Cortico-facial and cortico-trigeminal projections. A comparison by magnetic brain stimulation in man.
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Biomedical subjects
Publications and source records attributed to M Manfredi.
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The masseter inhibitory reflex (MIR) was investigated in 16 patients with localized brainstem lesions involving the trigeminal system. The MIR consists of two phases of EMG silence (S1 and S2) evoked by stimulation of the mental nerve during maximal clenching of the teeth. The extent of the lesions was assessed by neurological examination, nuclear magnetic resonance imaging (MRI), and recording of trigeminal reflexes with known paths (jaw jerk and blink reflex). The MIR appeared to be abnormal in lesions involving the pontine tegmentum, from the pontomedullary junction to midpons, and some lesions selectively affected one component of the MIR, proving that S1 and S2 are relayed by independent circuits. The results indicate that afferent fibres for S1, which reach the pons via the trigeminal sensory root, enter the ipsilateral trigeminal spinal tract and terminate at the level of the midpons; impulses are then relayed by interneurons to the ipsilateral and contralateral trigeminal motor nuclei. The afferent fibres for S2 follow a similar path, but descend to the pontomedullary junction; at this level impulses are conducted along bilateral interneuronal paths, which probably ascend through the lateral reticular formation, before connecting with the trigeminal motor nucleus on either side. Analysis of MIR recordings can be of particular value because brainstem inhibitory reflexes cannot be tested by clinical examination.
The trigeminal reflexes (corneal reflex, blink reflex, masseter inhibitory periods, jaw-jerk) and far field scalp potentials (nerve, root, brainstem, subcortical) evoked by percutaneous infraorbital stimulation were recorded in 30 patients with "idiopathic" trigeminal neuralgia (ITN) and 20 with "symptomatic" trigeminal pain (STP): seven postherpetic neuralgia, five multiple sclerosis, four tumour, two vascular malformation, one Tolosa-Hunt syndrome, and one traumatic fracture. All the patients with STP and two of those with ITN had trigeminal reflex abnormalities; 80% of patients with STP and 30% of those with ITN had evoked potential abnormalities. The results indicate that 1) trigeminal reflexes and evoked potentials are both useful in the examination of patients with trigeminal pain, and in cases secondary to specific pathologies provide 100% sensitivity; 2) in "symptomatic" and "idiopathic" paroxysmal pain the primary lesion affects the afferent fibres in the proximal portion of the root or the intrinsic portion in the pons; 3) primary sensory neurons of the A-beta fibre group are involved in both paroxysmal and constant pain, but in the latter the damage is far more severe.
To test whether calcium channel blockade plays a similar role in the coronary vasomotion of patients with syndrome X (n = 29) and patients with Prinzmetal's angina pectoris (n = 12), quantitative angiography was used to evaluate the effect of nifedipine (10 mg, sublingually) on the lumen diameter of proximal, mid and distal thirds of normal epicardial branches. The main differences in the coronary vasomotor reaction were uniform vasodilatation in Prinzmetal's angina and a variable response to syndrome X, and a greater increase in the coronary lumen in patients with Prinzmetal's angina as compared with those with syndrome X who showed vasodilatation. The variable response in syndrome X was not related to changes in diastolic pressure and cardiac output. Patients showing coronary constriction were those who responded to nifedipine with a higher degree of tachycardia, which might suggest a neural participation in the paradoxic reaction to this drug. In the Prinzmetal group, on the contrary, at a similar heart rate increase the pattern was invariably vasodilatation. Thus, calcium ions appear to have a different role in the coronary smooth muscle contractility of the 2 series of patients; in fact, in Prinzmetal's angina nifedipine relaxed the coronary arteries to a greater degree and made them unresponsive to stimuli that were still able to cause vasoconstriction in patients with syndrome X.
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Mechanical or electrical stimulations in the area of the mouth evoke two phases of inhibition in the masseter muscle (early and late inhibitory reflex, also called masseter silent periods). The question whether the afferents of the human masseter inhibitory reflex are nociceptive or non-nociceptive has not yet been settled. We showed that an innocuous stimulus, such as a fine jet of saline directed to the lips of healthy humans, evokes an early and a late masseter inhibitory reflex, similar to those following electrical stimulation. We measured the efferent and afferent delay of the masseter early inhibitory reflex in patients submitted to intracranial stimulation of the motor and sensory trigeminal root, and found that the reflex afferents belong to the intermediately-fast conducting fibre group.
