Bladder filling inhibits somatic spinal motoneurones.

OBJECTIVES: Despite evidence that the activation of visceral afferents modulates spinal motoneurone activity in humans the responsible circuits remain unclear. We investigated changes in spinal motoneurone excitability during bladder filling in 8 healthy subjects and in 8 patients with spinal cord lesions and 5 patients with multi-infarct encephalopathy. METHODS: Spinal motoneurone excitability was studied by analysing changes in H-reflex, F-wave and motor-evoked potential (MEP) size recorded from the calf muscles under different bladder filling conditions. RESULT: In normal subjects, maximal bladder filling significantly suppressed the H-reflex, F-wave and MEPs; after bladder voiding these responses returned to normal. In patients with encephalopathy maximal bladder filling strongly reduced H-reflex size; similarly to normal subjects H-reflex returned to control value after bladder voiding. In patients with spinal cord lesions, activation of bladder afferents left the H-reflex unchanged. CONCLUSIONS: These findings indicate that bladder distension induces post-synaptic inhibition of spinal motoneurones through a suprasegmental pathway, which is interrupted by rostral spinal cord lesions. This vesical-induced inhibition is probably mediated by the propriospinal system rather than by the diffuse noxious inhibitory control circuit.

Ia presynaptic inhibition after muscle twitch in the arm.

Contraction of upper limb muscles in healthy subjects was used to investigate presynaptic inhibition at spinal level. The H reflex recorded in the forearm flexor muscles in response to median nerve stimulation was depressed in amplitude from 400 ms to 1 s after a muscle twitch induced by transcranial stimulation, root stimulation, direct biceps stimulation, and triceps tendon tap. Stimulation of the cutaneous branch of musculocutaneous nerve, ipsilateral triceps and contralateral biceps, and biceps tendon tap did not alter H-reflex size. Forearm flexor H-reflex amplitude is therefore related to changes in proprioceptive inflow secondary to the biceps muscle twitch. Root and direct muscle stimulation both failed to reduce the size of the motor evoked potential (MEP) after transcranial magnetic stimulation, suggesting that the inhibition acts at presynaptic level. Attenuation of H-reflex amplitude was related to the size of the muscle twitch and was less pronounced during an isometric twitch than during free joint movement. Our results suggest that the biceps muscle twitch produces long-lasting inhibition of the Ia afferents from forearm flexor muscles. This is an important and a simple mechanism for suppressing proprioceptive input during movement.

Changes in the cortical silent period after repetitive magnetic stimulation of cortical motor areas.

The physiological mechanisms underlying the lengthening of the silent period (SP) evoked in active upper limb muscles by repetitive transcranial magnetic stimulation (rTMS) of the motor areas were studied in normal subjects. rTMS was delivered at frequencies of 1 Hz, 2 Hz, 3 Hz, 5 Hz, 10 Hz and 15 Hz and at an intensity just above the motor threshold (Mth). Trains delivered at 2 Hz, 3 Hz, 5 Hz, 10 Hz and 15 Hz significantly prolonged the cortical SP, whereas stimuli at 1 Hz did not. The first few stimuli in the train already prolonged the duration of the cortical SP: the other stimuli did not prolong it further. Motor evoked potentials remained unchanged in amplitude regardless of the frequencies and number of stimuli in the train. The effect of intensity of stimulation was studied by delivering trains at suprathreshold intensity (110% and 140% of Mth) and 3-Hz frequency and with trains at subthreshold intensity and 5-Hz and 10-Hz frequencies. SPs had a longer duration at 140% than at 110% Mth intensity. SPs elicited by 3-Hz trains at 140% and 110% Mth intensity lengthened to a similar extent over the course of the train. rTMS delivered at an intensity below Mth did not evoke cortical SPs over the course of the trains. Repetitive stimulation of the cortical forearm motor areas prolonged the duration of the cortical SP in forearm flexor muscles but failed to evoke SPs in the biceps muscles. The maximal single stimulus intensity and less intense stimuli delivered in short trains evoked SPs of similar duration. We propose that rTMS delivered in trains at frequencies higher than 1 Hz and at suprathreshold intensity prolongs the cortical SP mainly through temporal summation of inhibitory interneurones.

