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The Neurological Aspects of Coma
The Neurological Aspects of Coma SIMEON LOCKE, M.D.*
Considering how often coma constitutes one of the presenting physical signs in patients admitted to a large hospital, it is disappointing that the mechanism of the disorder is so little understood. Perhaps this relates to the difficulty in dealing scientifically with the notion "consciousness." Recognized by introspection, or evident through the intercession of motor behavior, consciousness remains difficult to define. Its study has been of interest to philosophers, psychologists, and physicians, who have searched for its location. Advocates of the concept of centers of consciousness have located this function in the frontal lobes 12 and corpus striatum. 5 More recently, the thesis of "centers" has been discarded, 2 • 19 with emphasis rightly placed on the distinction between function and its anatomical substratum. As used in a medical setting, consciousness implies awareness of the environment with responses appropriate to evoking stimuli. Usual stimuli must retain their adequacy. 14 Conscious awareness is an accompaniment of cortical activity, but "a healthy cerebral cortex cannot by itself maintain the conscious state." 3 Cortical activity is necessary for the content of consciousness, but not for its existence. Its activating or on-off aspect sets the bias, so to speak, on which specific input functions.
NEUROMECHANISMS The organization of the central nervous system is best viewed as being vertical in construction, with generalized core components near the central canal and specialized structures laterally disposed. 18 The core components, an interlacing of medullated fibers and neuronal aggregates distinct from the brain stem nuclei of classical neuroanatomy, constitute the reticular formation. This nonspecific or extralemniscal brain stem system receives its input by way of collaterals from the specific or lemniscal tracts. 25 It projects to cortex by two pathways. One is thalamic, with projection through the nucleus ventralis anterior, the centrum medianum, and the intralaminar nuclei. The secFrom the Department of Neurology, Harvard Medical School, and the Neurological Unit, Boston City Hospital *Assistant Professor of Neurology, Harvard Medical School
Surgical Clinics of North America- Vol. 48, No. 2, April, 1968
251
252
Al·T3
SIMEON LOCKE
260
T3·C3
~v
C3·C4 ~~~~~~~~~~~~~~~~~~MN~~~~~t~A
C4·T4
~~-~~~~'~A~~~(\~~~~~~~~~~--~~~NV~
F4·F3 F3·F7
Figure 1. Above, Electroencephalogram obtained one day after the onset of coma in a 54-year-old woman who was flaccid, areflexic, devoid of eye movements, had bilateral extensor plantar responses, and ultimately developed intermittent decerebration. Below, At postmortem examination ten days later, hemorrhagic necrosis of medulla, central pons, and base of mesencephalon was disclosed. The clinical coma contrasted sharply with the desynchronized electroencephalogram.
ond, extrathalamic, projection is capsular. 24 In thalamus the specific and nonspecific projection systems remain distinct. Lemniscal input terminates in the relay nuclei which project to cortex in a point-to-point manner. The extralemniscal input terminates in the nonspecific thalamic nuclei which project diffusely to cortex. 2 ° Cortical feedback is received by the reticular formation of the cephalic brain stem from frontal oculomotor area, cingulate gyrus, orbital surface of frontal
THE NEUROLOGICAL ASPECTS OF COMA
253
lobes, sensorimotor cortex, posterior parietal and paraoccipital regions, and the superior temporal gyrus. 11 Electrical stimulation of the reticular formation of the brain stem produces activation or desynchronization of the electroencephalogram, an effect which can be also achieved by physiological stimulation of lemniscal pathways in a sleeping individual. Presumably this electrographic arousal results from the distribution of impulses by collateral lemniscal branches to the reticular activating system. Although sleep and coma are usually characterized by synchronous, slow activity in the electroencephalogram, paradoxical sleep occurs in which behavioral sleep accompanies electroencephalographic desynchronization. 22 Drugs also may dissociate behavioral and electrographic sleep. Atropine produces behavioral alertness with a synchronized electroencephalogram, while reserpine produces drowsiness without synchronization of the electroencephalogram. 10 Lesions of the central cephalic brain stem produce behavioral and electrical sleep or coma, but, following long survival, electroencephalographic activation may return. 18 Behavioral unresponsiveness without associated synchronization of the electroencephalogram occurs with posterior hypothalamic lesions, while lesions of the reticular formation of the brain stem may be associated with electroencephalographic sleep in a waking preparation. 6 Structures in the medulla, located in the region of the rostral solitary tract, are antagonistic to the reticular activating system and cause synchronization of the electroencephalogramY Lesions of the medulla and low pons in isolation do not produce coma (Case 1, ref. 23). Higher centrally located brain stem lesions may produce behavioral unresponsiveness without altering the resting electroencephalogram 16• 17 (Fig. 1). The clinical relation between coma and mesencephalic tegmental lesions is well substantiated,9 and probably correlates with the experimental demonstration of suppression of the electrical activity of the medial reticular formation of the Inidbrain following cerebral concussion,8 with sensory-evoked potentials in the reticular system absent at a time they are still present in the lemnisci. 7 The occurrence of an akinetic, mute state with third ventricular lesions 4 may correlate with the function of the posterior hypothalamus, stimulation of which produces an excitatory response. 1 Akinetic mutism may be mimicked by a brain stem lesion. 13 Then, a patient deprived of ability to communicate may be SJibject to the cruelty of intact awareness.
