PVL (Periventricular Leukomalacia) - Imaging

Two Forms of PVL

Cranial Ultrasound (US)

• Days 1-7: Periventricular hyperechogenic "flares" (increased echogenicity of white matter)
• Days 8-25: Flares evolve into coalescent macrocysts or microcysts within the periventricular white matter

Fig. 76.75 (A) Day 10: sagittal US showing increased heterogeneous echogenicity of periventricular white matter (arrow). (B) Day 25: multiple periventricular cysts (arrows). (C,D) MRI at 2.5 months: T1 axial images showing white matter thinning, irregular lateral ventricular outline (arrows). - Grainger & Allison's Diagnostic Radiology

Important: Ultrasound often fails to identify subtle diffuse white matter injury. The true incidence of PVL is likely underestimated by US alone. MRI is more sensitive.

MRI Findings

Acute/Subacute fPVL

• Restricted diffusion (DWI) within periventricular and deep white matter in the acute phase
• Cystic lesions: T1 low signal, T2 high signal, with central free diffusion (as opposed to restricted)
• Cysts coalesce, then are progressively resorbed over time

Established/Chronic fPVL

• Ventricular enlargement with an irregular outline of the body of lateral ventricles
• Thinning of periventricular white matter
• Focal signal abnormality extending from ventricular margins (especially posteriorly) - reflecting white matter gliosis

Diffuse PVL (dPVL) on MRI

• Ventriculomegaly with regular (smooth) outlines of the lateral ventricles
• Thinning of periventricular white matter without the irregular/cystic changes of fPVL

Fig. 76.76 T2-weighted axial MRI showing thinning of periventricular white matter with regular outline of lateral ventricles (dPVL). - Grainger & Allison's Diagnostic Radiology

Punctate WMI (current predominant form)

Different severities of WMI. (A,C) Cystic necrotic WMI: cavitations seen as T1 hypointensity on sagittal image. (B,D) Punctate WMI: signal hyperintensities on T1 (arrowheads). - Bradley and Daroff's Neurology in Clinical Practice

Prognostic MRI Marker

Summary: US vs MRI in PVL

Clinical Context

• Incidence: Detected by US in 5-15% of very-low-birth-weight infants; true incidence higher
• Risk factors: IVH, cardiopulmonary instability, sepsis, hypocarbia, metabolic acidosis, placental abruption, twin-twin transfusion syndrome
• Sequelae: Spastic diplegia (most common - lower extremity motor fibers traverse periventricular area), or quadriplegia/cognitive/visual/auditory impairment with more severe injury

Cerebral Abscess - Imaging

Stages of Abscess Formation

CT Findings

• Ill-defined area of low attenuation (hypodensity)
• Enhancement usually absent early; can appear irregular and peripheral in late cerebritis

• Central hypodensity (pus/necrotic debris)
• Rim of slightly higher attenuation surrounded by hypodense vasogenic oedema
• Ring enhancement after contrast - smooth inner margin, with characteristic thinning of the medial (deep/ventricular) wall
• Centre does NOT enhance on delayed images (unlike cerebritis)
• Gas within the abscess is rare - when present, suggests surgical intervention, sinus communication, or gas-forming organism

MRI Findings (Superior to CT)

• Early cerebritis stage (CT often fails to show it)
• Posterior fossa abscesses
• Identifying satellite lesions and adjacent complications

Signal characteristics of mature abscess:

Fig. 57.2 Pyogenic Brain Abscess in a 40-year-old female. (A) FLAIR: ring-like low signal lesion with surrounding high signal oedema. (B) T2 coronal: hyperintense centre, hypointense rim. (C) DWI: bright centre (restricted diffusion). (D) ADC: low signal (confirming restriction). (E) Perfusion map. (F) Post-contrast T1: smooth ring enhancement. - Grainger & Allison's Diagnostic Radiology

The Key DWI Finding - and Its Limitations

• The degree of diffusion restriction is inversely correlated with the viable cell count inside the abscess
• Important caveat: restricted diffusion does NOT always reliably distinguish abscess from tumour - necrotic tumours and other lesions can occasionally show restricted diffusion

Fig. 145-1 Pyogenic brain abscess. (A) T1+Gad: prominent ring enhancement. (B) DWI: hyperintense centre. (C) ADC: dark centre confirming restricted diffusion. - Harrison's Principles of Internal Medicine

Location of Abscesses

• Frontal sinusitis → frontal lobe (directly beneath involved sinus)
• Mastoiditis/otitis media → temporal lobe or cerebellar hemisphere
• Haematogenous spread → predilection for gray-white matter junction (MCA territory, frontoparietal region); can occur anywhere
• Abscesses are multiple in 10-50% of cases
• Often subcortical or periventricular
• Frequently medial wall thinner than lateral wall (closer to ventricle, lower vascularity)

Fig. 79.1 Brain abscess. (A) T2/FLAIR: large ring lesion with perilesional oedema. (B) Post-contrast T1: smooth ring enhancement, thin medial wall (arrowhead). - Bradley and Daroff's Neurology in Clinical Practice

Differential Diagnosis of Ring-Enhancing Lesion

A thick, irregular rim of enhancement is more suggestive of tumour. Abscess more likely shows small satellite lesions and a smooth inner margin.

