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PubMedDate not supplied

Giant repeater F-wave in patients with anterior horn cell disorders. Role of motor unit size.

Conventional F-wave responses as well as single motor unit F-wave responses together with the volitionally recruited motor unit action potentials (MUAP) were studied in hand and feet muscles of 10 healthy subjects and 32 patients with anterior horn cell disorders. The amplitude of the largest F-wave (Fl) was significantly greater in the affected patients compared with healthy subjects. Giant repeater F-wave responses "up to 4 mV" were recorded in muscles having volitionally recruited giant MUAPs. Although, the group mean percentage of motor unit F-wave responses per stimulation in all tested orthodromic MUAPs was significantly decreased in amyotrophic lateral sclerosis patients, the group mean percentage of motor unit F-wave responses per stimulation in all tested orthodromic MUAPs that gave motor unit F-wave response was significantly increased compared with healthy subjects. The responding orthodromic MUAP gave identical motor unit F-wave response, even for complex polyphasic units. Enhanced monosynaptic (H-) reflex, proximal axon reflex (A-wave), and repetitive muscle response as possible explanations for the giant F-wave responses could be discounted. The electrophysiologic behavior of the giant late responses described here fits well with the criteria of F-waves modulated by newly formed distal (and or proximal) axonal branching.

Aged↗
PubMed1985

Thyrotropin-releasing hormone mimics descending slow synaptic potentials in rat spinal motoneurons.

Thyrotropin-releasing hormone (TRH) produced a depolarization in lumbar motoneurons of neonatal rats. The depolarization by TRH persisted after extracellular Ca2+ was replaced by Mg2+ or Mn2+, indicating its direct action upon motoneurons. Stimulation of the ventral descending tract at the lower thoracic segment evoked slow excitatory postsynaptic potentials (e.p.s.ps) lasting 20-30 s in every motoneuron. Both the TRH-induced depolarization and descending slow e.p.s.p. were accompanied by a decrease in input conductance of motoneurons. When the membrane potential of the motoneuron was shifted, both the TRH-induced depolarization and slow e.p.s.p. became larger in amplitude during depolarization and smaller during hyperpolarization. However, they could not be reversed in polarity by hyperpolarization. During the depolarization of motoneuron produced by TRH application, the slow e.p.s.p. was markedly reduced in amplitude, suggesting the involvement of identical ionic mechanisms in the two responses. After incubation of the isolated spinal cord with antisera to TRH, the depolarizing response produced by TRH as well as the descending slow e.p.s.p. was greatly diminished. In contrast, monosynaptic reflexes evoked by dorsal root stimulation remained unchanged under this condition. These results suggest that TRH serves as a neurotransmitter mediating the descending slow e.p.s.p. in motoneurons.

Animals↗
PubMed1978

Deep tendon reflex in Eaton-Lambert syndrome.

The mechanism of absent or decreased deep tendon reflex in Eaton-Lambert syndrome was studied. There was no evidence suggestive of the presence of a neuropathy. On the other hand, a brief (about 10 seconds) maximal voluntary contraction made the absent deep tendon reflexes elicitable, which suggests that the block of neuromuscular transmission in Eaton-Lambert syndrome is responsible for the absent or decreased deep tendon reflex. Such enhancement of the decreased deep tendon reflex in Eaton-Lambert syndrome might be helpful in differentiating neuropathy and Eaton-Lambert syndrome.

Bronchial Neoplasms↗
PubMed2000

Depression of group Ia monosynaptic EPSPs in cat hindlimb motoneurones during fictive locomotion.

The effects of fictive locomotion on monosynaptic EPSPs recorded in motoneurones and extracellular field potentials recorded in the ventral horn were examined during brainstem-evoked fictive locomotion in decerebrate cats. Composite homonymous and heteronymous EPSPs and field potentials were evoked by group I intensity (<= 2T) stimulation of ipsilateral hindlimb muscle nerves. Ninety-one of the 98 monosynaptic EPSPs were reduced in amplitude during locomotion (mean depression of the 91 was to 66 % of control values); seven increased in amplitude (to a mean of 121 % of control). Twenty-one of the 22 field potentials were depressed during locomotion (mean depression to 72 % of control). All but 14 Ia EPSPs were smaller during both the flexion and extension phases of locomotion than during control. In 35 % of the cases there was < 5 % difference between the amplitudes of the EPSPs evoked during the flexion and extension phases. In 27 % of the cases EPSPs evoked during flexion were larger than those evoked during extension. The remaining 38 % of EPSPs were larger during extension. There was no relation between either the magnitude of EPSP depression or the locomotor phase in which maximum EPSP depression occurred and whether an EPSP was recorded in a flexor or extensor motoneurone. The mean recovery time of both EPSP and field potential amplitudes following the end of a bout of locomotion was approximately 2 min (range, < 10 to > 300 s). Motoneurone membrane resistance decreased during fictive locomotion (to a mean of 61 % of control, n = 22). Because these decreases were only weakly correlated to EPSP depression (r 2 = 0.31) they are unlikely to fully account for this depression. The depression of monosynaptic EPSPs and group I field potentials during locomotion is consistent with the hypothesis that during fictive locomotion there is a tonic presynaptic regulation of synaptic transmission from group Ia afferents to motoneurones and interneurones. Such a reduction in neurotransmitter release would decrease group Ia monosynaptic reflex excitation during locomotion. This reduction may contribute to the tonic depression of stretch reflexes occurring in the decerebrate cat during locomotion.

