CASE REPORT The Journal of TRAUMA威 Injury, Infection, and Critical Care Survival after Severe Penetrating Non-Missile Brainstem Injury: Case Report Sami Khoshyomn, MD, Paul L. Penar, MD, Keith Nagle, MD, and Steven P. Braff, MD J Trauma. 2004;56:1131–1134. N on-fatal penetrating injuries to the brainstem are rare.1,2 A careful review of the literature reveals that nearly all such reports involve superficial or tangential injury to the pons or midbrain.3–5 Salam et al.2 report the only true and well-documented case of functional survival after brainstem penetration. In that report, a crossbow arrow had penetrated and passed through the posterior midbrain tegmentum just above the ponto-mesencephalic junction. The patient was initially comatose and quadriplegic. Four months after the injury, he recovered with unspecified functional limitations. We describe a 49-year-old man with an excellent functional recovery after a true complete penetration of the midbrain and upper pons by a metallic hook, which entered in an anterior-posterior direction. CASE REPORT Clinical Presentation In August 1998, a 49-year-old, right-handed man was emergently transported to the Medical Center Hospital of Vermont (now the MCHV campus, Fletcher Allen Health Care). He had been found 2 hours earlier, unresponsive on the ground next to a metallic hook attached to a bungee cord at a campsite. At the scene, he was briefly unresponsive and had a large clot of blood protruding from his right nostril. On admission, he was alert and oriented with a Glasgow Coma Scale score of 15. He recalled that he had been securing a tent post to the ground with a self-made bungee cord and metallic hook construct (Fig. 1) when he was hit in the face by the object. He had massive facial swelling, predominantly on the right side. A general medical examination was otherwise unremarkable, and his blood pressure was 140/80. His pupils were 3 mm and briskly reactive, and extraocular movements were intact without nystagmus. The corneal reflex on the left side was weakly present. Although difficult to verify initially Submitted for publication: November 22, 2002. Accepted for publication: March 14, 2003. Copyright © 2004 by Lippincott Williams & Wilkins, Inc. From the Division of Neurosurgery, Department of Surgery (S.K., P.L.P.), the Department of Neurology (K.N.), and the Department of Radiology (S.P.B.), University of Vermont College of Medicine, Burlington, Vermont. Address for reprints: Paul L. Penar, MD, University of Vermont, College of Medicine, Division of Neurosurgery, 507 Fletcher House, 111 Colchester Avenue, Burlington, VT 05401; email: Paul.Penar@vtmednet.org DOI: 10.1097/01.TA.0000071299.31349.D6 Volume 56 • Number 5 due to facial swelling, the patient had left central facial nerve palsy with decreased sensation in the distribution of all three branches of the left trigeminal nerve. The gag reflex was present bilaterally, although the right-sided palate did not elevate as much as the left side. When protruded, the tongue slightly deviated to the left. Dysarthric speech was also evident. There was left hemiparesis (4⫹/5 throughout) with left hyperreflexia, positive Hoffman’s sign, and an up-going toe to plantar stimulation (Babinski sign). Proprioception was severely impaired in the left limbs. The patient was treated with steroids and antibiotics and admitted to the surgical intensive care unit. Neuroradiological Examination At the time of initial admission, computer tomographic (CT) and magnetic resonance imaging (MRI) of the head was performed. CT angiography and formal 4-vessel angiography were additionally done to rule out vascular injury. Noncontrast CT with bone windows showed opacification of right-sided ethmoid cells and sphenoid sinus, a fracture of the right posterior clinoid process, and a linear midbrain and upper pontine hemorrhage, suggesting direct penetrating trauma (Fig. 2). Additional small amounts of intraventricular and subarachnoid hemorrhage were also evident. Despite displacement of a fragment of posterior clinoid process in the proximity of the P1 segment of the right posterior cerebral artery (PCA), CT and formal angiography showed good filling of the right PCA via a prominent right posterior communicating artery . The MRI showed a linear hypointensity on both proton density and T2-weighted imaging consistent with acute hemorrhage. The location of injury appeared to be medial to the right cerebral peduncle of the midbrain, extending just lateral to the midline through the entire anterior-posterior diameter of the midbrain. The upper pons was involved via a similar trajectory beginning from just lateral to the midline and extending to just below the inferior colliculus (Fig. 3A-D). The pituitary was spared. Clinical Course and Follow-Up The patient’s neurologic exam remained unchanged during 10 days of acute hospitalization. He subsequently was discharged to a rehabilitation unit. A deep venous thrombosis of the left leg and an incidental diagnosis of chronic lymphocytic leukemia complicated his hospital stay. 1131 The Journal of TRAUMA威 Injury, Infection, and Critical Care Fig. 1. Photograph of the metallic hook that was part of a bungeecord-and-hook