NEUROPHYSIOLOGY Flashcards

1
Q

Action potential
initiated?
numbers?
- resting membrane potential
- threshold potential
- positive level
what in and out when?

A

At the axonal hillock
resting membrane - -70
threshold- -55
NA channels go IN
+40
K GO out
hyperpolarised

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2
Q

3 types of snapses

A

–> chemical- excitatory or inhibitory
sometimes just help build up but not release an actual (facilitaton) - spatial summation when several other help cause AP. Temporal summation when just one cuases AP
–> electrical
–> cojoint

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3
Q

Eating
full?
hungry?
outside CNs?

A
  • ventromedial =. sateity centre
  • lateral hypothalamus = feeding centre
    ghrelin + neuropetite Y = increase appetite
  • leptin, cholecystokinin and seretonin = feel full
    ghrelin only of these subtences produced outside CNS

food increase dopaminergic activity in nucelus accumbens (reward centre)

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4
Q

Temperature
hypothalamus has 2 centres controlling body temp

A

1) pre-optic anterior hypothalamus = hypothermic centre –> parasympathetic mediated sweating and vasodilation.

2) posterior hypothalamus = hyperthermic –> sympathetic drive, shivers + vasoconstriction

diurnal variation = median eminence (lesions here damage it)

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5
Q

Pain
where detects
which fibres

FAST?
SLOW?

receptors modulates?

A

thalamus - perception
cortical centres- localisation
C fibres. / A delta fibres carry pain to dorsal horn spinal cord
fast –> LATERAL SPINOTHALAMIC - localisation
slow –> reticulothamaic - subjective

receptors modulate- opioid in dorsal horn + descending fibres in seretonergic raphe nuceli (explains TCA help pain)

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6
Q

Thirst
areas ?
neurotransmitter?

A

subfornical organ + organum vasculosum of lamina terminalis - perception of thirst
+ hypothalamic paraventricular nuceleus

Angiotensin 2 + (hypotension stimulates via baroreceptiors)

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7
Q

Kluver-Bucy syndrome

A

Bilateral lesions of amygdala and hippocampus –> placidity with decreased aggressive
behaviour. oral exploratory behaviour + hypersexuality. Hypermetamorphosis
(objects are repeatedly examined as if novel)

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8
Q

LaurenceMoon-Biedl Syndrome

A

Obesity and hypogonadism along with low IQ, retinitis pigmentosa, and polydactyly. Diabetes insipidus
Autosomal recessive with genetic locus at 11q13
No hypothalamic lesions have been found.

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9
Q

Prader-Willi Syndrome

A

Hypotonia, obesity with hyperphagia, hypogenitalism, mental retardation, short stature, impaired glucose tolerance.
Abnormal control of body temperature and daytime
hypersomnolence is related to hypothalamic disturbances.
A reduction in oxytocin neurons and satiety neurons is noted. Associated with paternal deletion

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10
Q

Kleine-Levin Syndrome

A

Compulsive eating behaviour with hyperphagia, hypersomnolence, hyperactivity,
hypersexuality and exhibitionism. A hypothalamic abnormality sometimes preceded by a viral illness; often resolves by the third decade of life.

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11
Q

Psychogenic polydipsia

A

Psychogenic
polydipsia Excessive water consumption in the absence of hypovolemia or hypernatremia. May lead to water intoxication and serious electrolyte imbalance

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12
Q

Neurogenesis

where zones start?

  • where continuous
A

Subventricular zone - neruones migrate out from here to cortical plate
- axons project to subplate neurones + detatch in development but in schizphrenia abnormal persistence of subplate neurones

  • continuous at dentate gyrus of hippocampus and olfactory bulb
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13
Q

neuronal migration (begins first 6 months gestation)
2 types

myelination = beings 4th gestational month + complete by 2 yrs

A

1) Radial migration (form scaffolding)- form radial stacks of cells (Dakics cortical columns)

2) Tangential migration
failure of migration = heterotopia

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14
Q

Synaptogensis

synaptic pruning

A

occurs 2nd trimester –> 10 yrs old (mainly 2yrs)

pruning- commences early teen years
can measure neuronal numbers by d2 receptor density
d2 receptor loss faster men than women, fastest in schizophrenics

excessive pruning in schizophrenia, under pruning in autism

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15
Q

pituitary
- anterior
- posterior

A

pituitary
anterior - GH, LH, FSH, ACTH, TSH, prolactin

posterior
- Vasopressin (ADH)
- oxytocin (synthesised in magnocellular cells of supraoptic nuceli + paraventricular nuceli)

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16
Q

hypothalamus hormones

A

CRH
GHRH
GnRH
TRH
SST
PIF

17
Q

Thyroid gland
TRH –> increases TSH

A

blunted response to TRH in depression
t3 +t4 can accelerate response to antidepressant treatment
nerve growth factor genes activated by T3 in early development

hypothyroidism - trigger rapid cycling mood pattern in previous stable bipolar

18
Q

Hypothalamic-pituitary Adrenal Axis

A
  1. CRH released from hypothalamus –>
  2. ACTH from anterior pituitary
  3. ACTH –> cortisol from adrenal cortex
  4. Cortisol inhibits CRH

chronic stress = HPA feedback fails, decreased hippocampal neurogenesis + shrinking + impaired memory

Compensatory increase in dendritic arborisation of neurones in basolateral amygdala occurs- memory bias towards negative events and chronic stress.

