Early detection of Huntington's disease. Blink reflex and levodopa load in presymptomatic and incipient subjects.

Esteban, Ángel; Mateo, D; Giménez-Roldán, S

doi:10.1136/jnnp.44.1.43

Cited by 26 publications

(15 citation statements)

References 9 publications

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“…First, blocking the excessive GABAergic inhibition of the superior colliculus of 6-OHDA-lesioned animals with a GABA antagonist, bicuculline, virtually eliminated reflex blink hyperexcitability. The GABA blockade of the superior colliculus exerted its strongest effect on the long-latency R2 component of the blink, the component most profoundly altered in experimental animals with dopamine depletion and in humans with Parkinson's disease (Pearce et al, 1968;Penders and Delwaide, 1971;Messina et al, 1972;Kimura, 1973;Esteban et al, 1981;Caliguiri et al, 1987;Masumoto et al, 1992). Second, reducing the inhibitory output of the nigro-collicular pathway by microinjecting the GABA agonist muscimol into the SNr decreased reflex blink amplitude of the long-latency R2 component in normal rats.…”

Section: Discussionmentioning

confidence: 99%

“…For example, lesions of the ascending dopaminergic pathway with 6-hydroxydopamine (6-OHDA) dramatically increase excitability and reduce habituation of the blink reflex in rats (Shallert et al, 1989;Basso et al, 1993). Similar increases in reflex blink excitability and loss of habituation occur in humans with Parkinson's disease (Pearce et al, 1968;Penders and Delwaide, 1971;Messina et al, 1972;Kimura, 1973;Esteban et al, 1981;Caliguiri et al, 1987;Masumoto et al, 1992).…”

Section: Abstract: Parkinson's Disease; Blink Reflex; 6-hydroxydopammentioning

confidence: 99%

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An Explanation for Reflex Blink Hyperexcitability in Parkinson’s Disease. I. Superior Colliculus

Basso¹,

1996

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Hyperexcitable reflex blinks are a cardinal sign of Parkinson's disease. We investigated the neural circuit through which a loss of dopamine in the substantia nigra pars compacta (SNc) leads to increased reflex blink excitability. Through its inhibitory inputs to the thalamus, the basal ganglia could modulate the brainstem reflex blink circuits via descending cortical projections. Alternatively, with its inhibitory input to the superior colliculus, the basal ganglia could regulate brainstem reflex blink circuits via tecto-reticular projections. Our study demonstrated that the basal ganglia utilizes its GABAergic input to the superior colliculus to modulate reflex blinks. In rats with previous unilateral 6-hydroxydopamine (6-OHDA) lesions of the dopamine neurons of the SNc, we found that microinjections of bicuculline, a GABA antagonist, into the superior colliculus of both alert and anesthetized rats eliminated the reflex blink hyperexcitability associated with dopamine depletion. In normal, alert rats, decreasing the basal ganglia output to the superior colliculus by injecting muscimol, a GABA agonist, into the substantia nigra pars reticulata (SNr) markedly reduced blink amplitude. Finally, brief trains of microstimulation to the superior colliculus reduced blink amplitude. Histological analysis revealed that effective muscimol microinjection and microstimulation sites in the superior colliculus overlapped the nigrotectal projection from the basal ganglia. These data support models of Parkinsonian symtomatology that rely on changes in the inhibitory drive from basal ganglia output structures. Moreover, they support a model of Parkinsonian reflex blink hyperexcitability in which the SNr-SC target projection is critical.

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Section: Discussionmentioning

confidence: 99%

Section: Abstract: Parkinson's Disease; Blink Reflex; 6-hydroxydopammentioning

confidence: 99%

An Explanation for Reflex Blink Hyperexcitability in Parkinson’s Disease. I. Superior Colliculus

Basso¹,

1996

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“…The dopaminergic properties of lisuride have been clearly established [10,12] as well as its antiparkinsonian efficacy related to a specific interaction with the D2 receptors [12][13][14], An involvement of these receptors has been hypothesized to explain clinical im provement in Huntington's chorea (HC) after acute administration of lisuride [17]. The habituation of the blink reflex in HC is en hanced [18] and this electrophysiological alteration can be worsened by L-dopa admin istration, probably in relation to a hypersen sitivity versus overinhibition of dopaminer gic receptors at the striatum level [19], These data suggest that D2 receptors may have an important role in blink reflex habit uation. Therefore, a cortical role in blink reflex habituation has been supposed by dif ferent authors [5,17,20] and D2 receptors are preferably located on axon of descending corticostriatal trait [13].…”

Section: Discussionmentioning

confidence: 99%

Effects of Lisuride on Blink Reflex Habituation in Parkinson Disease

et al. 1985

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The blink reflex presents a tendency to habituation (a gradual diminution of the amplitude of the response during repetitive stimulation). Electromyographic analysis of this reflex makes it possible to quantify this phenomenon. A lack of the habituation of the blink reflex is a typical feature of Parkinson disease. L-Dopa and amantadine, but not anticholinergic drugs, are able to partly reverse these abnormalities in blink reflex habituation to a normal pattern. Lisuride, a dopamine agonist with serotoninergic activity, has been recently proposed as antiparkinsonian agent. In our study we observed that lisuride has a positive effect on blink reflex habituation in Parkinson disease. A good correlation between the improvement of this electrophysiological parameter and clinical akinesia was seen. Mechanisms underlying the therapeutic effect of lisuride are complex, but this drug usually has a postsynaptic effect on D₂receptors. Our data suggest that these receptors play an important role in blink reflex habituation.

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“…[2,[9][10][11] However, the onset of disease is only clear after a collection of symptoms become apparent and unambiguous, so early diagnosis is delayed with these physical tests. Any single behavioral change is not necessarily related to the onset of HD.…”

Section: Introductionmentioning

confidence: 99%

Raman spectroscopy of fibroblast cells from a Huntington's disease patient

Tsikritsis

Elfick

Downes

2016

Spectroscopy Letters

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We present a Raman spectroscopy case study of living fibroblast (skin) cells from a patient who developed Huntington's disease, with fibroblasts from a healthy volunteer as a control. Spectra were processed to remove cosmic rays, had a spectrum of the quartz substrate subtracted, and were flattened to remove cellular autofluorescence. We achieved an accuracy of 95% in discriminating individual cells, and assign spectral differences to (i) the reduction of cholesterol, (ii) the reduction of lipids, and (iii) an increase in beta-sheet proteins for fibroblasts with Huntington's disease. All these biochemical changes have been previously measured by other methods. Averages over all the cells in this study yield a difference which is extremely statistically significant [p < 0.0001]. ARTICLE HISTORY

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Early detection of Huntington's disease. Blink reflex and levodopa load in presymptomatic and incipient subjects.

Cited by 26 publications

References 9 publications

An Explanation for Reflex Blink Hyperexcitability in Parkinson’s Disease. I. Superior Colliculus

An Explanation for Reflex Blink Hyperexcitability in Parkinson’s Disease. I. Superior Colliculus

Effects of Lisuride on Blink Reflex Habituation in Parkinson Disease

Raman spectroscopy of fibroblast cells from a Huntington's disease patient

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