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Pontomedullary infarction from sustained cervical spine hyperflexion
282
Surg Neurol 1986;26:282-6
Pontomedullary Infarction from Sustained Cervical Spine Hyperflexion Walter J. Faillace, M.D., and Shige-Hisa Okawara, M.D., Ph.D. Division of Neurological Surgery, University of Rochester Medical Center, Rochester, New York
Faillace WJ, Okawara S-H. Pontomedullary infarction from sustained cervical spine hyperflexion. Surg Neurol 1986;26:282-6.
A paraplegic but independent 26-year-old man developed pontomedullary infarction from a fall which placed him in a position of sustained cervical spine hyperflexion. An early noncontrast computed tomography scan displayed infarction of the pontomedullary region. The patient made partial recovery of his neurologic deficits. The infarct was thought to arise from compromise of blood flow through the vertebrobasilar vessels during hyperflexion of the cervical spine. The mechanisms that impeded blood flow in the vertebrobasilar territory and the prognostic factors of ischemic infarction in this area are discussed.
of maximal movement of the cervical spine during turning of the head. In addition, blood flow in this artery can be compromised almost anywhere along its course in the neck [6,15,18]. This paper reports a patient who acquired an infarction of the pontomedullary region of the brain as a result of sustained cervical spine hyperflexion. There was no associated spinal fracture, and the infarct was visualized by noncontrast computed tomography (CT) scan during the early, acute phase. The patient's neurologic deficits resolved partially and he was successfully rehabilitated. To our knowledge there is no other report of pontomedullary infarction from sustained cervical spine hyperflexion.
KEV WORDS: Brainstem; Cerebral infarction; Spinal cord hyperflexion; Vertebrobasilar insufficiency; Pontomedullary
Case R e p o r t
Syndromes of vertebrobasilar insufficiency or infarction have been reported after nonpenetrating, forceful, traumatic occlusion of the vertebral artery during cervical fracture [14], chiropractic manipulation [7], calisthentics [9], and yoga [4]. These syndromes have been observed even after head movements considered within a comfortable range of motion such as ceiling painting [ i0], automobile driving [1], and archery [17]. In all of these instances the vascular insult is thought to occur from compromise of blood flow through the vertebral arteries while the cervical spine is in a position of hyperextension, or hyperextension with lateral rotation. Angiographic studies and autopsy findings show that the pathophysiologic mechanism of stroke in these patients is due to injury to the intima of the vertebral artery with thrombotic vessel occlusion, and in some instances, the formation of an embolus with its subsequent migration into the posterior circulation [ 16]. The vertebral artery is most often injured at the atlantoaxial joint, the site
Addre.~s reprint requests to: Walter J. Faillace, M.D., University of Rochester Medical Center, Division of Neurosurgery, Box 661,601 Elmwood Avenue, Rochester, New York 14642.
~; 1986 by Elsevier Science Publishing Co., Inc.
The patient is a 26-year-old man who fell from a motorcycle in May 1982, and was rendered paraplegic with a compression fracture of the T-5 vertebral body with anterior dislocation of the bodies of T-4 on T-5. H e was treated by immobilization in a body cast until the thoracic fractures fused, he underwent a rehabilitation program, and he was discharged in a wheelchair from the hospital 9 weeks after injury. H e subsequently gained part-time employment. Seventeen months after the motor cycle injury, while in the midst of a transfer from a wheelchair to a living room couch, the wheelchair turned down backward and the patient was thrown backwards coming to lie on his neck and occiput with his body flipped over him. His neck was in a position of hyperflexion, and he remained in this position for approximately 10 minutes, until he was discovered and extricated by his mother. The patient did not lose consciousness. H e experienced an onset of bilateral upper extremity weakness and numbness and he was brought to the hospital. The physical examination on admission revealed normal vital signs. There was no external evidence of craniocervical trauma. The patient was irritable, photophobic, nauseated, and complaining of biparieto-occipital headache. H e could follow simple commands, but he 0090-3019/86/$3.50
Pontomedullary Infarction
