complete loss of smell (many etiologies) |
|
|
Term
|
Definition
| diminished sense of smell (number of etiologies) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| What may accompany anosmia and hyposmia? |
|
Definition
|
|
Term
| What are some etiologies of diminished/loss of smell? |
|
Definition
| upper respiratory infections; nasal polyps; head trauma; age (around age 60); smoking (longer you smoke, the worse it is; recovers after you quit-fully recovered in 30 years) |
|
|
Term
| How do you test smell in clinic? |
|
Definition
| small tube/swab of odorant; Univ of Penn Smell ID Test (40 item scratch and sniff test) |
|
|
Term
| What is the relationship of olfactory dysfunction an neurodegenerative disease (Alzheimer's, Parkinson's)? What do you see in Alzheimer's specifically? |
|
Definition
| olfactory epithelium begins to deteriorate early in AD and PD; may be linked to excess Tau proteins; can use smell test to predict onset of these diseases; AD patients have profound deficity in odor discrimination and 2 other odor-related tasks |
|
|
Term
| What percentage of strokes do hemorrhagic strokes comprise? |
|
Definition
|
|
Term
| What causes hemorrhagic strokes? What is the distribution (percentage of each)? |
|
Definition
| equally divided between hemorrhage into brain (intracerebral hemorrhage and parenchymal hemorrhage) and hemorrhage into subarachnoid space |
|
|
Term
| What are the 4 distinct types of cerebral hemorrhage? |
|
Definition
| subarachnoid; intracerebral; epidural; subdural |
|
|
Term
| What are major causes of hemorrhagic strokes? (there are 11 listed- other questions will address some of them specifically) |
|
Definition
| berry aneurysm; vascular malformation; traumatic; mycotic aneurysm; hyperT; tumor; bleeding diatheses; anticoagulant complication; congophilic angiopathy; vasculitis; illict drug use |
|
|
Term
| What is the distribution of congenital cerebral (berry) aneurysms? (there is a schematic in the notes illustrating this) |
|
Definition
| anterior circulation aneurysms comprise 85% with 30% occuring in the anterior cerebral artery and its branches, 30% in the internal carotid artery and its branches, and 25% in the middle cerebral artery; posterior circulation arteries comprise 15% with 2% in the posterior cerebral artery and its branches, 10% in the basilar artery (trunk and bifurcation), and 3% in the vertebral-posterior inferior cerebellar artery/area |
|
|
Term
|
Definition
| developmental defects in blood vessel wall that tend to enlarge with time; 80% of subarachnoid hemorrhages are due to berry/saccular aneurysm rupture |
|
|
Term
| What is the significance of the size of a berry aneurysm/defect in brain blood vessel wall? |
|
Definition
| 20% of population have an aneurysm/detectable defect measuring ≤2mm in diameter (rarely rupture); 5% of population has cerebral aneurysum 2-5mm that occassionally bleeds; aneurysms >5mm rupture and bleed at rate of 1-3% per year (less common and cause about 30,000 SAH in the US each year) |
|
|
Term
| What are some risk factors for SAH? |
|
Definition
| tobacco and alcohol use; hyperT; oral contraceptives; stimulant drugs (cocaine, etc); low cholesterol; genetics (polycystic kidneys, Marfan's) |
|
|
Term
| What is the natural history of SAH? |
|
Definition
| 10-15% die before reaching ER; 25% die during next 3 months; overall mortality of 40%; patients who survive have 40% chance of having neurologic sequelae |
|
|
Term
| What are the symptoms of SAH? |
|
Definition
| "worst headache of my life"; rapid loss of consciousness (some but not all patients) due to large pulse pressure change delivered to brainstem (result of arterial blood entering SA space); neck stiffness/pain, photophobia, phonophobia; nausea/vomiting; focal neurological signs are frequently MINIMAL or ABSENT |
|
|
Term
| Which symptoms of SAH are later symptoms? What do they reflect? |
|
Definition
| Neck stiffness/pain, photophobia, phonophobia reflect irritation and inflammation of meninges secondary to breakdown products of RBC lysis (follow rupture within hours) |
|
|
Term
| What symptoms distinguish hemorrhagic from ischemic stroke? |
|
Definition
| focal neurologic signs are not typical of SAH |
|
|
Term
| What are some signs of SAH? |
|
Definition
| abnormal vital signs (elevated BP, arrythmias); if focal neurologic signs are present, they can help pinpoint arterial site of aneurysm; meningeal signs typically present but often delayed after rupture/onset of headache; retinal hemorrhages |
|
|
Term
| What are some examples of focal neurologic signs in SAH? |
|
Definition
| CN III paresis- dilated pupil and ophthalmoparesis consistent with an aneurysm at junction of ICA and posterior communicating arteries; paraperesis (bilateral leg weakness)-suggests aneurysm of anterior cerebral artery; hemiparesis- suggests middle cerebral artery aneurysm |
|
|
Term
| What are the meningeal signs of SAH? |
|
Definition
| Kerning's sign: resistance to full extension of leg at knee when hip is flexed ≤135°; Brudzinski's sign: flexion of both hips and knees when neck is passively flexed |
|
|
Term
| What are some diagnostic tests for SAH? |
|
Definition
| non-contrast CT scan (most helpful non-invasive test); lumbar puncture (only method to 100% rule OUT SAH); MRI; DSA (4-vessel digital subtraction arteriogram- GOLD STANDARD) |
|
|
Term
| What does a non-contrast CT scan tell you about SAH? |
|
Definition
| amount of blood and location helps determine site of berry aneurysm and likelihood of delayed complication called vasospasm; might be NEGATIVE if bleeding is slight or CT is delayed for several days- perform LP if CT is neg and you suspect SAH |
|
|
Term
| Why do you delay LP for at least 4 hours after symptom (headache) of SAH? |
|
Definition
| allow time for RBCs in SA space to lyse and release Hb into CSF- present of Hb/breakdown products in CSF allows you to distinguish between blood in CSF occurred from nicking a vein while peforming LP and blood from ruptured aneurysm |
|
|
Term
| What do you do if CSF from LP appears bloody or discolored? |
|
Definition
| immediately centrifuge and examine for xanthrochromia- RBCs from nicked vein remain intact and are spun down, leaving a cyrstal clear supernatant; red tinge/discoloration of supernatant indicates Hb dissolved in CSF from RBCs that hae been in CSF for several hours; xanthochromia/yellow discoloration indicates breakdown of Hb (takes a day or more after rupture to develop) |
|
|
Term
| What do you do once you confirm your diagnosis of SAH with CT scan or LP? |
|
Definition
| MRI- to ID the site of ruptured blood vessel; will reveal aneurysms > 5 mm; or DSA is gold standard for diagnosing one or more aneurysms (may be multiple, espeically if associated with polycystic kidney disease) |
|
|
Term
|
Definition
| place small coils within aneurysm through an intra-arterial catheter to cause it to clot and seal itself; surgical placement of metal clip at neck of aneurysm; combination of aforementioned 2 |
|
|
Term
| What is the most common cause of parenchymal brain hemorrhage? |
|
Definition
| trauma is more frequent; hypertension is 2nd; arteriovenous malformations (often appear on DSA and CT scans) |
|
|
Term
| How does hypertension cause parenchymal hemorrhage? |
|
Definition
| chronic elevation of BP injures small cerebral BV and produces microaneurysms called Charcot Bouchard aneuryms |
|
|
Term
| Where do Charcot Bouchard develop? |
