Biomedical subjects
J Bogousslavsky
Publications and source records attributed to J Bogousslavsky.
Different predictors of neurological worsening in different causes of stroke.
OBJECTIVES: To investigate clinical determinants of neurological worsening and to delineate its predictors. DESIGN: Restrospective analysis of the data from the Lausanne Stroke Registry. PATIENTS: A total of 3038 patients with first-ever stroke consecutively admitted to a primary-care stroke center. MAIN OUTCOME MEASURES: Neurological worsening in the acute phase of stroke. RESULTS: Neurological worsening was observed in 38% of 300 patients with brain hemorrhage, 34% of 1968 patients with noncardioembolic infarction, and 15% of 770 patients with cardioembolic infarction (P<.001). Neurological worsening was significantly less frequent in patients with small-artery disease than in those with large-artery atherosclerosis or other causes. A logistic multiple regression model in patients with noncardioembolic infarction showed age less than 65 years, hypertension, lesion outside the superficial anterior circulation, absence of transient ischemic attack, and reduced level of consciousness as the independent factors in the patients with small-artery disease, while it showed involvement of the posterior circulation and reduced level of consciousness in the patients with large-artery atherosclerosis. Severe functional disability or death was more common in patients with neurological worsening, both in patients with large-artery atherosclerosis and in those with small-artery disease (18% vs 9%; P<.001). CONCLUSIONS: Determinants of neurological worsening may include causative aspects rather than just the evolution of the ischemic or hemorrhagic process itself. For a better comprehension and treatment of neurological worsening, the causative and pathophysiological conditions underlying stroke should be differentiated as early as possible.
Preventing stroke recurrence in patients with patent foramen ovale: antithrombotic therapy, foramen closure, or therapeutic abstention? A decision analytic perspective.
Emphasis on the role of patent foramen ovale as a potential risk factor for ischemic paradoxical stroke has recently increased. Current therapeutic options for secondary stroke prevention include long-term antithrombotic therapies and invasive closure of the defect, but selective indications have not been evaluated. Therefore we developed a Markov-based decision analysis model for a hypothetical cohort of patients 55 years of age with presumed paradoxical embolism, measuring for each therapy the risks of stroke recurrence, treatment-related complications, and death after 5 years and the quality-adjusted life-years. Over a wide range of stroke risk recurrence (0.8% per year to 7% per year), the gain provided by closure of the defect exceeded the one obtained by other therapeutic options. When the risk exceeded 0.8% per year and 1.4% per year, respectively, this was also verified for anticoagulation and antiplatelet therapies compared with therapeutic abstention. Therapeutic abstention was the preferred strategy under 0.8% per year. Sensitivity analyses identified key parameters influencing the choice of therapy. These included estimates of stroke recurrence, bleeding rates, surgery-related case fatality rates, and age. Considering the risks of treatment and the devastating consequences of a recurrent stroke, our model suggests that if the estimated risk of paradoxical stroke recurrence is > 0.8% per year, therapeutic abstention becomes the worst option. Above this threshold secondary stroke prevention with anticoagulation therapy or surgical closure of the defect is the preferred strategy, and assessment of both the risk of stroke recurrence and the risk related to therapeutic options should guide individual therapeutic decision making.
Diagnosis as a guide to stroke therapy.
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Familial cardiomyopathy and distal myopathy with abnormal desmin accumulation and migration.
Desminopathies form a heterogeneous group of myopathies characterised by pathological aggregations of desmin. We report a family, where mother and daughter presented with an atrioventricular block and a slowly progressive distal muscular weakness, with non-homogeneous focal atrophy on computed tomography scans. The mother developed a severe global heart insufficiency necessitating a heart transplantation at 56 years of age. Skeletal muscle biopsies were characterised by inclusion bodies strongly expressing desmin and alpha B-crystallin, with a predominantly subsarcolemmal localisation. Ultrastructurally most inclusions corresponded to non-membrane bound granulo-filamentous material with disruption of myofibrils. An immunoblot showed a hyperintense desmin band at 53 kDa and a second band at 49 kDa, the latter being absent in controls. The cardiac muscle of the explanted heart showed very similar inclusions. These cases illustrate that in this distinct subtype of desminopathies the cardiac muscle alterations are comparable with those observed in skeletal muscle, and suggest the possibility of a primary desmin pathology.
