Term
| What is demyelination vs dysmyelination |
|
Definition
demyelination - destruction of previously normal myelin with inflammatory response
dysmyelination- myelin delayed or arrested in development or maintenance is disturbed |
|
|
Term
| What are some non MS demyelinating diseases? Their presentations? |
|
Definition
Subacute combined degeneration - b12 deficiency,
central pontine meylinosis - rapid Na changes;
ADEM - post infection or vaccination;
PML - jc virus in oligodendrocytes |
|
|
Term
| What are the triggers, onset age and details of MS |
|
Definition
| autoimmune, inflammatory CNS disease - strikes anytime from 15-55 or older, involves a genetic predisposition(MNAY SNP's) but environmental trigger |
|
|
Term
| How do you dx MS, are there treatments? |
|
Definition
| using clinical presentation, csf and MRI, there are treatments - tysabari, gilenya, copaxone, |
|
|
Term
|
Definition
| demyelinating + axonal damage |
|
|
Term
| DO we have any ideas about genesis? |
|
Definition
| participating microbial infections that through mimicry or antigens induce an autoimmune response in a genetically predisposed host - genetic, environmental, and immune trigger |
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|
Term
| By what mechanism do the current treatments work? |
|
Definition
| immune system modification |
|
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Term
|
Definition
| visual, sensory, fatigue, disziness, impaired coordination, heat sensitivity, burning/electrical sensation, bowel, bladder, cognitive, motor, depression (mood) |
|
|
Term
| If some one presents with blurred vision - what are things that should be considered? |
|
Definition
| one eye or both? tracking or visual processing? pain? |
|
|
Term
|
Definition
| relevant afferent pupillary defect - found with flashlight swing, when going from unaffected eye to affected eye puils do not constrict , symptoms are like optic neuritis. |
|
|
Term
| Causes of RAPD? Why does unaffected eye cause restriction in both? |
|
Definition
| optic nerve lesion between retina and optic nerve, because the afferent (CN2) may be damaged but the intact efferent (CN3) is not |
|
|
Term
| Where would a lesion be to cause ON |
|
Definition
-optic nerve
-Medial longitudinal fassiculus ( info about eye directions, crosses through brain stem) |
|
|
Term
| What are the creiteria for MS sx |
|
Definition
lesions/sx disseminated in time in space with clinical presentation, and mimicers ruled out
needs sx spread over time (at least month) and MRI lesions in dif typical areas (juxtacortical, paraventricular, spinal cord, ventricular enlargement)
CSF maybe useful |
|
|
Term
| Why is CSF not a strong tool? |
|
Definition
| Only present in 85% of MS patients (showing as two oligoclonal bands ) |
|
|
Term
|
Definition
| DMT's and corticosteroids for fast resolution of acute attacks |
|
|
Term
| How are reflexes effected? |
|
Definition
| because its an UMN disease it results in hyperreflexia |
|
|
Term
| What's the basic mechanism for MS disease pathologies? |
|
Definition
| Activsted T cells cross the BB and attack matching antigens causing WBC's to multiple. These rally B cells and antibodies to increase immune response, attack myelin, oligodendrocytes and nerves |
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|
Term
|
Definition
| danaged areas that harden |
|
|
Term
| what is an activated Monocyte? |
|
Definition
|
|
Term
| Why is meyelin important? |
|
Definition
| its needed for the rapid conduction of impulses, trophic support and to protect nerve fibers |
|
|
Term
| how does the begining of MS different from later on in the disease course ? |
|
Definition
| early on it presents with more T2 lesions - later on T1 are more present and there is more atrophy |
|
|
Term
| WHy is Tysabari different from most drugs? |
|
Definition
| the alpha 4 integrin antagonist as selective adhesion molecule can block leukocytes - it keeps t cells from crossing the BBB |
|
|
Term
| Where is the future of MS drugs |
|
Definition
| neuroprotection and looking at myelination (opc and axon health) |