|
Definition
| in small, penetrating microvessels located in basal ganglia (30%), thalamus (20%), pons (5%), cerebellum (10%)- those are the most common sites for intraparenchymal hemorrhages by hyperT |
|
|
Term
| Where else might you see Charcot Bouchard develop, although this site is unrelated to hypertension? |
|
Definition
| in deep white matter (no microvessels here- why development is not related to hyperT) |
|
|
Term
| How do you treat hypertensive parenchymal hemorrhages? |
|
Definition
| correct bleeding problem (vit K, FFP, rFVIIa, prothrombin complex concentrate); reduce BP to <160/100 or MAP < 130 mmHg; monitor for and treat elevated ICP/herniations appropriately- with hyperventilation, osmotic agents, neurosurgical intervention to maintain CPP between 60-80 mmHg |
|
|
Term
| How do you treat AVM parenchymal hemorrhages? |
|
Definition
| intravascular occlusion of AVM with coils, followed by surgical removal or gamma knife obliteration of AVM |
|
|
Term
| What is an ischemic stroke? |
|
Definition
| injury to brain caused by interruption of its blood flow- comprises 80% of all strokes |
|
|
Term
| What is the clinical appearance if ischemic strokes? |
|
Definition
| abrupt onset of focal neurologic deficits (from loss of blood supply to one area); may be reversible and resolve within one hour (TIA-transient ischemic atatck); may be reversible and take more than 1 hour to resolve; may be irreversible leading to permanent neurologic deficits |
|
|
Term
| What are TIAs warning signs of? |
|
Definition
|
|
Term
| If strokes is reversible but takes more than 1 hour to resolve, what do you call it and why? |
|
Definition
| associated with detectable injury on MRI brain scans though neuro deficits may have resolved- "silent stroke" or "resolving ischemic neurologic deficits" (RINDs) |
|
|
Term
| What is the pathogenesis of ischemic stroke? |
|
Definition
| atherosclerotic occlusion of intra/extracerebral blood vessel (20%); embolus from heart or cerebral blood vessel (20%); disease of lumen of small arerioles aka lacunar infarcts (25%); cryptogenic aka unknown etiology (30%) |
|
|
Term
| What are nonmodifiable stroke risk factors? |
|
Definition
| age (doubles each decade after 55 y); gender (male > female by 1.5x); race (blacks 2x>whites); family history/genetics |
|
|
Term
| What are some modifiable stroke risk factors? |
|
Definition
| hypertension (relative risk is low but prevalence is high); diabetes; hyperlipidemia; somking; carotid artery stenosis; atrial fibrillation (relative risk is very high but prevalence is low); obesity; physical inactivity |
|
|
Term
| What is cerebral infarction? |
|
Definition
| focal necrosis of all cellular elements of brain (neurons, glia, other supporting cells) |
|
|
Term
| What is the pathological consequence of focal brain ischemia/ |
|
Definition
|
|
Term
| What is selective ischemic necrosis? |
|
Definition
| only brain neurons injured; most common in patients with transient global brain sichemia from cardiac arrest and successful resuscitation; only specific populations of highly vulnerable neurons (CA1 pyramidal neurons of hippocampus or cerebellar Purkinje cells) |
|
|
Term
| How long can brain survive in absence of blood supply providing glucose? |
|
Definition
| each 100 mg of brain has sufficient energy to last only 2.5 min- so not very long! |
|
|
Term
| What do hyperthermia and hyperglycemia do to brain during stroke? |
|
Definition
| accelerate and worsen the injury; increased brain temperature exacerbates catabolism in the brain (mechanism by which the cells die); elevated circulating glucose provides further fuel for glycolysis (results in higher concentrations of lactic acid that also exacerbates ischemic brain injury) |
|
|
Term
| In regards to energy/metabolism, what happens under normal conditions of cerebral blood flow? |
|
Definition
| neurons metabolizes glucose delivered by blood via aerobic metabolism; mitochondria generate adequate ATP and PCr to sustain membrane ion pumping mechanisms that maintain fluctuating membrane ion gradients and mebrane potential associated with normal depolarization and repolarization |
|
|
Term
| In regards to energy/ metabolism, what happens with loss of cerebral blood flow? |
|
Definition
| brain energy stores are depleted within minutes b/c glucose is metabolized via glycolytic pathways with accumulation of lactic acid; must reverse condition or catabolic mechanisms begin and cells die |
|
|
Term
| What is the goal for acute stroke intervention? |
|
Definition
| normalize elevated body temperatures and rapidly treat hyperglycemia |
|
|
Term
| What is the pathogenesis of ischemic stroke when caused by an embolus? |
|
Definition
| artery occluded by embolus; area distal/downstream to embolus experiences reduced blood flow (reduction is NOT uniform); the ischemic core experiences the most severe loss of blood flow and suffers irreversible injury within 1 hour or less; the ischemic penumbra may survive for 4-6 hours |
|
|
Term
| What is the ischemic core? |
|
Definition
| central area of territory most remote from surrounding blood vessels that could provide collateral blood flow to area distal to embolus during stroke (area experiencing most severe loss of blood flow) |
|
|
Term
| What is the ischemic penumbra? |
|
Definition
| the peripheral area w/less severe ischemia b/c it is supported by collateralizations |
|
|
Term
| What is the therapeutic window in stroke caused by embolus? |
|
Definition
| 4-6 hours in which acute intervention could restore blood supply to salvage brain tissue |
|
|
Term
| What are some neurologic signs and symptoms of stroke? |
|
Definition
| acute onset of weakness or paralysis in one limb or one side of body; loss of sensation in one limb or one side of body; loss of vision in one eye (amaurosis fugax) or one visual field; difficulty with language; clumsiness or loss of balance; difficulty with cognitive abilities- organization or perception |
|
|
Term
| What are the subtypes of ischemic stroke subtypes (characterized by blood vessel location/size)? |
|
Definition
| occlusion of...anterior: ICA, MCA, ACA, and any branches; posterior: PCA, VA, SCA< AICA, PICA, and any branches OR large diameter: ICA, MCA< ACA, PCA, VA, SCA< AICA, PICA; small diameter: long and short penetrating branches of large vessels |
|
|
Term
| Describe the normal curve of in autoregulation of cerebral blood flow (CBF). |
|
Definition
| CBF= MAP/CVR; sigmoid curve with plateau of CBF between MAPs of 55 and 155 mmHg; in this range, CBF is relatively constant and independent of MAP |
|
|
Term
| Why is the range of MAP in which CBF is constant important? |
|
Definition
| MAP can fluctuate rapidly and widley with changing position but CBF does NOT fluctuately with body position changes in normal individuals |
|
|
Term
| What happens when MAP falls out of its normal range? (should refer to graph in notes) |
|
Definition
| CBF becomes proportionately related to MAP- severe hypoT leads to decreased CBF and syncope; severe hyperT leads to hypertensive encephalopathy |
|
|
Term
| What happens to the CBF curve with chronic hyperT? (should refer to graph in notes) |
|
Definition
| if BP is elevated for more than 2 weeks, CBF curve shifts right and range of MAP becomes 75-175 mmHg (so less severe hypoT or even levels of BP that would be considerd normal now result in decreased CBF)- important to not acutely lower BP b/c of risk of further reducing CBF to an already ischemic vascular bed |
