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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic stroke in the vertebrobasilar arterial territory often presents stunning signs and symptoms, and poses little difficulty in the clinical diagnosis. But in less dramatic cases, it is often difficult to make accurate clinical diagnosis and to document the precise extent of an infarct. The purpose of the present study is to demonstrate clinicotopographic correlations in patients with various brainstem and cerebellar infarctions and to reevaluate the importance of bedside clinical examinations for understanding pathophysiology and planning management of the patient. One hundred forty-three patients with clinical diagnosis of the vertebrobasilar infarction confirmed by MRI were studied. MRI is superior to CT scanning in delineating areas of infarction in the territory of posterior cerebral circulation because of the three dimensional approach and the lack of bone artifact. MRI also allowed very precise clinicotopographic correlations even in patients with good recovery, in whom pathologic verification of the lesion is not possible. There are some restrictions of MRI diagnosis to detect the clinical features which change from hour to hour, because of the mechanical limitation in spatial resolution and of the temporal uncertainty of the lesions such as reversible edema or coincidental asymptomatic old lesions. Clinical importance of ocular signs (eg. skew deviation, gaze limitations, nystagmus, pupillary abnormalities and so on) was discussed. Some eye-movement abnormalities (eg. gaze paresis, MLF syndrome, 'one-and-a-half' syndrome, lateropulsion or contrapulsion of eyes, and vertical nystagmus at the primary position) served as useful localizing signs, and especially their consecutive observations were of importance for clinical local diagnosis. Clinical syndromes, caused by lacunar lesions located either in the supratentorial or in the infratentorial structures, such as pure motor hemiparesis and ataxic hemiparesis were also discussed. In some cases of these syndromes, MRI failed to document the precise lesion responsible for the episode due to the multiplicities of small asymptomatic lesions. Even in such cases, detailed clinical informations (temporal profiles of the episode, past medical histories, neuro-ophthalmic signs and so on) may enable the differential diagnosis. It is concluded that the use of new imaging techniques such as MRI may provide new insights in the diagnosis of cerebrovascular diseases, but the importance of clinical observations can not be overemphasized.
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PMID:[Clinical aspects of brainstem infarction]. 209 72

A 67-year-old woman with medial medullary infarction is reported, including clinical manifestations, MRI and angiographical findings, and results of evoked potentials. She suffered from contralateral hemiplegia and disturbance of deep sensation. Motor paresis of the tongue was absent. Magnetic resonance imaging revealed a lesion in the medial portion of the medulla oblongata. The 17 cases previously reported with medial medullary infarction are reviewed. Only 3 cases had triad of medial medullary infarction, contralateral hemiparesis, deep sensory disturbance, and ipsilateral hypoglossal paresis. Therefore, lesion detection is necessary to diagnose medial medullary infarction. Most infarctions limited to the upper third of the medulla were caused by occlusions of vertebral arteries or their branches and prognosis was good. In contrast, infarctions in the lower two thirds were caused by occlusions of anterior spinal arteries and their branches and the prognosis was poor. Thus localization of the lesion using MRI plays an important role to predict the prognosis.
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PMID:[Medial medullary infarction demonstrated by MRI]. 218 65

We report 5 patients with unilateral infarct and 1 with hemorrhage limited to the genu of the internal capsule. The most prominent finding was contralateral facial and lingual hemiparesis with dysarthria. Three patients also showed unilateral mastication-palatal-pharyngeal weakness, and 1 had unilateral vocal cord paresis. Mild limb involvement was limited to hand weakness in 4 patients. Our findings suggest that the majority of motor corticopontine and corticocobulbar fibers are located in the genu of the internal capsule. The faciolingual syndrome and its variants are highly suggestive of capsular genu stroke.
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PMID:Capsular genu syndrome. 179 70

