Wednesday, 15 January 2014

Lithium

 

Lithium

FAQ 01

What are the indications for lithium?

We use lithium in the prophylaxis and treatment of mania, prophylaxis of bipolar disorder, as an augmentation strategy for patients with treatment-resistant depression.

What are the common signs of lithium toxicity?

Thirst, polyuria, memory problems, tremor, weight gain, tiredness, diarrhea. Cognitive dysfunction is the most common symptom that leads to non-compliance. Side effects are dose-related.

What is the concentration at which toxic effects reliably occur?

Toxic effects reliably occur at 1.5mmol/l but toxic effects can occur at MUCH LOWER LEVELS in many patients, especially in older patients, systemically ill patients, and in use of alcohol or other CNS active meds

What are the two systems lithium causes the most damage to?

Thyroid and kidneys

What are the differences between the brands of lithium?

There are differences in bioavailability, and recommendations are to keep to the patient on the same brand. If it is necessary to change formulations, lithium levels must be monitored closely until a patient reaches a steady state.

What are the distinct forms of lithium found in different formulations?

Tablets have lithium carbonate; liquid has lithium citrate.

How is lithium administered, timing-wise?

We give it as a single daily dose at night. 

When should blood for serum lithium estimation be taken?

12 hours after the last dose. IF you're on liquid then you take the blood before the morning dose.

What can cause increased lithium concentrations?

A low-salt diet, diarrhoea, vomiting, excessive sweating, systemic illness of any origin, renal impairment, NSAIDs, ACE inhibitors, ARBs, diuretics.

Tell me about lithium and surgery?

Lithium is probably safe in minor surgery but is usually discontinued before major procedures and restarted once electrolytes normalize. The following points should be considered if you will take lithium during the period. Lithium prolongs the action of muscle relaxant, electrolyte imbalance can precipitate lithium toxicity, dehydration can too. increased, increased arrhythmia

What is your dose determined by?

Blood levels.

What is the therapeutic range of lithium?

0.4 to 1 mmol/l

What kind of damage does lithium cause to the thyroid?

It can cause both hyper and hypothyroidism.

What is lithium's lag phase?

5–7 days

What are the neurochemical effects of lithium?

It enhances serotonergic activity, reduces cholinergic activity, and inhibits PI and cAMP.

How is lithium transported across the cell membrane?

It is actively transported across membranes using a voltage-sensitive sodium channel and sodium-potassium ATPase.

Tell me about lithium and signal transduction?

It increases inositol monophosphate. It depletes free inositol. Adrenergic, cholinergic, serotonergic, and dopaminergic receptors are coupled to Pi turnover in the CNS. There is possibly a compensatory stabilization of biogenic amine imbalance. cAMP accumulation is inhibited. All of this is mediated by G proteins. Chronically, it may have effects through protein kinase C and expression of neuromodulators and components of secondary messenger systems.

Tell me about lithium's mechanism of action?

It affects serotonin precursor uptake, synthesis, release, storage, catabolism, receptors, and receptor effector interaction primarily presynaptically. It increases DA turnover, decreases DA formation, decreases striatal DA activity. Facilitates the release of NA through presynaptic autoreceptor. Stimulates Ach synthesis and release.

What percentage of people relapse when on lithium? What percentage relapse on a placebo?

34% relapse on lithium while 81% relapse on placebo.

What percentage relapse and after abrupt termination of lithium?

50% relapse within 5 months.

What can reduce the risk of relapse when you stop the lithium?

Tapering slowly

What percentage of bipolar patients will show an inadequate response to lithium alone and will require the addition of ADT or anticonvulsant?

50%

What patterns of bipolar show reduced the efficacy of lithium?

Rapid cyclers or mixed states. Personality disorders and substance abuse are also associated with poorer response.

Is MDI better or DMI better in lithium treatment?

MDI pattern which is preceding depression responds better to lithium while DMI which is when you get severe episodes of depression don’t respond as well.

How long does lithium take to work in bipolar depression?

3–4 weeks

What percentage of bipolar patients respond to lithium as an antidepressant vs how many unipolar patients respond to it as an antidepressant?

79% of bipolar patients and 36% of unipolar patients.

What percentage of treatment-refractory patients respond to lithium augmentation?

50%

What other ailments is lithium used to treat?

Schizoaffective disorders, cluster headache, preliminary use in HIV treated patients with zidovudine.

Give me the side effects of lithium by the system?

Neuromuscular: fine tremor, slowed cognition. GI: Nausea, diarrhea, weight gain. Thyroid: hypothyroid, hyperthyroid, raised TSH. Cardio: ST and T-wave changes, sinus Brady, T-wave depression. Renal: polyuria and polydipsia, diabetes insipidus, interstitial nephritis

Why does lithium cause organic damage?

