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V Biousse

Publications and source records attributed to V Biousse.

At least 19 recordsLinked to original sources

Central retinal artery occlusion associated with head or neck pain revealing spontaneous internal carotid artery dissection.

PURPOSE: To report two cases of head or neck pain and central retinal artery occlusion associated with spontaneous dissection of the ipsilateral internal carotid artery. METHODS: Case reports. RESULTS: We describe two cases of sudden visual loss caused by central retinal artery occlusion. Both cases were preceded by ipsilateral headaches or neck pain and tinnitus. The patient had no other neurological signs or history of trauma. In both cases, cerebral angiography revealed ipsilateral internal carotid artery dissection. CONCLUSION: Ipsilateral headache or neck pain with tinnitus preceding central retinal artery occlusion is highly suggestive of internal carotid artery dissection. Early diagnosis and treatment may reduce the risk of hemispheric stroke.

Adult

Coffee and doughnut maculopathy: a cause of acute central ring scotomas.

AIMS: To report the clinical features of five patients with non-progressive central ring scotomas of acute onset associated with excellent retained visual acuity. METHODS: Complete neuro-ophthalmological examinations were performed. Visual fields were performed by tangent screen, Goldmann, or Humphrey perimetry. In some cases further testing was carried out including fundus photography, fluorescein angiography, ERG, VEP, and neuroimaging. RESULTS: The patients were three women and two men whose ages ranged from 25 to 57 years. Four patients were heavy caffeine consumers while the fifth patient experienced an episode of hypotension. Vision loss was acute in all cases. The onset of vision loss was bilateral/simultaneous in three cases, bilateral/sequential in one case, and unilateral in one case. All affected eyes retained visual acuities of 20/25 or better. Colour vision was subnormal in three of four cases. Visual field defects were characterised by a central ring scotoma having an outer diameter less than 10 degrees. Fundus examination demonstrated temporal optic nerve pallor in three patients (five of 10 affected eyes) and reddish, petaloid macular lesions in one patient. Good visual acuity was maintained for the duration of follow up in all five patients. CONCLUSION: Central ring scotomas with excellent retained visual acuity may present as an acute, bilateral syndrome in patients who are heavy caffeine consumers. The configuration of visual field loss and its location, combined with the presence of temporal pallor in five eyes, suggest that the defect localises to the inner layers of the macula. While these cases could be considered an expansion of the clinical spectrum of acute macular neuroretinopathy, some may represent a distinct entity.

Adult

Isolated intracranial hypertension as the only sign of cerebral venous thrombosis.

BACKGROUND: Cerebral venous thrombosis (CVT) is often overlooked when intracranial hypertension (ICH) is isolated, hence mimicking idiopathic intracranial hypertension (IIH). OBJECTIVE: To describe the characteristics of patients with CVT and ICH. METHODS: We examined 160 consecutive patients with CVT between 1975 and 1998. They were separated into two groups according to their clinical presentation--isolated ICH and other neurologic symptoms and signs. RESULTS: Fifty-nine patients with CVT (37%) presented with isolated ICH. Neuroimaging showed involvement of more than one sinus in 35 patients (59%). Brain CT was normal in 27 of 50 patients (54%). Lumbar puncture was performed in 44 patients and showed elevated opening pressure in 25 of 32 (78%) and abnormal CSF content in 11 (25%). Etiologies and risk factors included local causes in 7 of 59 (12%), surgery in 1, inflammatory diseases in 18 (30.5%), infection in 2, cancer in 1, postpartum state in 1, coagulopathies in 11 (19%), oral contraception in 7 (12%), and remained unknown in 11 (19%). Anticoagulants were used in 41 of 59 patients (69.5%), steroids or acetazolamide in 26 (44%), therapeutic lumbar puncture in 44 (75%), and surgical shunt in 1. Three patients had optic atrophy with severe visual loss, 1 died from carcinomatous meningitis, and 55 (93%) had complete recovery. CONCLUSIONS: Central venous thrombosis (CVT) can present with all the classical criteria for idiopathic intracranial hypertension (IIH), including normal brain CT with normal CSF content. Because the recognition of CVT has crucial prognostic and therapeutic implications, MRI, with magnetic resonance venography when necessary, should be performed in patients with isolated intracranial hypertension. The outcome of CVT is unpredictable, and management of patients with CVT should not differ whether they present with isolated raised intracranial pressure or with other neurologic symptoms and signs. Therefore, isolated raised intracranial pressure from CVT differs in management from IIH and should be classified neither as "IIH" nor "pseudotumor cerebri."

