Stroke in neuroborreliosis.

Abstract

A 20-year-old man suffered two thalamic infarctions during the course of neuroborreliosis and was successfully treated with intravenous ceftriaxone. Review of 11 additional cases of stroke and cerebral vasculitis in neuroborreliosis suggests that there is a meningovascular form of the infection with predilection for the posterior circulation and an association with the European strains of Borrelia burgdorferi. (Stroke 1990;21:1232-1235) L yme disease is a systemic disease caused by infection with the tick-transmitted spirochete / Borrelia burgdorferi. The first stage of the disease is often manifested by a skin lesion, erythema chronicum migrans, at the site of the tick bite. This may be followed weeks to months later by a second stage, during which neurologic and cardiac symptoms and signs appear. Approximately 15% of patients with Lyme disease develop neurologic complications, the most common of which are meningoencephalitis, cranial neuritis, and radiculoplexitis.1 Strokes or vasculitis as complications of neuroborreliosis have been reported only rarely.2 " 8 In fact, some recent reviews of neurologic manifestations of Lyme disease fail to mention stroke as a complication. 1 -9 - 10 We report a patient with bilateral thalamic infarction associated with infection with B burgdorferi and review the subject of stroke in this disorder. Case ReportThe patient is a previously healthy 20-year-old man from California in the United States Army, stationed in southern Germany from late 1987 through the onset of his illness. In January 1989, he began to experience intermittent occipital headaches and was treated symptomatically with ibuprofen until March 15, when he suddenly developed lightheadedness, vertical diplopia, and dysarthria. He was found to be afebrile and without meningismus. The neurologic examination disclosed dysarthric speech, a right central facial weakness, and mild clumsiness of the right upper extremity. Computed tomography (CT) and magnetic resonance imaging (MRI) (FigFrom Multiple lumbar punctures showed persistent lymphocytic pleocytosis with elevated protein content and hypoglycorrhachia (Table 1). Serum and cerebrospinal fluid (CSF) bacterial, fungal, acid-fast bacillus, and viral cultures and titers were negative. Serum fluorescent treponeural antibody assay and serum and CSF VDRL were negative.On April 19 the patient became acutely confused. On examination he was oriented to self and place only. His speech was accurate but slurred with occasional perseveration of answers to simple questions. There was a marked impairment of his short-term memory but good recall of remote events. He had a mild left central facial paralysis. Computed tomography and MRI of the head with contrast injection revealed a new area of infarction in the right anterior thalamus (Figure 1, right) and a resolving left posterior thalamic infarct.The patient's problems with short-term memory and orientation improved over the next 24 hours but he remained hypersomnolent.Immunofixation assays for antibody to B burgdorferi in ser...

Cerebral Vasculitis and Stroke in Lyme Neuroborreliosis

“…Our patient 2, and several reports in the literature, show that unrecognized LNB can lead to recurrent cerebral ischemia and multiple infarcts [6, 7, 12, 18]. Serological screening for Bb-specific antibodies in an unselected cohort of stroke patients is of little value [8].…”

“…This assumption is supported by occasional findings of Bb spirochetes or Bb DNA in brain tissue samples of affected patients [10], and the fact that excellent responses to a single course of antibiotic treatment have been repeatedly reported [7, 11, 15, 17]. As opposed to direct spirochetal invasion, neurological damage may also result from a response to molecular mimicry by sharing of antigenic determinants between Bb and human tissue [21].…”

“…Most patients have a ‘prodromal stage’ lasting several weeks to months with complaints such as headache, fatigue, difficulty concentrating, loss of appetite and weight, and episodes of nausea and vomiting. In other patients, cranial neuritis and radiculoneuritis precede or accompany stroke symptoms [6,7,8,9, 13, 14]. …”

“…A substantial number of reports on stroke due to LNB described patients younger than 30 years [6, 7, 10, 11, 14, 15, 17, 18, 20]. However, the observation that LNB might be more common in young stroke patients is probably biased, as workup of stroke etiology tends to be more extensive in young stroke victims.…”

“…Stroke due to LNB may manifest as subarachnoid hemorrhage [3, 4], intracerebral hemorrhage [5] and, most frequently reported, ischemic infarction [6,7,8,9,10,11,12,13,14,15,16,17,18,19,20]. We report on 2 patients with cerebral vasculitis and stroke due to LNB, and provide a review of current knowledge.…”