A simple composite probe for surface acoustic and electromyographic recording is described. A piezoceramic transducer, glued to a flexible printed circuit board etched to form 3 copper strips, taped firmly onto the skin can pick up fibre acoustic noise and electrical activity.
Transcranial stimulation (TCS) in intact human subjects was used to investigate the corticobulbar projections and the functional organization of the trigeminal motor system. Both electrical (with the anode overlying the face area of the motor cortex) and magnetic TCS (with the coil at the vertex) excite the upper motoneurons projecting to the trigeminal motor nucleus, evoking motor potentials (C-MEPs) in the jaw-closing and suprahyoid muscles, but only during voluntary contraction. At least 30% of jaw-closing motoneurons are reached by direct fast-conducting corticobulbar fibres; these projections are mainly crossed. Suprahyoid motoneurons are also reached by fast-conducting corticobulbar fibres; these projections are probably bilateral. In the masseter, electrical TCS also evokes an ipsilateral motor response (R-MEP), followed by a later wave (U), and bilateral inhibitory periods. The R-MEP is secondary to excitation of the motor trigeminal root; the U wave probably results from the simultaneous excitation of Ia afferents in the root and ipsilaterally projecting corticofugal fibres; the inhibitory periods are largely due to activation of exteroceptive afferents in the root. Magnetic TCS, avoiding spread of current to the trigeminal root, evokes C-MEPs but not R-MEPs or U waves. The masseter inhibitory period after magnetic TCS may be due to excitation of corticofugal inhibitory fibres and to mechanical activation of Golgi tendon organs.
By raising the body temperature of 0.5 degrees C the critical fusion frequency of a flickering light increases in normal subjects but decreases in multiple sclerosis (MS) patients. The change was present in 14 patients with definite MS and in 5 of 10 patients with probable MS. No clinical worsening was observed during the procedure or in the following hours.
The descending volley evoked in humans by transcranial electrical stimulation of the scalp was recorded with epidural and spinal electrodes. It consisted of an early wave, which increased in amplitude and decreased in latency when the strength of the stimulus was increased. The mean conduction velocity of the early wave was 66, SD 2.5 m/s. At high stimulus intensity this wave was followed by later and smaller waves, which travel at the same speed as the initial potential. The recovery cycle of the descending volley was studied by delivering paired cortical stimuli at time intervals ranging from 0.5 to 10 ms. The early wave evoked by the test stimulus recovered to about 50% at a 1 ms interval and to 100% at a 3.5 ms interval. The later waves could not be tested at short time intervals but with time intervals longer than 3.5 ms they recovered to 100%. It is suggested that the initial and later waves after scalp stimulation are equivalent to the D and I waves seen in animal experiments.
From 1976 to 1986, 681 patients with drug-refractory trigeminal neuralgia (TN)--typical in 641, symptomatic of multiple sclerosis in 23 and of tumor in 10, atypical in 5, and postherpetic in 2--were treated with various percutaneous procedures. Controlled differential thermocoagulation of the gasserian ganglion and/or retrogasserian rootlets was performed in 533 patients; glycerolization of the trigeminal cistern in 32; and compression of the gasserian ganglion by balloon catheter in 159. Results and complications of each procedure are assessed at a mean follow-up of 6.5 years for thermocoagulation, 5 years for glycerolization, and 3.5 years for compression. The following therapeutic protocol is proposed: 1) in TN patients at first operation: a) gasserian compression (or glycerolization, if experience warrants it) is indicated in all cases of typical TN, unless the 3rd division alone is affected; b) in the latter case and in symptomatic TN, we suggest thermocoagulation; 2) in recurrences: a) after glycerolization or gasserian compression, gasserian compression (or glycerolization) is indicated; b) after thermocoagulation or open surgery, thermocoagulation is suggested.
