Guillain-Barré syndrome

Case contributed by Dr Hoe Han Guan


Sudden onset of bilateral lower limbs weakness with rapid ascending weakness to involve bilateral upper limbs. History of upper respiratory tract infection one week prior to weakness.

Patient Data

Age: 5 years
Gender: Male

Smooth thickening and abnormal enhancement of the cauda equina including both anterior and posterior nerve roots. The upper thoracic spinal cord nerve roots show mild abnormal enhancement. Otherwise normal exam. 

No “sugar-coated” spine to suggest diffuse leptomeningeal contrast enhancement in spinal cord. Normal alignment of the vertebra bodies and they return normal signal intensity. Intervertebral discs are preserved and maintain normal signal. No disc herniation. The spinal cord ends at L1. No abnormal enlargement of the spinal cord.
The spinal cord and conus medullaris return normal signal intensity.  No abnormal T2/STIR sequence hyperintensity within the spinal cord. No intraspinal or intramedullary lesion.


Normal study. 

No focal brain parenchymal lesion or abnormal signal intensity. No abnormal leptomeningeal enhancement. No midline shift or hydrocephalus. Cerebral sulci, gyri and CSF-containing spaces are normal. Basal cisterns are not effaced. No abnormal restricted diffusion on DWI/ADC or abnormal blooming artefacts on GRE sequence.
The brainstem and cerebellum are normal. Bilateral optic nerves are symmetrical and normal in size. No abnormal signal intensity within the optic nerves.

Case Discussion

Given clinical history of acute presentation (<6 weeks) and rapid ascending weakness, the imaging features are highly suggestive Guillain-Barre syndrome. No MR evidence of compressive causes of polyradiculopathy or transverse myelitis.

No significant abnormality in the brain and optic nerves, unlikely to be NMOSD(neuromyelitis optica spectrum), acute disseminated encephalomyelitis and myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD) as no abnormal signal intensity in brain and optic nerves.

Patient was treated with intravenous immunoglobulin.

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