construct. Fig. 3. T2-weighted-MRI images after injury (A and B) showing a linear hypointensity consistent with acute hemorrhage. The injury track traverses the anterior-posterior diameter of the midbrain from the mesial right cerebral peduncle to the quadrigeminal plate. (C) Sagittal T1 image and (D) T2-weighted MRI 2 years after injury showing atrophy of right cerebral peduncle and linear hypointensity consistent with hemosiderin. Arrow in C points to injury track. Fig. 2. Non-contrast CT of the brain showing a linear hematoma traversing the right midbrain (large arrow) and a displaced fragment of bone from the fractured right posterior clinoid (small arrow). In September 2000, nearly 2 years after his injury, the patient was re-evaluated. He had not been able to return to work due primarily to a left hemiparesis and hemisensory loss. In addition, he had been suffering from a fluctuating but constant burning pain of the left side of his body, including the back of his head. These dysesthetic sensations, relieved partially by movement, caused chronic insomnia. Closer examination was remarkable for marked decrease in sensation to pain and temperature, with patchy variations on the order of a 20 –100% relative to the right side. Sensation to vibration and joint position were nearly absent on the left side, result1132 ing in difficulty with finger movements. Examination of limbs revealed increased reflexes in left upper and lower extremities with normal strength, including intrinsic hand muscles. His gait was confident, with minimal left armassociated movements and circumduction of the left leg. Romberg sign was negative, and cerebellar signs were absent. The eye examination was normal. Sensation in his face was significantly decreased, predominantly in the V1 and V2 distributions of left trigeminal nerve, and there was a mild decrease in the left nasolabial fold consistent with central facial nerve palsy. Rinne and Weber tests were normal. The cognitive examination was normal. However, the patient and his wife both reported a change in his personality and referred to it as a flat affect. He no longer would tell or laugh at jokes. Spontaneous speech was also somewhat decreased. The remainder of his neurologic exam was normal. MRI at this time showed significant atrophy of right cerebral peduncle and a linear hypointensity on both T1- and T2-weighted images, extending from interpeduncular cistern mesial to right cerebral peduncle to just lateral to the quadrigeminal plate (Fig. 3C and 3D). This finding was consistent with hemosiderin from the initial hemorrhage. A “blooming artifact” on gradient-echo sequences at this location was also evident, verifying hemosiderin. May 2004 Survival after Penetrating Brainstem Injury Neurophysiological Examination In September 2000, brainstem auditory evoked responses (BAERs) as well as median and posterior tibial nerve (PTN) somatosensory evoked potentials (SSEPs) were recorded. The BAERs were normal, as were the SSEPs generated by stimulation of the right median nerve and PTN. However, after stimulation of the left corresponding nerves, there were no responses proximal to Erb’s point and a stationary lumbar potential, respectively. These findings confirmed a conduction defect of the large fiber sensory pathway, which in this clinical context is most consistent with a lesion affecting the right medial lemniscus. DISCUSSION Penetrating non-missile injuries to the brainstem are rare and often fatal.2 Cases in which such brainstem injury is compatible with patient survival, let alone functional recovery, are extremely unusual.2 Although occasional survival from low-velocity penetrating injuries has been reported in the literature, nearly all of these involve superficial or tangential injury to pons or midbrain.3–5 Well-documented, true, non-fatal penetrating injury with complete traversal of brainstem has been reported only once in the literature. Salam et al.2 in 1990 reported the case of a 24-year-old man who had sustained a non-fatal penetrating brainstem injury from a crossbow bolt. CT scan of the brain of this patient showed a linear hemorrhagic track between the tegmentum and tectum of the midbrain at the pontomesencephalic junction. This patient was initially comatose and quadriplegic. At four months after the injury, he had recovered to the point that he could feed and dress himself and walk with a walker. Another report by Bauch et al.3 in 1999 describes the case of a 24-year-old man who had sustained a nail gun injury to the posterior fossa. The CT and MRI images of the brain of this patient, however, indicated an injury track posterior to pons through the middle cerebellar peduncles. Recently, Nathoo et al.6 reported a series of 17 patients with penetrating stab injuries to the brainstem. Four patients in their report survived with unspecified functional impairments. The majority of their patients had injuries that typically ended in the brainstem and did not traverse the brainstem. CT and cranial autopsy in their series revealed only three cases where track hematomas (indicating penetrating injury) had traversed the brainstem. All three injuries were fatal. In the present report, we