Cranial
Neuropathy, Myeloradiculopathy,
Complications Ted L. Rothstein, MD,
of
George
Mycoplasma pneumoniae E.
Myositis
Infection
Kenny, PhD
\s=b\ Polymyositis, transverse myelitis, ascending polyneuritis, bilateral optic neuritis, and hearing loss developed in a patient with high complement-fixing antibody titers to Mycoplasma pneumoniae. Each of her three children had primary atypical pneumonia with isolation of the organism. The neurologic disturbance is thought to represent a postinfectious complication of M pneumoniae infection. (Arch Neurol 36:476-477, 1979)
Ty/Tycoplasma pneumoniae can be associated with a variety of neurologic disorders. We followed up a patient with serologically and epidemiologically associated M pneumoniae ' '-'
infection who had simultaneous in¬ volvement of multiple cranial nerves, spinal cord, peripheral nerves, and skeletal muscle. REPORT OF A CASE
A 28-year-old woman was hospitalized because of dysesthetic pains in her chest and abdomen. Two weeks previously, she had had headache, diarrhea, coryza, and a nonproductive cough. Initial examination disclosed a pruritic papulovesicular rash involving the ears. The following day, she complained of diffuse muscle pain and tenderness, had severe proximal weakness of her lower extremities, and was areflexia There was loss of pain sensibility below the neck in an asymmetric pattern affecting the left upper extremity and trunk and
Accepted for publication Oct 10, 1978. From the Neurology Department, Northwest Memorial Hospital, and the Department of Pathobiology, School of Public Health and Community Medicine, University of Washington,
Seattle. Read in part before the 11th World
and
Congress of Neurology, Amsterdam, Sept 15, 1977. Reprint requests to 1570 N 115th St, Seattle, WA 98133 (Dr Rothstein).
both lower extremities. Lhermitte's sign present. Loss of urinary sphincter control necessitated catheter drainage. Routine laboratory test results were normal except for a WBC count of 18,000/ cu mm, with 89% neutrophils, and the following serum enzyme values: creatinine was
phosphokinase, mostly isozyme III, >40,000 units; SGOT, 2,000 units; and lactic dehydrogenase, 5,920 units. The urine contained 15,000 Mg/L of myoglobin. The Westergren sedimentation rate was 26 mm/hr. Rheumatoid factor, ABO-Rh anti¬ body screen, lupus erythematosus cell preparation, antinuclear antibodies, and serologie test for syphilis were normal. Serum C3 complement level was 100 mg/ dL (normal, 105 to 180), and serum C4 complement level was 13 mg/dL (normal, 10 to 40). Anti-DNA antibody was under 1.0 ug of DNA bound per milliliter (normal,
1.0). Serum collected on the second hospi¬ day disclosed cold agglutinins present at 1:512 dilution, and M pneumoniae anti
Neuropathy, Myeloradiculopathy,
Complications Ted L. Rothstein, MD,
of
George
Mycoplasma pneumoniae E.
Myositis
Infection
Kenny, PhD
\s=b\ Polymyositis, transverse myelitis, ascending polyneuritis, bilateral optic neuritis, and hearing loss developed in a patient with high complement-fixing antibody titers to Mycoplasma pneumoniae. Each of her three children had primary atypical pneumonia with isolation of the organism. The neurologic disturbance is thought to represent a postinfectious complication of M pneumoniae infection. (Arch Neurol 36:476-477, 1979)
Ty/Tycoplasma pneumoniae can be associated with a variety of neurologic disorders. We followed up a patient with serologically and epidemiologically associated M pneumoniae ' '-'
infection who had simultaneous in¬ volvement of multiple cranial nerves, spinal cord, peripheral nerves, and skeletal muscle. REPORT OF A CASE
A 28-year-old woman was hospitalized because of dysesthetic pains in her chest and abdomen. Two weeks previously, she had had headache, diarrhea, coryza, and a nonproductive cough. Initial examination disclosed a pruritic papulovesicular rash involving the ears. The following day, she complained of diffuse muscle pain and tenderness, had severe proximal weakness of her lower extremities, and was areflexia There was loss of pain sensibility below the neck in an asymmetric pattern affecting the left upper extremity and trunk and
Accepted for publication Oct 10, 1978. From the Neurology Department, Northwest Memorial Hospital, and the Department of Pathobiology, School of Public Health and Community Medicine, University of Washington,
Seattle. Read in part before the 11th World
and
Congress of Neurology, Amsterdam, Sept 15, 1977. Reprint requests to 1570 N 115th St, Seattle, WA 98133 (Dr Rothstein).
both lower extremities. Lhermitte's sign present. Loss of urinary sphincter control necessitated catheter drainage. Routine laboratory test results were normal except for a WBC count of 18,000/ cu mm, with 89% neutrophils, and the following serum enzyme values: creatinine was
phosphokinase, mostly isozyme III, >40,000 units; SGOT, 2,000 units; and lactic dehydrogenase, 5,920 units. The urine contained 15,000 Mg/L of myoglobin. The Westergren sedimentation rate was 26 mm/hr. Rheumatoid factor, ABO-Rh anti¬ body screen, lupus erythematosus cell preparation, antinuclear antibodies, and serologie test for syphilis were normal. Serum C3 complement level was 100 mg/ dL (normal, 105 to 180), and serum C4 complement level was 13 mg/dL (normal, 10 to 40). Anti-DNA antibody was under 1.0 ug of DNA bound per milliliter (normal,
1.0). Serum collected on the second hospi¬ day disclosed cold agglutinins present at 1:512 dilution, and M pneumoniae anti