remained lethargic and fatigued easily. Eye examination revealed see-saw nystagmus in all directions of gaze, and fundoscopy showed no papilledema or retinopathy. His cranial nerve deficits included: symmetrical weakness of muscles of mastication, and depressed corneal reflexes, left greater than the right; mild left peripheral facial paralysis; depressed gag reflex, palate deviation toward the left, hypophonic, nasal tone of voice; symmetrical weakness of the sternocleidomastoid and trapezius muscles; tongue deviation toward the left, with incomplete crossing toward the right. Motor examination revealed: 4 +/5 strength of all major motor groups of the right arm and hand; 3 +/5 strength of the same motor groups in the left arm; deep tendon reflexes were symmetrically 1 +/4 hyporeflexic. Examination of the legs showed old spastic paraplegia. Sensory examination showed symmetrical hypesthesia to pinprick and touch above the T1 dermatome, bilateral impairment of position and vibration sense of upper extremities, and loss of all sensory modalities below the T4 dermatome. There was staccato speech and dysrnetria of the upper extremities. The cervical spine was immobilized with a rigid Philadelphia collar. Roentgenograms of the cervical spine disclosed no fracture or dislocation. A noncontrast CT scan of the brain performed 5 hours after injury showed a lowdensity lesion extending from the medulla to the pons compatible with infarction (Figure 1). The patient was admitted to the surgical intensive care unit for treatment aimed at reduction of cerebral edema. This was accomplished by elevation of his head to 30 °, fluid volume restriction to two-thirds daily maintenance, diuresis with a regimen of 25% mannitol I g/kg load and 50 g every 8 hours, and dexamethasone 10 mg
Figure 1. Noncontrast CT scan of the head 5 hours after sustained cervical spine lzyperflexion illustrates low-density midline area in the pons and medulla compatible with ischemic infarction.
Surg Neurol 1986;26:282-6
283
intravenous load followed by 4 mg every 6 hours. Fortyeight hours after injury, a noncontrast CT scan of the head with views of the cervical spine was obtained. This scan revealed a well-delineated area of infarction of the ports, medulla, and swelling of the upper cervical spinal cord (Figure 2 A and B). At 72 hours after injury, examination of the patient showed that he was no longer irritable and photophobic, his voice was euphonic and without a staccato quality, and there was partial resolution of all cranial nerve deficits. There was residual nystagmus and dysmetria of both upper extremities. The motor strength of all major muscle groups of the left arm had improved to 4 +/5. Sensory appreciation improved above the T1 dermatome in both arms. Mannitol was discontinued and decadron was tapered over the course of 5 days. Physical and occupational therapy was started to improve upper extremity strength and coordination, sitting balance, bed mobility, and to commence activities of daily living. The patient successfully completed the rehabilitation program and he was discharged 8 weeks after injury. At the time of discharge, his residual deficits included a mild left peripheral facial paresis, spasticity, and weakness of 4 +/5 strength of the upper extremities. A noncontrast CT scan performed 7 weeks after injury showed that the previously described area of infarction was less well defined. Discussion We report this case to document that pontomedullary infarction can result from sustained cervical spine hyperflexion without an accompanying injury to bone. The vertebral artery has been shown to be susceptible to extraluminal compression from surrounding structures at three sites: (a) at its entrance in the foramen transversarium of C-6 by skeletal muscle fascial bands [6]; (b) compression by osteophytes throughout its upward
284
Surg Neurol 1986;26:282-6
Faillace and Okawara
A
B
course through the cervical spine [15]; (c) compression or elongation of the artery during rotation of the head in its relatively fixed position at the atlantoaxial joint [18]. Blood flow through the vertebral artery of our patient may have been compromised by extraluminal compression along any one or all of these three critical areas. A wealth of scientific investigations have been performed to study the cerebral circulation of humans and select animals. In a study on human cadavers, Toole and Tucker [ 19] demonstrated that flow through the carotid
Figure 2. (A) Noncontrast CT scan of the head48 hours after sustained cervical spine hyperflexion illustrates ischemic infarctio~ of the pontomedullary region. (B) Noncontrast CT scan through the cervical spine areas 1 and 2 shows swelling of the cervical spinal cord.
