neurology 3 Flashcards

1
Q

cerebellar deep nuclei names

A
lateral to medial are 
dentate
emboliform 
globose 
fastigial
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2
Q

what medial structures of cerebellum gives rise to truncal ataxia, head tilting and nystagmus

A

vermis
fastigial medial most deep nucleus
flocullonodular lobe

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3
Q

medial cerebellar lesions give rise to uni/ bilateral weakness

A

bilateral truncal and proximal extremity weakness

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4
Q

lateral cerebellar lesions can give rise to

A

tendency to fall on affected side

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5
Q

parts of striatum of basal ganglia

remember to imagine coronal section for striatum structures

A

caudate

putamen

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6
Q

what are components of lentiform nucleus of BG

remember to imagine axial section

A

putamen

globus pallidus

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7
Q

Direct BG pathway receptors are

A

D1 - excitatory- stimulates and increases motion

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8
Q

Indirect BG pathway receptors are

A

indirect is inhibitory for motion and receptors are D2.

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9
Q

three components of blood brain barrier

A

TIGHT junctions between NON FENESTRATED endothelial cells
complete encircling BASEMENT MEMBRANE
FOOT PROCESSES OF ASTROCYTES

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10
Q

3 places not having blood brain barrier

A
  1. AREA POST TREMA-post chemo vomiting has CTZ
  2. OVLT- organum vasculosum lamina terminalis– osmoreceptors
  3. NEurohypophysis – for ADH release
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11
Q

why is area post trema, OVLT and neurohypophysis devoid of blood brain barrier

A

because their capillary endothelial cells are fenestrated.

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12
Q

Vomiting centre is located in

A

medulla known as Nucleus tractus solitarius (one of the three vagal nuclei)

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13
Q

inputs to Vomiting centre in medulla is recieved from

A

CTZ from area post trema
GIT via vagus nerve (remember vomiting centre NTS is a vagal nuclei)
vestibular system
CNS

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14
Q

5 major receptors in CTZ and vomiting centre

A

H1 and M1—- antagonists used to treat motion sickness

Neurokinin NK1, D2 and 5HT3 serotonin—– antagonists are used to treat chemotherapy induced vomiting

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15
Q

treatment of hyperemesis gravidarum

A

H1 antagonists – doxylamine

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16
Q

regulation of circadian rhythm is done by

A

suprachiasmatic nucleus of hypothalamus after recieving signals from eyes.

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17
Q

what products are seen in night – nocturnal release under circadian rhythm

A

ACTH
prolactin
melatonin
norepinephrine

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18
Q

how is melatonin secreted by pineal gland

A

at night – suprachiasmatic nucleus releases Norepinephrine

which stimulates pineal gland to release melatonin at night

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19
Q

what causes reduction in REM sleep

A

nor -epinephrine – remember stress increases NE and in stress u cant sleep

Alcohol
Benzodiazepines and barbiturates

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20
Q

what is the mechanism of action of opoids in nociception

A

inhibition of release of substance P

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21
Q

Fast pain is carried by —- fibres and is —–localised

slow pain is carried by —–fibres and is —–localised

A

Fast pain is carried by type III fibres and is WELL localised
slow pain is carried by C-fibres and is POORLY -localised

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22
Q

NAME THE 4 MECHANORECEPTORS

A

PACINNIAN —- in subcu skin for vibration
MEISSEINERS— in non hairy skin for fine touch velocity
RUFFINI —-for pressure
MERKEL DISC– position seen in skin

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23
Q

REM sleep is characterised by

A

rapid eye movements
loss of muscle tone but penile erection
pupillary constriction.
DREAMS

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24
Q

REM sleep EEG resembles

A

awake person EEG -beta waves
and
stage 1 of NREM

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25
Q

source of waves in EEG

A

synaptic evoked potential btw the purkinje cells of cerebral cortex

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26
Q

EEG waves in awake person

A

with eyes open — alert person – beta waves

with eyes closed — alpha waves

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27
Q

what are the stages of non REM sleep

A

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

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28
Q

in which phase of sleep bruxism occurs

A

Stage 2 NREM— sleep spindles and K complexes on EEG

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29
Q

in what phase of sleep nightmares and dreams occurs

A

REM sleep

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30
Q

difference between nightmares and night terrors

A

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.

