444 lines
31 KiB
Markdown
444 lines
31 KiB
Markdown
---
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title: "Wallerian Degeneration"
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docid: "e4bb682d-6534-4176-9d39-34c1a42f3771"
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authors:
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- key: "1fa14dfd-71ea-4960-908e-e720313bc63a"
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value: "Santhosh Gaddikeri, MD"
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- key: "a25c450b-3d34-4f64-bba3-cc0834813df6"
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value: "Miral D. Jhaveri, MD, MBA"
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breadcrumbs:
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-
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name: "Brain"
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slug: "brain"
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treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
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name: "Diagnosis"
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slug: "diagnosis"
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treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
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name: "Pathology-Based Diagnoses"
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slug: "pathology-based-diagnoses"
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treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
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name: "Acquired Toxic/Metabolic/Degenerative Disorders"
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slug: "acquired-toxicmetabolicdegenerativ-"
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treeNodeId: "ba3cfeaf-64d9-4117-91e8-d2ce58783fc5"
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name: "Dementias and Degenerative Disorders"
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slug: "dementias-and-degenerative-disorde-"
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treeNodeId: "6381104d-7a4c-4be5-bb19-3cd90837d547"
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-
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name: "Wallerian Degeneration"
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slug: "wallerian-degeneration"
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treeNodeId: null
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category: "Brain"
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documentVersionId: "7ea6d768-c200-42ac-9b53-89abb08709d4"
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imageCount: 21
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lastUpdated: "08/07/20"
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pageDescription: "Wallerian Degeneration"
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pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Acquired Toxic/Metabolic/Degenerative Disorders, Dementias and Degenerative Disorders, Wallerian Degeneration"
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pageTitle: "Wallerian Degeneration | STATdx"
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enhancedTitle: "Wallerian Degeneration"
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type: "DX"
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references: true
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breadcrumbs:
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- "Brain"
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- "Diagnosis"
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- "Pathology-Based Diagnoses"
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- "Acquired Toxic/Metabolic/Degenerative Disorders"
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- "Dementias and Degenerative Disorders"
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- "Wallerian Degeneration"
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---
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# KEY FACTS
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- ## Terminology
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- Wallerian degeneration (WaD)
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- Progressive secondary anterograde degeneration of axons and their myelin sheaths caused by interruption of axonal integrity or damage to neuron
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- ## Imaging
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- Primary lesion is cortical or subcortical with WaD in descending white matter (WM) tracts ipsilateral to neuronal injury
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- WaD can be seen in fibers crossing corpus callosum, fibers of optic radiations, fornices, and cerebellar peduncles
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- CT is not sensitive for WaD in acute-subacute stages
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- Detects atrophy of corticospinal tracts (CSTs) in chronic stage
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- Time-dependent changes in CSTs on MR
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- Strong correlation between WaD detected on T2WI and DWI and long-term morbidity
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- DWI findings precede development of WaD assessed by conventional MR
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- DTI may distinguish between primary lesion and associated WaD
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- Reduced fractional anisotropy (FA) with ↑ mean diffusivity (MD) in infarct
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- Reduced FA with preserved MD in CST
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- ## Top Differential Diagnoses
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- Normal CST can appear T2/FLAIR hyperintense on high-field-strength MR
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- Neurodegenerative diseases
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- Brainstem glioma
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- Demyelinating and inflammatory diseases
