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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The majority of pediatric neoplasias of the brain are midline growths in the posterior fossa. These mass lesions lead to obstruction of cerebrospinal fluid circulation and cause increased intracranial pressure. Affected children typically present with insidious complaints of headache and vomiting. Ataxia, cranial nerve palsies, or pyramidal tract signs may be present at the time the diagnosis is entertained. In the reports describing pathognomonic clinical features of posterior fossa tumors, an accelerated presentation with minimal prodromal events has not been emphasized. This report details the case of a child with a cerebellar medulloblastoma who presented with abrupt onset of fever, nuchal rigidity, and altered mental status. Emergency department misdiagnosis occurred.
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PMID:Erroneous diagnosis within the cranial vault. 140 86

This review focuses on the features of pseudotumor cerebri in the pediatric age group. There is no sex predilection in children, and obesity does not appear to be an important factor. Infants and young children may present with irritability, apathy, or somnolence, rather than headache. Dizziness and ataxia may also occur. Papilledema is infrequently noted in pediatric patients if the fontanelles are open or the sutures are split. Pre-adolescents appear more likely than adults or adolescents to have manifestations of their pseudotumor cerebri other than headache and papilledema, including lateral rectus pareses, vertical strabismus, facial paresis, back and neck pain. Among the etiologies that are particularly pertinent to children are tetracycline therapy, malnutrition or renutrition, and the correction of hypothyroidism. Children with pseudotumor cerebri are at risk for visual loss and their visual function must be closely monitored. Surgical intervention is imperative when vision is threatened.
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PMID:Pediatric pseudotumor cerebri (idiopathic intracranial hypertension). 147 50

This study represents a secondary data analysis of two double-blind and placebo-controlled clinical trials of lithium, performed to contrast side effects associated with lithium administration to those associated with placebo. The sample consisted of 91 hospitalized children, aged 5.12 to 12.92 years (mean 9.16), diagnosed as having conduct disorder characterized by severe aggressiveness and explosiveness. Daily doses of lithium ranged from 250 to 2100 mg. During the entire treatment period, more side effects were seen in the lithium group than in the placebo group, whereas during the therapeutic dose period, the difference between side effects in the two groups diminished. The most common side effects seen exclusively with lithium administration included enuresis, fatigue, and ataxia. Increased aggressiveness was observed in 4 children who received placebo. Vomiting, headache, and stomachache were the most common side effects experienced by patients in both lithium and placebo groups. However, more patients experienced these side effects in the lithium group than in the placebo group.
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PMID:Side effects associated with lithium and placebo administration in aggressive children. 148 Jul 37

Symptomatic ventricular coaptation, or the slit ventricle syndrome, is frequently described and recognized as a clinical entity in the pediatric population. It is characterized by symptoms of shunt failure (i.e., ataxia, obtundation, nausea, vomiting, lethargy, irritability, and complaints of headache) and the CT findings of ventricular coaptation (slit-like ventricles). This study of twenty-two children with this syndrome reflects the variety of possible clinical presentations, and the variety of available treatment modalities. Multiple therapeutic approaches were required in seven of the patients. This illustrates not only an evolving treatment regimen, but also that a single treatment modality is not universally effective. Six patients needed only occasional symptomatic support. Blockage and/or removal of the shunt system was the definitive therapy in six patients, pressure augmentation in nine patients, and subtemporal craniectomy in one. This article outlines the theoretical pathophysiology, and a scheme for the management of patients with this syndrome.
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PMID:Slit ventricle syndrome in children: clinical presentation and treatment. 151 32

The term "papilledema" describes optic disc swelling resulting from increased intracranial pressure. A complete history and direct funduscopic examination of the optic nerve head and adjacent vessels are necessary to differentiate papilledema from optic disc swelling due to other conditions. Signs of optic disc swelling include elevation and blurring of the disc and its margins, venous congestion, and retinal hard exudates, splinter hemorrhages and infarcts. Patients with papilledema usually present with signs or symptoms of elevated intracranial pressure, such as headache, nausea, vomiting, diplopia, ataxia or altered consciousness. Causes of papilledema include intracranial tumors, idiopathic intracranial hypertension (pseudotumor cerebri), subarachnoid hemorrhage, subdural hematoma and intracranial inflammation. Optic disc edema may also occur from many conditions other than papilledema, including central retinal artery or vein occlusion, congenital structural anomalies and optic neuritis.
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PMID:Papilledema: clinical clues and differential diagnosis. 154 98

Neuro-cryptococcosis is a common opportunistic infection in AIDS or HIV infected patients. From a series of 10 neuro-cryptococcosis the four of them studied by magnetic resonance (MR) are reported. In AIDS patients a high suspicion of opportunistic infection of the CNS is needed as exemplified by two of the four patients who only presented cephalalgia. The other two patients suffered additional symptoms and signs of meningeal and CNS involvement, such as nuchal rigidity, cranial nerve palsies, papilloedema, gait ataxia and dismetria. Diagnosis was achieved (confirmed) by a positive culture, serology or indian ink test in CSF. CT scan did not contribute to the diagnosis and management of the patients. In contrast MR, showed in three of them a peculiar pattern of small, confluent, high-signal lesions, roughly symmetrically placed in the basal ganglia and the internal capsule. They probably correspond to the dilated Virchow-Robin spaces through which torulae migrate from the subarachnoid space.
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PMID:[Use of magnetic resonance in the diagnosis of neuro-cryptococcosis in the acquired immunodeficiency syndrome: study of 4 patients]. 155 79

