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Muscle tone was increased on the left compared to the right, and the left plantar response was extensor. The radiologist reported that there were fragments of metal embedded in the skull over the right frontal lobe. Pupillary size and reactions Moderately dilated pupil, usually ipsilateral to primary lesion Constricts sluggishly c. Motor responses at rest and to stimulation Appropriate motor response to noxious orbital roof pressure. Contralateral paratonic resistance Contralateral extensor plantar reflex Figure 3­9. The patient confirmed that the boyfriend had actually tried to shoot her, but that the bullet had struck her skull with only a glancing blow where it apparently had fragmented. The right frontal lobe was contused and swollen and downward pressure had caused transtentorial herniation of the uncus. Following right frontal lobectomy to decompress her brain, she improved and was discharged. The lapse into coma may take place over just a few minutes, as in the patient above who was uncooperative with the x-ray technician and 10 minutes later was found by the neurologist to be deeply comatose. Hemiparesis may be ipsilateral to the herniation (if the midbrain is compressed against the opposite tentorial edge) or may be contralateral (if the paresis is due to the lesion damaging the descending corti- cospinal tract or to a herniating temporal lobe compressing the ipsilateral cerebral peduncle). Breathing is typically normal, or the patient may lapse into a Cheyne-Stokes pattern of respiration (Figure 3­10). Respiratory pattern or Regular sustained hyperventilation Rarely, Cheyne-Stokes b. Pupillary size and reactions ipsilateral pupil widely dilated Does not constrict c. Motor responses at rest and to stimulation Decorticate or decerebrate responses Figure 3­10. Structural Causes of Stupor and Coma 107 may fix at midposition, and neither eye elevates, depresses, or turns medially with oculocephalic or caloric vestibular testing. Initially, subjects might find it difficult to concentrate and may be unable to retain the orderly details of recent events. As the compression of the diencephalon progresses, the patient lapses into torpid drowsiness, and finally stupor and coma. Respiration in the early diencephalic stage of central herniation is commonly interrupted by sighs, yawns, and occasional pauses (Figure 3­11). As the sleepiness deepens, many patients lapse into the periodic breathing of Cheyne-Stokes respiration. The pupils are typically small (1 to 3 mm), and it may be difficult to identify their reaction to light without a bright light source or a magnifying glass. However, the pupils typically dilate briskly in response to a pinch of the skin over the neck (ciliospinal reflex). There is typically a diffuse, waxy increase in motor tone (paratonia or gegenhalten), and the toe signs may become bilaterally extensor. The appearance of a patient in the early diencephalic stage of central herniation is quite similar to that in metabolic encephalopathy. This is a key problem, because one would like to identify patients in the earliest phase of central herniation to institute specific therapy, and yet these patients look most like patients who have no structural cause of coma. For this reason, every patient with the clinical appearance of metabolic encephalopathy requires careful serial examinations until a structural lesion can be ruled out with an imaging study and a metabolic cause of coma can be identified and corrected. During the late diencephalic stage (Figure 3­12), the clinical appearance of the patient becomes more distinctive. The patient becomes gradually more difficult to arouse, and eventually localizing motor responses to pain may disappear entirely or decorticate responses may appear. Initially, the upper extremity flexor and lower extremity extensor posturing tends to appear on the side contralateral to the lesion, and only in response to noxious stimuli.