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- Hypertrophic olivary degeneration
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- Metabolic diseases
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- Intoxication (heroin inhalation)
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# TERMINOLOGY
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- ## Abbreviations
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- Wallerian degeneration (WaD)
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- ## Definitions
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- Progressive secondary anterograde degeneration of axons and their myelin sheaths caused by interruption of axonal integrity or damage to neuron
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- Contiguous T2 hyperintensity along topographic distribution of corticospinal tract (CST) in internal capsule (IC) and brainstem in patients with various cerebral pathologies
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- ### Location
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- Primary lesion: Cortical or subcortical
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- WaD: Descending white matter (WM) tracts ipsilateral to neuronal injury
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- CST, corticobulbar, corticopontocerebellar tracts
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- Corpus callosum, posterior column of spinal cord, limbic circuit, and optic pathway
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- Center of cerebral peduncle may reveal WaD of CST
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- Lateral side of cerebral peduncle may show WaD of corticopontine tract
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- WaD can be seen in corpus callosum, optic radiations, fornices, and cerebellar peduncles
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- WaD in distal optic radiations after infarction at their root
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- Pontine infarct can cause WaD in middle cerebellar peduncle
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- Corpus callosum has been shown to be susceptible to atrophy in Alzheimer disease mainly as correlate of WaD of commissural nerve fibers of neocortex
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- Callosal atrophy is present predominantly in latest stage of Alzheimer disease
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- Seizure-induced damage may cause secondary WM degeneration along tapetum and through splenium of corpus callosum
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- ### Size
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- Acute stage: Normal size
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- Chronic stage: ↓ (atrophy)
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- ### Morphology
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- Signal changes conforming to WM tract shape
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- Oval regions in posterior limb of IC and cerebral peduncle; thin curvilinear regions in pons
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- ## CT Findings
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- ### NECT
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- Not sensitive for WaD in acute-subacute stages
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- Detects atrophy of CSTs in chronic stage
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- ↓ size of corresponding aspect of brainstem
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- ## MR Findings
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- ### T1WI
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- Time-dependent changes in descending WM tracts
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- Stage 1: No changes
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- Stage 2: T1 hyperintense
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- Stage 3: T1 hypointense
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- Stage 4: Ipsilateral brainstem atrophy ± hypointensity
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- ### T2WI
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- Time-dependent changes in descending WM tracts
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- Stage 1: No changes in adult CNS
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- Stage 2: T2 hypointense
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- Stage 3: T2 hyperintense
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- Stage 4: Atrophy, best seen in brainstem
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- Sometimes, T2 hyperintense signal may persist
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- Neonates and infants: Identification of WaD by T2WI complicated by high water content and lack of myelination in immature WM
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- Adults: Strong correlation between T2WI-detected WaD and long-term morbidity
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- ### FLAIR
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- Same as T2WI
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- ### DWI
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- Can demonstrate acute injury to descending WM tracts < 10 days after primary injury such as infarction
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- Neonates and infants: Indicates acute WM injury
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- DWI findings precede development of WaD assessed by conventional MR
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- May portend poor clinical outcome
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- Adults: Correlation of DW changes in descending motor pathways at presentation with long-term neurologic disability
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- ↑ signal intensity in descending WM tract ipsilateral to territorial infarct at level of IC or cerebral peduncle or both
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- ↓ ADC values in involved WM tract compared with normal WM
