SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
In a patient of generalised dystonia treated with bilateral pallidal stimulation, serial surface EMGs recorded from the neck muscles during alternating head movements revealed progressive reduction in hypertonic activity and reversal of co-contraction to reciprocal contraction, which preceded clinical improvement.
We describe a 21-year-old man with essential palatal tremor. The patient had rhythmic contractions not only of tensor veli palatini but also of facial, lingual, temporalis, pharyngeal, and neck muscles. He had some voluntary control of palatal tremor and ear clicks. He was treated with 5 units of botulinum toxin-A (BOTOX) injected into each tensor veli palatini, and had complete resolution of all the symptoms.
We determined the frequency of dropped head syndrome in Parkinson's disease (PD) in Japan and evaluated its clinical correlates. A total of 252 consecutive patients with PD who visited our hospital were studied. Dropped head syndrome was found in 15 patients (6.0%) (3 men, 12 women; mean age at onset of PD, 62.8 +/- 11.5 years). The interval before emergence of dropped head after disease onset was 5.4 +/- 4.3 years (-0.5 to 15 years). The Hoehn-Yahr score at the on stage was 3.2 +/- 0.7; at the off stage 3.5 +/- 0.8. Of those 15 patients, 8 had major symptoms of rigidity and akinesia. In 2 patients, administration of a dopamine agonist appeared to evoke dropped head syndrome. An increase in and/or the addition of antiparkinsonian drugs alleviated head drop in 4 patients and reduced head drop in 7 patients. Any medication was not effective for 4 patients. Dropped head syndrome in PD is not rare in Japan. It is more often observed in women and is associated with patients who primarily suffer rigidity and akinesia. Dropped head syndrome in these patients appears to be produced by disproportionate tonus of the neck muscles. It is modulated by antiparkinsonian drugs and is considered to be a type of dystonia.
Isolated dystonia of trunk and neck muscles without involvement elsewhere has been termed segmental axial dystonia--a rare disorder. We report a 31-year-old man who developed marked dystonia of paraspinal muscles and progressive scoliosis 6 months after a closed head injury. Computed tomography (CT) disclosed three small areas of encephalomalacia, one involving the head of the caudate nucleus. Treatment with trihexyphenidyl resulted in significant improvement of the dystonia and scoliosis.
Botulinum toxin A (btx) is used to treat focal dystonias. From accidental intoxications it is known that btx can cause generalized pathologic single-fiber electromyography (SFEMG) findings. We monitored the onset and course of these disturbances in eight patients who received a small dose of btx (2-22 ng) for therapy of focal dystonias in the head/neck region for the first time via repeated SFEMG investigations at days 0, 3, 6, 9, 12, 28, and 56. Recordings were performed in the extensor digitorum brevis muscle, and in two patients additionally in the tibialis anterior muscle. In six of these patients we found an increase of jitter and blocking. The onset of these changes was in the range of 3-13 days after injection. Fiber density showed a tendency to increase. There was no correlation between SFEMG findings and the dose of injected btx. Possible mechanisms for these observations may be either a very efficient local uptake and retrograde axonal transport via the spinal motor neurons or a systemic distribution via the blood circulation.
We observed abnormal involuntary movements, involving principally the facial and neck muscles, in 23 patients with stuttering. These movements were similar to involuntary movements seen in distinct dystonic syndromes. There was a history of stuttering in the first degree relatives of six patients. The association of stuttering with degenerative neurologic disorders and focal brain lesions, cerebral blood flow changes in patients with developmental stuttering, its occurrence as a side effect of centrally acting drugs, induction and alleviation of stuttering by mechanical perturbation, or by electrical stimulation of the thalamus, a strong genetic predisposition with male preponderance, and the statistically significant occurrence of stuttering in the family history of patients with idiopathic torsion dystonia suggest an organic basis for developmental stuttering. These findings and the reported similarities between the involuntary movements associated with stuttering and dystonic involuntary movements support the hypothesis that stuttering is a form of segmental or focal action dystonia.