|
|
Term
| How was SZ differentiated from other manic depression? |
|
Definition
|
|
Term
| What are some positive symptoms of SZ |
|
Definition
| delusion, hallucination, bizzarre thoughts, |
|
|
Term
| What are some negative sx of SZ |
|
Definition
| apathy, poor motivation, social withdrawl, cognitive dysfunction |
|
|
Term
| What the the dx creiteria for SZ |
|
Definition
| 1-2 pos/neg sx for the better part of a month, social occupational dysfunction, signs of disturbance for 6 month, relation to other develomental disorfers |
|
|
Term
| What are some of the disease course for SZ |
|
Definition
| young adult onset, progressive, chronic, relapse remitting. |
|
|
Term
|
Definition
| genetic component determined from twin studies and environmental risks from gestational problems or viral infection |
|
|
Term
| Explain the Dopamine hypothesis for origin of Sz |
|
Definition
abnormal LTP in limbic syst, striatum, B gang, and cingulate - sx due to hyperactiver dA signal transduction or overactivtation of D2 receptors,
antiphyschotics work because they are DA antagonists |
|
|
Term
| Decribe the glutamate hypotheses |
|
Definition
| Most likely originates from a problem w/ mgluR 1 and 5 which results again n an enhancement of LTP. the hypofunction of glutamtergic NMDA receptors. PCP an antagonist of NMDA causes both pos and neg sypmtoms |
|
|
Term
| does the glutamate theory discount the DA theory? |
|
Definition
|
|
Term
| What are some anatomical brain changes associated with SZ |
|
Definition
| ventricular enlargement, volume reduction of hippocampus, frontal and temporal lobes. |
|
|
Term
| What are some imaging techniques usale in analyzing SZ |
|
Definition
PET?SPECT - measure blood flow and glucose metabolism and montitor changes
FMRI/ cortical hyperactivation |
|
|
Term
|
Definition
| a mental disintegration of thinking and emotional responsiveness. |
|
|
Term
| Describe the neurodevelomental hypotheses |
|
Definition
| caused by gestational insults that cause the formation of parallel circuits later activated in adolescence, triggered by psychological stressors, effect of normal plastic mechanisms, genisis via infection or pregnancy abnormality, few physical anomalies |
|
|
Term
| Decribe the glutamate hypotheses |
|
Definition
| Most likely originates from a problem w/ mgluR 1 and 5 which results again n an enhancement of LTP. the hypofunction of glutamtergic NMDA receptors. PCP an antagonist of NMDA causes both pos and neg sypmtoms |
|
|
Term
| does the glutamate theory discount the DA theory? |
|
Definition
|
|
Term
| What are some anatomical brain changes associated with SZ |
|
Definition
| ventricular enlargement, volume reduction of hippocampus, frontal and temporal lobes. |
|
|
Term
| What are some imaging techniques usale in analyzing SZ |
|
Definition
PET?SPECT - measure blood flow and glucose metabolism and montitor changes
FMRI/ cortical hyperactivation |
|
|
Term
|
Definition
| a mental disintegration of thinking and emotional responsiveness. |
|
|
Term
| Describe the neurodevelomental hypotheses |
|
Definition
| caused by gestational insults that cause the formation of parallel circuits later activated in adolescence, triggered by psychological stressors, effect of normal plastic mechanisms, genisis via infection or pregnancy abnormality, few physical anomalies |
|
|
Term
WHAT TYPE OF DAMAGE WOULD RESULT IN A SIMILAR MRI?
[image] |
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Definition
|
|
Term
| WHAT TYPE OF DAMAGE WOULD RESULT IN A SIMILAR MRI?[image] |
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Definition
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|
Term
WHAT TYPE OF DAMAGE WOULD RESULT IN A SIMILAR MRI?
[image] |
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Definition
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|
Term
WHAT TYPE OF DAMAGE WOULD RESULT IN A SIMILAR MRI?
[image] |
|
Definition
|
|
Term
WHAT TYPE OF DAMAGE WOULD RESULT IN A SIMILAR MRI?
[image] |
|
Definition
|
|
Term
WHAT TYPE OF DAMAGE WOULD RESULT IN A SIMILAR MRI?
