Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The course of lethal Plasmodium berghei infection was examined in nu/+ and T cell-deficient nu/nu BALB/c mice. A rapidly fatal neurologic syndrome, including ataxia, hemiparesis, and seizures, was seen in the nu/+ mice early in the infection, whereas this syndrome was absent in the nu/nu mice. The nu/nu mice also developed anemia more slowly, had lower levels of immune complexes and total IgG, and had smaller decreases in serum C3 compared with the nu/+ mice. Histopathologic examination of the brains revealed cerebral malaria lesions, including vascular plugging and micro-hemorrhages, in the nu/+ mice but not in the nu/nu mice. Cerebral lesions similar in frequency and severity to those in nu/+ mice developed in nu/nu mice given spleen cells from normal nu/+ mice. The results suggest that an intact immune system is necessary for the expression of cerebral malaria.
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PMID:Virulent P. berghei malaria: prolonged survival and decreased cerebral pathology in cell-dependent nude mice. 674 88

The mechanisms of death and neurologic sequelae in African children with cerebral malaria are undetermined. Because pathologic features are confined to the cerebral vasculature, perturbations in cerebral hemodynamics may be responsible. We compared the transcranial Doppler findings in 50 children with cerebral malaria with those of 115 conscious Kenyan children. In addition, 10 children with cerebral malaria were studied during intracranial pressure monitoring and nine children were studied during the agonal stages. In the children with cerebral malaria, cerebral blood flow velocity was increased in 30%, usually associated with seizures. Of the 11 children who developed neurologic sequelae, six had sonographic abnormalities associated with lateralizing deficits, including four children with hemiparesis (in two children the contralateral middle cerebral artery could not be insonated and two had transient increases in blood flow velocity associated with seizures). In the children with severe intracranial hypertension, there was a significant linear relationship between the cerebral perfusion pressure and blood flow velocity, suggesting that autoregulation was impaired. Sonographic features of progressive intracranial hypertension, were observed in three children with cerebral malaria who died. Perturbations of cerebral hemodynamics are associated with a poor outcome in Kenyan children with cerebral malaria.
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PMID:Perturbations of cerebral hemodynamics in Kenyans with cerebral malaria. 885

A 67-year-old man was referred to us for tonic-clonic convulsions. A review of his history revealed that he had been hospitalized for loss of consciousness, hypotension, and suspected apoplexy at age 67. He had experienced prior tonic-clonic convulsions at age 72 and age 74. He had malaria and tuberculosis in his history but had been otherwise generally well. Physical examination was normal, and his blood pressure was 100/80 mmHg. Laboratory findings were normal except alcalinephosphatase (292 U/l) and gamma-glutamyl transpeptidase(60 U/l). Neurological examination showed alert consciousness, mild upper gaze palsy, slight right-side hemiparesis and left Babinski signs was present. Cranial magnetic resonance imaging showed no abnormality, but cerebral angiography revealed bilateral carotid artery occlusion. There were abundant leptomeningeal anastomoses, and the posterior communicating artery was supplied by the left vertebral artery. Electroencephalography showed a spike wave in the temporal lobe and rebuild-up phenomenon in the right hemisphere. Brain atrophy in the anterior and temporal lobes progressed, and the patient experienced gradual disorientation, delirium and hypobulia. He was eventually bedridden. He also demonstrated repetitive tonic-clonic convulsions. After one convulsion, he remained unconscious and died of pneumonia. Autopsy revealed thickening of the intima and internal elastic lamina in the occluded internal carotid artery. The anterior and middle cerebral arteries showed the same pathological changes. Multiple small infarctions restricted to grey matter were present in the cerebral cortex and may have caused the progressive brain atrophy. There was no myelin pallor in the white matter of the cerebrum. Atherosclerotic changes, senile plaque, and neurofibrillary tangles were seen but were within normal limits. These pathological findings were strongly suggestive of moyamoya disease.
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PMID:[An autopsy case of bilateral carotid artery occlusion with repetitive epilepsy and brain atrophy in a senile patient]. 1068 97

The numerous extrapulmonary manifestations of tuberculosis have been well described. Intracranial localizations, including brain stem tuberculoma, are very rare. The authors report a case of brain tuberculoma in a patient with a history of primary pulmonary tuberculosis successfully treated more than twenty years earlier. The patient presented with signs of infection, although the fever disappeared temporarily after successive treatments for malaria (confirmed Plasmodium faiciparum), as well as neurological signs with left hemiparesis. Chest radiographs showed no signs of progressive pulmonary tuberculosis, and blood tests, cerebrospinal fluid testing, and HIV serology were all negative. Treatments for maxillary sinusitis, the malaria, bacterial meningitis, and cerebral abscess were equally ineffective. Brain stem tuberculoma was diagnosed only when the patient was transferred to a hospital equipped with neuroimaging equipment and was confirmed after histopathological examination of the intracranial lesion biopsies and the detection of mycobacterium DNA by polymerase chain reaction (PCR) in the cerebrospinal fluid. A review of 147 cases of intracranial tuberculoma reported in Africa between 1985 and 2001 points out the difficulties of both the differential diagnosis (tuberculoma or other intracranial space-occupying lesions) and treatment in African areas where neuroimaging is unavailable. Our patient's brainstem tuberculoma probably resulted from reactivation of latent tuberculosis.
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PMID:[Intracranial tuberculoma in Africa, with no available neuroimaging. Case report and review of the literature]. 1469 80