[Skew deviation].
BACKGROUND: Skew deviation is a vertical ocular misalignment of prenuclear origin. Although well described in the literature, it is still probably underdiagnosed. Natural history of skew deviation is not well described in the literature. PURPOSE: To describe the clinical presentations, etiologies and follow-up of skew deviation. METHODS: Retrospective study of 29 patients diagnosed with skew deviation between 1993 and 1996. RESULTS: The commonest cause was cerebrovascular accident (12/29) and the commonest localisation was mesencephalic (9/29). Other causes included surgery (7/29), tumor (4/29), trauma (3/29), degeneration (3/29), inflammatory (2/29), increased intracranial pressure (1/29). Other localisations included cerebellum (5/29), ponto-mesencephalic (3/29), and medulla (2/29). Vertical diplopia was always accompanied by other neuro-ophthalmologic abnormalities. 69.2% (18/26) patients were totally asymptomatic after 7.5 months. 30.8% (8/26) were still symptomatic (diplopia). One patient required surgery, three patients were relieved with prisms, one patient needed monocular occlusion. One patient died during follow-up and precise data were lacking in two symptomatic patients. CONCLUSION: Skew deviation is not so rare, 10% of the cases referred to us for diplopia in 3 years. The diagnosis of skew deviation should be entertained when vertical diplopia cannot be explained by pathology of extraocular muscles, peripheral or central cranial nerve III or IV palsies, myasthenia, or orbital pathology. Prognosis for recovery in patients with skew deviation is good. 70% will recover, after a median time of 7.5 months. Surgery should be postponed at least for 12 months.
Mechanisms of second and further strokes.
OBJECTIVES: The mechanisms underlying recurrent stroke may be complex and multifactorial, but they have not been studied systematically. The aim was to analyse the different patterns and pathophysiological mechanisms of second and further strokes. METHODS: Recurrent stroke patterns and mechanisms were studied in 102 patients admitted with second or further strokes to the stroke centre in Lausanne University Hospital. RESULTS: The patients with an initial cardioembolic stroke experienced recurrent stroke of the same type most often, followed by those with initial non-lacunar non-cardioembolic stroke, brain haemorrhage, and lacunar stroke (77%, 65%, 58%, and 48% respectively). Forty two per cent of the recurrent strokes in patients with an initial brain haemorrhage were ischaemic, whereas patients with ischaemic stroke only occasionally suffered brain haemorrhage (5%). In patients with brain haemorrhage, the lobar location predominated in both the first and all episodes (69% and 78% respectively), suggesting a small, occult arteriovenous malformation or cerebral amyloid angiopathy rather than hypertensive small artery disease. The functional disability of patients after an initial lacunar stroke was significantly better than in patients with other stroke subtypes (p<0.001), but the difference became non-significant after recurrent stroke (p=0.26). CONCLUSIONS: Most of the recurrent strokes were of the same type as the first episode for both cardioembolic and non-lacunar non-cardioembolic stroke, however, about half of the patients with an initial brain haemorrhage or a lacunar stroke experienced other types of stroke recurrently. The findings suggest that the coexistence of multiple aetiologies may play a major part in determining the mechanism of stroke recurrence. The study is an important step in understanding the patterns of stroke recurrence, which may be critical for better prevention.
Face-arm-trunk-leg sensory loss limited to the contralateral side in lateral medullary infarction: a new variant.
Two patients are reported on who experienced loss of pain and temperature sensation in the entire contralateral hemibody but sparing the ispsilateral face (pure sensory stroke pattern) related to acute lateral medullary infarction. In both patients MRI showed a notch-like retro-olivary ischaemic lesion in the ventromedial tegmentum with preservation of the far lateral medulla. The mediolateral lesion involved the crossed lateral spinothalamic tract and the ventral trigeminothalamic tract, corresponding to sensory loss in the contralateral face, arm, and upper trunk. The ventrolateral extension of infarct damaged the far lateral part of the spinothalamic tract, corresponding to sensory loss in the contralateral lower trunk and leg. The findings suggest that hemisensory loss of the spinothalamic type involving-and limited to-the whole hemibody can occur in infarction in the lower brainstem. This form of pure sensory stroke may be classified as type IV of sensory loss in lateral medullary infarction.