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- Extent and severity of territorial ischemia is related to development of descending WM tract injury detectable by DWI
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- Hyperintense DW signal intensity and ↓ ADC values within territorial infarct and ipsilateral CST
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- DW and ADC time courses in region of territorial injury and CST injury may be different
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- Relatively delayed development of diffusion abnormality in descending WM tracts
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- Subacute period after territorial infarction in adults
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- Within infarct, WM ADC reduction > that in GM
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- DW signal intensity abnormality in descending WM tracts may persist, even as DW hyperintensity in ipsilateral cerebral hemisphere fades
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- WaD of inferior cerebellar peduncle (after lateral medullary infarction) depicted by thin slice DWI has been reported
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- ### T1WI C+
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- No contrast enhancement of degenerated tracts
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- ### MRS
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- ¹H-MRS enables in vivo assessment of axonal injury based on signal intensity of N-acetyl aspartate (NAA)
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- ↓ NAA concentration in normal-appearing WM in pons and cerebellar peduncles in early stages of relapsing-remitting multiple sclerosis (MS)
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- Evidence of early WaD outside MS plaques
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- Correlates best with disability, MS duration, and relapse rate
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- DTI
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- Myelin breakdown leads to ↓ diffusion anisotropy
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- DTI may distinguish between primary lesion and associated WaD
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- Difference in diffusion properties between primary lesion and degenerated tract
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- Fractional anisotropy (FA) = measure of directionality of water diffusion
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- Mean diffusivity (MD) = measure of amount of water diffusion
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- Reduced FA with ↑ MD in infarct
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- Reduced FA with preserved MD in CST
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- In patients with motor pathway infarction, diffusion indices in degenerated CST stabilize within 3 months and early changes in CST FA may predict long-term clinical outcomes
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- ## Imaging Recommendations
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- ### Best imaging tool
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- MR
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- ### Protocol advice
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- DWI allows early detection (stage 1)
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- T2WI detects changes after 4 weeks
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# DIFFERENTIAL DIAGNOSIS
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- ## Normal CST
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- CST can appear T2/FLAIR hyperintense on 3T MR (normal fully myelinated brain)
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- ## Neurodegenerative Diseases
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- [Amyotrophic lateral sclerosis (upper &/or lower motor neuron involvement)](/document/amyotrophic-lateral-sclerosis-als/23de52b7-d9bd-441c-a18c-95c8afccb470)
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- Bilateral hyperintensities along CST extending from corona radiata to brainstem on T2WI/PD/FLAIR
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- Primary lateral sclerosis and infantile-onset hereditary spastic paraplegia
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- Upper motor neuron degeneration only
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- [Brainstem Glioma](/document/brainstem-tumors/657b37eb-c286-42bf-b8e6-55b5c20e5e50)
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- T2 hyperintense mass ± enhancement
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- ## Demyelinating and Inflammatory Diseases
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- [MS: Periventricular T2 hyperintensity](/document/multiple-sclerosis/7892b2a2-f52a-4d7f-9858-a326f2b7ab04)
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- [ADEM: Asymmetric T2 hyperintensity in WM and gray matter (GM) after viral prodrome](/document/adem/a3fafeb7-5861-4364-beb8-c0e30220564e)
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- [Behçet disease: Enlarged T2 hyperintense brainstem ± thalamus](/document/behet-disease/4e447bb6-0f14-40e1-929a-4c1465feec0a)
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- [Hypertrophic Olivary Degeneration](/document/hypertrophic-olivary-degeneration/78257543-6d52-4879-84b1-445f3611d996)
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- Secondary degeneration of inferior olivary nucleus (ION), usually caused by primary lesions in dentato-rubro-olivary pathway
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- Time-dependent T2 changes of ION
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- Hyperintense signal without hypertrophy of ION: Within first 6 months of ictus
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- Both ↑ signal and hypertrophy of ION: Between 6 months and 3-4 years after ictus
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- Only ↑ signal in ION: Begins when hypertrophy resolves and can persist indefinitely