[image] |
|
Definition
|
|
Term
WHAT IS THIS AN IMAGE OF? (MS RELATED)
[image] |
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Definition
|
|
Term
WHAT IS THIS AN IMAGE OF? (MS RELATED)
[image] |
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Definition
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|
Term
WHAT IS THIS AN IMAGE OF? (MS RELATED)
[image] |
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Definition
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|
Term
WHAT IS THIS AN IMAGE OF? (MS RELATED)
[image] |
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Definition
|
|
Term
| what are the 3 main associated FALS genes? |
|
Definition
|
|
Term
|
Definition
| its a superoxide disumtase 1 - in 20% of ALS |
|
|
Term
|
Definition
| Transactivated response region DNA binding protein of 43 kilodaltons |
|
|
Term
|
Definition
| an increase in transcription caused by a foriegn process |
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|
Term
| What chromosome is the FUS gene on? |
|
Definition
| its codes for an RNA binding protein on the 16p chromoosme |
|
|
Term
| Whats an example of candidate gene studies being worse than darts |
|
Definition
| its just a publication pusher - thought reelin may be important in SZ becuase it guides post mitotic cells - after much testing and research realized its not the case |
|
|
Term
| WHats a great graph to look at GWAS study info? how do you know something is significant? |
|
Definition
| Manhattan plot which is a scatter plotwith gene location on the x and -log of p value on the y axis , if data exceesd the beonferonni threshold |
|
|
Term
|
Definition
| single nucleotide polymorphisms. they can be synonymous or non synonymous |
|
|
Term
| What are the problems and benefits to Manhattan plots? |
|
Definition
| they eliminate falso positives but introduce the chance for false negatives |
|
|
Term
| whats necessary for a good gwas study? |
|
Definition
| large cohorts and sharinnnggg |
|
|
Term
| What was traynor's solution to not finding good data even with large cohorts? |
|
Definition
| to use a homogenous population - less polymorphisms because very little population drift |
|
|
Term
| What does the 1p33 gene influence in FALS? |
|
Definition
| age of onset - making it a good target because that coould delay disease - its assumed we will all one day develop ALS, but what matters is when |
|
|
Term
| WHy was finland a good choice for homogeneity in ALS |
|
Definition
| They are a founder population with high rates of ALS specifically featuring a mutation in the D90A allele of the SOD1 gene, the excess number of cases means they may all be to some degree familial |
|
|
Term
| What was the new gene found in the finnish population? |
|
Definition
| the 9p21 gene involved in 2% of FALS |
|
|
Term
| Why is exon sequencing so popular - what are some downsides? |
|
Definition
| its now faster and cheaper and 85% of diseases come from exon coding errors - it give torrents of info which is hard to sort through even with filters |
|
|
Term
| what did this 9p21 gene code for? |
|
Definition
| the VCP (valosin conting protein) an ER atpase used in proteolysis during autophagy |
|
|
Term
|
Definition
| alleles around a locus inherited as a group, or highly statistically associated SNP's on a single chromosome |
|
|
Term
| Insequencing what does coverage refer to? what is the standard coverage? What coverage did traynor use? |
|
Definition
| coverage refers to how much of an area is sequenced, usually its 6x, traynor did 300x |
|
|
Term
| What was the structural defect the coverage gap allowed traynor to identify |
|
Definition
| identified a hexanucleotide expansion in c9orf72, something in about 7% of FALS cases |
|
|
Term
| what problem does this c9orf72 hexanucleotide repeat cause? |
|
Definition
| its a gain of function problem- repeat contains sticky c's and g's - act like a toxic sponge that halts translation |
|
|
Term
| how was this mutation spread - what other diseases is c9orf72 linked to? |
|
Definition
| it was spread by the vikings and norsemen, and it has implications in AD and FTD |
|
|
Term
| What is the highes rated disease burden by ilness? |
|
Definition
|
|
Term
| WHat are the factors of mania |
|
Definition
mood - elated or iritable, expansice
attitude - Imperious or grandiose
vitality - speed thinking, no need for sleep, |
|
|
Term
| what is the characteristic progression of depression? |
|
Definition
| episodic with depressive states - relapse/remitting b/w unipolar or bipolar |
|
|
Term
| what does lithium do as a treatment? |
|
Definition
| decreases manic/depresive alterations - stops mood swings, |
|
|
Term
| What are the factors of depression |
|
Definition
mood - sad apathetic, numb,
attitude - low self esteem, decreased self confidence
