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

Tuberculosis of the craniovertebral region is very rare. Neural deficit in this region is reported in between 24% and 64% of cases, and mainly takes the form of quadriparesis. Hemiplegic and monoplegic presentation among this set of patients is rarer. Out of 32 patients treated at our institution between May 1989 and February 2001, only one had hemiplegia, while two had monoplegia. These three cases are discussed. Case 1 involved a 45-year-old woman who presented with hemiplegia following a trivial fall. Plain radiographs and computed tomographic (CT) scans of the skull appeared normal, but CT scans of C1-C2 and the craniovertebral junction revealed destruction of the dens and atlantoaxial subluxation. The patients in cases 2 and 3 had monoplegia. Plain radiographs in both cases showed an increased prevertebral soft tissue shadow in front of C1-C2. CT in case 2 and magnetic resonance imaging (MRI) in case 3 revealed destruction of the arch of C1 and the dens, with subluxation. All three patients were successfully treated with rest, skull traction, anti-tubercular drugs and suitable braces. Case 3 required stabilization. All three patients achieved complete neural recovery. Patients 1, 2 and 3 had 22, 48 and 4 months' follow-up respectively. Patient 3 was subsequently transferred to a neurosurgery ward for stabilization of the occipito-C3 vertebrae. Hemi/monoplegic presentation is extremely rare; no author in the literature is able to give reason for the rarity or the pathomechanics of the condition. We believe that if medullary cervical junctional involvement extends slightly higher (in rare circumstances), with involvement of one of the branches of the vertebral or lower basilar artery, medial medullary syndrome will occur, sparing medial lemniscus and emerging hypoglossal nerve fibres. Thus the pyramids will be involved, causing contralateral hemiparesis, and if the pyramids are selectively involved, it will cause contralateral monoparesis.
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PMID:Hemiplegic/monoplegic presentation of cervical spine (C1-C2) tuberculosis. 1180 97

Cerebral palsy is an established symptom complex that results from heterogeneous etiologies. Our understanding of the relative contribution of underlying etiologies to the occurrence of cerebral palsy is largely derived from studies lacking systematic neurologic evaluation or the application of contemporary imaging modalities. Throughout a 10-year inclusive period, the case records of all consecutive patients diagnosed with cerebral palsy in a single pediatric neurology practice were reviewed with reference to clinical features and diagnostic yield. A total of 217 cases of cerebral palsy were identified (129 male, 88 female): 77 (35.5%) spastic quadriplegic, 68 (31.3%) spastic hemiplegic, 39 (18%) spastic diplegic, five (2.7%) spastic monoplegic, 12 (5.5%) mixed, 12 (5.5%) ataxic-hypotonic, two (0.9%) dyskinetic, two (0.9%) Worster-Drought syndrome. Overall etiologic yield was 82.0%, varying according to type of cerebral palsy: 50% dyskinetic, 59% diplegia, 80% monoplegia, 80.9% hemiplegia, 90.9% quadriplegia, 91.7% ataxic hypotonia, and 100% mixed/Woster-Drought. The top five etiologic entities identified were periventricular leukomalacia, 24.9%; intrapartum asphyxia, 21.7%; cerebral dysgenesis, 17.1%; intracranial hemorrhage, 12.9%; and vascular, 9.7%. Although a single etiology was apparent in 144 (66.4%) of the cases, multiple etiologies were believed to be contributory in 34 (15.6%) of the cases. The etiologic profile varied according to such features as the type of cerebral palsy, gestational age, and the source (high-risk neonatal population or not) of the patients. Features of the child's cerebral palsy, such as microcephaly, neonatal difficulties, prior or coexisting epilepsy, and high-risk source, were found to be predictive of eventual etiologic yield. This contemporary evaluation of cerebral palsy etiologic yield suggests that it is much higher than previously reported and varies, depending on key clinical features.
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PMID:Etiologic yield of cerebral palsy: a contemporary case series. 1287 96

