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CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE
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taken place when she was in the akinetic mute state This rare state of apparent vigilance in an imperceptive and unresponsive patient has been referred to by French authors as coma vigile, but the same term has been applied to the vegetative state 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, leaving intact the motor and sensory pathways; the patient is profoundly apathetic, lacking to an extreme degree the psychic drive or impulse to action (abulia) (pages 359 and 394) However, the abulic patient, unlike Cairns s patient, registers most of what is happening about him and intensely stimulated, may speak normally, relating events observed in the recent and distant past The psychiatric 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 re ex abnormalities Oculocephalic responses are preserved, as in the awake state ie, the eyes move concurrently as the head is turned There is usually resistance to eye opening, and some patients display a waxy exibility of passive limb movement that gives the examiner a feeling of bending a wax rod ( exibilitas cerea); there is 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 suggest the possibility of seizure activity The EEG shows normal posterior alpha activity that is attenuated by stimulation Catatonia is discussed further on pages 359 and 1311 Since there is considerable imprecision in the use of terms by which these states are designated, the physician would be 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 frequently or over a longer period than the several minutes usually devoted to this portion of the neurologic examination
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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 arti cial means Mollaret and Goulon referred to this condition as coma depasse (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 (Beecher et al) RD Adams, who was a member of the committee, de ned the state as one of complete unresponsiveness to all modes of stimulation, respiratory arrest, 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 posed a number of important ethical, legal, and social problems as well as medical ones The various aspects of brain death have since been the subject of close study by several professional committees, which have for the most part con rmed the 1968 guidelines for determining that the brain is dead The monograph by our colleague Wijdicks is a thorough and modern source on the subject of brain death and also addresses the subject from an international perspective
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The central considerations in the diagnosis of brain death are (1) absence of cerebral functions; (2) absence of brainstem functions, including spontaneous respiration; and (3) irreversibility of the state Following from the last criterion, it is necessary to demonstrate an irrefutable cause of the catastrophic brain damage (eg, trauma, cardiac arrest, cerebral hemorrhage) and to exclude reversible causes such as drug overdose The absence of cerebral function is judged by the presence of deep coma and total lack of spontaneous movement and of motor and vocal responses to all visual, auditory, and cutaneous stimulation Spinal re exes may persist in some cases, and the toes often ex slowly in response to plantar stimulation; but a well-developed Babinski sign is unusual in our experience (although its presence does not exclude the diagnosis of brain death) Extensor or exor posturing is seen from time to time as a transitional phenomenon just after brain death becomes evident The absence of brainstem function is judged by the loss of spontaneous eye movements, midposition of the eyes, and lack of response to oculocephalic and caloric (oculovestibular) testing; presence of dilated or midposition xed pupils (not smaller than 3 mm); paralysis of bulbar musculature (no facial movement or gag, cough, corneal, or sucking re exes); an absence of motor and autonomic responses to noxious stimuli; and absence of respiratory movements The clinical ndings should show complete absence of brain function, not an approximation that might be re ected, for example, by small or poorly reactive pupils, slight eye deviation with oculovestibular stimulation, posturing of the limbs, and the like As a nal test of this last component, it has become customary to perform an apnea test to demonstrate an unresponsivity of the medullary centers to a high carbon dioxide tension This test is conducted by rst employing preoxygenation for several minutes with 90% inspired oxygen, the purpose of which is to displace nitrogen from the alveoli and create a reservoir of oxygen that will diffuse down a gradient into the pulmonary blood The patient can then be disconnected from the respirator for a few minutes (during which time 100% oxygen is being delivered by cannula); this allows the PCO 2 to rise to 50 to 60 mmHg (typically, carbon dioxide rises 25 mmHg per minute at normal body temperature slower if the patient is hypothermic) If no breathing is observed and examination of the blood gases shows that an adequate level of PCO 2 has been attained, the presence of this component of brain death is corroborated Most but not all patients have the signs of diabetes insipidus when the other criteria for brain death are ful lled, re ecting the imprecision of clinical features in detecting the total loss of brain function Other ancillary bedside tests may be conducted Among the ones we use from time to time is an absence of pulse response to the injection of atropine; this re ects the loss of innervation of the heart by vagal neurons The authors have observed a number of dramatic spontaneous movements when severely hypoxic levels are attained by apnea testing or terminal disconnection from the ventilator for several minutes These include opisthotonos with chest expansion that simulates a breath, raising the arms and crossing them in front of the chest or neck (which we have termed the Lazarus sign), head-turning, shoulder-shrugging, and variants of these posturing-like movements (Ropper 1984) For this reason it is advisable that the family not be in attendance immediately after mechanical ventilation has been discontinued The EEG provides con rmation of cerebral death, and most institutions prefer corroboration of the clinical features by the dem-
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