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NSB > Intro to Neuropath > Flashcards

Intro to Neuropath Flashcards

1
Q

Glial Cell Type and Functions:

A
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2
Q

What protects the brain?

A

The blood brain barrier and the 3 meninges

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3
Q

Is the CNS ‘immune priveleged’?

A
  • believed to have been shielded away from the
    rest of the body’s immune response
  • however there may be a connection between
    lymphatic system and brain
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4
Q

What is the main immune cell of the brain?
Where is it derived from?
Actions?

A
  • microglial cell = APC
  • from embryonic yolk sac progenitor cells
  • major antigen presenting cells
  • dendritic cells (checkpoint inhibitor)
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5
Q

Neuroinflammation:

A
  • facilitates the delivery of effector molecules to
    aid repair through signals
  • vascular dilatation = increased permeability =
    alterations in adhesion
  • microglia activate and macrophages outside
    the CNS are recruited
  • astrocytes repair
  • demyelination
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6
Q

Neuroinflammation Flowchart:

A
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7
Q

Two types of neuroinflammation are:

A
  • vasogenic = extracellular
  • cytotoxic = intracellular
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8
Q

What is shown below?

A

Neuroinflammation

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9
Q

What is shown below?

A

Microglia (L-R)
1) resting
2) become activated, larger, higher turnover of
ATP = more circular, spherical cells
3) evidence of inflammation, larger, angrier
4) resting state in older patients; more worn
down cells, impairs function of microglia

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10
Q

Which types of oedema correspond to the CAT below?

A
  • left is vasogenic, cellular ‘ boundaries are seen,
    clear grey and white differntiation
  • right is cytotoxic and less clear differentiation
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11
Q

Chronic changes to neural damage (3):

A
  • neural degeneration
  • demyelination
  • gliotic scars: possible epileptic foci
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12
Q

Retrograde Neural Degeneration:

A

when the main axon is damaged there is degeneration of the neurone as well as the classical distal degeneration of the axon

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13
Q

Trans-Synaptic Degeneration:

A

injured neurons spread injury to previously uninjured neurons connected by a synapse (diaschisis)

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14
Q

VITAMIN C:

A
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15
Q

What is a meningioma?

A

a tumour of the meninges

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16
Q

What is now used to define patient subgroups in oncology?

A

Molecular classification
precision cancer medication

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17
Q

Paraneoplastic Syndrome:

A
  • remote effect of a cancer
  • abnormal immune response to a cancer eg
    lung/breast/ovarian
  • antibodies to T-cells begin to fight the normal
    brain (AUTOIMMUNE)
  • symptoms develop over days to weeks
  • involve peripheral (Lambert Eaton (small cell
    lung cancer, causes weakness that improves
    over time) or cns (NMDA encephalitis(presents
    with psychosis but is actually ovarian tumour)
  • rare but presentation may be the first
    symptom of an underlying malignancy
18
Q

Meningoencephalitis:

A
  • non-localised/diffuse problem
  • meningitis = inflammation of the meninges
    - presents as headache, nuchal rigidity (neck
    stiffness), and photophobia
    - leptomeninges (pia+arachnoid) = infection
    - pachymeninges (arachnoid + dura) =
    cancer (both are usually not always)
  • encephalitis = alteration in the
    sensorium/cognitive state due to
    inflammation (infection/autoimmune)
    - drowsy, confused, less responsive
19
Q

Decompression of the spinal compartment for example during a lumbar puncture could result in a brain herniation when

A

there is unequal pressures in the intracranial compartment eg cerebellar tumour

removal of fluid can cause the brain to fall and herniation

STOP = shift, trauma, obstruction, posterior fossa mass

20
Q

Causes of Meningoencephalitis:

A
21
Q

What are coup and contre-coup injuries?

A

direct and indirect

22
Q

Traumatic Brain Injury: Blunt Force:
- concussion
- contusion
- secondary consequences of blunt force
trauma c

A
  • concussion: clinical syndrome with immediate
    and transient alteration in brain function can
    result in headache, drowsiness, concentration
    and amnesia for months
  • contusion: pathological term (seen on scan)
    meaning bruising of the brain tissue, can result
    in confusion, altered consciousness and focal
    neurological deficits within days or weeks
  • due to moving the brain backwards = contre-
    coup
  • eg boxer is punched and becomes blind, but
    not because of punch to eye but due to
    contusion at visual cortex at the back of the
    skull
  • secondary effects:
    • cerebral oedema and ischaemia
    • vascular damage
23
Q

Traumatic Brain Injury: Acceleration-Deceleration:
- examples of such injuries
- caused
- what scans are needed

