The jaw reflexes. The International Federation of Clinical Neurophysiology.
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Electromyography↗
Biomedical subjects
G Cruccu
Publications and source records attributed to G Cruccu.
The orbicularis oculi reflexes. The International Federation of Clinical Neurophysiology.
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Blinking↗
Mandibular nerve involvement in diabetic polyneuropathy and chronic inflammatory demyelinating polyneuropathy.
Sensory complaints in the area of the mandible and mouth often escape notice or remain undiagnosed. Using electromyographic recording of the trigeminal reflexes and motor responses, we sought trigeminal dysfunction in 50 patients with peripheral neuropathy, and tried to gain pathophysiological information on the mechanisms provoking trigeminal damage. Trigeminal reflex recordings (early and late blink reflex after supraorbital stimulation, early and late masseter inhibitory reflex after mental stimulation, and jaw jerk) disclosed abnormalities caused by sensory trigeminal neuropathy in 8 out of 15 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 13 out of 23 patients with severe diabetic polyneuropathy, and in none of 12 patients with mild diabetic polyneuropathy. Six patients had abnormal motor responses in facial or masseter muscles. The response affected most frequently was the masseter early inhibitory reflex (also called first silent period, SP1) after mental nerve stimulation, its latency being strongly delayed. We found these long delays not only in patients with CIDP, but also in diabetic patients with severe polyneuropathy. We conclude that peripheral polyneuropathies often cause subclinical damage to the trigeminal nerve, especially to its mandibular branch. We believe that the nerve fibers running along the alveolar-mandibular pathway are more exposed to damage because of their cramped anatomical route in the mandibular canal and below the internal pterygoid muscle and fascia.
Adolescent↗
Jaw-opening reflex after CO2 laser stimulation of the perioral region in man.
CO2 laser pulses selectively excite A-delta and C mechano-thermal nociceptors in the superficial layers of the skin. To study the jaw-opening reflex elicited by a purely nociceptive input, we delivered laser pulses to the perioral region in 15 subjects. Sensory threshold was very low (9 mJ/mm2). High-intensity noxious laser pulses (more than 4 x sensory threshold) evoked a single phase of electromyogram suppression (laser silent period, LSP) at an onset latency of 70 ms in the contracted masseter and temporal muscles, bilaterally. Even maximum-intensity laser pulses failed to activate the suprahyoid muscles. The recovery curves to paired laser stimuli showed that at short interstimulus intervals the test LSP was strongly suppressed. At about 380 ms it recovered to 50%, i.e. its recovery curve resembled that of the masseter late silent period after electrical mental nerve stimulation (SP2). In experiments studying the interaction with heterotopic stimuli and non-nociceptive responses, chin-taps or electrical shocks delivered to the supraorbital, infraorbital or mental nerves before laser stimulation strongly suppressed the LSP. A preceding perioral laser pulse strongly suppressed the masseter SP evoked by supraorbital stimulation and the SP2 evoked by mental stimulation, but left SPI unaffected. We conclude that the perioral A-delta fibre input elicits a jaw-opening reflex simply by inhibiting the jaw-closers. The LSP response is mediated by a multisynaptic chain of brainstem interneurons and shares with the masseter SP2 part of the central circuit in the ponto-medullary region. We also propose that a common centre processes the various inputs for jaw opening.
Adult↗
Rapid decline of fertility in a case of adrenoleukodystrophy.
Adrenoleukodystrophy/adrenomyeloneuropathy (ALD/AMN) is a group of genetically determined peroxisomal disorders associated with progressive central demyelination, primary adrenal cortical insufficiency (Addison's disease) and, frequently, primary hypogonadism. Recently, testicular dysfunction was described in ALD/AMN patients but no information on sperm characteristics was provided. In this paper we studied the reproductive function of a patient with adult cerebral ALD, focusing our attention on sperm characteristics. At the time of diagnosis the patient was 22 years old, had high plasma C26 and C24 very-long-chain fatty acid (VLCFA) concentrations and adrenal insufficiency. Plasma testosterone concentration was in the normal range. The patient was prescribed a low-fat diet and 'Lorenzo's oil', which led to normalization of plasma VLCFA concentrations within 3 months of therapy. Semen analysis showed normal sperm count, gross morphological alterations and reduced motility. Electron microscopy analysis of sperm cells showed pathological changes in the head, the plasma membrane and the nucleus in 60% of the spermatozoa examined. However, isolated motile spermatozoa showed normal molecular dynamics of phospholipid bilayer surface and physiological responsiveness to progesterone. At the 12 months follow-up, the patient became azoospermic and testicular histology showed arrested maturation. To our knowledge, this is the first description of sperm alterations in a post-pubertal ALD patient, in which severe impairment of spermatogenesis and rapid progression to azoospermia occurred despite normalization of plasma VLCFA concentrations.
