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Neurology Flashcards

1
Q

Diseases associated with syringomyelia

A

trauma
Extrinsic compression
Arnold chiari malformation

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2
Q

Common location of syringomyelia

A

C8-t1
Cape like sensory loss
Due to involvement of anterior commisure in cord
Bilateral pain and temperature sensation lost
Fine touch and proprioception preserved because carried by dorsal columns which do not cross

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3
Q

What runs in lateral horn of spinal cord

A

Hypothalamospinal tract

Sympathetic outflow for face at T1

If affected because of syringomyelia causes horners syndrome

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4
Q

What are features of horners syndrome

A

Ptosis
Miosis
Anhidrosis

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5
Q

What is affected in poliomyelitis

A

Anterior horn cells

Lmn signs flaccid paralysis, weakness with atrophy, impaired reflexes with
Negative babinski—- downward going toes

DD is werdnig hoffman disease - floppy baby syndrome— AR INHERITED ANT MOTOR NEURON DEGENERATION DEATH IN FEW YEARS

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6
Q

What is floppy baby syndrome

Werdnig hoffman syndrome

A

It is an autosomal recessive inherited degeneration of anterior horn cell
Mimics polio symptoms
Death in few years after birth

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7
Q

What is amyolateral sclerosis

A

Degenerative upper and lower motor neuron disease ie of corticospinal tract

Anterior horn involvement —-LMN SIGNS

LATERAL CORTICOSPINAL TRACT INV—-UMN SIGNS

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8
Q

How can ALS and syringomyelia be differentiated

A

ALS is pure motor disorder no cape like sensory loss

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9
Q

What mutation can be seen in familial cases of ALS

A

Zine- copper superoxide dismutase

SOD Is important mechanism to manage oxygen free radical by converting it to hydrogen peroxide

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10
Q

What is freidreichs ataxia

A

Degenerative disorder of cerebellum and spinal cord tracts

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11
Q

Symptoms of freidrichs ataxia

A

Ataxia
Loss of vibration and proprioception
Muscle weakness in lower extremities
Loss of DTR

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12
Q

Genetic abnormality in freidrichs ataxia

A

AR
unstable GAA trinucleotide repeats in frataxin gene

Fra taxin—- iron toxin —- iron is toxic in mitochondria because abnormal iron metabolism in mitochondria generates free radicals

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13
Q

What age friedrichs ataxia presents

A

Childhood

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14
Q

Association of freidrichs ataxia

A

Hypertrophic cardiomyopathy

High yield

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15
Q

3 most common causes of

Meningitis in neonates

A

Grp B STREPTO
E COLI
L MONOCYTOGENES

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16
Q

Menignitis causes in children and teenages

A

Neisseria meningitidis

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17
Q

Meningitis in adults and elderly

A

Strep pneumo

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18
Q

Meningitis in. Non vaccinated infants

A

H influenza

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19
Q

Most common viral cause of meningitis

A

Coxsackie

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20
Q

LP FINDINGS IN BACTERIAL MENINGITIS

A

Neutrophils with low glucose
Positive gram stain
Positive culture

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21
Q

LP IN VIRAL MENINGITIS

A

Lymphocytes with normal CSF glucose

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22
Q

LP IN FUNGAL MENINGITIS

A

Lymphocytes with low CSF GLUCOSE

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23
Q

Causes of global cerebral ischemia

A

Low perfusion
Acute reduction in blood flow— SHOCK
chronic hypoxia— ANEMIA
repeated hypoglycemia—- INSULINOMA

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24
Q

Mild GCI resolves
Severe does cerebral necrosis and death or vegetative comma state

What are features of moderate or intermdiate form of GCI

A

Classic example is low perfusion hypotension

Infarcts in watershed areas
Damage to highly vulnerable areas of brain

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25
Q

What are the high vulnerable areas prone to damage in moderate global cerebral
Ischemia

A

Cortex neurons in layer 3 5 6 pyramidal neurons triangular appearence
Giving line of necrosis in 356
Ie cortical laminar necrosis

And pyramidal neurons of hippocampus ( long term memory)
Purkinje cells of cerebellum

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26
Q

Embolic stroke is

A

Haemorrhagic infarction

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27
Q

Lacunar stroke is due to

A

Hyaline arteriosclerosis

Cmnly in lenticulostriate vessels

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28
Q

Histology of ischemic stroke

A

Leads to liquefactive necrosis
1st sign— red neurons 12 hrs

2nd sign— cells come in - neutrophils and microglia for granulation tissue by 1 week

