Ebook Case-Based brain imaging (2nd edition): Part 2

(BQ) Part 2 the book Case-Based brain imaging presents the following contents: Neurodegenerative/white matter diseases/metabolic, trauma, congenital/developmental malformations and syndromes, cranial nerves.

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Section IV

Neurodegenerative/

White Matter Diseases/

Metabolic

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• Microvascular ischemic disease (older patient, typically sparing of corpus callosum and subcortical

U fibers, lack of enhancement)

• Vasculitis (small chronic infarctions and leptomeningeal enhancement may be seen)

• Neoplasm (typically more mass effect, rarely involves the corpus callosum unless glioblastoma or lymphoma)

Fig 85.1 Multiple axial T2-W FLAIR images

demon-strate scattered periventricular foci of T2 prolongation radiating from ventricles (A), within the left brachium

pontis (B), and within the splenium of the corpus

cal-losum (C) in a pattern typical of demyelination as seen

with multiple sclerosis The lesion within the corpus losum demonstrates enhancement on the postcontrast T1W image (D) and restricted diffusion on the DWI (E)

cal-with matching ADC (F) signal consistent with an active

region of demyelination

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412 CASE-BASED BRAIN IMAGING

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IV NEURODEGENERATIVE/WHITE MATTER DISEASES/METABOLIC 413

• ated and myelinated white matter, monophasic, and often fatal

Balo's concentric sclerosis type: characterized by large lesions with alternating zones of demyelin-Pathology Gross

• Acute plaques are edematous and have a pink-gray color

• Chronic plaques show atrophy and cystic change

Microscopic

• There is a variable degree of perivenular inflammation, macrophage infiltration, myelin loss, edema, and gliosis, with varying axonal loss

• Necrosis, hemorrhage, and calcification are rare

• Cystic change may occur in large lesions

Imaging Findings Computed Tomography

• Lesions are typically isodense or hypodense on noncontrast scan

• Acute lesions may show enhancement postcontrast

Magnetic Resonance

• get” appearance: a hyperintense center representing demyelination with a slightly less hyperintense pe-riphery representing vasogenic edema A rim of hypointensity separates these two regions When lesions are large and masslike with or without edema they may mimic neoplasm, tumefactive MS (see Case 86)

Lesions are typically homogeneously hyperintense on T2W imaging Large acute lesions may have a “tar-• Lesions may be iso- or hypointense on T1W imaging, and may demonstrate a rim of T1 shortening attributed to free radicals in infiltrating macrophages T1 black holes are MS plaques with decreased signal on T1 If acute and enhancing the decreased signal is likely due to edema Chronic decreased signal within a plaque on a T1W image is thought to be secondary to associated axonal loss

• Acute lesions often enhance following gadolinium administration, and the pattern may be nodular, arclike, or ringlike

• New disease inflammation disrupts the blood–brain barrier resulting in enhancement Enhancement may precede T2 abnormalities Enhancement generally lasts 4 weeks and then resolves (range 1–16 weeks)

• Acute lesions may demonstrate diffusion restriction, or enlargement of preexisting T2 lesions secondary to acute inflammation

• Lesions typically affect the corpus callosum, periventricular white matter, and arcuate fibers; they may also occur in the posterior fossa and in gray matter structures such as the basal ganglia The periven-tricular WM lesion are often ovoid and perpendicular to the ventricular surface “Dawson’s fingers.”

• Cerebral volume loss greater than expected for age is often seen and diffuse or focal loss of volume

of the corpus callosum may be seen due to intrinsic corpus callosum plaques or due to axonal loss secondary to more peripheral MS plaques

• MR spectroscopy may demonstrate reduced NAA peaks with a reduced NAA:creatine ratio and an elevated choline within plaques

Treatment

• Corticosteroids, particularly acutely

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Prognosis

Highly variable depending on the form of the disease and its responsiveness to therapy

PEARLS

• MR is much more sensitive and specific than CT for the diagnosis of MS, as MR’s multiplanar

capability better demonstrates callosal involvement and “Dawson’s fingers” (ovoid lesions with

Fig 85.2 (A–K) Examinations from multiple patients The

typical MRI appearance of “Dawson’s fingers” is shown with ovoid T2 hyperintense lesions radiating from the corpus callosum on (A) axial and (B) sagittal T2W FLAIR (C, D) The

second patient illustrates the use of contrast to identify acute areas of inflammatory demyelination (D) in a patient with

severe underlying chronic disease on axial T2W FLAIR (C).

