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dial part of the medulla, the rhythm of breathing is chaotic, being irregularly interrupted and each breath varying in rate and depth (Biot breathing; also called ataxia of breathing not an appropriate term) This pattern progresses to one of intermittent prolonged inspiratory gasps that are recognized by all physicians as agonal in nature and nally to apnea; in fact, respiratory arrest is the mode of death of most patients with serious central nervous system (CNS) disease 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 (CSR-CNH-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 may cause sudden respiratory arrest without any of the aforementioned abnormalities of breathing; presumably this results from fulminant pontomedullary 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, and subhyaloid retinal hemorrhages are immediate clues to the presence of increased intracranial pressure, usually from one of the types of cerebral hemorrhage Papilledema develops within 12 to 24 h in cases of brain trauma and hemorrhage, but if it is pronounced, it usually signi es brain tumor or abscess ie, a lesion of longer duration Increased intracranial pressure produces coma by impeding global cerebral blood ow; but this occurs only at extremely high levels of pressure High pressure within one compartment produces shifts of central structures and a series of false localizing signs due to lateral displacements and herniations, as noted in the above discussion of herniation The syndrome of acute hydrocephalus, most often from subarachnoid hemorrhage or from rapid obstruction of the ventricular system by a tumor in the posterior fossa, induces a state of abulia (page 359) followed by stupor and then coma with bilateral Babinski signs The pupils are small and tone in the legs is increased These signs may be accompanied by headache and systemic hypertension This subject is discussed further in Chap 30.

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Unless the diagnosis is established at once by history and physical examination, it is necessary to carry out a number of laboratory procedures In patients with evidence of a cerebral mass or acute hydrocephalus, as manifest by signs of raised intracranial pressure or indications of brain displacements (asymmetry of limb movements, pupillary enlargement), a CT scan or MRI should be obtained as the primary procedure As discussed in Chap 2, lumbar puncture, although carrying a certain small risk of promoting further herniation, is nevertheless necessary in some instances to exclude bacterial meningitis or encephalitis If poisoning is suspected, aspiration and analysis of the gastric contents is sometimes helpful, but greater reliance should be placed on chromatographic analysis of the blood and urine ( toxic screen ) Accurate means are available for measuring the blood concentrations of phenytoin and other anticonvulsants, opiates, diazepines, barbiturates, alcohol, and a

wide range of other toxic substances A specimen of urine is obtained by catheter for determination of speci c gravity and for glucose, acetone, and protein content Proteinuria may also be found for 2 or 3 days after a subarachnoid hemorrhage or with high fever Urine of high speci c gravity, glycosuria, and acetonuria occur almost invariably in diabetic coma; but transient glycosuria and hyperglycemia may result from a massive cerebral lesion Blood counts should be obtained, and in malarial districts a blood smear should be examined for parasites Neutrophilic leukocytosis occurs in bacterial infections and also with brain hemorrhage and infarction, although the elevation of leukocytes in the latter conditions rarely exceeds 12,000/mm3 Venous blood should be examined for the concentrations of glucose, urea, carbon dioxide, bicarbonate, ammonia, sodium, potassium, chloride, calcium, and SGOT (serum glutamic oxaloacetic transaminase); analysis of blood gases and carboxyhemoglobin should be obtained in appropriate cases It should be kept in mind that disorders of water and sodium balance, re ected in hyper- or hyponatremia, may be the result of cerebral disease (excess ADH secretion, diabetes insipidus, atrial natriuretic factor release), as well as being the proximate cause of coma An EEG may be highly informative if no adequate explanation for coma is forthcoming from the initial examinations This is the only way to reveal nonconvulsive status epilepticus as the cause of a stupor

Classi cation of Coma and Differential Diagnosis (See also Table 17-3)

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The demonstration of focal brain disease or of meningeal irritation with abnormalities of the CSF is of particular help in the differential diagnosis of coma and serves to divide the diseases that cause coma into three classes, as follows: I Diseases that cause no focal or lateralizing neurologic signs, usually with normal brainstem functions CT scan and cellular content of the CSF are normal A Intoxications: alcohol, barbiturates and other sedative drugs, opiates, etc (Chaps 42 and 43) B Metabolic disturbances: anoxia, diabetic acidosis, uremia, hepatic failure, nonketotic hyperosmolar hyperglycemia, hypo- and hypernatremia, hypoglycemia, addisonian crisis, profound nutritional de ciency, carbon monoxide, thyroid states including Hashimoto encephalopathy (Chaps 40 and 41) C Severe systemic infections: pneumonia, peritonitis, typhoid fever, malaria, septicemia, WaterhouseFriderichsen syndrome D Circulatory collapse (shock) from any cause E Postseizure states and convulsive and nonconvulsive status epilepticus (Chap 16) F Hypertensive encephalopathy and eclampsia (Chap 34) G Hyperthermia and hypothermia H Concussion (Chap 35) I Acute hydrocephalus (Chap 30) J Late stages of certain degenerative diseases and Creutzfeldt-Jakob disease II Diseases that cause meningeal irritation, with or without fever, and with an excess of WBCs or RBCs in the CSF, usually without focal or lateralizing cerebral or brainstem

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