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Pathophysiology - Neurology > Introduction to Neuropathology and Mass Lesions > Flashcards

Introduction to Neuropathology and Mass Lesions Flashcards

1
Q

What germ layer gives rise to each type of glial cell?

A

Neuroectoderm -> Macroglia, including astrocytes, oligodendrocytes, and ependymal cells

Mesoderm -> microglia (macrophages are derived from mesenchyme, like blood vessels)

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2
Q

What germ layer gives rise to the meninges? Include the two special terms for meninges.

A

Leptomeninges - pia / arachnoid mater - neural crest

Pachymeninges - dura mater - mesoderm

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3
Q

Other than the leptomeninges, what else does the neural crest give rise to?

A

Schwann cells
Melanocytes
Entire peripheral nervous system (note: CNS is derived from neuroectoderm)

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4
Q

Why are neurons so susceptible to damage?

A

They last for a lifetime of the individual and are not replaced if lost -> insults throughout life cause damage

Furthermore, they need constant oxygen and glucose since they are so metabolically active

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5
Q

What is Wallerian degeneration?

A

Degeneration of axon distal to the site of injury (i.e. transection). Proximal area of axon is preserved

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6
Q

What are the two types of trans-synaptic degeneration which can occur?

A

Retrograde - loss of synaptic target cell (the cell that was damaged undergoing Wallerian degeneration) leads to death of afferent neuron

Anterograde / orthograde - loss of afferent cell (the cell that was damaged undergoing Wallerian degeneration) leads to death of target neuron

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7
Q

What are the supporting cells of the PNS?

A

Schwann cells - myelinate only one axon

Satellite cells - also derived from neural crest, a form of Schwann cell which encapsulates some sensory ganglion cells

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8
Q

What are the major functions of astrocytes?

A 
Physical support
Repair
Extracellular K+ buffer with depolarization
Removal of excess neurotransmitter
Formation of blood-brain barrier
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9
Q

What is gliosis and what is it called acutely?

A

Gliosis - chronic changes of “glial scar” associated with an increase in astrocytes and their cell processes. Basically, the CNS version of fibrosis

Acutely = Astrocytosis, hypertrophy and hyperplasia of astrocytes

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10
Q

What marker is used for the detection of astrocytes?

A

GFAP - glial fibrillary acidic protein

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11
Q

What is metabolic astrocytosis?

A

Proliferation of gray matter astrocytes in response to metabolic injury -> i.e. hepatic or renal failure

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12
Q

What is the difference between primary and secondary demyelination? Give a process which causes each type?

A

Primary - selective destruction of myelin with sparing of axon (attack of oligodendrocytes or Schwann cells)
-> Multiple sclerosis (CNS) or Guillain-Barre (PNS)

Secondary - breakdown of myelin secondary to loss / destruction of axon
-> Wallerian degeneration

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13
Q

When do dysmyelination and remyelination occur?

A

Dysmyelination - formation of abnormal myelin, occurs in some leukodystrophies

Remyelination - occurs poorly in CNS but okay in PNS (Regeneration of myelin following Wallerian degeneration)

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14
Q

Where is CSF produced?

A

In the choroid plexus of the lateral ventricle (anterior and inferior/temporal horns only, no posterior), 3rd ventricle, and 4th ventricle

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15
Q

Describe the flow of CSF from lateral ventricle to systemic circulation?

A

CSF made in lateral ventricle -> interventricular foramen of Monro -> 3rd ventricle -> cerebral aqueduct thru midbrain -> 4th ventricle -> Foramen Magendie (midline) or lateral Luschkia -> subarachnoid space

Subarachnoid space pads brain -> reabsorption into superior sagittal sinus thru arachnoid granulations

Flow of CSF maintained by intracranial pressure > venous pressure

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16
Q

How does CSF compare to blood with regards to protein, chloride, glucose, and WBCs? Is it constant along the spinal cord?

A

Protein - increases towards lumbar cord (non-constant). Normal is <50 mg/dL

Chloride - Higher than blood

Glucose - comparable but slightly lower than blood

WBCs - very few 0-5 cells / mL, elevations suggest meningitis

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17
Q

What are normal CSF pressures and does the rate of production vary with pressure?

A

50-200 mmHg

Secretion is constant at 0.5 L/day, does not depend on ventricular pressure

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18
Q

What does xanthochromia vs cloudiness of CSF mean?

A

xanthochromia - yellow color, due to degenerating RBCs - caused by bilirubin, most commonly following subarachnoid hemorrhage

Cloudiness - due to increased protein and WBCs - protein commonly due to infection, tumor, or tissue destruction

19
Q

What is a non-communicating hydrocephalus and what causes it?

A

Also known as obstructive -> due to blockage of CSF flow within the ventricular system

20
Q

What happens to intracranial pressure in hydrocephalus?

A

Can be elevated or normal

Hydrocephalus just means increased CSF volume with ventricular dilation

21
Q

What is communicating hydrocephalus and what causes it? What will happen to ICP

A

Impaired flow or resorption of CSF outside the ventricular system

  • > i.e. scarring of arachnoid granulations post-meningitis
  • > will increase ICP
22
Q

What is it called when there is a compensatory enlargement of ventricles due to loss of brain parenchymal volume? What will happen to ICP?

A

Hydrocephalus ex vacuo (dilation secondary to atrophy)

ICP is normal despite ventricular enlargement.

23
Q

What is normal pressure hydrocephalus and the associated triad? What happens to ICP?

A

Hydrocephalus affecting elderly which is idiopathic, causes stretching of corona radiata with progress dementia

Triad: Wet, Wobbly, Wacky
Wet - Urinary incontinence
Wobbly - Ataxia
Wacky - Cognitive dysfunction

ICP is usually normal and may be periodically elevated

24
Q

What is the function of the blood brain barrier and how is it formed?