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- ## Metabolic Diseases
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- [X-linked adrenoleukodystrophy: Enhancing peritrigonal demyelination](/document/x-linked-adrenoleukodystrophy/0543abe3-8086-488b-85d2-483ce458f345)
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- [Wilson disease: WM and GM lesions involving basal ganglia, dentate nucleus, brainstem](/document/wilson-disease/3d4d4876-4ce4-4af0-9e75-1a419bdd813c)
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- [Hypoglycemic coma: Reversible CST changes](/document/adult-hypoglycemia/38e4de6e-07c4-485e-bac1-f4dd4815b3b8)
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- [Heroin Inhalation](/document/drug-abuse/e4502a67-4b96-4d98-a167-6e90f6b65faf)
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- Symmetric T2 hyperintensity in posterior WM, including posterior limb of IC
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# PATHOLOGY
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- ## General Features
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- ### Etiology
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- Infarction, hemorrhage, neoplasm, encephalitis
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- Demyelinating disease, trauma, arteriovenous malformations
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- Reported also in patients with movement disorder
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- ### Genetics
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- Process of axonal degeneration is genetically regulated
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- ### Associated abnormalities
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- Primary lesion/disorder that caused secondary WM tract degeneration
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- ## Staging, Grading, & Classification
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- Stage 1 (0-4 weeks)
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- Degradation of axon; mild changes in myelin
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- Stage 2 (4-14 weeks)
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- Myelin protein breakdown; lipids remain intact
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- Stage 3 (> 14 weeks)
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- Myelin lipid breakdown, gliosis, changes in water content and structure
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- Stage 4 (after months to years)
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- Atrophy of ipsilateral brainstem
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- ## Gross Pathologic & Surgical Features
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- Brainstem asymmetry due to atrophy in chronic stage
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- ## Microscopic Features
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- Stage 1: Beginning of myelin and axon breakdown
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- Myelin sheaths break up into ellipsoids and spheres but retain myelin-staining properties
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- Stage 2: ↓ protein:lipid ratio
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- Stage 3: ↑ edema and further lipid breakdown
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- Stage 4: Atrophy due to volume loss; removal of axonal debris by microglia continues for 2 years (vs. completed in 3 weeks in peripheral nervous system)
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- Expression of transcription factors *ATF3* and *JUN* by nonneuronal cells during WaD
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- *ATF3*/*JUN* heterodimers may play role in regulating changes in gene expression necessary for preparing distal segments of injured peripheral nerves for axonal regeneration
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- Absence of *ATF3* and *JUN* from CNS glia during WaD may limit their ability to support regeneration
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- In CNS, astrocyte-dominated matrix fails to accommodate new axonal growth
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# CLINICAL ISSUES
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- ## Presentation
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- ### Most common signs/symptoms
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- WaD in CST is associated with persistent hemiparesis
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- ## Demographics
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- ### Age
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- Reported in all ages
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- ### Sex
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- No preference
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- ### Epidemiology
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- WaD commonly follows CNS lesions
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- WaD in pyramidal tract reported in 78.6% of cases of capsular infarct
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- ## Natural History & Prognosis
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- WaD may begin within 1 week of fiber tract damage
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- Demyelination can continue during next 6 months
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- Signifies irreversible loss of neuronal function
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- Little evidence of axonal regeneration in CNS
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- Presence or absence of WaD may influence clinical outcome after stroke
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- Extent of WaD is related to severity of motor deficit
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- Abnormal DWI signal in CST can be acute predictor of motor outcome in childhood infarction
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- Contralesional CST abnormal DWI signal predicts severe hemiparesis