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31
Q

Night terrors, bedwetting and sleep walking occurs in which phase of cycle

A

stage N3 of NREM –slow wave sleep that is delta sleep

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32
Q

what regulates REM sleep

A

REM -ON neurons in Locus coeruleus

REM-OFF neurons in pedunculopontine tegmentum

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33
Q

Acetylcholine levels increase and oxygen consumption by brain occurs in which phase of sleep

A

REM sleep

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34
Q

what is REM sleep latency

A

period of time between onset of sleep to first REM episode – 90 -120 min
Latency is increased in elderly
reduced in depression

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35
Q

cause of extraocular movements in REM sleep

A

activity of PPRF— paramedian pontine reticular formation

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36
Q

changes of sleep phases in elderly are

A

increased latency — difficulty falling asleep

reduced N3phase and REM phase —- once they fall asleep their sleep is shorter in duration

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37
Q

why is REM sleep paradoxical

A

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

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38
Q

changes of sleep in major depression

A

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

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39
Q

thermoregulation and sexual behaviour are controlled by

A

PRE-OPTIC NUCLEUS OF HYPOTHALAMUS

which releases GnRH

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40
Q

failure of GnRH neuron migration from olfactory pit/placode to preoptic nucleus leads to

A

Kallmann syndrome
olfactory bulb is absent no sense of smell
NO GnRH so congenital hypogonadism

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41
Q

Anterior and posterior nucleus of hypothalamus controls ?

A

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.

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42
Q

Leptin acts on both lateral and ventromedial nucleus of hypothalamus but ghrelin acts only on

A

lateral nucleus

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43
Q

craniopharyngioma can cause obesity because

A

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

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44
Q

core temperature and set point temperature sensing portion in hypothalmus is

A

anterior nucleus

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45
Q

Molecules involved in set point temperature changes in hypothalamus

A

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

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46
Q

difference between heat stroke and heat exhaustion

A

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

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47
Q

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

A

in eye-
photoreceptor – light causes reduced inward current— more negative potential – hyperpolarisation develops to activate the signal

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48
Q

name the three membranous canals of cochlea

A

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

49
Q

What forms the organ of corti

A

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

50
Q

what causes action potential to be generated in hair cells in auditiory sensation

A

bending of cilia which are touching the tectorial membrane changes K ion conductance

51
Q

route of auditory sensation

A

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

52
Q

only neuron in humans that regularly replace themselves

A

olfactory neurons–replaced by undifferentiated stem cell at the basal layer of olfactory epithelium

53
Q

receptor for olfaction is

A

endings of true unmyelinated C neurons which detect olfaction

54
Q

olfactory epithelium has two nerve supply

A

one is cn 1– olfactory nerve

second is Cn V for painful stimuli or noxious smell –like that of ammonia

55
Q

In fractures of cribriform plate leading to anosmia– ammonia smell will still be detected why

A

because it is painful noxious subtance — stimuli is carried by trigeminal V nerve

56
Q

taste sensation pathway

A

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

57
Q

what two senses are relayed in ventral posteromedial nucleus of thalamus

A

face sensation — trigeminal nerve

taste —from NTS from 7, 9, 10 CN

58
Q

all nuclei in thalamus are sensory relays except

A

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

59
Q

what part of thalamus takes part in limbic system

A

anterior thalamic nuclei

60
Q

what three structures of brain are directly connected with mamillary bodies

A
  1. hippocampus– via fornix
  2. Thalamus — via mamillothalamic tract to anterior nuclei
  3. tegmentum of midbrain -via mamillary peduncle and mamillotegmental tract
61
Q

role of superior olive in hearing.

A

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

62
Q

what are positive symptoms in dopaminergic pathways

A

hallucinations delusions are called positive symptoms

63
Q

what pathway if has increased activity causes positive psyhotic symptoms

A
mesolimbic pathway (reward) if has increased activity leads to hallucinations and delusions. 
Mesolimbic pathway is the site of action for majority of antipsychotic medications.
64
Q

what are negative symptoms in psychosis

A

anerygia, apathy, lack of spontaneity are negative symptoms

65
Q

what causes negative symptoms in psychosis

A

reduced activity of mesocortical pathway (tegmentum to prefrontal cortex) leads to negative symptoms

66
Q

what is gerstman syndrome

A

lesion in angular gyrus of dominant parietal cortex, leads to ———
1 finger agnosia
2 left right disorientation
3 agraphia and acalculia

67
Q

intramedullary cord metastasis from lung would lead to

A

brown sequard syndrome

68
Q

what is brown sequard syndrome

A

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.

