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Proton MR spectroscopy of cerebellitis
Magnetic Resonance Imaging 20 (2002) 619 – 622
Proton MR spectroscopy of cerebellitis Laura Guerrinia, Giacomo Bellib, Martino Cellerinic, Patrizia Nencinid, Mario Mascalchia,* a
Radiodiagnostica I, Dipartimento di Fisiopatologia Clinica, Universita` di Firenze, Viale Morgagni 85, Firenze, Italy b Fisica Sanitaria, Azienda Ospedaliera di Careggi, Viale Morgagni 85, Firenze, Italy c Neuroradiologia, Azienda Ospedaliera di Careggi, Viale Morgagni 85, Firenze, Italy d Clinica Neurologica III, Universita` di Firenze, Viale Morgagni 85, Firenze, Italy Received 11 August 2002; accepted 9 September 2002
Abstract Single voxel proton MR spectroscopy (1H-MRS) of the vermis was obtained in two patients with cerebellitis. In the acute phase 1H-MRS revealed low N-acetyl-aspartate (NAA)/creatine (Cr) and NAA/choline (Cho) and normal Cho/Cr ratios. Decrease of the concentration of NAA was confirmed by quantitative analysis in one patient. The NAA/Cr and NAA/Cho ratios and NAA concentration were increased in 1 H-MRS examinations obtained 10 and 24 months after the acute episode. 1H-MRS demonstrates reversible metabolite changes in cerebellitis. © 2002 Elsevier Science Inc. All rights reserved. Keywords: Proton MRS; Cerebellum; Cerebellitis
1. Introduction Cerebellitis is a disease of children and adults in which a selective damage of the cerebellum ensues during or after an infectious disease [1–3]. Differential diagnosis with other conditions causing acute ataxia is sometimes difficult on clinical ground. MR imaging may be normal or demonstrate characteristic signal changes in the cerebellar folia [1–3]. We evaluated with single voxel proton MR spectroscopy (1H-MRS) two patients with cerebellitis in the acute phase and many months after the episode.
2. Case histories Case n. 1. A 36-year-old man presented with fever, headache, ataxia, and dysarthria after a non-specific virus infection. One plain and contrast enhanced cranial computed tomography and two unenhanced cranial MRI were negative. A further cranial MRI 6 days after onset demonstrated symmetric areas of subtle hyperintensity in T2 weighted images in the folia of the upper portion of the cerebellar hemispheres and vermis which were slightly swollen (Fig. 1). There was no abnormal contrast enhance* Corresponding author. Tel.: ⫹055-4377673; fax: ⫹055-431970. E-mail address: [email protected] (M. Mascalchi).
ment. Initial 1H-MRS was obtained one week later. Routine laboratory blood and urine examinations were normal. CSF examination showed a mild increase of the cells (6/ml, N.V. ⬍5/ml). An extensive search for antibodies to viruses and bacteria in the serum and CSF was negative. He was treated with ceftriaxone, steroids and acyclovir and recovered completely in one month. Ten months after discharge MRI demonstrated complete disappearance of the areas of signal changes in the cerebellum and 1H-MRS was obtained in the same session. Case n. 2. A 19-year-old man was admitted to hospital because of headache, dysarthria and transient left lower limb weakness which appeared 3 months after bronchopneumonia. Plain and contrast enhanced cranial computed tomography and a cranial MR imaging performed 6 days after onset of the neurological symptoms were negative as well as a digital four vessel arteriography. A second cranial MR imaging three days later showed areas of increased signal in T2 weighted images in the folia of the cerebellar hemispheres and vermis which were slightly swollen. There was no abnormal contrast enhancement. Initial 1H-MRS was obtained the next day. Increased titers of IgM antibodies to mycoplasma pneumoniae were detected twice in the serum, with a maximum of 1:128 (N.V. ⬍ 1:8), but not in the CSF which showed 106 cells/ml (99 mononucleates and 7 polynucleate) and a mild increase of protein content (0.53 g/l, N.V. ⬍ 0.5 g/l). He was treated with ceftriaxone, doxy-
0730-725X/02/$ – see front matter © 2002 Elsevier Science Inc. All rights reserved. PII: S 0 7 3 0 - 7 2 5 X ( 0 2 ) 0 0 6 0 0 - 8
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L. Guerrini et al. / Magnetic Resonance Imaging 20 (2002) 619 – 622
Fig. 1. (A–D) Case 1. Coronal T2 weighted (TR 4400 ms, TE110 ms, echo train length 15) TSE image in the acute phase (A) shows areas of subtle hyperintensity (arrows) in the folia of the upper portion of the cerebellar hemispheres and vermis which are slightly swollen. 1H-MR spectra of the cerebellar vermis obtained with PRESS sequence (TR 2000 ms, TE 272 ms) in case 1 at presentation (B) and in a healthy control subject (C) show low NAA/Cr and NAA/Cho ratios in (B). 1H-MR spectrum in case 1 obtained 10 months later (D) demonstrates increased NAA/Cr and NAA/Cho ratios.
