Study of the Excitability Cycle of the Blink Reflex in Huntington’s Chorea

Caraceni, T.; Avanzini, G.; Spreafico, Roberto; Negri, S.; Broggi, G.; Girotti, F.

doi:10.1159/000114774

Cited by 44 publications

(18 citation statements)

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“…By considering the whole group of HC patients, we have not found an increased R2 habituation, as reported previously by other authors (1)(2)(3). Our impression is that in this regard the HC patients are not homogeneous.…”

Section: Discussionsupporting

confidence: 82%

Correlation between facial involuntary movements and abnormalities of blink and corneal reflexes in Huntington's chorea

Agostino¹,

Berardelli²,

Cruccu³

et al. 1988

Movement Disorders

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Blink and corneal reflexes were studied in 11 patients with Huntington's chorea and the results compared with the severity of the disease. The latency of the R2 component of the blink reflex was delayed and the duration of R2 and of the corneal reflex (CR) prolonged. A greater habituation of the R2 component was found in the patients with involuntary movements in the face, and in some patients a long-lasting depression of R2 was present. A correlation was found between: (a) severity of involuntary face movements and R2 and CR latency and (b) severity of involuntary movements in the neck and latency of R2.

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Section: Discussionsupporting

confidence: 82%

Correlation between facial involuntary movements and abnormalities of blink and corneal reflexes in Huntington's chorea

Agostino¹,

Berardelli²,

Cruccu³

et al. 1988

Movement Disorders

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“…Changes in excitability of the trigeminofacial reflex in extrapyramidal diseases have been hypothesized to be related to a presynaptic damage [21]. Our data suggest an im portant role for the postsynaptic mechanism too.…”

Section: Discussionmentioning

confidence: 51%

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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“…This reduction in nigro-collicular inhibition should increase collicular activity. As predicted from the superior colliculus microstimulation experiment and the SNr muscimol experiment, patients with Huntington's disease typically exhibit hypoexcitable reflex blinks (Esteban and Giminez-Roldan, 1975;Caraceni et al, 1976). Thus, increasing inhibition of the superior colliculus enhances reflex blink excitability, whereas decreasing inhibition of the superior colliculus reduces reflex blink excitability.…”

Section: Discussionmentioning

confidence: 95%

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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Study of the Excitability Cycle of the Blink Reflex in Huntington’s Chorea

Cited by 44 publications

References 0 publications

Correlation between facial involuntary movements and abnormalities of blink and corneal reflexes in Huntington's chorea

Correlation between facial involuntary movements and abnormalities of blink and corneal reflexes in Huntington's chorea

Effects of Lisuride on Blink Reflex Habituation in Parkinson Disease

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

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