Neurophysiology Flashcards
1
Q
Where is an action potential initiated?
A
Axonal hillock
2
Q
How is an action potential initiated?
A
- Synaptic signals received by dendrites and soma
- These signals raise intracellular resting membrane potential from -70mV to -55mV
- Na + channels in axons initial segment open
- Na+ influx causes rapid reversal of membrane potential from negative values to +40mV
- Na+ channels close, k+ channels open
- As K+ ions move out of axon, cell membrane gets repolarized
3
Q
What is the threshold potential?
A
-55mV
4
Q
At what mV do the Na+ channels open?
A
-55mV
5
Q
At what mV do the Na+ channels close?
A
+40mV
6
Q
At what mV do the K+ channels open?
A
+40mV
7
Q
What is a synapse?
A
Junction between 2 cells
8
Q
What types of synapses are there?
A
Chemical
Electrical
Conjoint
9
Q
What are conjoint synapses?
A
They have both electrical and chemical properties.
10
Q
What are electrical synapses?
A
Bring response by electrical communication, without chemical exchange.
11
Q
How do chemical synapses work?
A
Presynaptic neuron releases chemical molecule on stimulation. This molecule acts on next neurone to bring on molecular effect or propagate the impulse further down.
12
Q
What happens to postsynaptic neurons at excitatatory synapses?
A
They are depolarized
13
Q
What does inhibitory synaptic activity do to postsynaptic neurons?
A
Hyperpolarizes them
14
Q
What is facilitation?
A
When postsynaptic changes induced by excitatory synapse is not sufficient to induce action potential but may serve to facilitate likelihood of generating an action potential with further stimulation.
15
Q
What is spatial summation?
A
When additional input from several other presynaptic cells through other synapses lead to an action potential.
16
Q
What is temporal summation?
A
When recurrent stimulation by same synapse results in action potential.
17
Q
What are the centres in the hypothalamus that control feeding?
A
Ventromedial hypothalamus
Lateral hypothalamus
18
Q
Where is the satiety centre?
A
Ventromedial hypothalamus
19
Q
Where is the feeding centre?
A
Lateral hypothalamus
20
Q
What are the neurochemical mediators of increased appetite?
A
Ghrelin
Neuropeptide Y
21
Q
What is the word to describe neurochemical mediators of increased appetite?
A
Orexigenic
22
Q
What is the word to describe neurochemical mediators of satiety?
A
Anorexigenic
23
Q
What are the neurochemical mediators of satiety?
A
Leptin
Cholecystokinin
Serotonin
24
Q
Which orexigenic substance is produced outside of the CNS?
A
Ghrelin
25
Where is Ghrelin produced?
Gastric mucosa
26
How is Ghrelin synthesized?
Adipose cells synthesize leptin
27
How does food affect the hypothalamus?
Food/food cues increase dopaminergic activity in nucleus accumbens (reward centre).
28
What happens to dopamine receptors in obesity?
D2 receptors are reduced in striatum.
29
What are the centres for temperature in the hypothalamus?
Preoptic anterior hypothalamus
| Posterior hypothalamus
30
What is the hypothermic centre called?
Preoptic anterior hypothalamus
31
What is the hyperthermic centre called?
Posterior hypothalamus
32
What happens if the preoptic anterior hypothalamus is stimulated?
Parasympathetic-mediated sweating and vasodilation, resulting in hypothermia.
33
What happens if the posterior hypothalamus is stimulated?
Sympathetic drive, shivers and vasoconstriction leading to hyperthermia.
34
What type of lesion reduces diurnal temperature variation?
Lesions in median eminence
35
What causes malignant hyperthermia?
Abnormal excitation-contraction coupling in skeletal muscle.
36
What happens in Neuroleptic Malignant Syndrome?
Hyperthermia induced by neuroleptic use or levodopa withdrawl.
37
Which subcortical centre plays a role in pain?
Thalamus
38
Which fibres carry pain sensation?
Unmyelinated C fibres
| Sparsley myelinated A-delta fibres
39
Where do C and A-delta fibres carry pain sensation to?
Dorsal horn of spinal cord
40
Are C fibres myelinated?