A,B

D

C

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Suggested Readings

Fox RJ, Rudick RA Multiple sclerosis: disease markers accelerate progress Lancet Neurol 2004;3(1):10 Gean-Marton AD, Vezina LG, Marton KI, et al Abnormal corpus callosum: a sensitive and specific indicator of multiple sclerosis Radiology 1991;180(1):215–221

Mullins ME Emergent neuroimaging of intracranial infection/inflammation Radiol Clin North Am 2011;49(1):47–62 Polman CH, Reingold SC, Banwell B, et al Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria

Ann Neurol 2011;69(2):292–302 Sajja BR, Wolinsky JS, Narayana PA Proton magnetic resonance spectroscopy in multiple sclerosis Neuroimaging Clin N

Am 2009;19(1):45–58

K

Fig 85.2 (continued) The third patient illustrates the increased conspicuity

of posterior fossa MS lesions on (F) T2W compared to T2W FLAIR images (E)

(G) The fourth patient presented with a hypodense lesion in the left parietal

lobe on CT This tumefactive MS case can be distinguished from tumor by its hypodensity on CT (compared to isodense or hyperdense in tumor), relative lack of mass effect on surrounding brain that would be expected for tumor

on (H) axial T2W FLAIR and (I) irregular rim of enhancement on postcontrast

T1W imaging (J, K) Same patient as in Fig 85.2H, I In patients where it is

unclear if the lesion in tumefactive MS or tumor, follow-up imaging may be obtained Four months after treatment with steroids (and also after biopsy) (J) axial T2W FLAIR demonstrates decreased size of the lesion and nearly

complete resolution of enhancement on (K) postcontrast T1W imaging.

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sion within the left posterior parietal white matter Axial

(B, C) and sagittal (E) T2-FLAIR sequences demonstrate

two dominant rounded T2 hyperintense white matter

lesions within the left parietal lobe; these lesions

dem-onstrate surrounding more pronounced T2

prolonga-tion suggesting vasogenic edema Lesions have minimal

local mass effect and mildly efface the regional sulci

The sagittal T2-FLAIR sequence (E) also demonstrates a

lamellated, or onion-skin, appearance of the more rior lesion (D) Axial and (F) sagittal postcontrast T1W

ante-images demonstrate ringlike enhancement of these lesions A tiny contralateral periatrial white matter lesion does not enhance (C).

D,E

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Diagnosis

Tumefactive multiple sclerosis (MS)

Differential Diagnosis

• Neoplasm (typically more mass effect, more surrounding vasogenic edema, rare to have lamellated appearance, rare to be hypodense on CT)

• Abscess (typically restricted diffusion centrally within the rim enhancing lesion, T2 hypointense rim with “shaggy” enhancement)

• mon and colossal involvement uncommon, but may be indistinguishable from the first episode of MS)

Acute disseminated encephalomyelitis (more common in children, deep gray nuclear involvement com-• Vasculitis (areas of infarction and leptomeningeal enhancement are common)

• Encephalitis (patients are typically acutely ill with fever and alteration in consciousness)

• Progressive multifocal leukoencephalopathy (corpus callosum is not typically involved—only 2% of white matter diseases other than MS involve the corpus callosum, typically also involves the sub-cortical U fibers)

Discussion Background

MS is the most common neurologic disorder in young adults, generally having onset between 20 and

45 years of age, although 13% of cases present before age 20 and 15% after age 50 MS is more common

strate evidence of lesions separated in time and space Separation in time requires two attacks each lasting at least 24 hours involving different parts of the CNS and separated by at least 1 month Separa-tion in space requires clinical evidence of distinct neurologic deficits and/or MR imaging evidence of separate CNS lesions Pathologically, MS is a disease of oligodendroglia and results in multifocal areas

in women than men with a ratio of 3:2 The clinical definition of MS requires that the patient demon-of well-demarcated demyelination with or without axonal degeneration

Etiology

The cause is unknown, but it is likely an autoimmune reaction in genetically susceptible individuals

Clinical Findings

The presentation varies with the location of lesions Focal motor and sensory deficits are typical, with headache or seizures being less common presenting symptoms Optic nerve involvement is common, and patients may present with acute visual changes due to optic neuritis Spinal cord involvement may cause myelopathic symptoms Most patients have a chronic relapsing and remitting course, although some patients may demonstrate steady progression of deficits

