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
name the three membranous canals of cochlea
scala VESTIBULI— perilymph- high in Na ions and lined by Reissners membrane
Scala MEDIA— endolymph– high in K ions, is bordered by basilar memb and has organ of corti
scala TYMPANI— again perilymph– high in Na ions
What forms the organ of corti
in scala media– basilar membrane has inner and outer hair cells embedded.
Hair cells have cilia which are embedded in tectorial membrane
hair cells synapse with auditory nerve endings in spiral ganglion
what causes action potential to be generated in hair cells in auditiory sensation
bending of cilia which are touching the tectorial membrane changes K ion conductance
route of auditory sensation
VIII nerve nucleus– ascends in lateral leminiscus– inferior colliculus in tectum of midbrain —– reaches medial geniculate nucleus of thalamus— transmitted to auditory cortex of temporal lobe
only neuron in humans that regularly replace themselves
olfactory neurons–replaced by undifferentiated stem cell at the basal layer of olfactory epithelium
receptor for olfaction is
endings of true unmyelinated C neurons which detect olfaction
olfactory epithelium has two nerve supply
one is cn 1– olfactory nerve
second is Cn V for painful stimuli or noxious smell –like that of ammonia
In fractures of cribriform plate leading to anosmia– ammonia smell will still be detected why
because it is painful noxious subtance — stimuli is carried by trigeminal V nerve
taste sensation pathway
Cn 7, 9 and 10 reach medulla
from medulla they ascend in solitary tract and reach nucleus tractus solitarius
relay in ipsilateral ventral posteromedial of thalamus
then reach primary somatosensory cortex
what two senses are relayed in ventral posteromedial nucleus of thalamus
face sensation — trigeminal nerve
taste —from NTS from 7, 9, 10 CN
all nuclei in thalamus are sensory relays except
VENTRAL LATERAL nucleus which is a motor relay to go back into cortex
it recieves input of modulating the motor activity by cerebellum and basal ganglia
what part of thalamus takes part in limbic system
anterior thalamic nuclei
what three structures of brain are directly connected with mamillary bodies
- hippocampus– via fornix
- Thalamus — via mamillothalamic tract to anterior nuclei
- tegmentum of midbrain -via mamillary peduncle and mamillotegmental tract
role of superior olive in hearing.
superior olive situated from mid pons to upper medulla
receives input from both ears
can tell the angular direction from which ear the sound arises
&
time difference between arrival of sound from both ear
what are positive symptoms in dopaminergic pathways
hallucinations delusions are called positive symptoms
what pathway if has increased activity causes positive psyhotic symptoms
mesolimbic pathway (reward) if has increased activity leads to hallucinations and delusions. Mesolimbic pathway is the site of action for majority of antipsychotic medications.
what are negative symptoms in psychosis
anerygia, apathy, lack of spontaneity are negative symptoms
what causes negative symptoms in psychosis
reduced activity of mesocortical pathway (tegmentum to prefrontal cortex) leads to negative symptoms