No
41
What happens once pain sensation arrives at dorsal horn of spinal cord?
Fast transmission via lateral spinothalamic route
| Slow transmission via reticulothalamic tract
42
Purpose of transmission of pain along lateral spinothalamic tract?
Aids localization of pain
43
Purpose of slow transmission of pain sensation via reticulothalamic tract?
Aids subjective sensation
44
Which receptors modulate pain sensitivity?
Opioid receptors in dorsal horn + periaqueductal grey matter (brain stem)
45
Which fibres modulate pain perception?
Descending fibres from serotonergic raphe nuclei
46
How does thalamic pain syndrome occur?
Stroke involving thalamoperforating branches of posterior cerebral artery.
47
Signs of thalamic pain syndrome?
Contralateral loss of sensation with burning or aching pain triggered by light cutaneous stimulation.
48
Which parts of the brain are involved in thirst?
Subfornical organ
Organum vasculosum of the lamina terminalis
Hypothalamic paraventricular nucleus
49
Which neurotransmitter is used to propagate thirst signals?
Angiotensin II
50
Where do neurotransmitters propagate thirst signals to?
Hypothalamus
51
How does hypotension stimulate thirst?
Via baroreceptors on aorta and carotid
52
Organic/anatomical cause of SIADH?
Damage to paraventricular and supraoptic hypothalamic nuclei
53
What causes Kluver-Bucy syndrome?
Bilateral lesions of amygdala and hippocampus
54
Symptoms in Kluver-Bucy syndrome?
Decreased aggressive behaviour.
Prominent oral exploratory behaviour and hypersexuality.
Hypermetamorphosis (objects repeatedly examined as if novel)
55
What is the cause of Laurence-Moon-Biedl Syndrome?
Autosomal recessive with genetic locus at 11q13 in most cases
56
Symptoms in Laurence-Mood-Biedl Syndrome?
```
Obesity
Hypogonadism
Low IQ
Retinitis pigmentosa
Polydactyly
Diabetes insipidus
```
57
Cause of Prader-Willi syndrome?
Reduced in oxytocin neurons and satiety neurons noted.
| Associated with paternal deletion (genomic imprinting) at 15q11-q13.
58
Signs in Prader-Willi syndrome?
```
Hypotonia
Obesity with hyperphagia
Hypogenitalism
Short stature
Impaired glucose tolerance
Abnormal control of body temperature
Daytime hypersomnolence
```
59
Cause of Kleine-Levin syndrome?
Hypothalamic abnormality sometimes preceded by viral illness - often resolves by third decade of life.
60
Signs in Kleine-Levin syndrome?
Compulsive eating behaviour with hyperphagia, hypersomnolence, hyperactivity, hypersexuality, exhibitionism.
61
Where is active nerve cell production seen in early fetal lfe?
Subventricular zone - around ventricles of neural tube.
62
What happens to neurons produced in subventricular zone?
Migrate out towards cortical plate.
63
In neurogenesis, what happens to thalamic axons?
Thalamic axons that project to cortical plate synapse on a transient layer of neurons called subplate neurons.
These axons then detach from subplate neurons and synapse on true cortical cells.
Subplate neurons degenerate.
64
What happens to thalamic axons in schizophrenia (occasionally)?
Abnormal persistence of subplate neurons, suggestive of failure of axonal path-finding.
65
Where does neurogenesis in adults particularly take place?
Dentate gyrus of hippocampus
| Olfactory bulb
66
What reduces hippocampal neurogenesis?
Stress
67
What increases hippocampal neurogenesis?
Enriched environments
Exercise
Antidepressants
68
When does neuronal migration take place?
First 6 months of gestation
69
What are the types of neuronal migration?
Radial
| Tangential
70
What is radial migration?
Primary mechanism by which excitatory neurons reach cortex.
Radial glial cells form scaffolding through foot processes to guide migrating neuronal cells.
Successive populations f migrating neurons travel past previously settled neurons to form radial stacks of cells.
71
What is the radial stack of cells created in radial migration called?
Rakic's cortical columns
72
What is tangential migration?
Most inhibitory interneurons in external and internal granular layers migrate tangentially.
73
What is heteropia?