ETIOLOGY Disorders of conscious awareness may result from systemic disease or intracranial lesion. Coma without focal abnormality and unconsciousness with lateralizing signs should not be equated with systemic or focal etiology respectively, for a previously well compensated neurologic abnormality may be re-expressed as a result of a systemic depression of function. Contrariwise, focal lesions, if strategically located, may produce global depression of consciousness without evident focal abnormality.
254
SIMEON LOCKE
Exogenous and Endogenous Poisons In unconsciousness from systemic disorder the etiology must be sought in ancillary findings, for nothing about the coma itself indicates its cause. Exogenous poisons are frequently responsible. Of these, in the patient population of a large municipal institution, ethyl alcohol and its less palatable substitutes are among the important offenders. Methyl alcohol ingestion productive of coma may be recognized by the associated metabolic acidosis and ethylene glycol ingested in antifreeze can be suspected on the basis of oxalic acid crystals in the urine. Odor of alcohol must not be accepted as presumptive evidence of the causal agents as other ingestants may be simultaneously employed or systemic conditions may occur in association with alcoholism. Opiates, barbiturates, bromides, and proprietary preparations to induce or prevent sleep can be identified by appropriate laboratory methods. Carbon monoxide intoxication is of less frequent occurrence. Hypogylcemia in the insulin-treated diabetic individual may be recognized by the characteristic symptomatology of an insulin reaction and by the finding of low blood sugar. However, reactions without the usual warning of anxiety, tachycardia, headache, perspiration, and weakness are not uncommon; even the blood sugar level at the time of arrival to the hospital may be deceptive, for mobilization of glycogen stores or emergency first aid treatment prior to obtaining a blood sample may deprive the physician of important laboratory evidence. Endogenous intoxications may occur with hepatic or renal decompensation, carbon dioxide retention, disorders of calcium metabolism, other electrolyte abnormalities, and diabetic ketoacidosis. Usually the stigmata of the underlying disorder are sufficiently evident so that inference about the nature of the coma may be made. Included among the extracranial causes of unconsciousness should be: (1) overwhelming systemic sepsis, particularly in the very young or very old; (2) circulatory disorders which only rarely produce more than short-lived depression of awareness unless associated with intracranial focal abnormality; (3) nutritional disorders such as Wernicke's disease, which, though the result of systemic deprivation, undoubtedly exert effects through strategically disposed lesions of brain stem; and finally, (4) disorders of temperature regulation.
