Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 66-year-old woman was admitted to our hospital because of vomiting, dizziness and vertigo. Neurological examination on admission revealed only upbeat nystagmus without cranial nerve symptoms, paresis, cerebellar signs or sensory disturbances. Magnetic resonance(MR) images demonstrated a new T 2 high intensity and T 1 iso-intensity signal lesion in the right upper medial medulla. This medial medullary infarction caused central vestibular dysfunction. MR angiography and digital subtraction angiography demonstrated a persistent primitive hypoglossal artery (PPHA) originating from the right internal carotid artery to the vertebrobasilar artery associated with the stenosis of the right internal carotid artery at the level of the cervical bifurcation. This is the first report of medullary infarction with persistent carotid-basilar anastomosis. We suspected this medullary infarction was caused by artery to artery embolism in the branch of the right vertebral artery through the PPHA distal originated from the stenosis of the right internal carotid artery.
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PMID:[A case of medial medullary infarction with persistent primitive hypoglossal artery]. 1199 64

Vertebral artery dissection (VAD) has been infrequently recognized in children. The authors have reviewed 68 reported cases of VAD in children in the existing literature. An association between routine types of neck movement in sports and the evolution of VAD was recognized in half of the reported cases. Boys outnumbered girls by a ratio of 6.6 to 1, in contrast to adults, for whom the male to female ratio is approximately equal (1.3 to 1). Neck pain, one of the hallmark symptoms of VAD in adults, was infrequently noted in this young population (12%). Most children presented with various combinations of symptoms and signs, including ataxia (53%), headache (38%) and vomiting (34%). Eye signs or symptoms were noted in 72% of patients, and paresis/paralysis of one or more extremity occurred in 54%. Angiography was the method most frequently used to diagnose VAD (63/68; 93%). Magnetic resonance angiography (MRA) revealed pathognomonic signs of VAD in only 3 out of 13 patients evaluated (23%). In this series of 68 patients, 48 reports failed to indicate whether or not a cervical X-ray was performed, but in the 20 patients for whom such information was recorded, half had skeletal abnormalities in the occipital/atlas/axis region. The most common treatments were antiplatelet therapy (n = 15) and anticoagulation with (n = 8) or without (n = 7) supplemental antiplatelet therapy. Asymptomatic recovery occurred in 12 of the 15 patients (80%) who received antiplatelet therapy compared with 4 of the 15 patients (27%) who received anticoagulation therapy with or without antiplatelet therapy. There is a very high incidence of associated cervical anomalies in children with VAD. Further studies are required to determine if noninvasive examinations such as magnetic resonance imaging, ultrasonography, computed tomography angiography and MRA could replace angiography as the modality of choice in establishing the diagnosis of VAD in children. The role of different therapies for children presenting with symptoms related to VAD is unclear.
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PMID:Vertebral artery dissection in children: a comprehensive review. 1237 9

The characteristic symptoms for acute porphyrias are caused by the inherited decreased activity of the enzymes of the heme biosynthesis pathway. Usually there is an exogenous or endogenous factor inhibiting the heme biosynthesis or increasing the consumption of heme produced in already decreased amount. The most important precipitating factors are the therapeutic drugs. Therefore, certain therapeutic drugs ordered for carriers or patients with acute porphyria are serious risk factors. It is very important to identify patients and carriers with acute porphyria as early as possible and to make a close follow-up so the development of the symptoms of the life threatening acute attack could be prevented. It is very difficult to suspect the diagnosis of acute porphyria. There is a very characteristic discrepancy between the serious complaints and the actual clinical findings. The severe cramping abdominal pain, nausea, vomiting, muscle weakness of the limbs and sensory loss are the main signs at the beginning. The specific symptoms which help to establish the diagnosis--red-colored urine, hyponatremia, tachycardia, hypertension, subileus, acute psychosis, gradually developing paresis of the lower and then the upper limbs--are characteristic for the later phase of the acute attack. Very often there is a rapid progression with Landry-type paralysis developing in days or even in hours, following respiratory paralysis or serious arrhythmia is the cause of the death. In case of suspicion of acute porphyria the patient should be directed to a department where the specific laboratory methods--measurement of the porphyrin precursors, porphyrins and their isomers in urine and feces, quantitation of protoporphyrin in red blood cells, measurement of the plasma porphyrin and enzyme activity--to diagnose the different types of the disease and the immediate specific treatment with heme arginate are possible if needed. All of these are available in the National Porphyria Center.
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PMID:[Acute porphyrias in differential diagnosis]. 1276 67

