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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surface electromyographic "EMG" activity in biceps brachii (agonist muscle) and triceps brachii (antagonist muscle) as well as the discharge behaviour of motor units "MUs" (needle recording) in biceps brachii muscle were recorded during slow (0.33 Hz) and fast (0.66 Hz) voluntary elbow flexion movements (auditory matching task) in fifty patients with spastic hemiplegia. In the spastic limbs, a long lasting, small amplitude tonic co-contraction of antagonist muscles was seen during slow flexions (SF) in 29 cases. This effect was strongest during the fast elbow flexion movements (FF). In 33 patients a triphasic pattern of muscle activation was observed on the unaffected side but not on the spastic side. The amplitude of the agonist surface EMG was significantly reduced and the amplitudes of the MU potentials recruited during maximal effort were generally smaller on the spastic side compared to the unaffected side. The agonist-antagonist activation pattern was analysed with respect to three clinically identifiable functional recovery stages of voluntary movements in the spastic limbs, namely synergistic, isolated and useful movements. The MU amplitudes and the amplitude of the surface EMG activity in the agonist muscle recorded during FF movements became significantly larger whereas the amplitude of the antagonist tonic activity became smaller with increasing functional recovery of the limb. It is concluded that impaired recruitment of type II motor units in the agonist muscles and the inability to selectively activate the agonist muscle contribute to the deficit in motor performance in spastic paresis.
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PMID:Impaired activation pattern in antagonistic elbow muscles of patients with spastic hemiparesis: contribution to movement disorder. 835 30

Two cases of traumatic internal carotid artery occlusion probably related to the seat belt shoulder strap are reported. Case 1. A 20-year-old woman was driving and was struck on the right front side of her car by another car. There were neither bruises, abrasions on her neck, nor weakness in her extremities. About 4 hours later, she developed left hemiplegia, and CT scan taken on the following day revealed low density areas in the capsulostriatal area on the right. The right carotid angiography revealed occlusion of the internal carotid artery about 3 cm distal to the bifurcation. Case 2. A 43-year-old man was driving and was struck on the front of his car by a hard iron railing. He sustained a sternum fracture, but there was no disturbance of consciousness or paresis of the extremities. His neck was unremarkable externally. About 50 days later, he developed left hemiplegia. CT scan and MRI revealed a massive infarction in the distribution of the right middle cerebral artery territories. The carotid angiography revealed occlusion of the right internal carotid artery about 3 cm distal to the bifurcation. In each cases, the driver was wearing a three-point shoulder seatbelt when the car was struck on the front or on the right front. Previous experimental studies have revealed in these situations the neck is flexed right anteriorly, and then quickly overextended left posteriorly. The overextension of the neck probably injured the intima of the internal carotid artery ipsilateral to the shoulder fixed in the seatbelt, resulting in the subsequent occlusion by a thrombus.
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PMID:[Internal carotid artery occlusion related to seat belt shoulder strap: report of two cases]. 890 87

We reported five patients having presented only with clumsy hand and dysarthria which resulted from motor paresis confined to one side of the fingers and the ipsilateral face and tongue. All of them were right-handed, and their manifestation was transient. They had no abnormalities of muscle tonus and sensation, and no ataxia. The features of these cases differed from those of the dysarthria-clumsy hand syndrome because of absence of ataxia, and could be distinguished from pure motor hemiplegia by a motor paresis with cheiro-oral topography. MRI examinations showed a localized lesion at the border between internal capsule and corona radiata (two cases), or in the corona radiata just over this region (three cases). In the former cases in which the internal capsule was involved, we confirmed the lesion in the genu and anterior half of the posterior limb of the internal capsule. The lesion was on the left side in all five patients. It has been known that the pyramidal tract consists of the large and small fibers. The large ones are localized in the posterior part of the posterior limb of the internal capsule, and the damage of them produces sustained and serious motor paralysis. The small ones are widely distributed in the genu and the posterior limb of the internal capsule. The findings of our study suggest that the small fibers have adjacent somatotopy for the hand and mouth in the region of the genu and the anterior part of the posterior limb of the internal capsule, and that the damage of them may lead to mild, transient motor paresis without spasticity.
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PMID:[Motor paresis with cheiro-oral topography due to small infarct in the internal capsule or the corona radiata]. 914 66