A
  • car accidents, shaken baby syndrome
  • rotational movements of the brain in the skull
    result in shearing forces causing axons to
    stretch = diffuse axonal injury
  • can result in loss of consciousness or coma
  • may need MRI with T2 flair images; may be a
    delay in injury showing up on scan
24
Q

Increased Cerebral Pressure:

A
  • brain expands in very small space available
  • results in herniation
  • headaches, meningism, vision changes, CN6
    palsy
  • high bp, redlexive bradycardia,, irregular
    respiration = Cushings reflex (high bp, low
    heart rate, erratic breathing)
25
Q

Chronic Traumatic Encephalopathy:

A
  • recurrent head injuries
  • deposition of beta amyloid plaques. diffuse
    plaques and tau mostly TAU
  • below pia mater
  • was classified as a tauopathy
  • present with dementia like features decades
    after recurrent head injuries
26
Q

Headaches: Categories:

A
  • Primary: tension-type, migraine, trigeminal
    autonomic cephalagias
  • Secondary: infection, neoplasm, stroke, meds,
    toxins
27
Q

Headaches: Red Flags:

A
  • worsens with valsalva
  • wakes you up whilst sleeping
  • change in character:
  • age of onset
  • sudden onset
  • focal neurological deficits
  • constitutional symptoms: fever, weight loss,
    meningism, rash
28
Q

Mneumonic for headache history taking = SNNOOP10:

A
29
Q

Primary Headaches: Tension-Type:

A
  • 90% headaches
  • featureless,, band-like pressure, stress
  • pathophysiology is unknown
  • episodic: frequent if at least 10 headaches on
    1-14 days a month for >3 months
  • chronic: headaches on >14 days/ month for
    >3months
30
Q

Primary Headaches: Migraine:

A
  • photophobia
  • incapacity
  • nausea/vomiting
  • episodic: without aura, with aura ( visual:
    zigzags, olfactory hallucinations)
  • chronic: at least 15 days/month for more than
    3 months, which on at least 8 days a month
    has the features of a migraine headache
  • status migrainosus: an attack lasting longer
    than 72 hours
31
Q

Primary Headache: TACs:

A
  • trigeminal parasympathetic reflex with clinical
    signs of cranial sympathetic dysfunction being
    secondary
  • cluster headache: male predisposition,
    excruciating pain causing agitation, autonomic
    features
  • paroxysmal hemicrania
  • short-lasting unilateral neuralgliform
    headache attacks
  • hemicrania continua
32
Q

Primary Headache: Summary:

A
33
Q

Pathophysiology of Headache (Migraine):

A
  • neurovascular theory
  • sensory neurons of the
    trigeminocervicocomplex is the source of pain
    resulting in the release of inflammatory and
    noiciceptive mediators which over time can
    result in central sensitisation responses
34
Q

Trigeminal Nerve: Sensory Pathway:

A
  • 1st order
  • 2nd order
  • 3rd order = ventromedial nucleus of the
    thalamus
  • 4th order = sensory cortex, insula, cingulate
    cortex

trigeminal cervical complex is a physiological complex

probably one of the reasons there is neck pain and pain is not localised

35
Q

Trigeminocervical Complex:

A
  • physiological complex not anatomic
  • how head and neck sensory information
    combine
  • innervation of large cerebral vessels, pia
    vessels, dura mater, large venous sinuses
  • anterior = mostly V1 (ophthalmic)
  • posterior = mostly upper cervical roots
36
Q

Trigeminal Autonomic Reflex pathway explains why

A

autonomic system activates running nose, eyes on the same side as the headache pain is felt

ipsilateral autonomic features from cranial parasymapthetic activation (lacrimation) and sympathetic hypofunction due to neurpraxic effect of the carotid wall swelling

afferent = trigeminal
efferent = superior salivatory nucleus via the 7th (facial) cranial nerve to synapse nicotinic post-ganglionic parasympathetic neurons)

37
Q

We prevent medication overuse for headaches by

A

limiting monthly use of the medications eg
triptans < 10 days
non-opiod analgesics < 15 days
opiods < 10 days

chronic headaches should be managed with preventative strategies

38
Q

Anoxic Brain Injury:

A
  • hypoxia: drowning, strangulation, CO, asphyxia
  • ischaemia: cardiac arrest, increased intracrania
    pressure, hypovolaemia
  • may result in:
    - seizures and myoclonus
    - coma
    - minimally conscious state
    - unresponsive wakefulness syndrome
    - brain death
39
Q

What is shown below?

A

anoxic brain injury

40
Q

Histopathology classifies the tumour but genotyping will dictate treatment in the future.

True or False?

A

True

NSB (50 decks)

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