We report the case of a 59-year-old man with primary intestinal T-cell non-Hodgkin's lymphoma who developed abnormal facial twitching synchronous with small palatal movements induced by attempts at speaking or swallowing. At rest, the electromyogram (EMG) showed no spontaneous muscular activity. Phonation triggered trains of synchronous, rhythmic EMG bursts at a frequency of 3-4 Hz lasting 10-20 s, with an average burst of 150 ms, which simultaneously involved palatal, facial, and neck muscles bilaterally with left-sided predominance. An enhanced blink reflex recovery curve was observed after stimulation of either side. Backaveraging electroencephalographic study revealed no activity that was time locked with the jerks. Axial T2-weighted magnetic resonance imaging showed an increased signal intensity and bilateral enlargement of the inferior olives. No antineuronal-specific antibodies were found in the blood or in the cerebrospinal fluid. All of these clinical findings were consistent with a symptomatic palatal tremor (PT). Because it was triggered by activation of cranial muscles, we termed this movement disorder action PT. To our knowledge, this is the first report of symptomatic PT displaying these features.
Three cases of adverse reactions to repeated intramuscular botulinum toxin A (BTA) injections are described: a persistent rash on the face at the site of injection, a localized anaphylactic reaction following BTA injection into one leg, and bilateral ptosis repeatedly following BTA injection into neck muscles. The mechanisms for these idiosyncratic adverse responses are not known.
A model of the saccadic system of salamanders on the basis of electrophysiological and anatomical results is presented. The model includes centers found to be significant for the guidance of saccades in these comparatively simple vertebrates. In particular, these are the optic tectum, the bulbar reticular formation and the motor system. The latter consists of two pairs of neck-muscles, an epaxial and a hypaxial one driven by their respective motoneurons. The model includes a visual, a sensori-motor, and a motor level. At the sensory level, the retinal coordinates are transferred to the optic tectum to establish an orthogonal map of visual angles. A secondary visual map of the ipsilateral eye with a pointsymmetrical organization exists in addition. The premotor system of the tectum was modelled according to an ensemble-coding principle. Thus, local activation of the visual map results in recruitment of an appropriate number of tectal premotor units. Simulation of the model reproduces correct metric properties of salamander saccades under varying stimulus presentations.
The activity of 52 single auditory units in the central nucleus of the inferior colliculus (IC) was recorded along with cortical and hippocampal (CA1) electrograms and neck muscle electromyograms in behaving, head-restrained guinea pigs during paradoxical sleep (PS) and wakefulness. Sixteen (30%) of the IC auditory units showed positive correlation with the hippocampal theta (theta) rhythm: 8 (15%) were theta rhythmic with theta phase-locking (type 1), 8 (15%) showed only theta phase-locking with no rhythmicity (type 2), while 70% did not show any correlation to hippocampal theta rhythm (type 3). During wakefulness IC neurons (4 of 13) showed a higher synchrony with hippocampal theta when sound-stimulated at the unit's characteristic frequency. During PS all IC auditory neurons recorded presented some hippocampal theta correlation: 40% were rhythmic and phase-locked to the theta frequency and 60% were nonrhythmic maintaining the theta phase-locking. Shifts in the angle of phase-locking to the theta rhythm were observed during PS. It is suggested that the hippocampal theta rhythm may play the part of an internal clock, adding a temporal dimension to the processing of auditory sensory information.
The profile of integration in a sample of 183 interneurones localized in the subnucleus-gamma of the oral nucleus of the spinal trigeminal tract (NVspo-gamma) has been analyzed. 134 neurones were tested for inputs from primary afferents of the trigeminal, facial and cervical nerves as well as for inputs from the midbrain and from the cervical spinal cord. The remaining 49 neurones were tested for inputs from the primary afferents and for descending convergence from defined sites within the oro-facial primary projections of the cerebral cortex. It was found that the interneurones, mainly recorded in the dorsal and dorsomedial aspect of the NVspo-gamma, receive short latency inputs from the low threshold oral and perioral afferents and longer latency inputs from the high threshold jaw and neck muscle afferents. There was evidence for convergence from the cervical segmental level (29%) and some of the neurones had axon terminals in the superior colliculus. However, the interneurones did not receive a descending tectal input. About 80% of the NVspo-gamma interneurones were activated from the orofacial primary projection fields within cytoarchitectonic areas 3a and 3b of the coronal gyrus. This input was topographically organized and the neurones were activated from the same oral and perioral region of the periphery as the cortical region from which the descending projections themselves originated. Minimum latencies indicated a monosynaptic connection. The convergence profile onto the NVspo-gamma interneurones appeared unique as compared with interneurones located in the intertrigeminal area. Aspects of the possible functional roles of the NVspo-gamma neurones are discussed in relation to ongoing oro-facial ("masticatory") movements. The properties of a selected sample of NVspo-gamma interneurones, which were antidromically activated from the digastric subnucleus of the trigeminal motor nucleus, are reported in a companion paper (Olsson and Westberg 1991).
