Mineralization of the basal ganglia: implications for neuropsychiatry, pathology and neuroimaging

Casanova, Manuel F.; Araque, Julio M.

doi:10.1016/s0165-1781(03)00202-6

Cited by 74 publications

(74 citation statements)

References 188 publications

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Section: Introductionmentioning

confidence: 99%

“…Historically recognized as Fahr's syndrome, they can vary in presentation from accidental findings to severe neuropsychiatric syndromes [1][2][3][4] . Researchers have found that lesions are usually located at the basal ganglia and cerebellum and may reach the internal capsule and the thalamus, regardless the etiology 1,3 . The reason for this tropism is unknown, but recent findings suggest that cellular and histochemical specificities, such as vascular permeability and the presence of other electrolytes (iron, zinc and magnesium), may contribute to the process [3][4][5] .…”

Section: Introductionmentioning

confidence: 99%

“…The reason for this tropism is unknown, but recent findings suggest that cellular and histochemical specificities, such as vascular permeability and the presence of other electrolytes (iron, zinc and magnesium), may contribute to the process [3][4][5] . CC development is slow and may remain asymptomatic for long periods of time 3,4 .…”

Section: Introductionmentioning

confidence: 99%

“…Pathologies most statistically associated to CC are calcium and phosphorus metabolic disturbances (endocrinopathies and genetic syndromes) 3,4 . Even though uncommon, hypoparathyroidism is a possible cause of severe psychiatric disturbances, whether these be related or not to CC 5 .…”

Section: Introductionmentioning

confidence: 99%

“…Parathormone (PTH) deficiency results in a reduction in serum calcium levels and an increase in serum phosphate levels, thus producing mineral deposits in the skin, retina and cerebrum 1 . Clinical symptoms of calcium imbalance previously demonstrated include: tetany, Chvostek sing (facial muscle cramps), laryngeal stridor, muscle stiffness, movement disturbances (freezing), and seizures [1][2][3][4][5] . The last of which may be the only manifestation of this condition 1 .…”

Section: Introductionmentioning

confidence: 99%

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Cerebral calcifications and schizophreniform disorder

Meyer

Jozef²,

Taborda³

et al. 2013

J. bras. psiquiatr.

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objectives: Discuss pathophysiological aspects of cerebral calcifications (CC) and highlight its importance related to the occurrence of neuropsychiatric syndromes. Method: Single case report. result: Man 52 years old, 20 years after going through a total thyroidectomy, starts showing behavioral disturbance (psychotic syndrome). He was diagnosed as schizophrenic (paranoid subtype) and submitted to outpatient psychiatric treatment. During a psychiatric admission to evaluate his progressive cognitive and motor deterioration, we identified a dementia syndrome and extensive cerebral calcifications, derived from iatrogenic hypoparathyroidism. Conclusion: The calcium and phosphorus disturbances, including hypoparathyroidism, are common causes of CC. Its symptoms can imitate psychiatric disorders and produce serious and permanent cognitive sequelae. The exclusion of organicity is mandatory in any psychiatric investigative diagnosis in order to avoid unfavorable outcomes, such as in the present case report. resUMo objetivos: Discutir aspectos fisiopatológicos das calcificações cerebrais (CC) e ressaltar sua importância na ocorrência de síndromes neuropsiquiátricas. Método: Relato de caso individual. resultado: Homem 52 anos de idade, 20 anos após tireoidectomia total, iniciou com alteração comportamental (síndrome psicótica), foi diagnosticado como portador de esquizofrenia paranoide e encaminhado para ambulatório de psiquiatria. Durante internação psiquiátrica, para avaliação de importante deterioração cognitivo e motora, foi verificada a vigência de síndrome demencial e extensas CC, secundários a hipoparatiroidismo iatrogênico. Conclusão: Os distúrbios do metabolismo do cálcio e do fósforo, incluindo o hipoparatiroidismo, são causas frequentes de CC. Seus sintomas podem mimetizar transtornos psiquiátricos e provocar sequelas cognitivas permanentes. A exclusão de organicidade é mandatória durante toda investigação diagnóstica na psiquiatria, a fim de evitar desfechos desfavoráveis, como no presente relato de caso.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Cerebral calcifications and schizophreniform disorder

Meyer

Jozef²,

Taborda³

et al. 2013

J. bras. psiquiatr.

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The risk of myocardial infarction and pharmacologic and nonpharmacologic myocardial infarction predictors in rheumatoid arthritis: A cohort and nested case–control analysis

Wolfe¹,

Michaud²

2008

Arthritis & Rheumatism

150

103

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Objective. To determine the risk of myocardial infarction (MI) in patients with rheumatoid arthritis (RA) compared with that in patients with noninflammatory rheumatic disorders and to determine risk factors for MI in RA, the relationship between cardiovascular risk factors and corticosteroid use, and the relationship between RA treatment and MI.Methods. We conducted a cohort study of MI in 17,738 patients with RA and 3,001 patients with noninflammatory rheumatic disorders who were assessed at 6-month intervals between 1999 and July 2006. We evaluated treatment effect in a nested case-control study of RA participants who were matched by age, sex, study duration, and date of study entry.Results. The covariate-adjusted risk of first MI in RA versus that in noninflammatory rheumatic disorders was 1.9 (95% confidence interval 1.2-2.9) (P ‫؍‬ 0.005). In RA, MI was predicted by age, sex, education level, hypertension, smoking, exercise, prior MI, diabetes, a comorbidity index, use of low-dose aspirin and antilipemic agents, RA severity and treatment variables, and corticosteroid use. Except for obesity, predictors were of equal strength in RA and noninflammatory rheumatic disorders. The increased risk for MI in RA compared with that in noninflammatory rheumatic disorders lessened when corticosteroid users were excluded. Use of corticosteroids was associated with future development of diabetes and hypertension.Conclusion. MI in RA is associated with demographic and cardiovascular risk factors and corticosteroid use. Study data support the hypothesis that RA activity causes MI and that corticosteroids are primarily a marker of RA activity. However, corticosteroids increase the risk of diabetes and hypertension and contribute to the overall risk of MI.The risk of ischemic heart disease is substantially increased in rheumatoid arthritis (RA). Recent large epidemiologic studies have provided quantitative evidence of the association between RA and the risk of myocardial infarction (MI). The relative risk of MI was 2.0 (95% confidence interval [95% CI] 1.2-3.3) in the 2003 Women's Health Study (1), 1.9 (95% CI 1.7-2.1) in a 2006 report from a British Columbia population registry (2), 1.8 (1.2-2.4) in a community registry (3), and 1.5 (95% CI 1.2-1.8) in the UK-based General Practice Research Database (4). Older studies, including those using different study designs, have shown the risk to range from 1.1 to 5.2 (5). The mechanism by which RA exerts its effect is not clear, but it has been suggested to be independent of traditional cardiovascular risk factors (5,6).Baseline demographic and cardiovascular risk factors have been compared in patients who subsequently developed MI (7). However, no epidemiologic studies of MI risk are available that include a wide range

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