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Brant - 5th Edition > Chapter 6 - Central Nervous System Infection > Flashcards

Chapter 6 - Central Nervous System Infection Flashcards

1
Q

TORCH infections

A
  1. Toxoplasmosis
  2. Other infections (syphilis, varicella zoster, lymphocytic choriomeningitis)
  3. Rubella
  4. Cytomegalovirus
  5. Herpes simplex
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2
Q

Most common congenital CNS infection

A

Cytomegalovirus

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3
Q

Symptoms of cytomegalovirus in neonates (5)

A
  1. Hepatosplenomegaly
  2. Jaundice
  3. Cerebral involvement (psychomotor retardation)
  4. Chorioretinitis
  5. Deafness
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4
Q

Important image finding of CMV

A

Periventricular calcification

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5
Q

These congenital infection results from hematogeneous stpread after a pregnant woman eats undercooked meat or is exposed to cat feces, both which can harbor viable oocytes.

A

Toxoplasmosis

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6
Q

Imaging finding of toxoplasmosis

A
  1. Atrophy
  2. Dilated ventricles
  3. Dystrophic calcification

The calcifications are scattered in the white matter, basal ganglia, and cortex. - as opposed to congenital CMV infection (perivetricular)

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7
Q

This is a rodent-borne arena virus which can closely mimic toxoplasmosis and CMV on neonatal imaging.

A

Lymphocytic choriomeningitis virus (LCMV)

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8
Q

It results from infection during descent through the birth canal when the mother has a genital infection with herpes virus (Type 2)

A

Herpes simplex encephalitis

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9
Q

Imaging finding of HSV

A
  1. US may show areas of increased parenchymal echogenicity
  2. CT = diffuse brain swelling or bilateral patchy areas of hypodensity in the white matter, cortex
  3. Sparing of the basal ganglia, thalami, and posterior fossa structures
  4. Hyposdense lesion = T2 hyperintensity
  5. Hemorrhage, calcification,
  6. Meningeal and patchy parenchymal enhancement
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10
Q

HIV encephalitis primarily affects what part of the brain?

A
  1. White matter
  2. Basal ganglia

Resulting in diffuse cerebral volume loss

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11
Q

Image findings of HIV encephalitis

A
  1. Symmetric calcifications in the basal ganglia, especially the globi pallidi = best seen in CT
  2. T2 hyperintense white matter
  3. Subtle enhancement of the basal ganglia
  4. MRA = associated vasculopathy with fusiform dilation and ectasia of the intracranial arteries
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12
Q

This was once a devastating fetal viral infection but is now very uncommon because of widespread immunization of females before childbearing age.

A

Rubella

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13
Q

Image findings of rubella

A
  1. CT = dystrophic calcifications in the deep gray nuclei and cortex
  2. MRI = demonstrates infarcts, white matter volume less, and delayed myelination
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14
Q

A flavivirus which originated in Africa and Southeast Asia and is transmitted by several species of mosquitoes, especially Aedes aegypti.

A

Zika virus (ZIKV)

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15
Q

Image finding of Zika virus

A
  1. CT - best demonstrates both punctate or linear calcifications which localize predominantly to the gray-white junction in the frontal and parietal lobes and, to a lesser extent, along the deep gray nuclei and periventricular zone
  2. MRI - volume loss, ventriculomegaly, abnormal myelination, callosal dysgenesis, heterotopia, lissencephaly, and polymicrogyria.
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16
Q

These extra-axial lesion result from paranasal sinusitis, otomastoiditis, orbital infections, penetrating injuries, surgery, or superinfection or pre-existing extra-axial collections.

A

Epidural and subdural abscesses or empyemas

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17
Q

What is more sensitive for evaluating epidural and subdural empyema, CT or MR?

A

MRI is more sensitive because the multiplanar capability of MRI alleviates the problem of patial volume averaging with the calvarium on CT.

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18
Q

Why is subdural empyema more acutely life threatening than epidural?

A

Because the can spread more easily through the subdural space.

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19
Q

What are complications of subdural/epidural empyema?

A
  1. Subjacent cerebritis

2. Cortical venous thrombosis and venous infarcts

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20
Q

It is a frontal sinusitis (in children) complicated by osteomyelitis, with subperiosteal, epidural, or subdural abscesses.

