Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
Yüklə 9,02 Mb. Pdf görüntüsü
|
|
raphe cells across the sleep-waking cycle and during cataplexy in narcoleptic dogs. J Physiol 554, 202–215, 2004.
50. Kolta A, Reader TA. Modulatory effects of catechol- amines on neurons of the rat visual cortex: single-cell iontophoretic studies. Can J Physiol Pharmacol 67, 615–623, 1989. 51. Sato H, Fox K, Daw NW. Effect of electrical stimu- lation of locus coeruleus on the activity of neurons in the cat visual cortex. J Neurophysiol 62, 946–958, 1989. 52. Bassant MH, Ennouri K, Lamour Y. Effects of ion- tophoretically applied monoamines on somatosensory cortical neurons of unanesthetized rats. Neuroscience 39, 431–439, 1990. 53. Lu J, Sherman D, Devor M, et al. A putative flip-flop switch for control of REM sleep. Nature 441, 589– 594, 2006. 54. Saper CB. Diffuse cortical projection systems: anato- mical organization and role in cortical function. In: F. Plum, ed. Handbook of Physiology. The Nervous System. V. Bethesda, Md.: American Physiological So- ciety, pp 168–210, 1987. 55. Welch MJ, Meltzer EO, Simons FE. H1-antihistamines and the central nervous system. Clin Allergy Immunol 17, 337–388, 2002. 56. Huang ZL, Qu WM, Li WD, et al. Arousal effect of orexin A depends on activation of the histaminergic system. Proc Natl Acad Sci 98, 9965–9970, 2001. 57. Parmentier R, Ohtsu H, Djebbara-Hannas Z, et al. Anatomical, physiological, and pharmacological char- acteristics of histidine decarboxylase knock-out mice: evidence for the role of brain histamine in behavioral and sleep-wake control. J Neurosci 22, 7695–7711, 2002. 58. Peyron C, Tighe DK, van den Pol AN, et al. Neurons containing hypocretin (orexin) project to multiple neu- ronal systems. J Neurosci 18, 9996–10015, 1998. 59. Bittencourt JC, Frigo L, Rissman RA, et al. The dis- tribution of melanin-concentrating hormone in the monkey brain (Cebus apella). Brain Res 804, 140–143, 1998.
60. Bittencourt JC, Presse F, Arias C, et al. The melanin- concentrating hormone system of the rat brain: an immuno- and hybridization histochemical character- ization. J Comp Neurol 319, 218–245, 1992. 61. Lin CS, Nicolelis MA, Schneider JS, et al. A major direct GABAergic pathway from zona incerta to neo- cortex. Science 248, 1553–1556, 1990. 62. Lee MG, Hassani OK, Jones BE. Discharge of iden- tified orexin/hypocretin neurons across the sleep- waking cycle. J Neurosci 25, 6716–6720, 2005. 63. Mileykovskiy BY, Kiyashchenko LI, Siegel JM. Behav- ioral correlates of activity in identified hypocretin/ orexin neurons. Neuron 46, 787–798, 2005. 64. Verret L, Goutagny R, Fort P, et al. A role of melanin-concentrating hormone producing neurons in the central regulation of paradoxical sleep. BMC Neurosci 4, 19, 2003. 65. Alam MN, Gong H, Alam T, et al. Sleep-waking dis- charge patterns of neurons recorded in the rat peri- fornical lateral hypothalamic area. J Physiol 538, 619– 631, 2002. 66. Gelineau JBE. De la narcolepsie. Gaz Hop (Paris) 53, 626–637, 1880. 67. Sakurai T, Amemiya A, Ishii M, et al. Orexins and orexin receptors: a family of hypothalamic neuropep- tides and G protein-coupled receptors that regulate feeding behavior. Cell 92, 573–585, 1998. 68. de Lecea L, Kilduff TS, Peyron C, et al. The hypo- cretins: hypothalamus-specific peptides with neuro- excitatory activity. Proc Natl Acad Sci 95, 322–327, 1998. 69. Willie JT, Chemelli RM, Sinton CMYM. To eat or to sleep? Orexin in the regulation of feeding and wake- fulness. Annu Rev Neurosci 24, 429–458, 2001. 70. Chimelli RM, Willie JT, Sinton CM, et al. Narcolepsy in orexin knockout mice: molecular genetics of sleep regulation. Cell 98, 437–451, 1999. 71. Lin L, Faraco J, Li R, et al. The sleep disorder canine narcolepsy is caused by a mutation in the hypocretin (orexin) receptor 2 gene. Cell 98, 365–376, 1999. 72. Peyron C, Faraco J, Rogers W, et al. A mutation in a case of early onset narcolepsy and a generalized ab- sence of hypocretin peptides in human narcoleptic brains. Nat Med 6, 991–997, 2000. 