Adolescent

Long-term follow-up of aneurysms developed during extracranial internal carotid artery dissection.

OBJECTIVE: To evaluate the clinical course of aneurysms developed during extracranial internal carotid artery (ICA) dissection. BACKGROUND: Aneurysms developed during extracranial ICA dissection are detected angiographically in 5 to 40% of cervical artery dissections. The clinical and radiologic course of these aneurysms is not known, and it is not known how they should be treated. METHODS: Fifty-eight consecutive patients with extracranial ICA dissection were reviewed, and those with radiographically detectable dissecting aneurysm at the acute stage or during early follow-up were included in this study. All patients had regular clinical and MR angiography examinations. Sixteen patients (27.5%) with a total of 20 ICA dissecting aneurysms were followed for a mean period of 36.9+/-21 months (range, 10 to 93 months). RESULTS: No clinical symptoms suggestive of aneurysmal rupture or embolization from the aneurysm were identified. Extracranial ICA aneurysms remained unchanged in 65% of patients, were resolved in 5% of patients, and decreased in size in 30% of patients. CONCLUSIONS: The clinical course of dissecting aneurysms was benign, although spontaneous radiologic resolution occurred rarely. Medical management with antiplatelet therapy alone (after early anticoagulation) is generally sufficient, and surgical management was seldom required.

Adult

Multiple sclerosis associated with uveitis in two large clinic-based series.

The authors reviewed records from consecutive patients in an MS clinic (n = 1,098) and in a uveitis clinic (n = 1,530) to select patients with "definite MS" and uveitis. A total of 28 of 2,628 patients (1%) were identified: 12 from the MS clinic (12 of 1,098; 1.1%) and 16 from the uveitis clinic (16 of 1,530; 1%). Pars planitis and panuveitis were most commonly encountered. The delay between the onset of neurologic and ocular symptoms (mean, 9 years) emphasizes the importance of a sequential diagnostic search throughout the patient's course.

Adult

Stroke-associated stuttering.

OBJECTIVE: To present patients with stuttering speech in association with stroke. DESIGN: Case series with follow-up for 5 years, or until the stuttering resolved. SETTING: University and community hospital neurology wards, and ambulatory neurology clinics. PATIENTS: Four patients who developed stuttering speech in association with an acute ischemic stroke. A 68-year-old man acutely developed stuttering with a large left middle cerebral artery distribution stroke. A 59-year-old man who had stuttered as a child began to stutter 2 months after a left temporal lobe infarction, as nonfluent aphasia was improving. Another childhood stutterer, a 59-year-old originally left-handed man developed severe but transient stuttering with a right parietal infarction. A 55-year-old man with a left occipital infarction had a right hemianopia and an acquired stutter, for which he was anosognosic. CONCLUSION: The clinical presentation of stroke-associated stuttering is variable, as are the locations of the implicated infarctions.

Aged

[Cervical artery dissection: recent data physiopathologic hypotheses].

INTRODUCTION: Cervicocranial arterial dissection is a major cause of cerebral infarction in young subjects. Traumatic and infectious factors are frequently suspected to be at the origin of cervicocranial artery dissection. However, they are usually too minor or too common to explain the vessel wall split-off. Underlying arteriopathy predisposing to dissections is therefore often suspected. CURRENT KNOWLEDGE AND KEY POINTS: The hypothesis of an underlying arteriopathy is based in certain cases on either the discovery of hereditary connective tissue disorders (or secondary signs of these diseases) or their frequent association with vascular and cardiac morphological abnormalities, thus suggesting extracellular matrix abnormalities. Current histological and biochemical data do not suggest the existence of a unique form of the disease but rather indicate the presence of various matrix abnormalities that could involve one of the fibrillar components or its enzymatic regulation. FUTURE PROSPECTS AND PROJECTS: Classification of dissections according to the various vascular wall alterations would therefore permit to better define recurrence and familial risks and to improve overall management of the patients.

