Impairment of central motor conduction in diabetic patients

Abbruzzese, Giovanni; Schenone, Angelo; Scramuzza, G; Caponnetto, Claudia; Gasparetto, B.; Adezati, L; Abbruzzese, M.; Viviani, Giorgio Luciano

doi:10.1016/0168-5597(93)90073-x

Cited by 39 publications

(27 citation statements)

References 22 publications

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“…We report that a short duration (8 weeks) of sustained hyperglycemia/hypoinsulinemia produced a marked attenuation of cerebral corticalϪevoked forelimb motor responses with a significant reduction of motor area topography. This novel finding is consistent with previous reports of decreased hippocampal synaptic plasticity (19,20) and disruption of neuronal function (6,7,21,22) in diabetes. This study extends these observations and suggests that dysregulation of central glucose and insulin in patients with poorly controlled diabetes may result in altered cerebral corticospinal motor function.…”

supporting

confidence: 82%

“…Subtle neuropsychological deficits observed in some children with type 1 diabetes have raised reasonable concerns about the effect this disease may have on cognitive development in school-age children (31,32). Mental and motor slowing have also been reported among both type 1 and type 2 adult diabetic subjects (33)(34)(35), and impaired central motor conduction, assessed by magnetic stimulation, in diabetic patients has been described (6,7). CNS motor systems appear uniquely sensitive to the effects of poorly controlled diabetes.…”

Section: Discussionmentioning

confidence: 99%

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Experimental Diabetes Attenuates Cerebral Cortical−Evoked Forelimb Motor Responses

et al. 2005

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Poorly controlled diabetes leads to debilitating peripheral complications, including retinopathy, nephropathy, and neuropathy. Chronic diabetes also impairs the central nervous system (CNS), leading to measurable deficits in cognition, somatosensory, and motor function. The cause of diabetes-associated CNS impairment is unknown. In this study, sustained hyperglycemia resulting from insulin deficiency was shown to contribute to CNS motor dysfunction. Experimental diabetes was induced in rats by streptozotocin (STZ) injection. CNS motor function was assessed by intracortical microstimulation of the sensorimotor cortex. Experimental diabetes significantly (P < 0.01; n ‫؍‬ 14) attenuated the number of motor cortical sites eliciting forelimb movements. The net area of the motor cortex representing the forelimb in diabetic rats was significantly reduced

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supporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Experimental Diabetes Attenuates Cerebral Cortical−Evoked Forelimb Motor Responses

et al. 2005

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“…The bar indicates the interval when no CMAP was obtained. *p < 0.05, **p < 0.01 cent studies of the central motor pathways in diabetic patients [3,19]. In contrast to the present study both these studies reported a prolonged CMCT in diabetic patients.…”

Section: Discussioncontrasting

confidence: 55%

“…These conflicting results may be ascribed to heterogeneity in type and duration of diabetes, and to a different frequency of renal complications in the study populations. The diabetic population in the studies by Abbruzzese et al [3] and Tchen et al [19] differed in several ways from the diabetic population in this study. The major differences were that about two-thirds of the patients had NIDDM, the mean age was higher and in the study by Abbruzzese et al more than 15 % had signs of nephropathy while Tchen et al did not report the prevalence of renal complications in the diabetic group.…”

Section: Discussioncontrasting

confidence: 50%

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Motor pathway function in normoalbuminuric IDDM patients

et al. 1995

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Summary Central motor pathways were studied in 17 normoalbuminuric insulin-dependent diabetic (IDDM) patients who had been diabetic for more than 20 years, and compared with findings in 17 age-, sex-, and height-matched control subjects. The central motor conduction time was calculated from recordings of the compound muscle action potentials of the abductor pollicis brevis muscle after single transcranial and spinal root magnetic stimulation. The central motor conduction time from motor cortex to cervical spinal roots was 9.8 + 1.65 ms in diabetic patients and 10.1 + 1.48 ms in control subjects. In diabetic patients with neuropathy the central motor conduction time was 9.5 + 1.76 ms vs 10.1 + 1.56 ms in patients without neuropathy. The excitability of the motor pathways was studied by paired transcranial magnetic stimulation at interstimulation intervals of 30-1000 ms. In normal control subjects, an early facilitation of the amplitude of the compound muscle action potential at an interstimulation interval of 30 ms was found, while no facilitation was present in diabetic patients. In addition the compound muscle action potential latencies were prolonged at interstimulation intervals of 30-50 ms in diabetic patients. The changes of excitability did not correlate with the presence of peripheral neuropathy, metabolic control or diabetes duration. It is concluded that long-term normoalbuminuric IDDM patients have impaired excitability but normal central conduction time of the motor pathways. [Diabetologia (1995[Diabetologia ( ) 38: 1191[Diabetologia ( -1196 Key words Magnetic stimulation, diabetic neuropathy, motor pathway, paired magnetic stimulation, diabetic encephalopathy.Motor, sensory and autonomic disturbances are concomitants with diabetic neuropathy. Sensory and autonomic dysfunctions have been well-studied and a battery of cutaneous perception threshold tests and autonomic function tests to characterize and monitor the neuropathy have been developed and validated.

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