Because of its accumulation and action of lithium on ion transport, second messenger, and receptor signaling systems.

Tell me all about lithiums damage to the thyroid?

It inhibits hormone synthesis and releases and inhibits the action of TSH. TSH induced hypothyroidism occurs between 5–35%. More common in females, 30% have elevated TFTs.

Give me lithium's important drug interactions?

Diuretics (loops<thiazide) increase lithium levels. Caffeine discontinuation can increase levels of NSAIDs to reduce Li clearance. Neuroleptics plus lithium worsen EPSEs.

What teratogenic effects does lithium have?

It has teratogenic effects on the cardiovascular system in the first trimester. Ebstein's anomaly.

What levels do you want lithium at?

0.6–0.8 in maintenance level 0.8–1.2 in an acute manic state.

How do you introduce lithium?

400–600mg given at night, increased weekly depending on serum monitoring to a maximum of 2g.

Describe the monitoring of lithium?

Check lithium level seven days after starting and seven days after each change of dose. Take blood samples 12 hours post-dose. Once the therapeutic serum level has been reached, continue to check lithium level/eGFR every three months and TFTs every six months. Keep an eye on the weight!

What are the side effects of lithium?

Fine tremor, Sedation impaired coordination  GI disturbances polyuria (more urine) Polydipsia (more thirsty)

 What are Signs of toxicity?

Lack of appetite Diarrhoea and vomiting  Blurred vision Marked tremor Drowsiness and confusion Slurred speech

What are the Interactions?

Diuretics, NSAIDS, HAloperidol, carbamazepine , antidepressants , ACEi,s ARBSs

How to counsel a  Patient?

Carry lithium cards will need regular blood tests. Be way of buying otcs, speak to pharmacist Maintain fluid and sodium intake. Women of childbearing age should use contraception to stay on the same brand should only be initiated in secondary care 

Monitoring?

Having a serum lithium concentration took 12 hours after the first dose. routine serum lithium Concentration took after initiation and after each dose change until stable and then every three months.

What type of medication is lithium? 

Mood stabilizer 

What is lithium used to treat? 

Gold standard preferred treatment for mania. 

What is the normal lithium blood serum level? 

0.6 – 1.2 millimoles per litre (mmol/L).

What are the short term adverse effects of lithium? 

Polyuria and polydipsia weight gain nausea and vomiting fine tremor headache metallic taste lethargy acne. 

What are the long term adverse effects of lithium?

Hyper or hypothyroidism kidney problems mild cognitive impairment and memory problems. 

What are the long term adverse effects of lithium?

Hyper or hypothyroidism kidney problems, mild cognitive impairment and memory problems. 

Why do patients taking lithium need to stay hydrated?

Because lithium interferes with regulating water and sodium dehydration, which worsen thyroid and kidney problems , 

What lithium concentration may show lithium toxicity?

1.5–2.0millimoles per liter (mmol/L). Lithium toxicity can also happen in therapeutic ranges (esp in the elderly) 

What are the symptoms of lithium toxicity?

Blurred vision, Vomiting, and diarrhoea, Coarse tremor, Muscle weakness, Confusion, Sluggishness, Ataxia, Dysarthria.

How/when would you monitor lithium blood serum levels?

If lithium toxicity signs are clear 5 days after starting restarting changing dose weekly during acute treatment then every 3 months once mental state and lithium levels are stable 

What diet would someone with lithium be on?

Regular diet with normal sodium and adequate fluid intake 

What is the side effect of sodium valproate?

Alopecia (hair loss)

Adverse effects of lithium?

Polyuria, Polydipsia, Weight Gain and Edema, Metallic Taste, TREMORS, Orthostatic Hypotension

Lithium has what effect during pregnancy?

Teratogenic

Lithium and NSAIDs cannot be given because?

NSAIDS causes lithium, Toxicity.

Lithium causes GI upset and should be taken with?

Food

They must avoid what type of beverages?

Caffeinated drinks

To which class of medications does lithium belong?

It is a mood stabilizer.

What conditions is lithium used to treat?

Used to treat bipolar disorder. Reduces frequency and severity of mania. It helps relieve depression, but more effective in treating mania. It helps to reduce the risk of suicide. Stabilises mood.

How long does it take to see results?

Takes up two weeks before seeing results.

Why are the Blood tests regularly taken?

because of the effect on kidneys and thyroids.

 What is the mechanism of action of lithium?

Though lithium is an effective way to treat bipolar disorder, it is still not clear how it works exactly. But studies have shown lithium affects the excitatory neurotransmitter, glutamate. Lithium changes inward and outward currents of glutamate receptors to help the body keep a healthy level.

What is the route of administration of lithium?

Oral

Side Effects?