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Fig 86.2 Multiple sclerosis Multifocal large

conflu-ent lesions demonstrating T2-hyperintensity (A),

T1-hypointensity (B), and heterogeneous enhancement (C)

in the periventricular white matter bilaterally (D) The

susceptibility-weighted image demonstrates the normal

periventricular white matter venules (arrows) crossing

through these confluent active MS plaques, a finding not usually seen with brain neoplasms

A

C

B

D

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• Gadolinium enhancement pattern may help differentiate tumefactive MS from neoplasm Although

the enhancement pattern may be nodular, asymmetric, or ringlike, incomplete or asymmetric ring of enhancement demonstrating the front of active demyelination is more specific for tumefactive MS

would be expected for a similarly sized tumor Additionally, the giant plaque may show an asym-• MR is highly sensitive for the detection of MS lesions, but it is nonspecific Therefore, imaging

Fig 86.3 A 2-month follow-up MRI of the index

patient in Fig 86.1 after 2 months of treatment

Tumefactive MS can frequently mimic tumor,

present-ing with mass lesions demonstratpresent-ing T2 prolongation

and enhancement (Fig 86.1A-F), but these lesions have

markedly decreased in size and enhancement as onstrated on the (A) axial T2-FLAIR and (B) postcontrast

dem-T1W images

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Fig 87.1 (A, B) Axial T2W FLAIR images demonstrate

multiple large and confluent T2 hyperintense white ter lesions with minimal associated enhancement (C) (D)

mat-The dominant portions of the lesions show decreased diffusivity on the apparent diffusion coefficient map (bright on DWI images [not shown])

A

B

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• Asymmetric areas of low density in the white matter may be seen

• Patchy bilateral asymmetric areas of T2 prolongation in the subcortical and deep white matter of the cerebral hemispheres ranging from punctate lesions to masslike Lesions are common in the cerebel-lum and brainstem, and deep gray matter involvement is also common, especially in children

• May see hemorrhage superimposed on areas of demyelination

• Lesions may occasionally show central cavitation

• Postgadolinium, there is variable enhancement of the lesions with a pattern that may be nodular, peripheral, or diffuse

• nent tissue injury

Diffusion is variable and may be reduced in acute lesions Reduced diffusion may indicate perma-• MR spectroscopy demonstrates decreased NAA, increased choline and lactate NAA can normalize with resolution of symptoms

Fig 87.2 Follow-up imaging after treatment for patient in

Fig 87.1 (A, B) Follow-up axial T2W FLAIR images following

immunomodulatory therapy demonstrate a dramatic

decrease in the size and number of the white matter lesions

(C) Some of the lesions developed intrinsic T1 shortening

after treatment which can be seen with remyelination

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Fig 88.1 (A) Nonenhanced axial CT demonstrates

hypo attenuation in the central pons (B) An axial

T2W image demonstrates prolongation in the pons correlating with the low density demonstrated

on CT (C) DWI and (D) ADC images demonstrate

diffusion restriction corresponding to the FLAIR signal abnormality in the pons (E) (F) The lesion centered in

the pons is demonstrated to be T1 hypointense and does not enhance on this sagittal postcontrast T1W image

A,B

D,E

C

F

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ODMS, formerly called central pontine myelinolysis (CPM) and/or extrapontine myelinolysis (EPM),

is acute demyelination (classically in the central pons) caused by rapid shifts in serum osmolality

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• Characteristic round or triangular shaped area of T2 prolongation in the central pons, with sparing

of a peripheral rim of tissue representing the corticospinal tracts

• Extrapontine lesions are commonly observed in the putamina and thalami, but may be seen in the periventricular white matter and at the corticomedullary junction

• Lesions are classically hypointense on T1W imaging, less commonly isointense to surrounding normal brain

Am J Neuroradiol 2004;25(2):210–213 Sharma P, Eesa M, Scott JN Toxic and acquired metabolic encephalopathies: MRI appearance AJR Am J Roentgenol 2009;193(3):879–886

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Case 89

Clinical Presentation

An 8-year-old girl with pharyngitis and febrile seizures presents with increasing lethargy

Radiologic Findings

Fig 89.1 (A) Diffusion weighted imaging with

corresponding ADC map (inset) shows abnormal

restricted diffusion along the left hippocampal cortex (B) FLAIR axial and (C) coronal images

demonstrate adjacent T2 hyperintensity (D) One

week follow-up DWI shows complete resolution of the previously noted abnormalities