69
Q

arygyll robertson pupil are seen in

A

tabes dorsalis — pupils accomodate but do not react. Tertiary syphillis

70
Q

kluver bucy syndrome is due to

A

bilateral amygdala damage most comn cause HSV1 encephalitis

71
Q

hypersexuality, difficulty in expressive speech disinhibitory behavioural changes –rage anger, hyperorality – putting various things in mouth is a sign of

A

kluver bucy syndrome which is bilateral amygdala damage.. HSV1 encephalitis is the cause

72
Q

child abuse shaken babies have which type of intracranial haemorrhage

A

subdural hematoma

73
Q

SAH pt on 3rd day onwards deteriorates but imaging shows no change— likely from

A

vasospasm

relieved by nimodipine CCB

74
Q

wernickes aphasia due to stroke is associated with what visual field defect. May at times have no motor defects

A

Pie on the sky— temporal lobe homonymous SUPERIOR QUADRANT anopia

75
Q

aphasias can be differentiated by

A

fluency – wernickes aphasia person speaks fluent jargon which means nothing or with grammatical error.

76
Q

What is rare delayed complication of thalamic stroke

A

central thalamic pain syndrome Mostly due to VPL nucleus stroke because it contain pain carrying spinothalamic tract.

77
Q

dorsolateral medulla stroke

A

PICA lateral medullary wallenberg sydrome

78
Q

in basilar artery stroke patient gets locked in syndrome just like CPMyelinolyis..what is spared

A

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

79
Q

facial nucleus is affected in what stroke

A

AICA

lateral pontine stroke

80
Q
Nucleus ambigues (vagus) is affected in what stroke 
leading to dysphagia, loss of gag and hoarseness
A

PICA lateral medullary syndrome

81
Q

out of AICA / PICA which stroke can lead to ipsilateral hearing loss

A

AICA leads to hearing loss SNHL because labyrinthine artery is a branch of AICA.
Remember AICA loops in IAM

82
Q

3 Hz spike wave discharges are seen with which seizure

A

absence petit mal

83
Q

a patient with metabolic abnormality has quick repititive jerks.. what type of epilepsy it is

A

myoclonic

84
Q

signs of anterior spinal artery/ vertebral artery stroke

A

medial medullary stroke Dejerine syndrome

  1. Corticospinal tract- contralateral motor weakness
  2. Medial leminiscus - loss of vibration and proprioception dorsal columns
  3. MLF- internuclear ophthalmoplegia of same side
  4. 12th nerve nucleus which is medial — tongue deviated to same side
85
Q

by what pathway parotid gland secretions occur

A

via CN 9
begins in inferior salivary nucleus -CN9 -Otic ganglion - auriculotemporal nerve –parasympathetic fibres to parotid gland

86
Q

NK1 antagonists are used to treat

A

Aprepitant
fosa-prepitant
are used to treat chemotherapy induced vomiting.

87
Q

what nerve exits mid pons— in axial sections if brachium pontis or middle cerebellar peduncle is seen it is mid pons

A

trigeminal nerve

88
Q

areas affected by transient ischemia in the order of susceptibility are

A

1st CA1 fibres of hippocampus– 3min

2nd cerebellar purkinje cell and pyramidal cells of neocortex – - min

89
Q

Why are pyramidal neurons damages in transient ischemia

A

these neurons of neocortex have high metabolic demand and once they depolarise during anoxia they are unable to repolarise

90
Q

histopatho in HIV dementia

A

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.

91
Q

CHEMICAL IMPLICATED IN MIGRAINE WITH AURA

A

SUBSTANCE P

CALCITONIN GENE RELATED PEPTIDE

92
Q

which spinal nerve does not have a dermatome

A

C1

it is a pure motor nerve.