A

Pott puffy tumor

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21
Q

How to distinguished subdural empyema from subdural effusion?

A

Subdural emypema is hyperintense on DWI

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22
Q

How to distinguished subdural hygroma from subdural empyema?

A

Subdural hygroma are similar to CSF density and signal intensity and do not enhance.

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23
Q

Mild, smooth dural or meningeal enhancement may be seen after craniotomies and in patients with ventriculostomy catheters, especially with MRI. This enhancement can persist for how long?

A

Can persist for years and should be considered benign in this clinical setting.

Intracranial hypotension from a spontaneous or iatrogenic CSF leak (including recent lumbar puncture) can also result in smooth symmetric dural enhancement, both intracranially and along the spinal canal.

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24
Q

Common etiology of bacterial meningitis in children?

A

Haemophilus influenzae

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25
Q

Common etiology of bacterial meningitis in teens and young adults?

A

Neisseria meningitidis

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26
Q

Common etiology of bacterial meningitis in older adults?

A

Steptococcus pneumoniae

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27
Q

Common etiology of bacterial meningitis in neonates?

A

Group B steptococcus and

Escherichia coli

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28
Q

Common etiology of bacterial meningitis in premature newborns?

A

Citrobacter

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29
Q

Other differential diagnostic considerations of meningitis (4)

A
  1. Ruptured aneurysm with subarachnoid hemorrhage
  2. Leptomeningeal metastases
  3. Neurosarcoidosis
  4. Lymphoma
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30
Q

Why is neuroimaging more important in the later course of meningitis?

A

To identify complications such as:

Hydrocephalus
Cerebritis or abscess
Arterial or venous infarction
Subdural effusio or empyema
Herniation
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31
Q

What is type of hydrocephalus is more common in mengitis, communicating or noncommunicating?

A

Communicating hydrocephalus

  • It reflects impaired CSF resorption by arachnoid granulations
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32
Q

This is the most common form of CNS tuberculosis.

A

Tuberculous meningitis

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33
Q

Imaging pattern of tuberculous meningitis

A

Thickened and enhancing meninges especially along the basal cistern, corresponding to a thick gelatinous inflammatory excudate

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34
Q

Differential diagnosis of tuberculous meningitis

A
  1. Fungal meningitis
  2. Racemose cysticercosis
  3. Neurosarcoidosis
  4. Carcinomatous menigitis
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35
Q

This occurs when the larvae of the pork tapeworm Taenia solium infest the subarachnoid space, especially the basal cisterns .

A

Meningobasal or racemose cystercosis

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36
Q

Imaging finding of meningobasal/ racemose cysticercosis

A

Cystic lesions - isodense on CT and isointense on MRI to CSF

No mural nodules or calcification

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37
Q

Imaging finding of intraventricular cysticercosis

A
  1. Subtle signal changes
  2. Lack of CSF pulsations within the cyst make them more visible on MRI than CT
  3. Enhancement may or may not be present
  4. A mural scolex can often be seen within these cysts.
  5. Can cause hydrocephalus
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38
Q

Most common cause of viral meningitis

A

Enteroviruses

But can also be caused by mumps, Epstein-Barr virus, togavirsus, lymphocytic choriomengitis, and HIV.

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39
Q

This is a noninfectious granulomatous disease of unclear etiology which involves the CNS in up to 14$ of patients at autopsy.

A

Sarcoidosis

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40
Q

Aside from biopsy what are other helpful methods use for diagnosis?

A
  1. Increased serum and CSF levels of angiotensin-converting enzyme (ACE)
  2. Pulmonary involvement
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41
Q

Imaging finding of CNS sarcoidosis

A
  1. Abnormal leptomeningeal and dural enhancement
  2. Thickening and enhancement of the cranial nerves and the hypothalamic-pituitary axis
  3. Focal enhancing intra-axial masses or nonenhancing small white matter lesions
  4. Calcifications are NOT typical
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42
Q

Differential diagnosis of sarcoidosis

A
  1. Granulomatous CNS infections
  2. Metastatic disease
  3. Wegener granulomatosis
  4. Langerhans cell histiocytosis
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43
Q

With infectious resulting from hematogenous spread, why are the frontal and parietal lobes most commonly involved?

A

Because of middle cerebral artery distribution.

The abscess are centered in the gray-white junction.

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44
Q

What lobe is commonly affected with spread of sinus infection?