|
|
Term
| What are the American Heart/Stroke Assoc guidelines for acute stroke therapy? |
|
Definition
| counsels against lowering BP in patients who are not candidates for thrombolytic therapy unless systolic >220 or diastolic > 120 and then to lower BP only 10-15% within first 24 hrs |
|
|
Term
| Where might you see neurological symptoms if you occlude the MCA? |
|
Definition
| toes, ankle, knee, hip, trunk, shoulder, arm, hand, fingers, thumb, face, lips, tongue, larynx |
|
|
Term
| Where might you see neurological symptoms if you occlude the ACA? |
|
Definition
| toes, ankle, knee, hip, trunk, shoulder, corpus calosum, pareital lobe, frontal lobe |
|
|
Term
| Where might you see neurological symptoms if you occlude the PCA? |
|
Definition
| visual radiations, hypothalmus, thalamus, pareital lobe, corpus callosum, occipital lobe, temporal lobe, hippocampus |
|
|
Term
| What is the function of the Circle of Willis? |
|
Definition
| to provide collateral blood flow in instances of proximal occlusions (closer to the heart) of cerebral blood vessels |
|
|
Term
| What region is affected in medial medullary syndrome? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| medial medulla; paramedian branches of vertebral and anterior spinal arteries; pyramidal tarct (contralateral arm or leg wekaness); medial lemniscus (contralateral decreased position and vibration sense); hypoglossal nucleus and exiting CN XII fascicles (ipsilateral tongue weakness) |
|
|
Term
| What region is affected in Wallenberg's syndrome (aka lateral medullary syndrome)? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| lateral medulla; vertebral artery (more commonly PICA); inferior cerebellar peduncle/vestibular nuclei (ipsilateral ataxia, vertigo, nystagmus, nausea); trigeminal nucleus and tract (ipsilateral facial decreased pain and temperature sense); spinothalamic tract (contraolateral body decreased pain and temperature sense); descending sympathetic fibers (ipsilateral Horner's syndrome); nucleus ambiguus (hoarseness, dysphagia); nucleus solitarius (ipsilateral decrased taste) |
|
|
Term
| What region is affected in dysarthria hemiparesis (pure motor hemiparesis)? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| medial pontine basis; paramedian branches of basilar artery, ventral territory; corticospinal and corticobulbar tracts (contralateral face, arm, and leg weakness, dysarthria) |
|
|
Term
| What region is affected in ataxic hemiparesis? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| medial pontine basis; paramedian branches of basilar artery, ventral territory; corticospinal and corticobulbar tracts (contralateral face, arm, and leg weakness, dysarthria) |
|
|
Term
| What region is affected in Foville's syndrome? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| medial pontine basis and tegmentum; paramedian branches of basilar artery, ventral and dorsal territories; corticospinal and corticobulbar tracts (contralateral face, arm, and leg weakness, dysarthria); facial colliculus (ipsilateral face waekness, ipsilateral horizontal gaze palsy) |
|
|
Term
| What region is affected in Pontine wrong-way eyes? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| medial pontine basis and tegmentum; paramedian branches of basilar artery, ventral and dorsal territories; corticospinal and corticobulbar tracts (contralateral face, arm, and leg weakness, dysarthria); abducens nucleus or paramedian pontine reticular formation (ipsilateral horizontal gaze palsy) |
|
|
Term
| What region is affected in Millard-Gubler syndrome? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| medial pontine basis and tegmentum; paramedian branches of basilar artery, ventral and dorsal territories; corticospinal and corticobulbar tracts (contralateral face, arm, and leg weakness, dysarthria); fascicles of facial nerve (ipsilateral face weakness) |
|
|
Term
| What region is affected in Other regions variably involved in focal vascular syndromes of pons? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| medial pontine basis and tegmentum; paramedian branches of basilar artery, ventral and dorsal territories; medial lemniscus (contralateral decreased position and vibration sense); medial longitudinal fasciculus (internuclear ophthalmoplegia (INO) |
|
|
Term
| What region is affected in Weber's syndrome? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| midbrain basis; branches of PCA and top of basilar artery; oculomotor nerve fascilces (ipsilateral 3rd nerve palsy); cerebral peduncle (contralateral hemiparesis) |
|
|
Term
| What region is affected in Claude's syndrome? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| midbrain tegmentum; branches of PCA and top of basilar artery; oculomotor nerve fasciles (ipsilateral 3rd nerve palsy); red nucleus, superior cerebellar peduncle fibers (contralateral ataxia) |
|
|
Term
| What region is affected in Benedikt's syndrome? Which vascular supply? Which anatomical structures? What are the clinical features of each anatomic structure affected? |
|
Definition
| midbrain basis and tegmentum; branches of PCA and top of basilar artery; oculomotor nerve fasciles (ipsilateral 3rd nerve palsy); cerebral peduncle (contralateral hemiparesis); red nucleus, substantia nigra, superior cerebellar peduncle fibers (contralateral ataxia, tremor, and involuntary movements) |
|
|
Term
| What are the signs and symptoms of anterior circulation stroke? |
|
Definition
| ipsilateral blindness or contralateral inferior quadrantanopsia (defect affecting quarter of visual field); ipsilateral gaze paresis; contralateral mono/hemiparesis and/or mono/hemisensory deficit; aphasia in dominant hemisphere or neglect in nondominant hemisphere; any combo of above signs |
|
|
Term
| Which blood supply is occluded if you see a right inferior quadrantanopsia? |
|
Definition
| pareital temporal branches of MCA |
|
|
Term
| Which blood supply is occluded if right side is affected with a mono/hemiparesis and/or mono/hemisensory deficit? |
|
Definition
|
|
Term
| What are the signs and symptoms of posterior circulation stroke? |
|
Definition
| unilateral, bilateral, or crossed (face, body) weakness or sensory deficits; contralateral homonymous hemianopsia or superior quadrantanopsia; vertigo, nausea/vomiting, gait ataxia, diplopia, dysphagi, Horner's syndrome, altered consciousness and amnesia, any combo of above |
|
|
Term
| Which vessel is occluded causing homonymous hemianopsia on right visual field? |
|
Definition
|
|
Term
| What is a lacunar stroke? |
|
Definition
| small areas of ischemic infarction caused by occlusion of small, penetrating brain arteries |
|
|
Term
| What are the 4 classic lacunar syndrome? |
|
Definition
| pure hemiparesis; pure hemisensory deficit; ataxia hemiparesis; dysarthria-clumsy hand syndrome |
|
|
Term
| What are the most common sites of of lesions causing pure hemiparesis and pure hemisensory deficits (lacunar strokes)? |
|
Definition
| may occur at severeal locations along corticospinal tract or spinothalamic but most commonly at internal capsule and pons; pure hemisensory deficits also commonly occur with lacunes involving VPL nucleus of thalamus |
|
|
Term
| What is the pathogenesis of lacunar stroke? |
|
Definition
| microatheroma; microemboli from heart and more proximal blood vessels; lipohyalinosis; fibrinoid necrosis |
|
|
Term