and vertebral arteries could be reduced to less than 10% of original flow during normal range of motions of the head. In performing angiography for vertebrobasilar insufficiency, George and Lurian [3] showed that a hemodynamic disorder could explain a bilateral cerebral lesion related to an infarct if there is a poorly developed
Pontomedullary Infarction
anastomotic network of arteries to the brainstem. Hence, to insure survival from a severe ischemic event in the vertebrobasilar territory, an adequate collateral circulation from the carotid system to the more deficient posterior circulation is a requirement. The circle of Willis is the most readily available collateral blood source. Other collateral sources include the distal branches of the thyrocervical and costocervical trunks, the occipital artery, muscular branches of the vertebral artery, and interspinal branches of the vertebral arteries. Reivich et al [12] performed quantitative measurements of blood flow through the carotid and vertebral arteries of a dog and observed a compensatory increase in blood flow in the carotid arteries of up to 4 5 % when flow through the vertebral artery was impeded. Scatliff et al [13] report that in humans, flow rate per se is important in permitting reflux through an occluded vertebral artery; reflux of the vertebral artery is inversely related to anterograde circulatory flow rate during times of occlusion in this artery. The symptoms of vertebrobasilar insufficiency or infarction may be protean because of the close proximity of multiple cranial nerve nuclei, motor, sensory, cerebellar, and autonomic tracts in the ischemic area. The particular clinical and anatomopathologic entities of vertebrobasilar insufficiency have been reviewed by Marshall [8]. Our patient showed deficits compatible with patchy, bilateral ischemic lesions of the pontomedulla. In a study of the temporal profile of vertebrobasilar infarction, Patrick et al [11] concluded that the group of patients who were in coma from the onset have a dismal prognosis. Their second group of patients with slow neurologic deterioration, but with stabilization of deficits had an excellent prognosis. An early, adequate collateral circulation was thought to account for the survival and successful recovery o f the second group. The third group with stabilized deficits but with subsequent deterioration had presumed failure of collateral circulation. Caronna and Levy [2], in a prospective study designed to identify the clinical variables associated with recovery from an acute ischemic stroke, found there was a reduced chance of recovery if there was severity of the early, focal deficit, and if there was evidence of a large infarction. A reduced density on the initial early CT scan was observed in less than 25% of their patients, and this was associated with a poor chance of regaining independent function. In their study patients with neurologic deficits localized to the vertebrobasilar territory and posterior cerebral artery faired better than those with involvement of the internal carotid-middle cerebral artery distribution. O f all ischemic infarcts, only half are imaged by CT scan within the first 48 hours. Those infarcts visible
Surg Neurol 1986;26:282-6
285
within 12-24 hours tend to be large and in the distribution of one or more major cerebral vessels [5]. Our patient was unique in showing a pontomedullary infarction within the first 5 hours of injury, and a follow-up scan performed 3 weeks later showed partial resolution of the infarct. We did not pursue an arteriogram to visualize vessel occlusion at the time of initial evaluation of our patient because the infarct was clearly imaged by CT scan. We report this case to reveal that sustained cervical spine hyperflexion could result in pontomedullary infarction. Obstruction of blood flow in the vertebrobasilar territory with resultant ischemic deficits can occur not only from cervical spine hyperextension, with or without rotation, but also from hyperflexion. Survival of a stroke in the pontomedullary region, an area with numerous intimately related neighboring structures, depends upon the existence of an adequate collateral blood circulation. An aggressive stance should be taken toward patient resuscitation despite an ominous lesion on CT scan, as recovery is likely, particularly if the patient is not comatose in the first 24 hours after injury.
