[Orbicularis oculi reflex in clinical and experimental neurology].
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Biomedical subjects
Publications and source records attributed to R Dengler.
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The recruitment pattern of single motor units (SMUs) was studied in the early (R1) and late (R2) blink reflex components in normal subjects (15), patients with parkinsonism (10) and with hemiplegia due to hemispheral lesions (5). Reflexes were evoked by constant current stimuli applied to the supraorbital nerve. SMU discharges were recorded in the preseptal part of the lower eyelid using a bipolar needle electrode. Thresholds of R1 and R2, latencies at the thresholds and the number of discharges in R2 were determined. In parkinsonism, the recruitment of SMUs in R1 was impaired, suggesting that the malfunction of the basal ganglia in this disorder is associated with a reduced excitability of neurons in the pontine brain-stem. In hemiplegia, the recruitment in both R1 and R2 could be impaired. The orderly function of neurones in the pontine and medullary pathways of these components appears to require facilitatory hemispheral influences. Signs of disinhibition occasionally found in R1 may point to an imbalance between facilitatory and inhibitory hemispheral influences upon the pontine pathway.
Discharges of several motor units (MU) were simultaneously recorded during slight isometric contractions of the first dorsal interosseus muscle using bipolar needle electrodes. Correlograms constructed by counting the relative discharge intervals (1-ms binwidth) between two MU frequently showed narrow central peaks reflecting the occurrence of more synchronies than expected by chance. Diagrams of the temporal distribution of these synchronies revealed that they tend to form clusters consisting of several subsequent events associated with an adjustment of the firing pattern of the two MU. The synchronization described here may be explained by similar mechanisms as the so-called 'short-term synchronization'.
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Membrane potentials, current-voltage relationships, and contractile parameters were studied in intact muscle cell bundles obtained from two patients with adynamia episodica hereditaria. In a normal extracellular medium, the cell membranes had resting potentials of about -80 mV and their current-voltage relationships were not significantly different from control curves. In contrast to normal muscles the afflicted cells were paralyzed in a medium having 6-10 mmol/liter potassium. The mechanisms of paralysis in the two specimens were different from each other. Many fibers from one patient were spontaneously active even in normal solution. In high potassium solution spontaneous activity was increased and the cells gradually depolarized to values at which excitatory sodium current is normally inactivated. This depolarization was connected with an increased sodium conductance and was reversed by the application of tetrodotoxin (TTX). The fibers from the other patient were not spontaneously active. In high potassium solution they were paralyzed at membrane potential values at which normal fibers would still contract. The reason for this paralysis was a reduced excitability.
The discharge pattern of single motor units in the early (R1) and late (R2) component of the electrically evoked trigemino-facial blink reflex was investigated by means of selective EMG-recording techniques. At low rate stimulation (0,1 Hz) the stimulus threshold of motor unit discharges in R1 was clearly above that in R2. Higher stimulation rates (1 Hz) were associated with an attenuation of motor unit discharges in R2 according to the well known habituation. The same motor units, however, revealed stable discharges in R1 or even signs of facilitation. These differences of motor unit recruitment in the two components indicate that R1 cannot be simply interpreted as a protective reflex like R2. At higher stimulus intensities, the characteristical firing pattern consisted of single discharges in R1 followed by high frequency multi-discharges of the same motor units in R2. This means that the motor unit discharges in R1 do not only evoke a single twitch of the eyelids but initiate a vigorous tetanic contraction with short latency. Thus, R1 yet reveals a protective function shortening the latency of the reflex blink upon stronger stimuli on the side of the affected eye.
The glabellar reflex (GR) was investigated in 15 patients with hemiplegia and in 10 control subjects. The reflex was elicited mechanically by a light tap on the glabella. The EMG-responses were recorded bilaterally from the orbicularis oculi muscles by pairs of surface electrodes. The EMG activities were averaged and integrated off-line. In addition, the latencies of the early and late components were determined. Two major types of the GR alterations could be distinguished. These two patterns probably indicate a lowered excitability of the brainstem trigeminal systems or brainstem facial systems respectively. A loss of facilitatory influences associated with the hemispheral lesion seems probable. The alterations of the early component showed essential linkage to those of the late component. The latencies of GR responses on both sides were frequently prolonged. This fact and the decrease of the GR responses on the unaffected side as well as on the affected side indicates that the glabellar reflex can be altered bilaterally in hemiplegic patients.
