Delayed Transient Worsening of Neurological Deficits after Ischaemic Stroke

Reuck, Jacques De; Groote, Liesbeth De; Maele, Georges Van

doi:10.1159/000092334

Cited by 23 publications

(13 citation statements)

References 92 publications

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“…It is speculated that, in addition to stretching, septation of the cisterns may lead to reduced clearance, and blood decay products may induce local pressure changes within cisterns that may then impact the nutritional supply of the cranial nerve. It is also speculated that another factor, such as toxicity of the clot itself and neurotoxic substances derived from the clot, might affect abducens nerve pareses [10,11,12,13,14]. Further investigation may reveal the pathogenesis of this finding more precisely.…”

Section: Discussionmentioning

confidence: 99%

Abducens Nerve Pareses Associated with Aneurysmal Subarachnoid Hemorrhage

Munakata

Ohkuma²,

Nakano³

et al. 2007

Cerebrovasc Dis

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Background: This study was performed to reveal the incidence and the etiology of abducens nerve pareses associated with aneurysmal subarachnoid hemorrhage. Methods: At the time of admission, CT scan was carried out, and the thickness of the prepontine subarachnoid clot was measured. Results: In total 101 patients met the study requirements and abducens nerve pareses was apparent in 6 patients (5.9%). There were significant differences between the group with abducens nerve pareses and the group without in regard to the thickness of the prepontine subarachnoid clot on CT scan. Conclusions: The prepontine subarachnoid clot seemed to be the factor inducing the abducens nerve pareses.

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Section: Discussionmentioning

confidence: 99%

Abducens Nerve Pareses Associated with Aneurysmal Subarachnoid Hemorrhage

Munakata

Ohkuma²,

Nakano³

et al. 2007

Cerebrovasc Dis

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“…It is not surprising that simple partial seizures appear to occur more frequently than complex partial seizures in patients with neotemporal cortical infarcts, as seizure activity can spread rapidly from these areas to the nearby primary motor and sensory cortex. Although not specifically investigated in this study, the high incidence of inhibitory seizures, mimicking transient ischaemic attacks, in patients with territorial infarcts, has to be mentioned [28]. …”

Section: Discussionmentioning

confidence: 99%

The Cortical Involvement of Territorial Infarcts as a Risk Factor for Stroke-Related Seizures

et al. 2007

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Background: The cortical involvement of territorial infarcts is considered to be a significant risk factor for the development of early- as well as late-onset seizures. However, it is not known which cortical regions are more susceptible to the development of stroke-related seizures. Patients and Methods: In this retrospective study of 687 patients with territorial infarcts, 184 with stroke-related seizures were compared to 503 without seizures. The extent and the location of the infarcts were determined by computed tomography (CT) scans and/or magnetic resonance imaging (MRI) scans of the brain. The infarcts of the seizure and the non-seizure group were compared on digital cerebral vascular maps by superimposing the CT and/or MRI slices. Results: In patients with late-onset seizures, the infarcts were significantly more frequent in the temporal and parietal branches of the middle cerebral artery in comparison to the non-seizure group. In patients with early-onset seizures and in those with seizures due to a recurrent stroke, the territory of the temporal and occipital branches of the middle cerebral artery was the predilection side of the infarcts. Generalized tonic-clonic seizures occurred mainly in cases of infarction in the deep territory of the middle cerebral and of the anterior choroidal artery. Status epilepticus was significantly correlated with infarcts in the posterior temporal region. Conclusion: Some infarct regions are the sides of predilection for stroke-related seizures according to their type and their onset-time.

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“…Stroke patients with diabetes also have an increased risk of delayed transient worsening of neurological deficit in the acute phase [4] as well as an increased long-term mortality compared to patients without diabetes [5]. The reasons for these observations are not fully understood although several factors may contribute, for example increased production of advanced glycation end-products [6], enhanced blood thrombogenicity [7, 8], reduced platelet responsiveness to aspirin [9], reduced collateral circulation [10], and greater cerebral susceptibility to ischaemia [11] all of which are associated with diabetes.…”

Section: Introductionmentioning

confidence: 99%

Histological Features of Symptomatic Carotid Plaques in Patients with Impaired Glucose Tolerance and Diabetes (Oxford Plaque Study)

Redgrave¹,

Lovett²,

Syed³

et al. 2008

Cerebrovasc Dis

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Background: Diabetes is associated with an increased risk of incident stroke and both early and late recurrent stroke after transient ischaemic attack. Some small studies have suggested that atherosclerotic plaques from diabetics have a higher prevalence of unstable features than plaques from non-diabetics but results have been inconsistent. Method: We made detailed histological assessments of 526 plaques from consecutive patients undergoing carotid endarterectomy for recently symptomatic stenosis and related these to the presence of diabetes and impaired glucose tolerance (IGT). Results: 53 (10.1%) patients had diabetes, 26 (5%) had IGT and 447 (84.9%) had normal glucose tolerance (NGT). The overall prevalence of unstable plaque features was similar across these groups. However, whereas plaques removed >60 days after last symptoms in patients with NGT had less surface thrombus (OR = 0.61, 95% CI = 0.40–0.92, p = 0.02), fewer plaque macrophages (OR = 0.78, 95% CI = 0.51–1.19, p < 0.001) and less marked overall instability (OR = 0.57, 95% CI = 0.35–0.88, p = 0.009) than plaques removed more acutely, these features tended to be more persistent in patients with diabetes/IGT (OR = 1.08, 95% CI = 0.42–2.77, OR = 1.16, 95% CI = 0.46–2.96 and OR = 1.51, 95% CI = 0.60–3.77, respectively). Conclusion: Overall, the prevalence of unstable histology features in recently symptomatic carotid plaques is similar in patients with diabetes, IGT and NGT. However, surface thrombus and plaque macrophages appear to persist for longer after ischaemic symptoms in plaques from patients with diabetes/IGT compared to plaques from patients with NGT. This may contribute to the increased risk of recurrent stroke that is associated with diabetes/IGT.

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Delayed Transient Worsening of Neurological Deficits after Ischaemic Stroke

Cited by 23 publications

References 92 publications

Abducens Nerve Pareses Associated with Aneurysmal Subarachnoid Hemorrhage

Abducens Nerve Pareses Associated with Aneurysmal Subarachnoid Hemorrhage

The Cortical Involvement of Territorial Infarcts as a Risk Factor for Stroke-Related Seizures

Histological Features of Symptomatic Carotid Plaques in Patients with Impaired Glucose Tolerance and Diabetes (Oxford Plaque Study)

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