73. Ripley B, Overeem S, Fujiki N, et al. CSF hypocretin/ orexin levels in narcolepsy and other neurological con- ditions. Neurology 57, 2253–2258, 2001. 74. Thannickal TC, Moore RY, Nienhuis R, et al. Reduced number of hypocretin neurons in human narcolepsy. Neuron 27, 469–474, 2000. 75. Marcus JN, Aschkenasi CJ, Lee CE, et al. Differential expression of orexin receptors 1 and 2 in the rat brain. J Comp Neurol 435, 6–25, 2001. 76. Saper CB. Organization of cerebral cortical afferent systems in the rat. II. Magnocellular basal nucleus. J Comp Neurol 222, 313–342, 1984. 77. Zaborsky L, Brownstein MJ, Palkovits M. Ascending projections to the hypothalamus and limbic nuclei from the dorsolateral pontine tegmentum: a biochem- ical and electron microscopic study. Acta Morphol Acad Sci Hung 25, 175–188, 1977. 78. Zaborsky L, Cullinan WE, Luine VN. Catecholami- nergic-cholinergic interaction in the basal forebrain. Prog Brain Res 98, 31–49, 1993. 79. Lee MG, Hassani OK, Alonso A, et al. Cholinergic basal forebrain neurons burst with theta during waking and paradoxical sleep. J Neurosci 25, 4365– 4369, 2005. 80. Richardson RT, DeLong MR. Nucleus basalis of Meynert neuronal activity during a delayed response task in monkey. Brain Res 399, 364–368, 1986. 81. Richardson RT, DeLong MR. Context-dependent responses of primate nucleus basalis neuron in a go/ no-go-go task. J Neurol Sci 10, 2528–2540, 1990. 82. Sherin JE, Shiromani PJ, McCarley RW, et al. Acti- vation of ventrolateral preoptic neurons during sleep. Science 271, 216–219, 1996. 83. Sherin JE, Elmquist JK, Torrealba F, et al. Inner- vation of histaminergic tuberomammilary neurons by GABAergic and alaninergic neurons in the ven- 36 Plum and Posner’s Diagnosis of Stupor and Coma trolateral preoptic nucleus of the rat. J Neurosci 18, 4705–4721, 1998. 84. Saper CB, Chou TC, Scammell TE. The sleep switch: hypothalamic control of sleep and wakefulness. Trends Neurosci 24, 726–731, 2001. 85. Gaus SE, Strecker RE, Tate BA, et al. Ventrolateral preoptic nucleus contains sleep-active, galaninergic neurons in multiple mammalian species. Neurosci- ence 115, 285–294, 2002. 86. Sallanon M, Denoyer M, Kitahama K, et al. Long- lasting insomnia induced by preoptic neuron lesions and its transient reversal by muscimol injection into the posterior hypothalamus in the cat. Neuroscience 32, 669–683, 1989. 87. Lu J, Greco MA, Shiromani P, et al. Effect of lesions of the ventrolateral preoptic nucleus on NREM and REM sleep. J Neurosci 20, 3820–3842, 2000. 88. Lu J, Bjorkum AA, Xu M, et al. Selective activation of the extended ventrolateral preoptic nucleus dur- ing rapid eye movement sleep. J Neurosci 22, 4568– 4576, 2002. 89. Hara J, Beuckmann CT, Nambu T, et al. Genetic ab- lation of orexin neurons in mice results in narcolepsy, hypophagia, and obesity. Neuron 30, 345–354, 2001. 90. Lydic R, Douglas CL, Baghdoyan HA. Microinjection of neostigmine into the pontine reticular formation of C57BL/6J mouse enhances rapid eye movement sleep and depresses breathing. Sleep 25, 835–841, 2002. 91. Lorente de No R. Cerebral cortex: architecture, intracortical connections, motor projections. In: JF Fulton, ed. Physiology of the Nervous System. New York: Oxford University Press, pp 291–340, 1938. 92. Hubel DH, Wiesel TN. Shape and arrangement of columns in cat’s striate cortex. J Physiol 165, 559– 568, 1963. 93. McCasland JS, Woolsey TA. High-resolution 2- deoxyglucose mapping of functional cortical columns in mouse barrel cortex. J Comp Neurol 278, 555– 569, 1988. 94. Gilbert CD, Wiesel TN. Columnar specificity of in- trinsic horizontal and corticocortical connections in cat visual cortex. J Neurosci 9, 2432–2442, 1989. 95. Hubel DH, Wiesel TN. The period of susceptibility to the physiological effects of unilateral eye closure in kittens. J Physiol 206, 419–436, 1970. 96. Frank MG, Issa NP, Stryker MP. Sleep enhances plas- ticity in the developing visual cortex. Neuron 30, 275– 287, 2001. 97. Hardcastle VG. Consciousness and the neurobiology of perceptual binding. Semin Neurol 17, 163–170, 1997. 