Pure sensory syndromes in thalamic stroke.
We studied 25 patients with an acute thalamic stroke (infarct or hemorrhage) on CT or MRI scan and sensory dysfunction, among the 3,628 patients with first-time stroke included in the Lausanne Stroke Registry. Twelve patients had a right-sided infarct, 11 a left-sided infarct, and 2 a left-sided thalamic hemorrhage. Sensory symptoms or signs were the only clinical abnormality. The presumed causes of stroke were small artery disease in 21 patients including both cases of hemorrhage, emboligenic heart disease in 2, while the etiology of ischemic stroke was undetermined in 2 patients. Nine patients had a loss of all modalities of sensation with faciobrachiocrural distribution, 5 patients suffered dissociated sensory loss with faciobrachiocrural distribution and 11 patients showed a dissociated involvement of sensation with a partial distribution pattern. The inferolateral region (thalamogeniculate arteries) was involved in all patients. Six patients complained of pain and/or dysesthesias during the stroke; 5 of them had involvement of the nucleus ventrocaudalis (in 3 with damage to the nucleus ventro-oralis intermedius, and in one to the pulvinar) and 1 patient had involvement of the nucleus ventro-oralis intermedius. Eighteen patients complained of paresthesias in the contralateral part of the body; 16 of them had involvement of the nucleus ventrocaudalis (in 4 with damage to the nucleus ventro-oralis intermedius, in 1 with damage to the nucleus ventro-oralis intermedius, and nucleus ventro-oralis externus, and in one with damage to the nucleus parvocellularis and pulvinar). Four patients developed delayed pain and/or dysesthesias; all of them had involvement of the nucleus ventrocaudalis (in 1 with damage to the nucleus parvocellularis and pulvinar). Time lag from stroke onset to developing pain ranged from 2 to 15 days (mean 10.5 days). One patient with dissociated involvement of sensation with a partial distribution pattern had paresthesias and dissociated hemisensory loss involving position sense without pain and temperature sensations. This patient had involvement of the posterolateral part of the nucleus ventrocaudalis. In conclusion, sensory dysfunction and delayed pain are more often found in thalamic lesions that involve the nucleus ventrocaudalis, and nucleus ventro-oralis intermedius. Restricted sensory abnormalities correlate with very small lesions located in critical areas within these nuclei.
Diagnosis of cerebral venous thrombosis with routine magnetic resonance: an update.
Magnetic resonance imaging and angiography is the technique of choice in the diagnosis and follow-up of cerebral venous thrombosis: Thrombosis appears as an absence of flow void on spin echo images and lack of signal in angiographic techniques. The thrombus signal intensity is different on T1 and T2 spin echo weighted images and evolves according to hemoglobin degradation. Recognition of pitfalls and artefacts related to the different magnetic resonance imaging techniques employed is essential to interpret dural venous sinus thrombosis. In this paper the imaging of 27 patients with cerebral venous thromboses is reviewed. We describe the type of signal abnormalities, the different types of clot- and flow-related artefacts, and the indirect signs of cerebral venous thrombosis.
Isolated internal ophthalmoplegia associated with IgG anti-GQ1b antibody.
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Ipsilateral hemiparesis and pyramidal tract abnormalities.
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Large infarcts in the middle cerebral artery territory. Etiology and outcome patterns.
