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MRCPsych Part A - Al-Rashid Hospital > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
Q

Where is an action potential initiated?

A

Axonal hillock

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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
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3
Q

What is the threshold potential?

A

-55mV

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4
Q

At what mV do the Na+ channels open?

A

-55mV

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5
Q

At what mV do the Na+ channels close?

A

+40mV

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6
Q

At what mV do the K+ channels open?

A

+40mV

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7
Q

What is a synapse?

A

Junction between 2 cells

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8
Q

What types of synapses are there?

A

Chemical
Electrical
Conjoint

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9
Q

What are conjoint synapses?

A

They have both electrical and chemical properties.

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10
Q

What are electrical synapses?

A

Bring response by electrical communication, without chemical exchange.

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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.

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12
Q

What happens to postsynaptic neurons at excitatatory synapses?

A

They are depolarized

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13
Q

What does inhibitory synaptic activity do to postsynaptic neurons?

A

Hyperpolarizes them

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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.

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15
Q

What is spatial summation?

A

When additional input from several other presynaptic cells through other synapses lead to an action potential.

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16
Q

What is temporal summation?

A

When recurrent stimulation by same synapse results in action potential.

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17
Q

What are the centres in the hypothalamus that control feeding?

A

Ventromedial hypothalamus

Lateral hypothalamus

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18
Q

Where is the satiety centre?

A

Ventromedial hypothalamus

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19
Q

Where is the feeding centre?

A

Lateral hypothalamus

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20
Q

What are the neurochemical mediators of increased appetite?

A

Ghrelin

Neuropeptide Y

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21
Q

What is the word to describe neurochemical mediators of increased appetite?

A

Orexigenic

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22
Q

What is the word to describe neurochemical mediators of satiety?

A

Anorexigenic

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23
Q

What are the neurochemical mediators of satiety?

A

Leptin
Cholecystokinin
Serotonin

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24
Q

Which orexigenic substance is produced outside of the CNS?

A

Ghrelin

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25
Q

Where is Ghrelin produced?

A

Gastric mucosa

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26
Q

How is Ghrelin synthesized?

A

Adipose cells synthesize leptin

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27
Q

How does food affect the hypothalamus?

A

Food/food cues increase dopaminergic activity in nucleus accumbens (reward centre).

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28
Q

What happens to dopamine receptors in obesity?

A

D2 receptors are reduced in striatum.

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29
Q

What are the centres for temperature in the hypothalamus?

A

Preoptic anterior hypothalamus

Posterior hypothalamus

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30
Q

What is the hypothermic centre called?

A

Preoptic anterior hypothalamus

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31
Q

What is the hyperthermic centre called?

A

Posterior hypothalamus

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32
Q

What happens if the preoptic anterior hypothalamus is stimulated?

A

Parasympathetic-mediated sweating and vasodilation, resulting in hypothermia.

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33
Q

What happens if the posterior hypothalamus is stimulated?

A

Sympathetic drive, shivers and vasoconstriction leading to hyperthermia.

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34
Q

What type of lesion reduces diurnal temperature variation?

A

Lesions in median eminence

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35
Q

What causes malignant hyperthermia?

A

Abnormal excitation-contraction coupling in skeletal muscle.

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36
Q

What happens in Neuroleptic Malignant Syndrome?

A

Hyperthermia induced by neuroleptic use or levodopa withdrawl.

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37
Q

Which subcortical centre plays a role in pain?

A

Thalamus

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38
Q

Which fibres carry pain sensation?

A

Unmyelinated C fibres

Sparsley myelinated A-delta fibres

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39
Q

Where do C and A-delta fibres carry pain sensation to?

A

Dorsal horn of spinal cord

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40
Q

Are C fibres myelinated?

A

No

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41
Q

What happens once pain sensation arrives at dorsal horn of spinal cord?

A

Fast transmission via lateral spinothalamic route

Slow transmission via reticulothalamic tract

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42
Q

Purpose of transmission of pain along lateral spinothalamic tract?

A

Aids localization of pain

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43
Q

Purpose of slow transmission of pain sensation via reticulothalamic tract?

A

Aids subjective sensation

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44
Q

Which receptors modulate pain sensitivity?

A

Opioid receptors in dorsal horn + periaqueductal grey matter (brain stem)

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45
Q

Which fibres modulate pain perception?