describe the case of a 49 year-old man with CT and MRI evidence of a linear-track hematoma at the right pontomesencephalic junction created by a metallic hook traversing the brainstem in an anteriorposterior direction. This injury had produced a number of neurologic deficits, including a left central facial palsy and spastic hemiparesis, left sensory loss including proprioception and vibration from the neck downward, and decreased left facial sensation including corneal sensation. The initial dysarthric speech, left central facial palsy, and spastic hemiVolume 56 • Number 5 Fig. 4. (A) Magnified T2-weighted image of the midbrain at the time of injury showing the injury track. (B) Anatomic structures of the midbrain and their relationship to the injury track: 1) Frontopontine tract; 2) corticospinal tract; 3) parieto-temporo-occipitopontine fibers; 4) substantia nigra; 5) medial lemniscus and spinothalamic tracts; 6) trigeminothalamic tract; 7) reticular formation and central tegmental tract; 8) rubrospinal tract; 9) decussation of superior cerebellar peduncle; 10) medial longitudinal fasciculus; 11) periaqueductal gray; 12) aqueduct; 13) lateral lemniscus; and 14) nucleus of inferior colliculus. paresis were consistent with an injury in proximity to the right frontopontine, corticobulbar, and corticospinal tracts, respectively (Fig. 4). At the time of follow-up 2 years later, a profound sensory decrease to pain and temperature were still evident on the left side, including the face. More striking was that sensation to vibration and joint position were absent on the left side. With intact pupillary response and extraocular eye movements, and in the absence of an internuclear ophthalmoplegia, it was apparent that the injury track had spared most of the midline structures within the midbrain, including the nuclei of the third and fourth cranial nerve, and the medial longitudinal fasciculus (MLF). These findings strongly suggest discrete damage to the right spinothalamic tract, medial lemniscus, and trigeminothalamic tract (originating from the left nucleus of spinal tract and principal sensory nucleus of cranial nerve V) at the pontomesencephalic junction.7 These tracts lie laterally within the tegmentum of the midbrain and within the injury path (Figs. 4A and B). This interpretation was further supported by the absent SSEPs proximal to Erb’s point and stationary lumbar potentials on stimulation of the left median and posterior tibial nerves, respectively. Normal bilateral BAERs suggest an intact inferior colliculus, lateral lemniscus, and medial geniculate body, which are located posteriorly to the anterolateral system within the midbrain. Table 1 matches the specific clinical findings discussed with their neuroanatomical correlates. The apathetic personality change may be due to injury to the locus ceruleus, which lies in a paramedian location at the level of the inferior colliculus, near the trochlear nucleus. This nucleus has widespread noradrenergic connections to the cortex, hippocampus, and hypothalamus. The dorsal tegmental nucleus also has extensive projections with contributions 1133 The Journal of TRAUMA威 Injury, Infection, and Critical Care Table 1 Neurological Signs and Their Anatomical Correlates Neurologic Signs and Anatomic Correlates Clinical Sign Anatomical Structures Left central facial weakness Left spastic hemiparesis Dysarthric speech Absence of internuclear ophthalmoplegia and intact extraocular eye movement Left sensory loss (including proprioception and vibration) from neck down Decreased left facial sensation including corneal sensation Right corticobulbar tracts medial in right cerebral peduncle Right corticospinal tracts lateral to corticobulbar tract in right cerebral peduncle Right frontopontine tracts medial in right cerebral peduncle Sparing of CN III, IV (medial midbrain), and VI (pontine) nuclei, and MLF Right medial lemniscus and spinothalamic tracts laterally located in tegmentum of midbrain Right trigeminothalamic tract from left nucleus of spinal tract and principal sensory nucleus of CN V, running together with spinothalamic and medial lemniscus tracts to the medial forebrain bundle. Injury to these regions can result in limbic system abnormalities. 2. CONCLUSION 3. The neurologic deficit resulting from this unusual penetrating injury is surprisingly restricted. The literature would suggest that all such injuries with traversal of the brainstem in anterior-posterior direction are fatal. This case provides a unique opportunity to study discrete and selective damage to neuroanatomical structures of the brainstem with clinical and neurophysiological correlates. Much like Vermont’s other famous case, that of Phineas Gage,8 this case provides a unique opportunity to study the clinical and functional outcome from an otherwise typically fatal traumatic injury to the brain. REFERENCES 1. Hammon WM. Analysis of 2187 consecutive penetrating wounds of brain from Vietnam. J Neurosurg. 1971;34:127–131. 1134 4. 5. 6. 7. 8. Salam AA, Eyres KS, Magides AD, Cleary J. Penetrating brain stem injury from crossbow bolt: a case report and review of the literature. 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