Temporal arteritis and Guillain-Barre syndrome.

ABSTRACT

The association of temporal arteritis and Guillain-Barre syndrome has rarely been reported. We describe a patient who sequentially suffered from both disorders. An 81-year-old woman presented with headache and loss of appetite. Analysis showed anemia and an erythrocyte sedimentation rate of 94 mm/hr. Temporal artery biopsy disclosed giant cell arteritis. Upon treatment with prednisone, all symptoms improved. A few weeks later, the patient began having low back pain, paresthesias, ascending weakness, and unexplained intermittent hypotension. Examination showed absent tendon reflexes in the knees. Cerebrospinal fluid contained one mononuclear cell/dL, and a protein level of 81 mg/dL. An electrophysiologic study revealed reduced nerve conduction velocities. Intravenous immunoglobulin therapy was instituted, and all symptoms slowly disappeared. This is the third reported case of Guillain-Barre syndrome in association with temporal arteritis. The other two patients recovered. Although the association of Guillain-Barre syndrome and temporal arteritis in these three patients could be coincidental, a common immunologic mechanism is also a possibility.

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NEUROLOGIC MANIFESTATIONS may occur in temporal arteritis, but the Guillain-Barre syndrome has rarely been observed in patients with this condition. (1,2) The following is a report of such an association.

CASE REPORT

An 81-year-old woman presented with a 4-week history of headache, photophobia, dizziness, and loss of appetite. Her medical history included diagnoses of hypertension, heart failure, type 2 diabetes mellitus, primary hypothyroidism, cataracts, and glaucoma. On physical examination, a grade 3/6 systolic murmur was heard in the aortic area, and the temporal arteries were not felt. Blood analysis showed a hemoglobin concentration of 11 g/dL, red blood cells that were normocytic and normochromic, and an erythrocyte sedimentation rate of 94 mm/hr; all other results were normal. An electrocardiogram revealed a right bundle branch block. Findings on chest radiographs, abdominal ultrasonography, and computed tomography of the head were normal. A biopsy of the right temporal artery disclosed changes typical of giant cell arteritis. Prednisone therapy (60 mg/day) was instituted, with improvement in all symptoms over the next several days.

Three weeks after starting prednisone therapy, the patient began having low back pain, with paresthesias and increasing weakness in the lower extremities. Over the next few weeks, she also had weakness in the upper extremities, mild dyspnea, and unexplained intermittent hypotension that necessitated intravenous dopamine for several days. Examination then showed severe weakness in the legs and absent tendon reflexes. Cerebrospinal fluid contained 1 mononuclear cell per deciliter, with a protein value of 81 mg/dL and glucose value of 126 mg/dL. Microbiology studies were negative, and results of new routine blood tests were normal. Magnetic resonance imaging of the thoracic and lumbar spine revealed no abnormalities. An electrophysiologic study disclosed reduced nerve conduction velocities. Treatment with intravenous immunoglobulin was instituted, prednisone was gradually tapered, and all symptoms slowly improved over the following weeks. Four months later, the patient was in good health and was able to walk wit hout help.

DISCUSSION

Our review of the literature shows only two more cases of Guillain-Barre syndrome in association with temporal arteritis. One of these patients was a 71-year-old woman who, in contrast to our patient, first had Guillain-Barre syndrome, and temporal arteritis developed several weeks later.' The other patient was a 73-year-old man who, like our patient, had temporal arteritis first and Guillain-Barre syndrome afterward. (2) Both patients eventually recovered.

Temporal arteritis is a systemic disease provoked by the inflammation of medium and large arteries. An autoimmune origin has been suggested. (3) The neurologic manifestations of this type of vasculitis are generally attributed to ischemic lesions of the nerves due to an arteritis of the vasa nervorum. But this mechanism does not appear to explain the occurrence of Guillain-Barre syndrome, a demyelinating symmetrical polyradiculoneuropathy that probably has also an immunologic origin. (4)

Although the association of Guillain-Barre syndrome and temporal arteritis in these three patients could be simply coincidental, a common immunologic mechanism is also a possibility that must be taken into account.

References

(1.) Corston RN: Temporal arteritis in association with the Guillain-Barre syndrome. BMJ 1980; 280:292-293

(2.) Tiab M, Raffi F, Hamidow M, et al: Syndrome de Guillain-Barre au course d'une maladie de Horton. Rev Med Interne 1994; 15:772-773

(3.) Neff AG, Greifenstein EM: Giant cell arteritis update. Semin Ophthalmol 1999; 14:109-112

(4.) Vedeler CA: Inflammatory neuropathies: update. Curr Opin Neurol 2000; 13:305-309

RELATED ARTICLE: KEY POINTS

* Neurologic complications are common in temporal arteritis.

* A patient with temporal arteritis and Guillain-Barre syndrome, a rare association, is reported.

* Temporal arteritis and Guillain-Barre syndrome may share a common immunologic etiology.

From the Department of Medicine, Hospital General of Castellon, Spain.

Reprint requests to Bernardino Roca, MD, Catalunya, 33-A, 4, 12004 Castellon, Spain.