Focal or Nonfocal Intracranial Disease Coma, when the result of a primary neurological lesion, may result from focal or nonfocal intracranial disease. Seizures, particularly when prolonged, may leave in their wake a period of unresponsiveness. The cause of this postictal depression may not be evident unless a history of seizures is obtained. Indeed, when trauma is an accompaniment of a flurry of convulsions, attention may be unnecessarily directed to the possibility of an underlying subdural hematoma as the cause of the unresponsiveness. Subdural hematoma may, of course, be remarkably elusive and diagnosable ultimately only by appropriate contrast studies. Signs of head trauma, a history of headache, fluctuating state of aware-
THE NEUROLOGICAL AsPECTS OF COMA
255
ness prior to coma, and xanthochromic spinal fluid under an elevated pressure are helpful when present. Unfortunately, one or all of these indications may be lacking without negating this diagnostic possibility. Subarachnoid hemorrhage from a ruptured vascular anomaly may also produce coma without focal sign. Headache, papilledema, subhyaloid hemorrhage, stiff neck, and bloody spinal fluid may be anticipated, but once again any or all of these usual accompaniments may be lacking without controverting the diagnosis. Pyogenic meningitis causing depression of consciousness need not always be associated with meningeal signs, fever, and leukocytosis, particularly early in the course of the illness in the elderly or very young. Diagnosis can be made only by cautious lumbar puncture on more than one occasion, if necessary. In this disorder, as in subarachnoid hemorrhage, subdural hematoma, or any intracranial process associated with elevated spinal fluid pressure, the decision as to whether lumbar puncture is indicated should rest on whether findings in the spinal fluid would change the course of therapy. Then, the procedure must be performe.d judiciously, removing through a small-bore needle only as much fluid as is absolutely necessary. Herniation of the temporal lobe at the incisura of the tentorium constitutes a hazard during lumbar puncture which is best handled preventively. Focal neurologic disorders associated with coma include vascular, neoplastic, and infectious processes that are circumscribed. The focal physical abnormalities help delineate the focus but not the nature of the lesion. Even this may be obscured by secondary brain stem findings which result from herniation, compression of peduncle, and Duret hemorrhages. Decision about etiology cannot be made on the basis of localization alone. Evidence of systemic cardiovascular disease associated with abrupt onset of a focal neurological process argues in favor of an intracranial vascular catastrophe. Neoplasm elsewhere raises the possibility of secondary deposits in brain. Infection in ear, paranasal sinus, bone, oral cavity, or chest sets the stage for intracranial abscess which may be epidural, subdural, or intracerebral. MANAGEMENT Because coma is the expression of a disease process, a significant part in management consists of identification and appropriate therapy of the underlying disorder. Certain principles, however, are applicable to the unconscious patient irrespective of the cause of coma. 15 In contrast to most medical emergencies, treatment should be instituted even before identification of the process at work. Patency of the airway must be guaranteed immediately. An oropharyngeal, or if necessary, an endotracheal tube should be employed. Access to a vein should be obtained, not only for the drawing of diagnostic blood samples, but also to initiate intravenous saline therapy until such time as appropriate fluid management can be instituted. This guarantees ability to support blood pressure during impending shock and to administer whatever fluids ultimately prove to be appropriate. A rapid search should then be made for occult
256
SIMEON LOCKE
hemorrhage which, if unrecognized, may terminate fatally. Only when these three processes are complete can a more leisurely evaluation be undertaken. If prolonged unconsciousness is anticipated, a pulsating air mattress should be employed to reduce the hazard of decubiti, which are best treated prophylactically. Frequent turning not only reinforces skin care but helps prevent hypostatic pneumonia. Nursing is best performed with the patient prone and the foot of the bed slightly elevated. This exploits the natural anatomy of the trachea, which slopes posteriorly, to induce dependent drainage. If hyperthermia develops, it should be treated with sponges or a cooling mattress. Elastic stockings, removed 15 or 20 minutes three times daily, help prevent phlebothrombosis and reduce the risk of pulmonary emboli. After the initial period of intravenous therapy, nutrition, hydration, and drugs may be best provided by an inlying nasogastric tube. A convenient regimen consists of feedings every two hours of about 180 cc. of fluid. The patient, supine, should be propped slightly to reduce the likelihood of regurgitation and aspiration. Prior to the introduction of fluid, the gastric contents should be aspirated. If more than 50 cc. is recovered, it should be returned and the feeding omitted. Feedings should include clear broth 9r juice with potassium supplements as needed, high protein fortified fluids, usually in a milk base, and saline, dextrose in saline, or dextrose in water with vitamins. Bladder care is best provided with external drainage if possible. If an indwelling catheter is employed, tidal drainage or similar technique is to be recommended. Systemic acidifying agents and instillation of mild antiseptic fluids into the bladder help reduce the liability to infection with urea-splitting organisms. Prophylactic antibiotics are best avoided. If infection occurs, isolation and identification of the organisms and their sensitivities allow treatment with the appropriate antibiotics in adequate dose. Physical therapy should be initiated at the beginning of hospitalization to prevent the development of painful contractures. Anticonvulsive medication if indicated can be given by nasogastric tube. Despite prolonged coma, remarkable recovery may occur; treatment of the unconscious patient is directed toward maintaining as physiological a state as possible until that time.
