The experiments were designed to test two hypotheses and their corollaries: 1. That adaptation of EMG responses to support surface rotations is due to a decrease in the gain of proprioceptively triggered long-loop stretch reflexes (Nashner 1976), and that the adaptation is dependent on a normally functioning vestibular system (Nashner et al. 1982); 2. That EMG responses to rotations are generated primarily by vestibulo-spinal reflexes triggered by head accelerations (Allum and Pfaltz 1985) and comprise a coactivation of opposing leg muscles (Allum and Büdingen 1979). Adaptation with successive dorsi-flexive rotations of the support surface was investigated in the EMG responses of the ankle muscles, soleus (SOL) and tibialis anterior (TA), as well as the neck muscles, trapezius (TRAP) and splenius capitis (SPLEN CAP), both for normal subjects and for patients with bilateral peripheral vestibular deficit. Both normals and patients who first received the stimulus with their eyes open demonstrated decreasing activation at medium latency (ML), that is, with an onset at about 125 ms, and long latency (LL) responses with an onset ca 200 ms. This was the case for both ankle and neck muscles when the EMG response areas for the first 3 and second 7 of 10 trials were compared. Ankle muscle responses in the patients were diminished in area with respect to normals both with the eyes open and with the eyes closed. Ankle torque recordings from the patients were also smaller in amplitude, and these attenuated differently from normal torque responses. Functional coupling of the opposing ML and LL SOL and TA muscle responses was confirmed by the nearly coincident onset times and significantly correlated EMG response areas. At ML, ankle torque was highly correlated with TA activity when the influence of SOL was controlled. At LL, SOL activity was highly correlated with torque when the influence of TA was controlled. The delay of torque adaptation beyond the period of ML activity in normals, but not in the patients was attributed to the proportionally balanced coactivated muscle patterns producing a consistent force output and level of stability in normals. The results indicate that the adaptation in EMG response amplitudes during a sway stabilisation task is not dependent on a normally functioning vestibular system nor on visual inputs but rather appears to be due to a generalized habituation in the postural control system.(ABSTRACT TRUNCATED AT 400 WORDS)

Vestibular, visual, and proprioceptive influences on muscle activity correcting for backwards body tilt were investigated in normals and patients with bilateral peripheral vestibular deficits. Body tilt was induced by a dorsi-flexion rotation of the feet about the ankle joints while the subject stood on a force measuring platform. Ankle muscle activity and torque were monitored as upright stance was reestablished, and correlated with head angular accelerations and neck muscle activity. In normals with eyes closed, soleus stretch reflex activity at 50-80 ms was followed by two bursts of tibialis anterior (TA) EMG activity at ca 80 and 125 ms from the onset of 36 deg/s, 3 deg amplitude platform rotations. Neck muscle activity rotated the head backwards at the same time as TA activity rotated the body forwards about the ankle joints. Under the influence of vision, i.e. eyes open, slight increases in the second burst of TA activity, and ankle torque were observed. When the subjects sat, and were instructed to activate TA rapidly on onset of the platform movement, TA EMG activity increased gradually at ca. 150 ms and not as a burst. In patients with long-lasting bilateral vestibular deficits, both bursts of TA activity were significantly less than normal with eyes closed. Consequently sway correcting torques were abnormally low and all but one of the patients fell over backwards. With eyes open, TA activity was slightly less than, and ankle torques were approximately equal to normal values. In contrast to normals, TA responses obtained in standing and sitting positions were not significantly different. Neck EMG activity varied from normal, consisting of a long burst 100 ms in duration. The present data indicate that a coordinated pattern of ankle, and neck muscle activity occurs during the first 150 ms following induced backward tilt. Ankle muscle activity corrects for the body sway, and neck muscle activity attempts to stabilise the head with respect to earth fixed coordinates. It is proposed that the vestibulo-spinal reflex system predominantly underlies the genesis and coordination of this muscle activity.

Preoperative and postoperative facial nerve and auditory function were reviewed retrospectively in 13 cases of cerebellopontine angle meningiomas. According to their location within the posterior fossa and with special reference to the internal auditory canal, they were classified into a premeatal and a retromeatal group. All the tumors were removed by an otoneurosurgical team by use of a retrosigmoid approach. Postoperative results (1 year after operation) were compared within the two groups with respect to preservation of hearing (normal hearing in 31% and preservation of preoperative hearing in 69% of the cases) and facial nerve function (no or mild postoperative impairment in 69% of the cases). Both preoperative and postoperative impairment of facial nerve and auditory function prevailed in the premeatal group. For preservation of vital vascular and central nervous structures, subtotal resection with consecutive fractionated radiation therapy had to be performed in 30% of the cases. Our results provide substantial evidence that in cerebellopontine angle meningiomas a precise preoperative study of tumor location will assist in improving individual operative strategy and thus postoperative functional results.

The effectiveness of any therapy in acute acoustic trauma or sudden hearing loss of unknown origin has not been demonstrated convincingly. The assessment is difficult because of a relatively high rate of spontaneous recovery. Nevertheless, many different forms of treatment are recommended. We tested one form, treatment with rheoactive substances, in a prospective, randomized, double-blind trial and compared treatment with (a) infusions of dextran-40 with pentoxifylline, (b) saline infusions with pentoxifylline, and (c) saline infusions with placebo medication. Pure-tone hearing thresholds served as control parameters and were taken before treatment and at 1 and 4 weeks after the onset of therapy. Three hundred eighty-two patients were included in the trial, 331 (87%) could be analyzed, 184 patients were treated because of sudden hearing loss, 147 because of acute acoustic trauma. The three treatment groups were comparable in their basic characteristics including the amount of initial hearing loss. In patients with sudden hearing loss, no significant differences of hearing recovery were detected between the three treatment groups. Hearing recovery was also similar in patients with acute acoustic trauma. A power analysis of the study revealed that possible true treatment differences of a hearing recovery of 10 dB would have lead to significance with a probability of over 90%. It is concluded that there were, in fact, no clinically relevant differences in hearing gains of sudden hearing loss or acute acoustic trauma between treatments with saline infusions together with placebo medication and treatment with dextran-40 and/or pentoxifylline.