Opalski syndrome detected on DWI MRI: A rare lateral medullary infarction. Case report and review.

INTRODUCTION: Wallenberg's syndrome and ipsilateral paresis due to combined infarction of the lateral medullary and cervical spinal infarction is known as Opalski syndrome. This rarely described syndrome was reported, to our knowledge, with DWI MRI, only once. CASE REPORT: We report the case of a 43-year-old man with autosomal dominant polycystic kidney disease who, after a brief episode of coma, developed Wallenberg syndrome and ipsilateral hemiparesis. Initial diffusion weighted-imaging MRI showed a high-intensity signal involving the lateral medulla oblongata and the spinal cord; but FLAIR MRI sequences showed bilateral high-intensity signals in the lateral medulla oblongata and spinal cord and high-intensity signals in the right and left cerebellar hemisphere in the PICA territories. MRI performed one year later showed an infarction involving the left medullary area and adjacent spinal segments alone. CONCLUSION: This observation illustrates a rare syndrome of lateral medullary infarction, associated with spinal cord infarction related to a possible transient basilar occlusion.

[Anosognosia for hemiplegia with pontine infarction]. / Anosognosie de l'hémiplégie dans un infarctus protubérantiel.

INTRODUCTION: Anosognosia for hemiplegia (AHP) is unawareness of unilateral motor deficit. This syndrome usually is reported in association with large lesions of the nondominant frontal and parietal lobes, the perithalamic lesions or their connexions with cortical or subcortical structures. Little is known about AHP in patients with brainstem's infarctions. CASE REPORT: A 79-year-old right handed woman, without history of intellectual deterioration or psychiatric diseases, with hypertension and paroxysmal atrial fibrillation, was admitted with acute left hemiplegia, somatosensory left deficit and slurred speech. Cerebral MRI indicated a recent infarct in the right anteromedial pontine territory. The patient had moderate anosognosia for hemiplegia (AHP) during the first week after the onset of stroke. There was no sign of left spatial hemineglect or left hemiasomatognosia, no persistant mental confusion and no associated significant cortical or subcortical lesions. CONCLUSION: We presumed that AHP is compatible with brainstem's lesions, particularly with pontine infarcts. The pathogenesis of AHP in pontine infarcts may result from the functional deactivation of frontal and parietal areas.

Pathogenesis of spontaneous cervico-cerebral artery dissection. A hypothesis and a review of the literature.

The pathogenesis of spontaneous cervico-cerebral artery dissection remains speculative due to the rarity of histopathological observations, which often correspond to late stage lesions. Transposition of theoretic data from experimental models, study of pathologies with morphological lesions of the same type, and review of some clinical cases, suggest a sequence for the pathological events leading to arterial dissection. Arterial dysplasia, aneurysms and dissections could all result from vascular remodeling in response to endothelial injury. It induces morphologic changes of the internal elastic lamina, smooth muscle cell proliferation, various matrix abnormalities involving the fibrillary components or their enzymatic regulation, arterial wall neoangiogenesis and dissection. Endothelial dysfunction could so play a key role in the imbalance between arterial degenerative and reparative processes and the initiation of cervico-cerebral artery dissection.

Diagnosis of acute ischaemic stroke with fluid-attenuated inversion recovery and diffusion-weighted sequences.

We evaluated the feasibility and use of diffusion-weighted and fluid-attenuated inversion-recovery pulse sequences performed as an emergency for patients with acute ischaemic stroke. A 5-min MRI session was designed as an emergency diagnostic procedure for patients admitted with suspected acute ischaemic stroke. We reviewed routine clinical implementation of the procedure, and its sensitivity and specificity for acute ischaemic stroke over the first 8 months. We imaged 91 patients (80 min to 48 h following the onset of stroke). Clinical deficit had resolved in less than 3 h in 15 patients, and the remaining 76 were classified as stroke (59) or stroke-like (17) after hospital discharge. Sensitivity of MRI for acute ischaemic stroke was 98%, specificity 100%. MRI provided an immediate and accurate picture of the number, site, size and age of ischaemic lesions in stroke and simplified diagnosis in stroke-like episodes. The feasibility and high diagnostic accuracy of emergency MRI in acute stroke strongly support its routine use in a stroke centre.

Diffusion-weighted magnetic resonance imaging in a case of cerebral venous thrombosis.

