Lyme disease

Ticks can be carriers of Lyme disease (illustration from Wikipedia article Lyme disease).

Lyme disease or Lyme borreliosis is a zoonotic disease transmitted by ticks and caused by several species of Borrelia spirochetes. North American Lyme disease and European borreliosis differ in many aspects: Whereas in North America infection by Borrelia burgdorferi sensu stricto almost invariably leads to erythema migrans, frequently followed by oligoarthritis in untreated individuals, most infections in Europe are caused by Borrelia garinii and Borrelia afzelii and are contracted asymptomatically (Egger, 2005). A minority of the infected individuals develop neuroborreliosis, consisting of various combinations of meningitis, radiculitis and (cranial) neuritis (Pfister and Rupprecht, 2006). Seropositivity alone is an insufficient finding for the diagnosis of Lyme disease and must be supported by the clinical findings and the patient's history.

Bull's-eye-like rash (erythema migrans) caused by Lyme disease (illustration from Wikipedia article Lyme disease).

It is known that recent-onset headaches resembling migraine are common in patients hospitalized with Lyme disease (Scelsa et al., 1995). According to the IHS ICHD-II criteria, these secondary headaches are classified as "Headache attributed to systemic bacterial infection" (ICHD-II 9.2.1). Headaches are classified as either primary or secondary. Primary headaches have no structural or metabolic cause, while secondary headaches are caused by an underlying pathologic or metabolic process. Migraine, tension-type, cluster, and analgesic-rebound headaches are all primary headache disorders. Secondary headaches are caused by conditions such as increased intracranial pressure, pseudotumor cerebri, subdural and intracerebral hematomas, hypertension, meningitis, temporal arteritis, brain tumours, and, last but not least, Lyme disease (Marks and Rapoport, 1997).

As has been acknowledged by Kristoferisch as early as 1991, "The great variety of neurological manifestations in Lyme borreliosis - most of them can also be attributed to other conditions - and the high rate of seropositivity for B. burgdorferi amongst the population living in endemic areas require strict criteria for the correct diagnosis of new and typical neurological manifestations." As "Lyme can masquerade as migraine", it has been characterised as a "disease in disguise" (Cowley and Underwood, 2004). The neurological symptoms of neuroborreliosis can in fact show considerable overlap with the symptoms of persistent aura without infarction, but despite many claims to the contrary by users of the Ezboard forum Visual snow or static (e.g. leahester [mother of subject #43], prismvision [subject #142] or ChodaKingandSprocket [subject #179]), there is no medical evidence that Lyme disease is a cause of persisting visual snow simultaneously in both temporal and nasal fields of both eyes, the most frequent symptom of the aforementioned migraine complication in the sample of respondents to Sofia Greene's internet survey, and the same holds true for persisting visual perseveration (e.g. increased afterimages, trails, palinopsia), which is also among the five most frequent symptoms of persistent aura without infarction in the given sample. Moreover, in addition to these differences in symptomatological spectrum, a patient with a definite diagnosis of persistent aura without infarction (see here) shows a specific temporal pattern of symptoms (i.e., a time course where one and the same phenomenon first occurs as a transitory and then as a persisting symptom) that is unlikely ever to be mimicked by the effects of the inflammatory CNS disorder of neuroborreliosis.

As has previously been noted in the Wikipedia article on Visual snow, "a variety of illnesses (e.g. Lyme disease...) ... have been blamed by sufferers in self-help internet forums as causes of persisting visual snow, but none of these claims have been supported by evidence-based medicine" (Podoll et al., 2006). It may be added that in general not even those reports from the internet that consider Lyme disease as the culprit for persistent visual snow claim or document that this particular persisting neurological symptom responds well to antibiotics. In summary, a critical review of the available evidence does not give support to the notion that Lyme disease is a cause of persisting visual snow and/or persisting visual perseveration. Misattribution of these two frequent symptoms of persistent aura without infarction to Lyme disease may cause costly and unnecessary examinations and therapies and distract sufferers from finding adequate diagnosis and therapy.

Reid et al. (1998) made an observational study on the adverse consequences of overdiagnosis and overtreatment of Lyme disease. In a sample of 209 patients of a University-based Lyme disease clinic with a presumptive diagnosis of Lyme disease previously assigned either by referring physicians, the patients themselves, or both, 44 (21%) met criteria for active Lyme disease, 40 (19%) had previous but not active Lyme disease, and 125 (60%) had no evidence of current or previous infection. In general, patients with active Lyme disease had good outcomes. Patients with previous Lyme disease and patients with no evidence of Lyme disease used considerable health resources, had frequent minor adverse drug events, reported significant disability, and had high rates of depression and stress. Thus, overdiagnosis and overtreatment of Lyme disease are associated with inappropriate use of health services, avoidable treatment-related illness, and substantial disability and distress. It seems safe to expect that this also applies to patients suffering from persistent aura without infarction who are misdiagnosed as having Lyme disease, as suggested by the above quoted case vignette.

The Lyme disease controversy (see here)

References

Cowley G, Underwood A. A disease in disguise. Lyme can masquerade as migraine, or as madness. Newsweek 2004; 23: 144(8): 62.
Egger M. [Lyme borreliosis--an overview]. Ther Umsch 2005 Nov; 62(11):731-736.
Kristoferisch W. Neurological manifestations of Lyme borreliosis. Infection 1991; 19: 268-271.
Marks DR, Rapoport AMPractical evaluation and diagnosis of headache. Semin Neurol 1997; 17: 307-312.
Pfister HW, Rupprecht TA. Clinical aspects of neuroborreliosis and post-Lyme disease syndrome in adult patients. Int J Med Microbiol 2006; 296 (Suppl 40): 11-16.
Podoll K, Dahlem M, Greene S. Visual snow. Wikipedia article, May 23, 2006.
Reid MC, Schoen RT, Evans J, Rosenberg JC, Horwitz RI. The consequences of overdiagnosis and overtreatment of Lyme disease: an observational study. Ann Int Med 1998; 128: 354-362.

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