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- ## Treatment
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- No specific therapy
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# DIAGNOSTIC CHECKLIST
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- ## Image Interpretation Pearls
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- In ischemic stroke: Important to differentiate DWI abnormality related to WaD from additional infarction
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- Time-specific signal intensity changes of WaD → able to ascertain age of primary lesion
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b1941e68-6700-4295-b371-61c4b12e78ad
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## References
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# Selected References
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1. [Zuo M et al: Wallerian degeneration in experimental focal cortical ischemia. Brain Res Bull. 149:194-202, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31051228%5Bpmid%5D)
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1. [Shen Y et al: Bilateral wallerian degeneration of the middle cerebellar peduncles secondary to pontine infarction: a case series. J Neurol Sci. 388:182-5, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29627018%5Bpmid%5D)
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1. [Zhang ZY et al: Clinical and radiological features of wallerian degeneration of the middle cerebellar peduncles secondary to pontine infarction. Chin Med J (Engl). 131(6):665-71, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29521288%5Bpmid%5D)
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1. [Chen YJ et al: Wallerian degeneration beyond the corticospinal tracts: conventional and advanced MRI findings. J Neuroimaging. 27(3):272-80, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28072502%5Bpmid%5D)
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1. [Jimenez-Gomez A et al: Teaching neuroimages: wallerian degeneration in evolving pediatric stroke. Neurology. 89(13):e166-7, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28947589%5Bpmid%5D)
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1. [Gandhi K et al: Progressive wallerian degeneration of the corpus callosal splenium in a patient with alexia without agraphia: advanced MR findings. Neuroradiol J. 27(6):653-6, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25489886%5Bpmid%5D)
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1. [Kleinman JT: Early wallerian degeneration on magnetic resonance imaging: underappreciated but highly relevant. Dev Med Child Neurol. 55(2):104-5, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23171080%5Bpmid%5D)
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1. [Saksena S et al: The corpus callosum wallerian degeneration in the unilateral brain tumors: evaluation with diffusion tensor imaging (DTI). J Clin Diagn Res. 7(2):320-5, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23543618%5Bpmid%5D)
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1. [Venkatasubramanian C et al: Natural history and prognostic value of corticospinal tract wallerian degeneration in intracerebral hemorrhage. J Am Heart Assoc. 2(4):e000090, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23913508%5Bpmid%5D)
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1. [Domi T et al: Corticospinal tract pre-wallerian degeneration: a novel outcome predictor for pediatric stroke on acute MRI. Stroke. 40(3):780-7, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19131656%5Bpmid%5D)
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1. [Liang Z et al: Progression of pathological changes in the middle cerebellar peduncle by diffusion tensor imaging correlates with lesser motor gains after pontine infarction. Neurorehabil Neural Repair. 23(7):692-8, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19244384%5Bpmid%5D)
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1. [Oh MY et al: Ipsilateral wallerian degeneration of the distal optic radiations after infarction at their root. J Neuroophthalmol. 29(2):146-8, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19491641%5Bpmid%5D)
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1. [Yu C et al: A longitudinal diffusion tensor imaging study on wallerian degeneration of corticospinal tract after motor pathway stroke. Neuroimage. 47(2):451-8, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19409500%5Bpmid%5D)
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1. [De Simone T et al: Wallerian degeneration of the pontocerebellar fibers. AJNR Am J Neuroradiol. 26(5):1062-5, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15891160%5Bpmid%5D)
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1. [Hunt D et al: ATF3 upregulation in glia during wallerian degeneration: differential expression in peripheral nerves and CNS white matter. BMC Neurosci. 5:9, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15113454%5Bpmid%5D)
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1. [Uchino A et al: Transient detection of early wallerian degeneration on diffusion-weighted MRI after an acute cerebrovascular accident. Neuroradiology. 46(3):183-8, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14991261%5Bpmid%5D)
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1. [Casanova B et al: Evidence of wallerian degeneration in normal appearing white matter in the early stages of relapsing-remitting multiple sclerosis: a HMRS study. J Neurol. 250(1):22-8, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12527988%5Bpmid%5D)
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1. [Mazumdar A et al: Diffusion-weighted imaging of acute corticospinal tract injury preceding wallerian degeneration in the maturing human brain. Am J Neuroradiol 24:1057-66, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12812927%5Bpmid%5D)
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1. [Pierpaoli C et al: Water diffusion changes in wallerian degeneration and their dependence on white matter architecture. Neuroimage. 13(6 Pt 1):1174-85, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11352623%5Bpmid%5D)
