A naturalistic study of methylphenidate in the treatment of negative symptoms in dementias

Galynker, Igor; Ieronimo, C.; Rosenblum, Jennifer; Miner, C.; Rosenthal, Richard N.

doi:10.1016/0006-3223(95)94620-c

Cited by 26 publications

(41 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is possible that the apparent inconsistencybetween the present results and those in studies that have found that MPH improved memory in humans (Aman et al, 1991;Camp-Bruno & Herting, 1994;Galynker et al, 1997;Mehta et al, 2000;Rapport et al, 1993) is due to species differences between samples. However, the dopaminergic systems of pigeons and mammals are highly similar (Karle, Anderson, Medina, & Reiner, 1996), and the neostriatum caudolaterale of pigeons is believed to be equivalent to the mammalian prefrontal cortex (Hartmann & Gunturkun, 1998), an area that is involved in memory, attention, and the effects of MPH (Mehta et al, 2000;Puumala & Sirvio, 1998;Ragozzino, 2000).…”

Section: Discussioncontrasting

confidence: 86%

“…However, experimental results have been equivocal. Galynker et al (1997) found that MPH (10-20 mg/day) improved the scores of 12 patients with AD and 15 with vascular dementia on the Mini-Mental State Examination, which assesses a variety of cognitive functions, including recall of recently presented words (Folstein, Folstein, & McHugh, 1975). However, this improvement was not statistically significant for the AD patients when the results of the two groups were analyzed separately.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effects of methylphenidate on working memory in pigeons

Wright

White

2003

Cognitive, Affective, & Behavioral Neuroscience

View full text Add to dashboard Cite

To assess the effects of methylphenidate on working memory, pigeons were trained in a delayed matching-to-sample task. Delay interval duration (0.2, 1, 3, 6, or 12 sec) was varied within sessions in order to separate delay-dependent from delay-independent effects of the drug on performance. A reduction in the sample response requirement from five responses to one response effectively reduced attention to the stimulus and impaired overall accuracy. Methylphenidate was administered in doses of 0.0 (saline control), 0.25, 2.5, and 10 mg/kg. Relative to performance with saline, accuracy was significantly reduced with 10 mg/kg methylphenidate to the same extent in both fixed ratio (FR) 1 and FR 5 conditions. The smaller doses had no effect, and there was no evidence that accuracy improved with drug administration. Intercepts and slopes of exponential functions fitted to measures of discriminability plotted as a function of delay showed that methylphenidate affected delay-independent aspects of performance (initial discriminability), but not delay-dependent aspects (rate of forgetting).

show abstract

Section: Discussioncontrasting

confidence: 86%

mentioning

confidence: 99%

Effects of methylphenidate on working memory in pigeons

Wright

White

2003

Cognitive, Affective, & Behavioral Neuroscience

View full text Add to dashboard Cite

show abstract

“…deprived of appropriate dopamine signaling, the latter structure becomes deficient in extracting the most appropriate response to be executed from intersected fronto-striatal circuits, Given PFc ventromedial areas are major targets of mesocorticolimbic dopamine projections 116 , and that there is experimental evidence of dopamine local modulation of goal-directed behavior 117 , it is reasonable to hypothesize that enhancement of dopaminergic neurotransmission might improve apathetic symptoms. Indeed, there are anecdotal successful reports using this pharmacological strategy [118][119][120][121] . Accordingly, czernecki and coworkers showed in a recent open label trial that Parkinson's disease patients, submitted to subthalamic nucleus stimulation, had unequivocal improvement in apathetic behavior measures after treatment with dopaminergic agonist 122 .…”

Section: Discussionmentioning

confidence: 99%

Neurobiology of apathy in Alzheimer's disease

Guimarães

Lévy²,

Teixeira

et al. 2008

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

-Apathy is considered the most frequent neuropsychiatric disturbance in dementia and its outcome is generally deleterious. Apathy can be related to a dysfunction of the anatomical-system that supports the generation of voluntary actions, namely the prefrontal cortex and/or the prefrontal-subcortical circuits. In Alzheimer's disease, pathological and neuroimaging data indicate that apathy is likely due to a dysfunction of the medial prefrontal cortex. Accordingly, in this review article, we propose a pathophysiological model to explain apathetic behavior in Alzheimer's disease, combining data from neuroimaging, neuropathology and experimental research on the role of orbito-frontal cortex, anterior cingulate cortex, basal ganglia and dopamine in decision-making neurobiology.Key words: apathy, Alzheimer's disease, decision-making, orbito-frontal cortex, anterior cingulate cortex, basal ganglia, dopamine. Neurobiologia da apatia na doença de alzheimerResumo -Apatia é considerada a alteração neuropsiquiátrica mais freqüente nas demências e suas conseqüências são habitualmente deletérias. Apatia pode ser relacionada à disfunção do sistema anatômico responsável pela geração de ações voluntárias, conhecido com córtex pré-frontal e/ou circuitos pré-frontais-subcorticais. Na doença de Alzheimer, evidências neuropatológicas e de neuroimagem funcional indicam que a apatia é provavelmente decorrente da disfunção do córtex pré-frontal medial. Assim, neste artigo de revisão, apresentamos uma proposta de um modelo fisiopatológico para explicar o comportamento apático na doença de Alzheimer, combinando dados de neuropatologia, neuroimagem e experimentação animal sobre o papel do córtex órbito-frontal, cíngulo anterior, núcleos da base e dopamina na neurobiologia da tomada de decisão.PAlAvrAs-chAve: apatia, doença de Alzheimer, tomada de decisão, córtex órbito-frontal, córtex cingulado anterior, núcleos da base, dopamina.