3rd sign— gliosis with fluid filled cystic spaces by 1 month

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29
Q

Common cause of intracranial haemorrhagd

A

Hypertension causes rupture of charcot bouchards microaneurysms

In basal ganglia

Other site— cerebellum

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30
Q

LP XANTHOCHROMIA

A

Yellow discolouration of csf due to SUBARACHNOID HAEMORRHAGE

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31
Q

Mst common cause of SAH

A

Berry aneurysms located in anterior circle of willis mostly near branch points of Acom

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32
Q

Diseases in which berry aneurysms are found

A

Marfans

AD PKD

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33
Q

Which vessel wall layer is lacking in berry aneurysm

Remember it is at branch point and it is a true aneurysm

A

Media layer

Muscle

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34
Q

Vessel most likely bleeding in epidural hematoma

A

Middle meningeal artery
Usually due to fractures of temporal bone

Lucid interval and herniation

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35
Q

Bleeding source in subdural

Hematoma

A

Bridging veins. Between dura and arachnoid

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36
Q

What structures are compressed due to uncal herniation

A

Cn 3 eye will be down out dilated and shut

PCA

Paramedian artery running on brain stem - gives rise to duret haemorrhages

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37
Q

What is the problem with leukodystrophies

A

Inherited disorders of enzymes needed for production and maintenance of myelin

Leads to demyelination

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38
Q

Which is the most common leukodystrophy

A

Metachromatic leukodystrophy

Def aryl sulfatase A

Myelin cannot be degraded.. sulfatides accumulates in neuron lysosomes

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39
Q

What is krabbes disease

A

Inherited leukodystrophy which has galactocerebroside- beta galatosidase

Galactocerebroside accumulates in macrophages

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40
Q

What is the biochemical problem

In adrenoleukodystrophh

A

Impaired addition of co enzyme A to VLCFA

Accumulates in adrenal gl and white matter

Xlr

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41
Q

What genetic suspceptibility does multiple sclerosis have

A

HLA DR2

Destruction of oligodendrocyte is main event
Hence leads to myelin loss

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42
Q

Scanning speach is seen in?

A

Multiple sclerosis

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43
Q

What structure involvement in multiple sclerosis leads to internuclear ophthalmoplegia

A

MLF

MEDIAL LONGITUDINAL FASCICULUS

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44
Q

What is internuclear ophthalmoplegia?

A

Both eyes do not turn together while looking at one direction

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45
Q

LP diagnosis of multiple sclerosis

A

Increased lymphocytes
Increased immunoglobulins
IgG oligoclonal bands
Presence of myelin basic protein

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46
Q

Locked in syndrome is seen in ?

A

Pontine lesions
Esp central pontine demyelination

All tracts in brainstem esp pons paralysed
Only cn 3 which is above pons is functioning
That is patient can move only eye and nothing else
Hence he gets locked in in his own body

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47
Q

MICTURITION CENTRE IN BRAIN IS LOCATED IN

A

MEDIAL FRONTAL LOBE - CINGULATE GYRUS

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48
Q

MANIFESTATIONS OF BILATERAL ACA OCCULUSION

A

BILATERAL SOMATOSENSORY AND MOTOR LOWER LIMB WEAKNESS
ABULIA (inability to take decisions)
SIGNIFICANT BEHAVIOURAL MALFUNCTION
MICTURITION CENTRE– URINARY INCONTINENCE

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49
Q

WHAT IS ANOSOGNOSIA

A

INABILITY TO IDENTIFY AND PERCEIVE HIS OR HER ILLNESS – FRONTAL LOBE INFARCTS MCA OCCLUSION

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50
Q

BROACAs aphasia

A

damage to dominant frontal lobe

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51
Q

damage to non dominant parietal lobe can lead to

A

hemineglect – loss of spatial sensation of opp half of body

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52
Q

MCA infarct leads to what type of blindness

A

cortex of temporal and parietal lobe affected – hence optic radiations are affected- ie contralateral homonymous hemianopia

53
Q

conjugate deviation towards the side of stroke

A

MCA infarct

54
Q

primary pathophysiology of lacunar infarcts

A

lipohyalinosis and microatheroma

55
Q

what is lipohyalinosis

A

cause of lacunar infarcts – it is leakage of plasma proteins into vessel wall due to damaged endothelium.
leads to hyaline thickeneing
collageneous sclerosis
accumulation of foamy macrophages in wall.