cycline and acyclovir. The patient’s symptoms rapidly improved. MR imaging 24 months after discharge showed disappearance of the areas of signal changes without atrophy of the cerebellum. Control 1H-MRS was performed in the same session.
3. MR spectroscopy 1
H-MRS was performed on a 1.5 T system (Philips Gyroscan NT ACS, Best The Netherlands) using a standard quadrature head coil. The voxel of interest in the two patients was a cube of 2 ⫻ 2 ⫻ 2 cm (8 ml) centered in the superior vermis. After automatic shimming and gradient tuning, water suppression was achieved with a selective excitation RF pulse. A point resolved proton spectroscopy
sequence (PRESS) technique was used for acquisition of the proton spectra with TR 2000 ms and 128 averages and an acquisition time of 4.24 minutes for each spectrum. In case 1, four echo times (80, 136, 272 and 400 ms) were obtained for computation of metabolites T2 and quantification of metabolites was performed with the external phantom calibration technique [4]. In case 2 only two echo times (136 and 272 ms) were obtained and no quantification was made. Reference normal values for metabolite ratios, T2 relaxation times and concentrations in the superior vermis were available in 5 age matched healthy subjects. Post-processing involved the following steps: zero filling, Gaussian filtering, exponential multiplication, Fourier transform and manual phase correction without baseline manipulation. The areas of the peaks at 2.07, 3.00 and 3.20 ppm corresponding to N-acetylaspartate (NAA), creatine (Cr) and choline (Cho)
L. Guerrini et al. / Magnetic Resonance Imaging 20 (2002) 619 – 622
and the ratios of NAA/Cr, Cho/Cr and NAA/Cho were calculated in the 272 ms spectra. No correction for CSF partial volumes which can affect determination of metabolite concentrations in the superior vermis due to variable contamination with CSF was made in case 1 and controls.
4. Results Initial 1H-MR spectra (Fig. 1) showed low, i.e. 2SD ⬍ the mean in the controls, NAA/Cr (case 1 ⫽ 0.98; case 2 ⫽ 0.96; N.V. 1.6 ⫾ 0.2) and NAA/Cho ratios (case 1 ⫽ 0.95; case 2 ⫽ 0.88; N.V. 1.3 ⫾ 0.1) with normal Cho/Cr ratio (case 1 ⫽ 1.03; case 2 ⫽ 1.08; N.V. 1.2 ⫾ 0.2) and no lactate. The metabolite T2 in case 1 were unchanged (NAA ⫽ 361 ms, N.V. 341 ⫾ 82 ms; Cr ⫽ 238 ms N.V. 217 ⫾ 26 ms; Cho ⫽ 400 ms, N.V. 374 ⫾ 77 ms). The NAA concentration in case 1 was 7.4 mmol/l (N.V. 9.8 ⫾ 2.7 mmol/ l), the Cr 12.4 mmol/l (N.V. 12.8 ⫾ 2.9 mmol/l) and the Cho 2.4 mmol/l (N.V. 3.0 ⫾ 1.0 mmol/l). Follow-up 1H-MR spectra showed increase of NAA/Cr (case 1 ⫽ 1.35; case 2 ⫽ 2.03), NAA/Cho (case 1 ⫽ 1.03; case 2 ⫽ 1.47) and Cho/Cr (case 1 ⫽ 1.31; case 2 ⫽ 1.37) (Fig. 1). In case 1 metabolite T2 relaxation times were normal (NAA 293 ms, Cr 207 ms and Cho 500 ms) and the concentration of NAA was increased (NAA ⫽ 10.8 mmol/l, Cr ⫽ 12.3 mmol/l, Cho ⫽ 2.3 mmol/l).
