Clinical meaning
Stroke results from either cerebral vessel occlusion (ischemic, 87% of cases) or rupture (hemorrhagic), causing acute neurological deficits corresponding to the affected vascular territory. Ischemic stroke triggers an ischemic cascade: neuronal energy failure leads to glutamate release, NMDA receptor activation, calcium influx, and activation of destructive enzymes (calpains, caspases) causing cell death — the ischemic penumbra is potentially salvageable tissue surrounding the infarct core that is the target of thrombolytic therapy (alteplase within 4.5 hours). Traumatic brain injury involves primary injury (direct mechanical damage) and secondary injury (cerebral edema, ischemia, excitotoxicity, and neuroinflammation that evolve over hours to days). The nurse managing neurological emergencies must perform serial neurological assessments using the Glasgow Coma Scale, monitor for signs of increased ICP (Cushing's triad: hypertension, bradycardia, irregular respirations), and implement neuroprotective interventions.
Exam relevance
Risk factors: - Hemorrhagic conversion after thrombolytic therapy - Secondary brain injury from cerebral edema post-TBI - Respiratory failure in ascending Guillain-Barre syndrome - Status epilepticus (seizure >5 minutes or repeated without recovery) - Vasospasm after subarachnoid hemorrhage (peak days 4-14) - Autonomic dysreflexia in spinal cord injury above T6