A

C

B

D

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Diagnosis

Reversible postictal cerebral edema; seizure edema

• Temporal lobe hyperintensity– Encephalitis (acute onset, often fever and personality change, often involvement of cingulum and insula)

– Neoplasm (insidious onset, mass effect, variable enhancement)– Mesial temporal sclerosis (MTS) (in addition to increased signal on T2W image see hippocampal atrophy and loss of gray white differentiation)

– Infarction (signal abnormality in a vascular territory)

Discussion Background

Reversible changes on CT and MR are known to occur following status epilepticus However, acute brain edema may also occur following a single or several seizures In these cases, the seizures are usually generalized or focal with secondary generalization The etiology of the observed parenchymal changes

is uncertain, but vasogenic edema due to focal blood–brain barrier disruption best explains the nomenon This is supported by the reversibility, relative lack of mass effect, and white matter predomi-nance of the transient radiologic abnormalities The lesions may predominate posteriorly secondary

phe-to regional variability of sympathetic vascular innervation, and because less innervation exists in the vertebrobasilar circulation, it is more prone to loss of autoregulation and disruption of the blood–brain barrier Cytotoxic edema and frank infarction due to acidosis and hypoxemia may, in some cases, com-plicate the picture and limit the reversibility of the changes Hippocampal swelling and/or T2 prolonga-tion may be observed as in the case above

The presentation varies with the location of the signal abnormality; postictal lethargy and confusion are common

Pathology

• It is rare for these cases to come to pathologic analysis

• Occasionally brain biopsies are done because of clinical concern for tumor

• Pathology may demonstrate acute neuronal loss, astrocytic infiltration with cytoplasmic swelling, and extracellular edema

– Findings distinguished from those seen with mesial temporal sclerosis when selective neuronal loss is observed in specific hippocampal subfields (Ammon’s horn sclerosis)

• Insensitive unless widespread abnormalities; variable enhancement

• Loss of gray-white distinction if the cortex is also edematous

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Case 90

A 34-year-old male burn victim with short-term memory loss, rigidity, and hyperreflexia

Fig 90.1 (A) Axial CT image shows focal

hypoden-sity in the globus pallidi bilaterally (B) Axial DWI

shows corresponding regions of diffusion restriction

(inset, ADC map) (C) Axial FLAIR demonstrates focal

T2-prolongation in the bilateral globus pallidi (D) Small

foci of gradient susceptibility may represent petechial hemorrhage, dystrophic calcification, or tissue break-down products

A

C

B

D

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Diagnosis

Carbon monoxide poisoning

• Other white matter toxins such as toluene or methanol (clinical history essential)

• Hypoxic injury (depending on degree may see involvement of other areas of brain including

thala-mus and cerebral hemispheres)

• Internal cerebral vein thrombosis (more typically thalamus is involved as well)

• Other toxins that affect the globi pallidi (i.e., cyanide poisoning, which is distinguished by clinical

history, cerebellar involvement, and lack of white matter changes)

• Inborn errors of metabolism such as methylmalonic acidemia or L-2-hydroxyglutaric acidemia

(typically present in childhood, need appropriate clinical history, and laboratory analysis)

Discussion

Background

CO poisoning most commonly occurs in the setting of attempted suicide or with the use of coal heaters

in poorly ventilated homes Three mechanisms of cellular toxicity in CO poisoning are thought to occur:

(1) the formation of carboxyhemoglobin (which cannot bind oxygen) causes hypoxia; (2) the

oxyhe-moglobin dissociation curve is shifted to the left, which decreases oxygen release to body tissues; and

(3) a direct toxic effect on mitochondria via CO binding to cytochrome a3 interferes with oxidative

phosphorylation

Clinical findings vary depending on the duration and intensity of the exposure Acute toxicity

typi-cally results in nausea, vomiting, and headache and may lead to confusion, cognitive impairment, loss

of consciousness, seizures, coma, or death Survivors may manifest movement disorders, hypertonia,

short-term memory loss, and mental deterioration Delayed neurologic sequelae has been reported in

10–30% of victims and occur weeks after initial recovery from acute CO poisoning

Pathology

• Bilateral necrosis (occasionally hemorrhagic) of the globus pallidus is the most common lesion

• Demyelination and areas of focal necrosis may occur in the white matter with sparing of subcortical

arcuate U-fibers (“Grinker myelinopathy”)

Imaging Findings

Computed Tomography

• Bilateral and symmetric low-attenuation lesions in the globus pallidus and white matter