Aortic Dissection

Sneddon syndrome with or without antiphospholipid antibodies. A comparative study in 46 patients.

Sneddon syndrome is characterized by the association of livedo reticularis and cerebral ischemic arterial events (stroke or transient ischemic attack). Reported prevalence of antiphospholipid antibodies is highly variable. We conducted this study to compare the clinical and pathologic features of patients with Sneddon syndrome according to the presence or absence of antiphospholipid antibodies. Forty-six consecutive patients with Sneddon syndrome were analyzed. All were examined by the same dermatologist who classified the livedo of the trunk according to the regularity of the fishnet reticular pattern and according to the thickness of the fishnet reticular pattern (> or = 10 mm = large; < 10 mm = fine). Skin biopsies were systematically performed, from both the center and the violaceous netlike pattern in 38 patients. Antiphospholipid antibodies-positive Sneddon syndrome was defined by the presence of lupus anticoagulant or abnormal titers of anticardiolipin antibodies on repeated determinations. Group I consisted of 27 antiphospholipid antibodies-negative patients and Group II, of 19 antiphospholipid antibodies-positive patients. All patients except I in Group II had irregular livedo reticularis. Large livedo racemosa was more frequently observed in Group I (89%) than in Group II (21%, p < 0.001). On skin biopsy, arteriolar obstruction was detected in only 8 patients (4 in each group). The following parameters were not statistically different between the 2 groups: gender, mean age at detection of livedo, mean age at first clinical cerebral event, hypertension, Raynaud phenomenon, patients with extracerebral and extracutaneous arterial or arteriolar thrombosis or stenosis, patients with venous thrombosis, and women with 2 fetal losses or more. In contrast, seizures (11% in Group I versus 37% in Group II, p < 0.05), mitral regurgitation on echocardiogram (19% versus 53%, p = 0.02), and thrombocytopenia < 150,000/muL (0% versus 42%, p < 0.005) were more frequently observed in Group II. The number of events per year of follow-up was lower with antiplatelet therapy (0.08 versus 0.5) in Group I, but was not different with anticoagulation (0.056 versus 0.06). Antiphospholipid antibodies-negative and -positive patients with Sneddon syndrome belong to close but different subsets of Sneddon syndrome.

Adolescent

Coagulation abnormalities and their neuro-ophthalmologic manifestations.

Congenital and acquired hypercoagulable states arise from an imbalance between procoagulant and anticoagulant forces. Although these conditions are present throughout the vascular tree, they typically give rise to local thrombotic lesions in discrete segments of the veins or arteries; this suggests that focal defects in the vascular wall or blood flow must be associated with a hypercoagulable state to produce thrombosis. Numerous new factors associated with hypercoagulability have been described in the past few years. Congenital and acquired hypercoagulable states are reviewed here, with an emphasis on recent data on focal thrombosis involving the eye and central nervous system.

Blood Coagulation Factors

Aneurysms and subarachnoid hemorrhage.

Most unruptured intracranial aneurysms that produce neuro-ophthalmologic signs arise from the junction of the internal carotid and posterior communicating arteries. These aneurysms typically compress the third nerve in the subarachnoid space. Compression of cranial nerves within the cavernous sinus is less common, resulting in single or multiple and often painful ocular motor nerve pareses. Unruptured aneurysms of the proximal and distal segments of the intracranial portion of the internal carotid artery can compress the anterior visual pathways and cause visual loss. Ocular symptoms and signs may be the presenting manifestations of intracranial aneurysms. Prompt recognition of an aneurysm prior to rupture can prevent devastating intracerebral or subarachnoid hemorrhage. Moreover, visual complications are a not infrequent source of morbidity in those patients surviving acute intracranial bleeding. Recent advances in noninvasive neuroimaging and endovascular therapies facilitate early diagnosis and treatment and therefore may limit such complications.