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of signal changes can appear several days after clinical onset [3], be subtle and not to enhance. Moreover MR imaging showed cerebellar T2 signal changes in only one of 46 children with acute cerebellar ataxia [2]. The failure of MRI in detection of cerebellar signal changes in patients with acute postinfectious cerebellar ataxia was recently confirmed in another study which advocated a role of SPECT for diagnosis of this condition due to its capability to show cerebellar hypoperfusion [7]. 1 H-MRS provides biochemical information in vivo non invasively and, to the best of our knowledge, has not been employed for evaluation of acute cerebellitis until now. Our observations indicate that 1H-MRS can demonstrate the reversible metabolite changes associated to cerebellitis and suggest that it may be more sensitive than MR imaging for diagnosis of this condition. The decrease of the NAA/Cr ratio and of the NAA concentration in the cerebellum we observed are not specific of cerebellitis. In fact they are reported in patients with medulloblastoma [8], degenerative ataxia [9], and Lehrmitte Duclos disease [10]. However clinical presentation and course and MR imaging findings generally allow differential diagnosis of these entities in which no reversal of 1H-MRS changes are expected. Acknowledgments The support of the National Ataxia Foundation, Minneapolis is acknowledged.
5. Discussion Cerebellitis is associated with several infectious illnesses, usually viral, and vaccinations [1–3]. However, in many cases, despite extensive serological tests, the causative agent of acute cerebellitis remains unknown [1,2]. The mechanisms underlying the damage to the cerebellum in acute cerebellitis are not established. In some cases a direct role of the infective agent is supported by its demonstration in the CSF [1], in other cases, an immunological alteration similar to that of acute disseminated encephalomyelitis is assumed [5]. The clinical presentation of acute cerebellitis usually entails a variable combination of tremor, ataxia, dysarthria, ophthalmoparesis, headache, altered mental status and fever. Hydrocephalus due to cerebellar swelling may require CSF shunting [3]. Although the course of the acute cerebellitis is usually benign with resolution of symptoms in few days/weeks, it may be fatal [6] or leave residual cerebellar ataxia. Since the clinical features of acute cerebellitis are nonspecific, demonstration with MRI of areas of signal changes in the cerebellar folia in T2 weighted images which can be symmetric or restricted to one cerebellar hemisphere and show contrast enhancement is important for the differential diagnosis of this condition with other causes of acute ataxia [1–3]. However, as confirmed by our observations, the areas
References [1] Sawaishi Y, Takahashi I, Hirayama Y, Abe T, Mizutani M, Hirai K, Takada G. Acute cerebellitis by Coxiella burnetii. Ann Neurol 1999; 45:124 –7. [2] Connolly AM, Dodson WE, Prensky AL, Rust RS. Course and outcome of acute cerebellar ataxia. Ann Neurol 1994;35:673–9. [3] Bakshi R, Bates VE, Kinkel PR, Mechtler LL, Kinkel WR. Magnetic resonance imaging findings in acute cerebellitis. Clin Imaging 1998; 22:79 – 85. [4] Keevil SF, Topp S, Leach MO, Ring P, Henriksen O, Barbiroli B, Cady EB, Carlier P, Gobbi B, Hennig J, Kugel H, Moser E, Mlynarik V, Podo F. A