19
Q

diurnal variation in cortisol levels occurs in humans, with peak cortisol levels

A

occurring around 6:00- 7:00 AM.
Hypercortisolema, loss diurnal variation = depression, mania and OCD.
some PTSD has hyPOcortisolemia in subgroup

20
Q

Dexamethasone suppression test (DST)

A

1mg dex given 11pm with baseline cortisol sampling
next day 8am, 4pm and 11pm levels measured again
any one sample >5mcg/L cortisol - indicates DST non-suppression
= failure feedback suppression of ACTH/CRH

DST non suppression seen in depression and other psych hyper-cortisol states
0 70% sensative in severe depression

Continued failure to suppress cortisol despite the apparent recovery from depression suggests an increased risk forrelapse,

21
Q

Pineal gland (contains Ca deposits more prominent with age)

A

Pinealocytes
- secreate seretonin: highest conc in body (day)
- melatonin (night) - regulates circadian rhythm

melatonin is synthesised from seretonin by seretonin- N-acetylase

melatonin synthesis = light-dark cycle + synthesis increased in darkness.
(B-antagonists such as propranolol decrease melatonin synthesis)

22
Q

Sleep latency:
Rem latency

A

sleep latency- time from ‘lights out’ to sleep onset
Rem latency- sleep onset to first REM episode ~90 mins

23
Q

NREM sleep - 75% sleep
stages
features
1,2, (3+4) = slow wave sleep

A

decreased muscle ton and upward deviating eyelids

1- drowsy period, low voltage theta and sharp V waves (deny being asleep)
2, 45% sleep- sleep spindles and K complexes
3, 12% sleep, <50% delta
4- 13% sleep- >50% Delta, physiological functions at the lowest

24
Q

REM Sleep = 25%

A

darting eye movements
paralysis of other muscles
EEG- low voltage theta and slow alpha. (similar to awake)

  • Increased sympathetic activity + autonomic functions active + protein synthesis

typical rotation through 5 episodes RM-non REM

25
Q

Sleep Spindles

K complex

v waves

A

Waves with upper alpha or lower beta frequency, seen in many stages but especially in stage 2. The waveform resembles a spindle with an initial increase in amplitude that decreases

K complex- D frequency - occur each time patient aroused partially from sleep

V waves- sharp waves - common stage 2 when disturbed, brief semi-arousals

26
Q

Sleep regulation
- master clock of brain
? free running

A

= suprachiasmatic nucelus (SCN) in ANTERIOR hypothalamus.
SCN resets each day via signals of light from retina
- specialised melanopsin-containing retinal ganglion cells project via retino-hypothalamic tract –>SCN

when sleep 24/hr- 26hr with no solar guidance

  • pineal melatonin secreted during darkness can reset the SCN
27
Q

what is the sleep switch nucleus?

A

VENTRO-LATERAL PREOPTIC NUCELUS induces sleep by stopping arousal nuclei
- has projections to ascending arousal system
- (damage to VLPO = chronic insomnia)
VLPO must be inhibited so people wake up- its stabilised by orexin neurones in hypothalamus

28
Q

when are Orexin neurones active?
- disorder associated

A

Orexin neurons are mainly active during wakefulness and
reinforce the arousal system. Patients with narcolepsy have reduced number of orexin neurons, leading to repeated somnolence during the day.

29
Q

EEG techniques

A

hyper-ventillation (most common)
photic (strobe light)
24 hout sleep deprivation

30
Q

Waves and frequency
alpha and beta are fast waves
Theta and delta slow waves

A

Beta- >13

Alpha 8-13

Theta- 4-8

Delta < 4hx

Mu 7-11 motor cortex

Lambda - single waves produced by visual scanning

31
Q

EEG Changes in different age groups
newborn
infant\early childhood
adolescence
adult

A

Newborns- D +T
Infants- Delta
Childhood- A develops
Teens- normal adult by 12-15
Adult- normal dominant alpha rhythm

32
Q

EEG in various disorders
Absence seizure (petit mal)

Angelmans

Diffuse atherosclerosis

Herpes simplex encephalitis-

Hepatic encephalopathy

A

Absence seizure- regular 3Hz complexes

Angelmans- prolonged runs high amplituden2-3Hz
EEG changes noted by age 2-same in patients with or without seizures

Diffuse atherosclerosis slowed alpha frequnecy, generalised theta slowing

Herpes simplex encephalitis- episodic discharges recurring every 1-3 seconds

Hepatic encephalopathy = triphasic waves

33
Q

Generally interpreted as?
Diffuse slowing of background

Focal slowing

A

diffuse- nonspecific and indicates encephalopathy

Focal slowing- local mass lesions eg oedema, haematoma,

34
Q

Effect drugs EEG
Antidepressant
Antipsychotic
Lithium
Sedating drugs
Recreational drugs

A

Antidep - slowing B, increase A, T and D
Antipsych- slowing B, increase A, T and D
Lithium- slow A
Sedating - decrease alpha
Recreational- increase alpha