| Where do lipohyalinosis and fibrinoid necrosis occur? |
|
Definition
| in smooth muscle and intima of small penetrating cerebral vessels as consequence of chronic hyperT |
|
|
Term
| What is included in the DD of ischeimc stroke? |
|
Definition
| hemorrhagic stroke; subdural hematoma; syncope/near syncope; radiculopathy; MS; hypo and hyperglycemia; bell's palsy; migraine; seizure; hypoxia; brain tumor |
|
|
Term
| What are the most common causes of ischemic stroke? |
|
Definition
| atherothrombosis/atheroemboli; lipohyalinosis and fibrinoid necrosis; cardiogenic emboli; vasculitis; hematologic disorders; drug related; fibromuscular dysplasia; carotid or vertebral artery dissection; increased homocysteine; other emboli (fat, air, bone marrow); vasospasm; migraine |
|
|
Term
| What are common sites for formation of atherothrombosis/atheroemboli in ischemic stroke? |
|
Definition
| origins of carotid and vertebral arteries; bifurcations of common carotid; ICA at carotid siphon and at branch points of MCA/ACA; M1 segment of MCA; basilar arteries |
|
|
Term
| What are major causes of cardiogenic emboli? Uncommon causes? |
|
Definition
| major: Afib (arrhythmia, valvular heart disease (mitral stenosis, bacterial endocarditis, prosthetic heart valves), mural thrombosis from MI; uncommon: atrial myxoma, valvular heart disease (mitral valve prolapse, nonbacterial endocarditis by cancer or SLE- Libman Sacks emboli), mural thrombosis from cardiomyopathy, paradoxical embolus (R-->L shunt) |
|
|
Term
| How does the neurogenic presentation of vasculitis induced ischemic stroke differ from usual ischemic stroke? |
|
Definition
| multiple cerebral blood vessels may be involved so multifocal neurological signs |
|
|
Term
| What are causes of CNS vasculitis? |
|
Definition
| Collagen vascular dx (SLE); giant cell temporal arteritis; infectious vasculitis (Syph, Lyme, AIDS, etc); hypersensitivity; Wegener's; Behcet's |
|
|
Term
| What are some hematologic disorders causing ischemic stroke? |
|
Definition
| hyperviscosity syndromes (polychtemia, multiple myeloma); hypercoagulable conditions (antiphospholipid, protein C/S deficiency, cancer, etc); hemoglobinopathies (sickle cell) |
|
|
Term
| What are the 6 tasks in approaching/managing ischemic stroke? |
|
Definition
| 1. evaluate and stabilize vital signs; 2. history (HPI to formulate anatomic diagnosis; PMI, FMH, Social Hx); 3. perform medical(pathology/etiology) and neuro (lesion location) exam; 4. working diagnosis- ask stroke or something else? Ischemic or hemorrhagic? vascular territory? etiology?; 5. routine lab evaluation; 6. special lab evaluation |
|
|
Term
| In evaluating a possible ischemic stroke, what do you do in your medical exam? |
|
Definition
| HR and rhythm, BP in both arms, listen for carotid bruits, peripheral vascular exam |
|
|
Term
| What are the routine lab evaluations when diagnosing a stroke? |
|
Definition
| EKG with rhythm strip, chest xray to evaluate heart size, CBC with differential and platelet count, chemistry profile (glucose, BUN, electrolytes), lipid profile, head CT w/o contrast, clotting time (INR, aPTT) |
|
|
Term
| What are the special lab evaluations in diagnosing an ischemic stroke? |
|
Definition
| RPR, coagulation profile (lupus anti-coag, anti-cardiolipin, protein C and S activity and levels, Factor V leiden), viscosity tests, vasculitis (ESR, FANA, etc), homocysteine levels, urine drug screen |
|
|
Term
| Which radiologic evaluations do you consider in ischemic stroke? |
|
Definition
| echocardiogram, carotid artery ultrasound, head MRI, head and neck MRA, CT arteriogram, DSA |
|
|
Term
| What is a head MRI good for in diagnosing ischemic stroke? |
|
Definition
| MRI diffusion weighted images (DWI) are useful in IDing ischemic areas (MRI FLAIR only show small hypersensitive areas) |
|
|
Term
| Is a CT arteriogram good for diagnosing ischemic stroke? |
|
Definition
| head CT scans detect evolving infarcts within 6-12 hours- not good to detect early ischemic stroke (like MRI FLAIR); highly sensitive to HEMORRHAGE and should be used in patients suspected of hemorrhagic stroke |
|
|
Term
|
Definition
| can place catheter via femoral artery to inject contrast to see extra/intracranial blood vessels |
|
|
Term
| What is the acute treatment for stroke? |
|
Definition
| treat w/ IV tissue plasminogen activtor if <4.5 hours from symptom onset and patient meets other strict criteria; treat with intra-arterial tPA if <6 hours from symptom onset and patients meets other strict criteria; retrieve clot with intra-arterial retrieving device if <8 hours from symptom onset and patientm eets other strict criteria |
|
|
Term
| What is the most effective way to deal with stroke? |
|
Definition
|
|
Term
| What is the prophylactic treatment for stroke? |
|
Definition
| medically treat hyperT, hyperlipidemia, and diabetes; add anti-platelet agent (aspirin) in cases of atherosclerosis to reduce recurrence of ischemic stroke; add warfarin in instances of cardiogenic emboli to signifcantly reduce recurrence of ischemic stroke (only use anticoagulatnts for cardiogenic emboli); smoking cessation; physical excericse; vascular stenting or endarterectomy for stenosis >70% of luminal diameter |
|
|
Term
|
Definition
| episode of abnormally synchronized and high frequency firing of neurons resulting in abnormal behavior or experience |
|
|
Term
|
Definition
| chronic brain disorder of various etiologies characterized byb recurrent, unprovoked seizures (excludes provoking factors: fever, acute head trauma, hypoglycemia, hyperglycemia, hyponatremia) |
|
|
Term
| In what age are epileptic seizures most common? |
|
Definition
| peaks in children and elderly, dipping between 20-60 years (increase in >60 years is due to increased rate of strokes in that age group) |
|
|
Term
| What are some causes of adult-onset epileptic seizures? |
|
Definition
| cerebrovascular disease, trauma, tumors, infections, cerebral degeneration |
|
|
Term
| What is a partial seizure? |
|
Definition
| focal onset seizures that emanate from a specific cortical head region and may sometimes spread to become secondarily generalized |
|
|
Term
| How do you differentiate simple and complex partial seizures? |
|
Definition
| simple: consciousness is preserved; complex: consciousness is impaired |
|
|
Term
| What does it mean for a seizure (partial) to be "secondarily generalized?" |
|
Definition
| consciousness lost + bilateral cerebral involvement |
|
|
Term
| What is a generalized seizure? |
|
Definition
| primary generalized seizure with no focal onset, thought to emanate from brainstem structures with spread to both hemispheres at same time |
|
|
Term
| Describe simple partial seizures. |
|
Definition
| signs/symptoms depend on focus (Jacksonian march indicates motor cortex is involved with focal seizure starting in hand and marching upwards ipsilaterally; somatosensory presents with focal tingling; autonomic presenting with rising epigastric sensations/nausea; psychic presenting with fear, deja vus, jamais vu); intact consciousness; EEG may appear normal; auras=brief simple partial seizures w/no overt behavior manifestations |
|
|
Term
| Describe complex partial seizures. |
|
Definition
| from temporal or frontal lobes; impaired consciousness; ictus duration of 1 minute; blank stare; oral/ipsilateral hand automatisms; contralateral dystonic posturing (indicates spread of seizure activity from temporal lobe-->ipsilateral basal ganglia); post-ictal amnesia/confusion; focal EEG abnormality |