REFERENCES 1. Akert, K., Koella, W. P., and Hess, R.: Sleep produced by electrical stimulation of the thalamus. Amer. J. Physiol., 168:260-267, 1952. 2. Brain, R.: Physiological basis of consciousness. Brain, 81:426-455, 1958. 3. Cairns, H.: Disturbances of consciousness with lesions of the brain stem and diencepha· lon. Brain, 75:109-146, 1952. 4. Cairns, H., Oldfield, R. C., Pennybacker, J. B., and Whitteridge, D.: Akinetic mutism with an epidermoid cyst of the third ventricle. Brain, 64:273-290, 1941. 5. Dandy, W. E.: Location of the conscious center in the brain: The corpus striatum. Bull. J. Hopkins Hosp., 79:34-57, 1946. 6. Feldman, S. M., and Waller, H. J.: Dissociation of electrocortical activation and behavioral arousal. Nature, 196:1320-1322, 1962.
THE NEUROLOGICAL ASPECTS OF COMA
257
7. Foltz, E. L., and Schmidt, R. P.: Role of the reticular presentation in the coma of head injury. J. Neurosurg., 13:145-154, 1956. 8. Foltz, E. L., Jenker, F. L., and Ward, A. A.: Experimental cerebral concussion. J. Neurosurg., 10:342-352, 1953. 9. French, J. D.: Brain lesions associated with prolonged unconsciousness. Arch. Neurol. Psychiat., 68:727-740, 1952. 10. French, J. D.: The reticular formation. Chapter 52, in Handbook of Physiology II, pp. 1281-1305. Washington, D. C., American Physiological Society, 1960. 11. French, J. D., Hernandez-Peon, R., and Livingston, R. B.: Projections from cortex to cephalic brain stem (reticular formation) in monkey. J. Nemophysiol., 18:74-95, 1955. 12. Jackson, J. H.: Selected Writings. Volume I. Ed. for the Guarantors of "Brain" by James Taylor, M.D. New York, Basic Books, Inc., 1958. 13. Kemper, T. L., and Romanul, F. C. A.: State resembling akinetic mutism in basilar artery occlusion. Neurology, 17:74-80, 1967. 14. Locke, S.: Neurology. Boston, Little, Brown & Co., 1966. 15. Locke, S.: Management of the unconscious patient. New Eng. J. Med., 274:787-788, 1966. 16. Loeb, C., and Poggio, G.: Electroencephalograms in a case with pontomesencephalic hemorrhage. EEG Clin. Neurophysiol., 5:295-296, 1953. 17. Lundervold, A., Hauge, T., and Loken, A. C.: Unusual EEG in unconscious patient with brain stem atrophy. EEG Clin. Neurophysiol., 8:665-670, 1956. 18. Magoun, H. W.: The Waking Brain. Springfield, Ill., Charles C Thomas, 1963. 19. Meyers, R.: Dandy's striatal theory of "The Center of Consciousness." Arch. Neurol. Psychiat., 65:659-671, 1951. 20. Morrison, R. S., and Dempsey, E. W.: A study of thalamocortical relations. Am. J. Physiol., 135:281-292, 1942. 21. Moruzzi, G.: Active processes in the brain stem during sleep. The Harvey Lectures, 58: 233-297, 1963. 22. Moruzzi, G.: Reticular influences on the EEG. EEG Clin. Neurophysiol., 16:2-17, 1964. 23. Plum, F., and Posner, J. B.: Diagnosis of Stupor and Coma. Philadelphia, F. A. Davis Co., 1966. 24. Starzl, T. E., Taylor, C. W., and Magoun, H. W.: Ascending conduction in reticular activating system with special reference to the diencephalon. J. Neurophysiol., 14:461477, 1951. 25. Starzl, T. E., Taylor, C. W., and Magoun, H. W.: Collateral afferent excitation of reticular formation of brain stem. J. Neurophysiol., 14:479-496, 1951. Neurological Unit, Boston City Hospital 818 Harrison Avenue Boston, Massachusetts 02118
Considering how often coma constitutes one of the presenting physical signs in patients admitted to a large hospital, it is disappointing that the mechanism of the disorder is so little understood. Perhaps this relates to the difficulty in dealing scientifically with the notion "consciousness." Recognized by introspection, or evident through the intercession of motor behavior, consciousness remains difficult to define. Its study has been of interest to philosophers, psychologists, and physicians, who have searched for its location. Advocates of the concept of centers of consciousness have located this function in the frontal lobes 12 and corpus striatum. 5 More recently, the thesis of "centers" has been discarded, 2 • 19 with emphasis rightly placed on the distinction between function and its anatomical substratum. As used in a medical setting, consciousness implies awareness of the environment with responses appropriate to evoking stimuli. Usual stimuli must retain their adequacy. 14 Conscious awareness is an accompaniment of cortical activity, but "a healthy cerebral cortex cannot by itself maintain the conscious state." 3 Cortical activity is necessary for the content of consciousness, but not for its existence. Its activating or on-off aspect sets the bias, so to speak, on which specific input functions.