References 1. Bauer R, Sheehan S, Meyer JS. Arteriographic study of cerebrovascular disease II. Cerebral symptoms due to kinking, tortuosity, and compression of carotid and vertebral arteries in the neck. Arch Neurol 1961;4:119-31. 2. CaronnaJJ, Levy DE. Clinical predictors of outcome in ischemic stroke. Neurol Clin 1983;1:103-17. 3. George B, Lurian C. Vertebrobasilar ischemia. Its relation to stenosis and occlusion of the vertebral artery. Acta Neurochir (Wien) 1982;62:287-95. 4. Hanus SH, Horner TD, Harter DH. Vertebral artery occlusion complicating yoga exercises. Arch Neurol 1977;34:574-5. 5. Houser OW, CampbellJK, Baker HLJr, Sundt TSJr. Radiologic evaluation of ischemic cerebrovascular syndromes with emphasis on computer tomography. Radiol Clin North Am 1982;20:123-42. 6. Husni EA, Bell HS, Storer J. Mechanical occlusion of the vertebral arteries. A new clinical concept. JAMA 1966;196:475-8. 7. Krueger BR, Okazaki H. Vertebral-basilar distribution infarction following chiropractic cervical manipulation. Mayo Clin Proc 1980;55:322-32. 8. Marshall J. A survey of occlusive disease of the vertebrobasilar arterial system. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology. Vol 12. Amsterdam: North Holland Publishing Co, 1972:1-12. 9. Nagler W. Vertebral artery obstruction by hyperextension of the neck: report of three cases. Arch Phys Med Rehabil 1973;54:237-40. 10. Okawara SH, Nibbelink D. Vertebral artery occlusion following hyperextension and rotation of the head. Stroke 1974;5:640-2. 11. Patrick BK, Ramirez-Lassepas M, Synder BD. Temporal profile of vertebrobasilar territory infarction. Prognostic implications. Stroke 1980;11:643-8. 12. Reivich M, Holling E, Roberts B, Toole JF. Reversal of blood
286
Surg N e u r o l 1986;26:282-6
Faillace and Okawara
flow through the vertebral artery and its effect on cerebral circulation. N Engl J Med 1961;265:878-84. 13. ScatliffJH, Hyde I, Gautot HJ. Vertebral artery reflux: a laboratory investigation of the nonobstructive causes of retrograde flow of contrast material into the contralateral vertebral artery. Radiology 1967;88:64-74. 14. Schneider RC, Schemm GW. Vertebral artery insufficiency in acute and chronic spinal trauma, with special reference to the syndrome of acute central cervical spinal cord injury. J Neurosurg 1961;18:348-60. l 5. Sheehan S, Bauer RB, Meyer JS. Vertebral artery compression
16. 17. 18. 19.
in cervical spondylosis: arteriographic demonstration during life of vertebral insufficiency due to rotation and extension of the neck. Neurology (Minneap) 1960;10:968-86. Sherman DG, Hart RG, Easton JD. Abrupt change in head position and cerebral infarction. Stroke 1981;12:2-6. Sorensen BF. Bow hunter's stroke. Neurosurgery 1978;2:259-61. Tatlow WFT, Bammer HG. Syndrome of vertebral artery compression. Neurology (Minneap) 1975;7:331-40. Toole JF, Tucker SH. Influence of head position upon cerebral circulation: studies on blood flow in cadavers. Arch Neurol 1960;2:616-23.
Surg Neurol 1986;26:282-6
Pontomedullary Infarction from Sustained Cervical Spine Hyperflexion Walter J. Faillace, M.D., and Shige-Hisa Okawara, M.D., Ph.D. Division of Neurological Surgery, University of Rochester Medical Center, Rochester, New York
Faillace WJ, Okawara S-H. Pontomedullary infarction from sustained cervical spine hyperflexion. Surg Neurol 1986;26:282-6.
A paraplegic but independent 26-year-old man developed pontomedullary infarction from a fall which placed him in a position of sustained cervical spine hyperflexion. An early noncontrast computed tomography scan displayed infarction of the pontomedullary region. The patient made partial recovery of his neurologic deficits. The infarct was thought to arise from compromise of blood flow through the vertebrobasilar vessels during hyperflexion of the cervical spine. The mechanisms that impeded blood flow in the vertebrobasilar territory and the prognostic factors of ischemic infarction in this area are discussed.
of maximal movement of the cervical spine during turning of the head. In addition, blood flow in this artery can be compromised almost anywhere along its course in the neck [6,15,18]. This paper reports a patient who acquired an infarction of the pontomedullary region of the brain as a result of sustained cervical spine hyperflexion. There was no associated spinal fracture, and the infarct was visualized by noncontrast computed tomography (CT) scan during the early, acute phase. The patient's neurologic deficits resolved partially and he was successfully rehabilitated. To our knowledge there is no other report of pontomedullary infarction from sustained cervical spine hyperflexion.
KEV WORDS: Brainstem; Cerebral infarction; Spinal cord hyperflexion; Vertebrobasilar insufficiency; Pontomedullary
Case R e p o r t
Syndromes of vertebrobasilar insufficiency or infarction have been reported after nonpenetrating, forceful, traumatic occlusion of the vertebral artery during cervical fracture [14], chiropractic manipulation [7], calisthentics [9], and yoga [4]. These syndromes have been observed even after head movements considered within a comfortable range of motion such as ceiling painting [ i0], automobile driving [1], and archery [17]. In all of these instances the vascular insult is thought to occur from compromise of blood flow through the vertebral arteries while the cervical spine is in a position of hyperextension, or hyperextension with lateral rotation. Angiographic studies and autopsy findings show that the pathophysiologic mechanism of stroke in these patients is due to injury to the intima of the vertebral artery with thrombotic vessel occlusion, and in some instances, the formation of an embolus with its subsequent migration into the posterior circulation [ 16]. The vertebral artery is most often injured at the atlantoaxial joint, the site
Addre.~s reprint requests to: Walter J. Faillace, M.D., University of Rochester Medical Center, Division of Neurosurgery, Box 661,601 Elmwood Avenue, Rochester, New York 14642.