93
Q

genes that can be abnormal in parkinsons disease

A

PINK 1
PARKIN
ALPHA SYNUCLEIN

94
Q

Pars reticularis of substantia nigra obtains signal from ——-releases—————-to inhibit ———-.

A

obtains signals from STRIATUM of BG, release inhibitory neurotransmittor GABA and inhibits THALAMUS

95
Q

important clinical features of parkinsons disease

A

resting pin rolling tremors
rigidity- cogwheel
brady, hypo and akinesia… it is a slow movement disorder
shuffling gait and postural instability

96
Q

what are causes of parkinsonism (parkinsons like symptoms in other disease )

A

lewy body dementia, picks disease and wilsons disease

drugs like — metoclopramide and antipsychotics like haloperidol

97
Q

deep brain stimulation for treatment of parkinsons disease is given to what part

A
subthalamic nucleus (indirect pathway high frequency stimulation stops the firing of these neurons)
Globus pallidus internus (common to both direct and indirect)
98
Q

what structure of brain is common / confluence of both direct and indirect nigrostriatal pathway

A

globus pallidus internus–

because it the only structure inhibiting thalamus.

99
Q

cause of rigidity and bradykinesia in PD is

A

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

100
Q

how does DBS deep brain stimulation improve movements

A

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

101
Q

high frequency stimulation of ventro-intermediate thalamic nucleus benefits

A

essential tremor

thalamus stops – excessive movements stops

102
Q

what portion of cerebellum is responsible for balance and eye movements

A

flocullonodular lobe
aka vestibulocerebellum
medial structure — if damaged causes vertigo and nystagmus

103
Q

what is webers syndrome

A

midbrain stroke from PCA branches occlusion
characterised by ipsilateral III cn palsy and contralateral hemiparesis
and contralateral parkinsonian rigidity if substantia nigra is involved.

104
Q

imaging alone cannot differentiate between weber syndrome or bendicts syndrome why

A

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

105
Q

genes abnormal in charcot marie tooth disease

A

Myelin protein named as -PMP 22 peripheral myelin protein duplication needed to take care of nerve myelin in day to day compression

106
Q

dysarthria - clumsy hand syndrome

A

lacunar infarct in genu of internal capsule

basal pons

107
Q

perception of flavours or different taste is dependent on

A

smell and taste of which smell is more important

anosmia after traumatic brain injury occurs due to olfactory nerve rootlets avulsion

108
Q

olfactory tract goes to which lobe

A

primary oflactory cortex in medial temporal lobe.

109
Q

semantic memory defination. FUnction of which part of brain

A

common knowledge memory ie colour, days of weeks etc

semantic memory is in anterior temporal pole.

110
Q

at times loss of taste sensation is accompanied by loss of general sensation causing numbness in anterior 2/3rd of tongue. why

A

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

111
Q

limitation of upward gaze (looking at floor preferred ) with papilloedema in a child shud prompt

A

parinaud syndrome from pinealoblastoma or germ cell tumour

112
Q

Dopamine and GH-RH

Are secreted by what nucleus of hypothalamus

A

Arcuate

113
Q

Cataract
Frontal baldness
Gonadal atrophy
Inability to release handshake or doorknob

A

Myotonic dystrophy

114
Q

Genetic abnormality in myotonic dystrophy

A

Trinucleotide CTG expansion
Myotonia protein kinase producing gene
Anticipation present

Myotonia- abnormally slow relaxation

115
Q

damage to what central structures can cause horners syndrome

A

posterolateral hypothalamus

lateral brainstem

116
Q

What is basis pontis

A

Ventral basal pons

Contains corticospinal tract

117
Q

Lacunar infarcts in basal pons will lead to

A

Pure motor hemiparesis —-equal measure of paresis of face arm leg

Dysarthria -clumsy hand syndrome

Ataxic hemiparesis

118
Q

Child with spastic diplegia
Developmental delays
Chorioathetoid involuntary movements
Elevated arginine level in plasma and csf

Has which diseaSe

A

Arginase deficiency

Only urea cycle enz def with no or mild hyperammonemia

Arginase converts arginine to urea and ornithine

119
Q

Gaba is formed by which enz

A

Gaba is formed from glutamate

By enz glutamate decarboxylase