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## Images
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### Selected Images
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*Coronal T2WI shows a cavernous malformation in left precentral gyrus <img src='img/arrows/CS.png'/>. T2 hyperintensity along the course of cortical spinal tract (CST) <img src='img/arrows/CC.png'/> indicating antegrade wallerian degeneration (WaD).*
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*Axial NECT shows changes of a remote right-sided craniotomy with right frontotemporal encephalomalacia <img src='img/arrows/CS.png'/> and atrophy of right cerebral peduncle <img src='img/arrows/CO.png'/> due to antegrade WaD. Also note ex vacuo dilation of right lateral ventricle <img src='img/arrows/CC.png'/>.*
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*Axial DWI in a patient with recent infarcts in the left occipital lobe <img src='img/arrows/CO.png'/> and left internal capsule <img src='img/arrows/CC.png'/> show restricted diffusion restriction along splenium <img src='img/arrows/CS.png'/>, indicating WaD.*
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*Left pontine remote infarct with WaD of bilateral middle cerebellar peduncles (MCPs) is shown. Axial FLAIR (A) shows left pontine small remote infarct <img src='img/arrows/CS.png'/>. Axial FLAIR (B) & diffusion weighted image (C) show hyperintense signal in MCPs <img src='img/arrows/CO.png'/> due to WaD.*
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*Axial ADC map in a newborn with acute infarcts in bilateral frontal and right occipital lobes <img src='img/arrows/CS.png'/> shows decreased ADC signal in the genu <img src='img/arrows/CO.png'/> and splenium <img src='img/arrows/CC.png'/> of the corpus callosum due to acute WaD.*
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*Axial T2WI in the same patient shows increased T2 signal in bilateral frontal and right occipital lobes <img src='img/arrows/CS.png'/> corresponding to acute infarcts. Subtle hyperintense signal in genu <img src='img/arrows/CO.png'/> & splenium <img src='img/arrows/CC.png'/> is difficult to assess due to high water content in the neonatal brain.*
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*Coronal T2WI in a 6-year-old boy with left-sided spasticity and history of perinatal insult shows periventricular cystic encephalomalacia <img src='img/arrows/CS.png'/> with ex vacuo dilation of the right lateral ventricle.*
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*Axial DTI in the same patient shows decreased fractional anisotropy in the right pontine corticospinal tract <img src='img/arrows/CO.png'/> due to WaD. Note intact CST on the contralateral side <img src='img/arrows/CS.png'/>.*
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*Axial FLAIR MR at the corona radiata level in a 65 year old with bilateral (left > > right) corona radiata infiltrative low-grade glioma and WaD of cerebral peduncles shows white matter (WM) hyperintense signal due to an infiltrative glioma <img src='img/arrows/CS.png'/>.*
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*Axial FLAIR image in the same patient shows mild atrophy and hyperintense signal in bilateral cerebral peduncles <img src='img/arrows/CC.png'/>. Considering atrophy of cerebral peduncles, WaD was considered more likely than tumor extension.*
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### Additional Images
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*Axial T2WI MR in a patient with left middle cerebral artery infarct (not shown) shows high signal intensity in the left cerebral peduncle <img src='img/arrows/WS.png'/>, consistent with WaD.*
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*Axial T2WI MR shows a large left middle cerebral artery infarct, which resulted in ipsilateral WaD (not shown).*
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*Axial T2WI MR in the same patient illustrates the hyperintense signal within the left cerebral peduncle <img src='img/arrows/WS.png'/> from WaD.*
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*Axial T2WI MR in the same patient shows hyperintense signal in crossing CSTs in the left side of the pons <img src='img/arrows/WS.png'/>, consistent with WaD.*
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*Axial T2WI MR in the same patient shows hyperintense signal in the right side of the medulla <img src='img/arrows/WS.png'/>, consistent with WaD.*
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*Axial T2WI MR in a patient with a left middle cerebral artery infarct shows no abnormal signal in the pons, although diffusion revealed abnormality from WaD (not shown).*
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*Anisotropy map in which high anisotropy values are seen in red shows diminished anisotropy in the left side of the pons despite normal T2WI in the same patient.*
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*Axial DTI trace image shows increased signal in the left corona radiata/CST related to an acute infarct <img src='img/arrows/WS.png'/>. DTI may distinguish between the primary lesion and associated WaD. Reduced fractional anisotropy may be seen in the affected CST.*
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*Axial DTI trace shows increased signal in the central cerebral peduncle <img src='img/arrows/WC.png'/> related to CST WaD. The lateral cerebral peduncle may show corticopontine tract involvement.*
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*Axial T2WI MR shows a heterogeneous hyperintense lesion involving the left corona radiata and CST <img src='img/arrows/WC.png'/> related to a glioblastoma. Note the internal curvilinear T2 hypointensity related to blood products or proteinaceous debris.*
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*Axial T2WI MR in the same patient shows cerebral peduncle hyperintensity <img src='img/arrows/WC.png'/> due to CST WaD from the tumor. There is slight volume loss with linear T2 hypointensity along the posterolateral margin <img src='img/arrows/WS.png'/>.*
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