Abnormalities in neuronal migration due to neurons failing to reach cortex and residing in ectopic positions.
74
When does myelination begin?
4th gestational month
75
When is myelination complete?
2 years postnatal
76
When does myelination reach its full extent?
Late in third decade of life
77
When does synaptogenesis occur rapidly?
From second trimester through to the first ten years of life.
78
When is the peak of synaptogenesis?
First 2 years postnatally.
79
When does synaptic pruning occur?
After mid-childhood.
80
What is synaptic pruning?
Synaptic elimination to select and preserve the most useful while eliminating unnecessary neuronal connections.
81
What can we use to study neuronal numbers?
Density of D2 receptors
82
When is density of D2 receptors greater than adult levels?
Before 5 years of age.
83
In which gender is dopamine receptor reduction fastest?
Males
84
Rate of dopamine receptor loss in adults?
2.2% reduction per decade
85
Rate of D2 receptor loss in schizophrenia?
6% loss per decade
86
What disorders are associated with under-pruning?
Autism
87
Where are neurohormones produced which regulate hormones from naterior lobe of the pituitary gland?
Parvocellular neurons of hypothalamus.
88
Where are the two hormones synthesized which are released from the posterior lobe of the pituitary gland?
Magnocellular cells of supraoptic nuclei
| Paraventricular nuclei of hypothalamus
89
What are the two hormones produced by the posterior pituitary?
Vasopressin/ADH
| Oxytocin
90
Which hormones are produced by the anterior pituitary?
```
Grown Hormone
Luteinizing hormone
Follicle Stimulating hormone
Adreno-corticotrophic hormone
Thyroid stimulating hormone
Prolactin
```
91
Which hormones produced by the anterior pituitary are gonadotrophins?
LH
FSH
ACTH
92
What increases GH release?
Exercise
Sleep
Stress
93
What alters the response of GH to GHRH?
Depressin
| Aneroxia
94
What inhibits prolactin release from hypothalamus?
Dopamine
95
What facilitates release of prolactin?
Thyrotrophin releasing hormone
96
During which activities are prolactin released?
Pregnancy
Nursing
Sleep
Exercise
97
How do antipsychotics lead to hyperprolactinaemia?
Remove inhibitory control of dopamine by blocking D2 receptors in tuberoinfundibular tract.
98
What does Vasopressin play a role in?
Attention
Memory
Learning
99
When is vasopressin release increased?
Pain
Stress
Exercise
100
What drugs increase vasopressin?
Morphine
Nicotine
Barbituates
101
What drug decreases vasopressin release?
Alcohol
102
What hormones are released from the hypothalamus?
```
Corticotrophin releasing hormone
Growth hormone releasing hormone
Gonadotrophin releasing hormone
Thyrotophin releasing hormone
Somatostatin
Prolactin inhibitory factor (dopamine)
```
103
Which hormone inhibits growth hormone?
Somatostatin
104
What stimulates secretion of TSH from the pituitary?
TRH from hypothalamus.
105
What stimulates thyroid gland to release T3 and T4?
TSH from anterior pituitary
106
Difference between T3 and T4?
T3 is more biologically potent.
| T4 is converted into T3 by target organs and the brain.
107
What happens if exogenous administration of TRH is given t depressed patients?
Blunted response to TRH
| Increases serotonergic transmission with decreased 5-HT1A sensitivity and increased 5-HT2A sensitivity.
108
What activates nerve growth factor genes in early development?
T3
109
Which MH problem is hypothyroidism implicated in?
Rapid cycling mood pattern in previously stable bipolar
110
What stimulates release of ACTH from anterior pituitary?
CRH from hypothalamus.
111
What stimulates release of cortisol from adrenal cortex?
ACTH from anterior pituitary.
112
What is the Hypothalamic-Pituitary-Adrenal axis?
CRH (hypothalamus) stimulates ACTH (anterior pituitary) which stimulates cortisol release (adrenal cortex) which inhibits CRH and ACTH.
113
What is the hypothalamic-pituitary-adrenal axis involved in?
Stress response
114
What happens to the hypothalamic-pituitary-adrenal axis in chronic stress?
Feedback fails
Continuous excess of cortisol produced, leading to deleterious consequences to hippocampus where there are glucocorticoid receptors.