vitality - fatigue, low energy, low concentration |
|
|
Term
| What are some diseases associated with depression ? |
|
Definition
| Parkinsons,, huntington, stroke, MS, TM, steroids, nicotine, hyperthyroidism, parturition, Transmeridian travel, seasonal variation |
|
|
Term
| How has depression shown to be heritable? Are there treatments? - |
|
Definition
| Yes there are many treatments, its heritable through GWAS many of the associated genes also involved in SZ |
|
|
Term
| What are some of the treatments depression? |
|
Definition
| antidepressants, ECT, TMS, supportive psychotherapy, cognitive psychotherapy. |
|
|
Term
| what are some types of antidepressants and what are the general flaws of the category as a whole? |
|
Definition
they are slow to work as wel as under/overperscribed
there are tricyclics ( need constant blood workups to watch for heart strain), SSRI's (need titration) and Lithium |
|
|
Term
| What is thought to be a general cause of depressions? |
|
Definition
| decreased concentration of monamine neurotransmitters |
|
|
Term
| What has eveidence of our ancestors headwounds suggested? |
|
Definition
| that we have naturally selected for better ability to self heal TBI |
|
|
Term
| in the past - what was TBI considered |
|
Definition
| it was considered shell shock, a form of cowardice or malingering - but thats not what data showed its what large forces pushed |
|
|
Term
| who's most suceptible to TBI |
|
Definition
| the very young and very old |
|
|
Term
| What are subtypes of tbi? |
|
Definition
|
|
Term
|
Definition
| temp impairment of neuro function |
|
|
Term
|
Definition
| shows white on ct scan it is bruise or microhemorhage in the brain, these damages spread with time from injury |
|
|
Term
|
Definition
| epidural hematoma - blood buildup between dura mater and skull - puts pressure on brain and can herniate brainstem into spinal cord disrupting maintenance functions - easily drained and recovered from - involves lacerations of meningeal vessels |
|
|
Term
|
Definition
| subdural hematoma - blood accumulateds between dura matter and arachnoid - actually bulges down onto brain - may cause much damage and also must be immediately surgically resolved with crainiectomy to drain - involves lacerations of bridging veins |
|
|
Term
|
Definition
| difuse axonal injury - extensice white matter lesions from shearing forces (tissue sliding over tissue), not usually focal (Difuse vasucular injury is focal) |
|
|
Term
| what are the grading quality for the categories of TBI |
|
Definition
| gasglow coma scale (physical/verbal text), amt of time of lost consciousness, amt of amneisia |
|
|
Term
| What can suceptibility weighted imaging find? |
|
Definition
| its a bold signal that can find microbleeds |
|
|
Term
| Dwi can identify two types of edema - what are they |
|
Definition
cytoxic - na/k pump failure that cause hyperpolarization and water influx
intersitial - astrocytes fail to remove k and water from ecf into vasculature |
|
|
Term
| What are the best ways to image TBI |
|
Definition
CT scans hardly show much MRI's are good, but best are apparent diffusion coefficient (adc) and dwi (shows damage bright (is a negative) )
flair can negate csf signals in order to better show hyperintensities |
|
|
Term
| why is the splenium a common source of damage |
|
Definition
| its attached to dura at 2 points no free range of motion in the skull |
|
|
Term
| Why is the intraventricular hematoma so bad? |
|
Definition
| it blocs CSF from entering the fourth ventrical - CSF cannot drain (we must drain all we make) and can quickly cause brainstem herniation or hemorrhage |
|
|
Term
| TBI damage isn't usually random - where does it usually occur? Why these places? |
|
Definition
| precuneus, posterior cingulate, superior parietal cortex, superior frontal cortex, - these arease are probably damaged because theya re active during the resting state |
|
|
Term
| What accounts for TBI's causing amneisia |
|
Definition
| tbi seems to have a large effect on hoppocampal connectivity |
|
|
Term
| what is the main function in memory of the hipocampus? |
|
Definition
| re encodes current events for storage |
|
|
Term
| Neural activity produces arteriole expansions follwoed by oxygenated blood, which is then deoxygenated. what can theses co2 levels tell us. |
|
Definition
| this hypercapnia allowes study of neural control of blood flow which tbi interferes with (when tbi interferes it increases radicals thereby causing more damage ) |
|
|
Term
| Whats the difference in what PWI and DWI identify in a stroke |
|
Definition
| DWI - indetifies dense infarct, PWI identifies areas getting enough blood to saty alive but not function |
|
|
Term
| does aphasia occur as a result of of hypoperfusion or structural damage? |
|
Definition
|
|
Term
How do we fix stroke damage?