Medial medullary infarction is characterized by ipsilateral hypoglossal nerve palsy, contralateral hemiparesis sparing the face, and contralateral disturbance of deep sensation. Although it is possible to make a clinical diagnosis in typical patients, diagnosis is difficult if hypoglossal nerve palsy is absent. We describe a patient with medial medullary infarction without hypoglossal nerve palsy. The patient suffered from left hemiplegia and homolateral disturbance of deep sensation. Magnetic resonance imaging revealed the site of the lesion to be in the medial portion of the upper medulla oblongata. The result of somatosensory evoked potential testing was compatible with disturbance of the medullary medial lemniscus. In a review of the literature, we examined the relation between clinical features and lesion location in 16 patients with medial medullary infarction and compared these to the present patient. Motor paresis was present in every patient, while disturbance of deep sensation was recorded in nine of 13 patients and hypoglossal nerve palsy in six of 14 patients. In atypical patients with medial medullary infarction (such as the present patient), magnetic resonance imaging is necessary to detect the lesion and to make a clinical diagnosis.
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PMID:Magnetic resonance imaging of medial medullary infarction. 234 1

Observation of neurosarcoidosis in a thirty-year-old black female characterised predominantly by bilateral facial nerve paralysis gave rise to a review of literature since 1978 and also to a comparison with an early study in 1963. As described 1963 the clinical picture is characterized by increased protein content of the CSF (33.8%), facial nerve paresis (25.5%), pleocytosis (23%), diabetes insipidus (21%), hemiparesis (17.2%), organic psychosis (16.9%), papilloedema (15.5%), ataxia (13%), convulsive seizures (12.5%), optic atrophy (12.5%), loss of hearing (12.2%), nystagmus (8.6%) and numerous other symptoms more rarely found. This corresponds to the symptoms of chronic basal meningitis with an infiltration in the neighbouring structures of brain and less frequently the spinal cord. In only 58.7% of the cases (presumably at the onset of sarcoidosis) was the bronchial tract (or the lungs) affected, in 11.5% the skin or the eyes. Although the clinical picture is clear enough the etiology has yet to be determined. Evidence of a pathogen or a pathogenic agent (analogous to berylliosis) has never been established to date. On the other hand there are some indications of a disturbance in the immune system, perhaps of a particular genetic foundation since sarcoidosis strikes black patients with conspicuous frequency. There exist more cases in one family. Exceeding expected random distribution, many patients have the HLA-Factor B 8 (on the chromosome 6) and DR 3. The Kveim-Test was in 71 cases positive, in 12 cases negative. The possibilities of carrying out studies of CSF - analogous to the studies of bronchial lavage - in the most cases of neurosarcoidosis have not been exhausted as to determine the activity of the T-lymphocytes, the interleucines, the angiotensin-converting enzyme while the Gallium 67 scintigraphy and other methods to determine the non-specific activity of the inflammation. The efficiency of the treatment with corticosteroids (Prednison or Triamcinolonacetonid) depends of the phase of the inflammatory process. 12% of the registered cases died.
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PMID:[Neurosarcoidosis. Comparative analysis of the clinical profile based on 537 cases from the world literature up to 1963 and from 1976-1988]. 240 26

This study presents a quantification of the impersistence in the EMG interference pattern (IP) produced during maximal effort by patients with chronic hemiparesis. Monopolar needles were used to record from the flexor carpi radialis (FCR) and extensor carpi radialis longus (ECR) muscles of both the paretic and non-paretic sides of 19 patients with a history of unilateral CVA and 10 healthy control subjects during maximal voluntary isometric wrist flexion or extension. We found more gaps in the IP and fewer total seconds of EMG activity in paretic than in non-paretic or control forearm muscles. The number of gaps was similar in paretic FCR and ECR, but the reduced active time in paretic ECR indicates proportionally more gaps per second of EMG activity. This method provides quantitative measures of both the lapses (gaps in the IP during maximal effort and the inability to sustain EMG activity (total seconds) during long contractions. The latter measure is sufficiently sensitive to distinguish the greater impairment of a paretic wrist extensor than a paretic wrist flexor muscle, and both may prove to be valuable for future comparisons of the severity of paresis and the progress of recovery. These results represent the first quantitative confirmation of previous qualitative descriptions of impersistent recruitment.
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PMID:Quantification of gaps in the EMG interference pattern in chronic hemiparesis. 247 27

