Hyperthermia and Chronic Pancerebellar Syndrome After Cocaine Abuse

Tanvetyanon, Tawee; Dissin, Jonathan; Selcer, Uzi M.

doi:10.1001/archinte.161.4.608

Cited by 9 publications

(1 citation statement)

References 15 publications

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“…Chronic cocaine consumption leads to a decrease in dopamine and norepinephrine binding in the dorsal striatum of non-human primates (Porrino et al, 2004) – a critical motor control hub, which receives input from the premotor cortex and sends information to the motor cortex via the thalamus. Although there are few large studies of motor control in chronic cocaine users, many smaller studies have demonstrated that chronic stimulant use is related to extrapyramidal symptoms – including tics, dystonia, and dyskinesia (Bauer, 1996; Pascual-Leone and Dhuna, 1990; Tanvetyanon et al, 2001; Preller et al, 2013). …”

Section: Introductionmentioning

confidence: 99%

A comprehensive study of sensorimotor cortex excitability in chronic cocaine users: Integrating TMS and functional MRI data

Hanlon

DeVries

Dowdle

et al. 2015

Drug and Alcohol Dependence

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Background Disruptions in motor control are often overlooked features of chronic cocaine users. During a simple sensorimotor integration task, for example, cocaine users activate a larger area of cortex than controls but have lower functional connectivity between the cortex and dorsal striatum, which is further correlated with poor performance. The purpose of this study was to determine whether abnormal cortical excitability in cocaine users was related to disrupted inhibitory or excitatory mechanisms, as measured by transcranial magnetic stimulation (TMS). Methods A battery of TMS measures were acquired from 87 individuals (50 cocaine dependent, 37 controls). Functional MRI data were acquired from a subset of 28 individuals who performed a block-design finger tapping task. Results TMS measures revealed that cocaine users had significantly higher resting motor thresholds and higher intracortical cortical facilitation (ICF) than controls. There was no between-group difference in either measure of cortical inhibition. Task-evoked BOLD signal in the motor cortex was significantly correlated with ICF in the cocaine users. There was no significant difference in brain-skull distance between groups. Conclusion These data demonstrated that cocaine users have disrupted cortical facilitation (as measured with TMS), which is related to elevated BOLD signal. Cortical inhibition, however, is largely intact. Given the relationship between ICF and glutamatergic agents, this may be a potentially fruitful and treatable target in addiction. Finally, among controls the distance from the scalp to the cortex was correlated with the motor threshold which may be a useful parameter to integrate into therapeutic TMS protocols in the future.

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