NEUROMECHANISMS The organization of the central nervous system is best viewed as being vertical in construction, with generalized core components near the central canal and specialized structures laterally disposed. 18 The core components, an interlacing of medullated fibers and neuronal aggregates distinct from the brain stem nuclei of classical neuroanatomy, constitute the reticular formation. This nonspecific or extralemniscal brain stem system receives its input by way of collaterals from the specific or lemniscal tracts. 25 It projects to cortex by two pathways. One is thalamic, with projection through the nucleus ventralis anterior, the centrum medianum, and the intralaminar nuclei. The secFrom the Department of Neurology, Harvard Medical School, and the Neurological Unit, Boston City Hospital *Assistant Professor of Neurology, Harvard Medical School
Surgical Clinics of North America- Vol. 48, No. 2, April, 1968
251
252
Al·T3
SIMEON LOCKE
260
T3·C3
~v
C3·C4 ~~~~~~~~~~~~~~~~~~MN~~~~~t~A
C4·T4
~~-~~~~'~A~~~(\~~~~~~~~~~--~~~NV~
F4·F3 F3·F7
Figure 1. Above, Electroencephalogram obtained one day after the onset of coma in a 54-year-old woman who was flaccid, areflexic, devoid of eye movements, had bilateral extensor plantar responses, and ultimately developed intermittent decerebration. Below, At postmortem examination ten days later, hemorrhagic necrosis of medulla, central pons, and base of mesencephalon was disclosed. The clinical coma contrasted sharply with the desynchronized electroencephalogram.
ond, extrathalamic, projection is capsular. 24 In thalamus the specific and nonspecific projection systems remain distinct. Lemniscal input terminates in the relay nuclei which project to cortex in a point-to-point manner. The extralemniscal input terminates in the nonspecific thalamic nuclei which project diffusely to cortex. 2 ° Cortical feedback is received by the reticular formation of the cephalic brain stem from frontal oculomotor area, cingulate gyrus, orbital surface of frontal
THE NEUROLOGICAL ASPECTS OF COMA
253
lobes, sensorimotor cortex, posterior parietal and paraoccipital regions, and the superior temporal gyrus. 11 Electrical stimulation of the reticular formation of the brain stem produces activation or desynchronization of the electroencephalogram, an effect which can be also achieved by physiological stimulation of lemniscal pathways in a sleeping individual. Presumably this electrographic arousal results from the distribution of impulses by collateral lemniscal branches to the reticular activating system. Although sleep and coma are usually characterized by synchronous, slow activity in the electroencephalogram, paradoxical sleep occurs in which behavioral sleep accompanies electroencephalographic desynchronization. 22 Drugs also may dissociate behavioral and electrographic sleep. Atropine produces behavioral alertness with a synchronized electroencephalogram, while reserpine produces drowsiness without synchronization of the electroencephalogram. 10 Lesions of the central cephalic brain stem produce behavioral and electrical sleep or coma, but, following long survival, electroencephalographic activation may return. 18 Behavioral unresponsiveness without associated synchronization of the electroencephalogram occurs with posterior hypothalamic lesions, while lesions of the reticular formation of the brain stem may be associated with electroencephalographic sleep in a waking preparation. 6 Structures in the medulla, located in the region of the rostral solitary tract, are antagonistic to the reticular activating system and cause synchronization of the electroencephalogramY Lesions of the medulla and low pons in isolation do not produce coma (Case 1, ref. 23). Higher centrally located brain stem lesions may produce behavioral unresponsiveness without altering the resting electroencephalogram 16• 17 (Fig. 1). The clinical relation between coma and mesencephalic tegmental lesions is well substantiated,9 and probably correlates with the experimental demonstration of suppression of the electrical activity of the medial reticular formation of the Inidbrain following cerebral concussion,8 with sensory-evoked potentials in the reticular system absent at a time they are still present in the lemnisci. 7 The occurrence of an akinetic, mute state with third ventricular lesions 4 may correlate with the function of the posterior hypothalamus, stimulation of which produces an excitatory response. 1 Akinetic mutism may be mimicked by a brain stem lesion. 13 Then, a patient deprived of ability to communicate may be SJibject to the cruelty of intact awareness.
