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Fig. 13.3 Hyperthermia (A) and hypothermia (B): Too much, or too little, of a good thing.
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corticosteroids in experimental models rather than the ostensible effect of these drugs on edema. Osterholm postulated that the initial event in acute impact injury was the release of norepinephrine from injured neurons in the central gray matter and that the subsequent vasoconstriction was responsible for both the central hemorrhagic and lateral white matter lesions. Later experimental work failed to substantiate this. Also, the contention that opioid release at the moment of trauma plays an important role in tissue damage has not been con rmed. The main problem with all the experimental work is that it only imperfectly reproduces the various types of spinal injury in humans. Clinical Effects of Spinal Cord Injury When the spinal cord is suddenly and virtually or completely severed, three disorders of function are at once evident: (1) all voluntary movement in parts of the body below the lesion is immediately and permanently lost; (2) all sensation from the lower (aboral) parts is abolished; and (3) re ex functions in all segments of the isolated spinal cord are suspended. The last effect, called spinal shock, involves tendon as well as autonomic re exes. It is of variable duration (1 to 6 weeks as a rule but sometimes far longer) and is so dramatic that Riddoch used it as a basis for dividing the clinical effects of spinal cord transection into two stages, that of spinal shock and are exia followed by the stage of heightened re ex activity. The separation of these two stages is not as sharp as this statement might imply but is nevertheless fundamental and useful for exposition. Less complete lesions of the spinal cord result in little or no spinal shock, and the same is true of any type of lesion that develops slowly. The features of complete spinal cord transection are presented later in detail for several reasons in addition to the practical value of understanding the evolution of cord lesions. They occupy a special place in classic neurology and are a guide to the processes that occur in nontraumtic and lesser types of cord damage. Stage of Spinal Shock or Are exia The loss of motor function at the time of injury tetraplegia with lesions of the fourth to fth cervical segments or above, paraplegia with lesions of the thoracic cord is accompanied by immediate atonic paralysis of bladder and bowel, gastric atony, loss of sensation below a level corresponding to the spinal cord lesion, muscular accidity, and almost complete suppression of all spinal segmental re ex activity below the lesion. As a result of their sudden separation from higher levels, the neural elements below the lesion fail to perform their normal function. However, the physiologic basis of this re ex segmental paralysis is incompletely understood as noted later. Also impaired in the segments below the lesion is the control of autonomic function. Vasomotor tone, sweating, and piloerection in the lower parts of the body are temporarily abolished. Systemic hypotension may be severe and contribute to the spinal cord damage. The lower extremities lose heat if left uncovered, and they swell if dependent. The skin becomes dry and pale, and ulcerations may develop over bony prominences. The sphincters of the bladder and the rectum remain contracted to some degree due to the loss of inhibitory in uence of higher central nervous system (CNS) centers, but the detrusor of the bladder and smooth muscle of the rectum are atonic. Urine accumulates until the intravesicular pressure is suf cient to overcome the sphincters; then driblets escape (over ow incontinence). There is also passive distention of the bowel, retention of feces, and absence of peristalsis (paralytic ileus). Genital re exes (penile erection, bulbocavernosus re ex, contraction of dartos muscle) are abolished or profoundly depressed. The duration of the stage of spinal shock with complete are-
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Issuing third nerve and cerebral peduncle Cerebral peduncle Supranuclear bers to third nerve, high midbrain tegmentum ventral to superior colliculus (nucleus of Cajal, nucleus of Darkschevich, rostral interstitial nucleus of the MLF, and posterior commissure) Dentatothalamic tract ( ) after decussation. Precise site of lesion unknown. Damage to motor tracts between red and vestibular nuclei
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FIGURE 8.I I P
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The McGraw Hill Companies, 2010
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Alcohol intoxication Hypothermia, hypotension, ushed skin, alcohol breath Elevated blood alcohol
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