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neurology 2 Flashcards

1
Q

what is anisocoria

A

asymmetry of pupils. one needs to determine which pupil is abnormal, It can be done by observing pupils in bright and dim light settings

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2
Q

For anisocoria evaluation the dim light should increase oculosympathetic input and cause pupillary dilatation

A

so if in dim light the asymmetry increases—- it means smaller pupil is paralysed —- unable to dilate and normal one dilates increasing the difference.
In bright light asymmetery will reduce because parasympathetic CN3 induced miosis woulld still occurs in both eyes.

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3
Q

if asymmetry in anisocoria increases in bright light —it indicates ?

A

it indicates larger pupil which should ideally constrict in bright light is paralysis ie CN3 is not working properly

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4
Q

what is relative afferent pupillary defect

A

afferent pathway problem in pupillary reflex – ie retina or optic nerve abnormal.
it is decreased bilateral pupillary constriction in response to light in affected eye
associated with mono-ocular vision loss.

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5
Q

which part is affected most in alzheimers disease

A

hippocampus and then temporoparietal lobes

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6
Q

what is clasp knife rigidity

A

seen in UMN lesions- spasticity
passive flexion should relax extensors because of stretch reflex.
However in UMN extensors are having increased tone and resists passive stretch
can be overcomed by continuing the movement. This is mediated by golgi tendon

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7
Q

nissls bodies in neurons are

A

rough endoplasmic reticulum

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8
Q

what are red neurons

A

disappearence of nissls granules (blue) from cytoplasm of neurons gives it red colour.
Seen in acute irreversible ischemic injury.

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9
Q

what is axonal reaction

A

seen in nerve transection.
Cell body enlarges, nucleus pushed to periphery, nucleolus enlarges and nissles bodies are dispersed. in an effort for protein and lipid synthesis to regenerate the transected axon.

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10
Q

normal function of trochlear nerve

A

supplies superior oblique muscle– it intorts the eye and depresses it when adducted.

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11
Q

signs of trochlear nerve palsy

patients say they cannot see FLOOR

A

eye is in extortion and hypertropia (visual axis above the normal eye) . Patient has vertical diplopia
patient usually chin tucks and head tilts away from the side affected to compensate.

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12
Q

signs of abducens palsy

A

horizontal diplopia and invard deviation (esotropia)

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13
Q

aneurysm of ICA can impinge

A

lateral fibres of optic chiasma leading to ipsilateral nasal hemianopsia.

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14
Q

aneurysm of PCA can impinge and compress

A

3rd CN

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15
Q

contralateral homonymous hemianopsia with macular sparing

A

right primary visual cortex- occipital lobe. due to occlusion of PCA
macula is supplied by MCA and PCA and hence spared.

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16
Q

what is dialysis associated nerve compression?

these compressions affects hands bilaterally

A

beta2 microglobulin accumulates in carpal tunnel leading to median nerve compression

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17
Q

convergence pathway and pupillary light reflex in eyes bypasses

A

MLF medial longitudinal fasciculus

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18
Q

what is lateral geniculate nucleus

A

it is visual information (sensory) relaying centre. It relays vision to cortex.
damage to lateral geniculate thalamic nucleus causes contralateral homonymous hemianopia

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19
Q

upward (vertical gaze palsy - superior colliculus), absent pupillary light reflex and absend / impaired convergence

A

tectal midbrain lesions where superior colliculus is there- parinaud syndrome.

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20
Q

examples of dystonia

A

spasmodic torticollis, blepharospasm, writers cramps etc

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21
Q

what causes hemiballism

A

contralateral injury in or near subthalamic nucleus… flinging of limbs on one side of body.

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22
Q

signs of spinal accessory nerve injury distally in posterior triangle of neck

A

shoulder drooping
no overhead abduction above 100 degrees
lateral displacement of scapula.

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23
Q

middle meningeal artery branch of maxillary artery - terminal branch of ECA enters skull via?

A

foramen spinosum

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24
Q

decreased acetylcholine levels in hippocampus and NUCLEUS BASALIS OF MEYNERT

A

ALZHEIMERS DISEASE

because of deficiency of choline acetyl transferase enzyme.