Adrenoleukodystrophy↗
Corneal reflex responses to mechanical and electrical stimuli in coma and narcotic analgesia in humans.
The corneal reflex, a bilateral eye-blink, can be elicited in humans either by mechanical or electrical corneal stimulation. Both in comatose patients and in normal subjects injected with the opiate fentanyl, the electrically-evoked corneal reflex was more suppressed than the mechanically-evoked reflex. We propose that the mechanical input yields a reflex more resistant to depression of the corticoreticular drive and to narcotic analgesia, because it exploits temporal summation at central synapses, whereas the electrical input exploits spatial summation.
Adult↗
Cortical mechanisms mediating the inhibitory period after magnetic stimulation of the facial motor area.
We studied the silent period (SP) that interrupts voluntary electromyographic activity (EMG) in facial muscles, after transcranial magnetic stimulation (TMS), in normal subjects. High-intensity magnetic stimulation with a 12-cm round coil centered at the vertex induced a long-lasting SP (215 ms), whereas supramaximal stimulation of the facial nerve only induced a short (< 20 ms) and incomplete EMG suppression, and cutaneous stimuli had no inhibitory effect at all. Cutaneous trigeminal stimulation delivered after TMS evoked blink-like reflexes, showing that facial motoneurons were not inhibited during the SP. Simultaneous recordings from perioral muscles (large cortical representation) and from orbicularis oculi and masseter muscles (small cortical representation) showed SPs of identical duration. Focal stimuli with a figure-of-eight coil showed that positioning of the coil was critical and that the optimal scalp sites for evoking the largest motor potentials and longest SPs coincided. Low-intensity stimulation occasionally elicited short SPs without a preceding motor potential. We conclude that the SP induced in facial muscles by TMS results from the excitation of cortical inhibitory interneurons surrounding the upper motoneurons.
Adult↗
Excitability of the central masticatory pathways in patients with painful temporomandibular disorders.
Much is unclear about the pathophysiological mechanisms underlying painful temporomandibular disorders. In addition to various other theories, masticatory muscle dysfunction and pain have also been attributed to primary central nervous system hyperactivity. We assessed this possibility in a study using recent neurophysiological techniques. From among outpatients whose diagnosis of temporomandibular disorders had been obtained in stomatognathic facilities, we studied 10 patients with bilateral pain and 15 patients with unilateral pain, in whom electromyographic examination of the trigeminal reflexes disclosed normal findings except for absence or amplitude asymmetry of the jaw jerk. Transcranial magnetic stimulation yielded masseter motor evoked potentials of normal latency and amplitude, but five patients had to exert a near-maximum contraction to obtain their responses. The masseter silent periods elicited by the double-shock technique recovered normally. Because these tests measure the excitability of the masticatory system (including motor cortex, corticobulbar and corticoreticular connections, reticular interneurones and lower motoneurones), the lack of facilitation in these patients' responses excluded central hyperactivity as the primary cause of their masticatory dysfunction and pain.
Adult↗
Silent period in upper limb muscles after noxious cutaneous stimulation in man.
We studied the effect of electrical stimulation of the C5-C8 dermatomes on voluntary electromyographic activity (EMG) recorded from the ipsilateral first dorsal interosseus (FDI), abductor digiti minimi, flexor and extensor carpi, triceps brachii, biceps brachii, and orbicularis oculi muscles of healthy humans. Finger stimulation (C6-C8) produced an EMG inhibition (silent period, SP), which progressively decreased in duration from distal to proximal muscles; in the biceps it induced a slight facilitation and in the orbicularis oculi muscle, it had no effect. Stimulation of the C5 dermatome induced no response in either distal or proximal muscles. Only high-intensity stimuli evoked clear silent periods. The threshold for evoking an SP was almost double that required for sensory action potentials, 3.25 times the sensory threshold, and decidedly above the pain threshold. An indirect estimation of the conduction velocity of SP afferent fibres placed them in the A-delta group of myelinated fibres. In double-shock experiments, used to study the recovery cycle of the SP in the FDI muscle after finger stimulation, neither low- nor high-intensity conditioning stimuli delivered 100-500 ms before the test stimulus changed test SPs. Experiments designed to evaluate motoneuronal excitability showed that in relaxed FDI muscle, finger stimulation markedly reduced the F wave at the 50 ms time interval, the time when the SP normally occurs. Our findings demonstrate that the activation of A-delta afferents from the fingers inhibits the C7-T1 motoneurons postsynaptically, through an oligosynaptic spinal circuit. We propose that the strong inhibitory effect exerted by noxious cutaneous stimuli on all distal muscles may contribute to a defence action which is specific for the human upper limb.
