Publications by authors named "Robert Loch MacDonald"

Chronic subdural hematoma (CSDH) is a common neurosurgical condition. Surgical evacuation has remained the primary treatment despite many advancements in the endovascular field. Regardless, recurrence requiring reoperation is commonly observed during the postoperative follow-up.

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Introduction: Cerebral infarction from delayed cerebral ischemia (DCI) is a leading cause of poor neurological outcome after aneurysmal subarachnoid hemorrhage (aSAH). We performed an international clinical practice survey to identify monitoring and management strategies for cerebral vasospasm associated with DCI in aSAH patients requiring intensive care unit admission.

Methods: The survey questionnaire was available on the European Society of Intensive Care Medicine (May 2021-June 2022) and Neurocritical Care Society (April - June 2022) websites following endorsement by these societies.

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Background A subset of good-grade patients with aneurysmal subarachnoid hemorrhage (aSAH) develop delayed cerebral ischemia (DCI) that may cause permanent disabilities after aSAH. However, little is known about the risk factors of DCI among this specific patient group. Methods and Results We obtained a multinational cohort of good-grade (Glasgow Coma Scale 13-15 on admission) patients with aSAH by pooling patient data from 4 clinical trials and 2 prospective cohort studies.

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Prior research suggests substantial between-center differences in functional outcome following aneurysmal subarachnoid hemorrhage (aSAH). One hypothesis is that these differences are due to practice variability. To characterize practice variability, we sent a survey to 230 centers, of which 145 (63%) responded.

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Antiplatelet and anticoagulant drugs (antithrombotic drugs) can cause or be associated with intracranial hemorrhage. Patients who take antithrombotic drugs are at higher risk for intracranial hemorrhage after trauma and are neurologically worse acutely compared with patients not on antithrombotic drugs. Treatment of patients on antithrombotic drugs who have intracranial hemorrhage includes reversal of anticoagulant drugs in almost all cases.

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Article Synopsis
  • Brain injury from intracerebral hemorrhage (ICH) affects both the cortex and white matter, potentially caused by the breakdown of blood products like bilirubin and its oxidation products.
  • Research showed that bilirubin significantly damages myelinated axons in brain slices, but unmyelinated axons are more susceptible to damage in live experiments.
  • The study suggests that preventing the toxic effects of bilirubin and its compounds, possibly using dimethyl sulfoxide, could be a therapeutic strategy to protect against axonal damage post-hemorrhagic stroke.
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Tice and colleagues pioneered site-specific, sustained-release drug delivery to the brain almost 30 years ago. Currently there is one drug approved for use in this manner. Clinical trials in subarachnoid hemorrhage have led to approval of nimodipine for oral and intravenous use, but other drugs, such as clazosentan, hydroxymethylglutaryl CoA reductase inhibitors (statins) and magnesium, have not shown consistent clinical efficacy.

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We studied whether endothelial nitric oxide synthase (eNOS) is upregulated and uncoupled in large cerebral arteries after subarachnoid hemorrhage (SAH) and also whether this causes cerebral vasospasm in a mouse model of anterior circulation SAH. Control animals underwent injection of saline instead of blood (n=16 SAH and n=16 controls). There was significant vasospasm of the middle cerebral artery 2 days after SAH (lumen radius/wall thickness ratio 4.

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Delayed cerebral vasospasm after subarachnoid hemorrhage is primarily due to sustained contraction of arterial smooth muscle cells. Its pathogenesis remains unclear. The degree of arterial constriction is regulated by membrane potential that in turn is determined predominately by K+ conductance (GK).

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Cerebral vasospasm is an important syndrome that afflicts 30% of patients in the aftermath of, and secondary to, subarachnoid hemorrhage. Starting approximately one week after the hemorrhage, the condition worsens the prognosis of the hemorrhage significantly. Apart from general supportive care, no treatment exists for cerebral vasospasm.

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