Headaches. Nausea. Diarrhea. Excessive Vomiting. Weakness or Muscle Fatigue Tremor. Ataxia. Muscle twitches. Seizures. Coma.

Acute and Chronic Toxicity Acute?

Intentionally or accidentally taking too much lithium Chronic. Taking Lithium every day for a lengthy period. 

Withdrawal Symptoms?

Studies have shown there are no withdrawal symptoms. There is usually no case of addiction when using lithium.

Schedule of drugs?

Not subjected to the controlled substances act, so not a federally scheduled drug.

What is the therapeutic range for lithium?

0.4 to 1 millimole per litter (mmol/l) is the normal therapeutic range. It is 0.8 to 1 millimoles per litter for acute episodes of mania or patients who have previously relapsed.

Can you enlist four tests for the monitoring of lithium?

Serum lithium concentration, renal function (baseline and every six months), cardiac function (before initiation and every six months, same for thyroid), thyroid function.

Lithium route of elimination?

It has a renal excretion, freely filtered at glomerulus with an eighty percent reabsorption rate. 

Enlist ten warning signs for lithium? 

Increasing Gastrointestinal (GI) disturbances (V&D)  Visual disturbances (e.g. blurred vision). central nervous system (CNS) disturbances (drowsiness, unsteadiness, confusion). Fine tremor (and worse)  incontinence, polyuria serum concentration over two millimoles per liter (mmol/L)  leading to seizures, coma, renal failure, arrhythmias, blood pressure changes, circulatory failure, sudden death, hypothyroidism renal dysfunction (polyuria and polydipsia) and benign intracranial hypertension (e.g. persistent headache and visual disturbance).

Enlist six counseling points for lithium?

See the doctor if any of the warning signs occur. Advise patients of staying on the same brand of lithium carbonate. Maintain constant water and salt intake (especially during hot weather and infection). Advise patients on interactions of lithium with over-the-counter (OTC) medications and to avoid alcohol. Do not stop lithium unless the doctor told you otherwise. 

List ten drugs that have increased risk of toxicity when lithium is comorbid with them?

Mainly any drugs that affect renal output: Angiotensin-converting enzyme (ACE) inhibitors, angiotensin-2 antagonists, loop diuretics, thiazides, Non-steroidal potassium-sparing diuretics, aldosterone antagonists, metronidazole, SSRIs, tricyclics. L.A.S.T. T.A.N. M.A.P.

With which drug, there is an increased risk of ventricular arrhythmias when lithium is given? 

Amiodarone

List five medications with which there is an increased risk of neurotoxicity when given with lithium alongside? 

Methyldopa, phenytoin, carbamazepine, diltiazem, verapamil MPCDV 

Increased risk of extrapyramidal side effects when lithium is given alongside these drugs? 

Clozapine, haloperidol, sulpiride, phenothiazines, risperidone, flupentixol, zuclopenthixol.  Mnemonic: CH(ie)FS  PR(e)Z

Safety of lithium in pregnancy? First, second, third trimester?

First trimester: Avoid due to teratogenicity, including cardiac abnormalities. Second and third trimester: Dose requirements are increased during the second and third trimesters, which return to normal after delivery.

Can mothers breastfeed while on lithium treatment?

lithium is present in breastmilk and can cause toxicity in the infant.

When should lithium concentration be monitored in regards to the last dose?

Twelve hours after the last dose.

How often should we carry out serum lithium tests when starting treatment?

Weekly after initiation and, after each dose change, weekly again.

How often should serum lithium be tested once a patient has achieved maintenance therapy?

Every three months, unless a patient develops the intercurrent disease, or has a significant change in sodium or fluid intake.

How should lithium be stopped?

Reduce gradually over four weeks to three months to lessen the risk of relapse.

What to do if the patient must stop lithium immediately, e.g. due to severe renal failure? 

Change to atypical antipsychotic or valproate.



Date: 02/06/2020

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Friday, 11 January 2013

Electroencephalography (EEG) Interpretation of Waves, including Sleep Waves, Effects of Medications and Neurological Conditions

Electroencephalography (EEG)

Electroencephalography (EEG) is a non-invasive electrophysiological method to measure the electrical activity of the brain. We can compare it with echocardiography of the heart that measures the electrical activity of the heart.

EEG measures voltage fluctuations resulting from ionic current within the neurons of the brain. Clinically, it refers to the recording of the brain's spontaneous electrical activity over a period, as recorded from multiple electrodes placed on the scalp.

Diagnostic features

Event-related potentials: These investigate potential fluctuations time-locked to an event, such as 'stimulus onset' or 'button press'.

Spectral content: This analyses the type of neural oscillations (popularly called "brain waves") that can be observed in EEG signals in the frequency domain.