multicentre trial of protocols and test objects for metabolite quantification by in vivo localised proton magnetic resonance spectroscopy. In: Podo F, Bovee´ WMMJ, de Certaines JD, Henriksen O, Leach MO, Leibfritz D, editors. Eurospin Annual 1995–1996. Rome: Istituto Superiore di Sanita`, 1996. p. 229 – 41. [5] Komatsu H, Kuroki S, Shimizu Y, Takada H, Takeuchi Y. Mycoplasma pneumoniae meningoencephalitis and cerebellitis with antiganglioside antibodies. Pediatr Neurol 1998;18:160 – 4. [6] Levy EI, Harris AE, Omalu BI, Hamilton RL, Branstetter BF 4th, Pollack IF. Sudden death from fulminant acute cerebellitis. Pediatr Neurosurg 2001;35:24 – 8. [7] Nagamisu S, Matsuishi T, Ishibashi M, Yamashita Y, Nishimi T, Ichikawa K, Yamanishi K, Kato H. Decreased cerebellar blood flow in postinfection acute cerebellar ataxia. J Neurol Neurosurg Psychiatry 1999;67:109 –12. [8] Wang Z, Sutton LN, Cnaan A, Haselgrove JC, Rorke LB, Zhao H, Bilaniuk LT, Zimmerman RA. Proton MR spectroscopy of pediatric cerebellar tumors. AJNR Am J Neuroradial 1995;16:1821–33.
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L. Guerrini et al. / Magnetic Resonance Imaging 20 (2002) 619 – 622
[9] Davie CA, Barker GJ, Webb S, Tofts PS, Thompson AJ, Harding AE, McDonald WI, Miller DH. Persistent functional deficit in multiple sclerosis and autosomal dominant cerebellar ataxia is associated with axonal loss. Brain 1995;118:1583–92.
[10] Klisch J, Juengling F, Speer J, Koch D, Thiel T, Buchert M, Arnold S, Feuerhake F, Schumacher M. Lhermitte-Duclos disease: assessment with MR imaging, positron emission tomography, single-photon emission CT, and MR spectroscopy. AJNR Am J Neuroradiol 2001;22:824–30.
Proton MR spectroscopy of cerebellitis Laura Guerrinia, Giacomo Bellib, Martino Cellerinic, Patrizia Nencinid, Mario Mascalchia,* a
Radiodiagnostica I, Dipartimento di Fisiopatologia Clinica, Universita` di Firenze, Viale Morgagni 85, Firenze, Italy b Fisica Sanitaria, Azienda Ospedaliera di Careggi, Viale Morgagni 85, Firenze, Italy c Neuroradiologia, Azienda Ospedaliera di Careggi, Viale Morgagni 85, Firenze, Italy d Clinica Neurologica III, Universita` di Firenze, Viale Morgagni 85, Firenze, Italy Received 11 August 2002; accepted 9 September 2002
Abstract Single voxel proton MR spectroscopy (1H-MRS) of the vermis was obtained in two patients with cerebellitis. In the acute phase 1H-MRS revealed low N-acetyl-aspartate (NAA)/creatine (Cr) and NAA/choline (Cho) and normal Cho/Cr ratios. Decrease of the concentration of NAA was confirmed by quantitative analysis in one patient. The NAA/Cr and NAA/Cho ratios and NAA concentration were increased in 1 H-MRS examinations obtained 10 and 24 months after the acute episode. 1H-MRS demonstrates reversible metabolite changes in cerebellitis. © 2002 Elsevier Science Inc. All rights reserved. Keywords: Proton MRS; Cerebellum; Cerebellitis
1. Introduction Cerebellitis is a disease of children and adults in which a selective damage of the cerebellum ensues during or after an infectious disease [1–3]. Differential diagnosis with other conditions causing acute ataxia is sometimes difficult on clinical ground. MR imaging may be normal or demonstrate characteristic signal changes in the cerebellar folia [1–3]. We evaluated with single voxel proton MR spectroscopy (1H-MRS) two patients with cerebellitis in the acute phase and many months after the episode.