A

Frontal lobes

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45
Q

What lobes are involved with spread from otomastoiditis

A

Temporal lobes and cerebellum

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46
Q

Stage of parenchymal infection that occurs first few days.

The infected portion of the brain is swollen and edematous.

Areas of early necrosis are filled with inflammatory polymorphonuclear leukocytes, lymphocytes, and plasma cells.

Organism are present in both the center and periphery of the lesion which has ill-defined margin

A

Early cerebritis

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47
Q

Imaging pattern of early cerebritis

A

CT: normal or show an area of low density
MR:
-hypointense/ isointense on T1
-hyperintense on T2W amd FLAIR

Mild mass effect and patchy areas of enhancement within the lesion on both CR and MRI.

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48
Q

Stage of parenchymal infection which occurs within 1 or 2 weeks.

Central necrosis progresses and begins to coalesce, with few organisms detected pathologically.

There is vascular proliferation at the periphery of the lesion, with more inflammatory cells and early granulation tissue, which represent the brain’s effort to contain infection.

A

Late cerebritis

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49
Q

Imaging pattern of late cerebritis

A 
CT: increased hypodensity
MR: 
-hypointense on T1
-hyperintense on T2W and FLAIR
-Increased signal intensity within the center on DWI

Irregular contrast enhancement on the edges of the lesion

Delay scan - late central enhancement

Worsening of vasogenic edema

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50
Q

Stage of parenchymal infection which occurs within 2 weeks.

The infection is walled off as a capsule of callagen and reticulin forms along the inflammatory vascular margin of the infection.

Macrophages, phagocytes, and neutrophils are also present in the capsule.

The necrotic center contains very few organism.

A

Early capsule

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51
Q

Imaging pattern of early capsule

A

Contrast CT and MR shows well-defined, usually smooth and thin, rim of enhancement.

The rim tends to be T2 hypointense.

Central:
Hypodense on CT 
T1 hypointense
T2 hyperintense 
DWI hyperintense
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52
Q

Stage of parenchymal infection where the rim of enhancement becomes even better defined and thicker, reflecting more complete collagen in the abscess wall.

Multiloculation is common.

A

Late capsule

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53
Q

Imaging pattern of late capsule

A

Hyperintense DWI
T1W isointense or hyperintense to white matter
T2W hypointense

54
Q

Differential diagnosis of bacterial cerebral abscess

A
  1. Neoplasm
  2. Subacute infarct
  3. Demyelination
55
Q

How can MRS assist in confirming cerebral abscess

A

If a combination of elevated lactate and amino acids is found in the center of the lesion.

56
Q

Infections that begin with septic embolus may have the typical appearance of an abscess.

True or false.

A

False.

The embolus frequently causes an infarct the dominates the imaging finding.

57
Q

Finding the is suggestive of septic embolus in the brain.

A

A thicker, more irregular ring of enhancement that persists within an area of infarct.

Septic emboli may lead to mycotic aneurysm formation, which can result in intraparenchyma or subarachnoid hemorrhage.

58
Q

Focal mycobaterial infection of the brain occurs in two forms.

A
  1. Tuberculoma
  2. Abscess

Tuberculoma - granuloma with central caseous necrosis

Tuberculous abscess - characteristic similar to pyogenic asbcess but usually develops in patients with impaired T-cell immunity

59
Q

Most tuberculomas in adults appear what part of the brain?

A

Supratentorial - involving the frontal and parietal lobes.

60% of tuberculomas in children are in the posterior fossa, usually the cerebellum.

60
Q

Imaging finding of tuberculomas

A

CT - one more more isodense or slightly hyperdense nodules or small mass lesions.

Multiple lesion 50% of the time

A target appearance with central calcification by rim enhancement

MRI - high/low signal intensity on T2 -depending upon the lesion and the water content of caseous necrosis.
Wall - usually hypointense n T2

61
Q

When are calcification seen in tuberculomas?

A

Calcification is present in fewer than 5% of cases at the initial diagnosis but is commonly seen as the lesion resolve.

62
Q

Differential diagnosis of tuberculoma

A
  1. Neoplasm
  2. Bacterial abscess
  3. Fungal and parasitic infections
  4. Neurosarcoidosis
63
Q

This is a rare complication seen in immunocompromised patient.