ETIOLOGY Disorders of conscious awareness may result from systemic disease or intracranial lesion. Coma without focal abnormality and unconsciousness with lateralizing signs should not be equated with systemic or focal etiology respectively, for a previously well compensated neurologic abnormality may be re-expressed as a result of a systemic depression of function. Contrariwise, focal lesions, if strategically located, may produce global depression of consciousness without evident focal abnormality.
254
SIMEON LOCKE
Exogenous and Endogenous Poisons In unconsciousness from systemic disorder the etiology must be sought in ancillary findings, for nothing about the coma itself indicates its cause. Exogenous poisons are frequently responsible. Of these, in the patient population of a large municipal institution, ethyl alcohol and its less palatable substitutes are among the important offenders. Methyl alcohol ingestion productive of coma may be recognized by the associated metabolic acidosis and ethylene glycol ingested in antifreeze can be suspected on the basis of oxalic acid crystals in the urine. Odor of alcohol must not be accepted as presumptive evidence of the causal agents as other ingestants may be simultaneously employed or systemic conditions may occur in association with alcoholism. Opiates, barbiturates, bromides, and proprietary preparations to induce or prevent sleep can be identified by appropriate laboratory methods. Carbon monoxide intoxication is of less frequent occurrence. Hypogylcemia in the insulin-treated diabetic individual may be recognized by the characteristic symptomatology of an insulin reaction and by the finding of low blood sugar. However, reactions without the usual warning of anxiety, tachycardia, headache, perspiration, and weakness are not uncommon; even the blood sugar level at the time of arrival to the hospital may be deceptive, for mobilization of glycogen stores or emergency first aid treatment prior to obtaining a blood sample may deprive the physician of important laboratory evidence. Endogenous intoxications may occur with hepatic or renal decompensation, carbon dioxide retention, disorders of calcium metabolism, other electrolyte abnormalities, and diabetic ketoacidosis. Usually the stigmata of the underlying disorder are sufficiently evident so that inference about the nature of the coma may be made. Included among the extracranial causes of unconsciousness should be: (1) overwhelming systemic sepsis, particularly in the very young or very old; (2) circulatory disorders which only rarely produce more than short-lived depression of awareness unless associated with intracranial focal abnormality; (3) nutritional disorders such as Wernicke's disease, which, though the result of systemic deprivation, undoubtedly exert effects through strategically disposed lesions of brain stem; and finally, (4) disorders of temperature regulation.