98. Revonsuo A. Binding and the phenomenal unity of con- sciousness. Conscious Cogn 8, 173–185, 1999. 99. Nishikawa T, Okuda J, Mizuta I, et al. Conflict of in- tentions due to callosal disconnection. J Neurol Neuro- surg Psychiatry 71, 462–471, 2001. 100. Alexander GE, DeLong MR, Strick PL. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annu Rev Neurosci 9, 357– 381, 1986. 101. Alexander GE, Crutcher MD, DeLong MR. Basal ganglia-thalamocortical circuits: parallel substrates for motor,oculomotor,‘‘prefrontal’’and‘‘limbic’’functions. Prog Brain Res 119–146, 1990. 102. Wyrtzes LM, Chatrian GE, Shaw CM, et al. Acute failure of forebrain with sparing of brain-stem func- tion. Electroencephalographic, multimodality evoked- potential, and pathologic findings. Arch Neurol 46, 93–97, 1989. 103. van der Knaap MS, Smit LS, Nauta JJ, et al. Cortical laminar abnormalities—occurrence and clinical sig- nificance. Neuropediatrics 24, 143–148, 1993. 104. Adams JH, Graham DI, Jennett B. The neuropathol- ogy of the vegetative state after an acute brain insult. Brain 123, 1327–1338, 2000. 105. Caplan LR. ‘‘Top of the basilar’’ syndrome. Neurology 30, 72–79, 1980. 106. Wechler B, Dell’Isola B, Vidailhet M, et al. MRI in 31 patients with Behcet’s disease and neurological involvement: prospective study with clinical correla- tion. J Neurol Neurosurg Psychiatry 56, 793–798, 1993.
107. Park-Matsumoto YC, Ogawa K, Tazawa T, et al. Mutism developing after bilateral thalamo-capsular lesions by neuro-Behcet disease. Acta Neurol Scand 91, 297–301, 1995. 108. Kinney HC, Korein J, Panigrahy A, et al. Neuro- pathological findings in the brain of Karen Ann Quinlan. The role of the thalamus in the persistent vegetative state. N Engl J Med 330 (21), 1469–1475, 1994. 109. Reeves AG, Plum F. Hyperphagia, rage, and demen- tial accompanying a ventromedial hypothalamic neo- plasm. Arch Neurol 20, 616–624, 1969. 110. Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma. Brain 126, 1524–1536, 2003. Pathophysiology of Signs and Symptoms of Coma 37
Chapter 2 Examination of the Comatose Patient OVERVIEW
HISTORY GENERAL PHYSICAL EXAMINATION LEVEL OF CONSCIOUSNESS ABC: AIRWAY, BREATHING, CIRCULATION Circulation Respiration PUPILLARY RESPONSES Examine the Pupils and Their Responses Pathophysiology of Pupillary Responses: Peripheral Anatomy of the Pupillomotor System
Pharmacology of the Peripheral Pupillomotor System Localizing Value of Abnormal Pupillary Responses in Patients in Coma Metabolic and Pharmacologic Causes of Abnormal Pupillary Response OCULOMOTOR RESPONSES Functional Anatomy of the Peripheral Oculomotor System Functional Anatomy of the Central Oculomotor System The Ocular Motor Examination Interpretation of Abnormal Ocular Movements MOTOR RESPONSES Motor Tone Motor Reflexes Motor Responses FALSE LOCALIZING SIGNS IN PATIENTS WITH METABOLIC COMA Respiratory Responses Pupillary Responses Ocular Motor Responses Motor Responses MAJOR LABORATORY DIAGNOSTIC AIDS Blood and Urine Testing Computed Tomography Imaging and Angiography Magnetic Resonance Imaging and Angiography Magnetic Resonance Spectroscopy Neurosonography Lumbar Puncture Electroencephalography and Evoked Potentials OVERVIEW
Coma, indeed any alteration of consciousness, is a medical emergency. The physician encoun- tering such a patient must begin examination and treatment simultaneously. The examina- tion must be thorough, but brief. The examina- tion begins by informally assessing the patient’s level of consciousness. First, the physician ad- dresses the patient verbally. If the patient does 38
