Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here a boy with infantile-onset fibromuscular dysplasia (FMD). At 8 months of age, he had the first cerebrovascular attack presenting with left facial palsy, followed by recurrent attacks of alternating hemiparesis. Involvement of systemic arteries was manifested by variable somatic symptoms: retarded growth of the right arm due to stenosis of the brachial artery, constipation and recurrent abdominal pain due to intestinal ischemia, and renovascular hypertension. Cerebral angiography disclosed stenosis of the bilateral internal carotid arteries and right vertebral artery, with development of moyamoya disease like collateral vessels. Systemic arteriography revealed stenosis of the right brachial and left femoral arteries, which was either tubular or mimicking a string of beads. This case was characterized by the early onset and involvement of many cerebral and systemic arteries resulting in severe and variable symptoms.
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PMID:[A boy with infantile-onset fibromuscular dysplasia showing recurrent cerebrovascular attacks]. 1275 58

The patient was a 19-year-old woman who presented with hemiatrophy and diminished superficial sensation on the left side of her body including her face. She had a past history of tonic-clonic seizures accompanied by left hemiparesis in late childhood. Brain CT demonstrated dilatation of the frontal sinus, calvarial thickening, cerebral hemiatrophy and dilatation of the lateral ventricle on the right side. Brain MRI showed atrophy of the right cerebrum and midbrain and dilatation of the lateral ventricle on T1-weighted images, as well as a high signal intensity area from the parietal to the occipital lobe on T2-weighted images. These findings are suggestive of an episode that may have caused a transient ischemia through the right cerebral hemisphere after the intrauterine period.
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PMID:Dyke-Davidoff-Masson syndrome manifested by seizure in late childhood: a case report. 1276 49

Although dissecting aneurysms appear not to be as rare as previously reported, their etiology remains unclear. We describe a rare case of a girl with ischemia in the region of the posterior cerebral artery (PCA). The patient complained of a mild headache and left upper paresthesia. Neurological findings revealed a mild left hemiparesis. Visual field was intact, and cardiac embolism was excluded due to the almost normal chest X-p, ECG, and UCG. Laboratory findings were within normal limits. However, MRA and angiography revealed a linear shadow and an irregular caliber change at the right P1-P2 segment. Conservative therapy was pursued and the patient showed full neurological recovery. After a 3-month follow-up period, MRI showed no recurrence and MRA showed that the lesion had returned to normal. Here, we report the case as well as review the literature relating to this disorder, including discussion of its etiology, clinical features, radiological findings, and management strategies. We conclude that this disorder should be taken into consideration as a differential diagnosis of cerebrovascular disease in young people.
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PMID:[Isolated posterior cerebral artery dissection--case report and review of the literature]. 1283 77

Incontinentia pigmenti (IP) is a multisystem disorder with characteristic cutaneous signs. After the skin, the central nervous system is the next most affected system. We report a child with IP and left-sided hemiparesis and cerebral periventricular leukomalacia on magnetic resonance imaging (MRI). The MRI findings would support ischemia sustained perinatally.
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PMID:Incontinentia pigmenti associated with cerebral palsy and cerebral leukomalacia: a case report and literature review. 1465 67

In 1891 Georg Avellis described a so-called "laryngeal hemiplegia" that can be caused by peripheral lesions of the vagal and glossopharyngeal nerves and rarely by infarctions of the medulla oblongata, thus representing a classical brainstem syndrome. In this study we describe two patients with an Avellis' syndrome caused by brainstem ischemia. Contemporary publications about Avellis' syndrome in brainstem lesions seem to be very inhomogenous. They report various diseases with unilateral laryngeal palsy due to nucleus ambiguus lesions with diverse additional neurological symptoms. We conclude that according to Avellis' original description only the combination of ipsilateral palatolaryngeal paresis and contralateral hemiparesis and/or hemihypesthesia should to be interpreted as Avellis' syndrome.
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PMID:[Avellis' syndrome in brainstem infarctions]. 1466 Nov 58

We report a case of a dissecting vertebral aneurysm with subarachnoid hemorrhage (SAH) after ischemic onset on the same day. A 48-year-old man had abrupt vertigo and nausea. CT & MRI on admission showed no abnormality, but he complained of left hemiparesis after admission. Twelve hours after the ischemic onset he suddenly complained of severe headache and his consciousness deteriorated. The follow-up CT showed diffuse SAH. Cerebral angiography showed occlusion of the right vertebral artery at the origin of the posterior inferior cerebellar artery (PICA) and segmental stenosis of the left vertebral artery at the portion distal to the vertebral PICA junction. We treated the patient conservatively. Four days later, he suddenly fell into a coma, but CT showed no bleeding. Because of this we suspected brain stem ischemia due to deterioration of vertebral dissection. The patient died 8 hours after the ischemic reattack. We report difficulty of treatment of a dissecting vertebral aneurysm with simultaneous ischemia and subarachnoid hemorrhage.
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PMID:[Dissecting vertebral aneurysm with subarachnoid hemorrhage after ischemic onset on the same day: a case report]. 1546 62