The recruitment of single motor units (MU) in the early (R1) and late (R2) components of the electrically evoked human blink reflex (BR) was studied using bipolar needle electrodes with a limited take-off area. It could be shown that the same MUs can discharge in R1 and R2 of a BR as well as during voluntary eyelid contraction. At repetitive stimulation (1 Hz), facilitation of MU discharges in R1 and habituation in R2 became apparent. The visible reflex eyelid contraction may mainly be due to repetitive MU discharges in R2. The discharges of the same MUs in R1, however, contribute to it and shorten the latency between stimulus and reflex response.
Electrically evoked blink reflexes were investigated in 18 patients with hemiplegia and in 15 control subjects, using common electromyographic techniques. The EMG activities of the early and late components were quantitatively and integration. In addition, the latencies of the single components were determined. Regarding the EMG activity of the late components two major types of BR alteration could be distinguished. In type I stimulation of the clinically affected side evoked significantly decreased late components on both the affected and the unaffected sides. This pattern points to a lowered excitability of the brain stem trigeminal systems and may be associated with predominantly sensory disorders. In type II the decrease of the late components was confined to the affected side independent of the side of stimulation. This pattern may indicate a lowered excitability of the brain stem facial systems and/or of the lateral bulbar reticular formation and may be correlated with predominantly motor deficits. Both types are presumably due to a loss of facilitatory influences associated with the hemispheral lesion. Although the early component was frequently decreased on the affected side there was no consistent pattern and no relation to the alterations of the late components. The latencies of both responses, predominantly of the late ones were frequently prolonged, in particular following stimulation of the affected side. Comparison of the seemingly normal components in the patients with the corresponding control values pointed to a generally lowered blink reflex excitability in hemiplegic patients.
Electrically evoked blink reflexes were recorded in 10 patients with unilateral tremor and/or rigor, mostly diagnosed as hemiparkinson syndrome. Five of the patients could be investigated before and after stereotaxic thalamo-subthalamotomy. The EMG activity of the early and late components was quantified by means of averaging and integrations techniques. In addition, the latencies of the reflex components were determined. The major finding was a unilateral decrease of the EMG activity of both the early and late components confined to the clinically affected side. This pattern points to a lowered state of excitability of neurons in or close to the facial nucleus, probably due to a dysfunction of contralateral EPMS structures. A loss of facilitatory influences from EPMS centers, e.g. the nigro-striatal system, on brain stem neurons in the area of the facial nucleus appears most probable. The latencies of the early and late components were mostly normal. After stereotaxic surgery, the BR activity was decreased bilaterally. The difference between the affected and unaffected sides, however, was nearly unchanged. At present an unspecific postoperative effect cannot be excluded.
Seven members of a family with histologically proven hereditary pressure-sensitive neuropathy (HPSN) agreed to be examine clinically and electrophysiologically. A sural nerve biopsy specimen taken from the propositus who suffered from a partial brachial plexus palsy showed typical 'sausage-like' myelin sheath thickenings reflecting a failure of axon-adjusted myelination. Reduced motor and sensory conduction velocities involving several nerves were found in the four family members with clinical signs of HPSN. In addition, central conduction times in the auditory and somatosensory pathways were determined measuring the interwave latency I-V in brainstem auditory-evoked potentials and the interpeak latency N14-N20 in median nerve sensory-evoked potentials. Central conduction times in both afferent systems were within normal limits. The absolute delay of peak N14 and N20 in median and P40 in tibial nerve-evoked potentials was probably due to an impaired conduction in the peripheral branch of the bipolar ganglion cell. Whether the central axon branch in the dorsal columns was also involved could not be decided.
The electrically evoked Orbicularis Oculi Reflex (OOR) consists of two separate components (R1 and R2). Within the last years the central pathways of R1 in pontine and R2 in medullary brainstem areas could be further elucitated. We have investigated the OOR in 66 patients with signs of a brainstem affection, obtaining pathological results in 67% of the cases. Five characteristic types of OOR-alterations could be differentiated. Type A with an isolated R1- and type B with an additional R2-Alteration point to pontine lesions. Type C, D, E with different R2-Alterations are indicative for medullary lesions. Disorders of the spinal trigeminal complex or the lateral bulbar reticular formation only can be distinguished from a combined lesion of these structures. Careful analysis of the alterations of the OOR-components and correlation with the known anatomical data provide a means to localize brainstem affections and to assess their extension.
