Ganong's Review of Medical Physiology, 23rd Edition

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248 SECTION III Central & Peripheral Neurophysiology FIGURE 16–7 A circuit drawing representing lesions produced in experimental animals to replicate decerebrate and decorticate deficits seen in humans. Bilateral transections are indicated by dashed lines A, B, C, and D. Decerebration is at a midcollicular level (A), decortication is rostral to the superior colliculus, dorsal roots sectioned for one extremity (B), and removal of anterior lobe of cerebellum (C). The objective was to identify anatomic substrates responsible for decerebrate or decorticate rigidity/posturing seen in humans with lesions that either isolate the forebrain from the brain stem or separate rostral from caudal brain stem and spinal cord. (Reproduced with permission from Haines DE [editor]: Fundamental Neuroscience for Basic and Clinical Applications, 3rd ed. Elsevier, 2006.)
CLINICAL BOX 16–2 Uncal Herniation Space-occupying lesions from large tumors, hemorrhages, strokes, or abscesses in the cerebral hemisphere can drive the uncus of the temporal lobe over the edge of the cerebellar tentorium, compressing the ipsilateral cranial nerve III (uncal herniation). Before the herniation these patients experience a decreased level of consciousness, lethargy, poorly reactive pupils, deviation of the eye to a “down and out” position, hyperactive reflexes, and a bilateral Babinski sign (due to compression of the ipsilateral corticospinal tract). After the brain herniates, the patients are decerebrate and comatose, have fixed and dilated pupils, and eye movements are absent. Once damage extends to the midbrain, a Cheyne–Stokes respiratory pattern develops, characterized by a pattern of waxing-and-waning depth of respiration with interposed periods of apnea. Eventually, medullary function is lost, breathing ceases, and recovery is unlikely. Hemispheric masses closer to the midline compress the thalamic reticular formation and can cause coma before eye findings develop (central herniation). As the mass enlarges, midbrain function is affected, the pupils dilate, and a decerebrate posture ensues. With progressive herniation, pontine vestibular and then medullary respiratory functions are lost. SPINAL SHOCK In all vertebrates, transection of the spinal cord is followed by a period of spinal shock during which all spinal reflex responses are profoundly depressed. Subsequently, reflex responses return and become hyperactive. The duration of spinal shock is A Upper pontine damage B Upper midbrain damage CHAPTER 16 Control of Posture & Movement 249 proportionate to the degree of encephalization of motor function in the various species. In frogs and rats it lasts for minutes; in dogs and cats it lasts for 1 to 2 h; in monkeys it lasts for days; and in humans it usually lasts for a minimum of 2 wk. The cause of spinal shock is uncertain. Cessation of tonic bombardment of spinal neurons by excitatory impulses in descending pathways undoubtedly plays a role, but the subsequent return of reflexes and their eventual hyperactivity also have to be explained. The recovery of reflex excitability may be due to the development of denervation hypersensitivity to the mediators released by the remaining spinal excitatory endings. Another possibility for which there is some evidence is the sprouting of collaterals from existing neurons, with the formation of additional excitatory endings on interneurons and motor neurons. The first reflex response to appear as spinal shock wears off in humans is often a slight contraction of the leg flexors and adductors in response to a noxious stimulus. In some patients, the knee jerk reflex recovers first. The interval between cord transection and the return of reflex activity is about 2 weeks in the absence of any complications, but if complications are present it is much longer. It is not known why infection, malnutrition, and other complications of SCI inhibit spinal reflex activity. Once the spinal reflexes begin to reappear after spinal shock, their threshold steadily drops. LOCOMOTION GENERATOR Circuits intrinsic to the spinal cord can produce walking movements when stimulated in a suitable fashion even after spinal cord transection in cats and dogs. There are two locomotor pattern generators in the spinal cord: one in the cervical region and one in the lumbar region. However, this does not mean that spinal animals or humans can walk without stimulation; the pattern generator has to be turned on by tonic discharge of a discrete area in the midbrain, the mesencephalic FIGURE 16–8 Decerebrate and decorticate postures. A) Damage to lower midbrain and upper pons causes decerebrate posturing in which lower extremities are extended with toes pointed inward and upper extremities extended with fingers flexed and forearms pronate. Neck and head are extended. B) Damage to upper midbrain may cause decorticate posturing in which upper limbs are flexed, lower limbs are extended with toes pointed slightly inward, and head is extended. (Modified from Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)
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Copyright © 2010 by The McGraw-Hil
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iv Key Features of the 23rd Edition
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About the Authors KIM E. BARRETT Ki
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viii CONTENTS 27. Digestion, Absorp
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2 SECTION I Cellular & Molecular Ba
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10 SECTION I Cellular & Molecular B
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80 SECTION II Physiology of Nerve &
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100 SECTION II Physiology of Nerve
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168 SECTION III Central & Periphera
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302 SECTION IV Endocrine & Reproduc
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430 SECTION V Gastrointestinal Phys
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490 SECTION VI Cardiovascular Physi
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588 SECTION VII Respiratory Physiol
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640 SECTION VIII Renal Physiology T
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642 SECTION VIII Renal Physiology m
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644 SECTION VIII Renal Physiology F
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646 SECTION VIII Renal Physiology N
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650 SECTION VIII Renal Physiology G
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652 SECTION VIII Renal Physiology t
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654 SECTION VIII Renal Physiology I
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660 SECTION VIII Renal Physiology C
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662 SECTION VIII Renal Physiology d
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668 SECTION VIII Renal Physiology p
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670 SECTION VIII Renal Physiology l
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672 SECTION VIII Renal Physiology A
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676 SECTION VIII Renal Physiology E
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678 SECTION VIII Renal Physiology o
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680 SECTION VIII Renal Physiology I
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682 SECTION VIII Renal Physiology C
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688 Answers to Multiple Choice Ques
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690 INDEX Angiotensin III, 671 Angi
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692 INDEX Cannabinoids, 145, 179 Ca
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694 INDEX Climbing fibers, 255 Clin
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696 INDEX Endocrine functions of pa
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698 INDEX Flaccid paralysis, 244 Fl
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700 INDEX Hearing (continued) affer
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702 INDEX Intrinsic system, 532 Int
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704 INDEX Monoamines (continued) hi
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706 INDEX Pacemaker (continued) imp
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708 INDEX Proprioceptors, 632-633 P
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710 INDEX Respiratory compensation,
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712 INDEX Supratentorial lesions, 2
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714 INDEX Vestibular system, 213-21
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Ganong's Review of Medical Physiology, 23rd Edition

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