A 34-year-old woman, housewife, with a history of seven weeks of evolution of cystic and hepatic lesions, multiple abscesses, with surgical drainage and prolonged treatment without antibiotics.
She was discharged with antibiotic therapy.
She was admitted to the Emergency Department of Hospital Sótero del Rio with a progressive onset of five days of evolution, characterized by nausea, vomiting, speech disorder and invalidating gait instability.
At admission, there were normal vital signs, absence of headache, fever or meningeal signs; in laboratory tests, normal AST and ALT (21 and 13 U/L, respectively), increased serum albumin levels (204 IU/ 360%).
On neurological examination, the patient was oriented, afflicted with dysarthria, acne is without nystagmus or cranial nerve alteration.
The motor examination showed no paresis, the osteotendinous reflexes were alive, with normal tone and plantar flexor reflexes.
No malformations were detected.
The cerebellar tests showed mild dysmetria in the upper limbs and marked ataxia and gait that prevented him from sit or sit down without assistance.
Initial evaluation with computed tomography of the brain and study of cerebrospinal fluid showed no alterations (cytochemical aspect: clear, colourless; glucose 52 mg/dL -with blood glucose 81 mg/dL-; proteins 0.24 g/dL).
Magnetic resonance imaging (MRI) of the encephalon showed bilateral, symmetrical, hyperintense lesions in T2 and FLAIR sequences located in the dentate nucleus and the dorsal region of the dentate globe, without diffusion effect.
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Based on the aforementioned studies, the possibility of an infectious, tumoral and unfavourable cause was ruled out, considering pharmacological toxicity as the most probable cause.
We reviewed the use of drugs since the diagnosis of liver abscess, highlighting the use of metronidazole for 49 days.
The total cumulative dose of metronidazole was 73.5 g.
In addition, he received other associated antibiotics: ceftriaxone (2 g per day for 29 days), ampicillin (1 g every 6 h for 3 days), then linezolid (600 mg every 12 h for 15 days),
Due to the suspicion of metronidazole neurotoxicity, the drug was suspended and antibiotic treatment was changed to linezolid and prednisone.
The patient was admitted with rapid regression of the cerebellar condition, which resolved completely on the fifth day of stopping metronidazole.
The patient subsequently suffered from dysesthesia and palmoplantar allodynia, with no apparent deficit on neurological examination.
Since the patient was impressive suggesting neuropatic involvement, treatment with amitriptyline was started, with partial improvement of symptoms.
No neurophysiological study was performed.
In a control 2 months after discontinuation of metronidazole, the patient did not present cerebellar alterations, although she persisted with paresthesia in palms and soles.
Neurological examination revealed the presence of live osteotendinous reflexes, with no signs of cerebellar dysfunction or long pathway deficits.
Control MRI performed at that time showed complete resolution of the lesions.
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Evaluated 8 months later, the patient reported only distal paresthesias in lower limbs, with neurological examination within normal limits.
An electromyograph (electromyocardial and conductive nerve, EMG/VCN) of the lower limbs was performed. Sensory polyneuropathy (PNP) was observed in the same control group. The other parameters were normal.
In her last control, 35 months after stopping the drug, the patient was able to perform her usual activities, reported minimal instability that prevented her from walking on a bicycle and persistence of plantar dysesthesia in the distal third, without objective physical examination.
A new MRI of the brain and EMG/CNV were performed, both without pathological findings.