Decreased hippocampal neurogenesis with atrophy of hippocampal dendrites.
Disrupts long-term potentian and impaired memory performance.
115
What compensations occur if hippocampal shrinkage occurs in chronic stress?
Compensatory increase in dendritic arborization of neurons in basolateral amygdala, contributing to memory bias towards negative events in chronic stress.
116
Cortisol level in Addisons?
High
117
Cortisol level in Cushings?
Low
118
When are cortisol levels at their peak?
6-7am
119
In what MH problem is hypercortisolaemia noted?
Depression
Mania
OCD
Schizoaffective disorder
120
In which MH problems is hypocortisolaemia noted?
PTSD
Chronic fatigue
Fibromyalagia
121
Describe the dexamethasone suppression test
1mg dexamethasone is given at 11pm with baseline cortisol sampling.
Next day, cortisol measured at 8am, 4pm and 11pm.
If any sample as >5mcg/L cortisol, this indicates DST non-suppression - failure of feedback suppression of ACTH/CRH.
122
Which MH problems is DST-suppression seen in?
Depression
| Hypercortisolaemic states
123
What physical conditions can lead to DST non-suppression?
Pregnancy
Severe weight loss
EtOH
Hepatic enzyme inducers
124
What is the epiphysis?
Pineal gland
125
What does the pineal gland contain?
Pinealocytes
| Calcium deposits - more prominent with age - brain sand.
126
What do pinealocytes do?
Secrete serotonin in the day, melatonin at night.
127
Where is the highest concentration of serotonin?
Pineal gland
128
Describe synthesis of Melatonin
Melatonin is synthesized from seretonin by action of serotonin-N-acetylase and 5 hydroxyindole-O-methyltransferase.
129
What regulates melatonin synthesis?
Light-dark cycle
130
What regulates the pineal gland?
Major-beta-adrenergic mechanism
131
What drugs decrease melatonin synthesis?
Beta-antangonists such as propranol
132
What regulates circadian rhythyms?
Melatonin
133
What hormone is increased at the start of sleep?
Testosterone
134
What hormone is increased at slow wave sleep?
GH
| SST
135
What hormone is reduced at slow wave sleep?
Cortisol
136
What hormone is reduced in REM sleep?
Melatonin
137
What hormone is increased in early morning sleep?
Prolactin
138
What happens in circadian rhythm development in first month?
Emergence of 24-hour core body temperature cycle
139
When is progression of nocturnal sleeping noted?
2 months
140
What are melatonin and cortisol rhythms established?
3 months
141
What type of dreams occur in REM sleep?
Illogical
| Bizarre
142
What type of dreams occur in non-REM sleep?
Thought-like
143
What is actigraphy?
used o quantify circadian wake-sleep patterns and detect movement disorders in sleep - uses a motion sensor.
144
What does polysomnography consist of?
EEG
| EMG
145
What can polysomnography help diagnose?
Sleep apnoea
Narcolepsy
Restless legs
REM behavioural disorder
146
What does sleep latency mean in polysomnography?
Time from lights out to sleep onset
147
What does REM latency mean in polysomnography?
Time from sleep onset to first REM episode.
148
What is normal REM latency in adults?
90 minutes
149
What is non-REM latency?
Time from sleep onset to first non-REM episode
150
What is sleep efficiency in polysomnography?
(total sleep time/total time in bed) x 100
151
What is multiple sleep latency test?
Used to assess daytime somnolence and daytime REM onset in narcolepsy.
152
Average length of sleep per night?
7.5 hours
153
How much of adult sleep is N-REM?
75%
154
What is NREM classified into?
4 stages based on increasing amplitude and decreasing frequency of EEG activity.
155
What is slow wave sleep?
Stages 3 and 4 of N-REM sleep.
156
What happens in Stage 1 NREM?
Drowsy period.
Low voltage theta activity, sharp V waves.
5% of sleep
157
Voltage activity in Stag
period.
| Low voltage theta activity, sharp V waves.
158
What % of sleep is Stage 1 NREM?
5%
159
What happens in Stage 2 NREM?
