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CNS > PATHOMA > Flashcards

PATHOMA Flashcards

1
Q

how is the CNS formed embryology? 3 steps

A

open neural plate —> envaginated neural plate (closing neural tube)—> neural tube and neural crest cells

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2
Q

what embryological structures lead to the following?
CNS:
PNS:
ventricles and spinal cord canal:

A

CNS:walls of neural tube
PNS: neural crest
ventricles and spinal cord canal: hollow lumen of the neural tube

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3
Q

cause of neural tube defect ?

A

folate deficiency PRIOR to conception

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4
Q

2 types of neural tube defects+def

A

1- anencephaly
(failure of closure at the cranial aspect: no skull/brain)

2- spina bifida
(failure of closure at the caudal aspect// failure of posterior vertebral arch to close)

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5
Q

frog like appearance is :

A

anencephaly

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6
Q

what can anencephaly lead to … and how?

A

MATERNAL POLYHYDRAMNIOS
-fetal swallowing of amniotic fluid is impaired (usually help reduce volume)
BECAUSE CNS contol swallowing centers are absent :) -no brain !

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7
Q

spina bifida occulta symptoms? main finding?

A

ASYMPTOMATIC

-dimple of patch of hair overlying vertebral defect

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8
Q

meningocele vs meningomyelocele

  • 1 similarity
  • 1 difference
A
  • both are spina bifida (not occulta!!) i.e cystic protrusion of underlying tissue
  • meningocele: meninges protrude
  • meningiomyelocele: meninges and spinal cord protrude
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9
Q

how can we detect neural tube defects?

A

elevated alpha-fetoprotein (AFP) in amniotic fluid and maternal blood !!!!!!!!!!!!!!!!!

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10
Q

alpha -fetoprotein AFP is made by: 2
(note its the most abundant protein in young fetus protein, remmeber its like the albumin of fetus!)
AFP elevation DD 5

A 
-made by fetal liver and yolk sac
DD:
-neural tube defects
-hepatocellular carcinoma
-liver metastasis
-yolk sac tumor
-germ cell tumor
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11
Q

most common cause of hydrocephalous in NEWBORNS

A

cerebral duct stenosis (3rd —>4th)

congenital

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12
Q
  • lateral ventricle to third ventricle what duct?
  • 3rd to 4th?
  • where is csf produced
A
  • interventricular (foramen of monro)
  • cerebral aqueduct (of sylvius)
  • choroid plexus
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13
Q

massively dilated 4th ventricle with almost absence of most of the cerebellum in imaging
diagnose

A

dandy walker malformation

d: dilated …
w: water hydrocephalus
s: small or absent vermis

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14
Q

newborn with:
hydrocephalus
increased ICP
MOTOR problem

A

dandy walker malformation

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15
Q

what is dandy walker malformation

A

congenital failure of cerebral vermis to develop :)

so 4th ventricle is massively dilated and cerebellum is absent (+hydrocephalus)

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16
Q

meningomyelocele or seringomyelia .. and herniated cerebullum

A

arnold chiari malformation

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17
Q

what is arnold chiari malformation

A

congenital downward displacement (mri) of cerebellar vermis and tonsils through foramen of magnum (leading to obstructive hydrocephalus)

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18
Q

symptoms of type 1 and 2 of arnold choari malformation

A

type 1 asymptomatic

type 2 obstruction of csf flow

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19
Q

what is seringomyelia?

sos sos

A

cystic degeneration of spinal cord

-arises w/ trauma or ass. w/ arnold chiari symptoms

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20
Q

where usually seringomyelia is found? how is it clinically relevant ?

A

C8-T1

symptoms in the UPPER EXTREMITY !

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21
Q
  • sensory loss of pain and temp in upper extremity
  • fine touch and position sense are spared
  • muscle atrophy and weakness
  • horners syndrome

diagnose?
each symptoms is due to what?

