[Acute tetraparesis of cerebral origin]. / Tétraparésie aiguë d'origine cérébrale.

INTRODUCTION: Thrombolytic treatment in the early stage of ischemic cerebral attacks requires rapid confirmation of the diagnosis and topographic localization. Unusual clinical features can lead to misdiagnosis with the risk of delaying optimal therapeutic management. OBSERVATION: We report the cases of two patients who experienced acute tetraparesis without any associated encephalic sign, consistent with the diagnosis of spinal cord injury. Cervical magnetic resonance imaging (MRI) was normal. Conversely, cerebral MRI displayed in both cases bilateral hemispheric infarction. Two ischemic lesions were revealed in the territory of both anterior cerebral arteries in the first patient, while the second patient had a bilateral infarction in the posterior arms of both internal capsules. CONCLUSION: In case of tetraparesis, emergency spinal cord MRI should be performed to rule out neurosurgical etiologies and ischemia. If negative, cerebral MRI should be performed at the same time to look for early cerebral infarction in both hemispheres and determine the indication for thrombolysis.

Dorsolateral infarction of the lower medulla: clinical-MRI study.

We describe a man with lateral medullary syndrome associated with a long-standing clumsiness of the ipsilateral upper limb. MRI showed that the clinical finding of ipsilateral clumsiness correlated with an extension of the infarction into the dorsal column nuclei but was not reflected in any involvement of the more ventral pyramidal tract. This deficit in movement control that appears superficially like a hemiparesis may result from a combination of lemniscal and spinocerebellar deficits.

[Cerebral venous thrombosis]. / Thromboses veineuses cérébrales.

Cerebral venous thrombosis shows remarkable clinical polymorphism: isolated intracranial hypertension, cerebrovascular accident or focal, subacute cerebral lesion. Magnetic resonance imaging permits easy identification of the thrombosis and its tissular consequences as well as long-term follow-up. Search for the cause should be meticulous, given the multiple possibilities, presently dominated by prothrombotic states (postpartum, haemostasis anomalies, systemic affections, haematologic diseases, birth control pill, etc.). The development of neuro-imaging is changing the classic severity of cerebral venous thrombosis. Anti-coagulant treatment is widely used, including during haemorrhagic infarction. This treatment probably contributes to improving the survival and functional prognosis.

[Non bacterial thrombotic endocarditis (marantic endocarditis). Apropos of a case and value of transoesophageal echocardiography]. / Endocardite thrombotique abactérienne (endocardite marastique). A propos d'un cas et de l'intérêt de l'échographie transoesophagienne.

Marantic or non-bacterial thrombotic endocarditis is a common complication of terminal malignancy, usually discovered at autopsy. The authors report a case of marantic endocarditis as a presenting sign of pancreatic carcinoma in which the diagnosis was made ante-mortem by transoesophageal echocardiography.

[Lateral bulbar infarctions. Distribution, etiology and prognosis in 40 cases diagnosed by MRI]. / Les infarctus latérobulbaires. Distribution, étiologies et pronostic de 40 cas identifiés par IRM.

Recent advances in lateral medullary syndrome have focused on otoneuro-ophthalmology and magnetic resonance imaging (MRI). To reevaluate lateral medullary infarcts, 40 non fatal cases (30 men and 10 women, mean age 57.5 years) accounting for 4.5 p. 100 of overall cerebral infarcts were consecutively included in a prospective study using MRI in all cases. Thirty three patients were investigated using transfemoral or magnetic resonance angiography. Besides classical symptomatology, visual disorders were usually noted: diplopia (n = 18), transient visual tilt of the surrounding (n = 4), skew deviation (= 4), esotropia (n = 2) or conjugate gaze deviation (n = 2). The middle part of the medulla was affected in 35 cases. When associated, ipsilateral peripheral facial palsy and/or deafness were linked to the involvement of the pontomedullary junction (n = 3) while ipsilateral hemiparesis (Opalski's syndrome, n = 4) was linked to the involvement of the lower medulla and the cervicomedullary junction. MRI showed an associated cerebellar infarct in 35 p. 100 of cases. Of 33 patients angiographically investigated, 27 (82 p. 100) had stenosis or occlusion of the ipsilateral vertebral artery, usually affecting the intracranial portion, when 3 had isolated posterior inferior cerebellar artery occlusion. Atherosclerosis was recognized as the main cause of lateral medullary infarcts (n = 25). Other miscellaneous etiologies were diagnosed: coagulopathy (n = 2), spontaneous arterial dissection (n = 2), dolichoectatic artery (n = 1), arteriolopathy (n = 1) or cardiogenic embolism (n = 1). At the term of follow-up (mean: 35 +/- 24 months), 33 patients were free of residual handicap, 8 had experienced recurrent vertebrobasilar infarcts, including 3 medullary infarcts (median ipsilateral, n = 1 or lateral contralateral, n = 2), and 3 were died of basilar artery thrombosis complicating extensive atherosclerosis of the intracranial vertebrobasilar system.

[Characterization of gestural disorders in primary progressive apraxia: diagnostic and nosographic contribution]. / Caractérisation du trouble gestuel dans l'apraxie progressive primaire: apport diagnostique et nosographique.

