Metronidazole induced cerebellar ataxia
A 31-year-old male patient, carpenter by occupation was admitted to the hospital on 25-01-2012 for instability of gait since 1 month duration. There was also slurring of speech since then. There was a history of tingling and numbness of both lower limbs, which had gradually ascended up to the knees for the past 1 month. The footwear used to slip off his feet while walking. Because of the numbness of the feet and the in coordination he was dependent on the family members for most of his daily activities. He experienced clumsiness while buttoning his shirt and mixing the food was also observed. Tremulous and overshooting of hand while eating, food was observed.\nThe patient had a generalized tonic-clonic seizure in the hospital, on the day of admission. There was a past history of 3 seizures 3 weeks earlier, on 15-12-2011 however, he was not evaluated at that time and was not on any antiepileptic medication at the time of admission. He was not a known epileptic before starting the anti-amoebic medication.\nThere was a history of weight loss of 11 kg in the past 4 months. He was admitted to the gastroenterology unit of the hospital 4 months ago, where he was diagnosed to be suffering amoebic liver abscess. The liver abscess was drained twice in 15 days’ time and he was administered metronidazole infusion in the hospital at that time and he was asked to stop alcohol. As the abscess was resolving, he was advised to continue metronidazole tablets 400 mg 5 tablets daily for a long period for another 2 weeks. Patient came for review after nearly 3 months with diarrhea. The patient was taking metronidazole for nearly 4 months before admission. In the last 1 month, Ornidazole 250 mg + Diloxanidee furoate 200 mg twice daily were added for control of diarrhea (without the knowledge that he was also taking metronidazole), The latter combination was taken for 3 weeks and discontinued, thereafter since the patient could not afford it.\nOn examination, he was alert and co-operative; there were no cranial nerve deficits. Speech was slurred with a scanning character. There was hypotonia in all 4 limbs. The muscle power on medical research council (MRC) grading scale was normal except minimal weakness of toe extensors bilaterally. The plantar reflexer were flexor, deep tendon reflexes were normal. There was intention tremor, dysmetria, dysdiadochokinesia in both upper limbs. In-coordination was noted in both upper and lower limbs. He was unable to stand on a narrow base. The gait was ataxic and he was unable to walk tandem. There was impairment of all modalities of sensation in both lower limbs below the knees.\nThe patient was investigated for his complaints. The laboratory work-up showed total leucocyte count of 8600/Cu mm with normal differential count. Platelets were adequate on smear and the count was 230,000/Cu mm. Random blood glucose was 143 mg/dl, blood urea was 37 mg/dl, and serum creatinine was 1.2 mg/dl. Liver function tests were normal. An ultrasound examination of the abdomen was normal, and the abscess had resolved. Nerve conduction study of the limbs suggested a length dependent axonal sensorimotor neuropathy. X-ray chest and electrocardiogram ruled out any cardiac involvement. Magnetic resonance imaging (MRI) scanning of the brain showed faint hyper-intense signals on T2 and FLAIR imaging from the dentate nucleus bilaterally more prominent on the left side [Figures -]. There was also hyper-intense signal in the splenium of corpus callosum.\nOn the day of admission, the seizures were controlled with diazepam. He was started on an anti-epileptic drug, levetiracetam. A diagnosis of post-infectious immune mediated disease like acute disseminated encephalomyelitis (ADEM) was considered initially as the seizures and ataxia followed a diarrheal illness. He was given one bolus of high-dose methylprednisolone as part of treatment for ADEM. When the MRI did not reveal typical lesions of ADEM, the history and clinical findings were reviewed. Metronidazole was suspected to cause the adverse reaction and was discontinued.\nThe patient was discharged after 7 days and followed-up after 10 days. Dysarthria and ataxia had resolved. There were no more seizures. Levetiracetam was also discontinued. The sensory symptoms in the lower limbs were persisting; however, he was able to walk independently.