show abstract

“…1995), bupropion (Corcoran ve ark. 2004) ve metilfenidat (Galynker ve ark. 1997) kullanýlmýþ ve elde edilen sonuçlar farklýlýk göstermiþtir ( Jansen ve ark.…”

Section: öZetunclassified

Amotivational Syndrome Caused by Cannabis Use: A Case Who Improved with Additional Testosterone Combination Treatment

Ekinci¹,

Kural²

2016

J Clin Psy

View full text Add to dashboard Cite

SUMMARYCannabis which is obtained from seeds and dried leaves of the cannabis sativa plant is widely used in the world due to its recreational effect. Epidemiological studies were suggested huge differences among countries in terms of using cannabis at least once. The percentiles of use for countries were determined as 41% in England, 17% in Denmark, 6% in Hungary, and 1.2-4% in Turkey.Lots of studies about cannabis use disorders, clinical classification, and treatment were conducted. However, amotivational syndrome caused by cannabis use is not only a clinically less known phenomenon but also we have limited clinical experience about this syndrome. Amotivational syndrome is a syndrome which is caused by cannabis use and which goes along with the cognitive and emotional dysfunctions such as decrease in energy and motivation, lack of social interaction, apathy, decrease in goal-oriented activities, poor judgement, lack of concentration, and memory problems. In studies, it was shown that clinical symptoms of motivational syndrome such as decrease in motivation and energy in 16-21% of people with cannabis use disorder was observed but motivational syndrome emerges as a clinical phenomenon which has been diagnosed less and we have a few studies about definitive diagnosis and treatment. For treatment, it is recommended that underlying problem should be eliminated and that cannabis use should be stopped.. In this article, a case which had amotivational syndrome caused by cannabis use and which had a recovery in clinical symptoms with the treatment of adding testosterone.Key Words: Cannabis use disorder, amotivational syndrome, testosteron, treatment ÖZET Esrar, cannabis sativa adlý bitkinin tohumlarýndan ve kurutulmuþ yapraklarýndan elde edilir, keyif verici etkisi nedeniyle dünyada yaygýn olarak kullanýlmaktadýr. Yapýlan epidemiyolojik çalýþmalarda, en az bir kez esrar kullanýmý ülkeler arasýnda büyük farklýlýklar göstermekte-dir. Ýngiltere'de %41, Danimarka %17, Macaristan %6, Türkiye'de %1.2-4 kullaným oranlarý belirlenmiþtir. Esrar kullaným bozukluklarýnýn, klinik sýnýflandýrýlmasý ve tedavisiyle ilgili bir çok çalýþma yapýlmýþtýr. Esrar kullanýmýna baðlý geliþen amotivasyonel sendrom ise klinik olarak az bilinmekte ve tedavisi ile ilgili günümüzde çok az klinik çalýþma bulunmaktadýr. Amotivasyonel sendrom, kronik esrar kullanýmý ile ortaya çýkan; enerjide azalma, motivasyon düþüklüðü, sosyal etkileþimsizlik, duygulanýmda küntleþme, amaca yönelik aktivitelerde azalma, zayýf muhakeme, konsantrasyon eksikliði, bellek kusuru gibi biliþsel ve duygusal fonksiyonlarda bozulmayla seyreden bir sendromdur.Yapýlan çalýþmalarda, kronik esrar kullaným bozukluðu olanlarda, motivasyon düþüklüðü, enerji azlýðý gibi amotivasyonel sendrom klinik belirtileri %16-21 oranýnda görülmekte buna raðmen amotivasyonel sendrom, az taný konulan, ayrýcý tanýsý ve tedavisi konusunda çok az çalýþmalarýn olduðu bir klinik tablo olarak karþýmýza çýk-maktadýr. Tedavisinde, öncelikle altta yatan nedenin ortadan kaldýrýlmasý, esrar kullanýmý varsa b...

show abstract

A naturalistic study of methylphenidate in the treatment of negative symptoms in dementias

Cited by 26 publications

References 0 publications

Effects of methylphenidate on working memory in pigeons

Effects of methylphenidate on working memory in pigeons

Neurobiology of apathy in Alzheimer's disease

Amotivational Syndrome Caused by Cannabis Use: A Case Who Improved with Additional Testosterone Combination Treatment

Contact Info

Product

Resources

About