Impaired T-cell function prevents the normal host response required for tuberculoma formation with caseous necrosis.

A

Tuberculous absecess

Imaging features are similar to that seen with bacterial abscesses.

64
Q

Fungal infections of the CNS can be group into what categries? (2)

A
  1. Endemic

2. Opportunistic

65
Q

These fungal infections are usually geographically restricted.

They can occur in both immunocompetent and immunosuppressed patients.

A

Endemic fungal infections

66
Q

These fungal infectios occur worldwide but usually in immunocomprised patients such as infects, the elderly, or chronically ill.

A

Opportunistic fungal infections

67
Q

Fungal infections that usually manifest as granulomatous meningitis

  • focal parenchymal lesions are unusual.
A

Endemic fungal infections

68
Q

What are the most common opportunistic fungal CNS infections?

A
  1. Cryptococosis
  2. Aspergillosis
  3. Mucormyscosis
  4. Candidiasis
69
Q

Fungal etiology that involves the CNS in 60% to 70% of patients with diseminated disease.

Infection may arise from hematogeneous spread or by direct aggressive extension from an infected paranasal sinus, leading to meningitis or meningoencephalitis.

A

Aspergillosis

70
Q

Image pattern of CNS aspergillosis

A

The abscesses are frequently T2 hypointense centrally on MRI due to hemorrhage or the presence of heavy metals concentrated by the fungus.

Subcortical or cortical infarcts from blood vessel invasion may occur.

71
Q

This fungal etiology invades the brain usually by direct extension from the sinuses, nose, or oral cavity but hematogeneous spread also occurs.

Almost all patients are diabetic or otherwise immunocompromised.

A

Mucormycosis

72
Q

Imaging pattern of CNS mucormycosis

A

Single or multiple mass lesions with the degree of peripheral enhancement and vasogenic edema

Smaller lesions show solid-enhancement pattern.

Lesions are often in the base of the brain, adjacent to disease sinuses.

Infarcts, intra-axial/ extra-axial hemorrhage, and meningeal enhancement can be seen with CT and MR.

73
Q

This finding is more likely to be mucormycotic abscess than an infarct.

A

Lesion with peripheral enhancement, cortical sparing, and nonvascular distritbution.

Often it is difficult to distinguish both.

74
Q

Most frequently reported CNS fungal infection.

A

Cryptococcosis

75
Q

Cryptococcosis etiology which is responsible for most cases in immunocompromised patients

A

Cryptococcus neoformans

76
Q

Cryptococcosis etiology which reported mostly in patients with normal immune function

A

Cryptococcus gattii

77
Q

CT scan finding of CNS cryptococcosis

A

CT scans in patients with cryptococcosis are frequently normal or demonstrate only mild meningeal enhancement and/or hydrocephalus.

Cryptococcomas are shown as small, usually multiple, solid enhancing, peripherally located parenchymal nodules with vasogenic edema.

Ring-like enhancement and calcifications are occasionally seen.

78
Q

MR findings of CNS cryptococcosis

A

Leptomeningeal nodules are often only seen on contrast-enhanced T1WI as multiple tiny enhancing lesions near the basal cisterns and within the sulci.

Diffuse meningeal enhancement is unusual.

Gelatinous pseudocysts (immunocompromised) = Dilated perivascular spaces filled with the organism and mucinous material.

They appear as rounded, smoothly marginated lesions in the basal ganglia that are nearly isodense and isointense to CSF.

There is minimal, if any, peripheral edema or enhancement.

79
Q

This is caused by the larvae of the pork tapeworm Taenia solium. Transmission occurs via the fecal-ral route.

A

Cysticercosis

80
Q

Stage of cysticercosis:

When viable parasitic cysts appear as small (usually 1 cm or less), solitary or multiple rounded lesions that are hypodense on CT and isointense to CSF on MRI.

A

Vesicular stage

The lesions are usually gray-white junction or in gray matter.

A small marginal nodule representing the scolex is sometimes seen.

There is usually no enhancement or edema.

81
Q

Stage of cysticercosis:

When the cyst dies and its fluid leaks into the surrounding brain inciting inflammation. This produces clinical symptoms of acute encephalitis, which may be severe depending on the number of lesions.

