technetium-tc-99m-bicisate and Cerebellar-Ataxia

It has been reported that autoimmune cerebellar ataxias, such as anti-glutamic acid decarboxylase (GAD)-antibody-positive cerebellar ataxia and gluten ataxia, are treatable. Here, we examined the therapeutic efficacy of intravenous immunoglobulin (IVIg) on autoantibody-positive cerebellar ataxia.. IVIg therapy was administered in seven autoantibody-positive cerebellar ataxia patients. Therapeutic efficacy was examined in terms of its effects on clinical symptoms and changes in brain perfusion using single photon emission computed tomography (SPECT).. Treatment was effective in four cerebellar cortical atrophy patients (two anti-GAD antibody-positive and two anti-gliadin antibody-positive) and in one anti-thyroid antibody-positive spinocerebellar ataxia type 3 (SCA3) patient, but not in two multiple system atrophy (MSA) patients. All four IVIg effective patients who underwent SPECT showed apparent increases in cerebellar perfusion.. If cerebellar ataxia with an autoimmune mechanism is suspected and radiological findings do not reveal MSA, it is worth considering immunotherapy including IVIg.

Topics: Aged; Aged, 80 and over; Autoantibodies; Cerebellar Ataxia; Cysteine; Female; Gliadin; Glutamate Decarboxylase; Humans; Immunoglobulins, Intravenous; Iodide Peroxidase; Male; Middle Aged; Organotechnetium Compounds; Radiopharmaceuticals; Tomography, Emission-Computed, Single-Photon; Treatment Outcome

A 69-year-old man was referred to our department because of acute onset nausea, vomiting, dysphagia, dysarthria and gait disturbance. He had a 50-day-history of amebic dysentery and had been treated with 1,500 mg metronidazole per day. Neurological examination revealed dysphagia, ataxic speech, ataxia of the left extremities and the trunk, and hyperactive deep tendon reflexes in all extremities. Sensory impairment of all modalities was apparent in a glove and stocking pattern, with mild paresthesia. Brain MRI showed T2 high signal lesions in the bilateral cerebellar dentate nuclei, more markedly on the left. On brain SPECT, obvious low blood perfusion was observed in the left cerebellar hemisphere. These findings well explained the ataxia of the left limbs. One month after discontinuing metronidazole, the cerebellar ataxia, dysphagia and MRI abnormalities completely cleared. Therefore, central nervous system damage induced by metronidazole is considered reversible. In spite of the presence of the MRI lesion in the right dentate nucleus, the patient had no ataxia of the right extremities and there was no hypoperfusion in the right cerebellar hemisphere. Thus, metronidazole does not appear to have a direct neurotoxic effect on the central nervous system. On the other hand, nerve conduction studies showed axonal polyneuropathy, which was not improved one month after cessation of the drug; thus metronidazole seems to exert more damage on peripheral nerves.

Topics: Acute Disease; Aged; Antiprotozoal Agents; Brain; Cerebellar Ataxia; Cysteine; Dysentery, Amebic; Humans; Magnetic Resonance Imaging; Male; Metronidazole; Organotechnetium Compounds; Radiopharmaceuticals; Tomography, Emission-Computed, Single-Photon