 

Uses

Most often we use EEG to diagnose epilepsy. It is also used to diagnose

1.       Sleep disorders

2.      Depth of anaesthesia

3.      Coma

4.     Encephalopathies

5.      Brain death.

 

In the past, they would use it to diagnose tumours, stroke, and other focal brain disorders.

Interpretation of Waves

Delta waves

These are 1-4 Hz waves which we can detect frontally in adults, posteriorly in children, and during slow-wave sleep and in babies. These waves should not be present when awake; presence while awake strongly suggests pathology. 

Theta waves

4-8Hz, generalised. Young children, drowsy and sleeping adults, with certain medications, meditation. We see a small amount in awake adults, an excessive amount when awake may show pathology. Theta waves have a 4-7 Hz frequency. Transient theta components encountered in 15 % of the normal population.

Alpha waves

These are 8-12 Hz waves that we identify posteriorly when the subject is relaxed and when the eyes are closed whilst awake.

Beta waves

12-30Hz, frontally. When busy or concentrating. principally fronto-lateral. Anxiety, alcohol, and drugs (barbiturates, benzodiazepines may enhance these)

Sigma waves

12-14Hz, frontal and central regions 

Sleep spindles 

Bursts of oscillatory activity that occur in stage 2 sleep. Along with K-complexes, they are the defining characteristic of stage 2 sleep.

Gamma waves

30-100 Hz. Meditation

Alpha (8-13 Hz):

These are prominent over the occipital region. Alpha waves are accentuated by eye-closure.  Attention attenuates them. A consistent difference of 1 Hz or more between hemispheres is pathological. We see slowing in early phenytoin toxicity.

Mu waves

These are arch-like, 7-11 Hz waves that we can notice over precentral areas—which are the motor areas. Mu waves relate to motor activity. They are attenuated by contralateral limb movements and increase when a person is at rest.

Lambda Waves

Lambda waves are single sharp waves that we see in the occipital region on the electroencephalograph. Usually, these are associated with visual ‘scanning’ and is related to ocular movements during visual attention. These occurs when eyes are open.

Vertex waves:

Vertex waves are electronegative sharp waves over the vertex that an auditory stimulus evokes.


Electroencephalographic Findings in Neurological Conditions

 

Sporadic CJD

In patients with sporadic CJD, early-on there are nonspecific slowing. Later in the course, they may have periodic biphasic and triphasic synchronous sharp wave complexes superimposed on a slow background rhythm.

 

Delirium

In patients with delirium, there is a diffuse slowing of background activity, decreased alpha, increased theta and delta activity. The diffuse slowing correlates inversely with the severity of the clinical symptoms.

 

Epilepsy

Initial interictal EEG is abnormal in 50-75 %, with repeated recordings, 90-95 % will show abnormalities. 2 % of the normal population have abnormalities considered to be epileptiform.

Absence seizures

Generalised, bilateral, synchronous, 3 Hz spike-and-wave pattern occurs in children and 4 Hz spike-and-wave in juveniles with absence seizures.

Generalised epilepsy Primary generalized tonic-clonic seizures:

Bursts of sharp spikes (25-30 Hz) and wave pattern during the ictal stage is diagnostically significant for generalized epilepsy. There is 10 Hz fast activity during the tonic phase and lower-frequency spike and wave complexes during the clonic phase. Generalized-slowing delta-range characterizes the postictal stage.

Partial epilepsy

In people with partial or focal epilepsy, focal spikes or sharp waves occur during the interictal state. When the patient is seizing, focal rhythmic discharges and periodic complexes occur.  

Myoclonic epilepsy

Generalised polyspike and wave activity. This can help for example, in patients who are on clozapine, where myoclonic seizures often develop before they proceed to generalised seizures.

 

 

Encephalopathy: Diffuse slowing

Delirium Tremens: Compared to delirium due to other causes, patients with delirium tremens have a hyperactive trace, fast activity.

Alzheimer's disease: Reduced alpha and beta, increased delta, and theta

Huntingdon’s Disease: In Huntington’s disease, patients have low-voltage waves and there are no alpha waves (flattening).

Normal ageing: Diffuse slowing, which can be focal or diffuse, if focal most seen in the left temporal region

polymorphic, arrhythmic, unreactive delta, periodic lateralized epileptiform discharges

Herpes simplex encephalitis

CJD (in late stages)

subacute sclerosing panencephalitis

Triphasic waves

liver, renal hypoxia, or metabolic encephalopathies

Frontal intermittent rhythmic delta activity (FIRDA)

metabolic encephalopathy

brain stem dysfunction

 

Alpha coma

Diffuse lesions

Rhythmic slowing, occasionally periodic discharges, Widespread, non-reactive alpha-range activity

Generalised encephalopathy

Burst suppression, High-voltage bursts, followed by periods of extreme suppression. Occurs within bi-hemispheric insult and deep anaesthesia