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25
Q

location and function of nucleus basalis of meynert

A

it is located in basal forebrain.
widely projects into neocortex
functions for memory and cognition.
impaired in alzheimers disease

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26
Q

where is raphe nucleus located, what is its primary neurotransmitter

A

located in medial portion of reticular formation in ENTIRE brainstem.
neurons are serotonergic
impaired anorexia, depression and CIRCARDIUM RHYTHM -sleep disturbances,

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27
Q

WHERE IS RETICULAR ACTIVATING SYSTEM LOCATED

A

THROUGHOUT THE BRAIN STEM

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28
Q

WHAT ARE THE 4 COMPONENTS / SUBPORTIONS OF RETICULAR ACTIVATING SYSTEM

A

LOCUS COERULEUS
RAPHE NUCLEUS
POSTERIOR TUBERO-MAMILLARY HYPOTHALAMUS
PEDUNCULO-PONTINE TEGMENTUM

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29
Q

FUNCTIONS OF RAS RETICULAR ACTIVATING SYSTEM

A

ATTENTION
AROUSAL
ABILITY TO FOCUS
MODULATES THE MUSCLE TONE

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30
Q

HOW IS RAS ACTIVATED

A

WHEN IT RECIEVES SIGNALS FROM LATERAL HYPOTHALAMUS

LATERAL HYPOTHALAMUS IN TURN RELEASES OREXIN WHEN LIGHT STRIKES EYE THAT IS WHN THE PATIENT IS AWAKE

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31
Q

WHERE IS LOCUS COERULUS LOCATED
HOW DOES IT GET ACTIVATED
WHAT DOES IT SECRETE

A

DORSOLATERAL PONS UPPER PART
OREXIN FROM LATERAL HYPOTHALAMUS ACTIVATES IT
IT SECRETES NOR EPINEPHRINE

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32
Q

WHAT DOES TUBEROMAMILLARY NUCLEI IN HYPOTHALAMUS SECRETE

A

HISTAMINE– THEY ARE PRIMARY HISTAMINE PRODUCING REGION

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33
Q

CAUSE OF PATIENT DEATH IN HUNTINGTONS DZ

A

SUICIDE

RESPIRATORY ASPIRATION

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34
Q

CAUSES OF NEURONAL DEATH IN HUNTINGTON DZ– ATROPHY OF CAUDATE AND PUTAMEN

A

DOPAMINE INCREASES
ACH AND GABA DECREASES
HENCE GLUTAMATE EXCITOTOXICITY — NMDA-R BINDING
NEURONS EXCITED TOO MUCH AND DEATH

because mutated huntingtin protein contains numerous glutamate residues due to CAG repeats – more excitotoxicity

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35
Q

what inclusions are found in frontotemporal dementia

A

picks inclusions these are intracytoplasmic round inclusions of hyperphosphorylated tau protein
or
ubiquitinated TDP-43 proteins

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36
Q

visual hallucinations are seen in which dementia

A

lewy body dementia

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37
Q

lewy body intracellular eosinophillic inclusions are seenn in

A

parkinsons disease

lewy body dementia (will be associated with visual hallucinations and REM sleep disturbances)

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38
Q

startle myoclonus is seen in

A

CJD disease

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39
Q

symptoms of CJD

A 
startle myoclonus 
dementia 
ataxia
with periodic sharp waves on EEG 
and elevated 14-3-3 protein in CSF highly specific
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40
Q

elevated 14-3-3 protein in CSF is diagnostic of

A

creutzfeldt jacob disease

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41
Q

opsoclonus myoclonus syndrome is

A

paraneoplastic syndrome associated with

  1. small cell lung ca
  2. neuroblastoma in babies
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42
Q

what is the pathophysiology of papilloedema

A

raised ICT causes break or obstruction in axoplasmic flow of optic nerve

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43
Q

papilloedema is seen on visual field mapping as

A

optic disc edema- -ie enlarged blind spot and peripheral visual field constriction.