Electrical stimulation of the superior colliculus (SC) in alert cats free to move their head, evoked coordinate eye and head movements. The characteristics of these movements as well as their mode of coordination differed according to the collicular region being explored. Three zones were distinguished. In the anterior zone, evoked eye saccades were retinotopic and the accompanying head movements were slow and small in amplitude. The vestibular slow phase velocity signal was continuously added to the eye saccadic command so that the evoked gaze shift was identical, with the head fixed or free. In the intermediate zone, evoked eye saccades were goal-directed and the synchronous head movements fast and of large amplitude. The vestibular slow phase signal was cancelled during the eye saccade so that the evoked gaze shift was the result of the eye plus head angular displacement. In the posterior zone, the evoked head movements were goal-directed. The pattern of eye movements was similar to a vestibular nystagmus. This zone probably directly commands body orienting movements. A model of SC function in gaze orienting behavior is proposed, calling upon at least two different modes of eye-head coordination.
Compensatory head movements, recorded in unrestrained frogs, were compared to compensatory eye movements recorded from animals that had their head fixed. Movements were evoked by oscillating the animal in the dark (vestibular stimulation) or in the light in front of an earth-fixed, patterned visual background (combined stimulation) or by rotating vertical black and white bars (optokinetic stimulation) around the stationary animal. Oscillations occurred in the horizontal plane at frequencies between 0.025 and 0.5 Hz. Gain and phase values of head and eye movements, relative to stimulus movements were calculated. Evoked eye movements were limited in amplitude to +/- 3-6 degrees, increasing with the size of the animal. Head movements were limited to +/- 30-40 degrees. Resetting fast-phases of both head and eyes were very rarely observed during sinusoidal stimulation and no eye movements were recorded in the absence of intended head movements. Vestibularly evoked head movements exhibited a frequency-dependent threshold that was not observed for vestibulo-ocular responses. Above threshold, the gain of evoked head responses increased and reached a frequency-dependent plateau at which the system behaved approximately linearly. Within the linear range, gain of vestibularly evoked responses increased with frequency (from 0.04 at 0.025 Hz to 0.75 at 0.5 Hz) and phase lead decreased (from about 80 degrees to 0 degrees). Vestibularly evoked eye movements similarly increased in gain from 0.05 to 0.56 and decreased in phase lead from about 56 degrees to 10 degrees over the same frequency range. Optokinetically evoked head and eye movements had their highest gains (about 0.8 and 0.5) at low constant velocities (less than or equal to 1-4 degrees/S) or frequencies (less than or equal to 0.025 Hz). At higher constant velocities or frequencies the gain dropped. The phase lag increased from close to zero (at 0.025 Hz) to about 60 degrees for the head and to about 20 degrees for the eye movements (at 0.25 Hz). These phase lags are explained by reaction times of the evoked movements of about 600 ms (head) and 200 ms (eyes). Combined stimulation evoked compensatory head movements with gain and phase values that were frequency-independent in the linear range. Head movements compensated for about 80-90% of the imposed gaze shift with a small phase lag (0-10 degrees). Evoked eye movements were found to be large enough in amplitude and fast enough in time to enable a frog to stabilize its gaze exclusively with slow phase compensatory movements for a large variety of frequency and amplitude combinations. The two motor systems controlling movements of the head and the eye are matched in such a way that the non-linearities of the evoked eye movements can compensate for the non-linearities of the evoked head movements.