Based on the results of several electrodiagnostic and biomechanical studies, the following classification of muscle dysfunction in spastic hemiplegia is proposed: changes in muscle activation (excess symptoms, e.g., spasticity, and deficit symptoms, e.g., paresis); changes in muscle stiffness; and changes in muscle length. The clinical significance of this classification is that different types of muscle dysfunction might require specific treatment. The authors have developed techniques to measure quantitatively each type of muscle dysfunction: free frequency repetitive movement (FFRM) and torque angle diagram (TAD). Surface EMGs of tibialis anterior, gastrocnemius, and soleus muscle are recorded during active (FFRM) and passive (TAD) ankle movements. EMG data are converted to parameters for abnormal muscle activation (excess and deficit symptoms). Parameters for muscle stiffness and muscle length are derived from the hysteresis curve of the TAD. This article describes the measurements and the results of a validation study. For the validation study, four hypotheses were formulated: 1) in nonimpaired control subjects, parameters expressing abnormal muscle activation are low; 2) in hemiplegic subjects, differences between the affected and the unaffected sides will be found for all types of parameters; 3) after local anaesthesia of the tibial nerve on the hemiplegic side, excess symptoms will decrease, while muscle stiffness remains unchanged; and 4) despite a uniform gait pattern, between-subject differences can be detected with regard to muscle activation, stiffness, and length. The first hypothesis was tested and confirmed in two controls; the remaining three were tested and confirmed in ten hemiplegic subjects (mean age 47.7 yrs, mean time since onset 10.7 yrs). However, the level of co-contraction of the gastrocnemius muscle was low, probably indicating that the clinical significance of this phenomenon might be limited. The results support the validity of the proposed classification and measurements.
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PMID:Measurement of impaired muscle function of the gastrocnemius, soleus, and tibialis anterior muscles in spastic hemiplegia: a preliminary study. 970 15

Twenty-four children with infantile cerebral palsy (6 girls and 18 boys aged 3-17 years), surgically treated in the years 1993-1997, were involved in the study. Neurological-orthopaedic examinations and computer tomography (CT) of the head allowed precise diagnosis and understanding of its pathology. The group consisted of 10 patients with hemiplegia, 10 with diplegia and 4 with severe quadriplegia. In 18 children changes in the brain were largely dependent on the clinical type of paresis. In hemiparesis, unilateral changes, such as cerebral cortex atrophy with enlarged ventricles, were predominant. Diplegia cases frequently showed periventricular damage to the white matter. Brain tomography in severe quadriplegia did not always correspond to the clinical condition. CT examinations revealed no abnormalities in the brain in 6 out of 24 cases. Since the results of rehabilitation were not satisfactory, 29 surgical procedures were performed in the presented group of patients, with improved the course of therapeutic rehabilitation or nursing care in all the children.
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PMID:Morphological brain damage, functional disorders and the possibilities of their treatment in children with infantile cerebral palsy. 997 49

We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.
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PMID:[A 96-year-old man with consciousness disturbance, convulsion, and left hemiplegia of acute onset]. 1006 67

Massive cerebral infarction is often accompanied by early death secondary to transtentorial herniation. Decompressive hemicraniectomy has been suggested as a lifesaving procedure. We report the case of a 61 year old man who had an acute infarction in the distribution area of the right middle cerebral artery. Initially, he was awake and suffered from total left-sided hemiparalysis. Over the next two days, his level of consciousness deteriorated to a Glasgow Coma Scale score of 5. Intracranial pressure (ICP) monitoring was then established. Three days later, the ICP increased from 20 to 40 mm Hg. We performed a right-sided decompressive hemicraniectomy, and the ICP was normalized immediately. Ten months after surgery the patient was at home and functioning with minimal assistance. He had moderate paresis of the left leg and was able to walk, but his left arm was paralytic. The presented case confirms that decompressive hemicraniectomy may prevent death and allow survival without severe disability in patients with massive cerebral infarction.
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PMID:[Decompression craniectomy--life-saving treatment in acute cerebral infarction]. 1066 83

