is probably of peripheral origin. Peripheral lesions of the hypoglossal nerve are generally classified into four categories depending on location [6]. These categories include extramedullary intracervical lesions, hypoglossal foramen lesions, extracranial lesions of the XII nerve at the base of the skull, and cervical hypoglossal nerve lesions. In our patient, investigations of the cervix and the base of the skull did not show abnormal findings. There are a few reports in the literature of isolated unilateral hypoglossal nerve palsy with a benign course, secondary to an infections process [3-5] or vaccination [7]. Although we could not establish the cause of our patient's disease, an awareness of this condition could relieve such patients from unnecessary invasive studies.
A physical examination revealed that he was completely well except for his difficulty in speaking. He was alert and cooperative and did not have lymphadenopathy or organomegaly. The pupillary diameters and reactions were normal. The palpebral fissures were symmetrical. There was no papilledema. The uvula was at midline and the gag reflex was intact. The movement of the neck was adequate and not restricted. At rest, the left side of the tongue appeared to be larger than the right side and there was no fasciculation. In addition, when the tongue was protruded, left side palsy was evident (Fig lA), and movement towards the left side was restricted. The routine blood laboratory data were normal. Since there were no sign of CNS infection, investigation of CSF was not performed. Furthermore, since he did not have fever, lymphadenopathy, or other clinical features commonly caused by viral infection, a test for EB virus was not performed. The X-ray of the skull was normal and the CT-scan of the brain did not reveal evidence of a brain tumor or ischemic lesions. The medulla, hypoglossal nerve, and hypoglossal foramen were easily detected by MR!. He was treated with multivitamins, periodically checked, and recovered completely within 12 weeks (Fig lB).
REFERENCES 1. Hemmings KW. Isolated hypoglossal nerve palsy as a presenting feature of prostatic carcinoma- a case report. Br J Oral Maxillofac Surg 1990;28: 125-7. 2. Vighetto A, Lisovoski F, Revol A, Trillet M, Almard G. Internal carotid artery dissection and ipsilateral hypoglossal nerve palsy. J Neurol Ncurosurg Psychiatry 1990;53:530-1. 3. Wright GDS, Lee KD. An isolated right hypoglossal nerve palsy in association with infectious mononucleosis. Postgrad Med J 1980;56: 185-6. 4. Rontal E, Rontal M. Lesions of the hypoglossal nerve- diagnosis, treatment, and rehabilitation. Laryngoscope 1982;92: 927-37. 5. Felix JK, Schwartz RH, Myers GJ. Isolated hypoglossal nerve paralysis following influenza vaccination. Am J Dis Child 1976;13:82-3.
DISCUSSION Since intramedullary lesions usually involve adjacent nuclei or tracts, the unilateral tongue palsy reported here
* The Efficacy of MR Imaging in Subdural Empyema Hironori Komori, MD, Tomoya Takagishi, MD, Etsuo Otaki, MD, Hirokazu Sasaki, MD, Toyojiro Matsuishi, MD, Toshi Abe, MD, Kazuyuki Kojima, MD and Kazuhiko Moritaka, MD
MRI findings of a 14-year-old boy with subdural empyema (SE) are reported and compared with those of serial CT-scan. He was admitted with fever, headache, right hemiplegia and facial palsy. Initial enhanced CT-scan revealed a slit left lateral ventricle and a shift in the mid-line structures, but failed to detect any SE. MRI at 10 days after admission clearly demonstrated SE as an area of low intensity on TJ-weigh (TI WI) and very high
*
* intensity on T2-weigh (T2WI). Post-contrast enhanced MRI (CE-MRI), using Gd-DTPA, showed a contrast enhancement in the wall of SE. However, no definite parenchymal abnormal intensity areas were detected, suggesting that the diagnosis was made sufficiently early for timely treatment and good neurological outcome. CE-MRI proved to be a more powerfUl and better diagnostic procedure than enhanced CT-scan, and was very useful in determining the state and development of the disease. Key words: Subdural empyema, MRI, CT. Komori H, Takagishi T, Otaki E, Sasaki H, Matsuishi T. Abe T. Kojima K. Moritaka K. The efficacy of MR imgaing in subdural empyema. Brain Dev 1992;14:123-5
Subdural empyema (SE) is a collection of pus in the space between the inner surface of dura and the outer surface of
Fig 1 A: An axial CT scan 2 days after admission, showing a shift in the mid-line structure from left to right. Band C: An axial plane CT-scan (B) and enhanced CT-scan (C) at 4 days after admission, showing a low density area suspected of being a subdural collection D: enhanced CT-scan at 9 days after admission.
