Abreu, P

Ferreira, C

Rodrigues, M

Santos, AF

English

Institutional repository of Hospital de Braga

LETTER TO THE EDITORReversible parkinsonism and cognitive deficits due to vitamin B12deficiencyAna Filipa Santos • Margarida Rodrigues •Pedro Abreu • Carla FerreiraReceived: 22 January 2015 / Accepted: 22 February 2015 Springer-Verlag Italia 2015Dear Sir,Vitamin B12 deficiency is responsible for many neuro-logical disorders and is normally sought in clinical practicein patients with dementia or ataxia [1, 2]. Parkinsonismsecondary to B12 deficiency is exceedingly rare [2, 3] withonly two previous reports, summarized in Table 1.A 71-year-old woman with chronic gastritis developed arapidly progressive gait disorder with very early fallswithin 1 month. She was slightly disoriented and presentedasymmetrical parkinsonism with marked facial hypomimia,hypophonia, bradykinesia and rigidity (more evident on theleft side and upper limbs), parkinsonian gait with posturalinstability (Unified Parkinson Disease Rating Scale partIII—26). Frontal release signs and ideomotor apraxia werealso present. She had no cerebellar nor pyramidal signs, herproprioception was normal and autonomic dysfunction,daily fluctuations, visual hallucination or delusions werenot present. No new medication had been started and noexposure to neuroleptics, carbon-monoxide or toxics wasrecorded.Levodopa was started, 150 mg/day for 2 weeks, then thedose was increased to 300 mg/day, at which point the pa-tient became more disoriented, needing help to attain dailyactivities and ultimately bedridden, with more markedmotor impairment. It was then suspended. At this timelaboratory studies showed a serious deficit of vitaminB12 (83 pg/ml, normal [250 pg/ml). Hemoglobin level,mean corpuscular volume, folate level, thyroid function,autoimmune and serological screen were normal. She hadno clinical signs or symptoms of myelopathy or neuropa-thy. Brain MRI revealed mild cortico-subcortical atrophy.Vitamin B12 replacement was started with injections at adose of 1000 mg/day for 7 days, than once a week for4 weeks and monthly thereafter, with progressive clinicalimprovement. Nine months later she was totally indepen-dent from the functional point of view. She was able to takecare of herself and her house chores including goingshopping on her own. Neurological examination was nor-mal with no frontal release signs.The most likely cause of this patient’s parkinsonism andcognitive deficits was, in our view, the serious B12 deficitdocumented, since we have observed full recovery withreplacement therapy and excluded other possible causes.Pathophysiology of extrapyramidal symptoms in patientswith vitamin B12 deficiency is far from clear. Vitamin B12has fundamental roles in CNS, especially the methionine-synthase mediated conversion of homocysteine to me-thionine [4]. This amino acid is a major source of S-adenosylmethionine, the most important methyl donor inthe brain and influences serotonin, norepinephrine, anddopamine synthesis [4]. A deficiency of vitamin B12 maylead to increased homocysteine levels. And there is evi-dence that increased homocysteine levels might acceleratedopaminergic cell death in Parkinson’s disease (PD),through neurotoxic effects [4]. Other known enzymaticreaction which is dependent on vitamin B12 is the con-version of methylmalonic acid to succinyl-CoA, so vitaminB12 deficiency can lead to increased levels of serummethylmalonic acid. Also, the methylmalonic acidemiausually presents with acute extrapyramidal syndrome ininfants and some cases respond to vitamin B12 replacementA. F. Santos (&)  M. Rodrigues  C. FerreiraServiço de Neurologia, Hospital de Braga, Sete Fontes,São Victor, 4710-243 Braga, Portugale-mail: filipasantos@hotmail.comP. AbreuServiço de Neurologia, Hospital de São João, Faculty ofMedicine, University of Oporto, Porto, Portugal123Neurol SciDOI 10.1007/s10072-015-2126-0[2]. Brain imaging and autopsy studies of this autosomalrecessive disorder have shown symmetrical involvement ofbasal ganglia [2]. Globus pallidus may be especially vul-nerable because of its high energy requirements [3].We alert that complicated extrapyramidal and cognitivemanifestations may be, sometimes, due to B12 deficiencyand this recognition is essential since we can easily andeffectively treat these patients.Conflict of interest The authors declare that they have no conflictof interests.References1. Shyambabu C, Sinha S, Taly AB et al (2008) Serum vitamin B12deficiency and hyperhomocystinemia: a reversible cause of acutechorea, cerebellar ataxia in an adult with cerebral ischemia.J Neurol Sci 273(1–2):152–1542. Kumar S (2004) Vitamin B12 deficiency presenting with an acutereversible extrapyramidal syndrome. Neurol India 52(4):507–5093. Sharrief AZ, Raffel J, Zee DS (2012) Vitamin B12 deficiency withbilateral globus pallidus abnormalities. Arch Neurol 69(6):769–7724. Qureshi GA, Qureshi AA, Devrajani BR et al (2008) Is thedeficiency of vitamin B12 related to oxidative stress and neuro-toxicity in Parkinson’s patients? CNS Neurol Disord Drug Targets7(1):20–27Table1DescriptionofreportedcasesofadultswithreversibleparkinsonismandB12deficitsReferencesAgeGenderInitialclinicalpresentationOtherneurologicalabnormalitiesbeyondparkinsonismSerumvitaminB12level(pg/ml)EvaluationforcausesofvitaminB12deficiencyB12supplementationClinicalimprovementLastfollowupKumar[2]55MaleBradykinesiaandtremorofhandsof10daysdurationMyeloneuropathy5AtrophicgastritisStartedonvitaminB12injectionsatadoseof1000mg/dayfor7days;thanonceaweekfor4weeks;monthlythereafterWithin3daysAt5years:noneurologicaldeficitsSharriefetal.[3]43MaleGaitabnormality(‘‘Stumbling’’)3monthsbeforehospitalizationMyeloneuropathyImpairedcognition254AutoimmunegastritisParenteralvitaminB12therapy(notspecified)Within1weekNotspecifiedNeurol Sci123

Reversible parkinsonism and cognitive deficits due to vitamin B12 deficiency

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Reversible parkinsonism and cognitive deficits due to vitamin B12 deficiency

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