A case of hypoglycemic hemiparesis in a fifteen-year-old girl with insulin dependent diabetes mellitus (IDDM) is described. The initial presentation included left facial paresis and muscular weakness of the left upper and lower extremities, associated with a blood glucose level of 31 mg/dL. The patient recovered completely after a glucose infusion. Her neurological examination became normal within 24 hours and remained so for a follow-up period of 6 months. Hypoglycemic hemiparesis is rarely described in children and adolescents.
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PMID:Hypoglycemic hemiplegia in an adolescent with insulin-dependent diabetes mellitus: a case report and a review of the literature. 266 69

We reported a 71-year-old male with lateral medullary syndrome presented acute respiratory arrest after ataxic respiration. The patient had experienced transient diplopia repeatedly for about 2 weeks and then the developed persistent diplopia and vertigo. On the third day he was admitted to our hospital because of neurological deterioration and aspiration pneumonia. He showed left Horner's sign and double vision. And he had sensory disturbances of pain and temperature in the left face and the right side of the body, left limb ataxia and truncal ataxia. He showed dysarthria, severe dysphagia and left mild central facial paresis, but no hemiparesis. This case was clinically considered to be a typical case of left lateral medullary syndrome. When he was admitted to our hospital, he showed hypoxia with hypercapnea in spite of no history of chronic obstructive pulmonary disease. This condition was considered to be a central alveolar hypoventilation. He had two episodes of sudden-onset respiratory arrest following ataxic respiration on the 4th and 5th days, but no cardiac arrest. He was supported his respiration by mechanical ventilation until he was able to breathe spontaneously on the 29th day. The 22nd day MRI disclosed high intensity area in the left lateral and dorso-medial medulla in T2-weighted image, and this lesion was 1.5 cm in length. Therefore this case was diagnosed medullary infarction. This case developed ipsilateral facial pain in chronic stage. Pain existed around the eye and in the cheek, and pain was like toothache and unbearable like thalamic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of medullary infarction presented lateral medullary syndrome and respiratory arrest after ataxic respiration]. 268 32

The drawings of 69 consecutive stroke patients with single cerebral lesions on CT and of 33 normal controls, were analyzed by two independent observers using a standardized scoring system. The drawings of left brain damaged subjects (LBD) were more impaired overall than those of right brain damaged subjects (RBD). RBD drawings displayed hemispatial neglect and impaired spatial relationships. LBD drawings were simplified and exhibited low level errors of execution. Lesion size correlated significantly with drawing impairment in RBD but not in LBD. No relationship between intrahemispheric lesion location and drawing quality was found. However, severity of hemiparesis correlated significantly with drawing impairment in LBD. Performance on a visuospatial perceptual task correlated better with overall drawing quality for RBD than for LBD. Our data suggest that neglect and a visuospatial deficit impair drawing in RBD while dominant hand paresis and a conceptual impairment which parallels comprehension impairment contribute to LBD drawing disability.
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PMID:Hemispheric contributions to drawing. 275 96

Three patients developed prominent neurologic symptoms and signs associated with Schoenlein-Henoch purpura. A 7 1/2-year-old boy was seen with status epilepticus after a 2-week history of generalized headaches, irritability, and intermittent colicky abdominal pain. A left hemiparesis and a left homonymous hemianopia with a right gaze preference that were present on initial examinations gradually resolved, but a mild left arm paresis persisted. Cutaneous, renal, and joint involvement followed initial CNS manifestations. The second patient, a 7-year-old girl, had a complex partial seizure with secondary generalization and a postictal hemiparesis seven days after presentation with classic signs of Schoenlein-Henoch purpura. Behavioral changes were noted during the acute phase of the illness. The third patient, a 13-year-old boy, developed signs of a left brachial plexopathy and transient weakness of his right leg during a complicated course of Schoenlein-Henoch purpura. Review of the world literature indicates that headaches and mental status changes are the most frequent neurologic complications of Schoenlein-Henoch purpura, followed by seizures, focal neurologic deficits, mononeuropathies, and polyradiculoneuropathies. The vasculitis of Schoenlein-Henoch purpura can involve the nervous system and may add significantly to the morbidity of the illness.
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PMID:Neurologic manifestations of Schoenlein-Henoch purpura: report of three cases and review of the literature. 298 37


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