A

Colloid stage

Imaging studies now reveal ring-enhancing lesions with surrounding vasogenic edema

The colloidal cyst fluid becomes increasingly dense on CT and hyperintense on MRI when compared with CSF. The dead cyst further degenerates in the nodular granular stage, becomes smaller and causes less edema, but shows increasing nodular or irregular peripheral enhancement.

82
Q

Stage of cysticercosis:

Where a dense residual calcification is left with no remaining edema or enhancement.

A

Nodular calcificied stage

CT without contrast excels at detecting these small, peripherally distributed calcifications.

With MRI, the calcifications are best seen on T2*-weighted gradient-recalled echo (GRE) sequences.

Once the cyst has degenerated, further drug therapy is not warranted.

83
Q

This is also known as hydatid disease.

A

Echinococcosis

84
Q

Etiologic agent of Echinococcosis

A

Echinococcus granulosis

85
Q

Imaging pattern of CNS echinococcosis

A

The cysts are usually solitary, unilocular or multilocular, large, round, and smoothly marginated.

Most often supratentorial and may rarely have mural calcifications.

CT - the fluid within the cyst is usually isodense with CSF. There is usually no surrounding edema or abnormal contrast enhancement, unless the cyst has ruptured, leading to an inflammatory reaction and more acute presentation.

MRI - lesions are usually nearly isointense with CSF but can have a T2- hypointense rim

86
Q

Most often implicated pathogens of Amebic meningoencephalitis. (3)

A
  1. Entamoeba histolytica
  2. Acanthamoeba
  3. Naegleria fowleri
87
Q

Imagining pattern of early amebic meningoencephalitis.

A

Early in the infection, there may be meningeal and/or gray matter enhancement.

Associated vasculitis and cerebral infarction can occasionally be observed.

88
Q

Imagining pattern of late amebic meningoencephalitis.

A

There is diffuse cerebral edema and hemorrhage may occur.

There are a few reports of amebic brain abscesses appearing as single or multiple lesions with solid or ring-like enhancement with surrounding edema .

Amebic abscesses are more common in debilitated or immunosuppressed patients.

89
Q

Imaging pattern of neurosyphilis

A
  1. Can be normal or demonstrate cerebral volume loss and nonspecific T2-hyperintense white matter lesions on MRI.
  2. Meningeal enhancement is unusual but cranial nerve enhancement in patients with syphilitic cranial neuritis has been described.
  3. Rarely, gummas (syphylitic granulomas) do develop. These usually appear as small enhancing nodules at the surface of the brain with adjacent meningeal enhancement.
90
Q

This presents as an acute stroke syndrome or subacute illness with variety of symptoms.

Pathologically, there is thickening of the meninges and a medium-to-large vessel arteritis.

A

Meningovascular syphilis

91
Q

Imaging finding of meningovascular syphilis

A

Imaging studies reveal small infarcts of the basal ganglia, white matter, cerebral cortex, or cerebellum.

The infarcts may exhibit patchy or gyriform enhancement and are best seen with MRI.

92
Q

MRA and conventional angiography findings in patients with meningovascular syphilis

A

Multiple segmental constrictions and/or occlusions of large and medium arteries, including the distal internal carotid, anterior cerebral, middle cerebral, posterior cerebral, and distal basilar arteries

93
Q

This is a multisystem spirochete infection which is most commonly caused by Borrelia burgdorferi

A

Lyme disease (or Lyme borreliosis)

94
Q

Modality of choice for CNS Lyme disease.

A

MRI

95
Q

Imaging pattern of cranial neuritis due to Lyme disease

A

MR scans may show thick, enhancing cranial nerves.

Cranial nerves III to VIII can be involved, with the facial nerve most commonly affected.

96
Q

Imaging pattern of parenchymal CNS Lyme disease

A

MR studies show multiple small white matter lesions, similar to that seen with multiple sclerosis.

The lesions can be found in the supratentorial and infratentorial white matter tracts.

They often enhance with contrast in a nodular or ring-like pattern, depending on their size. There may be meningeal enhancement.

97
Q

Differential diagnosis of CNS Lyme disease

A
  1. Multiple sclerosis and other demyelinating processes
  2. Neurosarcoidosis
  3. Vasculitis
98
Q

Imaging findings of herpes simplex encephalitis

A

CT: normal or show poorly defined hypodense regions in one or both temporal lobes

MRI: symmetric or asymmetric gyral pattern of hyperintensity on T2WI and FLAIR images in the temporal lobes with a predilection for the hippocampus and insular cortex but sparing of the subjacent putamen. This is best appreciated on FLAIR sequences.

