Reflection and Reaction 138 http://neurology.thelancet.com Vol 4 March 2005 Wee Yong and colleagues (Dec 2004) 1 provide an extensive review of the potential usefulness of minocycline in several neurological disorders. They describe also the side-effects and the exacerbation of neurological diseases possibly caused by minocycline. However, idiopathic intracranial hypertension (IIH) is not mentioned. IIH is characterised by optic disk oedema and a high opening pressure on lumbar puncture examination with normal CSF and brain imaging. The disease typically occurs in young obese females. Several drugs might precipitate IIH, including nalidixic acid, steroids, ciprofloxacin, and tetracycline. 2 Minocycline is currently used in young adults to treat acne vulgaris and has been repeatedly associated with IIH. 2–6 A study of 700 patients treated with minocycline for acne showed that the prevalence of IIH may be as high as 1·0–1·4%. 3 Kesler and colleagues 4 found that 16 of 243 patients with IIH (6·58%) were taking minocycline. The mechanism of increased intracranial pressure is unknown but is likely related to low CSF absorption at the arachnoid villi. 2 According to several reports, the long-term outcome of minocycline-related IIH may not be entirely benign and a significant visual-field loss may persist. 2,4–6 We recently observed a 19-year-old non-obese woman with headache, transient blurring of vision, and bilateral optic disk oedema who was on treatment with minocycline for acne. No abnormal findings were seen on MRI of the brain. The CSF opening pressure was as high as 450 mm H 2 O. Minocycline was discontinued and after 2 days the headache resolved. Although no case-controlled studies have been done, I believe the occurrence of IIH in patients taking minocycline is unlikely to be a chance association. In view of the possible use of mynocycline in several human neurological disorders, neurologists should be reminded that this drug might lead to IIH. This could be of particular importance, for instance, in a young female treated with minocycline for multiple sclerosis, who could eventually develop an optic disk oedema, thus raising problems of differential diagnosis. Fabio Bandini Department of Neurosciences, Ophthalmology and Genetics, University of Genoa, Via De Toni 5, Genoa, Italy fbandini@neurologia.unige.it Minocycline in neurological diseases clinical improvement as measured by the Alzheimer’s Disease Cooperative Study-Clinician’s Global Impression of Change (ADCS-CGIC). Tremor was more common in the rivastigmine-treated group, but scores on the motor subtest of the Unified Parkinson’s Disease Rating Scale (UPDRS) were not significantly different between the treated and control groups. The neuropsychological tests used in this study were tailored to assess the domains most commonly impaired in PDD (ie, visuospatial functioning, attention and concentration, and verbal fluency), and there were improvements in these secondary outcome measures. Although not rigorously assessed, symptoms and signs of orthostatic hypotension were not different in the treatment and control groups. Sleep measures were not assessed in this study. The implications of this study should be emphasised. First, the clinical syndrome of PDD can be recognised by multiple groups of investigators and across different cultures and native languages, at least in Europe where this study was conducted. Second, the findings are very similar to those in the rivastigmine in dementia with Lewy bodies study, 4 underscoring the commonality between the two dementias. The fact that parkinsonism (at least as measured by the motor subtest of the UPDRS) and orthostatic hypotension did not worsen bodes well for other drugs with cholinomimetic properties to be tested in PDD. Finally, and most importantly, rivastigmine and possibly other cholinesterase inhibitors can improve many of the cognitive and neuropsychiatric symptoms of PDD. Whether rivastigmine is superior to the other currently available and commonly used cholinesterase inhibitors—donepezil and galantamine—is unknown. Because the cholinesterase inhibitors rely on the amount of acetylcholine available at the synaptic cleft, and substantial degeneration of the cholinergic nucleus basalis of Meynert is well established in PD, cholinergic agonists may be as or more effective than the cholinesterase inhibitors in PDD. Although side-effects and aggravation of tremor can occur, rivastigmine and possibly other cholinesterase inhibitors should be considered part of the pharmacological armamentarium for treatment of patients with PDD. Bradley F Boeve Division of Behavioral Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota, 200 First Street SW, Rochester, Minnesota 55905, USA bboeve@mayo.edu I have no conflicts of interest. 1 Aarsland D, Larsen JP, Karlsen K, et al. Mental symptoms in Parkinson’s disease are important contributors to caregiver distress. Int J Geriatr Psychiatry 1999; 14: 866–74. 2 Aarsland D, Andersen K, Larsen JP, et al. Prevalence and characteristics of dementia in Parkinson disease: an 8-year prospective study. Arch Neurol 2003; 60: 387–92. 3 Apaydin H, Ahlskog JE, Parisi JE, Boeve BF, Dickson DW. Parkinson disease neuropathology: later-developing dementia and loss of the levodopa response. Arch Neurol 2002; 59: 102–12. 4 McKeith I, Del Ser T, Spano P-F, et al. Efficacy of rivastigmine in dementia with Lewy bodies: a randomized, double-blind, placebo-controlled international study. Lancet 2000; 356: 2031–36. 5 Emre M, Aarsland D, Albanese A, et al. Rivastigmine for dementia associated with Parkinson’s disease. N Engl J Med 2004; 351: 2509–18.