45% of sleep
| Development of sleep spindles and K complexes
160
What happens in Stage 3 sleep?
12% of sleep
| <50% delta waves
161
What happens in stage 4 NREM?
13% of sleep
>50% delta waves
Physiological functions at lowest
162
Features of NREM sleep
Increased parasympathetic activity - low HR and systolic BP, RR, cerebral blood flow.
Abolition of tendon reflexes.
Upward ocular deviation with few or no movements
Reduced recollection of dreams if awakren.
163
Is sleep terror NREM or REM disorder?
NREM
164
How much of adult sleep is REM?
25%
165
What characterizes REM sleep?
Darting eye movements, other muscles paralysed.
| High level of brain activity and physiological activity similar to those in wakefulness.
166
What happens in REM sleep behavioural disorder?
Muscular paralysis does not occur, resulting in violet movements coinciding with brain activity.
167
What does EEG show in REM sleep?
Low-voltage, mixed frequency (theta and slow alpha) activity similar to awake state.
Sawtooth waves.
168
How many episodes of nonREM/REM activity does a person cycle through in one night?
5 episodes, REM episodes increase in length.
169
Features of REM sleep
Increased sympathetic activity - increased HR, systolic, RR, cerebral blood flow
Autonomic functions active - penile erection/vaginal blood flow
Increased protein synthesis
Maximal loss of muscle tone with occassional myoclonic jerks
Vivid recall of dream if awakened
170
What are sleep spindles?
Waves with upper alpha or lower beta frequency
171
When do sleep spindles mainly occur?
Stage 2
172
Duration of sleep spindles
<1 second
173
What are K complexes?
Large amplitude delta frequency waves, sometimes with sharp apex.
174
Where are K complexes most prominent?
Bifrontal regions
175
Where are K complexes mediated from?
Thalamocortical circuitry.
176
When do K complexes occur?
When patient is aroused partially from sleep.
177
What is arousal burst?
When runs of generalized rhythmic theta waves follow K-complexes.
178
What are V waves?
Sharp waves that occur during sleep.
179
When are V waves largest?
Vertex bilaterally.
180
When do multiple V waves occur?
Stage 2 sleep
181
When do V waves often occur during sleep?
After sleep disturbances
182
By what age does REM sleep drop to less than <40%
3-4 months of age
183
What happens to sleep in old age?
Absolute reduction in both slow-wave and REM sleep.
| Increase in frequecy of awakenings after sleep onset
184
What is the master clock of the brain?
Suprachiasmatic nucleus in anterior hypothelamus
185
What synchronizes the suprachiasmatic nucleus?
Signals from retina
| Reset each day by signals of light.
186
How does suprachiasmatic nuceus receive input?
Specialized melanopsin-containing retinal ganglion cells project via retinaohypothalamic tract to SCN. This provides light input independent of vision.
187
What happens to 24 hour sleep cycle in absence of solar guidance?
Increases to 26 hours - called free running.
188
What can reset the SCN?
signals of light from retina
| pineal melatonin secretion during darkness
189
What is the sleep switch nucleus?
Ventrolateral preoptic nucleus
190
What is the anatomy of the ventrolateral preoptic nucleus?
Projections to main components of ascending arousal system.
191
Function of ventrolateral preoptic nucleus?
Induces sleep by putting brakes on arousal nuclei.
192
Signs of damage to ventrolateral preoptic nucleus?
Chronic insomnia
193
What must be inhibited for people to wake up?
Ventrolateral preoptic nucleus
194
What causes inhibition of VLPO?
Negative feedback from monoaminergic system.
| Switching to arousal is then stabilised by orexin/hypocretin neurons in hypothalamus.
195
When are orexin neurons activated?
During wakefulness.
196
What happens to patients with narcolepsy?
Reduced number of orexin neurons, leading to repeated somnolence during day.
197
Where are cholinergic neurotransmitters in ascending RAS?
Midbrain-pons nuclei
198
Where are nonadrenergic neurotransmitters in ascending RAS?
Locus coeruleus
199
Where are dopaminergic neurotransmitters in ascending RAS?
Periaqueductal gray matter
200
Where are serotoninergic neurotransmitters in ascending RAS?