Reduced diffusion on DWI is often present.

Meningeal and parenchymal enhancement or subtle evidence of hemorrhage may be present.

99
Q

This is also the cause of herpes zoster opthalmicus which can be complicated by ipsilateral cerebral angiitis causing cerebral infarction and contral lateral hemiparesis.

A

Varicella zoster virus

100
Q

Imaging pattern of VZV encephalitis

A

Typical infarcts, and angiography shows segmental areas of narrowing and/or beading of large- and medium-sized arteries.

Mycotic aneurysms may develop.

The brainstem can also be involved.

101
Q

VZV may infect any of the cranial nerves, but CNs VII and VIII are most commonly involved and result in herpes zoster oticus.

This is called what sydrome?

A

Ramsay Hunt syndrome

102
Q

This is a very rare condition caused by chronic infection by a variant of the measles virus.

Typically present in children and young adults with prior measles infection before age of 2 years and after an intervening asymptomatic period of up to years.

A

Subacute sclerosing panencephalitis.

103
Q

Imaging pattern of SSPE

A

Initial findings - often be normal but can reveal early asymmetric patchy or diffuse swelling with hypodensity and T2 hyperintensity of the cerebral white matter.

Enhancement is usually absent.

On DWI, inconsistent patterns of reduced diffusion involving cortex, white matter, corpus callosum, internal capsules, thalami, and brainstem have been documented in a small number of cases of early or rapidly progressive SSPE.

In the very late stages, profound cortical atrophy develops.

104
Q

Differential consideration for subacute sclerosing panencephalitis

A
  1. Demyelination,

2. Progressive multifocal leukoencephalopathy (PML), 3. HIV encephalitis.

105
Q

These are caused by arboviruses (insect borne) which preferentially affect the deep gray nuclei and brainstem.

A
  1. St Louis encephalitides
  2. Western equine encephalitides
  3. Eastern equine encephalitides
106
Q

This is a mosquito borne-virus, which incites a meningoencephalitis of widely variable clinical severity.

A

West Nile virus

107
Q

These encephalitides can demonstrate summetric swelling, hypodensity, and T2 hyperintensity of the thalami, basal ganglia, and brainstem.

A

West Nile and Japanese encephalitides

108
Q

Superimposed hemorrhage is seen in acute necrotizing encephalitis in children and has been associated with what viruse?

A

Influenza A and N viruses

109
Q

This is a devastating disease of childhood and of unknown etiology. Viral and/or autoimmune encephalitis are implicated.

The clinical course is characterized by intractable seizures, progressive neurologic deficits, and frequently, coma.

The disease usually affects one cerebral hemisphere.

A

Rasmussen encephalitis

110
Q

Imaging finding of Rasmussen encephalitis

A

The disease usually affects one cerebral hemisphere.

MR studies show focal cortical swelling and T2 hyperintensity with minimal, if any, enhancement in the involved hemisphere early on, but these progress to dramatic asymmetric atrophy later.

The affected hemisphere has been shown to be hypometabolic by SPECT and PET nuclear scans.

111
Q

This is an uncommon infectious or inflammatory process primarily affecting the cerebelllar hemispheres in a symmetric or asymmetric pattern

A

Cerebellitis

112
Q

This is an acute demyelinating disease that occurs most commonly after a recent viral illness or vaccination but sometimes spontaneously.

A

Acute disseminated encephalomyelitis (ADEM)

Autoimmune demyelination is the currently accepted mechanism, and infectious pathogens have not been isolated.

113
Q

This is a rare , severe variant of ADEM that is often fatal.

The major imaging feature is a rapid progression of white matter lesions over the course of several days.

A

Acute hemorrhagic leukoencephalitis

Pathologically, there is perivascular hemorrhagic necrosis, primarily in the centrum semiovale

114
Q

This is a transmissible spongiform encephalopathy caused by an infectious proteinaceous particle or “prion.” It is a rare, uniformly fatal, and rapidly progressive neurodegenerative disorder.

A

Creutzfeldt–Jakob disease (CJD)

Prions are protease-resistant particles resulting from altered conformation of a normal host cellular protein encoded by the PrP gene. Prions accumulate in the neural tissue and result in cell death.