arachnoid. SE remains an emergency condition of grave morbidity in spite of recent advances in antibiotic therapy [I, 2]. Recent advances in neuroimaging by CT -scan and MRI have enabled a noninvasive recognition of SE in its early stages [3,4] . Here we present a case of a 14-year-old boy with SE, and discuss the diagnostic usefulness of MRI with GdDTPA enhancement. CASE REPORT A 14-year-old boy was admitted to Kurume University Hospital, because of high fever, headache, right hemiplegia and right facial palsy. He had complained of nasal epistaxis for one month prior to admission. He had no history From the Departments of Pediatrics and Child Health (HK, TT, HS, HS, TM), Radiology (TA, KK), and Neurosurgery (KM), Kurume University School of Medicine, Kurume. Received for publication: July 27, 1991. Accepted for pUblication: January 15, 1992. Correspondence address: Dr. Hironori Komori, Department of Pediatrics and Child Health, Kurume University School of Medicine, 67 Asahi Machi, Kurume City 830, Japan.
124 Brain & Development, Vol 14, No 2, 1992
Fig 2 MRI, at IO days after admission, of the left temporal and left frontal regions, showing a low intensity area in Tl WI (A) which showed a high intensity in T2WI (B) suspected of being empyema. In TIWIwith Gd-DTPA (C, D), it became more clear that empyema existed between the dura and arachnoid more so than enhanced CT (D). Note the high intensity area in the frontal region, in which, no evidence of brain tissue damage was observed. There were high intensity areas due to inflammation in the left ethmoid and in the maxillary sinus (C).
of any allergic disorder or sinusitis. Four days before admission, he had a high fever, vomiting, and headache. He visited a local hospital, where right hemiparesiS was noticed, and meningitis was initially suspected because of neck stiffness and Brudzinski's sign. The CSF showed a cloudy appearance, the cell count being 740/mm 3 , consisting of 13% polymorphs and 87% lymphocytes. Glucose was 57 mg/dl and protein 84 mg/ dl. Cranial plain CT-scan showed the slit left lateral ventricle and a shift in the mid-line structures (rom left to right (Fig lA). A contrast CT-scan was not performed. In spite of vigorous antibiotic therapy with Cefotaxime (8 g/day), he developed cranial VIth and VIIth nerve palsies, and was then transferred to the Emergency Care Unit of our university hospital. On admission, he was alert, body temperature 40°C, heart rate 90/min, and blood pressure 120/54 mmHg. A redness of his left eyelid was noticed. Ocular fundus showed no papilledema. The right pupil was larger than the left, but both pupils reacted normally to light. Neurological examination revealed complete right Vlth and VlIth nerve palsies and right hemiplegia. Peripheralleuko-
cyte count was 13,600/mm 3 with a left shift of granulocytic series. CRP was 17.75 ng/ml (strongly positive). The serum electrolytes were within normal levels. The antibiotic therapy of 1.5 g Cefotaxime every 6 hours was started after admission. On the second day of admission, he showed semicoma and herniation signs due to high intracranial pressure (ICP). The X-ray demonstrated maxillary sinusitis with a diffuse opacity. Needle aspiration from bilateral maxillary sinuses yielded an evacuation of 5 ml of pus. In addition, 0.5 g/kg of mannitol was given every 6 hours to control the ICP. However, the condition aggravated progressively into semicoma, necessitating an intubation and mechanical ventilation support. On the fourth day of admission, a low density area became apparent in the axial plane of a CT -scan (Fig lB) and in the enhanced CT-scan (Fig lC), which suggested a subdural collection. The ICP increased despite using 0.5 g/kg mannitol every 4 hours. Cefotaxime was replaced by 1.0 g chloramphenicol IV every 6 hours because of expectation of better penetration to the subdural collection. Though a burr hole set at the left parietal area, twenty ml of pus was aspirated from the subdural space, from which Streptococcus milleri (S milleri) was cultured as did from the sinus fluid collection. They were found to be sensitive to gentamicin, cefotaxime, and chloramphenicol. A blood culture was negative. The patient