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Neurology > Neuroimaging > Flashcards

Neuroimaging Flashcards

1
Q

MRI TI, AKA?

A

Anatomical sequence because gray matter is gray and white matter is white.

This is as it appears in gross pathology.

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2
Q

Landmark on CT and MRI for central sulcus?

A

Omega sign. Anterior is frontal lobe, posterior is parietal lobe.

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3
Q

What level is this?

Identify structures.

A

Ventricles

Head of caudate, internal capsule, lentiform nucleus, thalamus, insular cortex, anterior temporal lobe.

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4
Q

Identify sylvian fissure (AKA). What artery runs along here?

What does the sylvian fissure separate?

A

Lateral sulcus

Middle cerebral artery

Frontal/Parietal lobe from temporal lobe

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5
Q

Identify Midbrain, basal cistern, medial temporal lobe “uncus”, temporal horn of lateral ventricle (what is specific for a normal appearance)?

Why is it important to local the medial temporal lobe?

What does it mean for the temportal horn of lateral ventricle to be dilated?

A

Uncus can herniate onto the midbrain

Temporal horn of lateral ventricle should normally be slit like.

Early sign of hydrocephalus if temporal horn of lateral ventricle is dilated.

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6
Q

What level is this?

Identify brachium pontins, direction of connection between brachium pontis and cerebellum, 4th ventricle, and cerebello-pontine angle.

A

Mid pontine level

Brachium pontins Will hug the 4th ventricle

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7
Q

Identify Medulla, 4th ventricle, and cerebellum

A
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8
Q

Identify foramen magnum and spinal cord

A
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9
Q

Steps for interpret Neuroimaging (5)

A

Identification - use landmarks

Symmetry

Density/Intensity

Pattern of Enhancement

Lesion location

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10
Q

What appears dense on CT?

Sensitivity to detect blood?

A

Mineralized structures such as calcified bone or chronic calcified lesions.

>90% sensitivity to detect blood

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11
Q

Identify hyperdense structures

A

Calvarium, lens, pineal gland, choroid plexus

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12
Q

Diagnosis?

A

Neurocysticercosis

Calcified scolex in cysticercosis

Scolex - the anterior end of a tapeworm, bearing suckers and hooks for attachment.

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13
Q

Diagnosis

A

Acute basal ganglia hemorrhage with intraventricular extension

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14
Q

Provide simple description

Diagnosis

A

Chalk outlining the sulci

Diffuse subarachnoid hemorrhage which is extraxial + intraventricular extension

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15
Q

For suspected extraxial epidural hematoma what can be done when reading the image?

A

Adjust to bone window to observe for calvarial sutures and fractures

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16
Q

Identify hyperdensities

A

Hyperdense MCA sign in the sylvian fissure

Between the cerebral peduncles in the interpeduncular cisterns -> Dense vessel sign (top of basilar artery)

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17
Q

Hypodense typically represent (4)?

A

Chronic lesions

Fluids

Cystic component

Edema

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18
Q

Define encephalomalacia

Define atrophy

A

Softening or loss of brain tissue after cerebral infarction, cerebral ischemia, infection, craniocerebral trauma, or other injury

Loss of NEURONS and the connections between them. Atrophy can be generalized, which means that all of the brain has shrunk; or it can be focal, affecting only a limited area of the brain and resulting in a decrease of the functions that area of the brain controls.

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19
Q

CT characteristics suggestive of chronic stroke vs traumatic brain injury?

A

Isodense to CSF

Follows vascular territory vs not

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20
Q

Is this intraxial or extraxial?

A

Fronto-temporal arachnoid cyst

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21
Q

Timeline for an acute stroke to present with hypodensity (edema) on CT?