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44
Q

what is optic nerve sheath fenestration surgery

A

nicks / incision on optic nerve meninges to relieve intracranial tension effects

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45
Q

triad of normal pressure hydrocephalus

A 
gait apraxia (magnetic gait- patient loses concentration over walking- tendency to freeze unable to initiate gait)
urinary incontinence 
cognitive dysfunction
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46
Q

painful unilateral vision loss with marcus gunn pupil is associated with

A

acute optic neuritis

seen in MS

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47
Q

Internuclear ophthalmoplegia is commonly seen with

A

MULTIPLE SCLEROSIS

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48
Q

WHAT IS THE MNEMONIC TO REMEMBER INTERNUCLEAR OPHTHALMOPLEGIA INO

A

INO
ipsilateral eye has adduction failure
nystagmus in opposite eye

eg in patient with right INO– the right eye remains central shows adduction failure and left normal eyes goes into nystagmus on lateral gaze

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49
Q

why does normal eye go into nystagmus in INO internuclear ophthalmoplegia

A

because opposite MLF is damaged leading to no cn 3 and medial rectus function and hence adduction failure
to over come it – normal eye overfires cn6 – lateral recuts over works – nystagmus

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50
Q

what is the name of symptom– electric shock like sensation in cervical spine on neck flexion

A

LHERMITTE PHENOMENON

SEEN IN MS

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51
Q

WHAT ARE DISEASE MODIFYING DRUGS IN MULTIPLE SCLEROSIS

A

BETA INTERFERON
GLATIRA-MER
NATALI-ZUMAB

52
Q

SPASTICITY OF MULTIPLE SCLEROSIS IS TREATED WITH

A

BACLOFEN

GABA -B RECEPTOR AGONISTS

53
Q

WHAT IS AIDP

A

ACUTE INFLAMMATORY DEMYELINATING POLYRADICULOPATHY

SUBTYPE OF GBS

54
Q

what is CSFhallmark of AIDP or GBS

A

albuminocytologic dissociated
albumin is raised
cell count is normal

55
Q

if GBS symptoms stay for more than 2 months it is called

A

chronic IDP inflammatory demyelinating polyneuropathy

56
Q

autoantibodies diagnositic in CIDP

A

GM1 gangliosides

57
Q

hereditory motor and sensory peripheral nerve neuropathy is

A

charcot marie tooth disease

58
Q

key clues in charcot marie tooth disease

A 
pes cavus 
hammer toes 
inverted bottle shaped atrophy in legs 
foot drop
sensory deficits
59
Q

which is the most common charcot marie tooth diease and its gene

A

CMT 1a

caused by PMP22 gene duplication

60
Q

PML progressive multifocal leukoencephalopathy is seen in

A

aids

natalizumab rituximab and immunosuppression recieving patients

61
Q

episcleral hemangioma is seen in

A

sturge weber syndrome—

can lead to increased IOP and early onset glaucoma

62
Q

genetic mutation in sturge weber syndrome

A

one copy of GNAQ (guanine nucleotide G(q) binding protein -alpha subunit)
this one copy undergoes somatic mosaicism activating mutation

63
Q

when GNAQ gene one of the copy gets activating mutation it lead to

A

sturge weber syndrome— proliferation of capillary sized vessels — leptomeningeal angiomatosis
why – GNAQ– alpha subunit binds GTP and causes signalling for regulation and development of blood vessels. a mutated GNAQ cannot be turned off… leads to angiomas.

64
Q

which tumor supressor genes are affected in tuberous sclerosis

A

TSC1 on chr 9

TSC2 on chr16

65
Q

sphenoid wing dysplasia leading to exophthalmos and facial asymmetry is seen in

A

NF 1

66
Q

what 4 diseases / characteristics can be seen in NF2

A

bilateral vestibular schwannoma
meningioma
ependymoma
juvenile cataracts

AD usually family history of meningioma or bilateral SNHL present

67
Q

two neurocutaneous syndrome which can have pheochromocytoma

A

VHL disease

NF1

68
Q

genetics of VHL mutation

A

VHL produces a protein which ubiquitinates (tags or marks) another protein HIF hypoxia inducible factor for degradation.
Normally HIF senses hypoxia and causes RBC proliferation by regulating erythropoeitin

when VHL is mutated. It cannot stop HIF and hence more erythropoeitin and BV proliferation tumour (hemangioblastomas) develop

69
Q

VHL gene mutation and hemangioblastoma has which hormone increase

A

erythropoietin — hence polycythemia

70
Q

three most common primaries metastatising to brain

A

lung
breast
kidney

71
Q

function of astrocytes

A 
physical support and BBB
repair and reactive gliosis formation 
extracellular K buffer 
glycogen fuel reserve
removes excess neurotransmitter
72
Q

why is meningioma common in female

A

because meningioma pathogenesis has positive growth role of estrogen

73
Q

pseudopalisading cells around necrosis is one feature of GBM
what is the other important features

A

endothelial cell proliferation- microvascular proliferation– these tumours have bleed areas on cut section

