Contrast MRI findings of Guillain-Barré Syndrome
TJ01-TJ02
Correspondence
Dr. Senthil Kumar Aiyappan,
Professor and Head, Department of Radiodiagnosis, SRM Medical College Hospital and Research Centre, SRMIST, Kattankulathur, Chengalpattu-603203, Tamil Nadu, India.
E-mail: asenthilkumarpgi@gmail.com
A 28-year-old female patient presented with complaints of progressive bilateral lower limb weakness for the past seven days, which had increased to involve bilateral upper limbs for the past two days. She also presented with difficulty in speaking for five days, associated with exhaustion after speaking more than 10 words. The patient also complained of diarrhoea for four days with bladder disturbances. Difficulty in initiation of micturition with incomplete evacuation of urine associated with dribbling was noted. The patient had a history of high-grade fever three weeks prior due to respiratory illness, which subsided with medications in three days. The patient also reported a history of tingling sensation and paresthesia in both lower limbs. There was no history of bronchial asthma, tuberculosis, cardiovascular abnormalities, chronic kidney disease, migraine, trauma, epilepsy, or transient ischaemic attacks.
On clinical examination, the patient was conscious, oriented, and afebrile. Deep tendon reflexes were absent. No signs of cyanosis, icterus, oedema, pallor, rash, or eschar were found. The patient had reduced finger grip in both toes and difficulty in squatting, suggestive of both proximal and distal muscle weakness in bilateral lower limbs. There was no history of cranial nerve involvement. The patient was normotensive with normal blood sugar levels. Clinically, a diagnosis of Guillain-Barre Syndrome (GBS) was considered. Blood and urine investigations were normal. A 24-hour urinary protein test was within normal limits. Urine culture and blood culture were negative. Cerebrospinal Fluid (CSF) analysis was normal with no evidence of albumin-cytological dissociation. Electrophysiological and nerve conduction studies were not classical of GBS and were inconclusive. Although GBS was suspected clinically, the CSF and nerve conduction studies did not contribute to the diagnosis.
Hence, the patient underwent contrast Magnetic Resonance Imaging (MRI) of the whole spine and brain for further evaluation and to rule out other causes. On plain study, the cord revealed normal signal intensity with normal cauda equina nerve roots without clumping (Table/Fig 1)a,b. Postcontrast administration showed smooth enhancement of the pial surface of the conus medullaris with smooth thickening and enhancement of all the cauda equina nerve roots (Table/Fig 2)a-c. Although the differential diagnosis for diffuse cauda equina nerve root enhancement were many, such as GBS, spinal meningitis or arachnoiditis, and chronic inflammatory demyelinating polyneuropathy, most of these were ruled out by correlating with clinical history, and GBS was considered an appropriate diagnosis. The patient then received Immunoglobulin therapy, with five daily infusions for a total dose of 1 g/kg/wt, resulting in the reversal of symptoms subsequently. The patient is presently on follow-up and is doing well.