FACIAL REFLEXES

FACIAL REFLEXES

242 FACIAL REFLEXES SiR,—I was delighted to see the clinical value of the facial reflexes confirmed by Dr. Olof Bynke (Jan. 16, p. 138). In a number o...

127KB Sizes 4 Downloads 144 Views

242 FACIAL REFLEXES SiR,—I was delighted to see the clinical value of the facial reflexes confirmed by Dr. Olof Bynke (Jan. 16, p. 138). In a number of publications I have demonstrated the considerable diagnostic utility of these reflexes. 1-3 By recording electromyographically from the orbicularis muscles on both sides, it is an easy matter to compare the amplitude and latency of the reflex responses on the normal side with those on the abnormal (or suspected abnormal) side. Many afferents converge on the facial motoneurone pool, but, in practice, it has been found that the facial reflexes are most useful in the assessment of Bell’s palsy, lesions of the various sensory components of the trigeminal nerve, lesions of the auditory nerve, and upper-motoneurone

lesions, including parkinsonism. A light touch to the cornea results only in a late reflex, but the normal reflex to glabella tap, or to sudden stretch of the orbicularis oculi, for example, has two components, an early synchronous reflex not subject to habituation, and a later asynchronous reflex which usually habituates after four or five elicitations. Following an upper-motoneurone lesion affecting the face, the first component is greatly exaggerated ipsilaterally while the second component is small, or even absent. In parkinsonism, the first component is also exaggerated, but the second component is greatly enhanced, and does not habituate on repeated stimulation. The second component is a " nociceptive " reflex, and is responsible for the actual closure of the eyelids. The first component of the reflex is too brief to produce actual lid-closure. These reflexes can also be produced by electrical stimulation of the supraorbital or infraorbital nerves, and it is then clear that the first component has a low electrical threshold and is ipsilateral, while the second component has a higher electrical threshold and is bilateral. Kugelbergshowed that the first component depended on afferents within the trigeminal nerve, and it seemed likely, from the method of elicitation and from the brief and more or less constant latency of the reflex, that it was a stretch reflex-a monosynaptic reflex of the brainstem. Dr. Bynke’s measurement of the central latency of this reflex during neurosurgical operations also points to its monosynaptic nature. Dr. W. F. Brown and I are currently studying this reflex in single facial motor units, with a view to establishing this. If the first component is a stretch reflex, this raises the question of the site and nature of the end-organs responsible. In reviewing this problem in 1966,5 I came down in favour of muscle spindles within the facial muscles themselves ; but muscle spindles, or other sensory endings, have not yet been demonstrated histologically in facial musculature, except, possibly, in the rabbit and the rat.6 Shahani and Youngargued that the first component of the blink reflex was of cutaneous origin. It is, of course, very difficult to stimulate, separately, the facial skin and the facial musculature, either mechanically or electrically. The first component has, however, many features of a stretch reflex, including its short central and peripheral latency, its and stability, and its exaggeration following upper-motoneurone lesions, but its afferents appear to be contained within the supraorbital and infraorbital nerves-

synchrony

usually regarded as cutaneous nerves. Whatever problems remain about the anatomical basis of some facial reflexes, they play a large part in this laboraRushworth, G. J. Neurol. Neurosurg. Psychiat. 1962, 25, 93. Rushworth, G. Trans. Ophthal. Soc. 1962, 82, 549. Rushworth, G. Electromyography, 1968, 8, 349. Kugelberg, Brain, 1952, 75, 385. Rushworth, G. in Control and Innervation of Skeletal Muscle (edited by B. L. Andrew). St. Andrews, 1966. 6. Bowden, R. E. M., Mahran, Z. Y. J. Anat. 1956, 90, 217. 7. Shahani, B., Young, R. R. J. Physiol., Lond. 1968, 198, 103p. 1. 2. 3. 4. 5.

tory in the electrophysiological diagnosis and assessment of certain upper-motoneurone lesions, including parkinsonism, as well as lesions within the brainstem and cranial nerves.

Unit of Clinical Neurophysiology, Churchill Hospital, Oxford.

GEOFFREY RUSHWORTH.

BLOOD FIBRINOLYTIC ACTIVITY IN DEEP-VEIN THROMBOSIS

SIR,-We have investigated blood fibrinolytic activity in 20 patients with deep-vein thrombosis of the lower limbs. 7 of the patients had had recurrent episodes of the disease,

and all of them had had at least three such episodes in the preceding two years. In the remaining 13 patients the diagnosis was confirmed either by lower-limb venography or by an ultrasonic doppler technique,l but (owing to lack of facilities) this could not be done in the 7 patients first mentioned.

Blood fibrinolytic activity in patients with deep-vein thrombosis.

On estimation by the euglobulin-lysis-time (E.L.T.) method, using an E.L.T. recorder,2the fibrinolytic activity in the 20 patients was found to be decreased when compared with age and sex matched normal controls (see accompanying figure). It was further shown that this activity was less in patients with recurrent deep-vein thrombosis than in patients who had had only one episode of the condition. It is suggested

that, at least in patients who have redeep-vein thrombosis, treatment with phenformin and ethylcestrenol, which increases blood fibrinolytic activity,3.4 may prove beneficial. We have achieved good current

1. 2. 3.

Evans, D. S., Cockett, F. B. Br. med. J. 1969, ii, 802. Menon, I. S., Martin, A., Weightman, D. Lab. Pract. 1969, 18, 1186. Fearnley, G. R., Chakrabarti, R., Hocking, E. D. Lancet, 1967, ii.

4.

Menon, I. S., Dewar, H. A. in Clinical and Physiological Aspects Fibrinolysis. London (in the press).

1008. of