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ABSTRACT: Interest in the use of antidepressants after stroke has been renewed by better knowledge of poststroke depression, but mainly by the capacity of some of them to promote functional recovery of nondepressed subjects. Recombinant tissue plasminogen activator thrombolysis within the first few hours after the stroke is currently the only validated treatment able to improve the spontaneous-and most of the time incomplete-recovery of neurological functions after stroke. However, we have learned from research over the last decade, in part based on the considerable improvement of neuroimaging techniques, that spontaneous recovery of neurological functions is associated with a large intracerebral reorganization of the damaged human brain. The question of whether lesioned-brain plasticity can be modulated by external factors such as pharmacological antidepressant agents is now being addressed with the aim of improving recovery and reducing the final disability of patients. Poststroke depression is known to be frequent and deleterious for patient outcome. We review the interest in the use of antidepressants after stroke in classic but often neglected poststroke depression and we strongly underline the action of some antidepressants in promoting functional recovery of nondepressed patients after stroke.
Current Neurology and Neuroscience Reports 01/2013; 13(1):318. · 3.45 Impact Factor
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ABSTRACT: We attempted to classify causes of ischemic stroke in young adults using a progressive diagnostic algorithm and the ASCO (atherosclerosis, small-vessel disease, cardiac source, other cause) classification system.
Patients aged 16-54 years consecutively treated for acute ischemic stroke in a tertiary stroke unit were included in this retrospective analysis. Causes of stroke were classified using the ASCO system, which assigns a graded level of likelihood to each potential cause in individual patients. The initial etiologic workup included brain imaging, magnetic resonance or CT angiography of cerebral and cervical vessels, EKG, and routine blood studies. Patients without a definite cause of ischemic stroke after initial evaluation underwent transesophageal echocardiography.
We included 318 patients (195 men and 123 women); 131 patients were aged 16-44 years, and 187 were aged 45-54 years. A definite cause of stroke (ASCO grade 1) could be identified in 145 patients (45.5%). An uncertain cause of stroke (ASCO grade 2) was found in 59 (18.5%) further patients. Most (130 of 145) definite causes were identified by initial evaluation. The 2 major definite or uncertain causes of stroke were patent foramen ovale associated with atrial septal aneurysm (PFO-ASA) (20 of 131 [15.3%]) and dissection of the cervical or cerebral artery (19 of 131 [14.5%]) in patients aged 16-44 years and large-vessel atherosclerosis (37 of 187 [19.8%]) and PFO-ASA (23 of 187 [12.3%]) in patients aged 45-54 years.
Our findings suggest that PFO-ASA may be a major cause of ischemic stroke in young adults.
Neurology 06/2011; 76(23):1983-8. · 8.31 Impact Factor
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ABSTRACT: Air embolism is a rare complication of various invasive medical procedures. Venous cerebral air embolism is usually the consequence of paradoxical embolism. We report a case of isolated cerebral air embolism resulting from a non-paradoxical mechanism.
A few minutes after his central venous catheter had been accidentally disconnected, a 63-year-old man developed left-sided rhythmic jerking movements followed by left hemiplegia. There were no associated cardiologic or pulmonary signs. Brain CT showed air bubbles in the right frontal cortical sulci. The brain MRI DWI and FLAIR sequences showed a high intensity right frontal cortical lesion without reduction in ADC. Transesophageal echocardiogram did not find a patent foramen ovale.
In this case of venous cerebral air embolism, the lack of any cardiopulmonary manifestation, the lack of a patent foramen ovale and the neuroradiological findings are not in favor of the hypothesis of paradoxical embolism. The hypothesis of retrograde venous cerebral air embolism is discussed.
Revue Neurologique 12/2010; 167(8-9):615-8. · 0.49 Impact Factor
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ABSTRACT: Isolated, non-traumatic, cortical subarachnoid haemorrhage (cSAH) is a rare type of cerebrovascular disease caused by various disorders. In a few cases, especially in the elderly, no apparent cause can be identified. We report a case series of patients without apparent cause of cSAH. We aimed to determine whether cerebral amyloid angiopathy (CAA) could be a common cause of cSAH.
We retrospectively analysed clinical and radiological data of consecutive patients admitted to a tertiary stroke unit with cSAH. All patients had brain MRI as a part of their initial evaluation and a repeat examination during follow-up.
Amongst 25 patients with cSAH, 10 patients had no apparent cause of cSAH (six men and four women; mean age ± SD: 73.8 ± 8.5 years). All patients with no apparent cause presented with single or recurrent focal transient neurological symptoms of short duration. Only one patient experienced headache. cSAH was limited to one or two sulci, mostly the central sulcus. MRI showed the evidence of prior asymptomatic bleeding in 9/10 patients: cortical hemosiderosis (9/10), lobar intracerebral haemorrhage (ICH) (6/10) and cortical microbleeds (9/10). Eight of ten patients met the Boston criteria for probable CAA and 2/10 for possible CAA. During follow-up, three patients had recurrent bleeding: cSAH (2) and lobar ICH (1).
Our findings suggest that CAA could be a common cause of cSAH in the elderly with a fairly uniform clinical presentation. In addition to prior cortical bleeding (ICH, MBs), most patients from the present series had evidence of focal cortical hemosiderosis likely corresponding with prior unrecognized cSAH and suggesting that cSAH was a recurrent event.
European Journal of Neurology 10/2010; 18(4):597-603. · 3.69 Impact Factor
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ABSTRACT: Our aim was to review the etiologic background of isolated acute nontraumatic cSAH. While SAH located in the basal cisterns originates from a ruptured aneurysm in approximately 85% of cases, a broad spectrum of vascular and even nonvascular pathologies can cause acute nontraumatic SAH along the convexity. Arteriovenous malformations or fistulas, cortical venous and/or dural sinus thrombosis, and distal and proximal arteriopathies (RCVS, vasculitides, mycotic aneurysms, Moyamoya, or severe atherosclerotic carotid disease) should be sought by noninvasive imaging methods or/and conventional angiography. Additionally, PRES may also be a source of acute cSAH. In elderly patients, cSAH might be attributed to CAA if numerous hemorrhages are demonstrated by GRE T2 images. Finally, cSAH is rarely observed in nonvascular disorders, such as abscess and primitive or secondary brain tumors.
American Journal of Neuroradiology 09/2010; 31(8):1355-62. · 2.93 Impact Factor