~; 1986 by Elsevier Science Publishing Co., Inc.
The patient is a 26-year-old man who fell from a motorcycle in May 1982, and was rendered paraplegic with a compression fracture of the T-5 vertebral body with anterior dislocation of the bodies of T-4 on T-5. H e was treated by immobilization in a body cast until the thoracic fractures fused, he underwent a rehabilitation program, and he was discharged in a wheelchair from the hospital 9 weeks after injury. H e subsequently gained part-time employment. Seventeen months after the motor cycle injury, while in the midst of a transfer from a wheelchair to a living room couch, the wheelchair turned down backward and the patient was thrown backwards coming to lie on his neck and occiput with his body flipped over him. His neck was in a position of hyperflexion, and he remained in this position for approximately 10 minutes, until he was discovered and extricated by his mother. The patient did not lose consciousness. H e experienced an onset of bilateral upper extremity weakness and numbness and he was brought to the hospital. The physical examination on admission revealed normal vital signs. There was no external evidence of craniocervical trauma. The patient was irritable, photophobic, nauseated, and complaining of biparieto-occipital headache. H e could follow simple commands, but he 0090-3019/86/$3.50
Pontomedullary Infarction
remained lethargic and fatigued easily. Eye examination revealed see-saw nystagmus in all directions of gaze, and fundoscopy showed no papilledema or retinopathy. His cranial nerve deficits included: symmetrical weakness of muscles of mastication, and depressed corneal reflexes, left greater than the right; mild left peripheral facial paralysis; depressed gag reflex, palate deviation toward the left, hypophonic, nasal tone of voice; symmetrical weakness of the sternocleidomastoid and trapezius muscles; tongue deviation toward the left, with incomplete crossing toward the right. Motor examination revealed: 4 +/5 strength of all major motor groups of the right arm and hand; 3 +/5 strength of the same motor groups in the left arm; deep tendon reflexes were symmetrically 1 +/4 hyporeflexic. Examination of the legs showed old spastic paraplegia. Sensory examination showed symmetrical hypesthesia to pinprick and touch above the T1 dermatome, bilateral impairment of position and vibration sense of upper extremities, and loss of all sensory modalities below the T4 dermatome. There was staccato speech and dysrnetria of the upper extremities. The cervical spine was immobilized with a rigid Philadelphia collar. Roentgenograms of the cervical spine disclosed no fracture or dislocation. A noncontrast CT scan of the brain performed 5 hours after injury showed a lowdensity lesion extending from the medulla to the pons compatible with infarction (Figure 1). The patient was admitted to the surgical intensive care unit for treatment aimed at reduction of cerebral edema. This was accomplished by elevation of his head to 30 °, fluid volume restriction to two-thirds daily maintenance, diuresis with a regimen of 25% mannitol I g/kg load and 50 g every 8 hours, and dexamethasone 10 mg
Figure 1. Noncontrast CT scan of the head 5 hours after sustained cervical spine lzyperflexion illustrates low-density midline area in the pons and medulla compatible with ischemic infarction.
