ABSTRACT:Background:A 1995 National Institute of Neurological Disorders (NINDS) study found benefit for intravenous tissue plasminogen activator (tPA) in acute ischemic stroke (AIS). The symptomatic intracranial hemorrhage (SICH) rate in the NINDS study was 6.4%, which may be deterring some physicians from using this medication.Methods:Starting December 1, 1998, patients with AIS in London, Ontario were treated according to NINDS criteria with one major exception; those with approximately greater than one-third involvement of the idealized middle cerebral artery (MCA) territory on neuroimaging were excluded from treatment. The method used to estimate involvement of one-third MCA territory involvement bears the acronym ICE and had a median kappa value of 0.80 among five physicians. Outcomes were compared to the NINDS study.Results:Between December 1, 1998 and February 1, 2000, 30 patients were treated. Compared to the NINDS study, more London patients were treated after 90 minutes (p<0.00001) and tended to be older. No SICH was observed. Compared to the treated arm of the NINDS trial, fewer London patients were dead or severely disabled at three months (p=0.04). Compared to the placebo arm of the trial, more patients made a partial recovery at 24 hours (p=0.02), more had normal outcomes (p=0.03) and fewer were dead or severely disabled at three months (p=0.004).Conclusions:The results of the NINDS study were closely replicated and, in some instances, improved upon in this small series of Canadian patients, despite older age and later treatment. These findings suggest that imaging exclusion criteria may optimize the benefits of tPA.
Although vascular dementia remains the only form of dementia that is preventable, available treatment is limited to the primary and secondary prevention of cerebrovascular disease. Strokes are highly responsive to different forms of prevention and treatment. The effectiveness of the same measures in the prevention of vascular dementia remains unclear, however, owing mainly to the lack of agreement on the definition and management of cognitive impairment. The successful treatment of "vascular dementia" involves the recognition of this term as obsolete, for it falsely implies that the underlying cognitive impairment has an unknown degenerative cause, is progressive, and responds neither to currently available preventive measures nor to treatments. Although dementia resulting from multiple strokes can be a terminal manifestation of this form of cognitive impairment, most patients have treatable cerebrovascular disease. A rational therapeutic approach to the treatment of this cognitive syndrome necessitates an understanding of its broad clinical spectrum and the diverse causes that may be responsive to currently available treatments, from the clinical asymptomatic "brain-at-risk" stage to full-blown dementia.
Background: Gadolinium-induced encephalopathy is a well documented complication due to the inadvertent entrance of a high dose of gadolinium into the intrathecal compartment. In lab animals, injecting gadolinium into the intrathecal compartment resulted in neurotoxicity and seizures. It is also well recognized that the presence of autologous blood in the intrathecal compartment can cause a broad range of neurological changes that can include seizures and mental status changes. At the time of writing this report, there were no references in the literature of simultaneous injection of gadolinium and blood into the subarachnoid space. Case: We present a case of a patient who received a high dose of gadolinium in the epidural space for needle placement confirmation during a fluoroscopically-guided epidural steroid injection for the treatment of lumbar radiculopathy. The injection was complicated by a wet tap necessitating an epidural blood patch for post-dural puncture headache. Shortly after the injection of the autologous blood, the patient developed grand-mal seizures and mental status changes requiring endotracheal intubation and admission to an intensive care unit. We describe the clinical course and management, as well as brain MRI findings and cerebrospinal fluid (CSF) changes. The patient made a complete recovery and was discharged. Conclusion: This case reinforces the need for using a low dose of gadolinium for the confirmation of needle placement in the epidural space, especially in procedures that carry the risk of inadvertent intrathecal injection. We attribute these findings to inadvertent simultaneous intrathecal injection of high dose gadolinium and autologous blood. A literature review of the cases of gadolinium-induced encephalopathy is provided followed by discussion. Key words: Postdural puncture headache, epidural blood patch, intrathecal gadolinium, seizures, mental status changes, encephalopathy
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