A

Descending fibres from serotonergic raphe nuclei

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46
Q

How does thalamic pain syndrome occur?

A

Stroke involving thalamoperforating branches of posterior cerebral artery.

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47
Q

Signs of thalamic pain syndrome?

A

Contralateral loss of sensation with burning or aching pain triggered by light cutaneous stimulation.

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48
Q

Which parts of the brain are involved in thirst?

A

Subfornical organ
Organum vasculosum of the lamina terminalis
Hypothalamic paraventricular nucleus

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49
Q

Which neurotransmitter is used to propagate thirst signals?

A

Angiotensin II

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50
Q

Where do neurotransmitters propagate thirst signals to?

A

Hypothalamus

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51
Q

How does hypotension stimulate thirst?

A

Via baroreceptors on aorta and carotid

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52
Q

Organic/anatomical cause of SIADH?

A

Damage to paraventricular and supraoptic hypothalamic nuclei

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53
Q

What causes Kluver-Bucy syndrome?

A

Bilateral lesions of amygdala and hippocampus

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54
Q

Symptoms in Kluver-Bucy syndrome?

A

Decreased aggressive behaviour.
Prominent oral exploratory behaviour and hypersexuality.
Hypermetamorphosis (objects repeatedly examined as if novel)

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55
Q

What is the cause of Laurence-Moon-Biedl Syndrome?

A

Autosomal recessive with genetic locus at 11q13 in most cases

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56
Q

Symptoms in Laurence-Mood-Biedl Syndrome?

A 
Obesity
Hypogonadism
Low IQ
Retinitis pigmentosa
Polydactyly
Diabetes insipidus
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57
Q

Cause of Prader-Willi syndrome?

A

Reduced in oxytocin neurons and satiety neurons noted.

Associated with paternal deletion (genomic imprinting) at 15q11-q13.

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58
Q

Signs in Prader-Willi syndrome?

A 
Hypotonia
Obesity with hyperphagia
Hypogenitalism
Short stature
Impaired glucose tolerance
Abnormal control of body temperature
Daytime hypersomnolence
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59
Q

Cause of Kleine-Levin syndrome?

A

Hypothalamic abnormality sometimes preceded by viral illness - often resolves by third decade of life.

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60
Q

Signs in Kleine-Levin syndrome?

A

Compulsive eating behaviour with hyperphagia, hypersomnolence, hyperactivity, hypersexuality, exhibitionism.

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61
Q

Where is active nerve cell production seen in early fetal lfe?

A

Subventricular zone - around ventricles of neural tube.

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62
Q

What happens to neurons produced in subventricular zone?

A

Migrate out towards cortical plate.

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63
Q

In neurogenesis, what happens to thalamic axons?

A

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.

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64
Q

What happens to thalamic axons in schizophrenia (occasionally)?

A

Abnormal persistence of subplate neurons, suggestive of failure of axonal path-finding.

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65
Q

Where does neurogenesis in adults particularly take place?

A

Dentate gyrus of hippocampus

Olfactory bulb

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66
Q

What reduces hippocampal neurogenesis?

A

Stress

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67
Q

What increases hippocampal neurogenesis?

A

Enriched environments
Exercise
Antidepressants

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68
Q

When does neuronal migration take place?

A

First 6 months of gestation

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69
Q

What are the types of neuronal migration?

A

Radial

Tangential

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70
Q

What is radial migration?

A

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.

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71
Q

What is the radial stack of cells created in radial migration called?

A

Rakic’s cortical columns

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72
Q

What is tangential migration?

A

Most inhibitory interneurons in external and internal granular layers migrate tangentially.

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73
Q

What is heteropia?

A

Abnormalities in neuronal migration due to neurons failing to reach cortex and residing in ectopic positions.

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74
Q

When does myelination begin?

A

4th gestational month

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75
Q

When is myelination complete?

A

2 years postnatal

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76
Q

When does myelination reach its full extent?

A

Late in third decade of life

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77
Q

When does synaptogenesis occur rapidly?

A

From second trimester through to the first ten years of life.

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78
Q

When is the peak of synaptogenesis?

A

First 2 years postnatally.

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79
Q

When does synaptic pruning occur?

A

After mid-childhood.

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80
Q

What is synaptic pruning?

A

Synaptic elimination to select and preserve the most useful while eliminating unnecessary neuronal connections.

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81
Q

What can we use to study neuronal numbers?