56
Q

features of thalamic stroke

A

complete (both anterior and dorsal column) sensory loss
gait disturbance due to loss of ataxia.
depending on thalamic nucleus involved – further symptoms arise.

57
Q

all sensory information relays in thalamus except

A

olfaction

58
Q

features of acute HIV

A

fever rash lymphadenopathy and painful oral tongue ulcers

59
Q

motor supply of tongue is

A

hypoglossal nerve with exception of anterior tonsillar pillar – ie palatoglossus muscle supplied by vagus nerve.

60
Q

general sensation of tongue

A

V3 division of trigeminal nerve in anterior 2/3rd
Glossopharyngeal in posterior 1/3rd
vagus nerve in the posterior most tongue – root area

61
Q

gustatory sensation is carried by

A

chorda tympani branch of facial nerve in anterior 2/3rd of tongue
for rest it is same as general sensation
ie posterior 1/3rd taste is carried by 9th
posterior most root, pharynx and upper esophagus taste is carried by 10th vagus

62
Q

contents of Superior orbital fissure

A

CN 3 -loss of adduction
NASOCILIARY BRANCH OF FACIAL NERVE - LOSS OF CORNEAL REFLEX
CN 4 AND 6 (LR 6 SO4)
SOV– Superior ophthalmic vein

63
Q

the only two contents of optic canal

A

optic nerve and ophthalmic artery

64
Q

contents of inferior orbital fissure – remember it has things which need to go to face

A

inferior orbital nerve and zygomatic nerve branches of V2 division of trigeminal nerve.
infraorbital vessels
ganglionic branches from pterygopalatine ganglion to V2 div
inferior ophthalmic vein

65
Q

when a patient tells a story with memory gaps and fills those gaps with his own story which he believes to be true– this is known as ?

A 
CONFABULATION 
due to thiamine deficiency 
inhibits new memory and learning also -- hence there is confabulation with anterograde amnesia
usually permanent despite treatment 
part of korsakoff syndrome
66
Q

korsakoff syndrome is damage to ?

A

anterior and dorsomedial thalamic nuclei

67
Q

structures affected in thiamine deficiency

A

paraventricular structures like mamillary bodies, anterior and dorsomedial thalamic nuclei
CN 3, 6 and vestibular nuclei – horizontal gase palsy and bilateral abducens palsy
cerebellar cortex – gait ataxia
mental status changes - disorientation, apathy, confabulation and anterograde memory loss

68
Q

What are the hall marks of korsakoffs syndrome

A

permanent memory loss and confabulation

69
Q

what is cerebral amyloid angiopathy

A

deposition of b amyloid in small and medium size cerebral vessel wall making it weak and prone to rupture.
It is seen as recurrent lobar haemorrhages in elderly

70
Q

most common cause of recurrent cerebral cortical haemorrhages in elderly

A

cerebral amyloid angiopathy

71
Q

Cerebral amyloid angiopathy is not associated with systemic amyloidosis. It has the same amyloid as in Alzimers diesae

A

true

72
Q

Vitamin E deficiency is extremely rare. Seen only in patients with ?

A

fat malabsorption - pancreatic insufficiency or cystic fibrosis
and
abetalipoproteinemia

73
Q

DD of vitamin E deficiency induced neuro symptoms

A

Vitamin B12 def –SACD of spinal cord due to dorsal column involvement
Fredrichs ataxia

74
Q

components of vitamin E def

A

hemolysis and neuro free radical damage
involvement of dorsal column - loss of vibration and proprioception
ATAXIA due to spinocerebellar tract involvement
Loss of DTR due to peripheral nerve degeneration eg sural nerve biopsy shows nonmyelination

75
Q

associations of berry aneurysm

A 
AD PKD
MARFANS AND EHLERS DANLOS SYNDROME
FMD
MOYA MOYA DZ
COARCTATION OF AORTA
76
Q

WHAT IS THE MEANING OF CROSSED SIGNS

A

IPSILATERAL CRANIAL NERVE PALSIES WITH CONTRALATERAL HEMIPARESIS
SEEN IN BRAINSTEM LESIONS

77
Q

WHAT IS VERNET JUGULAR FORAMEN SYNDROME

A

CRANIAL NERVE 9 10 11 PALSY
DYSPHAGIA HOARSENESS
LOSS OF GAG REFLEX
SHIFT OF UVULA TO NORMAL SIDE

78
Q

WHAT IS BABINSKI SIGN

A

IT IS KNOWN AS PLANTAR REFLEX IE ON STROKING LATERAL SOLE MARGIN TILL BALL THE TOE GOES IN PLANTAR FLEXION… THIS IS NORMAL PHENOMENON.
IF NOT - UMN PALSY