In this study we tested whether Ca++ has a similar part in the coronary vasomotion of patients with syndrome X (n = 29) and patients with Prinzmetal angina pectoris (n = 12). Through quantitative angiography we evaluated the influence of nifedipine (10 mg sl) on the lumen diameter of proximal, mid and distal thirds of normal epicardial branches. The main differences in the coronary vasomotor reaction were: uniform vasodilatation in Prinzmetal angina and a variable response in syndrome X; greater increase in the coronary lumen in patients in the former as compared to those in the latter group who showed vasodilatation. The variable response in syndrome X was not related to changes in diastolic pressure and cardiac output. Patients showing coronary constriction were those who responded to nifedipine with a higher degree of tachycardia; this might suggest a neural participation in the paradoxical reaction to this drug. In the Prinzmetal group, on the contrary, at similar heart rate increase the pattern was invariably vasodilatation. Thus, calcium ions appear to have a different role in the coronary smooth muscle contractility of the 2 series of patients; in fact, in Prinzmetal angina nifedipine relaxed the coronary arteries more potently and made them unresponsive to stimuli which were still able to cause vasoconstriction in syndrome X.
Rapid elbow flexion movements were studied in patients with an upper motor neuron syndrome following a stroke. The velocity of movements was slower than normal. The initial bursts of electromyographic (EMG) activity in both the agonist and antagonist muscles were prolonged. As in normal subjects, the first agonist burst increased in duration with larger movements, but it generally remained about 40 ms longer than normal. The size of the first agonist burst also increased with larger movements. A fixed linkage between burst duration and level of motor unit recruitment, together with a deficient corticospinal command, could explain the prolonged burst duration with preserved ability to modulate the burst.
Blink and corneal reflexes were studied in 11 patients with Huntington's chorea and the results compared with the severity of the disease. The latency of the R2 component of the blink reflex was delayed and the duration of R2 and of the corneal reflex (CR) prolonged. A greater habituation of the R2 component was found in the patients with involuntary movements in the face, and in some patients a long-lasting depression of R2 was present. A correlation was found between: (a) severity of involuntary face movements and R2 and CR latency and (b) severity of involuntary movements in the neck and latency of R2.
Percutaneous electrical stimulation of the motor cortex was used to evaluate corticospinal conduction to upper-limb motoneurons in 29 patients with multiple sclerosis. Central motor conduction abnormalities were correlated with clinical signs and somatosensory evoked potentials. Muscle responses to cortical stimulation were altered in 20 patients. The most common abnormality was increased central motor conduction time; in two cases the responses to cortical stimulation were absent. Abnormalities were also present in patients with no clinical evidence of corticomotoneuron deficit. Alterations of muscle responses and of somatosensory evoked potentials were usually correlated, but may appear independently. Both testing methods are useful in the study of patients with multiple sclerosis.
We studied masseter muscle function in 15 hemiplegic patients. Direct motor responses to stimulation of the masseteric nerve were normal. Voluntary activity at maximum strength was reduced on the paretic side. The jaw jerk was symmetric, but facilitation by teeth clenching showed on the nonparetic side only. Masseter silent periods were ill-defined and prolonged in recordings from the paretic side. The second silent period, but not the first, was reduced in size when the paretic side was stimulated, and showed an increased habituation. Though the masticatory nucleus receives bilateral innervation, the contralateral hemisphere exerts a predominant control on voluntary activity and multisynaptic reflexes.
The author provides some material for reflection on the issue of developing leadership in the health sector; in this case, in the specific area of nursing. Within this context, her proposition is that leadership is a process which comprises different levels of development, having an individual and collective dimension as well as conceptual, methodological and operational aspects. She proposes the adoption of policies which would point to the need of encouraging nurses to play an effective role in the processes that lead to the making of important decisions in the sector; she advocates that nurses participate in drawing up national health plans and in the management of community health services. It is pointed out that "the power of nursing as a profession lies in its practice"; this entails the need for basic changes, both in services and in the area of education, if the leadership position that has emerged in several countries during the last decade is to be strengthened. Lastly, the article suggests that in order to strengthen nurses' potential leadership and managerial skills, they should begin to receive leadership training at the undergraduate level, thus awakening in the students the greatest possible interest in the scientific method and in the epidemiological method for the analysis of health and related problems.
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