became fully oriented and afebrile after 23 hospital days. Right VIth and VIIth nerve palsies improved gradually within a period of 40 hospital days. On the 24th day of admission, he had another cranial burr hole into the temporal area to remove the residual pus. Before the second surgery, both MRI and CT-scan were performed. Although buth revealed the subdural collection, the lateral wall of the empyema was more clearly identified on MRI, with enhancement by Gd-DTPA (CEMRI) (Fig 2D) than on post contrast CT ·scan with enhancement (CE-CT) (Fig lD). The patient was treated with chloramphenicol for 2 months. At discharge, he had a mild right hemiparesis but no emotional or psychiatric problems. The right hemiparesis had completely disappeared within a follow-up period of 6 months. DISCUSSION SE is a rare and severe condition, and is know to be fatal on occasion. It has an incidence rate of about 20% of all localized intracranial infections. Most patients with SE demonstrate acute or chronic sinusitis, or otitis media [1-3]. The causative organism found in this patient was S milleri. S milleri are normally found in the mouth. Recently, it became apparent that S milleri have proclivity for purulent disease and abscess formation in immunologically compromised host [5], though we found no
evidence of any immunodeficiency state in our patient. CT-scan has been considered the most useful diagnostic method for early detection of SE. However some authors reported that CT-scan failed to demonstrate the subdural collection [3, 6, 7]. In our case, the initial axial CT-scan revealed only a shift in the mid-line structure and it was difficult to rule out herpes encephalitis (Fig 1A), though the subdural collection became apparent on a CT-scan at 4 days after admission (Fig 1B, C). Serial CT-scans should be performed for SE when intracranial empyema cannot be ruled out. Some reports emphasized that MRI is superior to CTscan in the detection of SE [4,8] and MRI was considered more powerful diagnostic method to detect venous thrombosis [9, 10] and others, even if CT-scan cannot detect those changes. In CE-MRI with Gd-DTPA, the cranial bone is detected as hypointense, but the inflammatory dura and arachnoid membrane are detected as a well-contrasted enhanced area. Consequently, we could assess the extent of the subdural collection more easily and more accurately by CE-MRI with Gd-DTPA than by enhanced CT. Furthermore, MRI could clearly indicate that there was no evidence of any brain tissue damage, allowing us a better neurological prognostication. We conclude that CE-MRI with Gd-DTPA can reveal not only the extent of the subdural fluid collection, but also the pathophysiological changes in the brain parenchyma, and can usefully predict the neurological prognosis of a patient with subdural empyema. REFERENCES l. Silverberg AL, DiNubile MJ. Subdural empyema and cranial epidural abscess. Med Clin N Am 1985 ;69: 361-73. 2. Small M, Dale BA. Intracranial suppuration 1968-1982a 15 year review. Clin OtolaryngoI1984;9: 315-21. 3. Moseley IF, Kendal BE. Radiology of intracranial empyema, with special reference to computed tomography. Neuroradiology 1984;26: 333-45. 4. Weingarten K, Zimmerman RD, Becker RD, Heier LA, Haimes AB, Deck MDF, Subdural and epidural empyemas: MR imaging. AIR 1989;152:615-21. 5. Singh KP, Morris A, Lang SD, MacCulloch OM, Bremner DA. Clinically significant Streptococcus anginosus (Streptococcus milleri) infection: a review of 186 cases. N Z Med I 1988; 101:813-6. 6. Dunker RO, Khakoo RA. Failure of computed tomographic scanning to demonstrate subdural empyema. lAMA 1981; 246:1116-8. 7. Luken MG, Whelan MA. Recent diagnostic ex perience with subdural empyema. I Neurosurg 1980;52:764-71. 8. Davidson HD, Steiner RE. Magnetic resonance imaging in infection of the central nervous system. AINR 1985 ;6:499504. 9. McMurdo SK Jr, Brant-Zawadzki M, Bradley WG Jr, Chang GY, Berg BO. Dural sinus thrombosis: study using intermediate field strength MR imaging. Radiology 1986; 161: 83-6. 10. Macchi PJ, Grossman RI, Gomori JM, Goldberg HI, Zimmerman RA, Bilaniuk LT. High field MR imaging of cerebral venous thrombosis. I Comput Assist Tomogr 1986; 10: 10-5.