A

6-8 hours

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22
Q

Describe

A

Vasogenic edema surround a metastatic lesion

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23
Q

MRI Brain without contrast

What are the basic sequences (4) + Optional

A
  1. T1WI
  2. T2WI + Fluid Attenuated Inversion Recovery (FLAIR)*
  3. DWI + Apparent Diffusion Coefficient**
  4. Gradient Echo Sequence (GRE)
  5. T1 with Gadolinium contrast

WI- Weighted Image

* Most filling and useful sequences

** Designed to diagnose energy failure and ischemia

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24
Q

What are some specialized MR sequences?

A

MR Angiogram and Venogram

Fat suppresion

Perfusion

Spectroscopy

Tractography

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25
Q

Detail

A

Neurovascular unit is an essential component to make up the blood brain barrier

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26
Q

Detail following ischemia

A

The cellular components of the nuerovascular unit becomes ischemic. Cannon maintain the sodium/potassium gradient leading to edema -> Cytotoxic edema

27
Q

Detail

A

T2WI is great to highlight fluid. This is an acute stroke.

28
Q

Detail

A

Leaky tight junction -> vasogenic edema (poor vessel integrity)

Occurs with neoplasm, abscess, trauma, and hypertensive emergency

29
Q

Describe

A

Heterogenous mass

30
Q

How does CT and MRI FLAIR relate in a stroke?

DWI?

A

Both require about 8 hours to demonstrate evidence of ischemia

Can detect ischemia within 30 minutes of onset.

31
Q

Why do we need DWI and ADC to confirm infarction?

T2 Shine through

A

DWI relates to T2WI (FLAIR) thus what is hyperintense on T2WI will be hyperintense on DWI.

T2WI (FLAIR) “shine through” to DWI

Thus if ADC is hyperintense, it is confirmed to be a T2 shine through

32
Q

Etiologies for T2WI (FLAIR) hyperintensities (6)

A

micro-hemorrhages

gliosis

damage to small blood vessel walls

breaches of the barrier between the cerebrospinal fluid and the brain

loss and deformation of the myelin sheath

Ischemia

33
Q

Discuss the nature of localization of pyogenic abscesses

A

Hematogenous spread following vascular territory territories thus majority of septic emboli locate in major vascular territories such as MCA -> frontal and pareital lobes being the most common locations in distribution of MCA

34
Q

What is a common location for metastatis?

A

Like bacteria hematogenous spread is common thus gray-white matter junctions are common.

Arterioles are just small enough at the junction to halt any further progression of emboli or metastatic cells.

35
Q

Most common brain metastasis (2)

Others (4)

A
  1. Lung
  2. Breast

Melanoma, Renal, Thyroid, Gastrointestinal

36
Q

Describe how transependymal flow of CSF will appear on FLAIR. What’s one reason this will occur?

A

Symmetrical smooth periventricular hyperintensities and hydrocephalus from eg. a posterior fossa mass -> communicating hydrocephalus.

37
Q

Describe Dawson Fingers.

Why does this occur?

A

Ovoid periventricular lesions

Central veins run perpendicular to the ventricles. Immune cells exit these veins and penetrate the brain parenchyma.

Axial View.

38
Q

Detail the difference.

A

Left: Ovoid periventricular hyperintense lesions - > MS

VERY COMMON - Right: Confluent periventricular and subcortical hyperintense lesions along with accompanying cerebral atrophy - > small vessel ischemic changes

39
Q

MR T1 hyperintense lesions caused typically by (4).

A

Paramagnetic substances (iron, copper, melanin, calcium)

Fat

Protein-rich lesions

Subacute hematoma

40
Q

MR T1

What is hyperintense in orbit?

A

Orbital fat

Orbital melanoma

41
Q

What MR sequence is this and what is the abnormality?

A

MR T1 and copper accumulation in the basal ganglia -> Wilson Disease

42
Q

What makes up the basal ganglia

A

Caudate nucleus, putamen, and globus pallidus in the cerebrum, the substantia nigra in the midbrain, and the subthalamic nucleus in the diencephalon

43
Q

What MR Sequence and Dx

A

Colloid cyst (Protein rich mass) leading to communicating hydrocephalus.