2. Case histories Case n. 1. A 36-year-old man presented with fever, headache, ataxia, and dysarthria after a non-specific virus infection. One plain and contrast enhanced cranial computed tomography and two unenhanced cranial MRI were negative. A further cranial MRI 6 days after onset demonstrated symmetric areas of subtle hyperintensity in T2 weighted images in the folia of the upper portion of the cerebellar hemispheres and vermis which were slightly swollen (Fig. 1). There was no abnormal contrast enhance* Corresponding author. Tel.: ⫹055-4377673; fax: ⫹055-431970. E-mail address: [email protected] (M. Mascalchi).
ment. Initial 1H-MRS was obtained one week later. Routine laboratory blood and urine examinations were normal. CSF examination showed a mild increase of the cells (6/ml, N.V. ⬍5/ml). An extensive search for antibodies to viruses and bacteria in the serum and CSF was negative. He was treated with ceftriaxone, steroids and acyclovir and recovered completely in one month. Ten months after discharge MRI demonstrated complete disappearance of the areas of signal changes in the cerebellum and 1H-MRS was obtained in the same session. Case n. 2. A 19-year-old man was admitted to hospital because of headache, dysarthria and transient left lower limb weakness which appeared 3 months after bronchopneumonia. Plain and contrast enhanced cranial computed tomography and a cranial MR imaging performed 6 days after onset of the neurological symptoms were negative as well as a digital four vessel arteriography. A second cranial MR imaging three days later showed areas of increased signal in T2 weighted images in the folia of the cerebellar hemispheres and vermis which were slightly swollen. There was no abnormal contrast enhancement. Initial 1H-MRS was obtained the next day. Increased titers of IgM antibodies to mycoplasma pneumoniae were detected twice in the serum, with a maximum of 1:128 (N.V. ⬍ 1:8), but not in the CSF which showed 106 cells/ml (99 mononucleates and 7 polynucleate) and a mild increase of protein content (0.53 g/l, N.V. ⬍ 0.5 g/l). He was treated with ceftriaxone, doxy-
0730-725X/02/$ – see front matter © 2002 Elsevier Science Inc. All rights reserved. PII: S 0 7 3 0 - 7 2 5 X ( 0 2 ) 0 0 6 0 0 - 8
620
L. Guerrini et al. / Magnetic Resonance Imaging 20 (2002) 619 – 622
Fig. 1. (A–D) Case 1. Coronal T2 weighted (TR 4400 ms, TE110 ms, echo train length 15) TSE image in the acute phase (A) shows areas of subtle hyperintensity (arrows) in the folia of the upper portion of the cerebellar hemispheres and vermis which are slightly swollen. 1H-MR spectra of the cerebellar vermis obtained with PRESS sequence (TR 2000 ms, TE 272 ms) in case 1 at presentation (B) and in a healthy control subject (C) show low NAA/Cr and NAA/Cho ratios in (B). 1H-MR spectrum in case 1 obtained 10 months later (D) demonstrates increased NAA/Cr and NAA/Cho ratios.
cycline and acyclovir. The patient’s symptoms rapidly improved. MR imaging 24 months after discharge showed disappearance of the areas of signal changes without atrophy of the cerebellum. Control 1H-MRS was performed in the same session.