Komori et al: MRI of subdural empyema 125
A physical examination revealed that he was completely well except for his difficulty in speaking. He was alert and cooperative and did not have lymphadenopathy or organomegaly. The pupillary diameters and reactions were normal. The palpebral fissures were symmetrical. There was no papilledema. The uvula was at midline and the gag reflex was intact. The movement of the neck was adequate and not restricted. At rest, the left side of the tongue appeared to be larger than the right side and there was no fasciculation. In addition, when the tongue was protruded, left side palsy was evident (Fig lA), and movement towards the left side was restricted. The routine blood laboratory data were normal. Since there were no sign of CNS infection, investigation of CSF was not performed. Furthermore, since he did not have fever, lymphadenopathy, or other clinical features commonly caused by viral infection, a test for EB virus was not performed. The X-ray of the skull was normal and the CT-scan of the brain did not reveal evidence of a brain tumor or ischemic lesions. The medulla, hypoglossal nerve, and hypoglossal foramen were easily detected by MR!. He was treated with multivitamins, periodically checked, and recovered completely within 12 weeks (Fig lB).
REFERENCES 1. Hemmings KW. Isolated hypoglossal nerve palsy as a presenting feature of prostatic carcinoma- a case report. Br J Oral Maxillofac Surg 1990;28: 125-7. 2. Vighetto A, Lisovoski F, Revol A, Trillet M, Almard G. Internal carotid artery dissection and ipsilateral hypoglossal nerve palsy. J Neurol Ncurosurg Psychiatry 1990;53:530-1. 3. Wright GDS, Lee KD. An isolated right hypoglossal nerve palsy in association with infectious mononucleosis. Postgrad Med J 1980;56: 185-6. 4. Rontal E, Rontal M. Lesions of the hypoglossal nerve- diagnosis, treatment, and rehabilitation. Laryngoscope 1982;92: 927-37. 5. Felix JK, Schwartz RH, Myers GJ. Isolated hypoglossal nerve paralysis following influenza vaccination. Am J Dis Child 1976;13:82-3.
DISCUSSION Since intramedullary lesions usually involve adjacent nuclei or tracts, the unilateral tongue palsy reported here
* The Efficacy of MR Imaging in Subdural Empyema Hironori Komori, MD, Tomoya Takagishi, MD, Etsuo Otaki, MD, Hirokazu Sasaki, MD, Toyojiro Matsuishi, MD, Toshi Abe, MD, Kazuyuki Kojima, MD and Kazuhiko Moritaka, MD
MRI findings of a 14-year-old boy with subdural empyema (SE) are reported and compared with those of serial CT-scan. He was admitted with fever, headache, right hemiplegia and facial palsy. Initial enhanced CT-scan revealed a slit left lateral ventricle and a shift in the mid-line structures, but failed to detect any SE. MRI at 10 days after admission clearly demonstrated SE as an area of low intensity on TJ-weigh (TI WI) and very high
*
* intensity on T2-weigh (T2WI). Post-contrast enhanced MRI (CE-MRI), using Gd-DTPA, showed a contrast enhancement in the wall of SE. However, no definite parenchymal abnormal intensity areas were detected, suggesting that the diagnosis was made sufficiently early for timely treatment and good neurological outcome. CE-MRI proved to be a more powerfUl and better diagnostic procedure than enhanced CT-scan, and was very useful in determining the state and development of the disease. Key words: Subdural empyema, MRI, CT. Komori H, Takagishi T, Otaki E, Sasaki H, Matsuishi T. Abe T. Kojima K. Moritaka K. The efficacy of MR imgaing in subdural empyema. Brain Dev 1992;14:123-5
Subdural empyema (SE) is a collection of pus in the space between the inner surface of dura and the outer surface of
Fig 1 A: An axial CT scan 2 days after admission, showing a shift in the mid-line structure from left to right. Band C: An axial plane CT-scan (B) and enhanced CT-scan (C) at 4 days after admission, showing a low density area suspected of being a subdural collection D: enhanced CT-scan at 9 days after admission.