A

SERINGOMYELIA
rem drawing of spinal cord
1- anterior white commissure degeneration (of spinothalamic tract)
-upper extremity b/c C8-T1 usually

2-dorsal column pathway is spared

3- anterior horn damage (motor neurons) d/t expansion of the damage from the ant white commissure

4- same expansion idea - but to lateral horns -hypothalamospinal tract damage (sympathetic input to face)

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22
Q

what is the fluid filled cyst called in seringomyelia

A

syrinx

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23
Q

what infection causes:
flaccid paralysis with muscle atrophy
babinski -ve
impaired reflexes
in addition to fever, sore throat, Abdominal pain, nausea, vomiting
-virus, transmission, pathophysio, dx name

A

-poliovirus infection
-fecal-oral transmission
infects oropharynx +small bowel
then spreads to cns via blood
-anterior horn neurons damage (LMN symptoms !!!!)

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24
Q 
floppy baby (hypotonia:decreased muscle tone) that dies within few years after birth 
-dx? -genetic? -pathophys?
A
  • werding-hoffman disease
  • AR
  • degeneration of anterior motor horn (like poliomyelitis)
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25
Q

degeneration of both LMN and UMN of corticospinal tract

what dx?

A

Amotrophic lateral sclerosis (ALS)

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26
Q

causes of ALS? 2

A

1- mostly sporadic
2- zinc-copper superoxide dismutase mutation (SOD1) causes free radical injury in neurons
remember: O2- —> H2O2 by SOD1

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27
Q

list LMN and UMN signs :

A 
Lower motor neuron signs:
Flaccid paralysis and muscle atrophy 
Fasciculations 
Negative Babinski
-
Upper motor neuron signs:
Spastic paralysis with hyperreflexia 
Increased muscle tone 
\+ve Babinski
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28
Q

DD between ALS and syringomyelia

both have atrophy and weakness of hand early sign

A

in ALS, the sensory system is intact

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29
Q

what neurological disease is associated with hypertrophic cardiomyopathy

A

fredrich ataxia

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30
Q 
presents in early childhood with: 
1- ataxia (indicates: ..)
2- 
-Loss of vibration and proprioception 
-Muscle weakness in lower extremities 
-Loss of deep tendon reflex
(indicates: … )

later on in few yrs will be WHEELCHAIR BOUND

A

disease: fredreich ataxia

ataxia indicates cerebellum involvement

others indicate: multiple spinal tract loss

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31
Q

unstable trinucelotide repeat GAA
in what gene causes what dx? what is it?
-mode of inheritance
-clinical importance of the gene

A

frataxin gene causes fredreich ataxia (degenerative disorder of cerebellum and spinal cord)
-AR

-frataxin gene is imp for mitochondrial iron regulation (loss results in iron buildup with free radical damage via fenton reaction!)

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32
Q

what is meningitis

A

inflammation of leptomeninges (arachanoid and pia)

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33
Q

classic triad of meningitis

A

HEADACHE
FEVER
NUCHAL RIGIDITY/stiffness

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34
Q

cause of meningitis in :

  • neonates:
  • non vaccinated infants:
  • teens/adults:
  • adults/elderly:
  • immunocompromised:
  • viral:
A
  • neonates: GBS (#1), E.coli, listeria
  • non vaccinated infants: H. flu
  • teens/adults: N. meningitis
  • adults/elderly: Strep pneumo
  • immunocompromised: fungi (Cryptococcus)
  • viral: coxackie (fecal oral transmission in kids)
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35
Q

where is LP is done in meningitis and why ? sos

A

needle between L4 and L5 (i.e level of iliac crest)
b/c SC ends at L2
cauda equina continues to S2

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36
Q

photophobia with meningitis is common in what cause?

A

viral

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37
Q

CSF findings of
bacterial, viral, fungal meningitis
in terms of cells and glucose level

A

1- bacterial: neutrophils, low gluc
2- viral: lymphocytes, normal gluc
3- fungal: lymphocyes, low gluc

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38
Q

what is the normal amount of glucose in CSF

A

2/3 of serum glucose

e.g 100 serum , 66 csf

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39
Q

when complications of meningitis are usually seen ? why 2?