A

Density of D2 receptors

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82
Q

When is density of D2 receptors greater than adult levels?

A

Before 5 years of age.

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83
Q

In which gender is dopamine receptor reduction fastest?

A

Males

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84
Q

Rate of dopamine receptor loss in adults?

A

2.2% reduction per decade

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85
Q

Rate of D2 receptor loss in schizophrenia?

A

6% loss per decade

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86
Q

What disorders are associated with under-pruning?

A

Autism

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87
Q

Where are neurohormones produced which regulate hormones from naterior lobe of the pituitary gland?

A

Parvocellular neurons of hypothalamus.

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88
Q

Where are the two hormones synthesized which are released from the posterior lobe of the pituitary gland?

A

Magnocellular cells of supraoptic nuclei

Paraventricular nuclei of hypothalamus

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89
Q

What are the two hormones produced by the posterior pituitary?

A

Vasopressin/ADH

Oxytocin

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90
Q

Which hormones are produced by the anterior pituitary?

A 
Grown Hormone
Luteinizing hormone 
Follicle Stimulating hormone
Adreno-corticotrophic hormone
Thyroid stimulating hormone
Prolactin
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91
Q

Which hormones produced by the anterior pituitary are gonadotrophins?

A

LH
FSH
ACTH

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92
Q

What increases GH release?

A

Exercise
Sleep
Stress

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93
Q

What alters the response of GH to GHRH?

A

Depressin

Aneroxia

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94
Q

What inhibits prolactin release from hypothalamus?

A

Dopamine

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95
Q

What facilitates release of prolactin?

A

Thyrotrophin releasing hormone

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96
Q

During which activities are prolactin released?

A

Pregnancy
Nursing
Sleep
Exercise

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97
Q

How do antipsychotics lead to hyperprolactinaemia?

A

Remove inhibitory control of dopamine by blocking D2 receptors in tuberoinfundibular tract.

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98
Q

What does Vasopressin play a role in?

A

Attention
Memory
Learning

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99
Q

When is vasopressin release increased?

A

Pain
Stress
Exercise

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100
Q

What drugs increase vasopressin?

A

Morphine
Nicotine
Barbituates

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101
Q

What drug decreases vasopressin release?

A

Alcohol

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102
Q

What hormones are released from the hypothalamus?

A 
Corticotrophin releasing hormone
Growth hormone releasing hormone
Gonadotrophin releasing hormone
Thyrotophin releasing hormone
Somatostatin
Prolactin inhibitory factor (dopamine)
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103
Q

Which hormone inhibits growth hormone?

A

Somatostatin

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104
Q

What stimulates secretion of TSH from the pituitary?

A

TRH from hypothalamus.

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105
Q

What stimulates thyroid gland to release T3 and T4?

A

TSH from anterior pituitary

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106
Q

Difference between T3 and T4?

A

T3 is more biologically potent.

T4 is converted into T3 by target organs and the brain.

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107
Q

What happens if exogenous administration of TRH is given t depressed patients?

A

Blunted response to TRH

Increases serotonergic transmission with decreased 5-HT1A sensitivity and increased 5-HT2A sensitivity.

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108
Q

What activates nerve growth factor genes in early development?

A

T3

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109
Q

Which MH problem is hypothyroidism implicated in?

A

Rapid cycling mood pattern in previously stable bipolar

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110
Q

What stimulates release of ACTH from anterior pituitary?

A

CRH from hypothalamus.

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111
Q

What stimulates release of cortisol from adrenal cortex?

A

ACTH from anterior pituitary.

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112
Q

What is the Hypothalamic-Pituitary-Adrenal axis?

A

CRH (hypothalamus) stimulates ACTH (anterior pituitary) which stimulates cortisol release (adrenal cortex) which inhibits CRH and ACTH.

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113
Q

What is the hypothalamic-pituitary-adrenal axis involved in?

A

Stress response

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114
Q

What happens to the hypothalamic-pituitary-adrenal axis in chronic stress?

A

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.

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115
Q

What compensations occur if hippocampal shrinkage occurs in chronic stress?

A

Compensatory increase in dendritic arborization of neurons in basolateral amygdala, contributing to memory bias towards negative events in chronic stress.

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116
Q

Cortisol level in Addisons?

A

High

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117
Q

Cortisol level in Cushings?

A

Low

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118
Q

When are cortisol levels at their peak?

