Toxic and Demyelinating Disorders of the CNS

Flashcards on Toxic and Demyelinating Disorders of the CNS

Toxic and demyelinating disorders of the CNS

Injury to myelin sheaths or axons caused by acquired and metabolic conditions.

Etiopathogenesis of toxic encephalopathies

Exogenous agents like drugs and toxins that cause direct neurotoxicity, mitochondrial dysfunction, or vascular compromise.

Hypoxic-Ischemic Toxic Encephalopathies

CO, cyanide, hydrogen sulfide.

Metabolic Toxic Encephalopathies

Hepatic, uremic, Wernicke.

Drug-induced Toxic Encephalopathies

Methotrexate, 5-FU, antipsychotics.

Heavy Metal/Alcohol Toxic Encephalopathies

Methanol, ethylene glycol.

MRI findings in Methanol Poisoning

Bilateral putaminal necrosis (T2/FLAIR hyperintensity), T1 hyperintensity and blooming on SWI with hemorrhage, acute diffusion restriction.

MRI findings in Carbon Monoxide Poisoning

Bilateral globus pallidus hyperintensity (T2/FLAIR), diffuse cerebral atrophy in chronic stages.

MRI findings in Radiation Necrosis

T2/FLAIR hyperintense WM changes, ring-enhancing necrotic lesions; acute (

MRI findings in Wernicke’s Encephalopathy

Symmetrical T2/FLAIR hyperintensity in mammillary bodies, thalami, periaqueductal gray; DWI shows early changes.

Putaminal necrosis

Hemorrhagic necrosis seen in Methanol poisoning

Trident Sign

Spares ventrolateral pons, seen in CPM

Soap bubble / Swiss cheese pattern

Enhancement pattern seen in Radiation necrosis

Hockey stick sign

Hyperintensity in pulvinar and medial thalamus, seen in Wernicke's and CJD

Panda sign

Midbrain involvement in Wernicke's encephalopathy

Reverse panda sign

Seen in Wilson's disease

Piglet sign

EPM pattern in basal ganglia, seen in Osmotic demyelination

Lentiform fork sign

Hyperintensity around lentiform nucleus, seen in metabolic encephalopathies

Central vein sign

Thin hypointense line at center of MS lesions on T2*/SWI or FLAIR

Paramagnetic rim sign

Peripheral hypointense rim on SWI/QSM in MS; chronic active lesions

Bright spotty lesions

T2 hyperintense, small (<2 mm) bright foci in spinal cord, seen in NMOSD

MOGAD H-sign

T2 hyperintensity restricted to gray matter forming H-shape in transverse myelitis, seen in MOGAD

Spectroscopy markers in Radiation necrosis

Lipid-lactate peak, ↓NAA

Spectroscopy markers in Methanol poisoning

Nonspecific unless complicated

Wernicke’s Differential Points

Periventricular gray matter + clinical history.

Etiopathogenesis of demyelinating disorders

Immune-mediated myelin injury (MS, ADEM), post-infectious or antibody-driven (ADEM, NMOSD, MOGAD).

Clinical features of demyelinating disorders

Visual loss, weakness, sensory symptoms, ataxia.

Variants of MS

Relapsing-remitting (RRMS), Secondary progressive (SPMS), Primary progressive (PPMS), Progressive relapsing.

MRI findings in Multiple Sclerosis (MS)

Ovoid periventricular plaques (Dawson’s fingers), juxtacortical/infratentorial/spinal cord lesions, active: Gd-enhancing; chronic: T1 black holes.

Dissemination in space (McDonald’s Criteria 2021)

≥1 lesion in ≥2 of 4 areas (periventricular, juxtacortical, infratentorial, spinal cord).

Dissemination in time (McDonald’s Criteria 2021)

Simultaneous enhancing/non-enhancing lesions or new lesion over time; CSF oligoclonal bands may replace dissemination in time.

MRI findings in ADEM

Large asymmetric WM lesions, basal ganglia/thalami may be involved, often monophasic.

MRI findings in Tumefactive MS

2 cm lesion with open ring enhancement; Mimics tumor; requires biopsy in some cases.

MRI findings in NMOSD

Longitudinal spinal cord lesions (>3 segments), periependymal and optic chiasm lesions, AQP4 IgG positive.

MRI findings in MOGAD

Cortical encephalitis, bilateral WM lesions, responsive to steroids, Anti-MOG IgG positive.

MRI findings in CPM (Central Pontine Myelinolysis)

T2 hyperintensity in central pons, sparing periphery; seen after rapid hyponatremia correction; Subtype of Osmotic Demyelination Syndrome (ODS).

MRI findings in MBD (Marchiafava-Bignami Disease)

Diffuse T2 hyperintensity in corpus callosum (central > peripheral), alcoholic background.

Spectroscopy markers in MS

↓NAA, ↑Choline, lipid-lactate peak in active plaques.

Spectroscopy markers in Radiation necrosis

Prominent lipid-lactate, ↓NAA.

Tumefactive MS spectroscopy findings

Preserved NAA, ↑Lipids without high Choline.

Tumors spectroscopy findings

↑Choline, ↑Cho:NAA ratio, ↓NAA.

CPM Differential points

Central pons, no enhancement.

MBD Differential points

Diffuse callosal involvement.

Radiologist’s approach

Assess lesion location and enhancement, use DWI, SWI, MRS to differentiate mimics, correlate with clinical history, antibody profiles.

Summary and Pitfalls

ADEM can mimic early MS but is monophasic; MOGAD and NMOSD are antibody-mediated; different management; Tumefactive MS may mimic neoplasm and need biopsy.