Animals↗
PubMed1973

Adrenergic control of tendon jerk reflexes in man.

1. Tendon jerk responses and H reflexes were recorded from conscious human volunteers before and after intravenous injection of methylamphetamine, thymoxamine and propranolol, and during intravenous infusion of noradrenaline.2. Methylamphetamine produced a significant increase in the amplitude of the tendon jerk, whereas noradrenaline had no effect in doses which caused a greater pressor response than methylamphetamine.3. Thymoxamine produced a dose-related reduction in the tendon jerk.4. Propranolol had no significant effect on the jerk.5. None of these drugs significantly affected the H reflex.6. It is suggested that central adrenoceptors, possibly alpha in type, exist in man, and that stimulation of these receptors facilitates tendon jerk reflexes by an action on the fusimotor system.

Blood Pressure↗
PubMed1977

Phenytoin, electric, ionic, and metabolic responses in cortex and spinal cord.

Post-tetanic potentiation (PTP) of monosynaptic reflex was estimated in spinal cords in the drug-free state after the administration of a convulsant dose of penicillin and after the administration of phenytoin. There was no apparent correlation between the degree of depression of PTP and the efficacy of controlling seizure activity by phenytoin. Extracellular potassium levels were measured with ion-selective microelectrodes. The post-stimulation clearing of [K+]0 was not accelerated by phenytoin, and frequently it was slowed. Post-stimulus undershooting of [K+]0 was diminished. Oxidation of NADH in cortex and of cytochrome a, a3 in spinal cord were measured by optical methods. Stimulus-evoked transient oxidation responses evoked by electrical stimulation were depressed by phenytoin. It is concluded that systemic administration of phenytoin in therapeutic doses does not stimulate Na+-K+-activated membrane ATPase in cortex and spinal cord. Unlike other depressants, phenytoin did not cause a reduction of "resting" redox levels of respiratory enzymes. The local regulation of blood flow remained unaltered after phenytoin administration. Phenytoin caused a moderate but consistent depression of the stimulus-evoked responses of potassium activity, electric potential, and oxidative enzymes, consistent with diminished outflow of potassium from cells, owing either to lesser activation of cells or to a lesser exchange of ions.

Animals↗
PubMedDate not supplied

Effects of zonisamide (AD-810) on tungstic acid gel-induced thalamic generalized seizures and conjugated estrogen-induced cortical spike-wave discharges in cats.

Effects of zonisamide (AD-810, CI-912) were examined on tungstic acid gel-induced thalamic generalized seizures and conjugated estrogen-induced cortical spike-wave discharges in gallamine-immobilized cats. Zonisamide prolonged the interictal periods of the generalized seizures by thalamic (centralis lateralis) application of tungstic acid gel (50 microliters) and, at the higher doses, abolished the seizures; its potency was near that of phenobarbital. Zonisamide abolished the spike-wave discharges by cortical (posterior lateralis) application of 2% conjugated estrogens (CE); its potency was stronger than that of dipropylacetate or trimethadione, but slightly less than that of phenytoin, phenobarbital, or carbamazepine. Zonisamide did not affect the posttetanic potentiation of the monosynaptic reflexes (ventral root potentials) in urethane-chloralose-anesthetized spinal rats. From these results, it is suggested that zonisamide suppresses both seizures originating from the thalamus and the cortex through the mechanism differing from that of phenytoin. Zonisamide appears to be effective in primary generalized seizures, especially the grand mal epilepsies, in addition to being effective in cortical epilepsies.

Animals↗
PubMed1984

The effect of the GABA-agonist, progabide, on stretch and flexor reflexes and on voluntary power in spastic patients.

