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The menace reflex
  1. Wouter J C van Ballegoij1,
  2. Peter J Koehler2,
  3. Bastiaan C Ter Meulen1,3
  1. 1Department of Neurology, St. Lucas Andreas Hospital, Amsterdam, The Netherlands
  2. 2Department of Neurology, Atrium Medical Center, Heerlen, The Netherlands
  3. 3Department of Neurology, Zaans Medisch Centrum, Zaandam, The Netherlands
  1. Correspondence to Wouter JC van Ballegoij, Department of Neurology, St. Lucas Andreas Hospital, Jan Tooropstraat 164, Amsterdam 1061AE, The Netherlands; w.vanballegoij{at}slaz.nl

Abstract

The menace reflex (blink reflex to visual threat) tests visual processing at the bedside in patients who cannot participate in normal visual field testing. We reviewed a collection of recently discovered historical movies showing the experiments of the Dutch physiologist Gysbertus Rademaker (1887–1957), exploring the anatomy of this reflex by making cerebral lesions in dogs. The experiments show not only that the menace reflex is cortically mediated, but also that lesions outside the visual cortex can abolish the reflex. Therefore, although often erroneously used in this way, an absent menace does not always indicate a visual field deficit.

  • Blink reflex
  • Menace reflex
  • Hemianopia
  • Rademaker
  • Garcin

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Introduction

The menace reflex (blink reflex to visual threat) is a frequently used bedside method for testing visual processing. In response to a sudden lateral movement directed towards the eyes, a person momentarily closes the eyelids. Despite the common use of this reflex in clinical practice, many clinicians are unfamiliar with its underlying physiology; this complicates the interpretation. Here, we briefly overview the menace reflex, including the early research, physiology and implications for its clinical use.

History

Gysbertus Rademaker (1887–1957), the Dutch professor of physiology (1929) and neurology (1945), was among the first to investigate the menace reflex in the 1920s and 1930s. He subsequently worked at the Universities of Utrecht and Leyden, performing operations on animals (pigeons, rabbits, cats, dogs and monkeys) to study the anatomical structures involved in various neurophysiological processes.1 A collection of 115 films showing these experiments, previously thought to be lost, was recently found. Due to the fire hazard of the highly inflammable cellulose-nitrate material of these films, they had been stored for decades in an old bunker in the dunes near The Hague. The films have been digitalised and one of us (PJK) has reviewed them. Most of the films address the physiology of body posture and show the results of experimental labyrinthectomies, cerebellectomies and brainstem sections. We found seven films concerning experiments on the visual system and optic reactions, including the menace reflex.2

At the time of these experiments, the afferent part (comprising the retina, optic nerve and optic tract up to the lateral geniculate body) and the efferent part (comprising the facial nerve and orbicularis oculi muscles) of the menace reflex were already known. However, the central pathways between these had not been defined. In the films, we see how various cerebral lesions in dogs affect the menace reflex (figure 1, see online supplementary video), implying that these areas form part of the reflex arc. As might be expected, Rademaker found that lesions to the visual cortex in the occipital lobe abolished the menace reflex. Interestingly though, cortical lesions outside the occipital lobe also resulted in an absent menace reflex.

Figure 1

(A) Blink reflexes to visual threat after removal of the left occipital cortex in a dog. The reflex is present when stimulating the left visual field (A), but absent when stimulating the right (B). (Stills from the movie available online.)

Physiology

Multiple stimuli can cause blinking, including hard sounds (cochleopalpebral reflex), sudden exposure to strong light and touching either the cornea (corneal reflex) or eyelids (blink reflex). While these are primitive reflexes with a purely subcortical course, the menace reflex is cortically mediated. This is illustrated by the fact that the reflex is absent in anencephaly (eg, in primitive animals) or after decortication. Even in newborns aged less than 4 months the menace reflex is absent, while the responses to light and corneal stimulation are already present.

Rademaker found various cerebral structures were involved in the menace reflex. He showed that the reflex is absent:

  • after removing parts of the striate area (visual cortex) in the occipital lobe,

  • in lesions of the ‘eyelid region'of the ipsilateral motor cortex (the part of motor cortex that causes closing of the eyelids when electrically stimulated),

  • in lesions of the parietal lobe between the striate area and the motor cortex.

From these observations, he concluded that the reflex arc for the menace reflex after stimulation of the left visual field (and vice versa) is as follows: right half of the retina of both eyes—right optic tract—right lateral geniculate body—right optic radiation—striate cortex in the right occipital lobe—parietal lobe—eyelid region of the right motor cortex—nuclei of the facial nerves—orbicularis oculi muscles (figure 2).

Figure 2

Schematic representation of the reflex arc of the blink reflex to visual threat, as deduced from the animal experiments (adapted from Rademaker and Garcin [3]).

Rademaker confirmed the existence of a similar reflex arc in humans through his observations from the Salpêtrière Neurology Clinic in Paris, cooperating with the French neurologist Raymond Garcin (1897–1971). They studied patients with an absent menace reflex, some of whom underwent surgery (trepanation of the skull). These patients were found to have lesions (meningiomas, tuberculomas, gliomas) in the same locations as the lesions that Rademaker made in his dogs. More recent imaging studies show similar results, with lesions in the occipital lobe, parietal lobe as well as the frontal lobe resulting in an absent menace reflex.4

Clinical implications

When testing the menace reflex in clinical practice, it is important to stand behind the patient so the threat cannot be anticipated. The investigator then suddenly moves a hand from a lateral position into the visual field, minimising sound or air movement into the eye, as this would activate the cochleopalpebral or corneal reflex instead. In a normal reflex, the patient briefly closes both eyelids.

The menace reflex is often used as an alternative to standard visual field testing (confrontation method); for example, in people with aphasia or delirium, since this does not need their cooperation. Although the reflex is absent in hemianopia, Rademaker's studies showed that the converse is not necessarily true—an absent menace reflex is not always caused by a visual field deficit. Lesions in several locations outside the visual cortex can lead to an absent menace reflex, while visual field testing is normal.

Making it more complex, there is debate as to whether the menace reflex is purely a reflex or is a higher order process requiring consciousness and intact mechanisms for visual attention. In a study of 91 patients in the vegetative state (of traumatic and non-traumatic origin), the menace reflex was absent in 45 patients (49%).5 However, it is not clear whether the decreased level of consciousness led to the reflex being absent. These patients might have had a lesion in the visual cortex or somewhere else in the reflex arc of the menace reflex, with the level of consciousness being of no influence. Moreover, the patients in whom the menace reflex was present had no other clinical signs of consciousness, implying that blinking to a visual threat differs from the conscious ‘awareness of a threat’.

The difficulties in interpretation might be why, to our knowledge, there is no literature on the sensitivity and specificity of the menace reflex in relation to visual field deficits. For daily clinical practice, one can use the next rule of thumb: the presence of the menace reflex excludes hemianopia, but its absence is of little localising value does not necessarily imply a visual field deficit.

Acknowledgments

We are grateful to Bas Agterberg (Institute for Sound and Vision, Hilversum, The Netherlands) for providing the pertinent digitalised films.

References

Supplementary materials

  • Supplementary Data

    This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.

    Files in this Data Supplement:

Footnotes

  • Contributors WJCvB was the lead writer of the article. PJK analysed the historical video material and selected relevant parts. PJK and BCTM assisted in writing the article.

  • Competing interests None.

  • Provenance and peer review Not commissioned. Externally peer reviewed. This paper was reviewed by Christian Lueck, Canberra, Australia.

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