Our objective was to determine the clinical spectrum of pediatric hemiparesis by identifying the relative frequency of various diagnoses and comorbid conditions seen in these children. Case records of all patients with hemiparesis in a single practice over an 11-year period were reviewed with reference to clinical features, etiologic determination, and comorbid conditions. Ninety-two children were identified: 73 (79.3%) had a congenital hemiparesis and 19 (20.7%) had an acquired hemiparesis. An abnormal perinatal history (P = .003), prematurity (P = .016), and younger age at onset of symptoms (P < .001) were associated with a congenital hemiparesis. The overall etiologic yield was 83.7% (82.2% in the congenital and 89.5% in the acquired). The top four etiologic entities were cerebrovascular ischemia (40.2%), periventricular leukomalacia (18.5%), intracranial hemorrhage (16.3%), and cerebral dysgenesis (13%). Factors predictive of establishing an underlying etiology included birth prior to 34 weeks' gestation (P = .034), global developmental delay (P = .048), epilepsy (P = .024), and having appropriate imaging modalities (P = .001). Half of these children had a concurrent global developmental delay, associated epilepsy (odds ratio 3.67; 95% confidence interval 1.40-9.72), and prematurity (odds ratio 5.41; 95% confidence interval 1.56-18.80). A third of these children developed epilepsy. Multivariate predictive factors for epilepsy included global developmental delay (odds ratio 4.20; 95% confidence interval 1.44-12.27), cerebrovascular ischemia (odds ratio 5.10; 95% confidence interval 1.76-14.77), and term birth (odds ratio 3.87; 95% confidence interval 1.20-12.56). The majority of children with hemiparesis have a congenital etiology. The diagnostic yield is higher than previously reported; however, specific underlying etiologies need to be better determined. Comorbid conditions of global developmental delay and epilepsy have a high prevalence in this population, contributing to overall morbidity.
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PMID:Profile of pediatric hemiparesis. 1599 94

A 46-year-old woman presented with weakness in the right arm and leg. She had developed difficulty in moving the right arm and leg while exercising and had noticed headache simultaneously. On admission, she had hemiparesis of the right side. Angiography on day 1 disclosed irregularity of the left anterior cerebral artery (ACA). We started argatroban and aspirin to prevent exacerbation of ischemia. Diffusion-weighted MR image on day 2 disclosed acute infarction in the territory of the left ACA. When she became able to move her leg against gravity (MMT 3/5), we discontinued antithrobotic therapy on day 3. MRI on day 10 disclosed enlargement of the infarcted area. Angiography on day 16 disclosed stenosis and dilation corresponding to pearl and string sign involving the left ACA. Spontaneous ACA dissection was established based on clinical features and angiographic findings. Antithrombotic therapy in patients with intracranial artery dissection remains controversial because subarachnoidal hemorrhage can complicate the course due to rupture of dissecting aneurysm, for there is no external elastic lamina in intracranial arteries. However, some cases of ACA dissection have showen progression of ischemic symptoms and enlargement of the infarcted area during the acute or subacute phase.
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PMID:[A case of anterior cerebral artery dissection causing enlargement of infarction]. 1631 74

We report an unusual case of systemic lupus erythematosus presented with protein-losing enteropathy. A 24-year-old girl was referred to our hospital with generalized edema, thrombocytopenia, hypoalbuminemia, hypercholesterolemia, hypocomplementemia, antinuclear antibody (ANA) (speckled pattern) and anti- SSA/Ro positivities, and elevated CA125 antigen appeared in the blood examination. On the radiological studies, she had mild pleural effusion and moderate ascites which were transudate. A diagnosis of protein-losing enteropathy was made on the basis of increased 99mTc-labelled human immunoglobulin scintigram showing abnormal radioactivity. Endoscopic gastric, duodenal and jejunal biopsies showed chronic inflammation, but vasculitis and immune complex deposition findings were not present. Renal biopsy revealed no definitive findings of lupus nephritis. By the administration of corticosteroids, hypoalbuminemia began to improve, but steroid doses were decreased due to steroid-induced myopathy. Temporary hemiparesis and facial paralysis developed in the patients' follow up. Her cranial magnetic resonance imaging revealed chronic ischemia, and the patient was considered to have neurological involvement due to systemic lupus erythematosus. protein-losing enteropathy and other symptoms then improved dramatically after monthly intravenous cyclophosphamide (three times) combined with oral low-dose corticosteroids. The combination of azathioprine and low-dose steroids was used as maintenance medication. Although about 30 protein-losing enteropathy -associated systemic lupus erythematosus cases have been reported, the patients having initial symptoms as protein-losing enteropathy are rare in the literature. Protein-losing enteropathy -associated systemic lupus erythematosus cases probably represent a subgroup of systemic lupus erythematosus, the characteristics of which are hypocomplementemia, protein-losing enteropathy, ANA positivity showing speckled pattern and anti-ds DNA negativities. In the patients with systemic lupus erythematosus with edema and hypoalbuminemia without renal protein loss, protein-losing enteropathy-associated systemic lupus erythematosus should be kept in mind.
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PMID:A case of systemic lupus erythematosus presenting with protein-losing enteropathy. 1694 Dec 61

In an effort to shed light on the mechanism of hemiparetic stroke-like events experienced by patients with congenital disorder of glycosylation type Ia, we evaluated 3 children with this disorder by brain imaging studies and continuous electroencephalogram monitoring during such events. No evidence of ischemia or infarction was revealed on imaging studies and electrographic seizures or intermittent epileptiform activity was demonstrated on electrographic recordings. All 3 patients showed clinical and electrographic improvement after administration of antiepileptic medication. Epileptic phenomena can complicate the stroke-like events of patients with congenital disorder of glycosylation type Ia, and the cause of the hemiparesis may indeed be an active epileptic inhibitory process. As such, electroencephalogram monitoring is warranted, and treatment with anticonvulsant agents is indicated.
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PMID:Radiologic and neurophysiologic aspects of stroke-like episodes in children with congenital disorder of glycosylation type Ia. 1730 46


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