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Psychiatry > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
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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2
Q

What is temporal summation?

A

When recurrent stimulation by same synapse results in action potential.

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3
Q

What are the neurochemical mediators of increased appetite?

A

Ghrelin

Neuropeptide Y

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4
Q

What are the neurochemical mediators of satiety?

A

Leptin
Cholecystokinin
Serotonin

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5
Q

Which orexigenic substance is produced outside of the CNS?

A

Ghrelin

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6
Q

Where is Ghrelin produced?

A

Gastric mucosa

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7
Q

What happens to dopamine receptors in obesity?

A

D2 receptors are reduced in striatum.

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8
Q

What are the centres for temperature in the hypothalamus?

A

Preoptic anterior hypothalamus

Posterior hypothalamus

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9
Q

What is the hypothermic centre called?

A

Preoptic anterior hypothalamus

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10
Q

What is the hyperthermic centre called?

A

Posterior hypothalamus

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11
Q

What type of lesion reduces diurnal temperature variation?

A

Lesions in median eminence

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12
Q

Which subcortical centre plays a role in pain?

A

Thalamus

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13
Q

Which fibres carry pain sensation?

A

Unmyelinated C fibres

Sparsely myelinated A-delta fibres

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14
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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15
Q

Purpose of transmission of pain along lateral spinothalamic tract?

A

Aids localization of pain

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16
Q

Purpose of slow transmission of pain sensation via reticulothalamic tract?

A

Aids subjective sensation

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17
Q

Which receptors modulate pain sensitivity?

A

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

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18
Q

Which fibres modulate pain perception?

A

Descending fibres from serotonergic raphe nuclei

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19
Q

How does thalamic pain syndrome occur?

A

Stroke involving thalamoperforating branches of posterior cerebral artery.

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20
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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21
Q

Which neurotransmitter is used to propagate thirst signals?

A

Angiotensin II

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22
Q

How does hypotension stimulate thirst

A

Via baroreceptors on aorta and carotid

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23
Q

Organic/anatomical cause of SIADH?

A

Damage to paraventricular and supraoptic hypothalamic nuclei

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24
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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25
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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26
Q

Symptoms in Laurence-Mood-Biedl Syndrome?

A 
Obesity
Hypogonadism
Low IQ
Retinitis pigmentosa
Polydactyly
Diabetes insipidus
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27
Q

When does neuronal migration take place?

A

First 6 months of gestation

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28
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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29
Q

When does myelination begin?

A

4th gestational month

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30
Q

When is myelination complete?

A

2 years postnatal

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31
Q

When does synaptogenesis occur rapidly?

A

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

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32
Q

When is the peak of synaptogenesis?

A

First 2 years postnatally.

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33
Q

What can we use to study neuronal numbers?

A

Density of D2 receptors

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34
Q

Rate of dopamine receptor loss in adults?

A

2.2% reduction per decade

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35
Q

Rate of D2 receptor loss in schizophrenia?

A

6% loss per decade

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36
Q

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

A

Parvocellular neurons of hypothalamus.

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37
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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38
Q

What increases GH release?

A

Exercise
Sleep
Stress

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39
Q

What facilitates release of prolactin?

A

Thyrotrophin releasing hormone

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40
Q

During which activities are prolactin released?

A

Pregnancy
Nursing
Sleep
Exercise

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41
Q

What does Vasopressin play a role in?

A

Attention
Memory
Learning

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42
Q

When is vasopressin release increased?

A

Pain
Stress
Exercise

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43
Q

What drugs increase vasopressin?

A

Morphine
Nicotine
Barbiturates

44
Q

What drug decreases vasopressin release?

A

Alcohol

45
Q

Which hormone inhibits growth hormone?

A

Somatostatin

46
Q

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

A

Blunted response to TRH

47
Q

What activates nerve growth factor genes in early development?

A

T3

48
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 potentiation and impaired memory performance.

49
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.

50
Q

What physical conditions can lead to DST non-suppression?

A

Pregnancy
Severe weight loss
ETOH
Hepatic enzyme inducers

51
Q

What drugs decrease melatonin synthesis?

A

Beta-antangonists such as propranolol

52
Q

What regulates circadian rhythms?

A

Melatonin

53
Q

What hormone is increased at the start of sleep?

A

Testosterone

54
Q

What hormone is increased at slow wave sleep?

A

GH

SST

55
Q

What hormone is reduced in REM sleep?