A

6-7am

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119
Q

In what MH problem is hypercortisolaemia noted?

A

Depression
Mania
OCD
Schizoaffective disorder

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120
Q

In which MH problems is hypocortisolaemia noted?

A

PTSD
Chronic fatigue
Fibromyalagia

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121
Q

Describe the dexamethasone suppression test

A

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.

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122
Q

Which MH problems is DST-suppression seen in?

A

Depression

Hypercortisolaemic states

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123
Q

What physical conditions can lead to DST non-suppression?

A

Pregnancy
Severe weight loss
EtOH
Hepatic enzyme inducers

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124
Q

What is the epiphysis?

A

Pineal gland

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125
Q

What does the pineal gland contain?

A

Pinealocytes

Calcium deposits - more prominent with age - brain sand.

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126
Q

What do pinealocytes do?

A

Secrete serotonin in the day, melatonin at night.

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127
Q

Where is the highest concentration of serotonin?

A

Pineal gland

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128
Q

Describe synthesis of Melatonin

A

Melatonin is synthesized from seretonin by action of serotonin-N-acetylase and 5 hydroxyindole-O-methyltransferase.

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129
Q

What regulates melatonin synthesis?

A

Light-dark cycle

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130
Q

What regulates the pineal gland?

A

Major-beta-adrenergic mechanism

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131
Q

What drugs decrease melatonin synthesis?

A

Beta-antangonists such as propranol

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132
Q

What regulates circadian rhythyms?

A

Melatonin

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133
Q

What hormone is increased at the start of sleep?

A

Testosterone

134
Q

What hormone is increased at slow wave sleep?

A

GH

SST

135
Q

What hormone is reduced at slow wave sleep?

A

Cortisol

136
Q

What hormone is reduced in REM sleep?

A

Melatonin

137
Q

What hormone is increased in early morning sleep?

A

Prolactin

138
Q

What happens in circadian rhythm development in first month?

A

Emergence of 24-hour core body temperature cycle

139
Q

When is progression of nocturnal sleeping noted?

A

2 months

140
Q

What are melatonin and cortisol rhythms established?

A

3 months

141
Q

What type of dreams occur in REM sleep?

A

Illogical

Bizarre

142
Q

What type of dreams occur in non-REM sleep?

A

Thought-like

143
Q

What is actigraphy?

A

used o quantify circadian wake-sleep patterns and detect movement disorders in sleep - uses a motion sensor.

144
Q

What does polysomnography consist of?

A

EEG

EMG

145
Q

What can polysomnography help diagnose?

A

Sleep apnoea
Narcolepsy
Restless legs
REM behavioural disorder

146
Q

What does sleep latency mean in polysomnography?

A

Time from lights out to sleep onset

147
Q

What does REM latency mean in polysomnography?

A

Time from sleep onset to first REM episode.

148
Q

What is normal REM latency in adults?

A

90 minutes

149
Q

What is non-REM latency?

A

Time from sleep onset to first non-REM episode

150
Q

What is sleep efficiency in polysomnography?

A

(total sleep time/total time in bed) x 100

151
Q

What is multiple sleep latency test?

A

Used to assess daytime somnolence and daytime REM onset in narcolepsy.

152
Q

Average length of sleep per night?

A

7.5 hours

153
Q

How much of adult sleep is N-REM?

A

75%

154
Q

What is NREM classified into?

A

4 stages based on increasing amplitude and decreasing frequency of EEG activity.

155
Q

What is slow wave sleep?

A

Stages 3 and 4 of N-REM sleep.

156
Q

What happens in Stage 1 NREM?

A

Drowsy period.
Low voltage theta activity, sharp V waves.
5% of sleep

157
Q

Voltage activity in Stag

A

period.

Low voltage theta activity, sharp V waves.

158
Q

What % of sleep is Stage 1 NREM?

A

5%

159
Q

What happens in Stage 2 NREM?

A

45% of sleep

Development of sleep spindles and K complexes

160
Q

What happens in Stage 3 sleep?

A

12% of sleep

<50% delta waves

161
Q

What happens in stage 4 NREM?

A

13% of sleep
>50% delta waves
Physiological functions at lowest

162
Q

Features of NREM sleep

A

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
Q

Is sleep terror NREM or REM disorder?

A

NREM

164
Q

How much of adult sleep is REM?

A

25%

165
Q

What characterizes REM sleep?

A

Darting eye movements, other muscles paralysed.

