(Neuro)physiology, statistics Flashcards

1
Q

ENG

A
  • Nerve Conduction Studies (NCV) involve three types: motor, sensory, and mixed.
  • Motor and sensory studies are most commonly ordered for clinical diagnosis.
  • Motor studies stimulate at both proximal (S2) and distal (S1) sites, recording muscle depolarization.
  • Distal latency measures time from stimulus to initial muscle depolarization.
  • Amplitude reflects the number of intact axons participating in depolarization.
  • Duration indicates the duration of the electrical impulse.
  • Conduction velocity is influenced by nerve diameter, myelination, and temperature.
  • Sensory studies only require stimulation at one site, assessing nerve function without muscle involvement.
  • Sensory studies calculate conduction velocity to measure nerve function.
  • Onset latency and amplitude are key metrics in sensory studies.
  • Sensory studies are valuable in conditions like carpal tunnel syndrome.
  • Temperature control is crucial for accurate NCV recordings.
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2
Q

Conduction velocity

A

Conduction velocity refers to the speed at which an electrical impulse travels along a nerve fiber. In the context of Nerve Conduction Studies (NCV), it is a measure of how quickly nerve impulses propagate along a nerve. Conduction velocity is influenced by various factors such as the diameter of the nerve, the presence of myelin sheath (which speeds up conduction), and temperature. In motor studies, conduction velocity is calculated by dividing the distance between the stimulation sites by the difference in latency between the proximal and distal sites. In sensory studies, conduction velocity is similarly calculated to assess nerve function, typically without muscle involvement. It is an important parameter in diagnosing nerve disorders and assessing nerve health.

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3
Q

SSEP

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4
Q

epilepsy symptoms by territory

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5
Q

epilepsy symptoms by location 2

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6
Q

Status epilepticus treatment algorithm

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7
Q

VEP

A
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8
Q

BAEP

A
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9
Q

SSEP

A

Somatosensory evoked potential (SSEP)- hátsó kötél pálya integritása
* Kevert idegek stimulálása- Ia izomrostok és a II típusú afferens rostok is ingerlésre kerülnek
Generátorok:
Felső végtag (N. medianus):
N9- Erb pont
N11-N13 komplexum- nyaki gerincvelő hátsó szarvi neuronjaink postsynapticus aktivitása
P14- ncl. cuneatus és a thalamus közt generálódik (felső agytörzs)
N20- első corticalis válasz, Broadman 3b area, P22- area precentralis

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10
Q

SSEP locations

A

Schematic representation of median nerve’s somatosensory evoked potentials (SSEP) responses localizations on brain MRI (a) and typical examples of their normal wave forms as well as recording electrodes montages (b). SSEP elicited by electric stimulation (15 mA) of median nerve at the wrist: N9, N13 and P14, respectively, the brachial plexus, cervical spinal cord, and cervico-medullary (subcortical) responses. N20 and P25 are responses of the primary sensory cortex. N9–N13 inter-peak latencies (IPL) represent a proximal peripheral nerve conduction time, and P14–N20 IPL the intracranial conduction time (ICCT). Recording and reference electrodes were placed at Cv7 (7th cervical vertebra)—Fz: for the N13 cervical spinal cord response and Cz-cSh (contralateral shoulder): for the subcortical far-field potential: P14. The cortical components, N20 and P25 were recorded at the contralateral C3′ or C4′ positions (2 cm behind C3 or C4) according to the international 10–20 system. Two sets of 500 sweeps were averaged

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11
Q

SSEP pathology

A
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12
Q

SSEP parameters

A

ENG in carpal tunnel syndrome: sensory latency > 3.7 ms is the most sensitive test

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13
Q

Inhaled anasthetic and SSEP

A

Nitrousoxide(N 2 O)reducestheamplitudeandincreasesthelatencyofcorticalcom- ponentsinadose-dependentfashion[43]. Inhalationalanesthetics,suchasIsoflurane,Halothane,andEnflurane,alldecrease theamplitudeandincreasethelatencyofthecorticalresponsesinadose-dependent fashion,especiallywhentheyareadministeredwithN 2 O[43].

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14
Q

IV anasthetics and SSEP

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IntravenousAgents PropofoldoesnotaffectthesubcorticalN13component,butitincreasesthelatencyby approximately10%oftheearlycorticalcomponentswithoutaffectingtheiramplitude. Latercorticalcomponentsusuallydisappear[43]. Benzodiazepines(e.g.,Diazepam,Midazolam)reducetheamplitudeofcortical SEPwaves[42]. Barbiturates(e.g.,Thiopental,Methohexital)increaseSEPlatencyinadose- dependentfashion,withaslightamplitudedecrease[43]. EtomidatehasasurprisingeffectonthecorticalSEPamplitude,whichcanbe augmentedbyasmuchas200–600%[43].However,italsoincreasesSEPlatencies. KetaminealsoincreasesSEPamplitudeandlatency[43,21]. Opiates,suchasMorphine,andsyntheticnarcotics,suchasFentanyl,Alfentanil, andSufentanil,causeaslightincreaseinSEPlatencywithoutaffectingtheampli- tude[42].