|
|
Term
| What happens during an absence (petit mal) primary generalized seizure? |
|
Definition
| brief loss of consciousness (10-20 sec); staring spell; no post-ictal confusion; subtle myoclonic movement, eyelid flutter; no baseline neurologic deficits; EEG shows bilteral and symmetrical spike and wave activity at 3 Hz spike (wave discharge) |
|
|
Term
| What happens during tonic-clonic (grand mal) primary generalized seizure? |
|
Definition
| cry, loss of consciousness; muscular rigidity (tonic); patient may fall; rhythmic jerking (clonic); tongue-biting/injury common; bladder/bowel incontinence; post-ictal confusion/sleep |
|
|
Term
| What happens during a myoclonic seizure? |
|
Definition
| brief, shock-like muscle contractions (head, upper extremities); usually bilateral and symmetrical; consciousness preserved; precipitated by awakening or falling asleep; may progress into tonic-clonic seizures; juvenile myoclonic epilepsy presents this way |
|
|
Term
| Describe an atonic seizure. |
|
Definition
| impaired consciousness; loss of muscle tone; head drop; fall; brief duration (few seconds); injury common |
|
|
Term
| What is the pathophysiology of seizure? |
|
Definition
| imbalance of between glutamate-mediated excitation and GABAergic ihibition (excitation>inhibition, especially during development of a focal seizure); hippocampus and thalamus are particular prone to abnormal electrical activity b/c of the types of ion channels expressed here (and patterns of inter-neuronal connections) |
|
|
Term
|
Definition
| activates GABAA receptors that mediate fast synaptic inhibition (IPSP)-->influx of Cl ions, resulting in hyperpolarization |
|
|
Term
|
Definition
| activates 3 classes of ion channels (AMPA, Kainate, NMDA) that mediate fast synaptic excitation-->rapid influx of Na and Ca ions |
|
|
Term
| How do you diagnose a seizure? |
|
Definition
| Hx from patient/witnesses; physical and neurologic exam (usually normal neuro exam); CBC, CMP, AED (anti-epileptic drug) levels; inter-ictal EEG; epilepsy protocol MRI; MRI; video EEG monitoring |
|
|
Term
| What does a metabolic panel tell you for diagnosing seizure? |
|
Definition
| hypoglycemia/hyponatremia may provoke seizure; AED may alert you to non-compliant or inadequately dosed patient |
|
|
Term
|
Definition
| initial EEG: detects epileptiform discharge in 29-55% of patients; serial EEGs: epileptiform discharges in 80-90% of patients; doing repeat studies with sleep deprivation and extended recording times increases chance of detecting epileptiform discharge in patients with epilepsy |
|
|
Term
| What sort of epileptiform discharges do you see in primary generalized seizures? |
|
Definition
| bilateral burst of epileptiform spike and slow wave discharges; occur simultaneously and symmetrically in both hemispheres |
|
|
Term
| What are some examples of epileptiform abnormoalities? |
|
Definition
| sharp waves, spikes, shapr-and-slow wave discharges |
|
|
Term
| What is an epilepsy protocol MRI? |
|
Definition
| coronal high resolution T1 weighted volume data set throughout whole brain; coronal T2 weighted sequence with 3 mm thin sections to detect hippocampal signal abnormalities (atrophic and sclerotic hippocampus in mesial temporal sclerosis) |
|
|
Term
| What will you see in reguar MRI for seizure diagnosis? |
|
Definition
| recent-onset epilepsy in adults requires imaging, including gadolinium-DPTA enhanced sequences to find primary or secondary tumors, infections, inflammation- might see cavernous malformation, focal cortical dysplasia, periventricular heterotropias (lesions are potentially resectable) |
|
|
Term
| What is a periventricular heterotropia? |
|
Definition
| abnormal neuronal migration; shows up as gray matter surrounding inferior border of left lateral ventricle and extending diffusely inferiorly and laterally to brain surface |
|
|
Term
| What occurs during video EEG monitoring? |
|
Definition
| record EEG and clinical behavior simultaneously; differentiate epileptic from non-epileptic seizures; good for characterizing seizure type; good for pre-surgical localization of seizure focus |
|
|
Term
| What is the goal of AED therapy? |
|
Definition
| restore excitation/inhibition balance (reduce glutamate-mediated excitation or increase GABA inhibition); medical remission (major goal) or disease remission |
|
|
Term
| Can surgery be used for anti-epileptic therapY? |
|
Definition
| yes, in well-selected cases, it may be used for disease remission (seizure free of ALL meds) |
|
|
Term
| How do you choose an AED? |
|
Definition
| specific seizure type of epilepsy syndrome; efficacy for co-morbid conditions; ineractions with other drugs; ease of inroduction and follow-up; drug safety; cost |
|
|
Term
| What considerations are there for co-morbid conditions in choosing an AED? |
|
Definition
| obesity, migraines, depression, bipolar; topamax (migraine prophylaxis) and zonegran can result in weight loss as SE; lamictal for depression and mood disorders; depakote for bipolar disorders |
|
|
Term
| What is the drug of choice for primary generalized seizures? |
|
Definition
|
|
Term
| What is used ONLY for partial onset seziures with or weithout secondary generalization? |
|
Definition
| trileptal, lyrica, carbamezapine |
|
|
Term
| What interactions are concerning when considering AEDs? |
|
Definition
| enzyme inducing AEDs might interfere with coumadin, statins, HIV meds (metabolism) |
|
|
Term
| What is the MOA of phenobarbital? Side effects? |
|
Definition
| enhance GABA receptor activity; depresses glutamate activity; reduces Na and K conductance/ hepatotoxicity, connective tissue disorder, SJS |
|
|
Term
| What is the MOA of phenytoin? Side effects? |
|
Definition
| blocks Na channels; inhibitory on Ca and Cl conductance/ Aplastic anemia, hepatic failure, SJS, lupus |
|
|
Term
| What is the MOA of carbamazepine? Side effects? |
|
Definition
| blocks neuronal Na channel conductance/ aplastic anemia, hepatotoxicity, SJS, lupus-like syndrome |
|
|
Term
| What is the MOA of valproate? Side effects? |
|
Definition
| affects GABA glutermagic activity; reduces threshold of Ca and K conductance/ Hepatotoxicity; hyperammonemia; leukopenia; thrombocytopenia; pancreatitis |
|
|
Term
| What is the MOA of ethosuxamide? Side effects? |
|
Definition
| inhibits Ca T-channel conductance/ Bone marrow depression, hepatotxocity |
|
|
Term
| What is the MOA of lamotrigine? Side effects? Elimination? |
|
Definition
| blockage of voltage-dependent Na conductance/ SJS, epidermal necrolysis/ hepatic elimination |
|
|
Term
| What is the MOA of oxcarbazepine? Side effects? Elimination? |
|
Definition
| Na channel blockage/ hyponatremia, rash/ hepatic, renal elimination |
|
|
Term
| What is the MOA of topiramate? Side effects? Elimination? |
|
Definition
| blockage of Na channels; enhances GABA-mediated Cl influx/ renal calculi, hypohidrosis/ renal elimination |
|
|
Term
| What is the MOA of Zonisamide? Side effects? Ellimination? |
|
Definition
| blockage of Na, K, and Ca channels; inhibits glutamate excitation; has lonest 1/2 life, good for once daily dosing/ renal calculi, hypohidrosis/ renal elimination |
|
|
Term
| What is the MOA of Gabapentin? Elimination? |
|
Definition
| modulation of N-type Ca channel/ renal elimination |
|
|
Term
| Which older AEDs are effective in partial and tonic-clonic seizusres? Absence seizures? |