Note this presentation of complete obstruction of the interventricular foramen (foramen of monro) can occur so acutely it can lead to imminent death

44
Q

What makes Blood on MR challenging to interpret.

A

Blood on MR evolves along with the intensity signals on T1 and T2.

45
Q

Acute hematoma

MR T1 vs T2

What is the form of Hgb?

A

(1-3 days)

Deoxyhemoglobin

46
Q

Subacute hematoma

MR T1 vs T2

What is the form of Hgb?

A

(3-14 days)

Methemoglobin (F3+, FerrIC ion)

47
Q

Chronic hematoma

MR T1 vs T2

What is the form of Hgb?

A

> 14 days (2 weeks)

Hemosiderin - iron-storage complex that is composed of partially digested ferritin and lysosomes

Essentially appears as a CSF filled hole. Rim of hypointense region on T2 is the ring of hemosiderin

48
Q

mnemonic for what can be identified on T2

A

S2HI2NE

Stroke, Subacute hematoma

Hydrocephalus

Ischemic changes, Inflammatory

Neoplastic

Edema

49
Q

Mnemonic for what can be seen using MR T1 sequence

A

SH IMMeR

Subacute hematoma

Iron

Metals

Melanoma

Rich in protein

50
Q

What is notable about hypdense lesions on T2

A

The same kinds of lesions that appear hyperintense on T1 will be hypointense on T2

Protein-rich masses

Flowing blood is not depicted but flow voids do appear

Paramagnetic substances (iron, copper, melanin, calcium)

In addition, acute hematoma

51
Q

MR sequence?

What are we highlighting here?

A

Flow voids

ICA, MCA, PCOM, PCAs, Confluence of venous sinuses

52
Q

Identify the pathology

A

Absent right ICA flow void - > occlusion

53
Q

Back pain

Exacerbating movements

Extension exacerbates _____ ?

A

Compressed cord

It decreases the diameter of the spinal canal, thus worsens compression. Flexed at the hips will increase the diameter of the canal and mitigate back pain.

54
Q

Back pain

Exacerbating movements

Flexion exacerbates _____ ?

A

Compressed root.

Radiculopathy may occur when the nerve root is compressed in the intervertebral foramina due to inflammatory changs causef by a herniated disk.

Flexion reduces the size of the intervetebral foramina.

55
Q

Chief complaints with spinal cord/nerve root pathology (6)

A

Back pain

Weakness

Gait abnormality (from weakness or disturbed position sense or damage to descending cerebellar pathways)

Neurogenic claudication (muscle cramp/spasm)

Bladder, bowel dysfunction (damage to descending pathways or sacral fibers)

Sensory level (“squeezing belt” with numbness and tingling below that level)

56
Q

Detail dorsal column topographically

A

Vibration, proprioception, fine touch

Arms are lateral, legs are medial

57
Q

Detail Anterolateral system topographically

A

Spinal thalamic tract

Pain, temperature, crude touch

58
Q

Detail lateral corticospinal tract topographically

A

Legs are lateral, arms are medial

59
Q

Symptoms of complete transverse lesion

Etiologies

A

Sensory level is most specific finding, bilateral weakness, urinary dysfunction, dysautonomia, respiratory distress, segmental anterior horn syndrome.

Note: Sensory fibers enter posterior cord, ascend 1-2 levels, then decussate in the anterior commissure. Thus sensory level typically present 1-2 segments below actual lesion.

Transverse myelitis

60
Q

Acute cord injury causes spinal shock - tone and reflexes?

A

Low tone and decreased reflexes.

Over days to weeks spasticity develops and hyper-reflexia

If descending micturition pathways are affected -> urinary dysfunction

61
Q

Damage to sympathetic pathways traveling in the intermediolateral columns can lead to ?

A

Serious dysautonomia

62
Q

Dangers of cervical lesions

A

Phrenic nerve can be affected causing paralysis of diaphragm

63
Q

Segmental anterior horn syndrome

A

Lower motor neuron pattern of weakness in the muscles innervated by that segment

64
Q
A

Neurology (6 decks)

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