High level of brain activity and physiological activity similar to those in wakefulness.

166
Q

What happens in REM sleep behavioural disorder?

A

Muscular paralysis does not occur, resulting in violet movements coinciding with brain activity.

167
Q

What does EEG show in REM sleep?

A

Low-voltage, mixed frequency (theta and slow alpha) activity similar to awake state.
Sawtooth waves.

168
Q

How many episodes of nonREM/REM activity does a person cycle through in one night?

A

5 episodes, REM episodes increase in length.

169
Q

Features of REM sleep

A

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
Q

What are sleep spindles?

A

Waves with upper alpha or lower beta frequency

171
Q

When do sleep spindles mainly occur?

A

Stage 2

172
Q

Duration of sleep spindles

A

<1 second

173
Q

What are K complexes?

A

Large amplitude delta frequency waves, sometimes with sharp apex.

174
Q

Where are K complexes most prominent?

A

Bifrontal regions

175
Q

Where are K complexes mediated from?

A

Thalamocortical circuitry.

176
Q

When do K complexes occur?

A

When patient is aroused partially from sleep.

177
Q

What is arousal burst?

A

When runs of generalized rhythmic theta waves follow K-complexes.

178
Q

What are V waves?

A

Sharp waves that occur during sleep.

179
Q

When are V waves largest?

A

Vertex bilaterally.

180
Q

When do multiple V waves occur?

A

Stage 2 sleep

181
Q

When do V waves often occur during sleep?

A

After sleep disturbances

182
Q

By what age does REM sleep drop to less than <40%

A

3-4 months of age

183
Q

What happens to sleep in old age?

A

Absolute reduction in both slow-wave and REM sleep.

Increase in frequecy of awakenings after sleep onset

184
Q

What is the master clock of the brain?

A

Suprachiasmatic nucleus in anterior hypothelamus

185
Q

What synchronizes the suprachiasmatic nucleus?

A

Signals from retina

Reset each day by signals of light.

186
Q

How does suprachiasmatic nuceus receive input?

A

Specialized melanopsin-containing retinal ganglion cells project via retinaohypothalamic tract to SCN. This provides light input independent of vision.

187
Q

What happens to 24 hour sleep cycle in absence of solar guidance?

A

Increases to 26 hours - called free running.

188
Q

What can reset the SCN?

A

signals of light from retina

pineal melatonin secretion during darkness

189
Q

What is the sleep switch nucleus?

A

Ventrolateral preoptic nucleus

190
Q

What is the anatomy of the ventrolateral preoptic nucleus?

A

Projections to main components of ascending arousal system.

191
Q

Function of ventrolateral preoptic nucleus?

A

Induces sleep by putting brakes on arousal nuclei.

192
Q

Signs of damage to ventrolateral preoptic nucleus?

A

Chronic insomnia

193
Q

What must be inhibited for people to wake up?

A

Ventrolateral preoptic nucleus

194
Q

What causes inhibition of VLPO?

A

Negative feedback from monoaminergic system.

Switching to arousal is then stabilised by orexin/hypocretin neurons in hypothalamus.

195
Q

When are orexin neurons activated?

A

During wakefulness.

196
Q

What happens to patients with narcolepsy?

A

Reduced number of orexin neurons, leading to repeated somnolence during day.

197
Q

Where are cholinergic neurotransmitters in ascending RAS?

A

Midbrain-pons nuclei

198
Q

Where are nonadrenergic neurotransmitters in ascending RAS?

A

Locus coeruleus

199
Q

Where are dopaminergic neurotransmitters in ascending RAS?

A

Periaqueductal gray matter

200
Q

Where are serotoninergic neurotransmitters in ascending RAS?

A

Raphe nuclei

201
Q

Where are histaminergic neurotransmitters in ascending RAS?

A

Tuberomammillary nucleus

202
Q

Function of cholinergic midbrains-pons nuclei

A

REM on neurons - activation brings on REM sleep.

203
Q

Function of noradrenergic neurotransmitter in locus coeruleus?

A

REM off neurons - activation reduces REM sleep.

204
Q

Function of dopaminergic neurotransmitters in periaquaductal gray matter?

A

D2 enhances REM sleep

205
Q

Function of serotonergic neurotransmitter in raphe nuclei?

A

5HT2 stimulation maintains arousal

206
Q

Function of histaminergic neurotransmittesr in tuberomammillary nucelus?

