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Coma is produced by one of two broad groups of problems: The rst is clearly morphologic, consisting either of discrete lesions in the upper brainstem and lower diencephalon (which may be primary or secondary to compression) or of more widespread changes throughout the hemispheres The second is metabolic or submicroscopic, resulting in suppression of neuronal activity The clinical examination in coma is designed to separate these various mechanisms and to gauge the depth of brain dysfunction The study of a large number of human cases in which coma preceded death by several days has disclosed three types of lesions, each of which ultimately deranges the function of the reticular activating system directly or indirectly In the rst type, a readily discernible mass lesion chie y a tumor, abscess, massive edematous infarct, or intracerebral, subarachnoid, subdural, or epidural hemorrhage is demonstrable Usually the lesion involves only a portion of the cortex and white matter, leaving much of the cerebrum intact, but nonetheless it distorts deeper structures In most instances, these mass lesions in or surrounding the hemispheres cause coma by a lateral displacement of deep central structures, sometimes with herniation of the temporal lobe into the tentorial opening, resulting in compression of the midbrain and subthalamic region of the reticular activating system (see below and also Chap 31) Likewise, a cerebellar lesion may secondarily compress the adjacent upper brainstem reticular region by displacing it forward and perhaps upward A detailed clinical record will show the coma to have coincided with these displacements and herniations The anatomic displacements caused by herniations are discussed in more detail below In a second type of anatomic lesion, less frequent than the rst, a destructive lesion is located in the thalamus or midbrain, in which case the neurons of the reticular activating are involved directly This pathoanatomic pattern characterizes brainstem stroke from basilar artery occlusion, thalamic and upper brainstem hemorrhages, as well as some forms of traumatic damage In a third type, widespread bilateral damage to the cortex and cerebral white matter is found the result of traumatic damage (contusions, diffuse axonal injury), bilateral infarcts or hemorrhages, viral encephalitis, meningitis, hypoxia, or ischemia, as occurs after cardiac arrest The coma in these cases results from interruption of thalamocortical impulses or from generalized.

destruction of cortical neurons Only if the cerebral lesions are bilateral and extensive is consciousness markedly impaired It should be mentioned, however, that in many of the diseases in this category there is severe thalamic damage, as mentioned earlier, and it is the latter that is responsible for coma Thus, the pathologic changes found in cases of coma are compatible with physiologic deductions namely that the state of prolonged coma correlates with lesions of all parts of the corticaldiencephalic system of neurons; but it is only in the upper brainstem that coma-producing lesions are small and discrete Recent studies by Parvizi and Damasio suggesting that lesions in the pons may cause coma are, in our opinion, subject to alternative interpretation, but further study is justi ed It should be noted again that in the largest group of cases of coma, no lesion is divulged by any technique of pathology; the lesion, caused by a metabolic or toxic abnormality or a generalized electrical discharge (seizure), is presumably subcellular or molecular, or the visible microscopic lesions are too diffuse for clinicoanatomic correlation

6:

Pathoanatomy of Brain Displacement and Herniations (See also Chap 31)

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As pointed out above, large, destructive, and space-consuming lesions of the cerebrum such as hemorrhage, tumor, abscess, or infarction with brain swelling impair consciousness in one of two ways One is by direct extension of the lesion into the diencephalon and midbrain The other, more frequent in clinical practice, is by lateral and downward displacement of the subthalamic upper brainstem structures with or without herniation of the medial part of the temporal lobe (uncus, hippocampus) into the opening in the tentorium One consequence of lateral displacement is that the upper midbrain, particularly the cerebral peduncle, is crushed against the opposite free edge of the tentorium (the resulting creasing of the lateral edge of the peduncle is called Kernohan s notch or, more properly, the Kernohan-Woltman phenomenon); this causes a Babinski sign ipsilateral to the hemispheral lesion The posterior cerebral artery may also be compressed at the edge of the tentorium, leading to hemorrhagic infarction of the occipital lobe (see also page 581) It follows from the foregoing discussion that unilateral destructive lesions of the hemispheres, such as infarcts or hemorrhages, do not cause coma unless they create some degree of mass effect, usually delayed in onset, which secondarily compresses the upper brainstem There are exceptions in which patients with massive strokes affecting the territory of the internal carotid artery are drowsy and inattentive from the onset, even before brain swelling occurs, but more often they are simply apathetic with a tendency to keep their eyes closed, a state that may be misinterpreted as stupor The term herniation, as in neurology and neurosurgery, refers to the dislocation of a portion of the cerebral or cerebellar hemisphere from its normal position to an adjacent compartment, a phenomenon that is evident at the autopsy table and may be appreciated by imaging of the brain Thus, herniations are termed transfalcine (across the falx) or transtentorial (through the tentorial aperture) or are named by the structure that is displaced cerebellar, uncal, etc These herniations between dural compartments are illustrated in Fig 17-1 and Table 17-2 Plum and Posner, following from earlier observations by McNealy and Plum, subdivided the transtentorial brainstem displacements into two groups: one a central.

Figure 17-1 Schematic depiction of brain herniations between dural compartments Transfalcial (1), transtentorial uncal-parahippocampal (2), cerebellar tonsillar (3), and horizontal (4), causing Kernohan-Woltman notch phenomenon Herniations are shown in blue

Now we just go into the pie chart type in the Chart Designer and go to the Pie overview screen and use the ExplosionOffset to expand the slices of the pie and separate them a bit to give some depth to the chart display In that same process, we can change the look and feel of the actual slices with some enhancements to the coloring We are using the primary and secondary colors with the gradient again in the Horizontal Position to give each of the slices some two-tone colors, as shown next

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