Because of its distinct anatomy, pathogens can quickly reach the middle ear of a child and cause acute otitis media. Depending on the age of the child, the clinical symptoms can vary from intense earaches, fever, pressure sensation and hearing loss to vomiting, diarrhea and refusal of food by infants. The progression of otitis media through four phases can be observed in an otoscopic examination. To improve Eustachian tube ventilation in uncomplicated cases, nose drops to reduce swelling along with pain therapy are employed first. Antibiotics can be administered to reduce the rate of complications from, for example, mastoiditis, paresis of the facial nerve, and labyrinthitis. In recurrent middle ear infections, an operative therapy should also be considered.
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PMID:[Acute otitis media in childhood]. 1536 65

Transient neurological deficits experienced by patients with Sturge-Weber syndrome can be caused by epilepsy, or may result from temporary ischaemia of the cortex underlying the vascular malformation. To show the difficulty in distinguishing seizures from ischaemic symptoms, two male children with episodes of acute unilateral weakness are presented here as well as a review of the literature. The first child presented at 2 years of age with a sudden increase in his pre-existing right hemiparesis accompanied by screaming. Ictal epileptiform activity was recorded at the moment of the attack, and subsequent seizures were controlled by adjustment of antiepileptic drug treatment. The second child presented at 4 years of age with attacks of vomiting and a coinciding increase in the pre-existing paresis of the left leg. Electroencephalogram (EEG) recording did not show ictal epileptiform activity. The origin was presumed to be vascular. Treatment with aspirin led to control of these transient ischaemic attacks. Ictal EEG is needed to differentiate between an epileptic and an ischaemic origin of transient focal deficit. Treatment with aspirin should be considered if an ischaemic origin cannot be excluded.
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PMID:Sturge-Weber syndrome and paroxysmal hemiparesis: epilepsy or ischaemia? 1554 Jun 41

We report clinical findings, risk factors and neurological and cognitive long-term outcome in three Italian children aged 7, 8 and 5, respectively, who experienced cerebral venous sinus thrombosis (CVST). All children presented with headache, associated to nausea, vomiting and papilloedema. None suffered from epileptic seizures. In two of them a paresis of the sixth cranial nerve with diplopia was found. Diagnosis was confirmed by magnetic resonance imaging angiography (angio MRI) in all cases. In all patients plasma levels of protein C, protein S, antithrombin III (AT III), antiphospholipid antibodies (ApA) and homocysteine were detected. Furthermore, factor V Leiden mutation, prothrombin mutation G20210A and MTHFR mutation were searched for. A Protein C reduction was detected in all patients at onset; this finding, however, was not confirmed at follow-up in all of them. At one-year follow-up, neurological examination was normal in all children and neuropsychological assessment, aimed at excluding linguistic and non-linguistic cognitive deficits, revealed normal performances in two of them. In the third child, cognitive assessment confirmed a previously diagnosed developmental dyslexia.
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PMID:Cerebral venous sinus thrombosis in childhood: clinical aspects and neurological and cognitive long-term outcome in three cases. 1562 88

Ten dogs with neuroendocrine carcinoma of the liver were selected for inclusion in the study. Clinical signs were anorexia (7), vomiting (5), polydipsia/polyuria (3), icterus (2), lethargy (2), weight loss (2), paresis (1), ataxia (1), weakness (1), collapse (1), and urinary tract infection (1). Hematologic and biochemical abnormalities included anemia (2/8), leukocytosis (4/8), high liver enzyme activity (serum alkaline phosphatase, 7/9; alanine transaminase, 7/9; aspartate transaminase, 8/9), and high total bilirubin (6/9). Grossly, the tumors were diffuse, involving all liver lobes in six dogs, and two dogs had various-sized nodules in addition to diffuse involvement. Histologically, there were eight tumors with solid or trabecular pattern (group A), one tumor with cords or rows of neoplastic cells (group B), and one tumor with multiple rosette-like structures (group C). Immunohistochemical studies revealed that all 10 neoplasms were positive for at least one of the endocrine markers used: neuron-specific enolase (NSE; 8/10), synaptophysin (5/10), and chromogranin-A (3/10). A panel of NSE, chromagranin-A, and synaptophysin detected 100% of the tumors in our series. Electron microscopy confirmed the diagnosis by the presence of intracytoplasmic neurosecretory granules in the two examined cases. Our results show that neuroendocrine markers commonly used in humans can be used for the diagnosis of hepatic neuroendocrine carcinoma in dogs, preferably a panel of synaptophysin, chromagranin-A, and NSE because chromogranin-A alone is not as useful in dogs as in humans.
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PMID:Canine hepatic neuroendocrine carcinoma: an immunohistochemical and electron microscopic study. 1575 67