Equinovarus deformity is one of the most common deformities seen in patients with cerebral palsy. During years between 1993 and 2004 in 36 patients with cerebral palsy 46 operative procedures of split posterior tibial tendon transfer to peroneus brevis muscle were performed to correct varus deformity of the foot. Additionally equinus was corrected by lengthening lengtheninglengthening of the calcaneal tendon in 42 cases and in 4 cases by gastrocnemius recession according to Baker modification of Vulpius procedure. Children's age at the time of operation was between 3.5 and 16 years of age (average 7.5). In our cohort of 36 patients there were 10 cases of quadriplegia (28%), 12 cases of hemiplegia (33%), 12 cases of paraparesis inferior (33%) and 2 cases of monoplegia (6%). 25 patients with 34 operated feet (73.9%) reported for final examination. Follow-up period was from 18 months to 11 years (average 5.5 years). At final examination we evaluated clinical effectiveness of gait, passive and active range of movement, plantograms, and subjective evaluation of patient and patients' parents. Wearing of orthoses and orthopaedic footwear was noted. The results were divided into groups according to Green's classification. There were 67.6% of very good results, 23.6% of good results and 8.8% of poor results. Basing on our experience in treatment of spastic equinovarus deformity of the foot in children with cerebral palsy we stand, that split posterior tibial tendon transfer can bring good results and is a valuable surgical technique in treatment of equinovarus deformity.
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PMID:[Split posterior tibial tendon transfer as a selected technique of treatment of spastic equino-varus deformity in children]. 2049 75

High-altitude cerebral oedema (HACO) is the most fatal high-altitude illness seen by rural physicians practising in high-altitude areas. HACO presents clinically with cerebellar ataxia, features of raised intracranial pressure (ICP) and coma. Early identification is important as delay in diagnosis can be fatal. We present two cases of HACO presenting with focal deficits mimicking stroke. The first patient presented with left-sided hemiplegia associated with the rapid deterioration in the sensorium. Neuroimaging revealed features suggestive of vasogenic oedema. The second patient presented with monoplegia of the lower limb. Neuroimaging revealed perfusion deficit in anterior cerebral artery territory. Both patients were managed with dexamethasone and they improved dramatically. Clinical picture and neuroimaging closely resembled acute ischaemic stroke in both cases. Thrombolysis in these patients would have been disastrous. Recent travel to high altitude, young age, absence of atherosclerotic risk factors and features of raised ICP concomitantly directed the diagnosis to HACO.
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PMID:High-altitude cerebral oedema mimicking stroke. 2467 73

We present the case of a 70 year-old smoker patient, who was admitted in hospital for removal of a tumour located on the left vocal cord. After direct suspension laryngoscopy (with tumorbiopsy sampling), preliminary histopathological exam revealed an in situ carcinoma. At 2 weeks after histopathological confirmation, the left vocal cord was removed by anterior approach, under general anesthesia. In the first 24 hours after surgery, the patient presented an ischaemic stroke, with a deep coma and left hemiplegia, which necessitated mechanical ventilation and specific neurological treatment. Under mechanical ventilation, the patient developed massive subcutaneous emphysema, bilateral pneumothorax and pneumomediastinum,which required tracheostomy and bilateralpleural drainage, in order to limit suddenly installed respiratory insufficiency. After an 18-day interval of intensive care therapy,the patient was released at home, considered to be surgically cured and had a moderate remaining left brachial monoplegia,which was almost totally cured in the next six months.
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PMID:Therapeutic management of massive subcutaneous emphysema, bilateral pneumothorax and pneumomediastinum after anterior cordectomy for in situ vocal cord carcinoma - case report. 2556 May 7

Hereditary neuropathy with liability to pressure palsies is an inherited disease associated with the loss of a copy of the PMP22 gene. The condition leads to mononeuropathy due to compression and easy strangulation during daily life activities, resulting in sudden muscle weakness and sensory disturbance, and displaying symptoms similar to cerebrovascular diseases. We report the case of an 80-year-old man with left paralysis due to chronic cerebral infarction. His medical history indicated remarkable recovery from about 4 months after the onset of left hemiplegia with predominant involvement of the fingers. Despite subsequent recurrent monoplegia of the upper or lower limbs, brain magnetic resonance imaging consistently revealed only previous cerebral infarction in the right corona radiata without new lesions. Medical examination showed reduced deep tendon reflexes in his extremities on both the healthy and hemiplegic sides. Nerve conduction studies showed delayed conduction at the bilateral carpal and cubital tunnels and near the right caput fibulae. Genetic analysis revealed loss of a copy of the PMP22 gene. Thus, he was diagnosed with a cerebral infarction complicated by hereditary neuropathy with liability to pressure palsies. Stroke patients develop sudden muscle weakness and sensory disturbance. However, if such patients have no hyperactive deep tendon reflexes and show atypical recovery of paralysis that does not correspond to findings of imaging modalities, nerve conduction studies and genetic analysis may be necessary, considering the complication of hereditary neuropathy with liability to pressure palsies.
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PMID:A Case of Apoplexy Attack-Like Neuropathy due to Hereditary Neuropathy with Liability to Pressure Palsies in a Patient Diagnosed with Chronic Cerebral Infarction. 2708 Jan 57


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