Action Potentials↗
Inhibition of hand muscle motoneurones by peripheral nerve stimulation in the relaxed human subject. Antidromic versus orthodromic input.
In active muscle, a supramaximal conditioning stimulus to peripheral nerve produces a classic silent period in the EMG. The present experiments examined the effect of this type of conditioning stimulus on motoneurone excitability in relaxed muscle. EMG responses evoked by transcranial magnetic stimulation of the brain were recorded from the first dorsal interosseus muscle (FDI) in 10 healthy subjects and 5 patients with sensory neuropathy. These responses (motor evoked potentials) were conditioned by supramaximal peripheral nerve stimuli given 0-150 msec beforehand. In the normal subjects, the classic silent period in the FDI lasted about 100 msec. The same conditioning stimulus only abolished motor evoked potentials when the conditioning-test interval was so short that the antidromic peripheral nerve volley collided with the orthodromic volley set up by magnetic brain stimulation. At longer conditioning-test intervals, although remarkably inhibited (65% mean suppression between 10 and 40 msec), the test motor potential was never completely abolished and gradually recovered by 100 msec. Inhibition of cortically evoked motor potentials did not depend upon activity set up by the conditioning stimulus in peripheral nerve sensory fibres. The patients with complete peripheral sensory neuropathy had the same extent and time-course of inhibition as the normal subjects. We conclude that in relaxed subjects the inhibitory effect of peripheral conditioning results almost exclusively from the motoneuronal inhibitory mechanisms consequent to antidromic invasion.
Adult↗
The Italian neurological "output".
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Bibliometrics↗
Human reflexes and late responses. Report of an IFCN committee.
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Electric Stimulation↗
Quantitative EEG modifications during the Cold Water Pressor Test: hemispheric and hand differences.
In a study designed to investigate the neurophysiological correlates of the Cold Water Pressor Test, a standardized experimental model of tonic pain, spectral EEGs were examined during the test in 15 young right-handed adults. Each subject performed a "cold water" and a "warm water" session. The subject immersed in cold water (0 degree C) either the right or the left hand alone, in a randomized way. EEG activity was recorded for an initial 3 min baseline and for the first and second minute epochs after immersion. A further EEG recording was obtained after a 30-min rest. Pain intensity was measured with a visual analogue scale. The EEG recordings showed several patterns of cortical activation during the test. Alpha 2 desynchronization was more evident on the contralateral parietal electrodes of the stimulated hand and lasted longer over all the right hemisphere. Delta activity increased bilaterally, predominantly in the frontal leads. Stimulation of the left hand resulted in a higher delta increase during the second minute after immersion.
Adult↗
Analgesic-antiinflammatory drugs inhibit orbicularis oculi reflexes in humans via a central mode of action.
1. A cross-over single blind study examined the possible central effects of non-opioid analgesic drugs on the trigeminal reflexes. 2. The corneal reflex and blink reflex (R1, R2) were recorded electromyographically and response areas measured in healthy volunteers before and after intramuscular injection of piroxicam (40 mg); and after intravenous injection of lysine acetylsalicylate (500 mg). After the last drug recording the subjects received intravenous naloxone (2 mg) followed 5 minutes later by further reflex testing. Saline was used as a placebo in control experiments. 3. Both analgesics reduced the corneal reflex: piroxicam induced a 27% and lysine acetylsalicylate a 21% a reduction that naloxone did not reverse. Neither drug reduced the early or the late component of the blink reflex. 4. The marked inhibitory changes that the two non-narcotic analgesics produced on the corneal reflex--a nociceptive response--indicate a centrally-mediated action. 5. Naloxone's failure to reverse the induced analgesia argues against opiate receptor mediation.
Adult↗
Pathophysiology of hemimasticatory spasm.
Two patients aged 21 and 50 years presented with facial hemiatrophy and unilateral spasms of the masticatory muscles. Masticatory muscle biopsy showed normal findings in both patients and facial skin biopsy specimens only showed atrophy, although morphoea (localised facial scleroderma) had been diagnosed nine years previously in the second patient. The involuntary movements consisted of brief twitches and prolonged contractions clinically and electromyographically similar to those of hemifacial spasm and cramps. The jaw jerk and the silent periods were absent in the affected muscles. Direct stimulation of the muscle nerve and transcranial stimulation of the trigeminal root demonstrated slowing of conduction and after-activity due to autoexcitation. Observations in other reported cases and these two patients suggest that hemimasticatory spasm is produced by ectopic activity secondary to focal demyelination of the trigeminal motor nerve fibres. The proposed cause of the neuropathy is focal damage to the masticatory nerves caused by compression, possibly resulting from the deep tissue changes that occur in facial hemiatrophy.
