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An 85-year-old man presented with a 3-week history of headache, reduced mobility and dysphasia. The headache was unilateral affecting the left side. His reduced mobility was associated with varying levels of weakness of the right arm and leg. His dysphasia was reflected in problems reading the newspaper, and speaking to his wife, as well as understanding what his wife was saying to him. On examination he was found to be alert and orientated in time, place and person, scoring an abbreviated mental test score of 9/10. Neurological examination revealed a right upper motor lesion of cranial nerve VII, increased reflexes in the right arm and leg, and a dysphasia which was both expressive and receptive. In addition he had a temperature of 37.5°C. He had a normal full blood count, routine biochemistry and chest X-ray. Blood cultures were negative. His C-reactive protein was 11 mg/l. Urgent computed tomography (CT) of the brain was organised (figure 1). Following treatment the patient's condition improved gradually over a month. At discharge he had minimal dysphasia and walked independently with ease. Two months later he developed a peripheral sensory neuropathy of a glove and stocking distribution. Serum vitamin B12, folate and thyroid function tests were normal. There was no history of alcoholism, diabetes mellitus or a connective tissue disorder. Following a further adjustment to his treatment he eventually fully recovered (figure2).
Cranial CT scan with contrast at presentation
Cranial CT scan with contrast after 8 months
Questions
- 1
- Might the medical history help?
- 2
- What is the probable initial diagnosis?
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- How would you manage his problem?
- 4
- Why did he develop peripheral neuropathy?
Answers
QUESTION 1
Yes. His medical history revealed that about 40 years earlier he had been diagnosed as having a left-sided cerebral abscess secondary to mastoiditis. Both were treated surgically. There are three main categories of predisposing factors for cerebral abscesses. Firstly, a contiguous source of infection such as dental abscess or otitis media accounts for approximately 47% of cases. Secondly, haematogenous spread from a distant focus such as bronchiectasis or bacterial endocarditis can account for 25% of causes. Cranial trauma accounts for approximately 8–13%. In 15–20% of cerebral abscess no cause can be found.1
QUESTION 2
Cranial CT scan showed ring-enhancing lesions in the left temporo-parietal area suggestive of cerebral abscesses or possibly metastatic malignant deposits (figure 1). The clinical picture supported the former diagnosis.
QUESTION 3
In consultation with local neurosurgeons a decision was made to opt for initial medical treatment and assess response with serial cranial CT scans. Treatment initially involved a 2-week regime of intravenous cefotaxime, metronidazole and ciprofloxacin. This was followed by long-term oral ciprofloxacin and metronidazole. There was resolution of the cerebral abscesses on CT scan 8 months after initiating antibiotics (figure 2). As no organism was isolated from the abscesses, treatment was empirical. The organisms isolated in cerebral abscesses include streptococci (Streptococcus intermedius group, including S angiosus) in 60–70% of cases, enterobacteriaceae in 23–30% of cases, bacteroides and parvotella in 20–40% of cases andStaphylococcus aureus in 10–15% of cases.2 Evidence for the use of metronidazole was provided by Ingham et al, who showed it to cross the blood–brain barrier and penetrate cerebral abscesses well.3 In Sjolin's series, a combination of cefotaxime and metronidazole was shown to be effective in treatment of cerebral abscesses.4 Success of ciprofloxacin in the treatment of cerebral abscesses has been reported.5
QUESTION 4
Metronidazole was stopped as it was suspected to be the cause of the peripheral neuropathy, and the patient was continued on ciprofloxacin 250 mg bid. His peripheral neuropathy had mainly resolved 6 months after discontinuation of metronidazole. This has been a well documented side-effect since 1976 when Coxon and Pallis first suggested metronidazole to be a cause of neuropathy.6 The degree of neuropathy is dose- and duration-dependent. Signs of neuropathy are reversed within 4–48 months of cessation of metronidazole treatment.7
Learning points
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beware of patients with stroke and a history of ear disease
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cerebral abscesses can recur late and be managed successfully medically
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long-term metronidazole can cause peripheral neuropathy
Final diagnosis
Cerebral abscesses, followed by peripheral neuropathy as a side-effect of metronidazole treatment.