Effects of repetitive cortical stimulation on the silent period evoked by magnetic stimulation.

The effects of repetitive transcranial stimulation (rTMS) on brain activity remain unknown. In healthy subjects, we studied the effects of rTMS on the duration of the cortical silent period (SP). Repetitive stimuli were delivered with a Cadwell High Speed Magnetic Stimulator and a figure-of-eight coil placed over the hand motor area. rTMS was delivered in trains of 11 or 20 stimuli at frequencies of 3 and 5 Hz and at stimulation intensities of 110 and 120% of motor threshold. The SP was recorded from the forearm muscles during a voluntary contraction (20% of maximum effort). rTMS delivered at a frequency of 3 and 5 Hz and intensities of 110 and 120% motor threshold prolonged the duration of the SP, without modifying either the size or the latency of the muscle-evoked potentials (MEP). A conditioning train of 11 stimuli at 3 Hz had no effect on the duration of the SP evoked by a single magnetic shock delivered 600 ms after the train. These findings show that rTMS increases the duration of the cortical SP, but does so only during the train of stimuli. rTMS probably changes the duration of the SP by facilitating cortical inhibitory interneurons.

Cortical excitability in patients with essential tremor.

We used transcranial magnetic stimulation in 10 patients with essential tremor and 8 matched healthy subjects. A round stimulating coil was placed over the vertex and electromyographic activity was recorded from the first dorsal interosseous muscle. Paired transcranial stimuli were delivered at interstimulus intervals of 3, 5, 20, 100, 150, and 200 ms. The intensity of the conditioning stimulus was 80% of motor threshold at short and 150% at long interstimulus intervals (ISIs). We also measured the silent period obtained after a single magnetic pulse delivered at 150% of motor threshold during a submaximal muscle contraction. Patients and controls had similar motor threshold and similar latencies. Paired magnetic stimuli given at short and long ISIs at rest, and during a voluntary muscle contraction, elicited similar responses in both groups. The silent period evoked by transcranial magnetic stimulation had a similar duration in patients with ET and controls. In conclusion, these findings suggest that patients with essential tremor have normal cortical motor area excitability.

Electrical stimulation over muscle tendons in humans. Evidence favouring presynaptic inhibition of Ia fibres due to the activation of group III tendon afferents.

Electrical stimulation over muscle tendons produces a transient suppression of voluntary EMG activity; its onset latency is approximately 55 ms in the forearm extensor muscles. This phenomenon has been attributed to the activation of a polysynaptic inhibitory pathway originating from Ib afferent fibres. To clarify its origin we conducted several experiments in 10 normal healthy subjects. The EMG silence after tendon stimulation appeared at relatively high stimulus intensities (> 50 mA); conditioning cutaneous stimulation left it unchanged, and the inhibition had a short recovery cycle (50 ms). Tendon stimulation still evoked EMG suppression during an ischaemic block of fast-conducting afferents. The motor potentials evoked by transcranial magnetic stimulation of the motor cortex during the EMG silence remained almost unchanged, whereas the H reflex was strongly inhibited. Hence we conclude that tendon stimulation activates slow-conducting tendon afferents, possibly group III fibres, connected not through a polysynaptic pathway originating from Ib afferents but through an oligo- or disynaptic inhibitory circuit. The EMG suppression after tendon stimulation probably represents a dysfacilitation of the alpha-motor neurons due to presynaptic inhibition of Ia fibres produced by tendon afferent input to the spinal cord.

Thrombosis of cerebral veins dural sinuses after paratyphi.

A 20 year old woman was admitted to our Department 15 days after the onset of typhoid fever treated with chloramphenicol. The patient showed intracranial hypertension with generalized seizures, slight right hemiparesis and a left VI cranial nerve deficit with diplopia. Magnetic Resonance Imaging (MRI) showed occlusion of the superior longitudinal, right transverse, right sigmoid sinus combined with a single hemorrhagic infarct in the left occipito-parietal area. Serum tests were positive for Salmonella Paratyphi A and B. The results of cerebrospinal fluid (CSF) examination were normal and blood cultures were negative. Clinical data, laboratory and MRI examinations indicate that the neurological signs are the result of aseptic cerebral sinus thrombosis; the physiopathologic mechanisms of the case are discussed.