A

Melatonin

56
Q

What hormone is increased in early morning sleep?

A

Prolactin

57
Q

What type of dreams occur in REM sleep?

A

Illogical

Bizarre

58
Q

What is normal REM latency in adults?

A

90 minutes

59
Q

How much of adult sleep is N-REM?

A

75%

60
Q

What is slow wave sleep?

A

Stages 3 and 4 of N-REM sleep.

61
Q

What happens in Stage 1 NREM?

A

Low voltage theta activity, sharp V waves.

5% of sleep

62
Q

What happens in Stage 2 NREM?

A

45% of sleep

Development of sleep spindles and K complexes

63
Q

What happens in Stage 3 sleep?

A

12% of sleep

<50% delta waves

64
Q

What happens in stage 4 NREM?

A

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

65
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 awaken.

66
Q

What does EEG show in REM sleep?

A

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

67
Q

What are sleep spindles?

A

Waves with upper alpha or lower beta frequency

68
Q

Where are K complexes most prominent?

A

Bi-frontal regions

69
Q

Where are K complexes mediated from?

A

Thalamocortical circuitry.

70
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

71
Q

What synchronizes the suprachiasmatic nucleus?

A

Signals from retina

Reset each day by signals of light.

72
Q

What can reset the SCN?

A

signals of light from retina

pineal melatonin secretion during darkness

73
Q

What is the sleep switch nucleus?

A

Ventrolateral preoptic nucleus

74
Q

What must be inhibited for people to wake up?

A

Ventrolateral preoptic nucleus

75
Q

What causes inhibition of VLPO?

A

Negative feedback from monoaminergic system.

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

76
Q

Where are histaminergic neurotransmitters in ascending RAS?

A

Tuberomammillary nucleus

77
Q

Function of cholinergic midbrain-pons nuclei

A

REM on neurons - activation brings on REM sleep.

78
Q

Function of noradrenergic neurotransmitter in locus coeruleus?

A

REM off neurons - activation reduces REM sleep.

79
Q

Function of dopaminergic neurotransmitters in periaquaductal gray matter?

A

D2 enhances REM sleep

80
Q

Function of serotonergic neurotransmitter in raphe nuclei?

A

5HT2 stimulation maintains arousal

81
Q

Affect of ETOH on sleep

A 
Increases SWS (chronic use causes loss)
Reduces initial REM but increases second half REM
82
Q

Affect of ETOH withdrawal on sleep

A

Loss of SWS
Increased REM
Intense REM rebound

83
Q

Affect of anxiety disorders on sleep

A

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

84
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.
85
Q

Affect of cannabis on sleep

A

Increased SWS

Suppress REM

86
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

87
Q

Affect of lithium on sleep

A

Suppresses REM
Increases REM latency
Increases SWS

88
Q

Affect of SSRIs on sleep

A

Alerting due to 5HT2 stimulation

May reduce REM latency

89
Q

Affect of tricyclics on sleep

A

REM suppression - especially clomipramine

Increased SWS and stage 1 sleep

90
Q

Where is beta waves seen?

A

Frontal, central position in normal waking EEG

91
Q

Where is alpha wave seen?

A

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

92
Q

Which waves are dominant in EEG when asleep?

A

Theta

93
Q

Which waves are dominant in newborns?

A

Delta

Theta

94
Q

What is seen in EEG during absence seizure?

A

Regular 3 Hz complexes

95
Q

What is seen in EEGs in Angelmans syndrome?

A

Noted by age of 2

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

96
Q

EEG in CJD

A

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

97
Q

EEG in herpes simplex encephalitis

A

Episodic discharges recurring every 1-3 seconds with variable focal waves over Temporal areas

98
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)

99
Q

What is a hallmark of seizure on EEG?

A

Epileptiform discharges seen interictally

100
Q

Effect of antipsychotics on EEG?

A

Slowing of beta activity

Increase in alpha, theta and delta

101
Q

Effect of antidepressants on EEG?

A

Slowing of beta activity

Increase in alpha, theta and delta

102
Q

Effect of lithium on EEG?

A

Slowing of alpha or paroxysmal activity

103
Q

Effect of benzos on EEG?

A

Increased beta

Decreased alpha

104
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

105
Q

What is decreased P300 amplitude related to in MH

A

Biological trait marker in schizophrenia

Psychiatry (10 decks)

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