A series of 17 patients aged from 9 months to 32 years with refractory epilepsy due to hypothalamic hamartoma were treated by total removal (one case) and disconnection (16 cases) between 1997 and 2002. The mean age at seizure onset was 16 months. Sixteen patients had gelastic seizures, 14 had partial seizures and three had generalized tonic-clonic seizures. The mean seizure frequency was 21 per day. Four patients had borderline intelligence quotient and the others were mentally retarded. Five patients presented with precocious puberty, one with acromegaly, and four suffered from obesity. Brain magnetic resonance imaging, performed at least twice in each patient, showed the hamartoma as a stable homogeneous interpeduncular mass implanted either on the mammilary tubercle or on the wall of the third ventricle with variable extension to the bottom. Ictal single photon emission computed tomography, performed in four patients, showed hyperperfusion within the hamartoma in two patients. Twenty-five operations were performed in the 17 patients. The first patient underwent total removal of the hamartoma, whereas the following 16 patients underwent disconnection through open surgery (14 procedures) and/or endoscopy (9 procedures). Eight patients became seizure-free, one patient had only brief gelastic seizures, and eight patients were dramatically improved with a mean follow up of 18.6 months (8 days to 43 months). Surgery was safe in all but two patients: the first patient had transient hemiplegia and the third cranial nerve paresis, and the other developed hemiplegia due to ischemia of the middle cerebral artery territory. The quality of life, and behavior and school performance were greatly improved in most patients. Our series illustrates the feasibility and relative safety of disconnection surgery for hypothalamic hamartomas with seizure relief in 53% of patients and dramatic improvement in the others. Surgical observations led us to propose a new anatomical classification according to the anatomical relationship between the hamartoma and the adjacent hypothalamus and third ventricle. Endoscopic disconnection seems to be a very safe way to treat hamartomas in intraventricular locations.
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PMID:Disconnecting surgical treatment of hypothalamic hamartoma in children and adults with refractory epilepsy and proposal of a new classification. 1262 81

We report a case of a bacterial brain abscess presenting symptoms of 'sudden stroke-like' onset, associated with infective endocarditis. A 59-year-old woman experienced a sudden stroke-like onset of left hemiplegia. Computed tomography (CT) and magnetic resonance imaging (MRI) were performed on the day of ictus. No lesion responsible for the symptom was seen on either CT or a T2 weighted image (T2WI), but a diffusion-weighted image (DWI) revealed focal increased signal intensity in the right frontal lobe. An initial diagnosis of acute embolic infarction associated with infective endocarditis was made. Although the patient's neurological state had been stable, motor paresis of her left extremities became worse starting one month after her admission. MRI with gadolinium-diethylenetriaminepenta-acid (Gd-DTPA) at 37 days after admission showed an irregular-shaped ring-enhancement lesion located at the same place as the initial infarction, and in the left frontal lobe. Surgical drainage of the lesion in the right frontal lobe was performed, and diagnosed as a bacterial abscess. The exact mechanism of a bacterial brain abscess presenting with 'sudden stroke-like' onset is unknown, but various hypotheses have been proposed. One is that paroxysmal septic emboli lead to abscess formation within or near the area of embolic infarction. Our case showed that the creation of a brain abscess followed embolic strokes, and that this hypothesis was demonstrated by MRI carried out on the day of ictus.
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PMID:[A case of a bacterial brain abscess presenting as symptoms of 'sudden stroke-like' onset]. 1270 27

Clinical-anatomic correlations were performed in 25 patients with focal infarcts in the basilar pons to determine whether pontine lacunar syndromes conform to discrete clinical entities, and whether there is topographic organization of the motor system within the human basis pontis. Twelve clinical signs were scored on a 6-point scale, neuroimaging lesions were mapped and defined with statistical certainty, and structure-function correlation was performed to develop a topographic map of motor function. Clinical findings ranged from major devastation following extensive lesions (pure motor hemiplegia) to incomplete basilar pontine syndrome and restricted deficits after small focal lesions (ataxic hemiparesis, dysarthria-clumsy hand syndrome, dysarthria-dysmetria and dysarthria-facial paresis). The syndromes are not absolutely discrete, and are distinguished from each other by the relative degree of involvement of each clinical feature. Structure-function correlations indicate that strength is conveyed by the corticofugal fibres destined for the spinal cord, whereas dysmetria results from lesions involving the neurons of the basilar pons that link the ipsilateral cerebral cortex with the contralateral cerebellar hemisphere. Facial movement and articulation are localized to rostral and medial basilar pons; hand coordination is medial and ventral in rostral and mid-pons; and arm function is represented ventral and lateral to the hand. Leg coordination is in the caudal half of the pons, with lateral predominance. Swallowing is dependent upon the integrity of a number of regions in the rostral pons. Gait is in medial and lateral locations throughout the rostral- caudal extent of the pons. Dysmetria ipsilateral to the lesion constitutes a disconnection syndrome, as it occurs when the hemipontine lesion is extensive and interrupts pontocerebellar fibres traversing from the opposite, intact side of the pons. The heterogeneity of manifestations reflects the well-organized topography of motor function in the human basis pontis, in agreement with the anatomic organization of the motor corticopontine projections in the monkey. Higher order impairments including motor neglect, paraphasic errors and pathological laughter result from rostral and medial pontine lesions, and may result from disruption of the pontine component of associative corticopontocerebellar circuits.
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PMID:The human basis pontis: motor syndromes and topographic organization. 1512 14


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