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A 68-year-old woman was admitted to the intensive care unit (ICU) after being diagnosed with poor-grade subarachnoid hemorrhage due to the rupture of a right middle cerebral artery aneurysm (World Federation of Neurosurgical Societies score = 5, Fisher score = 4, computed tomography [CT] in Fig. 1). The patient underwent craniectomy with hematoma evaluation and clipping of the aneurysm after the appearance of signs of a transient right mydriasis. Within 1 day after surgery, the patient presented with right then bilateral fixed nonreactive mydriasis suggesting midbrain injury. Repeated CT showed a temporal herniation with brainstem compression (Fig. 1). Given the extent of brain injury (CT and clinical examination), we held a multidisciplinary discussion, and further therapeutic interventions were not warranted. After the cessation of sedation on the third day, there was a possible course of evolution toward brain death.
Fig. 1
Clinical and electrophysiological monitoring during the progression to brain death. The top panel displays sequential CT scans showing the evolution of brain injury up to brain death confirmed with an angiographic CT (CTa at 60 s: opacification of superficial temporal arteries but not intracranial vessels [3]). The underneath table describes the evolution over time of clinical and neuromonitoring data over 7 days after injury. Every 6 h, the GCS scores and the maximum ICP (in millimeters of mercury) are documented, alongside the number of SDs detected and pupillary response (right and left pupil size and reactivity to light, denoted by “R” and “NR”). The orange color indicates the onset of brain injuries becoming permanent (red). The appearance of SD initiated NUP preceded the identification of brain death. The bottom panel presents electrographic tracing from the six-contact ECoG strip with a bipolar montage. The signal is split with the background activity on the AC band (1–30 Hz) in black, and the near-direct current (0.005–30 Hz) changes in red. Repeated SDs on day 2 can be observed with a near-direct current shift (red) leading to a transient depression of the background activity (black). At day 6, the SD is followed by an SD-initiated NUP (the direct current traces are described in Fig. 2) with a permanent depression of the background activity. CT, computed tomography, CTa, computed tomography angiography, ECoG, electrocorticography, GCS, Glasgow Coma Scale, ICP, intracranial pressure, NR, nonreactive, NUP, negative ultraslow potential, R, reactive, SAH, subarachnoid hemorrhage, SD, spreading depolarization, WFNS, World Federation of Neurosurgical Societies
These six bite-sized videos will equip you with insights into the pathophysiological processes underlying Lennox–Gastaut syndrome, the burden on patients and caregivers, and opportunities to increase diagnostic accuracy and optimize treatment strategies.
FND perplexes and frustrates patients and physicians alike. Limited knowledge and insufficient awareness delays diagnosis and treatment, and many patients feel misunderstood and stigmatized. How can you recognize FND and what are the treatment options?
