Neuropathology, Trauma, Radiology, & Tests Flashcards

1
Q

List the types of brain herniation

A

Cingulate/Subfalcine
Uncal/Transtentorial
Tonsillar

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2
Q

Cingulate/Subfalcine herniation

A

• Superior unilateral mass pushes ipsi cingulate gyrus under falx

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3
Q

Uncal/Transtentorial herniation

A
  • Ipsi uncus forced into tentorial notch
  • Commonly with mass of temporal lobe
  • May impinge oculomotor nerve = causes dilation of ipsi pupil (due to parasympathetics to ciliary body)
  • May compress contra cerebral peduncle into tentorial notch → ipsi hemiparesis
  • May compress ipsi posterior cerebral artery → infarct
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4
Q

Tonsillar herniation

A
  • Cerebellar tonsils protrude into foramen magnum

* Most commonly with mass in posterior fossa

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5
Q

Causes of brain herniation

A

Mass lesion (focal):
• Hemorrhage
• Tumor
• Infarct

Mass lesion (generalized)
•	Edema
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6
Q

Coup vs. Contrecoup

A

Coup = to injury at impact site
• Seen in trauma to stationary heads or those in motion
• Often at frontal, temporal, or occipital lobes

Contrecoup injury = occurrs remote from the impact focus
• Most commonly seen in abrupt deceleration of heads in motion.

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7
Q

Concussion

A
  • Transient diffuse cerebral cortical dysfunction (ex: confusion) with or without loss of consciousness
  • Other symptoms: headache, nausea
  • Usually resolves in seconds to hours
  • Historical definition = transient, but instant loss of neural function, followed by “recovery.”
  • This definition = problematic
  • Often have post-concussion syndrome (variable duration, headaches, subtle cognitive abnormalities, emotional dysregulation)
  • This is unaccompanied by visible antemortem acute pathologic findings upon brain imaging.
  • Actual structural changes include mitochondrial, membrane, and cytoskeletal abnormalities. Fiber injury may be present (DIA), with delayed axotomy, and continued pathology (i.e. CTE)
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8
Q

Chronic traumatic encephalopathy

A

Chronic progressive neurodenerative disease due to repetitive “mild” cranial trauma
• Delayed dementia
• Patients = athletes & military veterans.

Clinical features vary with pathologic stage:
• Early (I-II) include emotional explosivity, headache, and changes in short-term memory, concentration, & depression.
• Late (III-IV) include executive dysfunction, cognitive impairment, dementia and aggression (+/- motor issues)

Pathology:
• Gross includes:
o Atrophy, cavum septum pellucidum, pallor of pigmented nuclei, thalamic and mammillary atrophy.

Microscopic features:
o pTau intraneuronal and intraglial neurofibrillary inclusions, neuroaxonal loss, astrocytic tangles, and TDP-43 (transcriptional inhibitor) positive staining in effected areas.
o Tau = normally part of microtubules
o Tau becomes neurotoxic by being abnormally processed (phosphorylated, misfolded, cleaved).
o Interneuronal spreading of toxic Tau may occur by prion-like mechanism.

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9
Q

Cerebral Contusion

A
  • May occur without fracture

* Variable amounts of hemorrhage

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10
Q

Cerebral laceration

A
  • Generally accompanied by fracture or penetrating injury (not always)
  • Variable amounts of hemorrhage
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11
Q

Isolated epidural hemorrhage

A
  • Frequently = due to temporal head impact and laceration of middle meningeal artery
  • Bleeding under high pressure
  • The resultant ARTERIAL bleeding may enlarge rapidly = constitutes a medical emergency

A lucid interval may follow the time of trauma
• Initial concussion clears rapidly
• Followed by progressive diminishing arousal over minutes to hours
• Arterial bleeding → increased intracranial pressures
• Precedes recognition of clinical symptoms.

Imaging:
o	Lenticular shaped 
o	Can cross midline
o	Does not cross sutures
o	Associated with fractures and intracranial air
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12
Q

Isolated adult subdural hemorrhage

A
  • Most commonly = due to rupture of bridging VEINS from abrupt cranial deceleration
  • Bleeding under low pressure

Risk factors:
• Risk for falls
• Coagulopathies
• Atrophic brain diseases (stretches bridging veins)
• SDH in an infant = a marker for possible inflicted trauma (“shaking”).
• SDH may be acute, subacute, or chronic.

Imaging: 
o	Crescent shaped
o	Follows dural reflection
o	Does not cross midline
o	Crosses sutures
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13
Q

Non-adult abusive head trauma

A

• In infants and toddlers suffering shaking and/or impact cranial injury.

Pathology
• Acute subdural hemorrhage
• Ocular retinal hemorrhage
• Intracranial mass effect

Cellular pathology
• Axonal shearing injury with preference to centrum semiovale, dorsolateral brainstem, and corpus callosum with variable mass effect

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14
Q

Describe Computed tomography imaging

A

Based on same principle as x-ray
• Radiation passes successively through tissue from multiple directions
• Computers integrate information and construct image

Contrast: iodine-based (bright on CT)

Indications 
•	Trauma: fractures, hemorrhage
•	Stroke: initial evaluation
•	Hydrocephalus
•	Mass effect/midline shift

Advantages:
• Quick, readily available
• Excellent for visualizing bones
• Able to assess presence of calcification

Disadvantages
• Radiation
• Not as good as MR at evaluating soft tissues

When to order:
• Acute setting
• Situation where hemorrhage is on differential
• Initial screening test

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15
Q

Describe MRI

A

Based on magnets (not radiation)
• H+ atoms randomly arranged in body
• With magnetic field → H+ atoms line up
• Radiofrequency energy excites atoms
• H+ atoms relax/fall back to normal energy state → emit signal
• Relax at different rates depending on type of tissue