what is gerstman syndrome
lesion in angular gyrus of dominant parietal cortex, leads to ———
1 finger agnosia
2 left right disorientation
3 agraphia and acalculia
intramedullary cord metastasis from lung would lead to
brown sequard syndrome
what is brown sequard syndrome
hemisection of cord
features are –
1. LMN motor signs and loss of all sensation at the level of lesion
2. Ipsilateral UMN signs below the lesion.
3. Ipsilateral loss of dorsal column for below the lesion – loss of proprioception vibration
4. Crossed anterior spinothalamic of opp side is transected hence contralateral below lesion loss of TPT.
arygyll robertson pupil are seen in
tabes dorsalis — pupils accomodate but do not react. Tertiary syphillis
kluver bucy syndrome is due to
bilateral amygdala damage most comn cause HSV1 encephalitis
hypersexuality, difficulty in expressive speech disinhibitory behavioural changes –rage anger, hyperorality – putting various things in mouth is a sign of
kluver bucy syndrome which is bilateral amygdala damage.. HSV1 encephalitis is the cause
child abuse shaken babies have which type of intracranial haemorrhage
subdural hematoma
SAH pt on 3rd day onwards deteriorates but imaging shows no change— likely from
vasospasm
relieved by nimodipine CCB
wernickes aphasia due to stroke is associated with what visual field defect. May at times have no motor defects
Pie on the sky— temporal lobe homonymous SUPERIOR QUADRANT anopia
aphasias can be differentiated by
fluency – wernickes aphasia person speaks fluent jargon which means nothing or with grammatical error.
What is rare delayed complication of thalamic stroke
central thalamic pain syndrome Mostly due to VPL nucleus stroke because it contain pain carrying spinothalamic tract.
dorsolateral medulla stroke
PICA lateral medullary wallenberg sydrome
in basilar artery stroke patient gets locked in syndrome just like CPMyelinolyis..what is spared
pt has quadriplegia locked in syndrome with spared vertical eye movement (midbrain fn not supplied by basilar) and consciousness. Pts are usually conscious because of preserved RAS
facial nucleus is affected in what stroke
AICA
lateral pontine stroke
Nucleus ambigues (vagus) is affected in what stroke leading to dysphagia, loss of gag and hoarseness
PICA lateral medullary syndrome
out of AICA / PICA which stroke can lead to ipsilateral hearing loss
AICA leads to hearing loss SNHL because labyrinthine artery is a branch of AICA.
Remember AICA loops in IAM
3 Hz spike wave discharges are seen with which seizure
absence petit mal
a patient with metabolic abnormality has quick repititive jerks.. what type of epilepsy it is
myoclonic
signs of anterior spinal artery/ vertebral artery stroke
medial medullary stroke Dejerine syndrome
- Corticospinal tract- contralateral motor weakness
- Medial leminiscus - loss of vibration and proprioception dorsal columns
- MLF- internuclear ophthalmoplegia of same side
- 12th nerve nucleus which is medial — tongue deviated to same side
by what pathway parotid gland secretions occur
via CN 9
begins in inferior salivary nucleus -CN9 -Otic ganglion - auriculotemporal nerve –parasympathetic fibres to parotid gland
NK1 antagonists are used to treat
Aprepitant
fosa-prepitant
are used to treat chemotherapy induced vomiting.
what nerve exits mid pons— in axial sections if brachium pontis or middle cerebellar peduncle is seen it is mid pons
trigeminal nerve
areas affected by transient ischemia in the order of susceptibility are
1st CA1 fibres of hippocampus– 3min
2nd cerebellar purkinje cell and pyramidal cells of neocortex – - min
Why are pyramidal neurons damages in transient ischemia
these neurons of neocortex have high metabolic demand and once they depolarise during anoxia they are unable to repolarise
histopatho in HIV dementia
microglia is the infected cell
it gets activated and clusters around an area of necrosis forming MICROGLIAL NODULES
they also fuse to FORM MULTINUCLEATED GIANT CELL
HIV reaches brain by monocytes and infects resident macrophages ie microglia.
They dont infect neurons but release neurotoxins which causes dementia.
CHEMICAL IMPLICATED IN MIGRAINE WITH AURA
SUBSTANCE P
CALCITONIN GENE RELATED PEPTIDE
which spinal nerve does not have a dermatome
C1
it is a pure motor nerve.
genes that can be abnormal in parkinsons disease
PINK 1
PARKIN
ALPHA SYNUCLEIN
Pars reticularis of substantia nigra obtains signal from ——-releases—————-to inhibit ———-.