The action of the GABA-receptor agonist, progabide , was investigated in a double-blind study with cross-over to placebo. The stretch and flexor reflexes and voluntary power were measured in 16 patients with spasticity. 2-week treatment periods were used; the median daily oral dosage of progabide was 24.3 mg/kg. The Achilles tendon (T) reflex was significantly suppressed whereas the Hoffmann (H) reflex remained unchanged: the T/H ratio was thus reduced. Hmax /M (direct motor)max ratio and the vibration-induced suppression of the T- and H-reflexes were unchanged. These findings indicate an effect of progabide on the spindles or on the controlling fusimotor system (probably acting on spinal interneurons), whereas influence on presynaptic inhibition and alpha-motoneuron excitability is unlikely. The flexor reflex threshold was increased during progabide treatment and latency at threshold decreased towards normal latency. This indicates some influence of progabide on flexor reflex activity attributed to reinforcement of action of GABAergic interneurons at the spinal level. Isokinetic measurement of voluntary power of knee extension revealed particularly good progress for the fastest movements during progabide treatment, whereas isometric measurement of sustained handgrip remained unchanged, probably reflecting a reduction of spasticity without reduction of voluntary power in non-spastic muscles.

Achilles Tendon↗
PubMed1966

Presynaptic inhibition evoked by muscle contraction.

1. Contractions of flexor and extensor muscles of the knee and ankle were used to investigate presynaptic inhibition at the spinal level.2. Contractions evoked dorsal root potentials, and increased the excitability of the central terminals of group Ia, Ib and low threshold cutaneous primary afferent fibres.3. The monosynaptic reflexes recorded in response to stimulation of flexor or extensor muscle nerves were depressed, in the presence of strychnine hydrochloride 0.1 mg/kg I.V., by the contractions.4. It is suggested that these presynaptic inhibitory effects are largely due to the activation of Golgi tendon organs by contraction.

Journal Article↗
PubMed1977

An estimate of the secondary spindle receptor afferent contribution to the stretch reflex in extensor muscles of the decerebrate cat.

1. Vibration or stretch of the medial gastrocnemius muscle in the decerebrate cat each caused a significant increase in the tension of a synergist, the lateral gastrocenmius. 2. Simultaneous vibration and stretch of the medial gastrocnemius resulted in a substantial increase of lateral gastrocnemius tension which was greater that that produced by medial gastrocnemius vibration alone. The size of this force increase was proportional to the amplitude of medial gastrocnemius stretch, for the limited range of amplitudes examined. 3. Since the discharge of the medial gastrocnemius I a afferent fibres was held constant by vibration, the additional tension in lateral gastrocnemius provoked by medial gastrocnemius stretch must have resulted from the activation of an excitatory pathway separate from the I a afferent system. The secondary spindle afferent pathway was considered to be the most likely candidate. 4. The contributions of the Ia afferents and the additional stretch induced excitation to the stretch reflex were compared. The Ia potency was calculated from the ration of tonic vibration reflex force and the vibration frequency. The total Ia contribution to the stretch reflex, which was estimated from the product of this ratio and the primary ending stretch sensitivity, seemed modest, and was consistently smaller than the proposed secondary contribution. 5. The medial gastrocnemius nerve was subjected to anodal blockade at a strength sufficient to eliminate Ia transmission. Under these conditions, the lateral gastrocnemius excitation produced by medial gastrocnemius stretch or vibration was largely eliminated. When lateral gastrocnemius vibration was superimposed, the excitatory effect of medial gastrocnemius stretch was partly restored suggesting that some central facilitation by group Ia afferents may be necessary for group II pexcitatory effects to be manifested. 6. Although the additional excitatory actions of medial gastrocnemius stretch were examined exclusively in a synergist, it is suggested that similar effects are likely to occur in the homonymous stretch reflex.

Animals↗
PubMed1981

Two kinds of recurrent inhibition of cat spinal alpha-motoneurones as differentiated pharmacologically.

1. The effects of i.v. administration of the glycine-antagonist strychnine nitrate and the GABA-antagonists bicuculline hydrochloride and picrotoxin on the recurrent inhibition of lumbosacral alpha-motoneurones were studied in cats anaesthetized with pentobarbitone sodium. 2. As revealed from both monosynaptic reflex experiments and intracellular recordings, each of the drugs generally reduced, but rarely abolished, the recurrent inhibition. The amount of reduction was more or less identical for bicuculline and picrotoxin. 3. By applying de- and hyperpolarizing currents intracellularly it could be shown that both the strychnine-resistant and bicuculline/picrotoxin-resistant recurrent inhibitory potentials were genuinely post-synaptic in nature. 4. The strychnine-resistant part of the recurrent inhibition had a later maximum and a longer duration than the part which was resistant to bicuculline/picrotoxin. 5. The time course of the strychnine-resistant recurrent inhibition was more or less identical to that of the bicuculline/picrotoxin-sensitive recurrent inhibition. 6. The bicuculline/picrotoxin-resistant recurrent inhibition was blocked by strychnine and, vice versa, the strychnine-resistant recurrent inhibition was blocked by bicuculline/picrotoxin. The combined administration of strychnine and bicuculline/picrotoxin always resulted in a virtual abolition of the recurrent inhibitory effects. 7. The values for central delay suggested that both the strychnine-resistant and bicuculline/picrotoxin-resistant inhibitions were mediated via disynaptic pathways. 8. The results suggest that both glycine and GABA act as transmitter substances of Renshaw cells in mediating recurrent inhibition to alpha-motoneurones. 9. No organizational pattern of the two types of recurrent inhibition based on motor pool category or motor unit type could be detected.