79
Q

WHAT IS ABNORMAL BABINSKI SIGN

A

TOE IN EXTENSION WITH OR WITHOUT FANNING OF LITTLE FINGERS

80
Q

CHILDREN UNDER 12 YEARS WILL HAVE POSITIVE BABINSKI BECAUSE

A

OF INCOMPLETE MYELINATION OF CORTICOSPINAL TRACTS

81
Q

WHAT IS PRONATOR DRIFT

A

PRONATION BECOMES MORE POWERFUL THAN SUPINATION OF FOREARM IN UMN PALSY

82
Q

SIGNS OF UMN PALSY

A

HYPERREFLEXIA – -BRISK DTR
SPASTICITY
CLASP KNIFE RIGIDITY ON SUDDEN RELEASE OF PASSIVE FLEXION
INCREASED MUSCLE TONE
PRONATOR DRIFT
PYRAMIDAL WEAKNESS (LL FLEXORS AND UL EXTENSORS ARE MORE WEAK)

83
Q

WHAT IS PYRAMIDAL WEAKNESS

A

LOWER LIMB FLEXORS AND UPPER LIMB EXTENSORS HAVE MORE WEAKNESS IN UPPER MOTOR NEURON PALSY

84
Q

SIGNS OF LMN PALSY

A 
MUSCLE WEAKNESS WITH HYPOTONIA
LOSS OF DTR 
MUSCLE ATROPHY 
FASCICULATIONS OF SMALL GRP OF FIBRES 
BABINSKI WOULD BE NORMAL OR NO RESPONSE
85
Q

during passive limb movement, if the movement is interrupted due to rhythmic contractions of muscle fibres which gets rigid is known as

A

cog wheel rigidity — seen in extrapyramidal tract signs which functions normally to modulate a motor action

86
Q

what is cogwheel rigidity

A

increased muscle rigidity due to rhythmic muscle contraction during a passive movement. —sign of extrapyramidal tract lesion- parkinsons

87
Q

muscles supplied by superior gluteal nerve

A

gluteus medius minimus

tensor fascia latae

88
Q

difficulty in rising from seated position and climbing stairs

A

extension and external rotation of hip is not happening
gluteus maximus paralysed
inferior gluteal nerve palsy

89
Q

impaired thigh adduction and medial thigh sensory loss

A

obturator nerve injury

90
Q

location of red nucleus and its parts

A

ventral midbrain

divided into magnocellular and more important larger lower parvocellular

91
Q

decorticate rigidity

A

flexion of upper arms to the core of body – flexor posturing is decorticate
indicates intact red nucleus (leading to disinhibition of nucleus and more active rubrospinal tract ie lesion is above red nucleus)

92
Q

what is hypertrophic olivary degeneration

A

seen in direct damage to red nucleus
olives degenerated by shows hypertrophy
muscles like diaphragm, laryngeal muscles, soft palate and pharyngeal muscles shows rhythmic jerking motions
leads to palatal myoclonus and dysphagia

93
Q

pathophysiology of decorticate rigidity

A

lesion is above red nucleus - red nucleus is intact.

downward to red nucleus has UMN TYPE changes — hypertonic rigidity – flexors of upper limb get rigid

94
Q

CAFE AU LAIT SPOTS

LISCH NODULES ARE SEEN IN

A

NF1

95
Q

CHROMOSOME FOR NF

A

17 FOR 1 —NEUROFIBROMIN

22 FOR 2 —MERLIN PROTEIN

96
Q

PALISADES (natural cell and nuclear alignment stacking) ARE SEEN IN

A

SCHWANNOMA

97
Q

PSEUDOPALISADES (nuclear or cell alignment around an area of necrosis )ARE SEEN IN

A

GBM

98
Q

reticulin deposits and chronic inflammatory infiltrates are seen in which brain tumour

A

pleomorphic xanthoastrocytoma— mri cyst with solid enhancing nodule- peripherally location near leptomeninges and hence shows dural tail

99
Q

ependymal cells palisading around blood vessel and hence are called perivascular pseudorossettes