Personality disorder: increased slow waves (theta) in 31-58 % of psychopaths. Changes more right-sided ‘positive spike’ seen in 40-45 % of aggressive and impulsive psychopaths

Anxiety: Increased beta activity

Hypnosis: Like the normal relaxed, waking state

 

 

Effects of Medications on Electroencephalography Rhythms

Medication

Effect

Typical antipsychotics

Diffuse slowing (a)

Antidepressants

Slowing alpha waves, reduction of beta waves; increase other waves

Atypical antipsychotics

They have variable effects (b)

Lithium

Slowing

Benzodiazepines

Increase beta, decrease alpha (d)

Barbiturates

Increase beta

Stimulants

Increase alpha

Depressants

Decrease alpha

Cannabis

Increase alpha

Chlorpromazine

Increased delta, decreased beta

Phenytoin

Slowing of alpha

Benzodiazepines

Increased fast wave (beta) activity

Alcohol

Increased beta (i.e. Fast wave)

Carbamazepine

Increased fast wave

a) Which can be focal or diffuse, if focal most seen in the left temporal region

b) Clozapine has the most significant effect while quetiapine least has the significant.  Clozapine > Olanzapine > Risperidone > Typical > Quetiapine

i.e., increases the slow-wave activity

Sleep Waves on Electroencephalography

Stage 1

In stage 1 sleep, alpha waves disappear while desynchronised theta and delta activity appear. 

Stage 2

Low-voltages and delta waves with sleep spindles and K complexes are the characteristic waves that occur during this stage. 

Stage 3

High-voltage slow-waves appear during stage 3 of sleep. Less than 50% are delta waves. Sleep spindles and K complexes diminish.

Stage 4

During this stage, which we also know as slow-wave-sleep, delta waves grow over 50%.  Sleep spindles and K complexes absent.

Electrode Placement

We place electrodes according to the International 10-20 System, which entails measurements from:

  1. The nasion
  2. The inion
  3. The right auricular depression
  4. The left auricular depression

 

sphenoidal electrodes (between the mandibular coronoid notch and the zygoma) can obtain readings from the inferior temporal lobe

nasopharyngeal leads (in the superior part of the nasopharynx) can get readings from the inferior and medial temporal lobe

Wave characteristics

Amplitudes range from 5 to 150 μV

Frequencies range from 1 to 40 Hz

Spikes are transient tall peaks that last less than 80 ms

 

Sharp waves rise rapidly, fall more slowly, and last over eighty milliseconds

Frequency ranges

 

Normal Electroencephalographic findings

Infants have slower and higher amplitude rhythms. Initially, this is asynchronous and easily disturbing; mature rhythms develop between 2 and 6 years. Adults usually show either alpha posteriorly or beta anteriorly, but generalised low-amplitude beta may be present. 

These are present in all populations by puberty. When the subject is drowsy, alpha becomes intermittent and theta appears. In old age, alpha frequency slows, and delta activity is lower. 

 

 

What are the benefits of electroencephalography (EEG)


It has excellent time-resolution. Cognitive, perceptual, linguistic, emotional, and motor processes are fast and dynamic. For example, consider theta-band (4-8 Hz), rhythm but quiet for our conscious experience. Or consider gamma (30-80 Hz). A direct indicator of neuronal activity Multidimensional (time, space, frequency, power, phase (temporal), connectivity. Portability (observing the brain in action). Inexpensive + advanced analysis techniques on time series, e.g. single-trial classification methods using Fourier transform.


Limitations of EEG


It is not well-suited for precise functional localization. It is not well-suited for measuring deep brain structures (e.g., putamen, thalamus, nucleus accumbens). Sub-optimal method:  in the brain, where does process X occur or is information Y stored. It is also not very well-suited to study very slowly fluctuating process 'infra-slow' with uncertain and variable time course (but fMRI is)from Joy Interpretation issues:1) suffers from interpreting null results absence of proof is not the proof of absence.> ERP does not reveal all of EEG information (single trial)>  ERP does not capture non-phase locked responses2) ERP limited opportunity for linking results to actual neurophysiological dynamics > ERP less understood than oscillatory (is formed) and synchronous.


What type of neuronal activity does EEG capture?


postsynaptic potentials as opposed to action potential


What does EEG reflect?


EEG reflects the differences in electrical potential over time, created by the current flows originating from neuronal populations


What are chemical synapses?


Chemical synapses cause local changes in postsynaptic membrane potentials, through neurotransmitters. Information transmits with some delay about a millisecond.


What are the electrical synapses?


Electrical synapses or gap junctions. Ions flow directly through large channels into adjacent cells, with no time delay.


What is Postsynaptic Potential (PSP)?


An electrical potential started at a postsynaptic site that can vary in amplitude and spreads passively across the cell membrane, decreasing in strength with time and distance.