A

H1 stimulation maintains arousal

207
Q

What activates REM sleep?

A

Cholinergic neurotransmitters in midbrain-pons nuclei

208
Q

What turns off REM sleep?

A

Noradrenergic neurotransmitters in locus coeruleus

209
Q

Affect of EtOH on sleep

A 
Increases SWS (chronic use causes loss)
Reduces initial REM but increases second half REM
210
Q

Affect of EtOH withdrawl on sleep

A

Loss of SWS
Increased REM
Intense REM rebound

211
Q

Affect of anxiety disorders on sleep

A

Increased stage 1 (light sleep)
Reduced REM
Normal REm latency
Reduced slow wave sleep

212
Q

Affect of benzo on sleep

A 
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
Q

Affect on sleep on cessation of benzo

A

REM rebound

214
Q

Affect of cannabis on sleep

A

Increased SWS

Suppress REM

215
Q

Affect of Carbamazepine on sleep

A

Suppress REM
Increased REM latency
Increased SWS

216
Q

Affect of dementia on sleep

A

Increased sleep latency and fragmentation

Reduced sleep time

217
Q

Affect of depression on sleep

A

Loss of SWS slow wave sleep (first half)
Increased REM, leading on to early awakening
Reduced REM latency

218
Q

Affect of lithium on sleep

A

Supresses REM
Increases REM latency
Increases SWS

219
Q

Affect of opiates on sleep

A

Decreased SWS and REM

Withdrawl REM rebound

220
Q

Affect of schizophrenia on sleep

A

Inconsistent reduction in REM latency and slow wave sleep.

221
Q

Affect of SSRIs on sleep

A

Alerting due to 5HT2 stimulation

May reduce REM latency

222
Q

Affect of stimulants on sleep

A

Reduce sleep time by decreasing REM sleep and SWS

223
Q

Affect of cessation of SSRIs on sleep

A

REM rebound (except modafinil)

224
Q

Affect of tricyclics on sleep

A

REM suppression - especially clomipramine

Increased SWS and stage 1 sleep

225
Q

Affect on Z hypnotics on sleep

A

Zopiclone may increase SWS

226
Q

How is EEG placed?

A

21 electrodes, placed based on 10/20 international system of electrode placement.

227
Q

What is 10/20 international system of electrode placement?

A

Measures distance between readily identifiable landmarks on head, then locates electrode positions at 10% or 20% of that distance

228
Q

What activation procedures can be used to bring up abnormal discharges in EEG?

A

Strenuous hyperventilation
Photic stimulation via intense strobe light
24 hours of sleep deprivation can lead to activation of paroxysmal EEG discharges

229
Q

Types of waves in EEG

A 
Beta
Alpha
Theta
Delta
Mu
Lambda
230
Q

Frequency of beta wave

A

> 13 Hz

231
Q

Frequency of alpha wave

A

8-13 Hz

232
Q

Frequency of theta wave

A

4-8 Hz

233
Q

Frequency of delta wave

A

<4 Hz

234
Q

Frequency of Mu wave

A

7-11 Hz

235
Q

Frequency of lambda waves

A

Single waves

236
Q

Where is beta waves seen?

A

Frontal, central position in normal waking EEG

237
Q

Where is alpha wave seen?

A

Dominant brain wave frequency when eyes are closed and relaxing occipitoparietal predilection.

238
Q

When do alpha waves disappear?

A

Anxiety
Arousal
Eye opening or focused attention.

239
Q

What do alpha wave dominance reduce with?

A

Age

240
Q

When are theta waves seen?

A

Small amount of sporadic theta seen in waking EEG at frontotemporal area.
Pominent in drowsy or sleep EEG.

241
Q

What is excessive theta in awake EEG a sign of?

A

Pathology

242
Q

Where does Mu wave occur over?

A

Motor cortex

243
Q

What is Mu wave related to?

A

Motor activity

244
Q

What is Mu wave characterized by?

A

Arch like waves

245
Q

What attenuates Mu wave?

A

Movement of contralateral limb

246
Q

What does lambda wave look like?

A

Single occipital triangular, symmetrical sharp wave

247
Q

What produces lambda wave?

A

Visual scanning when awake such as reading

Light sleep

248
Q

Which wave is present on EEG when eyes are closed and relaxing?

A

ALpha

249
Q

Which waves are seen in EEG when awake?