Adult

Ischemic optic neuropathy associated with internal carotid artery dissection.

BACKGROUND: Ischemic optic neuropathy (ION) is an infarction of the anterior or, less frequently, posterior part of the optic nerve, usually due to a disease of small arteries supplying the optic nerve. Carotid stenosis or occlusions are rare causes, and among them, carotid dissections have been so far reported in only 5 cases. METHODS: We describe 4 patients with ION (2 anterior and 2 posterior) due to internal carotid artery dissection of a consecutive series of 110 patients with internal carotid artery dissection (3.6%). RESULTS: None of the patients had signs of central retinal artery occlusion or ischemic ocular syndrome. Ischemic optic neuropathy occurred after a mean of 5.3 days (range, 3-8 days) following the first symptom, which was headache in 1 patient, transient monocular blindness in 2, and hemispheric transient ischemic attack in 1. One patient had associated Homer syndrome, and 2 had severe ipsilateral headache and orbital pain. None of the patients developed a cerebral infarction. These features differ from those observed in "classic" nonarteritic anterior ION and might therefore point to carotid dissection. CONCLUSION: Ischemic optic neuropathy may occur as an early sign of carotid dissection: young age, previous transient monocular blindness, an association with pain, Horner syndrome, or hemispheric transient ischemic attacks are suggestive of this cause and should prompt confirmatory investigations.

Adult

Ophthalmologic manifestations of internal carotid artery dissection.

PURPOSE: To report the ophthalmologic symptoms and signs associated with extracranial internal carotid artery dissection. METHODS: One hundred forty-six consecutive patients with extracranial internal carotid artery dissection were evaluted; 29 were studied retrospectively from 1972 to 1984 and 117 prospectively from 1985 to 1997. RESULTS: Sixty-two percent of patients (91/146) with extracranial internal carotid artery dissection had ophthalmologic symptoms or signs that were the presenting symptoms or signs of dissection in 52% (76/146). Forty-four percent (65/146) had painful Horner syndrome, which remained isolated in half the cases (32/65). Twenty-eight percent (41/146) had transient monocular visual loss, which was painful in 31 cases, associated with Horner syndrome in 13 cases, and described as "scintillations" or "flashing lights"-often related to postural changes or exposure to bright lights-suggesting acute choroidal hypoperfusion in 23 cases. Four patients had ischemic optic neuropathy; one had diplopia. Among the 76 patients with ophthalmologic symptoms or signs as the presenting features of carotid dissection, a nonreversible ocular or hemispheric stroke later occurred in 27, within a mean of 6.2 days (range, 1 hour to 31 days). Eighteen patients had a stroke within the first week after the onset of neuro-ophthalmic symptoms and signs, and 24 had a stroke within the first 2 weeks. CONCLUSION: Ophthalmologic symptoms or signs are frequently associated with and are often the presenting features in internal carotid artery dissection. Painful Horner syndrome or transient monocular visual loss should prompt investigations to diagnose carotid artery dissection and begin early treatment to prevent a devastating ocular or hemispheric stroke.

Adult

The ophthalmology of intracranial vascular abnormalities.

PURPOSE: To provide a practical review of the ophthalmologic manifestations of intracranial vascular abnormalities. METHODS: We reviewed ocular manifestations of the most common intracranial vascular abnormalities: intracranial aneurysms, carotid-cavernous fistulas, arteriovenous malformations, and cavernous malformations. RESULTS: Unruptured aneurysms can compress the third cranial nerve and the anterior visual pathways. Ruptured aneurysms and subarachnoid hemorrhage can result in Terson syndrome and papilledema. Direct and indirect carotid-cavernous fistulas most commonly cause the classic triad of proptosis, conjunctival chemosis, and cranial bruit but can masquerade as chronic conjunctivitis. Arteriovenous malformations, with or without hemorrhage, may compress portions of the retrochiasmal pathways, causing visual field loss. Cavernous malformations, when in the brainstem, commonly cause abnormalities of supranuclear, nuclear, and fascicular ocular motility. CONCLUSIONS: The ophthalmologist may be the first physician to encounter clinical manifestations of intracranial vascular abnormalities that may herald devastating neurologic complications. Prompt diagnosis facilitates appropriate management and therapy.