How is a postsynaptic potential generated?


When AP reaches the presynaptic axon end, it releases a neurotransmitter into the synaptic cleft. The neurotransmitter binds to the receptor of the postsynaptic neuron by opening or closing an ion channel. This led to a graded change in membrane potential.


What two types of postsynaptic potential are there?


Two types of PSP Excitatory PSP (for excitatory synapse)


Inhibitory PSP (for inhibitory synapse)


what it requires for a postsynaptic neuron to fire?


A postsynaptic neuron will fire an action potential if a depolarization that exceeds the threshold reaches its axon hillock. It requires the combined effect of many excitatory synapses for a postsynaptic neuron to fire.


What are the two types of summation?


spatial and temporal


What is the spatial summation?


Is the summing of potentials that come from distinct parts of the cell? If the overall sum of EPSPs and IPSPs can depolarize the cell at the axon hillock, an action potential will occur.


What is temporal summation?


Temporal summation is the summing of potentials that arrive at the axon hillock at contrasting times. The closer together in time that they arrive, the greater the summation and possibility of an action potential.


What are EEG signals then?


EEG signals are primarily produced by the summation of postsynaptic potentials of millions of neurons summed millions of neurons/ firing in phase aggregated millions of PSPs 'note: EEG does not measure action potential


How is the AP aligned?


geometrically and in phase


What is EEG less sensitive to?


It is less sensitive to deep brain structures. Field strength decreases exponentially with distance. Neuronal populations in deeper structures are not arranged in a geometrically parallel fashion.


What EEG cannot measure?


It cannot measure individual molecular or synaptic events, nor it can isolate events that are produced by a specific neurotransmitter or neuromodulator. It is not very suitable to measure to slow (< 0.1 Hz) or very high (> 100 Hz) fluctuations.


What are electrodes made from?


Silver electrodes with a thin coating of silver- chloride, Tin Electrodes, Gold-cap Electrodes


The conductivity should be good between the electrode and the scalp, how?


Gel to reduce the impedance/resistance “Impedance below 5 Kilo Ohms Scalp preparation (removal of dead skin cells)also: Active Electrodes Integrated preamplifier.  Faster preparation time.


How many electrodes?


Traditional 19 Standard 32-64 (sufficient). High-density 128-256 (or more)


What are the pros of having more electrodes?


better spatial sampling better source reconstruction


What are the cons of having more electrodes?


long prep time electrolyte bridge poorer signal quality


What is an electrolyte bridge?


When the gel creates a short circuit between closely placed electrodes.


It amplifies the signal. Why and using what?


It amplifies the signal from a few ¼ Volts to a few Volts. The amplification is done by Differential Amplifiers.


What electrodes are associated with amplification?


Three electrodes: Active Electrode (A) placed at the desired site. Reference Electrode (R) placed elsewhere on the scalp Ground Electrode (G) placed elsewhere on the scalp/body. Elimination of ambient noise • Works best when impedances are the same (low) for A and R• Amplifier gain: 5-10 Ka. The optimal gain depends on the input potential and output range.


What are the usual reference sites?


Preferably a neutral site (tip of the nose, the earlobes, the mastoids, the chin, etc). Three practical criteria: Choose the site that is convenient and comfortable. Choose a site that does not induce hemispheric bias. Choose a site used by other researchers in your fields. Mostly used neutral references: the average of two earlobes average of two mastoids. Other referencing scheme: “Average of all electrodes Current source density maps Reference free method. Requires high-density recordings€¢ Less accurate for boundary electrodes Insensitive to deep sources Laplacia


What is aliasing?


When we are sampling a system (brain) with a sampling freq less than twice the maximum freq of interest. Because we monitor frame by frame - but at what rate? If it is not as fast as the original, then it is a POOR representation, as we haven't sampled enough to capture the information in the actual sample. Nyquist Criterion - sample at least twice as fast as the maximum freq (Sampling frequency (fs) should satisfy Nyquist Criterion fs > 2 fmax (fmax max. frequency of interest)This can be something like x5 the maximum - if we want to do alpha etc.


Why would we need to filter the signal?


to reduce artifacts


What filters are applicable?


Low pass High Pass Band pass band stop, notch


What is a high-pass filter?


0.5 Hz (or 0.1 Hz for slow brain responses)


What is a low-pass filter?


100 Hz


What is a notch filter (band stop)


50 Hz (for removing power line noise; 60 Hz in the USA)


We need to xxx analogue to xxxx


convert - digital


what resolution is EEG


16/24 bit Resolution (216 or 16192 different voltage values can be coded by the ADC)


What is aliasing?