(1) Compensatory slow phase movements were evoked by optokinetic, vestibular and combined optokinetic and vestibular stimulation. Superimposed fast phases resetting the position of the head (in space) and of the eye (in head) were recorded with a magnetic field search coil in unrestrained and head fixed frogs, respectively. (2) Head fast phases recorded during optokinetic stimulation covaried in the frequency of their occurrence with slow phase head velocity. Their amplitude was large (average 18.9 +/- 8.9 degrees), maximal velocity increased with amplitude by 6.6 degrees/s/deg, and duration (average 230 +/- 33 ms) was almost independent on amplitude. (3) Ocular fast phases rarely occurred during sinusoidal stimulation and neither optokinetic after nystagmus nor postrotatory nystagmus were observed. Fast phases, evoked by constant velocity optokinetic or acceleratory stimuli, consisted of two components: a primary resetting fast phase and a smaller fast movement in the opposite direction. The primary fast phase had a small amplitude (average 2.2 +/- 1.3 degrees). In different stimulus conditions fast phase parameters were very similar. Maximal velocity increased by 6.5 degrees/s/deg. Duration (average 165 +/- 23.4 ms) was variable. (4) During ocular fast phases the vestibulo-collic and the optokinetic-collic reflexes were suppressed. The slow phase head velocity either became zero or a small head fast phase in the direction of the ocular fast phase occurred. Fast phase head movements were accompanied by an ocular fast phase or by a retraction of one or both eyes, depending on the amplitude of the head fast phase. At the end of a head fast phase eye position was always recentered.
Oculomotor control in man was investigated during passive, sinusoidal, whole-body rotation under a conflict between the vestibulo-ocular reflex (VOR) and the eye tracking system (ETS), as to the appropriate direction of compensatory eye movements. ETS predominated at stimulus frequencies below 0.8 Hz, and VOR above 1.5 Hz. In the intermediate frequency range the dominance repeatedly flipped between ETS and VOR, suggesting that the interaction of the two systems is not linear, but rather governed by a switch.
Eye and head movements are strongly interconnected, because they both play an important role in accurately determining the direction of the visual field. The rostral brainstem includes two areas which contain neurons that participate in the control of both movement and position of the head and eyes. These regions are the caudal third of Field H of Forel, including the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and the interstitial nucleus of Cajal with adjacent reticular formation (INC-RF). Lesions in the caudal Field H of Forel in monkey and man result in vertical gaze paralysis. Head tilt to the opposite side and inability to maintain vertical eye position follow lesions in the INC-RF in cat and monkey. Projections from these areas to extraocular motoneurons has previously been observed. We reported a study of the location of neurons in Field H of Forel and INC-RF that project to spinal cord in cat. The distribution of these fiber projections to the spinal cord are described. The results indicate that: 1. Unlike the neurons projecting to the extra-ocular muscle motoneurons, the major portion of the spinally projecting neurons are not located in the riMLF or INC proper but in adjacent areas, i.e. the ventral and lateral parts of the caudal third of the Field H of Forel and in the INC-RF. A few neurons were also found in the nucleus of the posterior commissure and ventrally adjoining reticular formation. 2. Neurons in caudal Field H of Forel project, via the ventral part of the ventral funiculus, to the lateral part of the upper cervical ventral horn. This area includes the laterally located motoneuronal cell groups, innervating cleidomastoid, clavotrapezius and splenius motoneurons. At lower cervical levels labeled fibers are distributed to the medial part of the ventral horn. Projections from the caudal Field H of Forel to thoracic or more caudal spinal levels are sparse. 3. Neurons in the INC-RF, together with a few neurons in the area of the nucleus of the posterior commissure, project bilaterally to the medial part of the upper cervical ventral horn, via the dorsal part of the ventral funiculus. This area includes motoneurons innervating prevertebral flexor muscles and some of the motoneurons of the biventer cervicis and complexus muscles. Further caudally, labeled fibers are distributed to the medial part of the ventral horn (laminae VIII and adjoining VII) similar to the projections of Field H of Forel. A few INC-RF projections were observed to low thoracic and lumbosacral levels.(ABSTRACT TRUNCATED AT 400 WORDS)
A statistical study was done to determine the incidence of congenital torticollis. The aetiological relationship between torticollis and obstetrical paralysis was analysed in an attempt to clarify the possible cause of torticollis. There were forty-three cases of torticollis in the 2,160 babies delivered at the Otsu Red Cross Hospital from 1978 to 1981. The overall incidence of torticollis was 1.9%; 1.2% in cephalic presentations, 6.5% in double breech presentations, 4.2% in footling presentations and 34.0% in single (frank) breech presentations. In addition, forty-three cases of obstetrical paralysis treated in Kyoto University Hospital from 1961 to 1981 were reviewed. Torticollis was found in 26% of the cephalic presentations (6 out of 23) and in 80% of the breech presentations (16 out of 20) respectively. These findings suggest that a foetal posture with both the knees and the cervical spine extended seems to be closely related to the development of torticollis, which indicates that a direct cause may be stretching of the sternocleidomastoid muscle during delivery.
Explore the source record for details and available documents.