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Biomedical subjects

Valérie Biousse

Publications and source records attributed to Valérie Biousse.

32 records · Page 2Linked to original sources
PubMed2004

Cervicocranial arterial dissections.

Cervicocranial dissections are an increasingly recognized cause of stroke in the young. When the dissections narrow the vascular lumen, they often alter blood flow enough to cause transient ischemic attacks in the brain. Alterations in the endothelium activate the coagulation cascade, leading to the formation of intramural clot that may embolize distally to cause brain infarction. Pain and neuro-ophthalmic symptoms and signs are common manifestations.

Carotid Artery, Internal↗
PubMed2003

Cerebral Venous Thrombosis.

Because of its wide range of presentations, its highly variable mode of onset, its numerous causes, and its unpredictable outcome, cerebral venous thrombosis (CVT) remains a diagnostic and therapeutic challenge. Treatment of CVT consists primarily of symptomatic treatment of seizures and intracranial hypertension, antithrombotics, and etiologic treatment whenever possible. Heparin remains the first line of treatment for CVT; although its systematic use remains debated, recent studies have confirmed its safety even in patients with large hemorrhagic infarctions. The addition of local thrombolysis is indicated for patients with clinical worsening related to extension of the venous thrombosis, despite adequate anticoagulation and optimal symptomatic and etiologic treatment. In contrast to arterial stroke, complete recovery of prolonged or severe neurologic deficit is possible, justifying initiation of anticoagulation and eventually thrombolysis, even when the clinical situation seems desperate. New techniques using mechanical devices disrupting the clot may be used in addition to thrombolysis in rare cases. Ventricular drainage is indicated in cases of cerebellar infarction or deep venous thrombosis associated with hydrocephalus. Decompressive craniotomy may be performed acutely in patients with untractable intracranial hypertension and herniation.

Journal Article↗
PubMed2003

Cerebral Venous Thrombosis.

Because of its wide range of presentations, its highly variable mode of onset, its numerous causes, and its unpredictable outcome, cerebral venous thrombosis (CVT) remains a diagnostic and therapeutic challenge. Treatment of CVT consists primarily of symptomatic treatment of seizures and intracranial hypertension, antithrombotics, and etiologic treatment whenever possible. Heparin remains the first line of treatment for CVT; although its systematic use remains debated, recent studies have confirmed its safety even in patients with large hemorrhagic infarctions. The addition of local thrombolysis is indicated for patients with clinical worsening related to extension of the venous thrombosis, despite adequate anticoagulation and optimal symptomatic and etiologic treatment. In contrast to arterial stroke, complete recovery of prolonged or severe neurologic deficit is possible, justifying initiation of anticoagulation and eventually thrombolysis, even when the clinical situation seems desperate. New techniques using mechanical devices disrupting the clot may be used in addition to thrombolysis in rare cases. Ventricular drainage is indicated in cases of cerebellar infarction or deep venous thrombosis associated with hydrocephalus. Decompressive craniotomy may be performed acutely in patients with untractable intracranial hypertension and herniation.

Journal Article↗
PubMed2003

Anemia and papilledema.

PURPOSE: To elucidate the relationship between anemia and raised intracranial pressure (ICP). DESIGN: Interventional case series. METHODS: Retrospective case series and review of the literature. Only patients with documented papilledema, neuroimaging ruling out a space-occupying lesion, and anemia were included. RESULTS: Five women with confirmed idiopathic intracranial hypertension (IIH) (normal brain magnetic resonance imaging, normal cerebrospinal fluid, elevated intracranial pressure), and one man with presumed IIH (normal head computed tomography [CT], no lumbar puncture) were evaluated. All had bilateral papilledema associated with peripapillary hemorrhages. Two had retinal cotton-wool spots (CWS), and two had preretinal hemorrhages. All had severe iron deficiency anemia, which was discovered at the time of their ocular complaints in five of them. Their symptoms and signs improved dramatically after treatment of the anemia. We found 30 well-documented cases in the English and French literature. Among those, 13 were excluded from our analyses (11 had confounding disorders, and two had cerebral venous thrombosis). In the remaining 17 cases, isolated raised ICP associated with anemia was the most likely diagnosis, although in none of these cases was cerebral venous thrombosis excluded. CONCLUSIONS: Anemia may play a role in the occurrence of raised ICP and papilledema. Although only a few cases in the literature support this association, it may be more common than previously thought. Because most patients are not known to be anemic when papilledema is discovered, we suggest that a complete blood count be obtained in patients with IIH, especially in the absence of known associated factors such as obesity or medications or when treatment aimed at lowering ICP fails to improve the patient's symptoms. The underlying mechanisms remain unknown, but cerebral venous thrombosis should be carefully excluded.