When we are sampling a system (brain) with a sampling freq less than twice the maximum freq of interest.Because we monitor frame by frame - but what rate? If it is not as fast as the original, then it is a POOR representation, as we haven't sampled enough to capture the information in the actual sample.Nyquist Criterion - sample at least twice as fast as the maximum freq (Sampling frequency (fs) should satisfy Nyquist Criterion fs > 2 fmax (fmax   max. frequency of interest)This can be something like x5 the maximum - if we want to do alpha etc.


Why should we avoid aliasing?


Ro get a faithful representation of our sample


What should the sampling frequency satisfy?


Sampling frequency (fs) should satisfy Nyquist Criterion fs > 2 fmax (fmax   max. frequency of interest)


For an EEG signal with a maximum frequency of 70 Hz, aliasing occurs when. A fs 256Hz B. fs 1024 Hz C. fs 512Hz D. fs 128 Hz


128


What are EEG artifacts?


Problems in the EEG signal that need reducing/eliminating.


What are the 5 main artifacts?


1) Saccades 2) EMG (mastoid/jaw muscle/face muscles)3) EKG (pulsation of the heart)4) Skin potentials (leading to blocking)5) Alpha waves (mind wandering etc)


What is the brute force approach to rejection?


Brute force approach: Reject if over threshold (75-100 μV) as the brain doesn't create these frequency artifacts usually have much larger amplitude


Other factors in artefact rejection?


Blink (Check vEOG, Topography, Polarity) -measure the diff• Eye movement (Check hEOG, Step-like wave) - measure the diff• Electrode shift (Shifting of potentials)• Muscles (High frequency) beta - gamma Heart (Mostly in mastoid electrodes, Low frequency)


Three issues with artifact rejection?


Loss of a significant portion of data. Some participants are very prone to certain artifacts • Some tasks essentially call for artefacts. We lose TOO many trials


What is the alternative to artefact rejection?


artifact correction


What are the simple methods for artifact correction?


Subtraction method (variance-based) Filtering


What are the advanced methods for artifact correction?


Mathematical approaches:1) Dipole/Source modeling procedures2) Independent Component Analysis (ICA)


A brief description of Independent Component Analysis (ICA)?


a computational method to separate the sources of artifacts -  identifying the troublesome parts by certain characteristics and individual weights - then reverse the weights (reducing artifacts)


how to practically minimize Artifacts?


Electrical screening of the testing space (Faraday cage). Careful instruction of participants to minimize movement; blink pauses. Ensuring the participants in a relaxed condition (to reduce muscle activity). Careful electrode application to minimize impedance. Maintaining the cool temperature and low humidity level inside the lab (to reduce slow drift). Filtering (e.g., high-pass filter to remove slow-shifts [i.e.,low-frequency fluctuations in the EEG], and low- pass filter to avoid aliasing band-pass filter)


What are the 5 standard frequency bands?


Delta: < 4 Hz Theta:4-7Hz Alpha: 8-14 Hz Beta:15-30Hz• Gamma > 30 Hz5 frequency bands (FRE BAND in THE GAY BED)


What is the Fourier Analysis?


Transformation of the EEG into sine (sinusoidal) functions of various frequencies like a freq histogram (strength of particular freq)


What does Fourier Analysis lead to?


Leads to a power spectrum: power as a function of frequency


What are the applications of spontaneous EEG


Cognitive Research. Experiments with long-duration stimuli (i.e. task requiring sustained attention, ecologically appropriate stimuli)> Perhaps Mind-wandering? Monitoring sleep stages.  Clinical Research.  Epilepsy. Detection of seizures.  Localization of focus/foci. Prediction of seizure onset. Monitoring the level of anesthesia. Detection of brain death. Measurement of drug effects. Detection of cerebral pathology, e.g., through blood supply problems. Sleep disorders. Almost all neurological disorders have EEG correlates.


What is an event-related potential / evoked-potential?


The general class of potentials displaying a stable time relationship to a definable reference event.


What is an ERP reference event?


Reference event Onset/offset of a stimulus Motor response Decision moment. 


Who uses the term EP and who ERP Terminology?


EP: Perception and clinical research. ERP: Experimental cognitive research.


What characterizes an ERP?


ERPs are waveform characterized by a series of positive (P) or negative (N) deflections at different latencies  ERP Components Exogenous Components: Modulated by external characteristics of stimuli Endogenous Components: Modulated by internal characteristics


What is the ERP hypothesis?


ERP Hypothesis: ERP is a signal (s) that appears superimposed and without interaction on the background or ongoing EEG, which is considered random noise (n).


Assumptions of ERP?


ERP is uncorrelated with background EEG. Background EEG is random. ERP is invariant across trials (same ERP is repeated over trials - take the average as invariant) • Background EEG varies (randomly) from trial to trial. 


So how do we get an ERP?


Signal averaging


How does signal averaging work then?


