The pathophysiology of coma is complex, but simplification is possible. As with delirium, deficiency of substrates needed for neuronal function may occur as with hypoglycemia or hypoxia secondary to many different causes. Coma may occur from processes primary to the CNS or from systemic causes (T.a,b.l.§..221z8). With systemic causes, the brain is usually globally affected and signs that localize dysfunction to a specific area of the brainstem or cortex are usually lacking. In primary CNS causes, the coma may result from brainstem disease such as hemorrhage, herniation, vertebrobasilar artery thrombosis, or from bilateral cortical dysfunction. Signs localizing to specific areas of CNS dysfunction, such as hemiparesis or cranial nerve abnormalities, may be concomitantly present. A useful concept is that unilateral hemispheric disease, such as stroke, should not by itself result in coma. The function of either the brainstem and/or both hemispheres must be impaired for unresponsiveness.
A traditional view of reduced consciousness from mass lesions involves secondary compression of the brainstem by physical shifting of brain tissue. 19 In the uncal herniation syndrome, the most common of the herniation syndromes, the medial temporal lobe shifts to compress the upper brainstem, resulting in progressive drowsiness and then unresponsiveness. Usually, the pupillary light reaction on the same side of the mass is sluggish and the pupil may enlarge, eventually becoming widely dilated and nonreactive. The anatomic correlate of these events is suspected compression of the ipsilateral third cranial nerve by the medial temporal lobe herniating over the tentorium. In this scenario, the pupil ipsilateral to the mass first enlarges, then other signs of third nerve dysfunction progress with loss of extraocular movements. Hemiparesis may develop contralateral to the mass from compression of the descending motor tracts in the ipsilateral cerebral peduncle, reflecting dysfunction of the descending motor tracts prior to their decussation in the medulla. The above is the usual presentation of temporal lobe or uncal herniation; that is, ipsilateral third nerve palsy with contralateral hemiparesis. Less commonly, so-called falsely localizing signs are present with third nerve dysfunction contralateral, or hemiparesis ipsilateral, to the herniating temporal lobe. This is referred to as Kernohan's phenomenon and is thought to reflect compression of third nerve and midbrain structures against the tentorium contralateral to the mass. A central herniation syndrome is also described. These models spring from postmortem examination of brains from patients with expanding mass lesions.
The herniation syndromes serve as models, but their exact mechanism has been questioned. The fact that herniation syndromes may be reversed by interventions is evidence against simple physical displacement of the tissues and physical distortion of the brainstem. Additionally, the amount of midline shift of structures as evaluated by neuroimaging seemingly correlates with the level of consciousness without invoking physical herniation. In the patient with an acute lesion, the patient may be awake with up to 3 to 4 mm of pineal shift, with unresponsiveness deepening as the pineal shift increases to 10 mm.20 The perimesencephalic cisterns are invariably diminished in patients with pineal shift of about 9 mm. 20 The shift is in true dimensions as adjusted from the CT scan, which typically displays a miniaturized image. Less correlation of midline shift and consciousness has been noted with more anterior structures such as the septum.
Ischemia from compression of vessels is undoubtedly a factor in cerebral edema and effects of increased intracranial pressure. Increased intracranial pressure (ICP) may occur within regions of the brain, perhaps initiating a herniation syndrome or midline shift as described above. Increased ICP may also occur diffusely resulting in widely distributed CNS dysfunction. Cerebral blood flow (CBF) is usually constant between mean arterial blood pressures (MAP) of approximately 50 to 100 mmHg through the process of cerebral autoregulation. At MAP outside this range, CBF is reduced and ischemia may develop. Cerebral perfusion pressure (CPP) is equal to the MAP minus the intracranial pressure (CPP = MAP - ICP). It follows that in extreme uncontrolled elevation of the ICP, cerebral perfusion pressure is inadequate or lost as ICP approaches the MAP, and ischemia develops. Some authorities suggest that the upper range of MAP that allows constant CBF is about 150 mmHg, at least in the uninjured brain. There are many opinions, but little data to substantiate the exact range. (See Chap,...24Z for a more detailed discussion.)
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