Adult↗
PubMed2003

Magnetic resonance imaging abnormalities in cat-scratch disease encephalopathy.

A 23-year-old woman who presented with a branch retinal artery occlusion followed by encephalopathy showed, by brain magnetic resonance imaging, a nonenhancing lesion in the right parietal gray matter with normal diffusion-weighted imaging. Of 64 reported cases of cat-scratch encephalopathy with documented neuroimaging findings, only 12 (18.8%) have had abnormal imaging findings. The abnormalities have included cerebral white matter lesions, basal ganglia and thalamic lesions, and multifocal lesions in immunocompromised patients, but no gray matter lesions similar to those in this patient. The variety of neuroimaging findings supports multiple pathophysiologic mechanisms of central nervous system involvement in this disorder.

Adult↗
PubMed2003

The coagulation system.

Congenital and acquired hypercoagulable states arise from an imbalance between procoagulant and anticoagulant activity. Although these imbalances are present throughout the entire vascular tree, thrombotic lesions are usually localized in discrete segments of the veins or arteries and in certain organ systems. Thus, hypercoagulable states are likely to be associated with focal defects in the vascular wall to produce thrombosis. Many recently described factors are associated with hypercoagulability. Because thrombosis is a disease in which genetic and acquired risk factors interact dynamically, a thorough history, family history, and physical examination should be performed before ordering an extensive and costly coagulation panel.

Antiphospholipid Syndrome↗
PubMed2003

Leptomeningeal enhancement and venous abnormalities in granulomatous angiitis of the central nervous system.

A 68-year-old woman with a relatively acute onset of right homonymous hemianopia, Gerstmann syndrome, and global cognitive failure was found to have a lymphocytic pleocytosis and elevated protein on spinal fluid examination and displayed marked meningeal enhancement on magnetic resonance imaging and dilated cortical venules on cerebral angiography. Brain and meningeal biopsy disclosed a necrotizing granulomatous inflammation of small and medium-sized subarachnoid vessels. The brain parenchyma was normal. The angiographic presence of venous abnormalities, the lack of observable angiographic arterial involvement, and the lack of parenchymal pathology are distinctly unusual in granulomatous angiitis of the central nervous system. This case, therefore, extends the pathologic and imaging spectrum of this disorder.

Aged↗
PubMed2003

Neuro-ophthalmology of mitochondrial diseases.

PURPOSE OF REVIEW: To review recent data on mitochondrial diseases with emphasis on their neuro-ophthalmic manifestations. RECENT FINDINGS: Numerous studies have associated mitochondrial diseases with neuro-ophthalmic manifestations. Although there has been an explosion of studies on the genetics of mitochondrial diseases over the past few years, pathogenesis is only partly understood and therapy remains very limited. Over the past year, new mutations in Leber's hereditary optic neuropathy have been reported, and at least three genes associated with autosomal dominant chronic progressive external ophthalmoplegia have been described. These findings allow a better definition of the specific genetic mutations and gene products as well as pathophysiology of Leber's hereditary optic neuropathy and chronic progressive external ophthalmoplegia. The current development of animal models allows a better understanding of the pathophysiology of human mitochondrial diseases. SUMMARY: The afferent and efferent visual pathways within the central nervous system are frequently involved in mitochondrial diseases. Neuro-ophthalmic signs figure prominently and may be the presenting or even sole manifestation of these disorders. The four most common neuro-ophthalmic abnormalities seen in mitochondrial disorders are bilateral optic neuropathy, ophthalmoplegia with ptosis, pigmentary retinopathy, and retrochiasmal visual loss.

DNA Mutational Analysis↗
PubMed2002

Can Swedish interactive thresholding algorithm fast perimetry be used as an alternative to goldmann perimetry in neuro-ophthalmic practice?