Focal or Nonfocal Intracranial Disease Coma, when the result of a primary neurological lesion, may result from focal or nonfocal intracranial disease. Seizures, particularly when prolonged, may leave in their wake a period of unresponsiveness. The cause of this postictal depression may not be evident unless a history of seizures is obtained. Indeed, when trauma is an accompaniment of a flurry of convulsions, attention may be unnecessarily directed to the possibility of an underlying subdural hematoma as the cause of the unresponsiveness. Subdural hematoma may, of course, be remarkably elusive and diagnosable ultimately only by appropriate contrast studies. Signs of head trauma, a history of headache, fluctuating state of aware-
THE NEUROLOGICAL AsPECTS OF COMA
255
ness prior to coma, and xanthochromic spinal fluid under an elevated pressure are helpful when present. Unfortunately, one or all of these indications may be lacking without negating this diagnostic possibility. Subarachnoid hemorrhage from a ruptured vascular anomaly may also produce coma without focal sign. Headache, papilledema, subhyaloid hemorrhage, stiff neck, and bloody spinal fluid may be anticipated, but once again any or all of these usual accompaniments may be lacking without controverting the diagnosis. Pyogenic meningitis causing depression of consciousness need not always be associated with meningeal signs, fever, and leukocytosis, particularly early in the course of the illness in the elderly or very young. Diagnosis can be made only by cautious lumbar puncture on more than one occasion, if necessary. In this disorder, as in subarachnoid hemorrhage, subdural hematoma, or any intracranial process associated with elevated spinal fluid pressure, the decision as to whether lumbar puncture is indicated should rest on whether findings in the spinal fluid would change the course of therapy. Then, the procedure must be performe.d judiciously, removing through a small-bore needle only as much fluid as is absolutely necessary. Herniation of the temporal lobe at the incisura of the tentorium constitutes a hazard during lumbar puncture which is best handled preventively. Focal neurologic disorders associated with coma include vascular, neoplastic, and infectious processes that are circumscribed. The focal physical abnormalities help delineate the focus but not the nature of the lesion. Even this may be obscured by secondary brain stem findings which result from herniation, compression of peduncle, and Duret hemorrhages. Decision about etiology cannot be made on the basis of localization alone. Evidence of systemic cardiovascular disease associated with abrupt onset of a focal neurological process argues in favor of an intracranial vascular catastrophe. Neoplasm elsewhere raises the possibility of secondary deposits in brain. Infection in ear, paranasal sinus, bone, oral cavity, or chest sets the stage for intracranial abscess which may be epidural, subdural, or intracerebral. MANAGEMENT Because coma is the expression of a disease process, a significant part in management consists of identification and appropriate therapy of the underlying disorder. Certain principles, however, are applicable to the unconscious patient irrespective of the cause of coma. 15 In contrast to most medical emergencies, treatment should be instituted even before identification of the process at work. Patency of the airway must be guaranteed immediately. An oropharyngeal, or if necessary, an endotracheal tube should be employed. Access to a vein should be obtained, not only for the drawing of diagnostic blood samples, but also to initiate intravenous saline therapy until such time as appropriate fluid management can be instituted. This guarantees ability to support blood pressure during impending shock and to administer whatever fluids ultimately prove to be appropriate. A rapid search should then be made for occult
256
SIMEON LOCKE
hemorrhage which, if unrecognized, may terminate fatally. Only when these three processes are complete can a more leisurely evaluation be undertaken. If prolonged unconsciousness is anticipated, a pulsating air mattress should be employed to reduce the hazard of decubiti, which are best treated prophylactically. Frequent turning not only reinforces skin care but helps prevent hypostatic pneumonia. Nursing is best performed with the patient prone and the foot of the bed slightly elevated. This exploits the natural anatomy of the trachea, which slopes posteriorly, to induce dependent drainage. If hyperthermia develops, it should be treated with sponges or a cooling mattress. Elastic stockings, removed 15 or 20 minutes three times daily, help prevent phlebothrombosis and reduce the risk of pulmonary emboli. After the initial period of intravenous therapy, nutrition, hydration, and drugs may be best provided by an inlying nasogastric tube. A convenient regimen consists of feedings every two hours of about 180 cc. of fluid. The patient, supine, should be propped slightly to reduce the likelihood of regurgitation and aspiration. Prior to the introduction of fluid, the gastric contents should be aspirated. If more than 50 cc. is recovered, it should be returned and the feeding omitted. Feedings should include clear broth 9r juice with potassium supplements as needed, high protein fortified fluids, usually in a milk base, and saline, dextrose in saline, or dextrose in water with vitamins. Bladder care is best provided with external drainage if possible. If an indwelling catheter is employed, tidal drainage or similar technique is to be recommended. Systemic acidifying agents and instillation of mild antiseptic fluids into the bladder help reduce the liability to infection with urea-splitting organisms. Prophylactic antibiotics are best avoided. If infection occurs, isolation and identification of the organisms and their sensitivities allow treatment with the appropriate antibiotics in adequate dose. Physical therapy should be initiated at the beginning of hospitalization to prevent the development of painful contractures. Anticonvulsive medication if indicated can be given by nasogastric tube. Despite prolonged coma, remarkable recovery may occur; treatment of the unconscious patient is directed toward maintaining as physiological a state as possible until that time.
