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Pathoma > Neuro > Flashcards

Neuro Flashcards

1
Q

neural crest go on to develop

A

PNS,

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2
Q

The walls of the neural tube go on to form what?

A

The CNS

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3
Q

The lumen of the neural tube go on to form what?

A

The ventricles and the spinal cord canal.

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4
Q

What is the direction of formation of the neural tube?

A

cranial to caudal

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5
Q

Neural tube defects are associated with what?

A

Low folate levels PRIOR to conception.

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6
Q

How can neural tube defects be detected?

A

elevated AFP in amniotic fluid and/maternal blood.

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7
Q

What is Anencephaly?

A
  • Failure of the neural tube closing at the cranial aspect. •Eyes have a frog like appearance.
  • Results in maternal polyhydramnios.
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8
Q

What is maternal polyhydramnios?

A

Increased amniotic fluid.

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9
Q

What is Spina Bifida?

A

•Failure to close the caudal aspect of neural tube, specifically the posterior vertebral arch.

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10
Q

What are variations of Spina Bifida?

A
  • Spina Bifida Occulta→ dimple or patch of hair overlying the vertebral defect.
  • Spina Bifida→ meningocele or menignomylocele (see other flashcard)
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11
Q

What are the ‘true’ Spina Bifida?

A
  • Meningocele→ meninges only herniates through defect.

* Myelomeningocele→ meninges +/- spinal cord herniates through defect.

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12
Q

What is Cerebral Aqueduct Stenosis?

A
  • congenital stenosis of the channel that drains CSF from 3rd to 4th ventricle.
  • leads to accumulation of CSF in the ventricles and enlargement of head circumference.
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13
Q

What is Dandy -walker Malformation?

A

•Congenital failure of the cerebellar vermis presenting as massively dilated 4th ventricle with an absent cerebellum.
-often with hydrocephalus.

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14
Q

What is Arnold Chiari Malformation?

A

•Congenital extension of the cerebellar tonsils through the foramen magnum.
Two Types:
Chiari I: can be asymptomatic
Chiari II: obstruction of CSF flow.

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15
Q

What is Syringomyelia?

A
  • cystic degeneration of the spinal cord; •typically occurs at C8-T1 with sensory loss of pain and temperature.
  • fine touch and position sense are spared in the upper extremities.
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16
Q

What is the result of knocking out of the anterior white commissure

A

• pain and temp loss on both sides.

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17
Q

What is the route of the pain ⅋ temperature sensation from the stimulus entering to the cortex?

A

The pain-temp sensation comes from the sensory nerve⅋ synapses on the post-horn, the 2nd neuron decussates at the anterior white commissure, this nerve then enters the spinothalamic tract ⅋ synapses on the thalamus, then this travels to synapses again on the cortex.

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18
Q

What is Syrinx expansion?

A

•the cyst expands in syringomyelia and compresses other spinal tracts, if it involves:

  1. anterior horn→ Damaged LMN (LMN signs)
  2. lateral horn→ knocks out sympathetic tone to the face (ptosis, miosis)
19
Q

What is Poliomyelitis?

A
  • poliovirus damages anterior motor horn

* Signs are those of LMN lesions.

20
Q

What is the result of knocking out the anterior motor horn?

A

• the LMN gets knocked out, resulting in LMN signs.

LMN signs= flaccid paralysis w/ muscle atrophy, fasciculations, weakness, ↓muscle tone, ↓ reflexes, ⊖Babinski sign

21
Q

What is Werding-Hoffman Disease?

A
  • Inherited degeneration of the anterior motor horn, autosomal recessive
  • Presents as a ‘floppy baby’.
  • Baby will die in a few years.
22
Q

What is the disorder of ALS?

A
  • Degenerative disorder of UMN ⅋ LMN.

* Involves signs of both UMN ⅋ LMN lesions.

23
Q

What are signs of UMN degeneration?

A

•Degenerative UMN signs= spastic paralysis with hyperretlexia, increased muscle tone, and ⨁Babinski sign.