Surg Neurol 1986;26:282-6
283
intravenous load followed by 4 mg every 6 hours. Fortyeight hours after injury, a noncontrast CT scan of the head with views of the cervical spine was obtained. This scan revealed a well-delineated area of infarction of the ports, medulla, and swelling of the upper cervical spinal cord (Figure 2 A and B). At 72 hours after injury, examination of the patient showed that he was no longer irritable and photophobic, his voice was euphonic and without a staccato quality, and there was partial resolution of all cranial nerve deficits. There was residual nystagmus and dysmetria of both upper extremities. The motor strength of all major muscle groups of the left arm had improved to 4 +/5. Sensory appreciation improved above the T1 dermatome in both arms. Mannitol was discontinued and decadron was tapered over the course of 5 days. Physical and occupational therapy was started to improve upper extremity strength and coordination, sitting balance, bed mobility, and to commence activities of daily living. The patient successfully completed the rehabilitation program and he was discharged 8 weeks after injury. At the time of discharge, his residual deficits included a mild left peripheral facial paresis, spasticity, and weakness of 4 +/5 strength of the upper extremities. A noncontrast CT scan performed 7 weeks after injury showed that the previously described area of infarction was less well defined. Discussion We report this case to document that pontomedullary infarction can result from sustained cervical spine hyperflexion without an accompanying injury to bone. The vertebral artery has been shown to be susceptible to extraluminal compression from surrounding structures at three sites: (a) at its entrance in the foramen transversarium of C-6 by skeletal muscle fascial bands [6]; (b) compression by osteophytes throughout its upward
284
Surg Neurol 1986;26:282-6
Faillace and Okawara
A
B
course through the cervical spine [15]; (c) compression or elongation of the artery during rotation of the head in its relatively fixed position at the atlantoaxial joint [18]. Blood flow through the vertebral artery of our patient may have been compromised by extraluminal compression along any one or all of these three critical areas. A wealth of scientific investigations have been performed to study the cerebral circulation of humans and select animals. In a study on human cadavers, Toole and Tucker [ 19] demonstrated that flow through the carotid
Figure 2. (A) Noncontrast CT scan of the head48 hours after sustained cervical spine hyperflexion illustrates ischemic infarctio~ of the pontomedullary region. (B) Noncontrast CT scan through the cervical spine areas 1 and 2 shows swelling of the cervical spinal cord.
and vertebral arteries could be reduced to less than 10% of original flow during normal range of motions of the head. In performing angiography for vertebrobasilar insufficiency, George and Lurian [3] showed that a hemodynamic disorder could explain a bilateral cerebral lesion related to an infarct if there is a poorly developed
Pontomedullary Infarction
anastomotic network of arteries to the brainstem. Hence, to insure survival from a severe ischemic event in the vertebrobasilar territory, an adequate collateral circulation from the carotid system to the more deficient posterior circulation is a requirement. The circle of Willis is the most readily available collateral blood source. Other collateral sources include the distal branches of the thyrocervical and costocervical trunks, the occipital artery, muscular branches of the vertebral artery, and interspinal branches of the vertebral arteries. Reivich et al [12] performed quantitative measurements of blood flow through the carotid and vertebral arteries of a dog and observed a compensatory increase in blood flow in the carotid arteries of up to 4 5 % when flow through the vertebral artery was impeded. Scatliff et al [13] report that in humans, flow rate per se is important in permitting reflux through an occluded vertebral artery; reflux of the vertebral artery is inversely related to anterograde circulatory flow rate during times of occlusion in this artery. The symptoms of vertebrobasilar insufficiency or infarction may be protean because of the close proximity of multiple cranial nerve nuclei, motor, sensory, cerebellar, and autonomic tracts in the ischemic area. The particular clinical and anatomopathologic entities of vertebrobasilar insufficiency have been reviewed by Marshall [8]. Our patient showed deficits compatible with patchy, bilateral ischemic lesions of the pontomedulla. In a study of the temporal profile of vertebrobasilar infarction, Patrick et al [11] concluded that the group of patients who were in coma from the onset have a dismal prognosis. Their second group of patients with slow neurologic deterioration, but with stabilization of deficits had an excellent prognosis. An early, adequate collateral circulation was thought to account for the survival and successful recovery o f the second group. The third group with stabilized deficits but with subsequent deterioration had presumed failure of collateral circulation. Caronna and Levy [2], in a prospective study designed to identify the clinical variables associated with recovery from an acute ischemic stroke, found there was a reduced chance of recovery if there was severity of the early, focal deficit, and if there was evidence of a large infarction. A reduced density on the initial early CT scan was observed in less than 25% of their patients, and this was associated with a poor chance of regaining independent function. In their study patients with neurologic deficits localized to the vertebrobasilar territory and posterior cerebral artery faired better than those with involvement of the internal carotid-middle cerebral artery distribution. O f all ischemic infarcts, only half are imaged by CT scan within the first 48 hours. Those infarcts visible
Surg Neurol 1986;26:282-6
285
within 12-24 hours tend to be large and in the distribution of one or more major cerebral vessels [5]. Our patient was unique in showing a pontomedullary infarction within the first 5 hours of injury, and a follow-up scan performed 3 weeks later showed partial resolution of the infarct. We did not pursue an arteriogram to visualize vessel occlusion at the time of initial evaluation of our patient because the infarct was clearly imaged by CT scan. We report this case to reveal that sustained cervical spine hyperflexion could result in pontomedullary infarction. Obstruction of blood flow in the vertebrobasilar territory with resultant ischemic deficits can occur not only from cervical spine hyperextension, with or without rotation, but also from hyperflexion. Survival of a stroke in the pontomedullary region, an area with numerous intimately related neighboring structures, depends upon the existence of an adequate collateral blood circulation. An aggressive stance should be taken toward patient resuscitation despite an ominous lesion on CT scan, as recovery is likely, particularly if the patient is not comatose in the first 24 hours after injury.