A

Alpha

250
Q

Which waves are dominant in EEG when asleep?

A

Theta

251
Q

Which waves are prominent in EEG on deep sleep?

A

Deep sleep

252
Q

Which waves in EEG when awake suggest pathology?

A

Excessive theta

Focal/generalized delta

253
Q

Which waves in EEG are fast waves?

A

Beta

Alpha

254
Q

Which waves in EEG are slow waves?

A

Delta

Theta

255
Q

Which waves are dominant in newborns?

A

Delta

Theta

256
Q

What EEG is normal in infants?

A

Irregular medium to high voltage delta activity

257
Q

What EEG is normal in early childhood?

A

Alpha range develops in posterior areas

258
Q

What is seen in EEG during absence seizure?

A

Regular 3 Hz complexes

259
Q

What is seen in EEGs in Angelmans sndrome?

A

Noted by age of 2

Prolonged runs of high amplitude 2-3 Hz frontal activity with superimposed interictal epileptiform discharges.

260
Q

What is seen on an EEG in angelmans syndrome below the age of 12?

A

Occipital high amplitude rhythmic 4-6 Hz activity facilitated by eye closure.

261
Q

EEG abnormalities in ADHD

A

Upto 60% have EEG abnormality - spike waves

262
Q

EEG in BPD

A

Positive spikes - 14 and 6 per second in 25% of patients

263
Q

EEG in CJD

A

Generalised periodic 1-2 Hz sharp waves in 90% of patients with sporadic CJD.
Not in variant form.

264
Q

EEG in sharply focal head trauma

A

Focal slowing

265
Q

EEG in subdural haematoma

A

Focal delta slowing

266
Q

EECG in diffuse atherosclerosis

A

Slowed alpha frequency and increased generalised theta slowing

267
Q

EEG in herpes simplex encephalitis

A

Episodic discharges recurruring every 1-3 seconds with variable focal waves over emporal areas

268
Q

EEG in Huntington’s Dementia

A

Initial loss of alpha, later flattened trace

269
Q

EEG in infantile spasms

A

Hypsarrhythmia (diffuse giant waves, high voltage >400 microvolts) with chaotic background of irregular, asynchronous multifocal spikes and sharp waves.

270
Q

EEG association with clinical seizures in infantile spasms

A

Marked suppression of background - electrodecremental response

271
Q

EEG in infectious disorders

A

Diffuse, synchronous, high voltage slowing

272
Q

EEG in metabolic and endocrine disorders

A

Diffuse, generalised slowing.

Triphasic waves 1.5-3 per second high-voltage slow-waves (particularly in hepatic encephalopathy)

273
Q

EEG in neurosyphilis

A

Non-specific increase in slow waves occurring diffusely over scalp

274
Q

EEG in panic disorder

A

Paroxysmal EEG changes consistent with partial seizure in one third; focal slowing in 25% of patients

275
Q

EEG in seizures

A

Generalized, hemispheric, focal spike/spike wave discharge

276
Q

EEG in stroke

A

Focal or regional delta activity

277
Q

EEG in strutural lesions

A

Focal slowing/focal spike activity

278
Q

Most common EEG abnormality?

A

Diffuse slowing of background

279
Q

What does diffuse slowing of background on an EEG suggest?

A

Nonspecific

Signifies presence of encephelopathy

280
Q

What does focal slowing on EEG suggest?

A

Local mass lesions

281
Q

What is a hallmark of seizure on EEG?

A

Epileptiform discharges seen interictally

282
Q

What does lateralized epileptiform discharges on EEG suggest?

A

Acute destructive brain lesion

283
Q

Effect of antipsychotics on EEG?

A

Slowing of beta activity

Increase in alpha, theta and delta

284
Q

Effect of antidepressants on EEG?

A

SLowing of beta activity

Increase in alpha, theta and delta

285
Q

Effect of lithium on EEG?

A

Slowing of alpha or paroxysmal activity

286
Q

Effect of anticonvulsants on EEG?

A

No effect on awake EEG

287
Q

Main effect of sedating drugs on EEF?

A

Decrease alpha

288
Q

Effect of barbituates on EEG?

A

Opposite to EtOH:

Increased beta activity upon intoxication

289
Q

Effect of barbituate withdrawl on EEG?

A

Generalized paroxysmal activity and spike discharges

290
Q

Effect of benzos on EEG?