Large supratentorial infarctions play an important role in early mortality and severe disability from stroke. However, data concerning these types of infarction are scarce. Using data from the Lausanne Stroke Registry, we studied patients with a CT-proven infarction of the middle cerebral artery (MCA) territory that covered at least two of three MCA subterritories (deep, superficial anterior [superior] and posterior [inferior] territory). We compared these patients with patients presenting more limited infarction in the MCA territory. Our study group of large MCA (laMCA) infarction contained 208 patients, corresponding to 7.6% of all ischemic infarctions in the Lausanne Stroke Registry. Seventy-two patients had complete infarction in the whole MCA territory (coMCA). Internal carotid artery (ICA) occlusion (41%) and ICA dissection (12%) were more common than in limited superficial MCA (lsMCA) infarct and anterior circulation infarct (p < 0.001). Among the patients without ICA occlusion, atrial fibrillation (33%; p < 0.002) and cardiogenic embolism in general (54%; p < 0.001) were more frequent in laMCA than in lsMCA infarct. Severe neurologic deficit (hemiplegia and hemisensory loss in the face, arm and leg, hemianopia, global aphasia, reduced consciousness) was more common than in other types of infarct. A combination of these symptoms had a positive predictive value for laMCA infarction of 0.73 (sensitivity for left side laMCA infarcts, 0.56). Mortality (17%) and severe disability (50%) were higher with laMCA than for other infarcts (p < 0.001). Sixteen of the 35 deaths could be attributed to brain edema. Reduced consciousness, hemianopia, and coMCA infarction were independent predictors of death or severe disability; for death only, coma was an independent predictor. Patients who died because of brain edema were younger than patients whose death was due to other causes (mean age, 57 versus 73 years; p < 0.001); they also died sooner (mean time of death after stroke, 5 versus 37 days; p < 0.001). Furthermore, patients who developed coma on the day of admission were more likely to die because of brain death (p < 0.001). Large middle cerebral artery infarction is associated with cardiogenic embolism, ICA occlusion, and ICA dissection. It is a major predictor of death and severe disability, although a lower frequency of malignant brain infarction was found than previously reported.
Moriatic aphasia: a syndrome of acute carotid occlusion on the dominant side.
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Arterial territories of the human brain: cerebral hemispheres.
The development of neuroimaging has allowed clinicians to improve clinicoanatomic correlations in patients with stroke. Anatomic structures are well delineated on MRI, but there is a lack of standardization in their arterial supply. As in our previous study depicting the arterial supply of the brainstem and cerebellum, we present a system of 12 axial sections of the hemispheres depicting the dominant arterial territories, the most important anatomic structures, and Brodmann's areas. The area of variation of the cortical territory of the anterior, middle, and posterior cerebral arteries is also represented. These sections may be used as a practical tool to determine arterial territories on CT or MRI, and may help establish consistent clinicoanatomic correlations in patients with supratentorial stroke.
Persistent recurrence of hypomania and prosopoaffective agnosia in a patient with right thalamic infarct.
The authors report a 63-year-old man with a history of brief isolated manic episodes who became persistently hypomanic after a small right thalamic infarct. Detailed behavioral and neuropsychologic assessment were performed 18 months after the stroke and revealed a prosopoaffective agnosia as the foremost cognitive disorder, i.e., an impairment in the identification of emotional facial expressions with preserved discrimination of facial identity. Difficulties in reasoning on humorous material and other signs of mild right hemisphere dysfunction were present, but other perceptual, frontal and abstract-reasoning cognitive functions were unimpaired. Prosopoaffective agnosia has not been reported previously in thalamic lesions or in primary or secondary mania. The authors discuss the hypothetical relationships between a right hemisphere deficit in processing emotions and relapsing of the patient's hypomanic behavior.
Delayed segmental axial dystonia of the trunk on standing after lumbar disk operation.
We report four patients with various degrees of chronic, tonic, mildly painful, or non-painful, kyphoscolioses in orthostatism, which developed weeks, or months, after one or several laminectomies for lumbar disk hernia, in the absence of recurring radicular pain or acute lumbar pain. No family history or personal antecedent, of focal or generalized dystonia was found and the dystonia was not seen in any of the four patients pre-operatively, or during the immediate post-operative period. Only ill-defined lumbar 'discomfort', unlike their pre-operative lumbago, was reported by the patients, before and during the occurrence of the pathologic trunk posture on standing. Asymmetric lumbar muscle tonic contraction and hypertrophy was found on physical examination. In all patients, the kyphoscoliosis was maximal when standing, partially disappeared when seated, and completely when lying down. One patient responded well to clonazepam, but the other three showed no improvement with either clonazepam or local injections of botulinum toxin; L-dopa was ineffective in all cases, and trihexiphenidyle in three.