arachnoid. SE remains an emergency condition of grave morbidity in spite of recent advances in antibiotic therapy [I, 2]. Recent advances in neuroimaging by CT -scan and MRI have enabled a noninvasive recognition of SE in its early stages [3,4] . Here we present a case of a 14-year-old boy with SE, and discuss the diagnostic usefulness of MRI with GdDTPA enhancement. CASE REPORT A 14-year-old boy was admitted to Kurume University Hospital, because of high fever, headache, right hemiplegia and right facial palsy. He had complained of nasal epistaxis for one month prior to admission. He had no history From the Departments of Pediatrics and Child Health (HK, TT, HS, HS, TM), Radiology (TA, KK), and Neurosurgery (KM), Kurume University School of Medicine, Kurume. Received for publication: July 27, 1991. Accepted for pUblication: January 15, 1992. Correspondence address: Dr. Hironori Komori, Department of Pediatrics and Child Health, Kurume University School of Medicine, 67 Asahi Machi, Kurume City 830, Japan.
124 Brain & Development, Vol 14, No 2, 1992
Fig 2 MRI, at IO days after admission, of the left temporal and left frontal regions, showing a low intensity area in Tl WI (A) which showed a high intensity in T2WI (B) suspected of being empyema. In TIWIwith Gd-DTPA (C, D), it became more clear that empyema existed between the dura and arachnoid more so than enhanced CT (D). Note the high intensity area in the frontal region, in which, no evidence of brain tissue damage was observed. There were high intensity areas due to inflammation in the left ethmoid and in the maxillary sinus (C).
of any allergic disorder or sinusitis. Four days before admission, he had a high fever, vomiting, and headache. He visited a local hospital, where right hemiparesiS was noticed, and meningitis was initially suspected because of neck stiffness and Brudzinski's sign. The CSF showed a cloudy appearance, the cell count being 740/mm 3 , consisting of 13% polymorphs and 87% lymphocytes. Glucose was 57 mg/dl and protein 84 mg/ dl. Cranial plain CT-scan showed the slit left lateral ventricle and a shift in the mid-line structures (rom left to right (Fig lA). A contrast CT-scan was not performed. In spite of vigorous antibiotic therapy with Cefotaxime (8 g/day), he developed cranial VIth and VIIth nerve palsies, and was then transferred to the Emergency Care Unit of our university hospital. On admission, he was alert, body temperature 40°C, heart rate 90/min, and blood pressure 120/54 mmHg. A redness of his left eyelid was noticed. Ocular fundus showed no papilledema. The right pupil was larger than the left, but both pupils reacted normally to light. Neurological examination revealed complete right Vlth and VlIth nerve palsies and right hemiplegia. Peripheralleuko-
cyte count was 13,600/mm 3 with a left shift of granulocytic series. CRP was 17.75 ng/ml (strongly positive). The serum electrolytes were within normal levels. The antibiotic therapy of 1.5 g Cefotaxime every 6 hours was started after admission. On the second day of admission, he showed semicoma and herniation signs due to high intracranial pressure (ICP). The X-ray demonstrated maxillary sinusitis with a diffuse opacity. Needle aspiration from bilateral maxillary sinuses yielded an evacuation of 5 ml of pus. In addition, 0.5 g/kg of mannitol was given every 6 hours to control the ICP. However, the condition aggravated progressively into semicoma, necessitating an intubation and mechanical ventilation support. On the fourth day of admission, a low density area became apparent in the axial plane of a CT -scan (Fig lB) and in the enhanced CT-scan (Fig lC), which suggested a subdural collection. The ICP increased despite using 0.5 g/kg mannitol every 4 hours. Cefotaxime was replaced by 1.0 g chloramphenicol IV every 6 hours because of expectation of better penetration to the subdural collection. Though a burr hole set at the left parietal area, twenty ml of pus was aspirated from the subdural space, from which Streptococcus milleri (S milleri) was cultured as did from the sinus fluid collection. They were found to be sensitive to gentamicin, cefotaxime, and chloramphenicol. A blood culture was negative. The patient became fully oriented