NEUROPHYSIOLOGY Flashcards
Action potential
initiated?
numbers?
- resting membrane potential
- threshold potential
- positive level
what in and out when?
At the axonal hillock
resting membrane - -70
threshold- -55
NA channels go IN
+40
K GO out
hyperpolarised
3 types of snapses
–> 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
Eating
full?
hungry?
outside CNs?
- 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)
Temperature
hypothalamus has 2 centres controlling body temp
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)
Pain
where detects
which fibres
FAST?
SLOW?
receptors modulates?
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)
Thirst
areas ?
neurotransmitter?
subfornical organ + organum vasculosum of lamina terminalis - perception of thirst
+ hypothalamic paraventricular nuceleus
Angiotensin 2 + (hypotension stimulates via baroreceptiors)
Kluver-Bucy syndrome
Bilateral lesions of amygdala and hippocampus –> placidity with decreased aggressive
behaviour. oral exploratory behaviour + hypersexuality. Hypermetamorphosis
(objects are repeatedly examined as if novel)
LaurenceMoon-Biedl Syndrome
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.
Prader-Willi Syndrome
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
Kleine-Levin Syndrome
Compulsive eating behaviour with hyperphagia, hypersomnolence, hyperactivity, hypersexuality and exhibitionism.
A hypothalamic abnormality- proceeded by a viral illness; often resolves by the third decade of life.
Psychogenic polydipsia
Psychogenic polydipsia : Excessive water consumption in the absence of hypovolemia or hypernatremia.
May lead to water intoxication and serious electrolyte imbalance
Neurogenesis
where zones start?
- where continuous
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
neuronal migration (begins first 6 months gestation)
2 types
myelination = beings 4th gestational month + complete by 2 yrs
1) Radial migration (form scaffolding)- form radial stacks of cells (Dakics cortical columns)
2) Tangential migration
failure of migration = heterotopia
Synaptogensis
synaptic pruning
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
pituitary
- anterior
- posterior
pituitary
anterior - GH, LH, FSH, ACTH, TSH, prolactin
posterior
- Vasopressin (ADH)
- oxytocin (synthesised in magnocellular cells of supraoptic nuceli + paraventricular nuceli)
hypothalamus hormones
CRH
GHRH
GnRH
TRH
SST
PIF
Thyroid gland
TRH –> increases TSH
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
Hypothalamic-pituitary Adrenal Axis
- CRH released from hypothalamus –>
- ACTH from anterior pituitary
- ACTH –> cortisol from adrenal cortex
- 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.
diurnal variation in cortisol levels occurs in humans, with peak cortisol levels
occurring around 6:00- 7:00 AM.
Hypercortisolema, loss diurnal variation = depression, mania and OCD.
some PTSD has hyPOcortisolemia in subgroup
Dexamethasone suppression test (DST)
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,
Pineal gland (contains Ca deposits more prominent with age)
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)
Sleep latency:
Rem latency
sleep latency- time from ‘lights out’ to sleep onset
Rem latency- sleep onset to first REM episode ~90 mins
NREM sleep - 75% sleep
stages
features
1,2, (3+4) = slow wave sleep
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
REM Sleep = 25%
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
Sleep Spindles
K complex
v waves
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
Sleep regulation
- master clock of brain
? free running
= 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
what is the sleep switch nucleus?
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
when are Orexin neurones active?
- disorder associated
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.
EEG techniques
hyper-ventillation (most common)
photic (strobe light)
24 hout sleep deprivation
Waves and frequency
alpha and beta are fast waves
Theta and delta slow waves
Beta- >13
Alpha 8-13
Theta- 4-8
Delta < 4hx
Mu 7-11 motor cortex
Lambda - single waves produced by visual scanning
EEG Changes in different age groups
newborn
infant\early childhood
adolescence
adult
Newborns- D +T
Infants- Delta
Childhood- A develops
Teens- normal adult by 12-15
Adult- normal dominant alpha rhythm
EEG in various disorders
Absence seizure (petit mal)
Angelmans
Diffuse atherosclerosis
Herpes simplex encephalitis-
Hepatic encephalopathy
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
Generally interpreted as?
Diffuse slowing of background
Focal slowing
diffuse- nonspecific and indicates encephalopathy
Focal slowing- local mass lesions eg oedema, haematoma,
Effect drugs EEG
Antidepressant
Antipsychotic
Lithium
Sedating drugs
Recreational drugs
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
TRANSCORTICAL SENSORY APHASIA?
fluent, incomrehensible speech PLUS preserved repetition?
(werkenes but can repeat fine )
reduced 5hIAA in CSF?
increased aggression and suicidality
ADHD gene
DRD4