A

when it is bacterial meningitis

1- because pus and exudate pressures the brain causing herniation and cerebral edema thus death
2- d/t healing process (fibrosis) of the massive tissue damage, damages other parts leading to hydrocephalus, hearing loss, and seizures

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40
Q

revise

A

layers of LP

REMEMBER: never pierce the PIA !!!!! just cross arachnoid :)

41
Q

Neurons are susceptible to ischemia and undergo necrosis within

A

3-5 min

42
Q

types of strokes

A

1- ischemia 85%
focal 3 or global 3

2- hemmorhage 15%
intracerebral or subarachnoid

43
Q

causes of global cerebral ischemia 4

A 
1- low perfusion (ATHEROSCLEROSIS) 
2-acute decrease in BF 
(CARDIOGENIC SHOCK)
3-chronic hypoxia 
(ANEMIA)
4- repeated episodes of hypogylcemia (INSULINOMA)
44
Q

types of global cerebral ischemia

mild severe moderate

A

mild: transient confusion with prompt recovery (e.g insulinoma)
severe: DIFFUSE NECROSIS. if survives: “vegetative state”

moderate: 2 main points
-infarction on WATERSHED area
(b/w ant and mid cerebral artery)
-damage to HIGHLY VULNERABLE AREA
1-pyramidal neurons (layers 3 5 6 of cerebral cortex
2- pyramidal neurons of the hippocampus
3- purkinje layer of cerebellum

45
Q

what are the highly vulnerable areas to damage in the brain ?
esp in what type of stroke?

A

1-pyramidal neurons (layers 3 5 6 of cerebral cortex
SOS CORTICAL LAMINAR NECROSIS SOS
2- pyramidal neurons of the hippocampus
3- purkinje layer of cerebellum

moderate global ischemia

46
Q

regional (focal cerebral) ischemia vs TIA (time?)

A
  • Regional ischemia that causes focal neurological defects lasting >24 hours
    vs If symptoms last <24 hours, it’s called transient ischemic attack (TIA)
47
Q

subtypes of focal cerebral ischemia

A

thrombotic
embolic
lacunar

48
Q

most common location of the following focal cerebral ischemias

  • thrombotic
  • embolic
  • lacunar
A
  • thrombotic: mostly at BRANCH POINTS (e.g bifurcation of internal carotid and MCA at circle of willis)
  • embolic: MCA
  • lacunar: LENTICULOSTRIATE vessels (deep structures from the MCA
49
Q

most common cause of an embolic focal cerebral ischemia

A

emboli from left heart (AFib)

50
Q

hyaline arteriosclerosis as a complication of HTN and diabetes can lead to what type of stroke

A

LACUNAR FOCAL cerebral ischemia

51
Q

focal cerebral ischemias differences:
1- PALE infarct at periphery of cortex
2-PIN POINT hemorrhagic infarct 9over triangular area)
3- small cystic infarction

A

1- thrombotic
2- embolic
3- lacunar

52
Q

PURE MOTOR STROKE vs PURE SENSORY STROKE

  • what type of stroke? subtype?
  • what organ is involved /
A
  • focal lacunar
  • motor: internal capsule
  • sensory: thalamus
53
Q

what type of necrosis is seen in brain ischemia?

A

liquefactive necrosis

54
Q

first early sign of brain ischemia ? after how long?

A

red neurons (eoisinophilic chage)12-24 hrs

55
Q

time line of brain ischemia

A

firstly: 12hrs red neurons
1day to 1wk: neutro and macro (histiocytes)
1wk to 1 mo: granulation tissue-like (reactic astrocytes: gliosis)
result:fluid filled cystic space surrounded by gliosis

56
Q

main cause of intracerebral hemorrhage, involves what vessels?, what location?