and afebrile after 23 hospital days. Right VIth and VIIth nerve palsies improved gradually within a period of 40 hospital days. On the 24th day of admission, he had another cranial burr hole into the temporal area to remove the residual pus. Before the second surgery, both MRI and CT-scan were performed. Although buth revealed the subdural collection, the lateral wall of the empyema was more clearly identified on MRI, with enhancement by Gd-DTPA (CEMRI) (Fig 2D) than on post contrast CT ·scan with enhancement (CE-CT) (Fig lD). The patient was treated with chloramphenicol for 2 months. At discharge, he had a mild right hemiparesis but no emotional or psychiatric problems. The right hemiparesis had completely disappeared within a follow-up period of 6 months. DISCUSSION SE is a rare and severe condition, and is know to be fatal on occasion. It has an incidence rate of about 20% of all localized intracranial infections. Most patients with SE demonstrate acute or chronic sinusitis, or otitis media [1-3]. The causative organism found in this patient was S milleri. S milleri are normally found in the mouth. Recently, it became apparent that S milleri have proclivity for purulent disease and abscess formation in immunologically compromised host [5], though we found no
evidence of any immunodeficiency state in our patient. CT-scan has been considered the most useful diagnostic method for early detection of SE. However some authors reported that CT-scan failed to demonstrate the subdural collection [3, 6, 7]. In our case, the initial axial CT-scan revealed only a shift in the mid-line structure and it was difficult to rule out herpes encephalitis (Fig 1A), though the subdural collection became apparent on a CT-scan at 4 days after admission (Fig 1B, C). Serial CT-scans should be performed for SE when intracranial empyema cannot be ruled out. Some reports emphasized that MRI is superior to CTscan in the detection of SE [4,8] and MRI was considered more powerful diagnostic method to detect venous thrombosis [9, 10] and others, even if CT-scan cannot detect those changes. In CE-MRI with Gd-DTPA, the cranial bone is detected as hypointense, but the inflammatory dura and arachnoid membrane are detected as a well-contrasted enhanced area. Consequently, we could assess the extent of the subdural collection more easily and more accurately by CE-MRI with Gd-DTPA than by enhanced CT. Furthermore, MRI could clearly indicate that there was no evidence of any brain tissue damage, allowing us a better neurological prognostication. We conclude that CE-MRI with Gd-DTPA can reveal not only the extent of the subdural fluid collection, but also the pathophysiological changes in the brain parenchyma, and can usefully predict the neurological prognosis of a patient with subdural empyema. REFERENCES l. Silverberg AL, DiNubile MJ. Subdural empyema and cranial epidural abscess. Med Clin N Am 1985 ;69: 361-73. 2. Small M, Dale BA. Intracranial suppuration 1968-1982a 15 year review. Clin OtolaryngoI1984;9: 315-21. 3. Moseley IF, Kendal BE. Radiology of intracranial empyema, with special reference to computed tomography. Neuroradiology 1984;26: 333-45. 4. Weingarten K, Zimmerman RD, Becker RD, Heier LA, Haimes AB, Deck MDF, Subdural and epidural empyemas: MR imaging. AIR 1989;152:615-21. 5. Singh KP, Morris A, Lang SD, MacCulloch OM, Bremner DA. Clinically significant Streptococcus anginosus (Streptococcus milleri) infection: a review of 186 cases. N Z Med I 1988; 101:813-6. 6. Dunker RO, Khakoo RA. Failure of computed tomographic scanning to demonstrate subdural empyema. lAMA 1981; 246:1116-8. 7. Luken MG, Whelan MA. Recent diagnostic ex perience with subdural empyema. I Neurosurg 1980;52:764-71. 8. Davidson HD, Steiner RE. Magnetic resonance imaging in infection of the central nervous system. AINR 1985 ;6:499504. 9. McMurdo SK Jr, Brant-Zawadzki M, Bradley WG Jr, Chang GY, Berg BO. Dural sinus thrombosis: study using intermediate field strength MR imaging. Radiology 1986; 161: 83-6. 10. Macchi PJ, Grossman RI, Gomori JM, Goldberg HI, Zimmerman RA, Bilaniuk LT. High field MR imaging of cerebral venous thrombosis. I Comput Assist Tomogr 1986; 10: 10-5.
Komori et al: MRI of subdural empyema 125