• Bilateral basal ganglia DWI restriction is the best tool in the setting of acute exposure Low ADC

signal may persist for weeks following exposure

• Bilateral T2 hyperintensities are seen in the basal ganglia Caudate nucleus and putamen may also

be affected Subacute or chronic cases may show surrounding T2 hypointensity which may reflect hemosiderin

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• Diffuse symmetric T2 prolongation in hemispheric white matter, particularly the periventricular white matter and centrum semiovale Cortical involvement is less frequent

• Both T1 hypointense (likely reflecting necrosis) and hyperintense (likely reflecting hemorrhage) lesions have been reported

• Cerebellum may be involved as well as the cerebrum

Treatment

Hyperbaric oxygen therapy is most effective for acute CO exposure, ideally within 6 hours 100% oxygen therapy and hyperbaric oxygen may prevent long-term sequelae

Prognosis

• Varies with the severity and duration of exposure

• Long-term neurologic sequelae often occur in survivors

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Case 91

A 2-year-old boy presents with motor impairment and abdominal pain

Fig 91.1 (A) Coronal and (B) axial T2W FLAIR images

demonstrate confluent periventricular white matter T2

hyperintensity in a “butterfly” distribution with

promi-nent callosal involvement (C) Axial T2W image shows

“tigroid” perivascular sparing (arrows) (D) There is no

corresponding enhancement on the postcontrast T1W imaging

C

D

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Pelizaeus-Merzbacher disease: lack of myelination with cerebellar atrophy; manifests in the neona-• TORCH: white matter hyperintensity secondary to demyelination and gliosis Pattern is variable and may have associated calcifications

• Pseudo-TORCH: progressive demyelination with periventricular, basal ganglia, and brainstem calcifications

• Krabbe’s disease: increased thalamic density on CT; early white matter involvement in the cerebellum

Discussion Etiology

MLD is an autosomal recessive lysosomal storage disorder with a deficiency of arylsulfatase A (ARSA) resulting in defective desulfation of glycolipids and demyelination MLD is a rare disease with an affected birth rate of 1 in 40,000

There are three subtypes of the disease based on age of onset: late-infantile (ages 1–2), juvenile (ages 5–10), and adult The late-infantile subtype is the most common and characteristically presents with peripheral neuropathy, speech, and coordination difficulties The disease progresses to ataxia, quadriplegia, decere-brate posturing, and death within 4 years of onset The juvenile form presents with spasticity and dementia

The adult form may mimic multiple sclerosis clinically and lead to dementia in the third or fourth decade

Pathology Gross

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• Multiple sclerosis (white matter disease not typically confluent or symmetric)

Fig 92.1 (A) Axial T2W FLAIR and (B) axial T1W

images of the brain demonstrate abnormal ent bilateral decreased T1 and increased T2 signal throughout the posterior cerebral white matter

conflu-(C) A thin band of enhancement at the margins of

this signal abnormality on a postcontrast axial T1W image is thought to reflect active demyelination

(D) Axial DWI and the (E) corresponding ADC map

demonstrate a corresponding thin band of ally restricted diffusion

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lar inflammatory cells

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• Classic finding is low attenuation in the occipital white matter with involvement of the splenium of the corpus callosum

• Dystrophic calcifications occasionally seen

• Marked symmetric T1 and T2 prolongation in the occipital white matter and splenium of the corpus callosum Involvement of the retrolenticular portion of the posterior limb of the internal capsule

is often contiguous As the disease progresses, there is extension anteriorly to involve the frontal white matter

• T2 prolongation involving the corticospinal tracts in the pons and medulla The auditory pathways (lateral lemniscus, medial geniculate bodies, acoustic radiations) are involved as well

Lyon G, Fattal-Valevski A, Kolodny EH Leukodystrophies: clinical and genetic aspects Top Magn Reson Imaging 2006;17(4):

219–242

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• Multiple sclerosis (white matter disease not typically symmetric and more commonly

periven-tricular with plaques perpendicular to lateral ventricles often present)

Late Changes

• Include other inborn errors of metabolism leading to severe white matter loss and atrophy

Discussion

Background

Krabbe disease is an autosomal recessive lysosomal leukodystrophy marked by decreased

activ-ity of the lysosomal enzyme galactosylceramide b-galactosidase This causes accumulation of

Fig 93.1 (A) Axial and (B) sagittal T2W FLAIR images

demonstrate abnormal T2 prolongation in the periatrial

periventricular white matter as well as the posterior

body and splenium of the corpus callosum Volume loss

and ex-vacuo dilation of the atria of the lateral ventricles

is present Symmetric linear abnormal T2 hyperintensity

is also noted along the posterior limb of the internal capsules

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IV NEURODEGENERATIVE/WHITE MATTER DISEASES/METABOLIC 441 galactosylsphingosine, which interferes with myelin production and maintenance, and oligodendro-cytes are destroyed Onset can be early (infantile or late infantile), juvenile, or adult onset The early onset form (between 3 and 6 months) is the most common.