not respond to the physician’s voice, the phy- sician may speak more loudly or shake the pa- tient. When this fails to produce a response, the physician begins a more formal coma eval- uation. The examiner must systematically assess the arousal pathways. To determine if there is a structural lesion involving those pathways, it is necessary also to examine the function of brain- stem sensory and motor pathways that are ad- jacent to the arousal system. In particular, be- cause the oculomotor circuitry enfolds and surrounds most of the arousal system, this part of the examination is particularly informative. Fortunately, the examination of the comatose patient can usually be accomplished very quickly because the patient has such a limited range of responses.However, theexaminermust become conversant with the meaning of the signs elic- ited in that examination, so that decisions that may save the patient’s life can then be made quickly and accurately. The evaluation of the patient with a reduced level of consciousness, like that of any patient, requires a history (to the extent possible), phys- ical examination, and laboratory evaluation. These are considered, in turn, in this chapter. However, as soon as it is determined that a patient has a depressed level of consciousness, the next step is to ensure that the patient’s brain is receiving adequate blood and oxygen. The emergency treatment of the comatose pa- tient is detailed in Chapter 7. The physiology and pathophysiology of the cerebral circulation and of respiration are considered in the para- graphs below. HISTORY In patients with nervous system dysfunction, the history is the most important part of the examination (Table 2–1). Of course, patients with coma or diminished states of conscious- ness by definition are not able to give a history. Thus, the history must be obtained if possible from relatives, friends, or the individuals, usually the emergency medical personnel, who brought the patient to the hospital. The onset of coma is often important. In a previously healthy, young patient, the sudden onset of coma may be due to drug poisoning, subarachnoid hemorrhage, or head trauma; in the elderly, sudden coma is more likely caused by cerebral hemorrhage or infarction. Most pa- tients with lesions compressing the brain either have a clear history of trauma (e.g., epidural hematoma; see Chapter 4) or a more gradual rather than abrupt impairment of conscious- ness. Gradual onset is also true of most patients with metabolic disorders (see Chapter 5). The examiner should inquire about previous medical symptoms or illnesses or any recent trauma. A history of headache of recent onset points to a compressive lesion, whereas the his- tory of depression or psychiatric disease may suggest drug intoxication. Patients with known diabetes, renal failure, heart disease, or other chronic medical illness are more likely to be suffering from metabolic disorders or perhaps brainstem infarction. A history of premonitory signs, including focal weakness such as dragging Table 2–1 Examination of the Comatose Patient History ( from Relatives, Friends, or Attendants) Onset of coma (abrupt, gradual) Recent complaints (e.g., headache, depression, focal weakness, vertigo) Recent injury Previous medical illnesses (e.g., diabetes, renal failure, heart disease) Previous psychiatric history Access to drugs (sedatives, psychotropic drugs) General Physical Examination Vital signs Evidence of trauma Evidence of acute or chronic systemic illness Evidence of drug ingestion (needle marks, alcohol on breath) Nuchal rigidity (assuming that cervical trauma has been excluded) Neurologic Examination Verbal responses Eye opening Optic fundi Pupillary reactions Spontaneous eye movements Oculocephalic responses (assuming cervical trauma has been excluded) Oculovestibular responses Corneal responses Respiratory pattern Motor responses Deep tendon reflexes Skeletal muscle tone Examination of the Comatose Patient 39
