Biomedical subjects
Publications and source records attributed to Gert Jan Luijckx.
We describe a patient with successive attacks (40 to 90 minutes) of cluster-like headache associated with aphasia, and contralateral hemihypesthesia and hemiplegia. The condition can best be described as cluster-like headache aura status.
Neuroprotection of patients with acute ischemic stroke should start at the scene and continue in the ambulance with the assessment and treatment of the airway, breathing, circulation, body temperature, and blood glucose. The key goal in eligible patients should be fast vessel recanalization with intravenous recombinant tissue-type plasminogen activator Results from a meta-analysis suggest that systemic thrombolysis is effective when given within 4.5 hours after stroke onset. The time window extends to 6 hours for patients undergoing intravascular thrombolysis. Acute stroke patients should be admitted to stroke care units. A crucial component of neuroprotection is the prevention of secondary brain damage, which can be caused by hypoxemia, hypotension, hyperthermia and hyperglycemia. This can be achieved by avoiding complications, e.g. aspiration, and intensive control of oxygenation, hydration and blood pressure, body temperature, blood glucose, and cardiac monitoring. Neuroprotective agents are designed to try to salvage brain tissue within the penumbra. Thus far, despite promising preclinical studies, clinical trials with neuroprotective drugs in acute ischemic stroke have been disappointing. However, we have been able to identify many of the factors that were responsible for these failures, and better-designed clinical trials with neuroprotective drugs should look more promising. Mild induced hypothermia is another form of neuroprotective treatment that is currently being investigated in acute stroke.
BACKGROUND: Because elevated body temperature (BT) in acute ischemic stroke is associated with poor outcome, it is currently recommended to maintain normothermia with antipyretics. Whether this can be achieved by the administration of acetylsalicylic acid (ASA) or acetaminophen is uncertain. METHODS: Over a period of 9 months, patients admitted with acute hemiparetic ischemic stroke were monitored for BT in the first 48 h. When BT rose >37.5 degrees C, patients were treated with either ASA 500 mg intravenously or acetaminophen suppository 1,000 mg. When 6 h later the BT was still or again >37.5 degrees C, patients were further treated with acetaminophen suppository 1,000 mg up to 4 times a day. Primary outcome measure was normothermia (BT </=37.5 degrees C) within respectively 1 and 3 h after intervention. Secondary outcome parameters were any decrease in BT and the mean decrease in BT. RESULTS: Of a total of 132 patients, 63 (48%) developed a BT >37.5 degrees C. The effects of 43 injections of ASA and 89 administrations of acetaminophen were studied. After 1 h, treatment with acetaminophen produced both significantly more reductions in BT and normothermia (respectively in 60 and 20%) than treatment with ASA (respectively in 37 and 5%). At 3 h, both interventions had a similar effect, with normothermia being achieved in only 37-38%. Fever (>38.0 degrees C) and evidence of an infection were related to unresponsiveness to treatment. CONCLUSIONS: In the majority of patients with acute ischemic stroke, ASA and acetaminophen are insufficient for reducing an elevated BT to a state of normothermia.