obtains signals from STRIATUM of BG, release inhibitory neurotransmittor GABA and inhibits THALAMUS
important clinical features of parkinsons disease
resting pin rolling tremors
rigidity- cogwheel
brady, hypo and akinesia… it is a slow movement disorder
shuffling gait and postural instability
what are causes of parkinsonism (parkinsons like symptoms in other disease )
lewy body dementia, picks disease and wilsons disease
drugs like — metoclopramide and antipsychotics like haloperidol
deep brain stimulation for treatment of parkinsons disease is given to what part
subthalamic nucleus (indirect pathway high frequency stimulation stops the firing of these neurons) Globus pallidus internus (common to both direct and indirect)
what structure of brain is common / confluence of both direct and indirect nigrostriatal pathway
globus pallidus internus–
because it the only structure inhibiting thalamus.
cause of rigidity and bradykinesia in PD is
nigrostriatal pathway degeneration
which leads to excessive excitation of GP internus by subthalamic nuclei
leading to excessive inhibition of thalamus
no movement / less movements and excessive rigidity
how does DBS deep brain stimulation improve movements
high frequency stimulation leads to stop firing of neurons in subthalamic nucleus and GP interna
which in turn increases (causes dis-inhibition) of thalamo-cortical pathway
hence improved movements
high frequency stimulation of ventro-intermediate thalamic nucleus benefits
essential tremor
thalamus stops – excessive movements stops
what portion of cerebellum is responsible for balance and eye movements
flocullonodular lobe
aka vestibulocerebellum
medial structure — if damaged causes vertigo and nystagmus
what is webers syndrome
midbrain stroke from PCA branches occlusion
characterised by ipsilateral III cn palsy and contralateral hemiparesis
and contralateral parkinsonian rigidity if substantia nigra is involved.
imaging alone cannot differentiate between weber syndrome or bendicts syndrome why
both are midbrain stroke lesions
difference is clinically ascertained
both involve CN3
but benedict involves red nucleus in tegmentum as well hence will have CROSSED HEMIATAXIA AND CROSSED CHOREOATHETOSIS
genes abnormal in charcot marie tooth disease
Myelin protein named as -PMP 22 peripheral myelin protein duplication needed to take care of nerve myelin in day to day compression
dysarthria - clumsy hand syndrome
lacunar infarct in genu of internal capsule
basal pons
perception of flavours or different taste is dependent on
smell and taste of which smell is more important
anosmia after traumatic brain injury occurs due to olfactory nerve rootlets avulsion
olfactory tract goes to which lobe
primary oflactory cortex in medial temporal lobe.
semantic memory defination. FUnction of which part of brain
common knowledge memory ie colour, days of weeks etc
semantic memory is in anterior temporal pole.
at times loss of taste sensation is accompanied by loss of general sensation causing numbness in anterior 2/3rd of tongue. why
because chorda tympani fibres are carried by lingual nerve which is sensory afferent br of V3 trigeminal nerve.
hence taste and gen sensation are both lost together with lingual nerve injury
limitation of upward gaze (looking at floor preferred ) with papilloedema in a child shud prompt
parinaud syndrome from pinealoblastoma or germ cell tumour
Dopamine and GH-RH
Are secreted by what nucleus of hypothalamus
Arcuate
Cataract
Frontal baldness
Gonadal atrophy
Inability to release handshake or doorknob
Myotonic dystrophy
Genetic abnormality in myotonic dystrophy
Trinucleotide CTG expansion
Myotonia protein kinase producing gene
Anticipation present
Myotonia- abnormally slow relaxation
damage to what central structures can cause horners syndrome
posterolateral hypothalamus
lateral brainstem
What is basis pontis
Ventral basal pons
Contains corticospinal tract
Lacunar infarcts in basal pons will lead to
Pure motor hemiparesis —-equal measure of paresis of face arm leg
Dysarthria -clumsy hand syndrome
Ataxic hemiparesis
Child with spastic diplegia
Developmental delays
Chorioathetoid involuntary movements
Elevated arginine level in plasma and csf
Has which diseaSe
Arginase deficiency
Only urea cycle enz def with no or mild hyperammonemia
Arginase converts arginine to urea and ornithine
Gaba is formed by which enz
Gaba is formed from glutamate
By enz glutamate decarboxylase