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15
Q

EffectsofAnestheticAgentsonCorticalSEPAmplitude andLatency

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16
Q

TypicalSEPAmplitudeandLatencyValues ObtainedAfterMedianorPosteriorTibialNerveStimulation

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17
Q

MEP vs SSEP

A

SomatosensoryEPmonitoringmeasurestheintegrityofsensorytractsonly.There- fore,selectivedamagetomotortractsmaygoundetected.Additionally,sincethe ventralanddorsalportionsofthespinearesuppliedbydifferentbloodvessels,is- chemiaaffectingthemotortractsonlywillnotbedetectedbySEPs.Thus,MEPsare usedintraoperativelytoprotectthestructuralandfunctionalintegrityofthemotor tractsinthespinalcord.

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18
Q

tMEP intraoperative

A

Dependingonthesurgicalprocedure,stimulationcanbemonopolarorbipolar. Monopolarstimulationisdeliveredwithahand-heldsingle-tipstimulator,whichis usedasthecathode(negativestimulatingelectrode).Theanode(positiveelectrode) consistsofasterilesubdermalneedleplacedintoamuscleinsidetheincision.Bipo- larstimulationisdeliveredwithadoubletipelectrode,withthenegativetipplaced towardstherecordingsite. Constant-currentstimuli,eachhavingadurationof0.01msec,aredeliveredata lowrateof1or2Hztoavoidmusclefatigue.Stimulusintensityfordirectnerveor nerverootstimulationisgraduallyincreasedfrom0mAuntilanEMGresponseis seen,uptoamaximumofabout2mA[48].Forpedicleorpediclescrewstimulation, stimulusintensityisgraduallyincreaseduntilaresponseisseen,from0mAuptoa maximumofapproximately40mA[7,54].Thisprocedureisusedtominimizethe amountofcurrentdeliveredtoneuralstructures.

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19
Q

iOP EEG

A
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20
Q

iOP EEG ampl hz

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21
Q

ExampleofintraoperativeEEGrecording.

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22
Q

EffectsofAnestheticAgentsonEEGAmplitudeand FrequencyatTypicalDoses

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23
Q

ioSEP

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SEPsobtainedafterinadvertentocclusionoftheleftiliacartery.(a)Increased latencyanddecreasedamplitudeisseeninallresponsestoleft-legstimulation,while(b)the responsestorightlegstimulationremainunaffected.Lightcolortracescorrespondtothe baselinescollectedatthebeginningoftheoperation.

24
Q

ioSEP 2

A

SEPrecordingsobtainedaftercordinjuryduetomisplacedinstrumentation; (a)baselines;(b)normalvariationsduringthecase;and(c)cortical(peakN45)andcervical response(peakN30)disappearjustafterplacementofinstrumentation,whiletheperipheral response(peakPF)remainsunchanged.

25
Q

EEG electrode placement

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26
Q

epilepsy EEG parts

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27
Q

SEP elecrtodes

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28
Q

predictive values

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29
Q

NPV

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30
Q

PPV

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31
Q

sensitivity and specifity

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32
Q

sensitivity

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33
Q

specificity

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34
Q

three components of the ICP waveform

A

P1 = Percussion wave 🥁
Generated by arterial pulsations at the beginning of systole.
P2 = Tidal wave 🌊
Reflects the compliance of the ventricles, responding to increased pressure of the percussion wave.
Usually P2 is ~80% as tall as P1.(28169966) If P2 > P1 this suggests poor compliance, due to concerningly elevated ICP.
P3 = Dicrotic wave 📉
Reflects aortic valve closure at the end of systole.

Normally, P1 > P2 > P3, in a descending pattern.
As ICP elevates, the brain compliance is compromised. This causes P2 to increase higher than P1. Eventually, P1 and P2 may fuse into a single wave (figure above).
Abnormal waveforms may occur before the absolute value of the ICP is elevated. This may be an early signal of an impending ICP crisis.(34618757)
Dampened waveforms may also be seen in patients with catheter occlusion, catheter malposition, air bubbles, cerebral vasospasm, or in patients with an open skull (e.g., status post craniectomy).

35
Q

high ICP waveform

A
36
Q

(?) normal lundberg waves

A

B waves:
Waves last between ~30 seconds to several minutes.
Amplitude is ~20-30 mm Hg.
Significance is unclear; often suggest impaired intracranial compliance.
C waves:
Waves last ~7-15 seconds.
Amplitude is usually <20 mm Hg.
C-waves are a component of normal physiology, due to cardiac and respiratory cycles.