Raphe nuclei
201
Where are histaminergic neurotransmitters in ascending RAS?
Tuberomammillary nucleus
202
Function of cholinergic midbrains-pons nuclei
REM on neurons - activation brings on REM sleep.
203
Function of noradrenergic neurotransmitter in locus coeruleus?
REM off neurons - activation reduces REM sleep.
204
Function of dopaminergic neurotransmitters in periaquaductal gray matter?
D2 enhances REM sleep
205
Function of serotonergic neurotransmitter in raphe nuclei?
5HT2 stimulation maintains arousal
206
Function of histaminergic neurotransmittesr in tuberomammillary nucelus?
H1 stimulation maintains arousal
207
What activates REM sleep?
Cholinergic neurotransmitters in midbrain-pons nuclei
208
What turns off REM sleep?
Noradrenergic neurotransmitters in locus coeruleus
209
Affect of EtOH on sleep
```
Increases SWS (chronic use causes loss)
Reduces initial REM but increases second half REM
```
210
Affect of EtOH withdrawl on sleep
Loss of SWS
Increased REM
Intense REM rebound
211
Affect of anxiety disorders on sleep
Increased stage 1 (light sleep)
Reduced REM
Normal REm latency
Reduced slow wave sleep
212
Affect of benzo on sleep
```
Decreased sleep latency
Increased sleep time
Reduced stage 1 sleep
Increased stage 2 sleep
Reduce REM and SWS
Prevent transition from lighter stage 2 sleep into deep, restorative stage 3 and 4 sleep.
```
213
Affect on sleep on cessation of benzo
REM rebound
214
Affect of cannabis on sleep
Increased SWS
| Suppress REM
215
Affect of Carbamazepine on sleep
Suppress REM
Increased REM latency
Increased SWS
216
Affect of dementia on sleep
Increased sleep latency and fragmentation
| Reduced sleep time
217
Affect of depression on sleep
Loss of SWS slow wave sleep (first half)
Increased REM, leading on to early awakening
Reduced REM latency
218
Affect of lithium on sleep
Supresses REM
Increases REM latency
Increases SWS
219
Affect of opiates on sleep
Decreased SWS and REM
| Withdrawl REM rebound
220
Affect of schizophrenia on sleep
Inconsistent reduction in REM latency and slow wave sleep.
221
Affect of SSRIs on sleep
Alerting due to 5HT2 stimulation
| May reduce REM latency
222
Affect of stimulants on sleep
Reduce sleep time by decreasing REM sleep and SWS
223
Affect of cessation of SSRIs on sleep
REM rebound (except modafinil)
224
Affect of tricyclics on sleep
REM suppression - especially clomipramine
| Increased SWS and stage 1 sleep
225
Affect on Z hypnotics on sleep
Zopiclone may increase SWS
226
How is EEG placed?
21 electrodes, placed based on 10/20 international system of electrode placement.
227
What is 10/20 international system of electrode placement?
Measures distance between readily identifiable landmarks on head, then locates electrode positions at 10% or 20% of that distance
228
What activation procedures can be used to bring up abnormal discharges in EEG?
Strenuous hyperventilation
Photic stimulation via intense strobe light
24 hours of sleep deprivation can lead to activation of paroxysmal EEG discharges
229
Types of waves in EEG
```
Beta
Alpha
Theta
Delta
Mu
Lambda
```
230
Frequency of beta wave
>13 Hz
231
Frequency of alpha wave
8-13 Hz
232
Frequency of theta wave
4-8 Hz
233
Frequency of delta wave
<4 Hz
234
Frequency of Mu wave
7-11 Hz
235
Frequency of lambda waves
Single waves
236
Where is beta waves seen?
Frontal, central position in normal waking EEG
237
Where is alpha wave seen?
Dominant brain wave frequency when eyes are closed and relaxing occipitoparietal predilection.
238
When do alpha waves disappear?
Anxiety
Arousal
Eye opening or focused attention.
239
What do alpha wave dominance reduce with?
Age
240
When are theta waves seen?
Small amount of sporadic theta seen in waking EEG at frontotemporal area.
Pominent in drowsy or sleep EEG.
241
What is excessive theta in awake EEG a sign of?
