Hyperreflexia in Guillain-Barré syndrome: relation with acute motor axonal neuropathy and anti-GM1 antibody

Dr Satoshi Kuwabara, Department of Neurology, Chiba University School of Medicine, 1–8–1 Inohana, Chuo-ku, Chiba 260–8670, Japan. Telephone [phone] extension 5414; fax [phone]; email [email protected]

Guillain-Barré syndrome (GBS) is an immune mediated polyneuropathy clinically characterised by acute symmetric muscle weakness and areflexia.¹ Whereas most GBS is demyelinating neuropathy (acute inflammatory demyelinating polyneuropathy, AIDP) in western countries,^{2 3} an axonal form of GBS, termed acute motor axonal neuropathy (AMAN), has been recognised in northern China^{4 5} and in other countries.^{6 7} It is suggested that AMAN is associated with pure motor axonal involvement, antiganglioside GM1 antibodies, or precedingCampylobacter jejuniinfection.^7-9

Chinese patients with AMAN are reported to often develop hyperreflexia during the early phase of recovery,^{4 5} and other studies described patients with acute motor neuropathy with preserved tendon reflexes.^10-12 Preserved or exaggerated tendon reflexes do not usually occur in patients with AIDP and in patients with other peripheral neuropathies. We, therefore, investigated the incidence of hyperreflexia and its relation with electrophysiological subtypes (AMAN or AIDP), anti-GM1 antibodies, or C jejuniinfection in consecutive patients with GBS in Japan.

Patients and methods

PATIENTS

Fifty four patients with GBS who were seen at Chiba University Hospital and its affiliated hospitals between January 1992 and April 1998 were studied. The mean age was 40.1 years (range 3 to 78 years). Their first neurological examination and electrodiagnostic study were done within 2 weeks of onset. They fulfilled the clinical criteria for GBS,¹ except for two patients who had normal or brisk tendon reflexes in the first examination. The two patients were diagnosed as having AMAN because of electrophysiological evidence of motor axonal loss. Clinical disability was evaluated with the Hughes functional grading scale¹³ and patients were followed up for 3 months after onset. Hyperreflexia was regarded as present when there were increased amplitudes of tendon reflexes, abnormal reflex spread (finger jerks after tendon tapping of the biceps brachii or brachioradialis muscle, or thigh adduction after patella tendon tapping), and decreased reflex threshold (biceps contraction after tendon tapping of the brachioradialis, or quadriceps contraction after tapping of the midportion of the patella). Hoffmann’s and Babinski’s signs were also examined.

ELECTROPHYSIOLOGY

Nerve conduction and H-reflex...