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Something to think about. There seems to be an increase in both.
Holmes-Adie syndrome and Lyme disease
The Lancet, Volume 357, Number 9258, 10 March 2001
The Lancet, Volume 357, Number 9258, 10 March 2001
Correspondence
Holmes-Adie syndrome and Lyme disease
Sir—Paolo Martinelli (Nov 18, p 1760)provides an excellent clinical and historical overview of Holmes-Adie syndrome (tonic pupil [one pupil reacts much more slowly to light or focusing than the other. Ed.] and areflexia [slowed or no tendon reflexes - particularly the ankle and knee-jerk reflexes.Ed] ) more commonly known in the USA as Adie syndrome. Although the syndrome has not been associated with "infection of conventional bacterial or viral origin", it is occasionally linked to early syphilis, parvovirus B19, and herpes simplex virus infections. We now report an association with neurological Lyme disease.
Holmes-Adie syndrome and Lyme disease
Sir—Paolo Martinelli (Nov 18, p 1760)provides an excellent clinical and historical overview of Holmes-Adie syndrome (tonic pupil [one pupil reacts much more slowly to light or focusing than the other. Ed.] and areflexia [slowed or no tendon reflexes - particularly the ankle and knee-jerk reflexes.Ed] ) more commonly known in the USA as Adie syndrome. Although the syndrome has not been associated with "infection of conventional bacterial or viral origin", it is occasionally linked to early syphilis, parvovirus B19, and herpes simplex virus infections. We now report an association with neurological Lyme disease.
In a referral practice of about 140 patients with Lyme disease, we have seen three patients with predominant neurological symptoms who presented with Holmes-Adie syndrome (table). The diagnosis of Lyme disease was based on a history of tickbite, presence of an erythema migrans rash and positive serology for the spirochaete Borrelia burgdorferi. The duration of Lyme disease symptoms ranged from 2-16 years, and each patient developed a unilateral tonic pupil before the diagnosis of Lyme disease was made. All three patients had significant neuropsychiatric and cognitive defects, hyporeflexia, and facial dysaesthesia without anhydrosis. Rapid plasma reagin testing was negative in each case. Two patients had abnormal brain magnetic resonance imaging with white-matter lesions consistent with neurological Lyme disease. A decreased concentration of CD57 lymphocytes characteristic of chronic Lyme disease5 was found in two patients before antibiotic therapy. Of note, Holmes-Adie syndrome persisted in each case despite intravenous antibiotic therapy and partial resolution of other neurological symptoms of Lyme disease. [Table available on request. Ed.]
Neurological Lyme disease has been associated with various cranial nerve, meningeal, and neuropsychiatric abnormalities. Based on our clinical observation, it seems that Holmes-Adie syndrome might represent an early and unrecognised manifestation of Lyme disease. We suggest that patients presenting with this unusual neuro-ophthalmological syndrome should be tested for the Lyme disease spirochaete.
Raphael B Stricker, Edward E Winger,California Pacific Medical Center, San Francisco, CA 94120, USA; and Immunodiagnostic Laboratories, San Leandro, CA, USA
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