A

Increased beta

Decreased alpha

291
Q

Effect of benzo OD on EEG?

A

Diffuse slowing

292
Q

Effect of opioids on EEG?

A

Decreased alpha activity

Increased voltage of theta and delta waves

293
Q

Effect of opioid OD on EEG?

A

Slow waves

294
Q

Effect of recreational drugs generally on EEG?

A

Increased alpha

295
Q

Effect of EtOH on EEG?

A

Increased alpha and theta

296
Q

Effect of EtOH withdrawl on EEG?

A

Increased beta

297
Q

Effect of delirium tremens on EEG?

A

Beta (fast) wave activity

298
Q

Effect of marijuana on EEG?

A

Increased alpha in frontal area of brain

Overal slow alpha activity

299
Q

Effect of cocaine on EEG?

A

Same as marijuana but longer lasting:
Increased alpha in frontal area of brain
Overall slow alpha activity

300
Q

Effect of nicotine on EEG?

A

Increased alpha

301
Q

Effect of nicotine withdrawl on EEG?

A

Marked decrease in alpha activity

302
Q

Effect of caffeine withdrawl on EEG?

A

Increase in amplitude or voltage of theta activity

303
Q

What is magnetoencephalography?

A

Used to measure magnetic fields produced by electrical activity in the brain

304
Q

Difference between measuring magnetic and electrical fields in the brain?

A

Magnestic fields are less distorted y skull and scalp

305
Q

What are EEG and MEG sensitive to?

A

EEG: tangential and radial components
MEG: only tangential components

306
Q

What can EEG and MEG measure?

A

MEG: selectively measure activity in sulci
EEG: measure activity in both sulci and at top of cortical gyri

307
Q

What is an ERP?

A

Change in electrical brain activity stereotyped and time-locked to an event (stimulus).

308
Q

What do ERPs help with?

A

Allow investigation of specific types on information processing by brain

309
Q

What does it mean that ERPs have a low signal-to-noise ratio?

A

They are small relative to spontaneous brain activity (background EEG)

310
Q

How can we increase the ERP signal-to-noise ratio?

A

ERP averaging

311
Q

What do ERPs consist of?

A

Polarity (positive or negative)

Latency - moment of peak occurrence after stimulus is presented

312
Q

Positives of EEG/MEG/ERCP vs fMRI/PET

A

Higher temporal resolution

313
Q

Negatives of EEG/MEG/ERP compared to MRI/PET

A

Lack high spatial resolution

314
Q

How are time of occurrence ERPs classified?

A

Early
Mid
Late latency

315
Q

Advantage of early ERP?s

A

Basic sensory pathways can be studied

316
Q

Another name of early ERPs?

A

Evoked potentials

Brain stem evoked responses

317
Q

Examples of early ERPs

A

Response to sounds (auditory EP)
Flashes (visual EP)
electrical stimulation (somatosensory EP)

318
Q

When do midlatency ERPs occur?

A

After brain stem evoked responses

319
Q

What are three well known midlatency ERPs?

A

N100
P50
P200

320
Q

Characteristic of midlatency ERPs?

A

Amplitudes reduce with repetition (habituation response/sensory gating)

321
Q

What can late ERPs study?

A

Cognitive pathways related to execution of psychological events such as attention, emotion and memory tasks

322
Q

TWo examples of late ERPs

A

P300

MMN

323
Q

What is P300?

A

POsitive late ERP component after 300ms after stimulus presentation

324
Q

When is P300 generated?

A

When rare target stimulus is imbedded with more frequent stimuli

325
Q

What is P300 related to?

A

Maintenance of working memory

326
Q

What is decreased P300 amplitude related to in MH?

A

Biological trait marker in schizophrenia

327
Q

What is mismatch negativity/MMN?

A

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
Q

When is MMN best seen?

A

In difference wave between ERP in response to the standard and deviant sounds.

329
Q

What does MMN reflect?

A

Involuntary information processing in auditory context.

330
Q

What type of MMN is noted in schizophrenia?

A

Decreased MMN

331
Q

What is the contingent negative variation/CNV?

A

Slow negative shift in interval between two paired stimuli presented one after another.

332
Q

What type of CNV is noted in schizophrenia?

A

Reducted in central/midline electrodes, particularly in those with long duration of illness with positive symptoms

MRCPsych Part A - Al-Rashid Hospital (22 decks)

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