Etiology

Krabbe disease is caused by a deficiency of galactosylceramidase (galactocerebrosidase b- galactosidase),

a lysosomal enzyme that normally degrades galactosylceramide, a major component of the myelin sheath, to ceramide and galactose Accumulation of toxic metabolites leads to early destruction of oli-godendroglia, while accumulation of galactosylceramide itself elicits a globoid cell reaction The gene has been localized to chromosome 14q21 to q31 Approximately half of Krabbe disease patients have alleles that contain a large deletion in association with a C502YT polymorphism

T2 hyperintensity in the cerebellar white matter and pyramidal tracts and posterior corpus callo-• T1 hyperintensity can be seen in the basal ganglia, thalamus, and dentate nuclei

• Optic nerve and chiasmatic enlargement has been noted in some patients

• DWI may show reduced diffusion along active demyelination in the early stage of the disease but normalize in subacute or chronic stages

• May be a role for DTI in the diagnosis and monitoring infantile disease

• Rare cranial and peripheral nerve enhancement in Krabbe disease have been case reported

Treatment

• Stem cell transplant has been reported to halt progression in late onset disease

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• PMD-like disease (PMLD1) and spastic paraplegia 44

• Other hypomyelinating leukoencephalopathies

• Metachromatic leukodystrophy (butterfly appearance, sparing of subcortical U fibers)

Fig 94.1 (A) Diffusely abnormal T1 hypointensity and

(B) T2 hyperintensity is present throughout the white

matter with relative sparing of the corticospinal tracts,

consistent with severe hypomyelination for a 5-year-old child

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In classic PMD, patients often present with nystagmus and inspiratory stridor within the first few

months of life Spasticity, extrapyramidal features, and cerebellar ataxia are prominent Developmental

delay, seizures, and optic atrophy with blindness can also be present Brainstem and somatosensory

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Seitelberger F Neuropathology and genetics of Pelizaeus-Merzbacher disease Brain Pathol 1995;5(3):267–273 Steenweg ME, Vanderver A, Blaser S, et al Magnetic resonance imaging pattern recognition in hypomyelinating disorders

Brain 2010;133(10):2971–2982

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Fig 95.1 (A) Axial T2-FLAIR image demonstrates

symmetric T2 prolongation in the dorsal medulla and

dentate nuclei of the cerebellum (B) Symmetric T2

hyperintense signal is also present in the splenium

of the corpus callosum and adjacent periventricular white matter (C) DWI and (D) ADC maps demonstrate

normality in the corpus callosum

diffusionrestrictioncorrespondingtotheT2signalab-A

C

B

D

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MIE is seen with a prolonged course of the antibiotic metronidazole Metronidazole has been available for clinical use for over 30 years, and has played an important role in treating anaerobic bacterial and protozoal infections With good cellular penetration, it is believed that metronidazole readily enters the CSF and penetrates the central nervous system CNS lesions secondary to metronidazole are typically bilateral and symmetric involving the dentate nuclei of the cerebellum, dorsal medulla, dorsal pons, midbrain (tectum, red nucleus, and tegmentum), and the corpus callosum Symptoms and imaging findings typically resolve with discontinuation of metronidazole

Etiology

MIE is caused by prolonged metronidazole therapy The incidence is not well known Cytotoxic and vasogenic edema may be seen With cessation of metronidazole there is typically prompt resolution

of MIE However, although vasogenic edema lesions are reversible, residual signal abnormality may be seen on follow-up imaging secondary to cytotoxic edema

be similar to that of Wernicke encephalopathy as both of these encephalopathies have similar imaging features This may be due to the conversion of metronidazole to a thiamine analog with vitamin B1 antagonism

Pathology

Both cytotoxic and vasogenic edema are present

• Often normal

• May demonstrate hypodense nonenhancing lesions in the corpus callosum

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