Adult

[Sarcoidosis and pregnancy. A retrospective study of 11 cases].

PURPOSE: To analyze the evolutive profile of sarcoidosis together with reciprocal interactions between pregnancy and sarcoidosis. METHODS: All events that occurred during pregnancy in 11 women presenting with sarcoidosis were analyzed. Histological confirmation was obtained for the 11 cases. For all pregnancies were analyzed the course of both sarcoidosis and pregnancy, and the influence of pregnancy on the disease evolution. RESULTS: Among 33 pregnancies, 23 led to the birth of healthy fetuses (five spontaneous abortions, four voluntary abortions, and one therapeutic abortion). The major event was fetal hypotrophy in six cases. Three of them occurred during pregnancy in prednisone-treated patients with active sarcoidosis. No relapse of cured sarcoidosis or further evolution of sarcoidosis that was inactivated as of the beginning of pregnancy were observed. The course of active sarcoidosis varied, as improvement (one case), worsening (two cases) and stabilization (two cases) were observed. During the first year of follow-up after delivery, four relapses and, in two cases, preliminary signs of the disease were observed. CONCLUSION: Apart from the hypothetical but not definite risk of hypotrophy, no negative interaction between sarcoidosis and pregnancy could be established. Pregnancy does not seem to interfere with the course of sarcoidosis. Considering the risk of relapse after delivery, pregnant women presenting with sarcoidosis should benefit from clinical and radiological follow-up.

Abortion, Induced

[Angiitis of the central nervous system in systemic diseases].

PURPOSE: This review is aimed at presenting classification and diagnosis criteria of isolated central nervous system (CNS) angiitis, and at proposing guidelines for diagnosis and management of this disease. CURRENT KNOWLEDGE AND KEY POINTS: Isolated CNS angiitis are rare and most information has been provided by studies of very small series. Angiitis can be primitive or secondary to infectious, neoplastic diseases, or toxics. Clinical manifestations and radiologic abnormalities are not specific. A brain biopsy is therefore often required to confirm the diagnosis, as numerous non-inflammatory vascular diseases can mimic both clinically and radiologically isolated CNS angiitis. PERSPECTIVES AND PROJECTS: To help guide the diagnosis and therapeutical management of patients with CNS angiitis, strict classification criteria should be used: 1) rule out the various diseases that can mimic clinical and radiological CNS aspects related to isolated angiitis and differentiate "isolated CNS angiitis" from "CNS angiitis associated with systemic diseases"; 2) search for factors associated with the development of a "secondary CNS angiitis"; 3) check presumed mechanism at the origin of the cerebral vascular disease: "angiitis" versus "angiopathy"; 4) if the diagnosis of "primary CNS angiitis" is still suspected, it seems reasonable to perform cerebral and leptomeningeal biopsies. Treatment is still unknown and has to be discussed on a case by case basis according to the severity and progression of symptoms.

Arachnoid

Orbital pain as an isolated sign of internal carotid artery dissection. A diagnostic pitfall.

Head pain is one of the main presenting symptoms of internal carotid artery (ICA) dissection, usually in association with ischemic and/or local signs such as Horner's syndrome, lower cranial nerve palsies, or tinnitus. In rare cases, head pain remains isolated and mimics other conditions. We report a patient who suffered isolated prolonged orbital pain as the only sign of intrapetrous ICA dissection. Early recognition of such unusual facial pain may be crucial in decreasing the risk of secondary cerebral or retinal ischemia.

Aortic Dissection