References 1. Bauer R, Sheehan S, Meyer JS. Arteriographic study of cerebrovascular disease II. Cerebral symptoms due to kinking, tortuosity, and compression of carotid and vertebral arteries in the neck. Arch Neurol 1961;4:119-31. 2. CaronnaJJ, Levy DE. Clinical predictors of outcome in ischemic stroke. Neurol Clin 1983;1:103-17. 3. George B, Lurian C. Vertebrobasilar ischemia. Its relation to stenosis and occlusion of the vertebral artery. Acta Neurochir (Wien) 1982;62:287-95. 4. Hanus SH, Horner TD, Harter DH. Vertebral artery occlusion complicating yoga exercises. Arch Neurol 1977;34:574-5. 5. Houser OW, CampbellJK, Baker HLJr, Sundt TSJr. Radiologic evaluation of ischemic cerebrovascular syndromes with emphasis on computer tomography. Radiol Clin North Am 1982;20:123-42. 6. Husni EA, Bell HS, Storer J. Mechanical occlusion of the vertebral arteries. A new clinical concept. JAMA 1966;196:475-8. 7. Krueger BR, Okazaki H. Vertebral-basilar distribution infarction following chiropractic cervical manipulation. Mayo Clin Proc 1980;55:322-32. 8. Marshall J. A survey of occlusive disease of the vertebrobasilar arterial system. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology. Vol 12. Amsterdam: North Holland Publishing Co, 1972:1-12. 9. Nagler W. Vertebral artery obstruction by hyperextension of the neck: report of three cases. Arch Phys Med Rehabil 1973;54:237-40. 10. Okawara SH, Nibbelink D. Vertebral artery occlusion following hyperextension and rotation of the head. Stroke 1974;5:640-2. 11. Patrick BK, Ramirez-Lassepas M, Synder BD. Temporal profile of vertebrobasilar territory infarction. Prognostic implications. Stroke 1980;11:643-8. 12. Reivich M, Holling E, Roberts B, Toole JF. Reversal of blood
286
Surg N e u r o l 1986;26:282-6
Faillace and Okawara
flow through the vertebral artery and its effect on cerebral circulation. N Engl J Med 1961;265:878-84. 13. ScatliffJH, Hyde I, Gautot HJ. Vertebral artery reflux: a laboratory investigation of the nonobstructive causes of retrograde flow of contrast material into the contralateral vertebral artery. Radiology 1967;88:64-74. 14. Schneider RC, Schemm GW. Vertebral artery insufficiency in acute and chronic spinal trauma, with special reference to the syndrome of acute central cervical spinal cord injury. J Neurosurg 1961;18:348-60. l 5. Sheehan S, Bauer RB, Meyer JS. Vertebral artery compression
16. 17. 18. 19.
in cervical spondylosis: arteriographic demonstration during life of vertebral insufficiency due to rotation and extension of the neck. Neurology (Minneap) 1960;10:968-86. Sherman DG, Hart RG, Easton JD. Abrupt change in head position and cerebral infarction. Stroke 1981;12:2-6. Sorensen BF. Bow hunter's stroke. Neurosurgery 1978;2:259-61. Tatlow WFT, Bammer HG. Syndrome of vertebral artery compression. Neurology (Minneap) 1975;7:331-40. Toole JF, Tucker SH. Influence of head position upon cerebral circulation: studies on blood flow in cadavers. Arch Neurol 1960;2:616-23.