You are better off running than walking with acute vestibulopathy

You are better off running than walking with acute vestibulopathy

You are better off running than walking with acute vestibulopathy T Brandt, M Strupp, J Benson Patients with acute vestibular disorder balance better ...

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You are better off running than walking with acute vestibulopathy T Brandt, M Strupp, J Benson Patients with acute vestibular disorder balance better when running than when standing or walking slowly. We suggest that the automatic spinal locomotor programme suppresses destabilising vestibular input.

With acute unilateral vestibular failure, there is rotational vertigo, spontaneous horizontal-rotatory nystagmus away from the affected side, and postural imbalance with falls toward the affected side. The most common cause is vestibular neuritis. Slow motion is commonly believed much safer for these patients than fast motion; however, a chance observation of a dog with acute left unilateral vestibular failure (figure 1) suggested that running is safer. On waking one day, Tessa had a severe postural imbalance when standing still, and head movements caused falls to the left. When walking slowly, she veered to the left, staggering about in counterclockwise circles, and fell repeatedly. Surprisingly, once she was outside and began to run, she was able to follow her chosen course and obviously felt more confident as her raised, wagging tail indicated. As soon as she stopped trotting and began to slowly walk, she again showed severe imbalance. This observation prompted us to video record the balance during running and walking of patients with acute unilateral vestibulopathy and healthy volunteers with a post-rotatory transient vestibular tone imbalance. Four patients (all women, aged 57 to 67 years) had a confirmed Figure 1: The golden retriever, diagnosis of vestibular Tessa, with acute left neuritis. 3 to 5 days after labyrinthine failure the onset of the condition, Her head is tilted to the left and a few degrees of vertical divergence of the they were requested to eyes with right-over-left hypertropia close their eyes and slowly (ocular tilt reaction). There was a walk or run 10 m through spontaneous torsional nystagmus a 2·5 m wide corridor. All beating counterclockwise to the right and upward. four patients had gait deviation toward the affected ear when trying to slowly walk straight ahead. All touched the wall for support two to four times during the 10 m stretch. By contrast, when running slowly, they maintained their direction for over 10 m and felt much more secure. Increased walking speed also had a clearly stabilising influence on their balance. Ten blindfolded, healthy physical therapists (five women; mean age 26·5 [SD 3·7] years) were suddenly stopped after ten rotations in a chair at a constant angular velocity of 360°/s. They were then asked to either walk slowly or run straight ahead for 10 m. There was a mean deviation when they walked of 52·6 (12·4)° over 10 m (figure 2). By contrast, the mean deviation was 14·6 (9·2)° when they ran. The volunteers also felt it was easier to maintain their balance while running. Balance during locomotion requires that the input of the vestibular system in the head be integrated with the somatosensory input from the feet. However, locomotion can also be achieved solely by spinal cord mechanisms. Automatic locomotor patterns have been found in the chronic spinal cat1

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Figure 2: Deviation of gait during running and during walking in volunteers with a transient physiological vestibular tone imbalance Mean deviation when running was 14·6º (SD 9·2) and when walking 52·6º (12·4; paired t-test, p<0·001). Open square=mean; horizontal lines of the boxes=25th, 50th, and 75th percentiles; error bars above and below the boxes=5th and 95th percentiles; crosses=range.

and in paraplegic patients whose body weight was partly unloaded during suspension from a parachute harness connected to an overhead crane while walking on a moving treadmill.2 Such an automatic spinal programme of locomotion would explain our observation that you are better off running than walking with acute vestibulopathy. The programme would inhibit descending vestibular sensory inflow. This is compatible with the recent concept of sensory down-and-up chanelling for multisensory postural control.3 A misleading vestibular signal can thus be suppressed via downand-up chanelling. During walking, monosynaptic stretch reflex responses in the human leg are suppressed and spinal pathways of group I afferents are blocked.4 Moreover, a cortical analogue has been reported in positron emission tomographic studies that showed a reciprocal inhibitory visual-vestibular interaction to be a basic sensorimotor mechanism that ensures adequate self-motion perception.5 Postural control involves a complex of processes that are finetuned by repetition and learning. How they interact is determined not only by the pattern of actual motion stimulation, but also by the particular postural and locomotor task. It makes sense to suppress the vestibular (or somatosensory) input once a highly automatic locomotor pattern has been initiated. These findings may have important consequences for treatment of patients with vestibular disorders. 1

Grillner S. Control of locomotion in bipeds, tretrapeds, and fish. In: Brookhart M, Mountcastle M, eds. Handbook of physiology. The nervous system II. Washington DC: American Physiological Society, 1981: 1179–235. 2 Dietz V, Colombo G, Jensen L. Locomotor activity in spinal man. Lancet 1994; 344: 1260–63. 3 Mergner T, Rosemeier T. Interation of vestibular, somatosensory and visual signal for postural control and motion perception under terrestrial and microgravity conditions—a conceptual model. Brain Res Brain Res Rev 1998; 28: 118–35. 4 Dietz V. Human neuronal control of automatic functional movements: interaction between central programs and afferent input. Physiol Rev 1992; 72: 33–69. 5 Brandt Th, Bartenstein P, Janek A, Dieterich M. Reciprocal inhibitory visual-vestibular interaction. Visual motion stimulation deactivates the parieto-insular vestibular cortex. Brain 1998; 121: 1749–58.

Department of Neurology, Ludwig-Maximilians University of Munich, Klinikum Grosshadern, 81377 Munich, Germany (T Brandt FRCP, M Strupp MD, J Benson MA) Correspondence to: Dr T Brandt (e-mail: [email protected])

THE LANCET • Vol 354 • August 28, 1999