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protein 48 mg/dL, and sterile culture. Serum antibodies for dengue, scrub typhus, and Japanese encephalitis (JE) were negative. Herpes virus DNA was detected in the CSF by PCR. Due to the onset of new neurological symptoms in the second week of illness, CSF was collected and sent

protein 48 mg/dL, and sterile culture. Serum antibodies for dengue, scrub typhus, and Japanese encephalitis (JE) were negative. Herpes virus DNA was detected in the CSF by PCR. Due to the onset of new neurological symptoms in the second week of illness, CSF was collected and sent

protein 48 mg/dL, and sterile culture. Serum antibodies for dengue, scrub typhus, and Japanese encephalitis (JE) were negative. Herpes virus DNA was detected in the CSF by PCR. Due to the onset of new neurological symptoms in the second week of illness, CSF was collected and sent

protein C and S and high von Willebrand factor and lipoprotein (a) are present in higher proportions of patients with idiopathic ONFH compared with controls.41 Recurrent intraosseous hemorrhage from hemophilia, a bleeding disorder caused by decreased clotting factors, leads to occlusion of blood vessels and increased intraosseous

proteins (46%). Imaging abnormalities are present in 70% of symptomatic newborns, with intracerebral calcifications being the most commonly described feature. Causes of microcephaly include perinatal toxoplasmosis, rubeola, CMV, herpes simplex (TORCH) infections; some genetic syndromes; and maternal toxins such as alcohol, tobacco, drugs, or antiepileptics. Imaging Differential

protein-associated neurodegeneration, 98 Bifrontal bone defects, 329f Bilateral basal ganglia, 343 Bilateral cerebral palsy (spastic diplegia), due to periventricular leukomalacia, 92 Bilateral cortical/subcortical tubers, 296f Bilateral embolic strokes, in patient with cardiomyopathy, 257f Bilateral mixed-density subdural hematomas, 337f Bilateral striatal necrosis, 354 Bilateral subdural collections

viral encephalitis panel was negative. CT venogram showed no evidence of dural venous sinus thrombosis. EEG was abnormal with a mildly suppressed background, which suggested a generalized cerebral dysfunction of nonspecific etiology. Brain MRI revealed bilateral and relatively symmetric cortico-subcortical edema. Right parieto-occipital hemorrhage was noted

viral encephalitis panel was negative. CT venogram showed no evidence of dural venous sinus thrombosis. EEG was abnormal with a mildly suppressed background, which suggested a generalized cerebral dysfunction of nonspecific etiology. Brain MRI revealed bilateral and relatively symmetric cortico-subcortical edema. Right parieto-occipital hemorrhage was noted

protein-associated neurodegeneration, 98 Bifrontal bone defects, 329f Bilateral basal ganglia, 343 Bilateral cerebral palsy (spastic diplegia), due to periventricular leukomalacia, 92 Bilateral cortical/subcortical tubers, 296f Bilateral embolic strokes, in patient with cardiomyopathy, 257f Bilateral mixed-density subdural hematomas, 337f Bilateral striatal necrosis, 354 Bilateral subdural collections

proteins (46%). Imaging abnormalities are present in 70% of symptomatic newborns, with intracerebral calcifications being the most commonly described feature. Causes of microcephaly include perinatal toxoplasmosis, rubeola, CMV, herpes simplex (TORCH) infections; some genetic syndromes; and maternal toxins such as alcohol, tobacco, drugs, or antiepileptics. Imaging Differential