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EVOLVING CATASTROPHES IN THE NEURAXIS
Figure 8.12 Brain death diagnosis and guidelines for confirmatory testing. Evidence preferably based on computed tomographic scan or cerebrospinal fluid exam. Confirmatory test such as cerebral angiography,
nuclear scan, or transcranial Doppler ultrasonography may obviate observation over time. Criteria vary worldwide. PaCO2, partial pressure of arterial CO2; EEG, electroencephalogram.
tient. Cognition is intact, and patients may communicate through code systems. Mesencephalic damage usually is seldom seen in isolation and more commonly occurs from extension of a lesion in the thalamus (e.g., destructive intracranial hematoma) or as a result of occlusion of the tip of the basilar artery, producing simultaneous infarcts in both thalami and in the mesencephalic tegmentum. Bilateral thalamic damage resulting in coma most often involves the paramedian nuclei, but damage to interlaminar, ventrolateral, or lateral posterior nuclei may impair consciousness by interrupting the thalamic cortex and thalamocortical projections. Infarcts in the distribution of the penetrating thalamogeniculate or anterior thala-
mic perforating arteries are the most common causes of bilateral thalamic damage, but an infiltrating thalamic tumor or infiltrative intraventricular masses in the third ventricle can produce sudden coma. Ganglionic hemorrhages may extend into the thalamus and compress the opposite thalamus.16 Bithalamic hematoma is more commonly seen as an extension of pontine hematoma (see Chapter 14). Combined thalamic and mesencephalic damage may result in so-called slow syndrome, characterized by immobility, voicelessness, flat emotions, and somnolence most of the day.15 Bihemispheric structural damage may involve the white matter or cortex or both, and a diversity of disorders may produce damage severe