74
Q

whorled pattern of cells with psammoma bodies (laminated calcification)

A

meningioma

75
Q

s-100 positive tumour

A

schwannoma — s for s

76
Q

histology of schwannoma

A

dense and light cellular areas
dense cellular areas – have spindle cells (antoni A)
hypocellular areas have myxoid matrix (antoni B)

77
Q

fried egg cells— round nuclei with clear cytoplasm

chicken wire capillary pattern

A

oligodendroglioma

eggs and chicken

78
Q

most common tumour in children GFAP positive tumour in children

A

pilocytic astrocytoma- cystic with enhancing mural nodule

79
Q

histology of pilocytic astrocytoma

A

origin is astrocyte with shows pink thick ROSENTHAL CORKSCREW fibres.

80
Q

CELL WHICH GIVES RISE TO MOST COMMON TUMOUR IN CHILD AS WELL AS ADULT IS

A

ASTROCYTES
CHILD - PILOCYTIC ASTROCYTOMA
ADULT - GBM

81
Q

BELLS PALSY CAN BE PERIPHERAL OR CENTRAL

HOW TO ASCERTAIN

A

IN CENTRAL - pt is able to wrinkle forehead

in peripheral no wrinkling of forehead

82
Q

bilateral bells palsy is also known as facial diplegia. It is seen in

A

lymes disease
neurosarcoidosis
GBS
melkerson rosenthal syndrome— (lip and mouth swelling from granulomatosis, tongue furrows and recurrent bilateral facial palsy)

83
Q

what are homer wright rosettes

A

seen in medulloblastoma (type of PNET round cell tumour)

round blue cells rosette around pink areas of neuritic processes

84
Q

in exam histo shows palisading pattern with central vessel

A

ependymoma

85
Q

in exam histo —-palisading pattern with central acellular pink area ie necrosis

A

GBM

86
Q

patho signs of ependymoma

A

perivascular pseudorosettes and rod shaped basal ciliary bodies near nucleus (blepharoplasts)

87
Q

pituitary region tumour in a child gross cut surface shows motor oil like fluid what is it

A

they are cholesterol crystals in craniopharyngioma

88
Q

pinealoblastoma is associated with

A

precocious puberty because it secretes Bhcg
vertical gaze palsy - tectal compression parinaud syndrome
obstructive hydrocephalus because of aqueductal compression.

89
Q

pineal tumour closely resembles which other germ cell tumour

A

testicular seminoma

90
Q

grandfather gets huntingtons at 60
father gets at 50 and son gets at 40
what is this phenomenon of earlier onset in subsequent generations

A

ANTICIPATION
BECAUSE GERM CELLS CONTINUE AND HAVE INCREASED TRINUCLEOTIDE REPEATS
MORE IN SPERMATOGENESIS
HENCE FATHER TO SON TO SON WOULD HAVE ANTICIPATION PHENOMENON

91
Q

WHAT IS THE CAUSE OF SPONGIFORM ENCEPHALOPATHY

A

PRION PROTEINS
B SHEETS WHICH CANNOT BE DEGRADED AND ACCUMULATES IN NEURONS AND GLIAL CELLS
LEADING TO INTRACELLULAR VACUOLES

b sheets cause more conversion of pre-existing normal alpha sheet proteins to B sheets- hence are considered infection. Once a B sheet — exponential b sheet production due to this phenomenon

92
Q

WHAT IS VARIANT CJD

A

YOUNGER PATIENTS

BY CONSUMPTION OF MEAT OF COWS HAVING SPONGIFORM ENCEPHALOPATHY– MAD COW DISEASE– BOVINE SPONGIFORM ENCEPHALOPATHY

93
Q

WHAT IS FAMILIAL FATAL INSOMNIA

A

INHERITED PRION DISEASE HAVING
1 INSOMNIA
2 EXAGGERATED STARTLE RESPONSE

94
Q

WHAT IS LISSAUER TRACT

A

spinal cord posterolateral tract is also known as lissauer tract
it is just before the nerve from dorsal root ganglion enters posterior horn.