OBJECTIVE: To assess the potential role of Swedish Interactive Thresholding Algorithm (SITA) Fast computerized static perimetry, compared with that of Goldmann manual kinetic perimetry (GVF), for reliably detecting visual field defects in neuro-ophthalmic practice. BACKGROUND: Automated visual field testing is challenging in patients with poor visual acuity or severe neurological disease. In these patients, GVF is often the preferred visual field technique, but performance of this test requires a skilled technician, and this option may not be readily available. The recent development of the SITA family of perimetry has allowed for shorter automated perimetry testing time in normal subjects and in glaucoma patients. However, its usefulness for detecting visual field defects in patients with poor vision or neurological disease has not been evaluated. DESIGN AND METHODS: We prospectively studied 64 consecutive, neuro-ophthalmologically impaired patients with neurologic disability of 3 or more on the Modified Rankin Scale, or with visual acuity of 20/200 or worse in at least one eye. Goldmann manual kinetic perimetry and SITA Fast results were compared for each eye, with special attention to reliability, test duration, and detection and quantification of neuro-ophthalmic visual field defects. We categorized the results into 1 of 9 groups based on similarities and reliabilities. Patient test preference was also assessed. RESULTS: Patients were separated into 2 groups, those with severe neurologic deficits (n = 50 eyes) and those with severe vision loss but mild neurologic dysfunction or none at all (n = 50 eyes). Overall, GVF and SITA Fast were equally reliable in 77% of eyes. Goldmann manual kinetic perimetry and SITA Fast showed similar visual field results in 75% of all eyes (70% of eyes of patients with severe neurologic deficits and 80% of eyes with poor vision). The mean +/- SD duration per eye was 7.97 +/- 3.2 minutes for GVF and 5.43 +/- 1.41 minutes for SITA Fast (P<.001). Ninety-one percent of patients preferred GVF to SITA Fast. CONCLUSIONS: We found the SITA Fast strategy of automated perimetry to be useful in the detection, and accurate in the quantification of central visual field defects associated with neuro-ophthalmic disorders. Our results suggest that for the general ophthalmologist or neurologist, visual field testing with SITA Fast perimetry might even be preferable to GVF, especially if performed by a marginally trained technician, even in patients with severely decreased vision or who are neurologically disabled.

Adolescent↗
PubMed2002

Diffusion-weighted magnetic resonance imaging in Shaken Baby Syndrome.

PURPOSE: To evaluate the role of diffusion-weighted magnetic resonance imaging (DWIMRI) in the diagnosis and management of children with suspected or confirmed Shaken Baby Syndrome (SBS). METHODS: This was a retrospective interventional case series of all infants and children younger than 2 years of age admitted to a children's hospital. We retrospectively reviewed medical records and neuroimaging findings of all children younger than 2 years of age with confirmed or suspected SBS admitted to a children's hospital. Inclusion criteria were documented ocular examination by an ophthalmologist and a brain MRI with DWI. Twenty-six infants and children were included. Other children were excluded. Children with proven SBS were diagnosed with "confirmed SBS," while children in whom the diagnosis of SBS remained uncertain were diagnosed with "suspected SBS." RESULTS: Twenty-six infants and children with mean age of 7.1 months (range, 6 weeks-24 months) were included, 18 with confirmed SBS. All 26 patients had a subdural hematoma, 10 had associated occult bone fractures, and 18 had retinal hemorrhages. Seven of the eight cases without retinal hemorrhages had isolated subdural hematoma without parenchymal brain lesions on both conventional MRI and DWIMRI. SBS was confirmed in only one case with a normal fundus. Among the 18 patients with retinal hemorrhages, SBS was confirmed in all but one case. All 18 patients with confirmed SBS had an abnormal DWIMRI. In 13 patients, DWI showed lesions that were larger than on conventional MRI. In patients with brain parenchymal lesions, the DWIMRI characteristics suggested cerebral ischemia, which appears to play a major role in SBS. CONCLUSIONS: In all patients with confirmed SBS, DWIMRI was abnormal and suggested diffuse or posterior cerebral ischemia, in addition to subdural hematomas in the pathogenesis of this disorder.

Battered Child Syndrome↗
PubMed2002

Isolated acquired unilateral horizontal gaze paresis from a putative lesion of the abducens nucleus.

In three patients, acute horizontal gaze pareses developed that could not be overcome with the oculocephalic maneuver, indicating a putative lesion of the ipsilateral abducens nerve nucleus. None of the patients had a facial nerve paresis or evidence of a trigeminal sensory neuropathy. Although most lesions that affect the abducens nerve nucleus also damage the ipsilateral fasciculus of the facial nerve, small lesions in this region can produce an isolated horizontal gaze paresis.

Abducens Nerve Diseases↗
PubMed2002

The eyes of mito-mouse: mouse models of mitochondrial disease.

The recent creation of several mouse models of mitochondrial diseases has provided new insights into the understanding of human mitochondrial disorders. Whether these animals have clinical or histologic ophthalmologic abnormalities is of great interest given the high frequency of such abnormalities in humans with mitochondrial disorders. In this article, we describe the currently available mouse models for mitochondrial diseases with special emphasis on their ocular phenotype. These mouse models demonstrate multiple and varied ophthalmologic manifestations.

Animals↗