Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
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Decreased perfusion pressure can also occur when systemic blood pressure drops, such as when assuming a standing position. Some patients with increased ICP develop brief bi- lateral visual loss when they stand, called vi- sual obscurations, presumably due to failure to autoregulate the posterior cerebral blood flow. Failure of perfusion pressure can also occur focally (i.e., in a patient with an otherwise asymptomatic carotid occlusion who develops symptoms in the ipsilateral carotid distribu- tion on standing because of the resulting small drop in blood pressure). If the patient has bi- lateral chronic carotid occlusions, transient loss of consciousness may result. 16 Patients with elevated ICP from mass lesions often suffer sudden rises in ICP precipitated by changes in posture, coughing, sneezing, or straining, or even during tracheal suctioning (plateau waves). 17 The sudden rises in ICP can reduce cerebral perfusion and produce a variety of neurologic symptoms including confusion, stupor, and coma 18 (Table 3–2). In general, the symptoms last only a few minutes and then re- solve, leading some observers to confuse these with seizures. Finally, the loss of compliance of the intra- cranial system to further increases in volume and the rate of change in ICP plays an important role in the response of the brain to increased ICP. Compliance is the change in pressure caused by an increase in volume. In a normal brain, increases in brain volume (e.g., due to a small intracerebral hemorrhage) can be com- pensated by displacement of an equal volume of CSF from the compartment. However, when a mass has increased in size to the point where there is little remaining CSF in the compart- ment, even a small further increase in volume can produce a large increase in compartmental pressure. This loss of compliance in cases where diffuse brain edema has caused a critical in- crease in ICP can lead to the development of plateau waves. These are large, sustained in- creases in ICP, which may approach the mean arterial blood pressure, and which occur at in- tervals as often as every 15 to 30 minutes. 19,20 They are thought to be due to episodic arterial vasodilation, which is due to systemic vasomo- tor rhythms, but a sudden increase in vascular volume in a compartment with no compliance, even if very small, can dramatically increase ICP. 21
thus cause a wide range of neurologic parox- ysmal symptoms (see Table 3–2). When pres- sure in neighboring compartments is lower, this imbalance can cause herniation (see be- low). 22
Increase in Intracranial Pressure Impairment of consciousness Opisthotonus, trismus Trancelike state Rigidity and tonic extension/flexion Unreality/warmth of the arms and legs Confusion, disorientation Bilateral extensor plantar responses Restlessness, agitation Sluggish/absent deep tendon reflexes Disorganized motor activity, carphologia Generalized muscular weakness Sense of suffocation, air hunger Facial twitching Cardiovascular/respiratory disturbances Clonic movements of the arms and legs Headache
Facial/limb paresthesias Pain in the neck and shoulders Rise in temperature Nasal itch Nausea, vomiting Blurring of vision, amaurosis Facial flushing Mydriasis, pupillary areflexia Pallor, cyanosis Nystagmus Sweating Oculomotor/abducens paresis Shivering and ‘‘goose flesh’’ Conjugate deviation of the eyes Thirst External ophthalmoplegia Salivation Dysphagia, dysarthria Yawning, hiccoughing Nuchal rigidity Urinary and fecal urgency/incontinence Retroflexion of the neck Adapted from Ingvar. 18 Structural Causes of Stupor and Coma 93 Conversely, when a patient shows early signs of herniation, it is often possible to reverse the situation by restoring a small margin of com- pliance to the compartment containing the mass lesion. Hyperventilation causes a fall in arterial pCO
2 , resulting in arterial and venous vaso- constriction. The small reduction in intracranial blood volume may reverse the herniation syn- drome dramatically in just a few minutes. The Role of Vascular Factors and Cerebral Edema in Mass Lesions As indicated above, an important mechanism by which compressive lesions may cause symp- toms is by inducing local tissue ischemia. Even in the absence of a diffuse impairment of ce- rebral blood flow, local increases in pressure and tissue distortion in the vicinity of a mass le- sion may stretch small arteries and reduce their caliber to the point where they are no longer able to supply sufficient blood to their targets. Many mass lesions, including tumors, inflam- matory lesions, and the capsules of subdural hematomas, are able to induce the growth of new blood vessels (angiogenesis). 23 These blood ves- sels do not have the features that characterize normal cerebral capillaries (i.e., lack of fenes- trations and tight junctions between endothelial cells) that are the basis for the blood-brain bar- rier. Thus, the vessels leak; the leakage of Tight junction Astrocyte foot Vesicular transport across endothelial cells Capillary endothelial cells A C
Astrocyte foot Edematous astrocyte Edematous neuron
Edematous capillary endothelial cells
Opened tight junctions and escaping plasma Figure 3–1. A schematic drawing illustrating cytotoxic versus vasogenic edema. (A) Under normal circumstances, the brain is protected from the circulation by a blood-brain barrier, consisting of tight junctions between cerebral capillary endo- thelial cells that do not permit small molecules to penetrate the brain, as well as a basal lamina surrounded by astrocytic end-feet. (B) When the blood-brain barrier is breached (e.g., by neovascularization in a tumor or the membranes of sub- dural hematoma), fluid transudates from fenestrated blood vessels into the brain. This results in an increase in fluid in the extracellular compartment, vasogenic edema. Vasogenic edema can usually be reduced by corticosteroids, which decrease capillary permeability. (C) When neurons are injured, they can no longer maintain ion gradients. The increased intracel- lular sodium causes a shift of fluid from the extracellular to the intracellular compartment, resulting in cytotoxic edema. Cytotoxic edema is not affected by corticosteroids. (From Fishman, RA. Brain edema. N Engl J Med 293 (14):706–11, 1975. By permission of Massachusetts Medical Society.) 94 Plum and Posner’s Diagnosis of Stupor and Coma Yüklə 6,14 Mb. Dostları ilə paylaş:
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