Pathology
242
Where does Mu wave occur over?
Motor cortex
243
What is Mu wave related to?
Motor activity
244
What is Mu wave characterized by?
Arch like waves
245
What attenuates Mu wave?
Movement of contralateral limb
246
What does lambda wave look like?
Single occipital triangular, symmetrical sharp wave
247
What produces lambda wave?
Visual scanning when awake such as reading
| Light sleep
248
Which wave is present on EEG when eyes are closed and relaxing?
ALpha
249
Which waves are seen in EEG when awake?
Alpha
250
Which waves are dominant in EEG when asleep?
Theta
251
Which waves are prominent in EEG on deep sleep?
Deep sleep
252
Which waves in EEG when awake suggest pathology?
Excessive theta
| Focal/generalized delta
253
Which waves in EEG are fast waves?
Beta
| Alpha
254
Which waves in EEG are slow waves?
Delta
| Theta
255
Which waves are dominant in newborns?
Delta
| Theta
256
What EEG is normal in infants?
Irregular medium to high voltage delta activity
257
What EEG is normal in early childhood?
Alpha range develops in posterior areas
258
What is seen in EEG during absence seizure?
Regular 3 Hz complexes
259
What is seen in EEGs in Angelmans sndrome?
Noted by age of 2
| Prolonged runs of high amplitude 2-3 Hz frontal activity with superimposed interictal epileptiform discharges.
260
What is seen on an EEG in angelmans syndrome below the age of 12?
Occipital high amplitude rhythmic 4-6 Hz activity facilitated by eye closure.
261
EEG abnormalities in ADHD
Upto 60% have EEG abnormality - spike waves
262
EEG in BPD
Positive spikes - 14 and 6 per second in 25% of patients
263
EEG in CJD
Generalised periodic 1-2 Hz sharp waves in 90% of patients with sporadic CJD.
Not in variant form.
264
EEG in sharply focal head trauma
Focal slowing
265
EEG in subdural haematoma
Focal delta slowing
266
EECG in diffuse atherosclerosis
Slowed alpha frequency and increased generalised theta slowing
267
EEG in herpes simplex encephalitis
Episodic discharges recurruring every 1-3 seconds with variable focal waves over emporal areas
268
EEG in Huntington's Dementia
Initial loss of alpha, later flattened trace
269
EEG in infantile spasms
Hypsarrhythmia (diffuse giant waves, high voltage >400 microvolts) with chaotic background of irregular, asynchronous multifocal spikes and sharp waves.
270
EEG association with clinical seizures in infantile spasms
Marked suppression of background - electrodecremental response
271
EEG in infectious disorders
Diffuse, synchronous, high voltage slowing
272
EEG in metabolic and endocrine disorders
Diffuse, generalised slowing.
| Triphasic waves 1.5-3 per second high-voltage slow-waves (particularly in hepatic encephalopathy)
273
EEG in neurosyphilis
Non-specific increase in slow waves occurring diffusely over scalp
274
EEG in panic disorder
Paroxysmal EEG changes consistent with partial seizure in one third; focal slowing in 25% of patients
275
EEG in seizures
Generalized, hemispheric, focal spike/spike wave discharge
276
EEG in stroke
Focal or regional delta activity
277
EEG in strutural lesions
Focal slowing/focal spike activity
278
Most common EEG abnormality?
Diffuse slowing of background
279
What does diffuse slowing of background on an EEG suggest?
Nonspecific
| Signifies presence of encephelopathy
280
What does focal slowing on EEG suggest?
Local mass lesions
281
What is a hallmark of seizure on EEG?
Epileptiform discharges seen interictally
282
What does lateralized epileptiform discharges on EEG suggest?
Acute destructive brain lesion
283
Effect of antipsychotics on EEG?
Slowing of beta activity
| Increase in alpha, theta and delta
284
Effect of antidepressants on EEG?
SLowing of beta activity
| Increase in alpha, theta and delta
285
Effect of lithium on EEG?
Slowing of alpha or paroxysmal activity
286
Effect of anticonvulsants on EEG?
No effect on awake EEG
287
Main effect of sedating drugs on EEF?
Decrease alpha
288
Effect of barbituates on EEG?