of the leg or complaints of unilateral sensory symptoms or diplopia, suggests a cerebral or brainstem mass lesion. GENERAL PHYSICAL EXAMINATION The general physical examination is an im- portant source of clues as to the cause of unconsciousness. After stabilizing the patient (Chapter 7), one should search for signs of head trauma. Bilateral symmetric black eyes suggest basal skull fracture, as does blood be- hind the tympanic membrane or under the skin overlying the mastoid bone (Battle’s sign). Examine the neck with care; if there is a pos- sibility of trauma, the neck should be im- mobilized until cervical spine instability has been excluded by imaging. Resistance to neck flexion in the presence of easy lateral move- ment suggests meningeal inflammation such as meningitis or subarachnoid hemorrhage. Flex- ion of the legs upon flexing the neck (Brud- zinski’s sign) confirms meningismus. Examina- tion of the skin is also useful. Needle marks suggest drug ingestion. Petechiae may suggest meningitis or intravascular coagulation. Pres- sure sores or bullae indicate that the patient has been unconscious and lying in a single position for an extended period of time, and are especially frequent in patients with barbitu- rate overdosage. 1 LEVEL OF CONSCIOUSNESS After conducting the brief history and exami- nation as outlined above and stabilizing the patients’ vital functions, the examiner should conduct a formal coma evaluation. In assessing the level of consciousness of the patient, it is necessary to determine the intensity of stim- ulation necessary to arouse a response and the quality of the response that is achieved. When the patient does not respond to voice or vigor- ous shaking, the examiner next provides a source of pain to arouse the patient. Several methods for providing a sufficiently painful stimulus to arouse the patient without causing tissue dam- age are illustrated in Figure 2–1. It is best to begin with a modest, lateralized stimulus, such as compression of the nail beds, the supraor- bital ridge, or the temporomandibular joint. These give information about the lateralization of motor response (see below), but must be repeated on each side in case there is a focal lesion of the pain pathways on one side of the brain or spinal cord. If there is no response to the stimulus, a more vigorous midline stimulus may be given by the sternal rub. By vigorously pressing the examiner’s knuckles into the pa- tient’s sternum and rubbing up and down the chest, it is possible to create a sufficiently pain- ful stimulus to arouse any subject who is not deeply comatose. The response of the patient is noted and graded. The types of motor responses seen are considered in the section on motor responses (page 73). However, the level of response is important to the initial consideration of the depth of impairment of consciousness. In des- cending order of arousability, a sleepy patient who responds to being addressed verbally or light shaking, or one who responds verbally to more intense mechanical stimulation, is said to be lethargic or obtunded. A patient whose best response to deep pain is to attempt to push the examiner’s arm away is considered to be stu- porous, with localizing responses. Patients who A B C D Figure 2–1. Methods for attempting to elicit responses from unconscious patients. Noxious stimuli can be delivered with minimal trauma to the supraorbital ridge (A), the nail beds or the fingers or toes (B), the sternum (C) or the temporo- mandibular joints (D). 40 Plum and Posner’s Diagnosis of Stupor and Coma Box 2–1 Coma Scales A number of different scales have been devised for scoring patients with coma. The value of these is in providing a simple estimate of the prognosis for different groups of patients. Obviously, this is related as much to the cause of the coma (when known) as to the current status of the examination. Teasdale and Jennett’s Glasgow Coma Scale (GCS), 2 devised to categorize patients with head trauma, is reproduced below. Unfortunately, when used by emergency room physicians, in- terrater agreement is only moderate. 3 Two simple scales, ACDU (alert, confused, drowsy, unresponsive) and AVPU (alert, response to voice, response to pain, un- responsive) 4 are about as accurate as the GCS and much easier to use. 4 The
ACDU scale appears better at identifying early deterioration in level of con- sciousness. A recently validated coma scale, the FOUR scale (full outline of un- responsiveness), provides more neurologic detail than the GCS. However, no Yüklə 9,02 Mb. Dostları ilə paylaş:
|