37
Q

plateau wave - Lundberg A

A

Plateau waves result from a vicious cycle as shown above, which causes transient elevations in ICP.
The physiological prerequisites for plateau waves include the following:
(1) Tenuous brain perfusion.
(2) The brain is on the steep, right portion of the cerebral compliance curve (see figure below). The brain has expanded to the point where there is really no extra room to accommodate further edema. Thus, the mere dilation of cerebral vasculature is sufficient to increase the ICP.
(3) Preserved cerebral autoregulation.
Plateau waves themselves are self-limiting. Short plateau waves (e.g., ~5-15 min) pose no immediate threat, but longer pressure waves might cause neurologic insult. Regardless, the presence of pressure waves reflects a dangerous situation, where the brain has reached the limits of physiological compensation.
Plateau waves (a.k.a. pathological A waves) are transient, periodic severe elevations in ICP (up to 50-100 mm) usually lasting for ~5-30 minutes (but potentially up to two hours).(19565359) They may occur spontaneously, or may be precipitated by coughing, pain, or changes in position from lying to sitting or from sitting to standing.(26704760)
Plateau waves are often accompanied by clinical deterioration, with symptoms as listed below.(29329250) Arterial blood pressure remains roughly stable during a plateau wave, although dysautonomia can occur.

38
Q

High ICP treatment by Tier steps

A
39
Q

reasons to stop using mannitol

A

🛑 Mannitol is potentially nephrotoxic.
🛑 Mannitol often induces diuresis, which may lead to volume depletion and brain hypoperfusion. Diuresis may also promote electrolytic disarray (with hypokalemia, hypomagnesemia, and hypophosphatemia).(32440802) This risk can be mitigated by replacing the diuresed volume 1:1 with an isotonic solution (e.g., plasmalyte) for 6 hours after mannitol infusion.
🛑 Guidelines recommend monitoring the efficacy and safety of mannitol by following the serum osmolality to ensure that mannitol isn’t accumulating and thereby increasing the risk of kidney injury (e.g., an osmolality >320 mOsm and/or osmolal gap >55 mOsm suggests mannitol accumulation).(32227294) In reality, this is rarely performed properly.(32440802)
🛑 There may be a rebound elevation in ICP, due to mannitol which crosses the blood-brain barrier and eventually causes edema within damaged areas of the brain.
🛑 Meta-analysis of available studies shows that mannitol is less effective than hypertonic saline, while being associated with higher rates of kidney injury.(21242790) A Cochrane analysis found that mannitol might have detrimental effects on mortality, when compared to hypertonic saline.(32440802)
🛑 Guidelines recommend the use of hypertonic saline rather than mannitol for traumatic brain injury or intracranial hemorrhage.(32227294)

40
Q

moderately deep sedation with propofol

A

Propofol reduces brain metabolic activity, which may improve ICP and also avoid cellular hypoxemia.
For patients with ICP elevation, propofol sedation may be a sensible choice. Additionally, it may be reasonable to target a slightly deeper level of sedation than might otherwise be chosen.
Propofol has the advantage that it is easily titrated, thereby allowing for neurologic examinations to be performed intermittently. Propofol also has antiepileptic properties that will protect against seizure.

41
Q

barbiturate coma

A

The concept of a barbiturate coma is the same as that of propofol use above, with the difference that barbiturates can achieve a deeper coma. Barbiturates are ideally titrated using an EEG, to achieve a burst-suppression pattern (once a burst-suppression pattern is reached, barbiturate dose should not be increased further).(31659383)
**Pentobarbital is preferred over phenobarbital, because the half-life of pentobarbital is somewhat shorter. Nonetheless, pentobarbital still has a long half-life (15-50 hours). **Thiopental might be an attractive option here, but it’s unavailable in the United States, due to its history of being used for lethal injection.
A deep barbiturate coma has substantial side effects. Hypotension requiring vasopressor support may occur, as well as ileus. Barbiturates are **metabolized slowly, which may make it impossible to evaluate the patient’s neurological outcome for weeks. **This may lead to some very challenging situations. For example, it’s ethically impermissible to withdraw life-sustaining therapy in a patient who has been rendered comatose with pentobarbital.
⚠️ Due to inability to titrate or rapidly reverse this therapy, barbiturate coma is an intervention of last resort.

42
Q

p value

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43
Q

Odds ratio

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44
Q

odds ratio 2

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45
Q

evidence level

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46
Q

ICH scoring

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47
Q

ASIA scoring

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48
Q

Glasgow Outcome scale

csökken rossz

A
49
Q

mRS

növekszik rossz

A
50
Q

Koos classification

A
51
Q

Koos therapeutical cons

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52
Q

Cholinerg

A