We observed hyperreflexia in the course of the motor axonal neuropathy form of Guillain-Barre syndrome (GBS). Herein, we would like comment on a rare case. Acute motor axonal neuropathy (AMAN) is a type of GBS accompanied by peripheral axonal involvement where acute motor paralysis, loss of reflex or hyporeflexia, insignificant sensory loss, and albumino-cytologic disproportion in cerebrospinal f luid are seen with no demyelinating findings in electromyography (EMG). [1] Commonly known as acute inflammatory demyelinating polyneuropathy (AIDP), GBS’s spectrum has expanded in recent years to include variants with unusual attributes. Types such as AMAN and acute motor or sensorial axonal neuropathy have also begun to be more understood. In AMAN, there is an axonal damage with underlying inflammation of the peripheral nerves without demyelination. In the underlying etiology, Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, inf luenza, mycoplasma, coxsackie virus, and hepatitis viruses, previous surgery, delivery, or some vaccinations are shown to be related causes. [2,3] Motor conduction