Clinical neurophysiology practice · 2020
Brucellosis causing subacute motor polyradiculopathy and the pathological correlation of pseudomyopathic electromyography: A case report.
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Abuzinadah Ahmad R, Milyani Haneen A, Alshareef Aysha, Bamaga Ahmed K, Alshehri Abdulraheem, Kurdi Maher E
Аннотация
INTRODUCTION: Brucellosis is a rare cause of polyradiculopathy. We aim to present a case of subacute motor polyradiculopathy (SAMPR), along with the electromyographic pseudomyopathic changes, and their histopathological correlation.
CASE PRESENTATION: A 24-year-old man presented with gradually progressive bilateral lower limb weakness for three weeks that progressed to a loss of ambulation in seven weeks. He had no ocular, facial, or sphincteric weakness and no sensory symptoms. He showed normal cognitive, cranial nerve, and upper limb exams. His lower limb power was medical research council (MRC) grade 3 proximally, and 4 distally. His reflexes were grade 2+ in the upper limbs and grade 0 in the lower limbs. The nerve conduction studies were normal. Electromyography (EMG) showed active denervation with a short-duration motor unit potential (MUP) and early recruitment. MRI showed a diffuse enhancement of the lumbosacral nerve roots. Cerebrospinal fluid (CSF) showed a protein of 2.7 g/L and a white blood cells (WBC) count of 420 cells per microliter. Muscle biopsy revealed neurogenic changes with secondary degenerating and regenerating fibers, explaining the small and short MUPs in the EMG. CSF grew Brucella after fourteen days of incubation. Serum showed high antibody titers for the Brucella species "Melitensis" and "Abortus". The patient started to walk again, ten months after starting a course of antibiotics.
CONCLUSION: Neurobrucellosis can present primarily as SAMPR, sparing the sensory system. SAMPR, with ongoing degenerating and regenerating muscle fibers, may explain the pseudomyopathic changes found in electromyographic studies.
CASE PRESENTATION: A 24-year-old man presented with gradually progressive bilateral lower limb weakness for three weeks that progressed to a loss of ambulation in seven weeks. He had no ocular, facial, or sphincteric weakness and no sensory symptoms. He showed normal cognitive, cranial nerve, and upper limb exams. His lower limb power was medical research council (MRC) grade 3 proximally, and 4 distally. His reflexes were grade 2+ in the upper limbs and grade 0 in the lower limbs. The nerve conduction studies were normal. Electromyography (EMG) showed active denervation with a short-duration motor unit potential (MUP) and early recruitment. MRI showed a diffuse enhancement of the lumbosacral nerve roots. Cerebrospinal fluid (CSF) showed a protein of 2.7 g/L and a white blood cells (WBC) count of 420 cells per microliter. Muscle biopsy revealed neurogenic changes with secondary degenerating and regenerating fibers, explaining the small and short MUPs in the EMG. CSF grew Brucella after fourteen days of incubation. Serum showed high antibody titers for the Brucella species "Melitensis" and "Abortus". The patient started to walk again, ten months after starting a course of antibiotics.
CONCLUSION: Neurobrucellosis can present primarily as SAMPR, sparing the sensory system. SAMPR, with ongoing degenerating and regenerating muscle fibers, may explain the pseudomyopathic changes found in electromyographic studies.