Dyke-Davidoff-Masson syndrome is a disorder involving hemiatrophy or hypoplasia of 1 cerebral hemisphere secondary to an insult in the developing brain. Often this will manifest with seizures, hemiparesis, mental retardation, and facial changes. Associated with this pathology are the radiologically evident changes, such as thickening of the calvarium, hyperpneumatization of the sinuses, and dilation of the ipsilateral lateral ventricle among others. The following is a case presentation of an 18-year-old female emigrating from Ghana who presented to the emergency department with complaints of seizures diagnosed as being caused by cerebral malaria at 13 years of age. We hypothesize that the cerebral malaria and related vascular occlusion are the causes of her acquired cerebral changes. Included are computed tomography images.
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PMID:Dyke-Davidoff-Masson syndrome in postcerebral malaria. 1920 21

Francesco I de' Medici (1541-1587), the second Grand Duke of Tuscany, was one of the members of the Medici family who ruled Florence during the centuries of the Renaissance. When, in 1857, all members of the Medici family were exhumed and definitively buried in the place where they still lie buried today, a painter, Giuseppe Moricci (Florence 1806-1879), who attended the ceremony, depicted the corpse of Francesco I in a perfect state of preservation. The painting shows a right spastic hemiparesis with a facial droop, a claw-hand appearance, the right shoulder internally rotated, the calf muscle wasted and the clubfoot confirmed by an orthopedic footwear in the coffin. The hemiparesis and consequent disability were likely concealed when Francesco I was alive, since in official portraits the Grand Duke appeared in perfect physical condition. However, chronicles reported that he had suffered from malaria and syphilis. Later in his life, temper and behavioral changes as well as emotional instability were documented, together with handwriting deterioration and seizures. We postulate that Francesco I had suffered from a stroke consequent to syphilis, a new aggressive and rapidly spreading infectious disease at that time in Italy. Francesco's governmental skills were presumably altered due to these diseases. Disability consequent to stroke was likely concealed by official portrayers and biographers of Francesco I during his life, consistent with the King's two bodies theory common since the Middle Ages: while the King's physical body is destined to die, the political one is everlasting. Infectious diseases have remained a leading cause of stroke in underdeveloped countries until recently, but noncommunicable causes are now prevailing worldwide.
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PMID:Stroke in Renaissance time: the case of Francesco I de' Medici. 2269 46

A systematic study of thrombophilia markers in a large series of patients with cerebral venous thrombosis (CVT) from India is scarce. The present study was undertaken to know the prevalence of common hereditary thrombophilia in a large series of CVT patients from India. Six hundred and twelve (354 men, 219 women and 39 children) consecutive patients with CVT admitted to various hospitals in Mumbai between 2001 and 2010 were investigated for the common thrombophilia markers, that is, protein C (PC), protein S, antithrombin (AT), and factor V Leiden (FVL) mutation. The main presenting clinical manifestations included papilledema (62%), headache (62%), hemiparesis (48%), seizures (31%), and cranial nerve palsy (7%). All the patients were managed with heparin followed by warfarin during the succeeding 6 months. Superior sagittal sinus thrombosis was the commonest site (74%) followed by cortical venous thrombosis (15%). Associated clinical pathologies were dehydration, sepsis, pregnancy and puerperium, malaria, and tuberculosis; but in the majority of patients, there was no obvious cause. Eighteen percent of the patients had any of the thrombophilia markers studied; PC deficiency was the commonest thrombophilia marker followed by deficiency of protein S, FVL mutation and AT deficiency. The men below 45 years with PC deficiency (P=0.03) and women with protein S deficiency were significantly higher (P=0.04). In conclusion, CVT is not an uncommon cause of neurological deficit as was presented in earlier reports. Pregnancy and puerperium-related CVT was much less common. Thrombophilia markers accounted for approximately one-fifth of the patients. Death due to CVT has shown remarkable reduction (13%) because of early diagnosis and appropriate anticoagulation.
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PMID:Hereditary thrombophilia in cerebral venous thrombosis: a study from India. 2437 May 83