The term akinetic mutism has been applied to yet another group of patients who are silent and inert as a result of bilateral lesions of the anterior parts of the frontal lobes or in the thalamus, leaving intact the motor and sensory pathways. The patient is profoundly apathetic, lacking to an extreme degree the psychic drive or impulse to action. There is a marked delay in verbal and motor responses (abulia), however, the abulic patient, unlike Cairns’ patient, registers most of what is happening about him and if intensely stimulated, may speak normally, relating events observed in the recent and distant past.
The patient with catatonia appears unresponsive, in a state that simulates stupor, light coma, or akinetic mutism. There are no signs of structural brain disease, such as pupillary or reflex abnormalities. As in the normal awake state, oculocephalic responses are muted—that is, the eyes move concurrently with the head as it is turned. There is usually resistance to eye opening, and some patients display a waxy flexibility of passive limb movement that gives the examiner a feeling of bending a wax rod (flexibilitas cerea); there may also the retention for a long period of seemingly uncomfortable limb postures (catalepsy). Peculiar motor mannerisms or repetitive motions, seen in a number of these patients, may give the impression of seizures; choreiform jerking has also been reported, but the latter sign should also suggest the possibility of seizure activity. The EEG shows normal posterior alpha activity that is attenuated by stimulation. Catatonia is discussed further in Chaps. 19 and 49.
Because there is considerable imprecision in the use of terms by which the states of reduced consciousness are designated, the physician is better advised to supplement designations such as coma and akinetic mutism by simple descriptions indicating whether the patient appears awake or asleep, drowsy or alert, aware or unaware of his surroundings, and responsive or unresponsive to a variety of stimuli. This requires that the patient be observed more for a longer period and more frequently than the several minutes usually devoted to this portion of the neurologic examination. The aforementioned findings of responsiveness reflected by functional imaging in a clinically unresponsive patient further emphasizes the care with which these clinical diagnoses should be proffered.
In the late 1950s, European neurologists called attention to a state of coma in which the brain was irreversibly damaged and had ceased to function, but pulmonary and cardiac function could still be maintained by artificial means. Mollaret and Goulon referred to this condition as coma dépassé (a state beyond coma). A Harvard Medical School committee in 1968 called it brain death and established a set of clinical criteria by which it could be recognized (see Beecher et al; the report is often said to be from the “Beecher Committee”). R.D. Adams, who was a member of the committee, defined the state as one of complete unresponsiveness to all modes of stimulation, arrest of respiration, and absence of all EEG activity for 24 h. The concept that a person is dead if the brain is dead and that death of the brain may precede the cessation of cardiac function has over the years posed a number of important ethical, legal, and social problems, as well as medical ones. All aspects of brain death have since been the subject of close study by several professional and governmental committees, which for the most part have followed the 1968 guidelines for determining that the brain is dead and equating this state with the traditional version of death as the inevitable dissolution of the body after cardiac and respiratory function have permanently ceased. The American Academy of Neurology published guidelines on this subject in 1995 and affirmed them with some refinements in 2010. The monograph by Wijdicks is a comprehensive modern source on the subject of brain death and also addresses the subject from an international perspective.