A

ependymoma

100
Q

A beta amyloid is a broken down product of —- accumulated in alzeimers disease

A

App receptor

APP receptor if broken down by beta secretase gives beta amyloid protein

101
Q

What is definition of dementia

A

Cognitive + memory loss

Without any loss of consciousness

102
Q

Increased ApoE4 allele is associated with

A

Sporadic form of ALzeimers d

103
Q

ApoE2 form is associated with

A

Protective apo E2

Hence if reduced leads to ALZ DZ

104
Q

Associations of early onset alziehmers

A

Presenilin 1
Downs syndrome because trisomy 21
And App protein which breakdown leads to ALZ DZ is on chromosome 21 hence downs patients have too many APP proteins leading to early onset

105
Q

What is tau

A

Tau is a microtubule associated protein which is needed to organise microtubules
In cytoplasm

106
Q

Round aggregates of tau proteins in cortical neurons

A

Picks disease

Which is degenrstive dementia with behaviour and language symptoms due to frontal and temporal involvement

107
Q

MPTP neurotoxin

Methyl phenyl tetrapyridine

A

Parkinsons disease

108
Q

Features of parkinsons disease

Trap

A 
TRAP
Tremors- resting
Rigidity- cogwheel
Akinesia and bradykinesia— expressionless face
Posture—instability and shuffling gait
109
Q

Lewy body is composed of

A

Alpha synuclein

110
Q

In parkinsons disease histology shows

A

Loss of dopamingergic black neurons in substantia nigra pars compacta

Lewy bodies—round eosinophilic granular body

111
Q

In parkinsons disease dementia is a early or late feature?

A

Late feature

If early alternate diagnosis of lewy body dementia suggested

112
Q

which cranial nerve exits brain stem in post olivary sulcus of medulla

A

9th and 10th CN

113
Q

what is chorea

A

jerky fidgety involuntary movements

114
Q

what is the genetic defect in huntingtons chorea

A

AD CAG trinucleotide repeats causing gain of function mutation leading to huntingtin protein accumulation in neural cells

115
Q

what organ is affected in huntingtons disease

A 
caudate nucleus (striatum)
accumulation of huntingtin protein in caudate leads to loss and atrophy of inhibitory GABA neurons of caudate.
116
Q

what happens when GABA neurons of caudate are lost

A

in huntingtons dz– inhibitory GABA in caudate is lost. It would normally regulate motor and behaviour from cortex. Hence pts have behavioural abnormality and movement disorder

117
Q

what should u suspect in advanced dementia — severe memory loss, facial agnosia, bradykinesia, incontinence and near total absence of voluntary movements

A

huntingtons disease

118
Q

where is acetylcholine produced in brain

A

largest concentration is seen in amygdala– in nucleus basalis of meynert

119
Q

reduced concentration of NE and serotonin causes

A

in brain it causes depression. Treated with SSRI and SNRI

120
Q

anterior spinal artery occlusion symptoms would be ?

A

bilateral lower limb weakness with hyporeflexia LMN type

loss of pain and temperature becuase of spinothalamic tract involvement

121
Q

what is wallenberg syn?

A

lateral medullary PICA syndrome. Infarct in lateral medulla and inferior cerebellar peduncle

122
Q

features of lateral medullary pICA syndrome / wallenberg syn

A

lateral medulla and inferior cerebellar peduncle infarcted.
hence dysphagia, hiccups, hoarseness and vestibulocochlear sym… ataxia dizziness and nystagmus
SIADH because vagus mediated sensing of non osmotic stimuli from carotid sinus is not mediated and disinhibition of ADH occurs

123
Q

cause of hyperacusis

A

stapedius muscle paralysis causes stapes to vibrate violently. facial nerve palsy.

124
Q

treatment of hyperacusis

A

white noise – therapy with white noise

125
Q

what are diagnostic features of neuroblastoma

A

elevated catecholamine metabolites.
c-myc amplification
small round blue cells WITH HOMER WRIGHT ROSETTES on histo– remember it is a type of round cell tumour

126
Q

what movement disorder should prompt the diagnosis of neuroblastoma

A

non rhythmic conjugate eye movements
involuntary jerking movement of trunk and limbs
that is OPSOCLONUS MYOCLONUS SYN

127
Q

CNS LYMPHOMA HAS WHICH POSITIVE MARKERS

A

CD20 AND CD 79a

128
Q

which CNS tumour is associated with EBV genome

A

primary CNS lymphoma.

Flash Facts (23 decks)

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