The antimyotonic effect of the antiarrhythmic drug tocainide was tested in 14 patients. With 1200 to 1600 mg/d all patients reported good improvement. This was substantiated by objective tests. Only four patients noticed minor side effects.
The effect of prednisolone on indirectly stimulated rat muscle twitch was investigated at normal and prostigmine-treated neuromuscular junctions. In vivo, predenisolone up to 150 mg/kg body weight did not affect twitch contraction in normal animals. In neostigmine-pretreated animals, however, doses between 12.5 and 90 mg/kg could entirely abolish the anticholinesterase-induced twitch augmentation. In vitro, prednisolone produced a depressant effect on the twitch of a normal phrenic nerve diaphragm preparation which could amount to 20%. When the preparation was pretreated with neostigmine the augmented twitch could be depressed by 10(-3) to 10(-6) mol/l prednisolone to levels below the untreated control. Part of this effect is owing to a suppression of the neostigmine-induced, stimulus-bound repetitive firing of the motor nerve terminals, but to explain the full effect a further inhibitory action on neuromuscular transmission must be assumed. The latter could be accounted for by a depolarizing interaction of prednisolone and neostigmine on the nerve terminals resulting in conduction block. An action of prednisolone on postsynaptic receptors could also be considered. Such effects of the glucocorticoid might contribute to the exacerbation of muscular weakness occasionally observed in patients with myasthenia gravis at the beginning of steroid therapy.
The electrophysiological and metabolic responses to insulin of skeletal muscles from control and potassium-depleted rats were compared. Membrane potentials, action potentials, contraction parameters as well as oxygen uptake were measured in diaphragm strips or intact extremity muscles from the two groups, and similar measurements were made in vivo. The muscles were examined in solutions with normal potassium concentration [K]o , reduced [K]o, and in normal [K]o and in normal [K]o with ouabain, in each case before and after insulin, 400 mU/ml. In normal solution, the depleted muscle contractions were weaker and slower than control. The depleted muscles, already having low potassium conductance, are paralysed by the further reduction of potassium conductance after insulin. Hyperpolarising effects of insulin-induced Na/K pumping are offset in the depleted muscles with a high sodium conductance and low [K]o. Respiration is about normal at rest in depleted muscles, despite increased [Na]i, suggesting that the sodium is sequestered. After insulin, reduction of [K]o, or ouabain plus insulin, the depleted fibres take up more O2 than controls. In the presence of ouabain, this respiratory stimulation is believed to represent response to Ca++ influx. The K-depleted rat does not seem to be an entirely satisfactory model of the human disease hypokalaemic periodic paralysis.
The effects of the lidocaine derivative 2-amino-2',6'-propionoxylidide hydrochloride (tocainide, W-36095) on the contraction force and on membrane resting and action potentials of rat diaphragm were tested in vitro. In a concentration of 5 x 10(-4) mol/l, tocainide reduced the amplitude of the twitch by about 25% within 15 min. This reduction was reversible on washout of the drug. Tocainide had little effect on the membrane resting potential, but considerably affected the action potential: rate of rise, maximum amplitude and rate of fall were reduced, the duration increased. The conduction velocity of the action potential was reduced by 20%. Experimental myotonia produced in excised diaphragms or in anesthetized whole animals by anthracene-9-carboxylic acid was completely abolished by low doses of tocainide.
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Fourteen patients with paramyotonia congenita were examined clinically. Patients of 3 families had no myotonia in a warm environment while in a cold environment they developed paradoxical myotonia (myotonia aggravated by repeated muscle contraction). Patients of a 4th family had myotonia associated with after-activity in a warm environment which was not paradoxical. This myotonia was aggravated by cooling. In a warm environment the resting muscles of all patients showed no spontaneous electromyographic activity except for occasional myotonic runs. On cooling, spontaneous fibrillations developed. This was most intense at 32 degrees C-28 degrees C (muscle temperature). On deeper cooling it ceased. In contrast, 5 patients with myotonia congenita did not show such activity during cooling. In all paramyotonic patients cooling (30 degrees C-25 degrees C) produced muscle paralysis, which outlasted rewarming by several hours. At 32 degrees C-30 degrees C muscle relaxation was slowed. Recording of electromyographic activity and isometric contractions of the long finger flexors during cooling revealed that the slowing of muscle relaxation in paramyotonia is not as closely linked to after-activity as is the slowing of muscle relaxation in myotonia congenita.