Limbic Encephalitis following Guillain-Barré Syndrome Associated with <b><i>Mycoplasma</i></b> Infection

Abstract

A 12-year-old girl was admitted to the authors’ hospital due to muscle weakness, gait disturbance, dysarthria, dysphagia, and diplopia. She experienced prodromal fever 10 days before admission. On examination, deep tendon reflex was absent in the extremities, and nerve conduction velocity was decreased in the ulnar nerve. She was diagnosed with Guillain-Barré syndrome (GBS). Despite steroid pulse therapy following administration of intravenous high-dose γ-globulin, clinical manifestations remained unchanged. Therefore, plasma exchange was performed on day 10 of the illness. The titer of serum Mycoplasma immunoglobulin M level was increased. Immunological testing was positive for serum anti-galactocerebroside C antibody. On day 18 of the illness, however, she developed generalized convulsion. Brain magnetic resonance imaging revealed high intensity in the medial temporal lobes, including the hippocampus and thalamus on T2-weighted intensity imaging, which was consistent with limbic encephalitis. Further immunological tests revealed positivity for anti-N-methyl-D-aspartate-type glutamate receptor antibody in the cerebrospinal fluid. She was treated with additional plasma exchange; however, she exhibited residual manifestations including short-term memory disorder, emotional incontinence, and convulsions. This article describes a notable case of limbic encephalitis following GBS associated with prodromal Mycoplasma infection. It is interesting that autoimmune encephalopathy is concomitant with autoimmune polyneuropathy subsequent to Mycoplasma infection.

Enhancing Tone and Strength in a Patient With Autoimmune Encephalitis and Guillain-Barré Syndrome Using Rood’s Facilitatory Techniques and Neuromuscular Electrical Stimulation: A Case Report

“…These treatments, which included tapping, rubbing, brushing, heavy compression, and rapid icing, were used carefully to move the patient from a state of flaccidity to an enhanced muscular tone. Rood's facilitatory techniques were repeated and task-specific, which corresponded with motor learning principles, promoting adaptive alterations in brain pathways to improve neuromuscular coordination [18]. NMES, which used electrical impulses to activate muscles, provided a controlled environment for the nervous system to adapt and improve muscle strength.…”

“…GBS is characterized by the immune system attacking the peripheral nervous system, while AE involves inflammation of the brain. In some cases, there can be an overlap between these two conditions, as seen in Bickerstaff brainstem encephalitis (BBE) with GBS overlap, where patients may exhibit symptoms such as ataxia, ophthalmoplegia, altered consciousness, muscle weakness, and other neurological deficits [18,19]. The exact pathophysiology of this overlap is not entirely clear, but it is believed to involve autoimmune mechanisms and molecular mimicry triggered by infections like Chlamydia pneumoniae or other pathogens.…”