Five cases are reported of patients with so-called primary progressive apraxia, defined as a slowly worsening disturbance of gestural abilities, without other major cognitive changes during a long period, in relation to degenerative cortical atrophy. All five cases, as other cases in the literature, share the following common features: 1) asymmetrical onset of upper limb clumsiness, more often involving the left side, later involving the contralateral side and lower limbs; 2) after a variable delay, the occurrence of symptoms suggesting subcortical involvement (akinesia, limb stiffness, various kinds of movement disorders, dystonia, paresis of vertical gaze); 3) diffuse cortical atrophy typically more pronounced in the superior parietal cortex opposite to the first side affected. The unusual nature of apraxia in all these cases is pointed out and referred to as Luria's "kinesthaesic apraxia", ascribed to a loss of "selectivity" of distal elementary movements. This pattern of symptoms and their specific outcome could represent a distinct entity.

[Athymhormic syndrome caused by bilateral striato-capsular infarction. Moyamoya disease in adults]. / Syndrome athymhormique par infarctus striatocapsulaire bilatéral. Maladie de Moyamoya de l'adulte.

A 49 year-old women with no medical history suddenly presented bilateral striato-capsular infarct causing frontal-like behavioural disturbances associating inertia with loss of drive, interest and affect, and preservation of intellectual function ("athymhormic syndrome" or "loss of psychic self-activation"). Ischaemic lesions mainly affected right globus pallidus and left lentiform nucleus with no involvement of the caput of the nuclei caudati. Such changes were close to anoxic lesions known to cause the same symptomatology. Infarction was attributed to a Moyamoya disease on angiographic data. Bilateral involvement of basal ganglia, arterial borderzones or both, may explain the frequent occurrence of neuropsychological disturbances in Moyamoya disease.

Mutism and auditory agnosia due to bilateral insular damage--role of the insula in human communication.

We report a case of transient mutism and persistent auditory agnosia due to two successive ischemic infarcts mainly involving the insular cortex on both hemispheres. During the 'mutic' period, which lasted about 1 month, the patient did not respond to any auditory stimuli and made no effort to communicate. On follow-up examinations, language competences had re-appeared almost intact, but a massive auditory agnosia for non-verbal sounds was observed. From close inspection of lesion site, as determined with brain resonance imaging, and from a study of auditory evoked potentials, it is concluded that bilateral insular damage was crucial to both expressive and receptive components of the syndrome. The role of the insula in verbal and non-verbal communication is discussed in the light of anatomical descriptions of the pattern of connectivity of the insular cortex.

[Pseudovascular laterobulbar syndrome secondary to astrocytoma]. / Syndrome latérobulbaire pseudovasculaire secondaire à un astrocytome.

A patient presented with an atypical left lateral medullary syndrome (LMS) mimicking a stroke. Magnetic resonance imaging demonstrated a tumour in the left dorsolateral part of the medulla. Biopsy revealed a grade II astrocytoma. The patient died two weeks after surgery. Nine pathologically verified previous cases of LMS caused by a tumour are reviewed. LMS is invariably atypical because of associated supratentorial or extensive brainstem symptomatology. Onset is usually progressive but stroke-like onset has been occasionally reported. Glial tumours as a cause of LMS are less frequent than metastasis. Successful treatment has been reported in a case of low grade astrocytoma.

[Cerebral infarction in patients aged 16 to 35 years. Prospective study of 52 cases]. / Infarctus cérébraux artériels chez des patients âgés de 16 à 35 ans. Etude prospective de 52 observations.

OBJECTIVES: Aetiologies of cerebral ischemic events in young adults are various and often contraversial: atherosclerosis plays a role after age 35 years, cardioembolism is often recognized as the major cause, and numerous new predisposing conditions have been described. To evaluate very premature cerebral infarction, we studied prospectively 52 consecutive patients (34 women and 18 men) aged 16-35 years (mean 28.6 +/- 5.6 years) admitted over a 6-year period for an arterial cerebral infarct identified on CT, on MRI or both. METHODS: All patients were investigated using a standard protocol including cerebral angiography, transthoracic echocardiography, 24-hour Holter ECG monitoring, coagulation inhibitors levels, lupus anticoagulant testing, HIV and syphilitic serologies. Additional investigations were performed in a majority of patients: transesophageal echocardiography in 33, contrast echocardiography in 50, and anticardiolipin antibodies levels in 38. RESULTS: The arterial distribution of infarction did not differ from that of overall stroke patients. Sixteen cases were classified as certain aetiologies, including cardiac diseases with high embolic risk (n = 9), spontaneous arterial dissection (n = 4), moya-moya disease (n = 1), atherosclerosis (n = 1), and inherited antithrombine III deficiency (n = 1). Eighteen cases were classified as possible aetiologies including cardiac diseases with low embolic risk (n = 11) such as mitral valve prolapse or atrial septal aneurysm, miscellaneaous arteriopathies (n = 3) such as arterial dysplasia, antiphospholipid antibodies syndrome (n = 1) and migrainous stroke (n = 3). The 18 last cases were classified as unknown aetiologies, despite all patients but one had at least one vascular risk factor: this group significantly differed from the formers in that the patients were more frequently women using oral contraceptive associated with tobacco consumption, hypercholesterolemia, or both. Two patients died acutely and the survivors were followed 31 +/- 18 months. Three patients experienced recurrent stroke. Functional outcome was assessed using the Rankin scale on admission and 6 to 12 months after the onset of stroke: patients evaluated < or = 2 (no to mild handicap) were 31% on admission and 82% after recovery. Twenty six p. cent remained unable to resume a work. CONCLUSION: Despite extensive evaluation, identification and classification of aetiologies of cerebral infarction in young adults should be cautious because the risk as well as the pathogenesis of many potential causes still need to be defined.