BACKGROUND: Diffusion-weighted imaging (DWI) is the most sensitive MR sequence in acute arterial ischemic stroke but has not yet been evaluated in venous cerebral ischemia. We describe a patient with DWI performed at the acute phase of a venous ischemic stroke. CASE DESCRIPTION: A rapid cerebral MRI including DWI and fast fluid-attenuated inversion recovery (FLAIR) sequences was performed at the acute phase of a venous stroke confirmed by conventional angiography. DWI showed a slight decrease in apparent diffusion coefficient values 3 hours after onset (0.53+/-0.07x10(-3) mm2/s) and was normal 48 hours later (0.064+/-0.15x10(-3) mm2/s). Fast FLAIR sequences showed large left frontoparietal hyperintensities. The lack of a clear decrease in apparent diffusion coefficient values associated with marked FLAIR abnormalities may suggest prominent or early associated vasogenic edema. Physiopathological differences between arterial and venous ischemia may explain the different type of DWI FLAIR abnormalities during the acute phase as well as the better recovery of neurological deficit in venous stroke than in arterial ischemic stroke. CONCLUSIONS: In the context of an acute stroke, the contrast between marked FLAIR and subtle DWI abnormalities on MRI may reflect the venous mechanism of cerebral ischemia.

Evolving isolated hand palsy: a parietal lobe syndrome associated with carotid artery disease.

Six patients with cerebral ischaemia who presented evolving isolated hand palsy were studied, five prospectively and one retrospectively. The motor deficit involved only the hand and the wrist in some cases. In almost all cases the motor deficit was pseudo-ulnar. None of them had a Babinski sign, all had mild sensory symptoms or signs in the affected hand. CT and MRI disclosed recent infarctions contralateral to the affected hand, in the white matter of the angular gyrus, in a vascular borderzone. Five had a tight stenosis of the internal carotid artery. The pyramidal tract was anatomically spared in three cases, even considering its parietal origin. Consistent with previous data, our study suggests that the parietal lobe is involved in the control of the motor function of the hand. We propose the existence of a new entity, characterized by an evolving non-pyramidal motor deficit in the hand following infarction of the angular gyrus of the inferior parietal lobe.

Induction of myelination in the central nervous system by electrical activity.

The oligodendrocyte is the myelin-forming cell in the central nervous system. Despite the close interaction between axons and oligodendrocytes, there is little evidence that neurons influence myelinogenesis. On the contrary, newly differentiated oligodendrocytes, which mature in culture in the total absence of neurons, synthesize the myelin-specific constituents of oligodendrocytes differentiated in vivo and even form myelin-like figures. Neuronal electrical activity may be required, however, for the appropriate formation of the myelin sheath. To investigate the role of electrical activity on myelin formation, we have used highly specific neurotoxins, which can either block (tetrodotoxin) or increase (alpha-scorpion toxin) the firing of neurons. We show that myelination can be inhibited by blocking the action potential of neighboring axons or enhanced by increasing their electrical activity, clearly linking neuronal electrical activity to myelinogenesis.

[Contribution of position emission tomography in a case of Marchiafava Bignami disease: Morel's laminar sclerosis?]. / Apport de la tomographie par émission de positons dans un cas de maladie de Marchiafava Bignami: sclérose laminaire de Morel?

We report the case of a 26-year old alcoholic woman who abruptly presented with confusion associated with a major hypertonia. She evolved into a chronically vegetative state. Magnetic resonance imaging (MRI) was consistent with the diagnosis of Marchiafava Bignami disease. The corpus callosum first presented an oedematous aspect, then a central atrophy with an axial band. The clinical presentation and the functional imaging strongly suggest an association between the Marchiafava Bignami disease and diffuse cortical lesions, such as the laminar sclerosis of Morel.

Postneuroleptic laryngeal dyskinesias: a cause of upper airway obstructive syndrome improved by local injections of botulinum toxin.

We report a case of laryngeal dyskinesia resulting in severe rest and exercise dyspnea. A 51-year-old man treated for 2 years with flupentixol, an incisive neuroleptic, developed severe dyspnea due to intermittent, rhythmic, and dystonic movements of the vocal cords and upper airway. Local injections of botulinum toxin resulted in spectacular regression of laryngeal spasms and major improvement in breathing. This case emphasizes the risk of upper respiratory dyskinesias associated with neuroleptic treatment and shows the feasibility of a new local treatment in this life-threatening disorder.