|
Definition
| valproate, phenytoin, carbamazepine, phenobarbital; ethuosuxamide and valproate |
|
|
Term
| Which newer AEDs are effective for partial seizures? Broad spectrum for partial and generalized? |
|
Definition
| gabapentin and oxcarbazepine; lamotrigine, topiramate, levetiracetam, zonisamide |
|
|
Term
| What is the elimination of levetiracetam? |
|
Definition
|
|
Term
| What are the half-lives of the newer AEDs? |
|
Definition
| zonisamide (63 h)>lamotrigine (25h)>topiramate (21h)>oxcarbazepine (9h)> tiagabine (8h) >levetiracetam (7h) >gabapentin (6 h) |
|
|
Term
| What are the effects of dose on AED pharmacokinetics? |
|
Definition
| nonlinear (michaelis-mentis type)- clearance decreases as dose increases (phenytoin); nonlinear- clearance increases with dose (carbamazepine, valproate); linear- clearance remains constant as dose increases (phenobarbital) |
|
|
Term
| Which drugs are hepatic cytochrome p450 inducers? |
|
Definition
| carbamazepine, phenobarbital, phenytoin, oxcarbazepine (minimal), topiramate (minimal) |
|
|
Term
| What might CYP450 enzyme inducers do? |
|
Definition
| lead to failure of oral conctraceptives; cause osteopenia, osteoporosis, fractures; increase metabolism of androgens and estrogens |
|
|
Term
| In whom are CYP450 enzyme inducers undesirable? |
|
Definition
| women on oral contraceptives; patients on oral coagulation; transplant patients; AIDS patients on protease inhibitors; patients predisposed to osteoporosis; effects of inducers are not significantly reduced until TOTALLY discontinued |
|
|
Term
| What type of birth defects do older AEDs cause? |
|
Definition
| malformations in 4-8% of children (2x normal rate); increase risk with hier dose and polytherapy; category D drugs |
|
|
Term
| What type of birth defects are seen in newer AEDs? |
|
Definition
| not teratogenic in animals; hman experience limited but growing; Category C drugs |
|
|
Term
| How do you reduce birth defects when using AEDs? |
|
Definition
| lowest effective dose; monotherapy; preconceptual folic acid supplementation (0.8-4mg/day); prenatal diagnostic testing at 16-18 weeks (maternal serum alpha-fetoprotein; ultrasound studies) |
|
|
Term
| What is intractable/refractory epilepsy? |
|
Definition
| disabling seizures recurring despite optimized therapy- impaired quiality of life, limited educational or occupational opportunities, physical injuries, or social compromise; optimized therapy includes at least 2 AEDs at maximally tolerated dose and with good compliance |
|
|
Term
| Is intractable epilepsy common? |
|
Definition
| 70-80% of patients are effectively controled with AEDs (so not really) |
|
|
Term
| What is the therapy for inractable epilepsy? |
|
Definition
| AED polytherapy (3+ drugs simultaneously); vagal nerve stimulator; ketogenic diet; atkins diet; epilepsy surgery |
|
|
Term
| What is a vagal nerve stimulator? |
|
Definition
| electrical pulse generator implanted subQ on chest with lead attached to left vagus nerve (rarely seizure free but 40-50% see approx 50% reduction in seizures) |
|
|
Term
| What types of surgeries are peformed -ie what is removed during epilepsy surgery? |
|
Definition
| temporal lobectomy; lesionectomy; corticoectomy; corpus callostomy; multiple subpial transections; hemispherectomy (important to have correct seizure type diagnosis and have tried at least 2 AEDs with optimized use/good compliance; patient without major medical/psycho-social disturbance; need surgery for better quality of life) |
|
|
Term
| What is generalized convulsive status epilepticus (GCSE)? |
|
Definition
| continous, generalized, convulsive seizure lasting ≥ 5 mins or 2+ sequential seizures occurring w/o full recovery of conscoiusness |
|
|
Term
| what is non-convulsive status epilepticus (SE)? |
|
Definition
|
|
Term
|
Definition
| ABCs, IV access; labs, brief history and exam, 50 mLs of 50% glucose, thiamine; ativan (lorazepam as DOC- 0.1-0.15 mg/kg IV); order bedside EEG monitoring after giving ativan; start dilantin (20mg/kg bolus by slow IV- may give additional doses to toal 30 mg/kg) |
|
|
Term
| How do you treat refractory GCSE? |
|
Definition
| refractory if patient fails to respond to ativan; consider intubation if convulsive seizures persist; start continuous EEG monitoring and move patient to ICU; midazolam 0.2mg/kg bolus then 2-10 mg/kg/hr; pentobarbital 8mg/kg |
|
|
Term
| What are characteristics of psychogenic non-epileptic seziures (PNES)? |
|
Definition
| may be variable in apperance; occur in daytime; normal EEG; maybe prolonged in duration; rarely have tongue biting, injury, urinary incontinence, postictal confusion; epileptiform activity is NOT seen; motor activity is prolonged, uncoordinated, often with pelvic thrust; unrelated to medication changes; interictal and ictal EEGs are normal; commonly see presence of secondary gain and psychiatric disturbances |
|
|
Term
| What are characteristics of epileptic seizures? |
|
Definition
| usually stereotyped in appereance; can be nocturnal or daytime; abnormal interictal/ictal EEGs; uncommon to see presence of secondary gain or psychiatric disturbances; brief in duration; tongue biting and injury may occur with tonic-clonic seizures; urinary incontinence is frequent; epileptiform activity is present; automatisms or coordinated tonic-clonic motor activity is seen; common to have post-ictal confusion; usually related to medication changes |
|
|
Term
| What is a psychogenic non-epileptic seizure/pseudoseizure? |
|
Definition
| paroxysmal episode resembling epileptic seizures but are psychological in origin; patients can have both epileptic and non-epileptic events |
|
|
Term
| What some seizure precautions? |
|
Definition
| showers rather than baths; swimming should always be supervised; biking and rollerblading only if child wears a helmet; no driving for 6 months after seizure in TN |
|
|
Term
| What do you do if person has a seizure in the hospital? |
|
Definition
| ABC (place patient on side and adminster oxygen); administer benzodiazepine (no need to wait for EEG to treat if you know it is a seizure); consider loading with an anti-epileptic med; longer seizure lasts, the harder to treat |
|
|
Term
| What are some seizure first aid tips? |
|
Definition
| stay calm and with child; protect child from injury by moving sharp/hard objects; do not hold child down; put child on side; do not put anything in child's mouth or hold tongue; can place something soft under child's head; do not give meds/liquids PO during seizure; give diastat (rectal diazepam) for status epilepticus and seizure clusters |
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Term
| What are some features of the absence generalized seizure? |
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Definition
| begins during childhood with no aura/warning for each episode; onset is abrupt with duration very brief (seconds); termination is also abrupt; frequency may be muitiple seizures per day; no postictal phase; commonly triggered by hyperventilation; generalized spike and wave on EEG; normal MRI; simple automatisms |
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Term
| What are some features of a complex partial seizure? |
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Definition