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This can be done by grasping the head on either side with both hands and using the thumbs to reach across to the eyelids and hold them open. The head movements should be brisk, and when the head position is held at each extreme for a few seconds, the eyes should gradually come back to midposition. The head is then rotated in a vertical plane (as in head nodding) and the eyes are observed for vertical conjugate movement. In an awake patient, the voluntary control of gaze overcomes this reflex response. However, in patients with impaired consciousness, the oculocephalic reflex should predominate. There may also be a small contribution from proprioceptive afferents from the neck,112 which also travel through the medial longitudinal fasciculus. Because these pathways overlap extensively with the ascending arousal system (see Figure 2­8), it is quite unusual for patients with structural causes of coma to have a normal oculocephalic examination. In contrast, patients with metabolic encephalopathy, particularly due to hepatic failure, may have exaggerated or very brisk oculocephalic responses. Eye movements in patients who are deeply comatose may respond sluggishly or not at all to oculocephalic stimulation. In such cases, more intense vestibular stimulation may be obtained by testing caloric vestibulo-ocular responses. With appropriate equipment, vestibulo-ocular monitoring can be done using galvanic stimulation and video-oculography. The ear canal is first examined and, if necessary, cerumen is removed to allow clear visualization that the tympanic membrane is intact. The head of the bed is then raised to about 30 degrees to bring the horizontal semicircular canal into a vertical position so that the response is maximal. If the patient is merely sleepy, the canal may be irrigated with cool water (158C to 208C); this usually induces a brisk response and may occasionally cause nausea and vomiting. Fortunately, in practice, it is rarely necessary to use caloric stimulation in such patients. If the patient is deeply comatose, a maximal stimulus is obtained by using ice water. An emesis basin can be placed below the ear, seated on an absorbent pad, to catch the effluent. The ice water is infused at a rate of about 10 mL/minute for 5 minutes, or until a response is obtained. After a response is obtained, it is necessary to wait at least 5 minutes for the response to dissipate before testing the opposite ear. To test vertical eye movements, both external auditory canals are irrigated simultaneously with cold water (causing the eyes to deviate downward) or warm water (causing upward deviation). The cold water induces a downward convection current, away from the ampulla, in the endolymph within the horizontal semicircular canal. The effect of the current upon the hair cells in the ampulla is to reduce tonic discharge of the vestibular neurons. The left-hand side shows the responses to oculocephalic maneuvers (which should only be done after the possibility of cervical spine injury has been eliminated). The right-hand side shows responses to caloric stimulation with cold or warm water (see text for explanation). Normal brainstem reflexes in a patient with metabolic encephalopathy are illustrated in row (A). The patient shown in row (B) has a lesion of the right side of the pons (see Figure 2­8), causing a paralysis of gaze to that side with either eye. Row (E) illustrates a patient with a midbrain infarction eliminating both the oculomotor and trochlear responses, leaving only bilateral abduction responses. Hearing was intact, as were facial, oropharyngeal, and tongue motor and sensory responses. Motor and sensory examination was also normal, tendon reflexes were symmetric, and toes were downgoing. At that point, the pupils were pinpoint and the patient was unresponsive with flaccid limbs. The sudden onset of bilateral impairment of eye movements on the background of clear consciousness is rare, and raised the possibility of a brainstem injury even without unconsciousness.

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If transthoracic echocardiography is negative, a transesophageal echocardiogram may establish the diagnosis. However, cerebral infarcts or a fluctuating level of consciousness, with or without focal signs, should prompt a diligent search for a coagulopathy in a cancer patient. Patient 5­10 A 58-year-old man was admitted to the hospital for left-sided weakness. He had lost about 30 pounds over the previous 2 months, and on general examination he had a distended liver. On examination he was slightly lethargic, but other cognitive functions were intact. There was weakness of adduction of the left eye on looking to the right, with nystagmus in the abducting eye. He showed left upper motor neuron facial paresis and weakness of his left arm and leg. In addition, there was loss of appreciation of the position of his left limbs in space. Because these infarcts were apparently in two different vascular distributions, a central cause of emboli was suspected. Transthoracic and transesophageal echocardiogram was negative, as was heart rhythm monitoring. Blood coagulation testing showed a mild elevation of the prothrombin time and elevated fibrin degradation products. He subsequently had fluctuating drowsiness and passed into a coma, and a decision was made by the family to provide only comfort care. Examination of the heart disclosed vegetations on the mitral valve consisting of fibrin-platelet thrombi. There was diffuse thrombosis in both arteries and veins within the brain and the kidneys, but limited evidence of disseminated coagulation in other organs. Comment: Coagulopathies, including disseminated intravascular coagulation, venous thrombosis (which may cause paradoxic emboli), nonbacterial thrombotic endocarditis, or some combination of these syndromes, are a common cause of stroke in patients with cancer. Hematologic signs and involvement of other organ systems may be minimal, as in this case. Fibrin-platelet Sequelae of Hypoxia Following apparent recovery from an acute hypoxic insult, about 3%195 of patients relapse into a severe delayed postanoxic encephalopathy. Our own experience with this disorder now extends to well over 20 cases (Patient 1­1). The onset in our patients has been as early as 4 days and as late as 14 days after the initial hypoxia; reports from other authors give an even longer interval. Occasionally, however, relapse has been reported after a mild hypoxic insult that was sufficient only to daze the patient and not to cause full unconsciousness. The deterioration may progress to coma or death or may arrest itself at any point. Most patients have a second recovery period that leads to full health within a year,195 although some remain permanently impaired. Hyperbaric oxygen given at the initial insult does not appear to prevent the development of this neurologic problem. The typical distribution of lesions includes the deep white matter, particularly in the posterior part of the hemisphere, and the basal ganglia. This pattern is similar to the distribution of infarcts seen in patients with mitochondrial encephalopathies and may be due to the impairment of cellular oxidative metabolism in both cases. Patient 5­11 A 35-year-old electrical engineer was diagnosed with hypokalemic periodic paralysis. Attacks were often precipitated by eating foods rich in sugar, which caused a sudden drop in potassium. He became gradually weaker and called for help, but soon was so weak that he became apneic. Despite the eventual participation of bystanders in artificial ventilation, he suffered an estimated period of about 5 minutes of severe hypoxia. He was resuscitated by paramedics and brought to the hospital, where he awoke quickly and resumed normal activity. On the fourth day after his hypoxic event he became drowsy, then lapsed into a stuporous state and then a coma. After about a week he again woke up but was blind, and soon developed athetotic limb movements.

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