neurology 3 Flashcards
cerebellar deep nuclei names
lateral to medial are dentate emboliform globose fastigial
what medial structures of cerebellum gives rise to truncal ataxia, head tilting and nystagmus
vermis
fastigial medial most deep nucleus
flocullonodular lobe
medial cerebellar lesions give rise to uni/ bilateral weakness
bilateral truncal and proximal extremity weakness
lateral cerebellar lesions can give rise to
tendency to fall on affected side
parts of striatum of basal ganglia
remember to imagine coronal section for striatum structures
caudate
putamen
what are components of lentiform nucleus of BG
remember to imagine axial section
putamen
globus pallidus
Direct BG pathway receptors are
D1 - excitatory- stimulates and increases motion
Indirect BG pathway receptors are
indirect is inhibitory for motion and receptors are D2.
three components of blood brain barrier
TIGHT junctions between NON FENESTRATED endothelial cells
complete encircling BASEMENT MEMBRANE
FOOT PROCESSES OF ASTROCYTES
3 places not having blood brain barrier
- AREA POST TREMA-post chemo vomiting has CTZ
- OVLT- organum vasculosum lamina terminalis– osmoreceptors
- NEurohypophysis – for ADH release
why is area post trema, OVLT and neurohypophysis devoid of blood brain barrier
because their capillary endothelial cells are fenestrated.
Vomiting centre is located in
medulla known as Nucleus tractus solitarius (one of the three vagal nuclei)
inputs to Vomiting centre in medulla is recieved from
CTZ from area post trema
GIT via vagus nerve (remember vomiting centre NTS is a vagal nuclei)
vestibular system
CNS
5 major receptors in CTZ and vomiting centre
H1 and M1—- antagonists used to treat motion sickness
Neurokinin NK1, D2 and 5HT3 serotonin—– antagonists are used to treat chemotherapy induced vomiting
treatment of hyperemesis gravidarum
H1 antagonists – doxylamine
regulation of circadian rhythm is done by
suprachiasmatic nucleus of hypothalamus after recieving signals from eyes.
what products are seen in night – nocturnal release under circadian rhythm
ACTH
prolactin
melatonin
norepinephrine
how is melatonin secreted by pineal gland
at night – suprachiasmatic nucleus releases Norepinephrine
which stimulates pineal gland to release melatonin at night
what causes reduction in REM sleep
nor -epinephrine – remember stress increases NE and in stress u cant sleep
Alcohol
Benzodiazepines and barbiturates
what is the mechanism of action of opoids in nociception
inhibition of release of substance P
Fast pain is carried by —- fibres and is —–localised
slow pain is carried by —–fibres and is —–localised
Fast pain is carried by type III fibres and is WELL localised
slow pain is carried by C-fibres and is POORLY -localised
NAME THE 4 MECHANORECEPTORS
PACINNIAN —- in subcu skin for vibration
MEISSEINERS— in non hairy skin for fine touch velocity
RUFFINI —-for pressure
MERKEL DISC– position seen in skin
REM sleep is characterised by
rapid eye movements
loss of muscle tone but penile erection
pupillary constriction.
DREAMS
REM sleep EEG resembles
awake person EEG -beta waves
and
stage 1 of NREM
source of waves in EEG
synaptic evoked potential btw the purkinje cells of cerebral cortex
EEG waves in awake person
with eyes open — alert person – beta waves
with eyes closed — alpha waves
what are the stages of non REM sleep
N1 – light sleep – theta waves
N2 is largest in proportion – sleep spindles and K complexes occur
N3 is deepest slow wave sleep —delta wave– which are slow wave high amplitude
in which phase of sleep bruxism occurs
Stage 2 NREM— sleep spindles and K complexes on EEG
in what phase of sleep nightmares and dreams occurs
REM sleep
difference between nightmares and night terrors
Night mare— person will awaken after bad dream and will clearly recall it
Night terror—- person will get terrorised like shout, appear scared (asso with bedwetting) or sleep walk in their sleep but would hardly recall it in the morning.
Night terrors, bedwetting and sleep walking occurs in which phase of cycle
stage N3 of NREM –slow wave sleep that is delta sleep
what regulates REM sleep
REM -ON neurons in Locus coeruleus
REM-OFF neurons in pedunculopontine tegmentum
Acetylcholine levels increase and oxygen consumption by brain occurs in which phase of sleep
REM sleep
what is REM sleep latency
period of time between onset of sleep to first REM episode – 90 -120 min
Latency is increased in elderly
reduced in depression
cause of extraocular movements in REM sleep
activity of PPRF— paramedian pontine reticular formation
changes of sleep phases in elderly are
increased latency — difficulty falling asleep
reduced N3phase and REM phase —- once they fall asleep their sleep is shorter in duration
why is REM sleep paradoxical
because it is a very deep sleep associated with loss of muscle tone etc
it needs high waking threshold to wake up a person from REM sleep
but still the EEG pattern has beta waves which resembles awake person
hence it is paradoxical
changes of sleep in major depression
depressed people are already lethargic and lazy
they quickly fall asleep — REM latency is reduced.
N3phase is quickly passed to reach REM fast – N3 phase reduced
REM phase of sleep increased
More REM means more repeated night time awakenings
early morning awakening with terminal insomnia
thermoregulation and sexual behaviour are controlled by
PRE-OPTIC NUCLEUS OF HYPOTHALAMUS
which releases GnRH
failure of GnRH neuron migration from olfactory pit/placode to preoptic nucleus leads to
Kallmann syndrome
olfactory bulb is absent no sense of smell
NO GnRH so congenital hypogonadism
Anterior and posterior nucleus of hypothalamus controls ?
cold and heat regulation
anterior is cool – aage rehna cool dikhna — parasympathetic
posterior is heat — piche se HOT dikhte hai— remember brown fat –thermogenin sec has Beta receptors and hence sympathetic control.
Leptin acts on both lateral and ventromedial nucleus of hypothalamus but ghrelin acts only on
lateral nucleus
craniopharyngioma can cause obesity because
it destroys the ventromedial nucleus of hypothalamus– remember location of craniopharyngioma in relation to hypothalamus—
VM nucleus is satiety centre – which is destroyed
hence craniopharyngioma leads to hyperphagia and obesity
core temperature and set point temperature sensing portion in hypothalmus is
anterior nucleus
Molecules involved in set point temperature changes in hypothalamus
IL 1 from macrophages in ciruclation acts on receptors in anterior nucleus of hypothalamus
which in turn releases Prostaglandin E2
PGE2 increases the set point
leads to fever
hence steroids and aspirin can lower fever
difference between heat stroke and heat exhaustion
heat stroke strikes / damages the tissues – high ambient temperature builds up core temp because of inability to sweat (normal heat loss mechanism)– viscious cycle
heat exhaustion leads to fainting because excessive sweating to maintain core temperature— leads to dehydration, volume loss and low arterial BP
in all sensory receptors — opening of inward ion channel leads to depolarisation for excitation of sensory receptor.. This rule has an exception in which place
in eye-
photoreceptor – light causes reduced inward current— more negative potential – hyperpolarisation develops to activate the signal