Probably all of these erratic patterns of breathing are interrelated in some manner. Webber and Speck have shown that apnea, Biot breathing, and gasping could be produced in the same animal with lesions in the dorsolateral pontine tegmentum by altering the depth of anesthesia. As pointed out by Fisher and by Plum and Posner, when certain supratentorial lesions progress to the point of temporal lobe and cerebellar herniation, one may observe a succession of respiratory patterns (Cheyne-Stokes, then hyperventilation, then Biot breathing), indicating an extension of the functional disorder from upper to lower brainstem; but again, such a sequence is not always observed. Rapidly evolving lesions of the posterior fossa, mainly masses in the cerebellum, more often cause sudden respiratory arrest without any of the aforementioned abnormalities of breathing as intermediaries; presumably apnea results from fulminant medullary compression by the cerebellar tonsils.
Clinical Signs of Increased Intracranial Pressure
A history of headache before the onset of coma, vomiting, severe hypertension beyond the patient’s static level, unexplained bradycardia, or subhyaloid retinal hemorrhages (Terson syndrome) are immediate clues to the presence of increased intracranial pressure, usually from one of the types of intracranial hemorrhage. Papilledema develops within 12 to 24 h in cases of brain trauma and hemorrhage, and if it is apparent when coma supervenes, it usually signifies brain tumor or abscess, that is, a lesion of longer duration. Increased intracranial pressure produces coma by impeding global cerebral blood flow; but this occurs only at extremely high levels of pressure. Increased pressure within one compartment displaces central structures and produces a series of “false localizing” signs because of lateral distortion of deep brain tissue and herniations, as noted in the earlier discussion of this type. However, the absence of papilledema does not exclude the presence of increased intracranial pressure, particularly in the elderly.
The syndrome of acute hydrocephalus, most often from subarachnoid hemorrhage or from obstruction of the ventricular system by a tumor in the posterior fossa, induces a state of abulia (slowed responsivity), followed by stupor, and then coma with bilateral Babinski signs. The pupils are small and the tone in the legs is usually increased or there may be extensor posturing. The signs of hydrocephalus may be accompanied by headache and systemic hypertension, mediated through raised intracranial pressure. Chapter 29 discusses this subject further.
Laboratory Procedures for the Diagnosis
Unless the cause of coma is established at once by history and physical examination, it becomes necessary to carry out a number of laboratory procedures. In patients with signs of raised intracranial pressure or indications of brain displacements, CT scan or MRI should be obtained as the primary procedure. As discussed in Chap. 2, lumbar puncture, although carrying a small risk of promoting further herniation, is nevertheless necessary in some instances to exclude bacterial meningitis or encephalitis.