Opposite to EtOH:
| Increased beta activity upon intoxication
289
Effect of barbituate withdrawl on EEG?
Generalized paroxysmal activity and spike discharges
290
Effect of benzos on EEG?
Increased beta
| Decreased alpha
291
Effect of benzo OD on EEG?
Diffuse slowing
292
Effect of opioids on EEG?
Decreased alpha activity
| Increased voltage of theta and delta waves
293
Effect of opioid OD on EEG?
Slow waves
294
Effect of recreational drugs generally on EEG?
Increased alpha
295
Effect of EtOH on EEG?
Increased alpha and theta
296
Effect of EtOH withdrawl on EEG?
Increased beta
297
Effect of delirium tremens on EEG?
Beta (fast) wave activity
298
Effect of marijuana on EEG?
Increased alpha in frontal area of brain
| Overal slow alpha activity
299
Effect of cocaine on EEG?
Same as marijuana but longer lasting:
Increased alpha in frontal area of brain
Overall slow alpha activity
300
Effect of nicotine on EEG?
Increased alpha
301
Effect of nicotine withdrawl on EEG?
Marked decrease in alpha activity
302
Effect of caffeine withdrawl on EEG?
Increase in amplitude or voltage of theta activity
303
What is magnetoencephalography?
Used to measure magnetic fields produced by electrical activity in the brain
304
Difference between measuring magnetic and electrical fields in the brain?
Magnestic fields are less distorted y skull and scalp
305
What are EEG and MEG sensitive to?
EEG: tangential and radial components
MEG: only tangential components
306
What can EEG and MEG measure?
MEG: selectively measure activity in sulci
EEG: measure activity in both sulci and at top of cortical gyri
307
What is an ERP?
Change in electrical brain activity stereotyped and time-locked to an event (stimulus).
308
What do ERPs help with?
Allow investigation of specific types on information processing by brain
309
What does it mean that ERPs have a low signal-to-noise ratio?
They are small relative to spontaneous brain activity (background EEG)
310
How can we increase the ERP signal-to-noise ratio?
ERP averaging
311
What do ERPs consist of?
Polarity (positive or negative)
| Latency - moment of peak occurrence after stimulus is presented
312
Positives of EEG/MEG/ERCP vs fMRI/PET
Higher temporal resolution
313
Negatives of EEG/MEG/ERP compared to MRI/PET
Lack high spatial resolution
314
How are time of occurrence ERPs classified?
Early
Mid
Late latency
315
Advantage of early ERP?s
Basic sensory pathways can be studied
316
Another name of early ERPs?
Evoked potentials
| Brain stem evoked responses
317
Examples of early ERPs
Response to sounds (auditory EP)
Flashes (visual EP)
electrical stimulation (somatosensory EP)
318
When do midlatency ERPs occur?
After brain stem evoked responses
319
What are three well known midlatency ERPs?
N100
P50
P200
320
Characteristic of midlatency ERPs?
Amplitudes reduce with repetition (habituation response/sensory gating)
321
What can late ERPs study?
Cognitive pathways related to execution of psychological events such as attention, emotion and memory tasks
322
TWo examples of late ERPs
P300
| MMN
323
What is P300?
POsitive late ERP component after 300ms after stimulus presentation
324
When is P300 generated?
When rare target stimulus is imbedded with more frequent stimuli
325
What is P300 related to?
Maintenance of working memory
326
What is decreased P300 amplitude related to in MH?
Biological trait marker in schizophrenia
327
What is mismatch negativity/MMN?
Negative ERP component that is recorded between 100-200 ms in response to low-probability deviant sounds in a sequence of standard sound stimuli, when the aprticipant is not actively attending to teh deviants.
328
When is MMN best seen?
In difference wave between ERP in response to the standard and deviant sounds.
329
What does MMN reflect?
Involuntary information processing in auditory context.
330
What type of MMN is noted in schizophrenia?
Decreased MMN
331
What is the contingent negative variation/CNV?
Slow negative shift in interval between two paired stimuli presented one after another.
332
What type of CNV is noted in schizophrenia?
Reducted in central/midline electrodes, particularly in those with long duration of illness with positive symptoms