A

Prevents entrance of bacteria and large or charged (hydroPHILIC) molecules like drugs from entering brain

Formed by capillary endothelial tight junctions which are induced by perivascular astrocyte food processes

25
Q

Where in the brain is the BBB absent and why?

A

In specialized regions of the brain there are fenestrated capillaries so that blood products can act directly in the brain and influence function
-i.e. area postrema - vomiting center

OVLT - osmotic sensing

Neurohypophysis - ADH release

26
Q

What part of the brain does kernicterus affect?

A

Predominantly the basal ganglia - as bilirubin can deposit easily in premature infants with an underdeveloped BBB

27
Q

How is breakdown of the BBB radiologically useful?

A

Loss of BBB due to inflammation or injury can be recognized by radiocontrast being able to seep into brain parenchyma
-> recognized by CT or T1 MRI scans

28
Q

Where is the epidural space and what does it contain?

A

Space between dura mater and skull / bone, containing some fat and blood vessels

  • > more of a potential space in the skull
  • > loose connective tissue is real and prominent in vetebral canal
29
Q

What three voluminous compartments are within flux in the skull?

A

Tissue compartment - intracellular / extracellular (80%)

Vascular - blood vessels / intravascular blood (10%)

CSF - intraventricular and subarachnoid (10%)

30
Q

What are the purpose of the blood-choroid plexus barrier and how does it work?

A

Fenestrated capillaries within the choroid plexus are used to generate the CSF (sits in interstitial fluid until release)

CSF is released from the choroid plexus through the cells which form tight junctions with their choroidal epithelium

31
Q

What is vasogenic edema? Where does it especially affect?

A

“White matter edema” - Most pronounced in white matter. Increased interstitial fluid due to blood brain barrier breakdown secondary to inflammation, tumor, etc

Associated with increased protein in the interstitium

32
Q

What is interstitial edema? Where does it especially affect?

A

Increased resistance to CSF outflow leads to icreased intracranial pressure (obstructive or communicating hydrocephalus) and breakage of blood-CSF barrier, but will NOT cause a protein increase in the interstitium

Basically, edema caused by excess CSF

-> Affects predominantly the periventricular white matter (around where the CSF is)

33
Q

What is cytotoxic edema? Where does it especially affect?

A 
Cellular swelling (intracellular fluid accumulation -> increased water in brain) secondary to cell membrane ion pump dysfunction
-> usually caused by energy failure (secondary to hypoxia or ischemia) with injury to neurons / glia

-> affects cell bodies and thus “gray matter edema”

34
Q

How do you calculate cerebral perfusion pressure? When do symptoms of increased ICP develop?

A

CPP = MAP - ICP

MAP = 1/3 SBP + 2/3 DBP

Symptoms of increased ICP develop when CPP is below normal

35
Q

What are the characteristic signs of increased ICP?

A

Headache
Papilledema
Vomiting
Cushing’s triad: Bradycardia, high blood pressure, Cheyne-Stokes breathing
Focal neurological signs and dilated / blown out pupils
Abnormal posturing / altered mental status

36
Q

What are the mechanisms of treating increased ICP?

A

Hyperventilation - induce a hypocarbia which causes cerebral vasoconstriction

IV mannitol - osmotic relief

Corticosteroids - vasogenic edema treatment (restore BBB)

37
Q

What is a cingulate herniation also called and what issue can it cause?

A

Subfalcine - displacement of cingulate gyrus under the falx cerebri
-> can cause compression of anterior cerebral artery, leading to infarction

38
Q

What are the two types of transtentorial herniations? What might cause them?

A

These involve displacement of brain structures through tentorium cerebelli opening (incisure)

  1. Central - bilateral and symmetric, leading to caudal displacement and compression of entire brainstem -> i.e. due to diffuse brain swelling
  2. Uncal - unilateral, with herniation of medial temporal lobe into midbrain
    - > i.e. due to supratentorial hemorrhage
39
Q

What are the clinical complications of the two types of transtentorial herniations?

A
  1. Central - tends to cause Duret hemorrhages which are fatal
  2. Uncal - generally compresses ipsilateral CNIII - down-and-out pupil, as well as ipsilateral PCA (contralateral homonymous hemanopsia + macular sparing), + contralateral Crus cerebri problem. May cause Duret hemorrhage as well
40
Q

What is the crus cerebri problem which may be caused by uncal herniation?

A

Mass effect pushes contralateral cerebral peduncle into tentorium cerebelli edge (Kernohan notch)

This is a false localizing sign, because it will cause ipsilateral (to the mass lesion) UMN signs, when that would normally mean the lesion is contralateral

41
Q

What is a Duret hemorrhage?

A

Rupture of paramedian basilar artery branches on the pons -> usually fatal.

Can happen in both types of transtentorial hernation

42
Q

What is a tonsillar herniation and what is the usual clinical result?

A

Herniation of cerebellar tonsils into foramen magnum

Compression of brain stem (medulla) leads to cardiopulmonary arrest

43
Q

What is brain death and what causes it?

A

When intracranial pressure exceeds arterial perfusion pressure (ICP > MAP), cerebral perfusion stops

-> dead, non-perfused brain undergoes autolysis while on ventilator (respirator brain)

44
Q

What is persistent vegetative state?

A

Enough brainstem / hypothalamic function persists that an individual can regain spontaneous ventilation, autonomic control, and sleep-wake.

However, loss of cortical awareness = vegetable

Pathophysiology - Neurology (21 decks)

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