angioplasty/stenting? |
|
Definition
| manually widening narrow or obstructed arteries |
|
|
Term
How do we fix stroke damage?
embolectomy |
|
Definition
| surgically removing clots, can cause necrosis |
|
|
Term
How do we fix stroke damage?
thombolysis |
|
Definition
| breaking clots with pharmacology like tPA |
|
|
Term
| WHat are other ways we fix stroke damage? |
|
Definition
| surgical revascularization, induced bp elevation |
|
|
Term
| Why is reperfusion important immediately following stroke? |
|
Definition
| it allows for quick recoveries |
|
|
Term
| How does damage to broca's area play out? |
|
Definition
| Broca's area is the source of sentance production, reversible comprehension , articulation and spelling - so damage results in aphasia with nonfluent agramatic speech. speech is telegraphic at best with imparied repition and spelling, all with intact comprehension |
|
|
Term
| where would damage need to obstruct for a broca's area defect |
|
Definition
| superior MCA in order to cause damage to the posterior and inferiror frontal lobe |
|
|
Term
| How does damage to wernicke's area play out |
|
Definition
| results in fluent paragrammatic speech, extended jargons and neologisms, difficulty understanding written and spoken sentences , rep |
|
|
Term
| how does one damage wernickes area through stroke? |
|
Definition
| left inferior MCA - which cause damage to posterior and superior temporal lobe |
|
|
Term
|
Definition
can name tactile or verbally presented objects but not visually presented objects
cant read but knows word when spelled out |
|
|
Term
|
Definition
| fluent grammatical speecha nd comprehension -poor word retrieval |
|
|
Term
|
Definition
| no fluent speech - only utterances (tan,tan) poor comprehension, no spontanous speech - caused by damage to whole MCA distribution - |
|
|
Term
| do aphasia have a large degree of recovery? |
|
Definition
| yes - brain can compensate by switching function to other hemisphere (not recovery persay" |
|
|
Term
| conduction aphasia - cause |
|
Definition
| fluent but paragraphic speech okay comprehension, bad repitioun, conduit d'approoche phenomemnon - caused by lesion in the arcuate fasiculus it disconnects wernickes and brocas area |
|
|
Term
| Transcortical motor aphasia |
|
Definition
| telegraphic speech - caused by left aca damage |
|
|
Term
| Whats the difference b/w stroke and TIA? |
|
Definition
| TIA is tmeporary and usually slef resolves without much damage |
|
|
Term
| What are some causes of stroke? |
|
Definition
| obstruction, hemorrhage, infections (abcesss/encephalitis), metabolic problem (kidney/liver failure) |
|
|
Term
| which areas are most prone to hypotension? |
|
Definition
|
|
Term
|
Definition
| clinical presentation +imaging |
|
|
Term
|
Definition
| effects frontal and parietal lobes, sx usually, aphasia, neglect, weakness, contralateral face numbness |
|
|
Term
|
Definition
| effects frontal lobes resulting in contralateral leg weakness |
|
|
Term
|
Definition
| effects thalamus and occipital lobes results in contralateral sensory loss, visual field deficits, |
|
|
Term
|
Definition
| involves small deep penetrating vessels off MCA - good recovery rate - effects b gang, brainstem, cerebellum, thalamus and are usually thrombotic sx include hemiparesis, hemisensoryloss, dysarthria and ataxia |
|
|
Term
| What are some newer detectors of stroke? |
|
Definition
| increased homosystein, and c reactive protein, infarcts, infections, metabolic syndromes |
|
|
Term
| difference between thrombotic and embolitic stroke |
|
Definition
| embolitic blocks flow but not in the artery its in, not a focal blaock |
|
|
Term
|
Definition
|
|
Term
| whats the difference between arteriosclerosis and atherosclerosis |
|
Definition
| arterior is just vessel hardening, athero means its caused by fat buildup |
|
|
Term
| what are some genetic factors of stroke |
|
Definition
| apoE4 gene of AD is involved with cholesterol metabolism and asc with atherscleorsis |
|
|
Term
| asymptomatic strokes are usually what type? |
|
Definition
| lacunar, microbleesds or white matter diseased (from hardening - like leukoariosis |
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|