Adolescent↗
Blink reflex and the masseter inhibitory reflex in patients with dystonia.
The excitatory and inhibitory interneuronal pathways in the brainstem are tested by examining the blink reflex and the masseter inhibitory reflex, respectively. We studied the R2 component of the blink reflex and the SP2 component of the masseter inhibitory reflex and their recovery cycle in 56 patients with various forms of dystonia. In patients with cranial, cervical, and generalized dystonia, but not in patients with extracranial segmental dystonia, the recovery cycle of both reflexes was enhanced. The recovery cycle of R2 and SP2 can demonstrate subclinical changes in excitability of brainstem interneurons. The degree of enhancement of the recovery cycles did not correlate, however, with the severity of clinical facial muscle impairment. In addition, the recovery cycles correlated positively with each other, showing that excitatory as well as inhibitory interneuronal pathways in the brainstem are perturbed in dystonia. Study of the trigemino-facial and trigemino-trigeminal reflexes provides an objective tool for assessing functional abnormalities in dystonia.
Adult↗
Silent period evoked by transcranial stimulation of the human cortex and cervicomedullary junction.
1. The silent period evoked in the first dorsal interosseous (FDI) muscle after electrical and magnetic transcranial stimulation (TCS), electrical stimulation of the cervicomedullary junction and ulnar nerve stimulation was studied in ten healthy subjects. 2. With maximum-intensity shocks, the average duration of the silent period was 200 ms after electrical TCS, 300 ms after magnetic TCS, 43 ms after stimulation at the cervicomedullary junction and 100 ms after peripheral nerve stimulation. 3. The duration of the silent period, the amplitude of the motor-evoked potential, and the twitch force produced in the muscle were compared at increasing intensities of magnetic TCS. When the stimulus strength was increased from 30 to 70% of the stimulator output, the duration of the silent period lengthened as the amplitude of the motor potential and force of the muscle twitch increased. At 70 to 100% of the output, the amplitude of the motor potential and force of the muscle twitch saturated, whereas the duration of the silent period continued to increase. 4. Proximal arm muscle twitches induced by direct electrical stimulation of the biceps and extensor wrist muscles produced no inhibition of voluntary activity in the contracting FDI muscle. 5. The level of background activation had no effect on the duration of the silent period recorded in the FDI muscle after magnetic TCS. 6. Corticomotoneurone excitability after TCS was studied by means of a single magnetic conditioning shock and a test stimulus consisting either of one single magnetic shock or single and double electrical shocks (interstimulus interval 1.8 ms) in the relaxed muscle. A conditioning magnetic shock completely suppressed the response evoked by a second magnetic shock, reduced the size of the response evoked by a single electrical shock but did not affect the response evoked by double electrical shocks. Inhibition of the test magnetic shock was also present during muscle contraction. 7. Our findings indicate that the first 50 ms of the silent period after TCS are produced mainly by spinal mechanisms such as after-hyperpolarization and recurrent inhibition of the spinal motoneurones. If descending inhibitory fibres contribute, their contribution is small. Changes in proprioceptive input probably have a minor influence. From 50 ms onwards the silent period is produced mainly by cortical inhibitory mechanisms.
Adult↗
Piroxicam-induced analgesia: evidence for a central component which is not opioid mediated.
Piroxicam is a nonsteroidal anti-inflammatory drug with a potent analgesic effect. In order to establish whether the analgesic action of Piroxicam has a central component, we studied the effect of the drug on the nociceptive orbicularis oculi reflexes evoked by electrical stimulation of the cornea and supraorbital nerve in healthy subjects. Piroxicam significantly suppressed the corneal reflex and R3 component of the blink reflex by 28% (p < 0.05) and 50% (p < 0.01), respectively. This effect was not reversed by the i.v. injection of naloxone. Beta-endorphin levels did not change. Piroxicam administration induces distinct inhibitory changes in nociceptive reflexes, which suggests that the analgesic action of the drug has a central component. The ineffectiveness of naloxone, and the lack of beta-endorphin changes, indicate that this central action is independent of the opioid system; other pain regulatory systems are probably involved.
Adult↗