Neurosyphilis, a sexually transmitted disease that can cause neurologic damage, has become increasingly prevalent in the AIDS era. HIV carriers can contract neurosyphilis without the presence of other concurrent opportunistic infections. Because MR findings of neurosyphilis are seldom reported, we retrospectively reviewed and evaluated contrast-enhanced MR images of six young (average age, 33 years) HIV-positive men with high serum and CSF VDRL titers indicative of neurosyphilis. All six patients tested negative for concurrent opportunistic infections. Five patients had acute or subacute strokelike symptoms involving the basal ganglia or middle cerebral arteries; one had a parietal convexity mass mimicking meningioma with headache and ataxia. Contrast-enhanced MR images showed patchy enhancement involving the basal ganglia and middle cerebral artery territories in the first five patients and the convexity mass in the sixth patient. On the basis of brain biopsy, a convexity mass was diagnosed in the patient with syphilitic gumma. The imaging findings of the remaining five patients represented ischemic infarct caused by meningovascular syphilis. After penicillin treatment, serum and CSF VDRL titers decreased, and neurologic signs and symptoms improved in all six patients. A follow-up MR study in the patient with the gumma showed that the lesion resolved almost completely. In young HIV patients with stroke symptoms or a convexity mass, neurosyphilis should be considered. Contrast-enhanced MR can reveal the extent of involvement by neurosyphilis and should be used to facilitate diagnosis and proper treatment.
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PMID:Neurosyphilis in HIV carriers: MR findings in six patients. 159 Jan 35

Three siblings with inhaled elemental mercury toxicity are described, and the signs and symptoms of mercury toxicity, interpretation of mercury concentrations, and management of elemental mercury exposure are reviewed. A 4-year-old girl was admitted to the hospital with a history of fever and increasing irritability, fatigue, malaise, insomnia, headache, anorexia, and ataxia. She was discharged two days later with a diagnosis of acute cerebellar ataxia. During the following 18 days, the child's condition worsened, and she was rehospitalized. Meanwhile her 11-year-old sister was hospitalized for evaluation of fatigue, weakness, lower back pain, and ataxia. The older girl's blood mercury concentration, at 5.5 micrograms/dL, was in the toxic range. Twenty-four-hour urine mercury screening confirmed mercury intoxication in both children. Questioning revealed that the girls' brother had recently spilled 0.5-1 oz of elemental mercury in the house. All family members underwent blood and urine mercury testing. The brother underwent a dimercaprol challenge to determine his tissue mercury burden, which was found to be greater than 2.4 micrograms/dL. The sisters underwent two courses of chelation therapy with dimercaprol. Symptoms persisted in all three children, and they underwent five 10-day cycles of N-acetyl-D,L-penicillamine (NAP) therapy; the youngest underwent a third dimercaprol regimen. All siblings continued NAP chelation therapy because of extensive tissue mercury burden until the results of repeated urine mercury concentration determinations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elemental mercury poisoning. 174 59

ADD 94057, a metabolite of fluzinamide, manufactured by the A. H. Robins Company, blocks chemically- and electrically-induced seizures in animals. The primary objective of this open add-on study was to evaluate patient tolerability of ADD 94057 at ascending target plasma concentrations. Nine subjects with medically refractory seizures were receiving phenytoin (PHT, 3), carbamazepine (CBZ, 3), or both (3). A pharmacokinetic profile after a single oral 400-mg dose of ADD 94057 was used to calculate ADD 94057 dosages. After a 4-week baseline period, patients were treated for 4 weeks with weekly ADD 94057 dosage escalations. Two patients completed the study at their assigned highest dosage level; the other patients finished the study at lower dosages. The patients receiving PHT (but not CBZ) tolerated higher plasma concentrations of ADD 94057 than did patients receiving CBZ, alone or in combination with PHT. Adverse experiences included headache, ataxia, blurred vision, diplopia, dizziness, lightheadedness, and mild confusion. Eight of nine patients had reductions in seizure frequency from baseline.
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PMID:Pharmacokinetic and dose tolerability study of ADD 94057 in comedicated patients with partial seizures. 173 43

A 38 year-old laborer experienced solvent intoxication during each of two spray paintings of a dump truck and other heavy equipment in an enclosed, unventilated garage. The paint base consisted primarily of toluene and methyl ethyl ketone. Nausea, headaches, dizziness, respiratory difficulty and other symptoms began after exposures. Over the next several days he developed impaired concentration, memory loss and cerebellar signs including an intention tremor, gait ataxia and dysarthria. MRI of the brain and EGG early in the work-up were normal, although later MRIs demonstrated fluid collection over the left parietal area. Examination by a toxicologist and neurologist revealed likely toxic encephalopathy with dementia and cerebellar ataxia. Three formal neuropsychological assessments over 2 1/2 years quantified cognitive, motor and behavioral changes. Despite similar findings in chronic exposure to these solvents, lasting sequelae following acute exposure have not been widely reported.
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PMID:Chronic neuropsychological and neurological impairment following acute exposure to a solvent mixture of toluene and methyl ethyl ketone (MEK). 174 49


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