24
Q

How is syringomyelia distinguished from ALS?

A

• Syringomyelia has loss of pain and temperature

25
Q

Most cases of ALS are sporadic, but the familial cases may involve mutation of ___?

A

Zinc-copper superoxide dismutase (SOD)

26
Q

What is Friedreich Ataxia?

A
  • Degeneration of cerebellum and spinal cord → ataxia & multiple tracts involvement.
  • Involves Frataxin gene (mitochondrial iron regulation)
  • Associated with hypertrophic cardiomyopathy.
27
Q

What is the leptomeninges?

A
  • The Pia and arachnoid together

* This is the structure that is inflamed in meningitis.

28
Q

What is the most common causal organism of meningitis in neonates?

A
  • Group B streptococci,
  • E coli
  • Listeria monocytogenes
29
Q

What is the most common causal organism of meningitis in children and teenagers?

A
  • N. meningitidis

* this typically enters through the nasal pharynx and enters the blood.

30
Q

What is the most common causal organism of meningitis in adults and elderly?

A

•Streptococcus-pneumoniae

31
Q

What is the most common causal organism of meningitis in unvaccinated infants?

A

•H influenza

32
Q

How does a LP help diagnosed bacterial from viral meningitis?

A
  • Bacterial—neutrophils with low glucose; gram stain and culture help identify the organism.
  • Viral—lymphocytes with normal CSF glucose
  • Fungal—lymphocytes with low CSF glucose
33
Q

What layers are crossed in a lumbar puncture?

A
  • skin, ligaments, epidural space, dura, and arachnoid

* but you will NOT pierce the Pia.

34
Q

What are the clinical features of Global Cerebral Ischemia?

A

•based on duration and magnitude of the insult but can be boiled down three severities:

  1. Mild Global ischemia→ transient confusion
  2. Severe Global ischemia→ death or vegetative
  3. Moderate Global Ischemia→ cortico laminar necrosis
35
Q

What are two types of ischemia the brain can experience?

A

Global and focal.

36
Q

How do we distinguish a TIA from an ischemic stroke?

A

TIA→ focal defecit is less than 24hrs

Ischemic Stroke → deficits last more than 24hrs.

37
Q

What are the 3 main causes of stroke?

A
  • thrombotic→ rupture of an atherosclerotic plaque
  • embolic→ due to thromboemboli usually from Left side of the heart in a patient with A-fib.
  • lacunar→ secondary to hyaline arteriolosderosis. The wall thickens and the lumen narrows.
38
Q

Which is a pale stroke and which is a hemorrhagic stroke?

A
  • thrombotic stroke= pale infarction.

* embolic stroke = hemorrhagic infarction

39
Q

The brain undergoes ____ necrosis. _____ are early findings of this necrosis.

A

liquefactive; Red neurons;

40
Q

What occurs at 1 day, 1 week and 1 month in liquefactive necrosis of the brain?

A
  • 1 day→ Red neurons (12 hrs) then coagulative necrosis (1 day).
  • 1 week→ infiltration by neutrophils and microglial cells. with formation of granulation-like tissue
  • 1 month- formation of a fluid filled cyst (gliosis).
41
Q

What are the two types of hemorrhage in the brain?

A
  • Intracerebral hemorrhage

* Subarachnoid hemorrhage

42
Q

What is the cause of Intracerebral hemorrhage and where does it most commonly occur?

A
  • rupture of Charcot-Bouchard microaneurysms a complication of hypertension.
  • Basal ganglia is the most common site
43
Q

What is the cause of subarachnoid hemorrhage and where does it most commonly occur?

A

• (85%) due to rupture of a berry aneurysm in the anterior circle of willis at the branch points of the anterior communicating arteries.

44
Q

Why do berry aneurysms rupture so easily?

What other conditions are they associated with?

A
  • They lack a media layer.

* associated with Marfan and AD Polycystic Kidney disease.

Pathoma (2 decks)

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