| begins at any age with an aura/waring occurrig frequently with the gradual onset; duration is longer than that of absence seizures, lasting minutes; occasionally they occur with more frequency than once a day; there is a postictal phase characterized by confusion and fatigue; uncommon for it to triggered by hyperventilation; focal epileptic discharges or nonspecific lesions on EEG and lesion shown on MRI; more complex automatisms |
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Term
| Describe febrile seizures. |
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Definition
| most common type of childhood seizures affecting 2-5% of children in the US with peak incidence at 18 months; seizures occuring in febrile children between ages 6-60 mo do not have intracranial infection, metabolic disturbance, or history of afebrile seiqures |
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Term
| How do you classify febrile seizures? |
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Definition
| simple and complex; simple may be isolated (once in a 24 hr period), generalized, and brief (<15 min), and they constitute the majority of febrile seizures; complex may occur in multiples, may be focal, and may be prolonged (>15 min); complex are associated with higher risk of afebrile seizures but not of febrile seizure recurrence |
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Term
| Do you see recurrence of febrile seizures? |
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Definition
| 32% experience reucrrence with 90% of children having recurrence within 1 year of onset; risk factors for recurrence include young age at onset (≤18 mo), febrile seizure in 1st degree relative; low grade fever in ER; brief duration between fever and seizure (<1 hr) |
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Term
| What are the risk factors for epilepsy in children with febrile seizures? |
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Definition
| complex febriles seizures; family hx of epilepsy; neurologic impairement prior to febrile seizure |
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Term
| What do you do in your neurodiagnostic evaluation of a child with a FIRST SIMPLE febrile seizure? |
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Definition
| lumbar puncture (strongly considered if <12 mo, considered if ≥12 mo and ≤18 mo, strongly considered in all children on prior Abx treatment; not routine but recommended if meningeal signs are present in patient ≥18 mo); EEG (do not perform in evaluation of neurologically healthy child with first simple febrile seizure); blood studies (should not be routinely performed but directed towards IDing source of fever); neuroimaging/MRI (should not be peformed) |
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Term
| what is the long-term management of child with simple febrile seizures? |
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Definition
| neither continuous nor intermittent anti-convulsant tx is recommended for children w/ 2+ simple febrile seizures; if parents are anxious, they can give intermittent oral diazepam at fever onset; anti-pyreticsc will not prevent; can discharge with diastat but if child is on oral diazepam, family should not administer diastat unless given go-ahead by physician (SAFETY!) |
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Term
| What is the diagnostic approach for first non-febrile seizures in children? |
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Definition
| immediate evluation (stabilize, determine if a seizure has occurred and what is the cause); lab studies based on individual circumstances and toxicology screening if question of drug exposure (both optional); lumbar puncture (option b/c limited in value and used primarily with concern of meningitis/encephalits); EEG (wake/sleep/hyperventilation/photic stimulation, determine seizure type or epilepsy syndrome); neuroimaging (MRI is preferred) |
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Term
| What might you see on EEG in first non-febrile seizures (pediatrics)? |
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Definition
| focal slowing, epileptiform discharges predictive of seizure recurrence |
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Term
| How do you treat first non-febrile seizure? |
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Definition
| treatment after 1st appears to decrease risk of 2nd (partial onset or generalized tonic-clonic); no benefit of treatment in regards to prognosis of long-term seizure remission; AEDs carry risk of side effects; risk benefit analysis, indivdualized for each patient |
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Term
| What is status epilepticus? |
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Definition
| occurs when brain is in state of persistent seizure (lasting longer than 30 minutes) |
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Term
| What should you consider in assessing a child with status epilepticus? |
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Definition
| AED levels; toxicology testing; EEG; neuroimaging if clinically indicated or unkonwn etiology; unclear if blood cultures or LP should be done on routine basis if no clinical suspicion of infx |
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Term
|
Definition
| occurrence of multiple, unprovoked seizures separated by more than 24 hours |
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Term
| What are some common etiologies of infant epilepsy? |
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Definition
| perinatal injury, metabolic defect, congenital malformation, infection, postnatal trauma |
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Term
| What are some common etiologies of early childhood epilepsy? |
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Definition
| infection, genetic, brain tumors |
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Term
| What are some common etiologies of elderly epilepsy? |
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Definition
| brain tumors, vascular disease |
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Term
| What are some specific epilepsy syndromes? |
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Definition
| generalized: infantile spasms, Lennox-Gastaut, childhood absence epilepsy, juvenile myoclonic epilepsy; partial-onset: benign rolandic epilepsy (BRE) |
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Term
| What is the age of onset of infantile spasms? |
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Definition
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Term
| What occurs in infantile spasms? |
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Definition
| seizures/spasms are brief bilateral symmetric contractions of the muscles of the neck, trunk, and extremities; flexor spasms are most commonly seen- head flexed with arms and extended and legs drawn up (stomach crunches); patient may flush or turn pale or cyanotic; extensor spasms may occur with extension of arms, legs, and trunk; less commonly- head nodding or lightening attacks involving single, momentary shock-like contraction of entire body |
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Term
| What does the EEG show in ifnantile spasms? |
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Definition
| hypsarrhythmia (high voltage, chaotic activity between seizures and diffuse voltage depression during seizures); background slowing (high amplitude delta waves) and multifocal spikes |