115
Q

Imaging pattern of CJD

A

CT is not helpful and is usually normal or shows generalized cerebral volume loss.

MRI: hyperintensity in the striatum (caudate and putaminal nuclei) symmetrically and/or subtle ribbon- like hyperintensity in scattered areas of the cerebral cortex in early cases.

These features and cerebral atrophy become more apparent as the patient declines. Lack of enhancement is the rule.

116
Q

Pulvinar “Hockey-stick” sign is seen in what disease?

A

New variant Creutzfeldt–Jakob disease

117
Q

Differential diagnosis for CJD (3)

A
  1. Hypoxic-ischemic enchephalopathy
  2. Metabolic or toxic injury
  3. Encephalitis
118
Q

This is the most common manifestation of HIV infection of the brain on neuroimaging studies.

A

Diffuse atrophy

This is largely central atrophy, reflecting the predominant white matter involvement.

119
Q

Most common finding in MRI of HIV infection of the brain

A

A diffuse, symmetric, ill- defined, often hazy pattern of T2 hyperintensity in the deep and periventricular white matter or multiple small T2-hyperintense white matter lesions are the most common findings.

No mass effect or abnormal contrast enhancement should be seen

120
Q

Differential diangosis for HIV encephalitis in the young.

A
  1. CMV
  2. HSV
  3. PML
121
Q

This is the most common opportunistic CNS infection and brain mass in AIDS patients, occuring in about 13% to 33% of these patients with CNS complaints.

A

Toxoplasmosis

122
Q

What is the typical imaging appearance of CNS toxoplasmosis?

A

Multiple enhancing parenchymal lesions with surrounding vasogenic edema.

The lesions are usually relatively small, ranging between 1 and 4 cm in diameter, and exhibit surrounding vasogenic edema often with mass effect.

The lesions are hypodense on CT and T1 hypointense on MRI but may have a variable but typically hyperintense signal on T2WI and DWI.

123
Q

What is the favored stie of CNS toxoplasmosis?

A

Basal ganglia

But white matter and cortical lesions are also common

124
Q

Main differential diagnosis for CNS toxoplasmosis.

A

CNS lymphoma

125
Q

This an infection of immunosuppressed patients caused by reactivation of the latent JC polyomavirus

A

Progressive multifocal leukoencephalopathy (PML)

126
Q

Imaging pattern for PML

A

CT shows one or more hypodense lesions, usually asymmetrically distributed, within the subcortical and deep white matter.

On MRI, these exhibit decreased signal intensity on T1WI and increased signal on T2WI, FLAIR, and DWI sequences.

Mass effect and contrast enhancement are almost always absent, which are very important distinguishing features.

127
Q

This is by far the most common intracranial neoplasm in patients with AIDS.

A

Primary CNS lymphoma

Solitary or multiple enhancing mass lesions are found with neuroimaging studies.

128
Q

Location of primary CNS lymphoma

A

The lesions are usually centrally located within the deep white matter or basal ganglia, but cortical lesions occur occasionally.

There may be subependymal spread or extension across the corpus callosum, which do not usually occur with toxoplasmosis.

129
Q

Imaging pattern of primary CNS lymphoma

A

With CT, the lesions are often isodense or hyperdense compared with white matter.

With MRI, there is variable signal intensity which can be isointense or hypointense on T1WI and hypointense or hyperintense on T2WI and FLAIR sequences. The lesions almost always enhance with contrast in either a ring or solid pattern.

130
Q

What are the difference between primary CNS lymphoma and toxoplasmosis?

A
  1. Toxoplasmosis is more frequently multiple, and the lesions are usually smaller than with lymphoma.
  2. Lymphoma is favored if lesions demonstrate T2 hypointensity coupled with diffuse, homogeneous contrast enhancement on MRI.
  3. Central T2 hyperintensity, a T2-hypointense rim, and ring-like contrast enhancement favor toxoplasmosis.
  4. Lymphoma more commonly demonstrates associated reduced diffusion and hyperintensity on DWI, presumably due to hypercellularity.
  5. MRS shows increased choline and decreased N-acetyl aspartate (NAA) with lymphoma, while toxoplasmosis shows decreased choline and NAA with increased lipid and lactate.

Brant - 5th Edition (8 decks)

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