Contrast: Gadolinium-based (bright on T1-weighted images)

Indications
• Tumors, stroke, epilepsy, demyelination, infection, cranial nerve palsy

Advantages
• Broader palette of tissue contrast → greater anatomic detail, more comprehensive analysis of pathology
• Excellent for evaluating brain parenchyma
• No ionizing radiation
• Direct multi-planar imaging

Disadvantages 
•	Higher cost, limited access
•	Takes longer
•	Difficult for unstable patients
•	Claustrophobia 
•	Absolute contraindications (ex: pacemakers)
•	Not as good at evaluating bones

When to order:
• Characterize an abnormality initially seen on CT
• Characterize disease processes typically occult on CT
• Problem solving

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16
Q

Progression of ischemic stroke

A

• Interrupt blood flow → rapid (within minutes) breakdown of energy metabolism and ion exchange pumps

Result: massive shift of water from extra- to intracellular compartment = cytotoxic edema
• Intracellular water accumulation due to Na/K pump failure
• Pattern involves cortex and white matter
• Both gray and white matter are supplied by blocked vessel in embolic infarction
• Usually develops as response to ischemia or hypoxia

Produces high-intensity area on DWI (Cytotoxic edema)
• See cellular swelling
• Gray-white matter margin lost

17
Q

Vasogenic edema

A
  • Increased capillary permeability
  • White matter mostly affected
  • Allows movement of proteins from IV space → EC space
  • Response to trauma, tumors, focal inflammation, and late stages of cerebral ischemia
18
Q

Types of astrocytomas

A

Circumscribed = Pilocytic astrocytomas
o Cyst with enhancing mural nodule
o Optic nerves/chiasm (NF1)
o Pediatric patient population

Diffuse/infiltrating astrocytomas
Grade II
•	T2 hyperintense
•	No enhancement 
Grade III = anaplastic
•	Demographic: 30-40’s
•	Can evolve from grade II
•	Can de-differentiate into GBM (time to progression = 2 years)
Grade IV = glioblastoma multiforme
•	Variable surrounding T2 change
•	Hemorrhage, necrosis 
•	Heterogeneous enhancement 
•	Daughter lesions
19
Q

Name indications for lumbar puncture.

A
  • Subarachnoid hemorrhage
  • Meningitis & Encephalitis
  • Acute inflammatory demyelinating polyradiculoneuropathy
  • Multiple sclerosis
  • Some cancers metastasized to CSF (carcinomatous meningitis)
20
Q

Lumbar puncture for Subarachnoid hemorrhage

A

o Collect fluid in multiple tubes
o Helps distinguish bleeding from blood released during “traumatic tap” (from puncturing venous plexus around dura)
o If amount of collected blood clears = traumatic tap
o If stays constant = hemorrhage; also see xanthochromia (yellow tinge from centrifuged CSF due to RBC breakdown)

21
Q

Lumbar puncture for Meningitis & Encephalitis

A

o Bacterial cause: elevated WBCs (neutrophils predominant), low glucose concentration, elevated protein concentration
o Viral cause: elevated WBC (lymphocytes predominant), normal glucose, elevated protein (less than bacterial meningitis)
o Fungal cause: elevated WBC (lymphocytes predominant), normal glucose, elevated protein (less than bacterial meningitis)

22
Q

Lumbar puncture for Acute inflammatory demyelinating polyradiculoneuropathy

A

o Elevated lymphocytes with normal protein (albuminocytologic dissociation)

23
Q

Lumbar puncture for Multiple sclerosis

A

o Elevated immunoglobulin amount (due to autoantibody production in CNS)
o Oligoclonal bands on protein electrophoresis

24
Q

Lumbar puncture for some cancers metastasized to CSF

A

o Collect, stain, and examine cells

25
Q

Describe the function and indications for the electroencephalogram

A

Function:
o Uses scalp electrodes to record average electrical activity of cerebral cortical neurons
o Produces low voltage, random waveforms

Indications:
1) Monitor for seizures:
• Increased and synchronous neuronal firing → abnormal, higher voltage waves
• May see non-specific focal slowing
• Epileptiform discharges = waveforms that resemble brief moments of seizures
2) Delirium and other conditions = see diffuse slowing
3) Multiple sclerosis
• Use evoked potentials to assess response to certain visual stimuli
• If subclinical optic neuritis = may cause delayed potential due to demyelinated optic nerve conducting more slowly

26
Q

List the indications and results of electromyography.

A

o Insert needle electrodes into muscles and assess electrical activity
o Demyelination = usually normal, may see decreased amount of contraction

Axonal loss (denervation):
• Fibrillation potentials (spontaneous APs from myocytes at rest)
• Smaller amplitudes (loss and/or atrophy of motor units)
• Abnormal recruitment pattern (larger motor units due to remaining axons sprouting new terminals to denervated myocytes)

Myopathy
• Similar changes as axonal loss EXCEPT:
• Motor unit size not increased
• Nerve conduction studies = normal

27
Q

List the indications and results of nerve conduction studies

A

o Administer electricity to nerves or skin and record response
o Axonal loss = decreased amplitude
o Demyelination = slower action potential and/or conduction block
o Polyneuropathy = diffuse and distal changes
o Focal nerve or spinal nerve root dysfunction = changes at area of dysfunction and degenerated distal portions of axons
o Myasthenia gravis = decremental muscle response with repetitive stimulation

28
Q

Explain when biopsy is indicated for neurological syndromes.

A

Brain tumors

Autoimmune vascultis if involves CNS
o Meningeal or brain biopsy

Giant cell arteritis
o Temporal artery biopsy

Unusual polyneuropathies
o Sural nerve biopsy (sensory nerve of leg)

Myopathies
o Skeletal muscle biopsy (usually of quadriceps)