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Term
|
Definition
| triad of infantile spasms, hypsarrhythmia, and developmental arrest regression |
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Term
| How do you treat symptomatic infantile spasms (some have specific treatment, depending on etiology)? |
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Definition
| Vit B6 for pyridoxine dependent seizures; diet for phenylketonuria; diet for maple syrup urine disease; surgery for tumor/AVM; biotinidase for biotinidase deficiency; Cu histinidate for Menke's disase; Vigabatrin for tuberous sclerosis; ketogenic diet for glucose transporter deficiency; resection for cortical dysplasia |
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Term
| Overall treatments for infantile spasms? |
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Definition
| ACTH most commonly; also vigabatrin, topiramate, zonisamide, valproic acid, benzodiazepines, ketogenic diet |
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Term
| What is the age of onset for Lennox-Gastaut? |
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Definition
|
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Term
| What is the triad of Lennox-Gastaut? |
|
Definition
| specific seizure type, specific EEG, and mental deficiencies (at least 2 seizusre types, including tonic, atypical absence, and atonic); slowing of mental development; EEG slow spike and wave at 1.5-2 Hz |
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Term
| What are the seizures like in Lennox-Gastaut? May ti be compounded by any other epileptic syndromes? |
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Definition
| 9-39% have also had infantile spasms; seizures are life long and difficult to control |
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Term
| How do you treat Lennox-gastaut? |
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Definition
| valproic acid, lamotrigine, topiramate, zonisamide, felbamate, benzos, ketogenic diet, corpus callostomy, vagus nerve stimulator |
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Term
| What is the age of onset of childhood absence epilepsy? |
|
Definition
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Term
| Describe childhood absence epilepsy. |
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Definition
| normal neuro status; absence seizures occur multple times per day; generlized 3 Hz spike and wave discharges that may be triggered by hyperventilation; benign outcome (treat 2-3 years); normal EEG background |
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Term
| How do you treat childhood absence epilepsy? |
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Definition
| valproic acid, ethosuximide, lamotrigine, zonisamide, topiramate (NIH trial studying lamotragine, ethosuximide, and valproic acid); tegretol may worsen seizures |
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Term
| What is the age of onset for juvenile myoclonice epilepsy? |
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Definition
| adolescence (usually age 7-13 years for absence; 12-18 years for myoclonic jerks; 13-20 years for tonic-clonic) |
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Term
| Is juvenile myoclonic epilepsy genetic? |
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Definition
| hereditary- autosomal dominant linked to chromosome 6 |
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Term
| What are some triggers of juvenile myoclonic epilepsy? |
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Definition
| sleep deprivation, alcohol ingestion, stress, awakening from nocturnal or daytime sleep, menstruation, photic stimulation |
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Term
| What are seizures like in juvenile myoclonic epilepsy? |
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Definition
| may be tonic-clonic, myoclonic, or absence; myoclonic: brief, bilateral, not always symmetric, flexor jerks of arms (sometimes the legs, causing falls), highest frequency in morning, consciousness typically retained so patient is aware of jerking |
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Term
| What is diagnosis like for juvenile myoclonic epilepsy? |
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Definition
| usually delayed until onset of tonic-clonic seizures; neuro exam is typically normal and with normal neuroimaging |
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Term
| What is treatment for juvenile myoclonic epilepsy? |
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Definition
| lifelong- valproic acid, topiramate, levetiracetam, lamotrigine, zonisamide |
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Term
| How do you treat partial seizures (simple, complex, secondarily generalized)? Hint: these drugs are only used in partial as they may WORSEN generalized seizures |
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Definition
| phenytoin, carbamazepine, phenobarbital, gabapentin, tiagabine, levetiracetam, oxcarbazepine |
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Term
| How do you treat generalized and partial seizures? (aka broad spectrum agents) |
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Definition
| valproic acid, lamotrigine, topiramate, (felbamate), zonisamide, levetiracetan |
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Term
| What is ethosuximide ONLY used for? |
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Definition
|
|
Term
| What is ACTH ONLY used for? |
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Definition
|
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Term
| What else can you use to treat absence seizures? |
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Definition
| lamotrigine or valproate (+all broad spectrum agents) |
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Term
| What else MIGHT you be able to use for infantile spasms? |
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Definition
| topiramate, tiagabine, VGB (+ broad spectrum agents) |
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Term
| What is the most common form of benign partial onset epilepsy of childhood? |
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Definition
| Benign Rolandic Epilepsy (BRE) aka Benign Epilepsy w/centro-temporal spikes (BECDT) and benign focal epilepsy of childhood (BFEC) |
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Term
| From where do epileptiform discharges arise in BRE? |
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Definition
| from lower Rolandic area of brain |
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|
Term
| What is the age of onset and peak age of BRE? When does it stop? |
|
Definition
| 4-12 years with peak at 8-9 years; usually remits by age 14-16 years |
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Term
|
Definition
| normal neuro status and imaging with the most specific type of seizures (facial motor seizures) and most common presentation (nocturnal generalized tonic-clonic in 80% of patients); characteristic EEG finding is central-temporal spikes |
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Term
|
Definition
| carbamazepine or valproate but may not even need treatment |
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