[A study of 82 cerebral infarctions in the area of posterior cerebral arteries]. / Etude de 82 infarctus du territoire des artères cérébrales postérieures.

Of 598 consecutive non-selected cases of cerebral infarction included in a stroke registry, 82 cases (54 men and 28 women, mean age 66 +/- 14 years) of spontaneous and isolated posterior cerebral artery (PCA) territory infarction (right PCA in 36, left PCA in 35 and both in 11) were identified on the basis of CT combined with MRI in 51 cases. Infarction was superficial in 25 (group A), combined deep-superficial in 23 (group B) and deep in 34 (group C). Of 48 superficial lesions, 29 were massive while 19 were restricted to the territory of one branch. Of 57 deep lesions, 21 were located in the inferolateral thalamic territory, 10 in the paramedian thalamic territory, 12 in other midbrain or thalamic territories, and 14 in a combination of various midbrain and/or thalamic territories. Of 41 patients with unilateral superficial involvement, 39 had homonymous visual field defect. Unawareness of the visual defect and visual release hallucinations were observed with the same frequency in right and left lesions. Of 7 patients with bilateral superficial involvement, only 5 had bilateral visual field defect including incomplete cortical blindness in 3. The frequency of confusional state (n = 24) did not differ significantly in left versus right sided lesions while it was significantly higher in superficial or combined versus deep lesions (p = 0.05). Of 18 clinically evaluable patients with left PCA territory infarct, 14 had speech disorders including pure alexia in only one case. Of 15 patients with right territory infarction, 10 had spatial judgement disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Temporary forced laughter after unilateral strokes.

Forced laughter generally occurs in bilateral or diffuse lesions of the brain and is generally associated with pathologic crying. We report the cases of 3 patients in whom temporary forced laughter occurred after unilateral supratentorial infarction demonstrated by CT scan or MRI. In all cases, the lesion was exclusively subcortical and involved the striatocapsular region. For all patients the laughter occurred during the recovery phase of motor deficit and was 'pure' without associated weeping or other clinical features of pseudobulbar palsy. In all cases, the laughter attacks had become much less frequent or had totally disappeared 1 or 2 months after the stroke. According to a 'motor' hypothesis, a unilateral striatocapsular lesion may lead to temporary deregulation of the expression mechanisms.

[Lateral thalamic infarction. 22 cases]. / Infarctus thalamiques latéraux. 22 observations.

Isolated lateral thalamic infarcts (LThl) are rare. They often produce lacunar syndromes, and their main cause is thought to be an hypertensive arteriolopathy. To verify these data, we reviewed 639 cerebral infarcts demonstrated by CT and/or MRI and included in a hospital stroke registry over a 4-year period. We identified 22 cases (3.5 p. 100) of isolated LThl (right LThl: 15; left LThl: 7). Nineteen had MRI study. There were 13 men and 9 women of mean age 65 years. None had the complete Dejerine-Roussy syndrome: sensory disturbances 21 cases, hemiparesis 7, hemiataxia 5, involuntary movements 4. They were divided in group 1 (14 cases) with prominent sensory symptomatology and group 2 (8 cases) with prominent motor symptomatology. The pulvinar and the ventral posterior thalamic nucleus were affected in both groups while adjacent nuclei such as ventral lateral or lateral posterior were more often affected in group 2. All patients but one had good recovery but 13 developed thalamic pain severely interfering with social activities in 5 cases. Several findings suggested that rather an arteriolopathy than large vessels disease or cardiogenic embolism had been a major cause in this series: 1) all patients but one (including 2 with a potential cardiac source of embolism) were hypertensive or diabetic, 2) lesions were small infarcts in the territory of perforators, 3) patients did not experience premonitory as well as subsequent cerebral events suggestive of vertebrobasilar atherosclerosis while 2 experienced deep cerebral hypertensive hemorrhage, and 4) neuro-imaging found additional asymptomatic lacunes in numerous patients. However, in the absence of angiography in most patients, these results do not preclude a potential role of artery-to-artery microembolism.

Pure motor hemiparesis in a case of vertebrobasilar arterial ectasia.

A case of pure motor hemiparesis due to a pontine lacunar infarct is reported. Infarction was related to vertebrobasilar ectasia identified on CT, MRI and MR angiography. MR studies provide accurate information on anatomical location, residual lumen, partial thrombosis, mass effect on brain stem and CSF pathways and vascular complications.