Introduction
Guillain-Barre syndrome (GBS) is a rapid-onset muscle weakness cause by the immune system damaging the peripheral nervous system. The initial symptoms are typically changes in sensation or pain along with muscle weakness, beginning in the feet and hands.
We report a rare case of a patient with GBS who mainly had a symptom of severe sensory impairment.
Case
A 40-year-old man without any past medical history and infection history had tingling sensation of both hands one month ago, and the symptom progressed to both feet. Afterward, he began to have some difficulty of sit to stand independently. He was admitted to the Department of Neurology for evaluation.
Initial physical examination of the patient revealed muscle weakness at fingers, ankles, and big toe grade 3. He appealed reduced sensation at both hands and feet. In detail, pain and temperature was check 6-7 out of 10, and touch and vibration was 5-6 out of 10. Deep tendon reflex was hyporeflexic, and there is no facial palsy.
Brain MRI was normal, and there is no signal intensity change in spinal cord, small central herniated disc, C5/6, C6/7, and central extruded disc L5/S1 in spine MRI. NCS results on 1st and 23rd day of admission are presented in Table 1. Decreased CMAP was checked in both studies, which showed mild improvement on 23rd day compared to the 1st day. Both studies showed no sensory nerve action potential and no F-wave in both peroneal and Lt. tibial nerves, and increased latency in Rt. tibial nerve. Needle EMG done on 23rd day of admission confirmed abnormal spontaneous activity and reduced recruitment and polyphasic MUAP in Lt. abductor pollicis brevis, Lt. 1st dorsal interossei, Rt. Gastrocnemius, and Rt. Peroneus longus muscles. Cerebrospinal fluid test showed normal. Enzyme-linked immunosorbent assay for IgG and IgM antibodies against GM1, GD1b, GQ1b were negative. In laboratory test, HBsAg, anti-HBs, anti-HAV, anti-HCV were negative, and increased AST/ALT(293/293) was checked. Result of abdomen US was moderate fatty liver, mild splenomegaly.
Based on clinical features, laboratory findings, and electrophysiologic investigation, the patient was diagnosed the acute motor sensory axonal neuropathy (AMSAN), one of the subtype of GBS. He was treated with intravenous immunoglobulin for 5 days.
He was transferred to the Department of Rehabilitation on 10th day of admission. He could gait with minimal assist, however, he had severe sensory impairment at both hands and feet (Table 2). After 3 weeks of the physical and occupational therapies including sensory stimulation and sensory integration, he could gait with supervision, but his sensory impairment did not improve much (Table 2). K-MBI score was 92, and AST/ALT level became normalized.
Conclusion
This case shows a rare case of a patient with GBS who mainly had a symptom of severe sensory impairment which did not improve much. The long term follow up of the patient is needed for evaluation of prognosis. |