Animals↗
PubMed1973

Reflex compensation for variations in the mechanical properties of a muscle.

Soleus muscles of anesthetized cats were stretched and released by different amounts while their motor axons were stimulated. Muscle force increased, then gave way in response to large stretch. In the presence of active stretch reflexes in decerebrate cats, the give in force was absent. We demonstrate that autogenetic reflexes can compensate for variations in muscular stiffness revealed when responses to stretch and release are compared.

Animals↗
PubMed1973

Dynamic spindle reflexes and the rigidity of Parkinsonism.

The effects of stimulating the reflex arc from dynamic spindle endings were examined in patients with the rigidity of Parkinsonism and in control subjects. The arc was activated phasically by a tendon tap and by electrical stimulation in 15 patients. The effect of reinforcement by Jendrassik's manoeuvre was observed. The response to phasic activation indicated central facilitation of the reflex loop in the patients with Parkinsonism, with a concurrent decrease in fusimotor drive to dynamic spindles. These abnormalities could not be correlated with the severity of the patients' rigidity, and they did not alter when the rigidity was reduced by levodopa. The effect of activating dynamic spindle endings tonically by vibration at 50 Hz was also examined. The reflex contraction of the biceps and triceps muscles in response to vibration was found to be increased in 24 patients with rigidity compared with 24 control subjects. Patients with severe rigidity developed a more powerful contraction in response to vibration than patients with mild rigidity. The response to vibration was reduced by treatment with levodopa but the amount of this reduction could not be correlated with changes in the patients' rigidity.

Adult↗
PubMed1973

Modulation of postural reflexes by voluntary movement. II. Modulation at an inactive joint.

We have observed that there is a brief, 400 msec period of widespread facilitation of both the Hoffmann and the tendon-jerk reflexes associated with the initiation of a variety of local, voluntary, isometric efforts. It is suggested that the site of this facilitation lies within the spinal cord. We have also observed that this period is followed, for the Hoffmann reflex, by a period of spinal inhibition. By contrast, the tendon-jerk is facilitated, at a reduced level, for at least another 500 msec by mechanisms probably working at the muscle spindle. These results are discussed in comparison with experiments involving activation of the reflex agonist and antagonist muscles. It is proposed that voluntary control of the locomotor system is organized through separate mechanisms for muscle recruitment and for regulation of the sensitivity of the myotatic reflex loop.

Ankle Joint↗
PubMed1976

Central effect of bladder filling and voiding.

In normal subjects and in patients with spasticity and/or urological complaints changes in somatic muscle reflexes associated with filling of the urinary bladder were observed. Two different patterns of reflex changes occurred. One pattern was associated with easy initiation of voiding: it consisted of increasing H and T reflexes and decreasing flexor reflexes with concomitant decreasing sphincter muscle activity. The other pattern was associated with difficulty in initiation of voiding: it consisted of increasing flexor relfexes including sphincter muscle activity and decreasing H and T reflexes. The importance of these reflex patterns in disturbances of micturition is discussed. During voiding, decreasing flexor relfexes with increasing H and T reflexes occur as the general pattern.

Adult↗
PubMed1977

Conditioning of H reflex by a preceding subthreshold tendon reflex stimulus.

The soleus H reflex excitability cycle has been studied using, as conditioning stimulus, a mechanical tap, subthreshold for the tendon reflex, which was applied either on the Achilles tendon, the short biceps tendon, or the quadriceps tendon. In all cases there was an early facilitation followed by a longlasting inhibition of the test H reflex. The same results were obtained in patients with a complete spinal cord section. Wherever the site of the conditioning stimulation, these modifications disappeared after ischaemia of the leg. It is concluded that the effects observed are due to the activation by the tendon tap of the Ia nerve fibres from the soleus muscle, and that the longlasting inhibition is probably due to a transmitter depletion.

Adult↗