After averaging across trials, the noise will cancel out and only the event-related EEG response will remain. Background signal cancels out and leaves with the ERPs, which are invariant.


What are the advantages of ERP?


ERPs are simple, fast to computed ERPs require very few analyses or parameters. ERP has high temporal precision and accuracy. ERP literature is quite mature. ERP provides an excellent quality check.


What is an ERP component?


We can simply define an ERP component as one of the component waves of the more complex ERP waveform. So one part could be the One and another the Pe. An ERP component is a part of a waveform with a circumscribed scalp distribution (physiological substrate) and a circumscribed relationship to experimental variables (functional substrate).


What is an example of an ERP component?


Examples: MMN (mismatched negativity, 160-220 milliseconds at central sites) N170 (face-related potential at occipital sites)


Why do we study ERP components?

Common language linking diverse experiments, paradigms, etc 2. The base for integrating ERP with other measures of brain activity 3. Structure-function information


What is the baseline period?


In averaging, all trials are set (arithmetically)to have the same zero voltage at stimulus onset, so that only deviations from the baseline voltage are seen in the ERP, after stimulus presentation. if Baseline subtraction (mean of the baseline period is subtracted)


EEG


How many trials for electroencephalography?


As many as possible. The number of trials depends on signal-to-noise characteristics; the effect size and the type of analysis to be performed SNR (signal-to-noise-ratio) increases as a function of the square root of the number of trials. Practical suggestions. 50 trials / condition / participants. Similar number of trials for all conditions. Phase/power produce positive bias with fewer trials). If not possible, match trial count. Select the first N trials from each condition (N-the number of trials in the smallest condition). Select N trials at random. Select N trials based on some relevant behavioural or experiment variable (i.e. reaction time)


What is a VEP?


visual evoked potential


What is an AEP


Auditory evoked potential


What is an SEP


Somatosensory Evoked Potentials (SEP)


What is Contingent-Negative Variation (CNV)


Indicator of learning paired stimuli (Get Set – Go)• Reflection of attention, concentration &amp; readiness to S2 • Index of neuronal excitability


What ERP accompanies semantic violations ?


N400 in Semantic Violations


What accompanies violations in music


ERAN


What are the two major limitations of ERP?


The first concerns interpretational issues, particularly regarding interpreting null results - the absence of proof is not the proof of absence. An ERP reveals little EEG information (single-trial)– ERP does not capture non-phase-locked responses The ERPs provide limited opportunities for linking results to actual neurophysiological dynamics. ERPs are less understood compared to the neurophysiological mechanisms that produce neuronal oscillations and synchrony.


If ERP is evoked activity, what other types of activity are there?


Dynamic Brain Oscillations


And what two types of Dynamic Brain Oscillations are there?


Evoked oscillations have a strict phase relationship regarding the stimulus (every time brain respond same)Induced oscillations do not have a strict phase relationship (not always the same time-varying latency – e.g. (cognitive control / top-down / attention)


So what are the limitations of ERP regarding oscillations?


ERP takes the average (keep the same latency) but induced the response gets lost. The disadvantage as ERP only captures stimulus time-locked relationships.


Dynamic Brain Oscillations advantages


Logical interpretations.  Neurophysiological mechanisms. Ubiquitous oscillations.  Neuronal oscillations are the most promising bridge linking findings from multiple disciplines. Covers a more comprehensive multi-dimensional space. 


Methods for dynamic brain oscillation analysis?


short term Fourier transform of time-frequency time series or wavelet needs freq + time!!!


Oscillations in complex cognition 


then give them a hint ....brain oscillation structure - over occipital-parietal region - when higher (hint couldn't help) but if gamma is lower... then the hint is successfully utilised. Only worked in specific brain states (receptive) characterized by the oscillatory state if alpha was high in temporal - then also was more likely to solve the problem (when we focus on something, gamma increases, when diffuse attention, alpha is high. And for these types of problems, being too focused rarely works.  Need to be open (alpha) not fixed (gamma)so posterior gamma   focused attention (fixation)posterior alpha   diffuse (open to new solution)


Object Perception and feature binding


Gamma Band Synchrony


Visual binding in adults


in gamma band comparing kaniza triangle bind diff features - new perception represented by 40hz  - and is phase-locked


Attention to music in musicians


Gamma SYNCHRONY


Cognitive Insight 


Posterior Beta and anterior Gamma


Aha Moment! 


Posterior Gamma for sudden solutions


Which ERP for Semantic Violations?


N400


Music violations?


MRAN


Early Evoked potentials: AEP –SEP – N10CEP –Chemosensory has no early ERP


later Attention P1 / n1 p2


Early Evoked potentials: SEP


n10


Early Evoked potentials: CEP


Chemosensory has no early ERP


 


 


 

 

 

 

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