A 6-year-old dog, a 4-year-old dog and three 7-week-old puppies were diagnosed with thiamine deficiency caused by feeding sulphite treated meat. The 6-year-old dog presented with a history of inappetence, weight loss and vomiting that rapidly progressed to signs of multifocal intracranial disease including mental dullness, paresis, seizures, spontaneous nystagmus and strabismus. Thiamine pyrophosphate effect was elevated at 58% and magnetic resonance imaging revealed bilaterally symmetrical hyperintensity of the caudate nucleus and rostral colliculi. The dog recovered with thiamine supplementation. The 4-year-old dog and three 7-week-old puppies also presented with rapidly progressive multifocal central nervous system signs including ataxia, paresis, increased muscle tone, seizures, nystagmus and exophthalmos. The 4-year-old dog made a rapid recovery with thiamine supplementation. Euthanasia and necropsy of a puppy revealed malacia of multiple brainstem nuclei and oedema of the cerebral cortex. These findings were consistent with thiamine deficiency.
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PMID:Thiamine deficiency in dogs due to the feeding of sulphite preserved meat. 1603 79

Surgery for cochlear implantation (CI) bears the risks of complication associated with all major surgery, in addition to the particular risks associated with implanting a foreign body into the peripheral auditory system. Here we present a retrospective study involving 227 cochlear implant operations in 205 children to evaluate the rate of intra- and post-operative complications. Complications were defined as major complications, requiring explantation of the device or further operation, causing a significant medical problem, or leading to any degree of facial paralysis or requiring additional hospitalization for treatment; or defined as minor complications, namely those that settled spontaneously, with conservative treatment, with local care and/or with medication alone. In our study there were 15 (6.6 per cent) minor and 28 (12.33 per cent) major complications. The most frequent minor complication was dizziness and vomiting (3.08 per cent), followed by transient hemifacial oedema (1.76 per cent), head pain (1.32 per cent) and mild ataxia (0.4 per cent). The most frequent major complication was trauma to the device (9.69 per cent), followed by cerebrospinal fluid (CSF) gusher (2.2 per cent) and facial paresis (0.4 per cent). All of the device trauma cases were re-implanted. There were neither any life-threatening complications nor any facial nerve paralysis in our implanted children. This study confirms that CI is relatively safe and that major complications are few and within acceptable limits.
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PMID:Complications of paediatric cochlear implantation: experience in Izmir. 1610 14

The aim of this study was to describe the clinical characteristics of atypical lacunar syndrome (ALS) based on data collected from a prospective acute stroke registry. In total, 2500 acute stroke patients were included in a hospital based prospective stroke registry over a 12 year period, of whom 39 were identified as having ALS and radiologically proven (by computed tomography or magnetic resonance imaging) lacunes. ALS accounted for 1.8% of all acute stroke patients, 2.1% of acute ischaemic stroke, and 6.8% of lacunar syndromes. ALS included dysarthria facial paresis (n = 12) or isolate dysarthria (n = 9), isolated hemiataxia (n = 4), pure motor hemiparesis with transient internuclear ophthalmoplegia (n = 4), pure motor hemiparesis with transient subcortical aphasia (n = 3), unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarct syndrome, and hemichorea hemiballismus (n = 2). Atypical lacunar syndromes were due to small vessel disease in 96% of patients. Atherothrombotic infarction occurred in one patient and cardioembolic infarct in another, both presenting pure dysarthria. Outcome was good (in hospital mortality 0%, symptom free at discharge 28.2%). After multivariate analysis, the variables of speech disturbances, nausea/vomiting, ischaemic heart disease, and sensory symptoms were found to be significantly associated with ALS. In conclusion, atypical lacunar syndrome is an infrequent stroke subtype (one of each 14 lacunar strokes). ALS occurred in 6.8% of lacunar strokes. Isolated dysarthria or dysarthria facial paresis were the most frequent presenting forms. The prognosis of this infrequent non-classic lacunar syndrome is good.
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PMID:Clinical study of 39 patients with atypical lacunar syndrome. 1648 49


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