A

rupture of Charcot-Bouchard micro-aneurysm of lenticulostriate vessels in BASAL GANGLIA

57
Q

lenticulostriate vessels stroke DD

A

1- ischemic lacunar stroke (d/t arteriosclerosis)

2- intracerebral hemorrhage (charcot bouchard microaneurysm)

58
Q

what is an prevention to intracerebral hemmorhage by half!!?

A

HTN tx (since charcot bouchard microaneurysm is a complication of HTN and is the main cause of intracerebral hemorrhage)

59
Q

most common site of intracerebral hemorrhage

A

basal ganglia

60
Q

if you see bleeding at the BOTTOm of the brain, it is:

A

subarachnoid hemorrhage

61
Q

worst headache of my life or thundercloud headache , with nuchal rigidity

A

subarachnoid hemorrhage

62
Q

rupture of berry aneurysm can lead to what stroke? most common location sos?

  • what layer is the aneurysm missing and clinical importance?
  • what is an anneurysm?
A

hemorrhagic stroke
85% of SUBARACHNOID hemorrhage
-in branch point of anterior communicating artery !!!!

  • lacks media layer (has adventitia and intima)
  • thin, walled saccular outpouching easily ruptured
63
Q

berry aneurysm 2 associations sos

A

1- marfan syndrome

2- dominant polycystic kidney disease AD!!

64
Q

-what LP of subarachnoid hemorrhage shows? why?

A

XANTHOCHROMIA (yellow) b/c of bilirubin breakdown products

65
Q

talk and die dx

A

epidural hematoma

-lucod interval may precede nerologic sign

66
Q

lens shaped lesion on CT vs crescent shaped lesion on CT

A

epidural hematoma vs subdural hematoma

67
Q

what is a common cause of death in hematomas?

A

herniation !

68
Q

how is a subdural hematoma presented ?

A

progressive neruro sign (take mo’s for bleeding to accumulate)

sos: ct crescent shape
darker area (compared to parenchyma): chroic hemorrhage
lighter area: acute

69
Q

trauma—> fracture of the skull can lead to what and how?

A

epidural hematoma
d/t rupture of MIDDLE MENINGEAL ARTERY from trauma to temporal bone :)
it should be an artery (high pressure circut) to separate dura from skull

70
Q

what is the cause of subdural hematoma

A

d/t tearing of bridging veins that lie b/w dura and arachnoid
commonly with elderly (have atrophies brain) w/ trauma

71
Q

what is herniation ? d/t 2?

A

displacment of brain tisssue

d/t mass effect or increased ICP

72
Q

3 main types of brain herniation

A

1- tonsilar: Cerebellar tonsils herniates under foramen magnum

2- subfalcine: Cingulate gyrus herniates under falx cerebri

3-uncal: Temporal lobe uncus herniates under tentorium cerebeli

73
Q

what type of herniation can lead to: compression of brainstem and cardiopulmonary arrest

A

tonsilar herniation:

Cerebellar tonsils herniates under foramen magnum

74
Q

what type of herniation can lead to: compression of anterior cerebral artery leads to infarction

A

subfalcine: Cingulate gyrus herniates under falx cerebri

75
Q

how does uncal herniation (Temporal lobe uncus herniates under tentorium cerebeli) present ? 3

A

1- CN3 palsy - eye moving down and out and dialated pupil

2- Posterior cerebral artery compresion - infraction of posterior cerebral arery (contralateral homonymous hemianopsia)

3- Rupture of paramedian artery - Duret (brainstem) hemorrhage

76
Q

myelin in cns and pns

A

Schwann cells - myelinate PNS; single cell myelinate single neuron

77
Q

where is myelin in the brain ?

A

white matter is myelin !!!

78
Q

what is leukodystrophy and what are the 3 main dxs?

A

Inherited mutation in enzymes necessary to produce or maintain.
1- metachromatic leukodystrophy
2- krabbe disease
3- adreno leukodystrophy

79
Q

most common leukodystrophy

A

metachromatic leukodystrophy

80
Q

deficiency of arylsulfatase

-dx? inheritence? patho of enzyme ?