95
Q

what two tracts are the only ones spared in anterior spinal artery occlusion

A

dorsal column and posterolateral tracts (lissauer tract)

96
Q

what is artery of adamkiewicz

A

it is a dominant radiculomedullary artery (usually radicular ie nerve root arteries disappear post natally) but adamkeiwics is a named normally persistent artery
supplying cord below T8. It is largest spinal artery.
arises from left posterior intercostal artery

97
Q

where is spinal cord water shed area

A

mid thoracic ASA territory. Because below it there is artery of adamkeiwicz supplying at T8 to L2 level taking care of blood supply

98
Q

major and only feeder of anterior spinal artery below T8

A

artery of adamkeiwicz.. need to safeguard it during thoracic aortic repairs

99
Q

Dorsal column decussates in

A

Medulla

And then ascends contralaterally as the medial lemniscus

100
Q

Muscles of mastication which close jaw

A

Munchies
Temporalis
Medial pterygoid
Masseter

101
Q

Lateral pterygoid muscle action

A

Only muscle to open the jaw
Lateral pterygoid

Remember chewing is hard work hence needs more 3 muscles

102
Q

Components of corneal reflex

A

Afferent - nasociliary branch V1 of trigeminal n

Efferent is eye closure- facial nerve temporal branch supplying orbicularis oculi

103
Q

Name the three vagal nuclei

A

Nucleus tractus solitarius - visceral sensory— 7 9 10

Nucleus ambiguus— motor to pharynx larynx and upper esophagus—-9 10 11

Dorsal motor nucleus— parasympathetic to heart lungs upper GI— 10

104
Q

Mixed cranial nerve are

A

5 7 9 10

Are both motor and sensory

105
Q

Elevation of pharynx and larynx is by which muscle and nerve supply

A

Stylopharyngeus— glossopharyngeal nerve

106
Q

Which cranial nerve maintains uvula in midline

A

Vagus

Vagus also elevates soft palate

107
Q

Monitoring of carotid body receptors

A

9 th cranial nervd

108
Q

Monitoring of aortic arch receptors

A

Vagus

109
Q

Salivation in parotid gland is by

Salivation in submandibular and sublingual gland is by

A

Glossopharyngeal nerve

Smg and slg —seventh nerve facial

110
Q

Which cranial nerve arise medially

A

3 4 6

12

111
Q

Which cranial nerve arises dorsally

A

Cn4

Dorsal and medially

112
Q

Man in barrel syn

A

Bilateral proximal muscle weakness in both upper and lower limb

Due to bilateral watershed infarcts in ACA-MCA territories
Site of shlder arm and hip thigh region

113
Q

Location of wernickes area

A

Posterior portion of superior temporal gyrus

114
Q

Location of brocas area

A

Lower portion of left frontal lobe

115
Q

What is conduction aphasia

A

Lesion in perisylvian region affects arcuate fasciculus
Which are curved fibres connecting broaca and wernickes area

Pt is unable to repeat phrases but his own speech and comprehension is otherwise clear

116
Q

What are areas 44 and 45

A

Broaca speech area

Motor

117
Q

Area 22 broadmans is

A

Wernickes area

118
Q

PO2 regulates cerebral perfusion only in cases of

A

severe hypoxia. when PO2 falls below 50mmhg

Rest of the times PCo2 is the one maintaing perfusion

119
Q

two factors causing reduction in cerebral perfusion

A

reduced mean arterial pressure

increased intracranial pressure

120
Q

what is the effect of therapeutic hyperventilation

A

wash out of CO2
vasoconstriction intracranially
reduced blood flow and
reduction in ICT

used to treat acute cerebral edema secondary to stroke

121
Q

at what level of hypoxemia does CPP increase

A

when Po2 falls below 50 mmHg

CPP increases

122
Q

Pco2 directly affects Cerebral perfusion untill a threshold— after which no increase in CPP occurs. That value of pCO2 is

A

more than 90 mm Hg.
ie increase in PCO2 causes increase in cerebral blood flow and hence perfusion only till 90 mm Hg.
After this value further increase in CPP is prevented to avoid raised ICT.

123
Q

5F OF LIMBIC SYSTEM

A 
FEEDING
FLEEING
FIGHTING
FEELINGS 
SEX-- FUCK
124
Q

PARTS OF LIMBIC SYSTEM

A

HIPPOCAMPUS AND AMYGDALA
MAMILLARY BODIES AND ANTERIOR THALAMIC NUCLEI
CINGULATE GYRUS
ENTORHINAL CORTEX

125
Q

Where is entorhinal cortex

A

in medial temporal lobe
below hippocampus
it acts as an interface between hippocampus and neocortex

Flash Facts (23 decks)

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