REFERENCES 1. Akert, K., Koella, W. P., and Hess, R.: Sleep produced by electrical stimulation of the thalamus. Amer. J. Physiol., 168:260-267, 1952. 2. Brain, R.: Physiological basis of consciousness. Brain, 81:426-455, 1958. 3. Cairns, H.: Disturbances of consciousness with lesions of the brain stem and diencepha· lon. Brain, 75:109-146, 1952. 4. Cairns, H., Oldfield, R. C., Pennybacker, J. B., and Whitteridge, D.: Akinetic mutism with an epidermoid cyst of the third ventricle. Brain, 64:273-290, 1941. 5. Dandy, W. E.: Location of the conscious center in the brain: The corpus striatum. Bull. J. Hopkins Hosp., 79:34-57, 1946. 6. Feldman, S. M., and Waller, H. J.: Dissociation of electrocortical activation and behavioral arousal. Nature, 196:1320-1322, 1962.
THE NEUROLOGICAL ASPECTS OF COMA
257
7. Foltz, E. L., and Schmidt, R. P.: Role of the reticular presentation in the coma of head injury. J. Neurosurg., 13:145-154, 1956. 8. Foltz, E. L., Jenker, F. L., and Ward, A. A.: Experimental cerebral concussion. J. Neurosurg., 10:342-352, 1953. 9. French, J. D.: Brain lesions associated with prolonged unconsciousness. Arch. Neurol. Psychiat., 68:727-740, 1952. 10. French, J. D.: The reticular formation. Chapter 52, in Handbook of Physiology II, pp. 1281-1305. Washington, D. C., American Physiological Society, 1960. 11. French, J. D., Hernandez-Peon, R., and Livingston, R. B.: Projections from cortex to cephalic brain stem (reticular formation) in monkey. J. Nemophysiol., 18:74-95, 1955. 12. Jackson, J. H.: Selected Writings. Volume I. Ed. for the Guarantors of "Brain" by James Taylor, M.D. New York, Basic Books, Inc., 1958. 13. Kemper, T. L., and Romanul, F. C. A.: State resembling akinetic mutism in basilar artery occlusion. Neurology, 17:74-80, 1967. 14. Locke, S.: Neurology. Boston, Little, Brown & Co., 1966. 15. Locke, S.: Management of the unconscious patient. New Eng. J. Med., 274:787-788, 1966. 16. Loeb, C., and Poggio, G.: Electroencephalograms in a case with pontomesencephalic hemorrhage. EEG Clin. Neurophysiol., 5:295-296, 1953. 17. Lundervold, A., Hauge, T., and Loken, A. C.: Unusual EEG in unconscious patient with brain stem atrophy. EEG Clin. Neurophysiol., 8:665-670, 1956. 18. Magoun, H. W.: The Waking Brain. Springfield, Ill., Charles C Thomas, 1963. 19. Meyers, R.: Dandy's striatal theory of "The Center of Consciousness." Arch. Neurol. Psychiat., 65:659-671, 1951. 20. Morrison, R. S., and Dempsey, E. W.: A study of thalamocortical relations. Am. J. Physiol., 135:281-292, 1942. 21. Moruzzi, G.: Active processes in the brain stem during sleep. The Harvey Lectures, 58: 233-297, 1963. 22. Moruzzi, G.: Reticular influences on the EEG. EEG Clin. Neurophysiol., 16:2-17, 1964. 23. Plum, F., and Posner, J. B.: Diagnosis of Stupor and Coma. Philadelphia, F. A. Davis Co., 1966. 24. Starzl, T. E., Taylor, C. W., and Magoun, H. W.: Ascending conduction in reticular activating system with special reference to the diencephalon. J. Neurophysiol., 14:461477, 1951. 25. Starzl, T. E., Taylor, C. W., and Magoun, H. W.: Collateral afferent excitation of reticular formation of brain stem. J. Neurophysiol., 14:479-496, 1951. Neurological Unit, Boston City Hospital 818 Harrison Avenue Boston, Massachusetts 02118