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The Guillain–Barré syndrome is an immunologically mediated condition affecting the peripheral nervous system. There is evidence that Guillain–Barré syndrome, Miller–Fisher syndrome, and Bickerstaff brain stem encephalitis form a closely related spectrum of disorders.1 Magnetic resonance imaging (MRI) abnormalities in the spinal cord in these conditions have been well described,2 but intracranial findings are infrequent. We report resolution of sulcal changes on serial MRI of the brain concomitant with clinical recovery in a typical case of Guillain–Barré syndrome.
An 81 year old man had a one week history of progressive lower limb weakness and numbness associated with pain radiating down his right leg. There was no preceding history of infection or trauma. He had no significant past medical history.
On examination, he was alert and rational. There was no slurring of speech or paresis of the extraocular muscles. Cranial nerve and visual field examination was unremarkable and the neck was supple. He had mild proximal symmetrical upper limb weakness (MRC grade 4/5) and bilateral lower limb weakness (MRC grade 3/5). He had difficulty in walking unaided and in tandem walking. Sensory loss to touch was elicited in the distal lower extremities in stocking distribution. Reflexes in all four limbs were absent. The clinical features were consistent with the Guillain–Barré syndrome.
The patient was initially referred to an orthopaedic surgeon for possible lumbosacral spondylitic disease. Unenhanced MRI scans of the lumbar and thoracic spine showed mild degenerative changes and excluded intrinsic cord abnormalities or external compression. Subsequent enhanced cervical spine MRI scans were also negative. He was then referred for a neurological opinion.
Nerve conduction studies revealed significantly prolonged distal motor latency (median motor distal latency 6.7 to 9.8 ms; posterior tibial distal latency 7.7 to 9.4 ms) and reduced conduction velocities in the median (40.3 m/s), ulnar (39.6 m/s), and tibial nerves (35.7 m/s). F responses were prolonged (> 37 ms) or absent in all four limbs. Cerebrospinal fluid examination showed absent cells with raised protein of 0.8 g/l, normal glucose concentration, and positive globulin. Bacterial culture and viral studies were negative.
The first MRI of the brain, obtained to exclude a central cause for weakness and gait abnormalities during the first week of admission, showed left parietal and superior occipital sulcal hyperintensities on the fluid attenuated inversion recovery (FLAIR) sequences, in addition to subtle enhancement with contrast administration (fig 1). A repeat MRI one week later showed mild improvement. A third MRI two months after initial presentation showed resolution of the focal abnormalities.
In the related Miller–Fisher syndrome, MRI changes have been documented in the cranial nerves,3 spinocerebellar tracts, and pons.4 We postulate that our MRI findings represent a focal manifestation of a wider immunologically mediated reaction within the subarachnoid cerebrospinal fluid bathed space. This focal sulcal reaction probably represents a local concentration of proteinaceous fluid and correlates well with the CSF findings of high protein levels but an absence of cells.4 These MRI changes resolved with immunoblobulin treatment and clinical recovery. While MRI changes have been reported in the subcortical regions in demyelinating neuropathies, most probably from focal demyelination, sulcal changes have not been described. Serial MRI studies are a sensitive technique for documenting cerebral cortical abnormalities in this condition, even in the asymptomatic setting as demonstrated here.
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