Complications on Imaging

• Ventricular rupture: abscess breaks through medial wall into ventricle → ventriculitis (intraventricular debris, ependymal enhancement, FLAIR high signal within ventricles)
• Satellite abscesses: small additional ring lesions nearby
• Subdural empyema: crescentic fluid collection with restricted diffusion along the convexity or interhemispheric fissure
• Epidural abscess: lentiform extra-axial collection, can cross midline (unlike subdural)

Follow-up Imaging

• Recommended at biweekly intervals or when new symptoms arise
• Adequate treatment: resolution of rim enhancement or disappearance of T2 hypointense rim
• DWI superior to conventional MRI for monitoring response: low DWI signal = good response; increasing DWI signal = reaccumulation of pus

Demyelinating CNS Disease - Imaging

1. Multiple Sclerosis (MS)

MRI Lesion Characteristics

• Round to oval, typically a few mm to >1 cm
• Discrete and focal early; confluent in advanced disease, especially in posterior periventricular white matter
• Centred on medium-sized veins - "Dawson fingers": ovoid periventricular lesions whose major axis is perpendicular to the outer surface of the lateral ventricles (best seen on sagittal FLAIR)
• Central vein sign: visible on SWI - central punctate hypointensity within MS lesions (reflecting the perivenular origin); less frequent in non-MS white matter lesions

Fig. 58.2 Relapsing MS: axial T2-FLAIR showing typical periventricular demyelinating plaques with ovoid "Dawson finger" morphology (arrows). - Grainger & Allison's Diagnostic Radiology

Characteristic Locations (McDonald Criteria Regions)

Posterior fossa lesions preferentially affect the floor of the 4th ventricle, pons surface, intrapontine trigeminal tract, and cerebellar peduncles - unlike ischaemic lesions which involve central pontine WM.

Signal Characteristics by Sequence

Enhancement Patterns

• Nodular/homogeneous: common, especially small active lesions
• Ring enhancement in larger lesions - the MS ring is characteristically incomplete/open ring with the open margin facing cortical grey matter (unlike tumours and abscess which form complete rings)
• Simultaneous coexistence of enhancing and non-enhancing lesions is the rule in RRMS and is a key diagnostic clue

Spinal Cord MS

• Short-segment lesions: less than 2 vertebral segments (vs NMOSD which is ≥3)
• Less than half the cross-sectional diameter of the cord
• Peripheral location: predominantly lateral and dorsal columns
• Cervical region most commonly affected
• In progressive MS: diffuse subtle T1/PD/STIR abnormality and cord atrophy

2017 McDonald Criteria - MRI Requirements

2. Neuromyelitis Optica Spectrum Disorder (NMOSD)

Spinal Cord - Key Features

• Longitudinally extensive transverse myelitis (LETM): T2 hyperintensity extending ≥3 vertebral segments (vs <2 in MS)
• Enhancement in up to 90%; cervical cord: "shaggy ring enhancement" in ~30%
• Axial T2: "bright spotty lesions" = highly specific for NMO (reflects destructive inflammation)
• Progresses to atrophy, necrosis, and syrinx-like cavities on T1

Brain - NMO Features (distinct from MS)

• Lesions at sites of high AQP4 expression (circumventricular organs):
  • Periependymal areas around 3rd and lateral ventricles
  • Hypothalamus
  • Periaqueductal grey
  • Dorsal brainstem / area postrema (4th ventricle floor) - explains intractable vomiting/hiccup
  • Corpus callosum: ependymal surface, "arch bridge" or marbled oedematous appearance
  • Corticospinal tracts (posterior internal capsule → cerebral peduncle → longitudinally extensive)
• Enhancement: "cloud-like" - multiple patches with blurred margins (vs MS nodular/ring)
• No central vein sign on SWI (unlike MS)
• No hypointense rim on SWI (unlike chronic MS)

Fig. 50.2 Tumefactive MS: (A) FLAIR hyperintense peritrigonal lesion, (B) peripheral restricted diffusion on DWI, (C) post-contrast ring enhancement, (D,E) multiple T2 hyperintense spinal cord lesions with ring enhancement at C6-7. - Grainger & Allison's Diagnostic Radiology

MS vs NMOSD - Key Imaging Differences

3. Acute Disseminated Encephalomyelitis (ADEM)

Brain MRI

• Large, patchy, poorly marginated lesions (vs MS: small, well-defined)
• Predominant subcortical location with asymmetric hemispheric white matter involvement
• Often bilateral thalamic and basal ganglia involvement (helps distinguish from MS)
• Diffuse pontine involvement common
• Monophasic: no new lesions after 3 months on follow-up MRI (in contrast to MS)
• Complete MRI resolution within 6 months → favours ADEM diagnosis
• Persistence/new lesions after 3 months → suggests subsequent MS diagnosis

Enhancement in ADEM

• Gadolinium enhancement is uncommon (14-30%) overall
• When present, all lesions typically enhance simultaneously (unlike MS where enhancing and non-enhancing lesions coexist)
• Patterns: complete/incomplete ring, nodular, gyral, or spotty
• A normal brain MRI within the first few days does not exclude ADEM

Spinal Cord in ADEM

• Affected in one-third of patients, predominantly thoracic
• LETM: large, multi-segment lesions with cord swelling (like NMOSD, unlike MS)
• Variable enhancement; may affect grey matter, white matter, or both

Fig. 58.22 ADEM (A) vs MS (B) on T2-FLAIR and post-contrast T1: ADEM has larger, poorly marginated subcortical lesions without enhancement; MS has smaller, periventricular well-defined lesions with enhancement. - Grainger & Allison's Diagnostic Radiology

4. Tumefactive MS

• FLAIR: large hyperintense lesion, relatively well-defined, little mass effect for its size
• DWI: peripheral restricted diffusion (rim of restriction at the active demyelinating edge) - distinct from abscess (central restriction) and glioblastoma (variable)
• Post-contrast T1: open/incomplete ring enhancement with the open border facing cortical grey matter - the defining feature separating it from glioblastoma and metastasis (which show complete rings)
• Other MS lesions typically present elsewhere in the brain (key diagnostic clue)

Summary Comparison Table