A

metachromatic leukodystrophy
AR
sulfatides (myelin) can’t be degraded and accumulate in lysosome of oligodendrocytes :)

81
Q

deficiency in galactocerebrosidase

-dx? inheritence? patho of enzyme ?

A

krabbe dx
AR
galactocerebroside accumulates in macrophages

82
Q

damaged adrenal glands and WHITE matter of brain, in what dx? how ? inheritance?

A

adreno leukodystrophy
-damage because of accumulation of fatty acids
(d/t impaired addition of coenzyme A to long-chain FA)

X-linked

83
Q

most common chronic CNS dx of young adults (20-30)

- more in women

A

MS

84
Q

what dx is common with ppl who live far away from the equator

A

MS

85
Q

what genetic association is there with MS/

A

HLA-DR2

86
Q

MRI revealing white matter demyelination (white plaques on mri)
diagnose?
what other diagnostic method can be done?

A

MS

LP

87
Q

LP results:

  • increased lymphocytes and Ig
  • oligoclonal IgG bands on high resolution electrophoresis sos
  • myelin basic protein

diagnose

A

MS

88
Q

tx of acute attack MS

A

high dose steroids

89
Q

long term tx for MS

to slow dx progression

A

interferon beta

90
Q

how does MS present

list 4 and read others

A

Relapsing and remitting neurological features (comes and goes)
1- Vision:
SOS -Optic nerve damage - blurred vision in one eye
SOS -MLF (medial longitudinal fasiculus) damage - internuclear opthalmoplegia

2- Hearing:
SOS-Vertigo and scanning speech (like drunk)

3-ANS:
- Bowel, bladder, and sexual dysfunction
4- Spinal cord:
- Lower extremity loss of sensation and weakness
5- Cerebral white matter:
SOS - Hemiparesis or unilateral loss of sensation

91
Q

what infection leads to subacute sclerosing panencephalitis (DAWSON dx)

A

measles virus

NOTE: Primary infection occurs in infancy; neuro signs arise 6-15 years later

92
Q

Initially presents as dementia, personality alterations, and loss of
movement control. Slowly progresses to speech loss of speech, loss of
ability to walk and dysphagia. Then, pt will be blind, mute, loss bodily
functions and be in vegetative stage and/or comatose and evenually die.

diagnose

A

Subacute sclerosing panencephalitis (Dawson disease)

93
Q

most imp characteristic in Subacute sclerosing panencephalitis (Dawson disease)

A

-Viral (measles) inclusions in neurons (gray matter) and oligodendrocytes (white matter)
BOTHHHHHH—-diee

94
Q

if latent infection of JC virus get reactivated in the brain; mainly during immunesuppression - AIDS, Rituximab, or leukemia), leads to what: and what is it?

A

Progressive multifocal leukoencephalopathy
-Rapidly progressive neurologic signs (vision loss, weakness, dementia and eventually death in few months) caused due to JC virus damage of oligodendrocytes

95
Q

rapid correction of hyponatremia (in severly malnourished pts, alcoholics, liver dx) leads to:

A

Central pontine myelinolysis
(Focal demyelination of pons)

SOSOSOSOOS

  • Increasing Na concn too fast
    1- from low to high - makes your pons die
    2- from high to low - makes your brain blow
96
Q

what is locked in syndrome?

in what dx?

A

acute bilateral paralysis (except eyes)

-central pontine myelinolysis

97
Q

1- most common malignant tumor in adults
2- most common primary brain tumor in kids (B or M)
3- most common primary brain tumor in adults (B or M)

A

1- glioblastoma (astrocytes)
2- pilocytic astrocytoma (astrocytes) B
3- meningioma (FEMALES mainly) in meninges -B

98
Q

location of brain tumors in adults vs kids

A

adults: SUPRA tentorial
kids: INFRA tentorial

CNS (1 decks)

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