3. MR spectroscopy 1
H-MRS was performed on a 1.5 T system (Philips Gyroscan NT ACS, Best The Netherlands) using a standard quadrature head coil. The voxel of interest in the two patients was a cube of 2 ⫻ 2 ⫻ 2 cm (8 ml) centered in the superior vermis. After automatic shimming and gradient tuning, water suppression was achieved with a selective excitation RF pulse. A point resolved proton spectroscopy
sequence (PRESS) technique was used for acquisition of the proton spectra with TR 2000 ms and 128 averages and an acquisition time of 4.24 minutes for each spectrum. In case 1, four echo times (80, 136, 272 and 400 ms) were obtained for computation of metabolites T2 and quantification of metabolites was performed with the external phantom calibration technique [4]. In case 2 only two echo times (136 and 272 ms) were obtained and no quantification was made. Reference normal values for metabolite ratios, T2 relaxation times and concentrations in the superior vermis were available in 5 age matched healthy subjects. Post-processing involved the following steps: zero filling, Gaussian filtering, exponential multiplication, Fourier transform and manual phase correction without baseline manipulation. The areas of the peaks at 2.07, 3.00 and 3.20 ppm corresponding to N-acetylaspartate (NAA), creatine (Cr) and choline (Cho)
L. Guerrini et al. / Magnetic Resonance Imaging 20 (2002) 619 – 622
and the ratios of NAA/Cr, Cho/Cr and NAA/Cho were calculated in the 272 ms spectra. No correction for CSF partial volumes which can affect determination of metabolite concentrations in the superior vermis due to variable contamination with CSF was made in case 1 and controls.
4. Results Initial 1H-MR spectra (Fig. 1) showed low, i.e. 2SD ⬍ the mean in the controls, NAA/Cr (case 1 ⫽ 0.98; case 2 ⫽ 0.96; N.V. 1.6 ⫾ 0.2) and NAA/Cho ratios (case 1 ⫽ 0.95; case 2 ⫽ 0.88; N.V. 1.3 ⫾ 0.1) with normal Cho/Cr ratio (case 1 ⫽ 1.03; case 2 ⫽ 1.08; N.V. 1.2 ⫾ 0.2) and no lactate. The metabolite T2 in case 1 were unchanged (NAA ⫽ 361 ms, N.V. 341 ⫾ 82 ms; Cr ⫽ 238 ms N.V. 217 ⫾ 26 ms; Cho ⫽ 400 ms, N.V. 374 ⫾ 77 ms). The NAA concentration in case 1 was 7.4 mmol/l (N.V. 9.8 ⫾ 2.7 mmol/ l), the Cr 12.4 mmol/l (N.V. 12.8 ⫾ 2.9 mmol/l) and the Cho 2.4 mmol/l (N.V. 3.0 ⫾ 1.0 mmol/l). Follow-up 1H-MR spectra showed increase of NAA/Cr (case 1 ⫽ 1.35; case 2 ⫽ 2.03), NAA/Cho (case 1 ⫽ 1.03; case 2 ⫽ 1.47) and Cho/Cr (case 1 ⫽ 1.31; case 2 ⫽ 1.37) (Fig. 1). In case 1 metabolite T2 relaxation times were normal (NAA 293 ms, Cr 207 ms and Cho 500 ms) and the concentration of NAA was increased (NAA ⫽ 10.8 mmol/l, Cr ⫽ 12.3 mmol/l, Cho ⫽ 2.3 mmol/l).
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of signal changes can appear several days after clinical onset [3], be subtle and not to enhance. Moreover MR imaging showed cerebellar T2 signal changes in only one of 46 children with acute cerebellar ataxia [2]. The failure of MRI in detection of cerebellar signal changes in patients with acute postinfectious cerebellar ataxia was recently confirmed in another study which advocated a role of SPECT for diagnosis of this condition due to its capability to show cerebellar hypoperfusion [7]. 1 H-MRS provides biochemical information in vivo non invasively and, to the best of our knowledge, has not been employed for evaluation of acute cerebellitis until now. Our observations indicate that 1H-MRS can demonstrate the reversible metabolite changes associated to cerebellitis and suggest that it may be more sensitive than MR imaging for diagnosis of this condition. The decrease of the NAA/Cr ratio and of the NAA concentration in the cerebellum we observed are not specific of cerebellitis. In fact they are reported in patients with medulloblastoma [8], degenerative ataxia [9], and Lehrmitte Duclos disease [10]. However clinical presentation and course and MR imaging findings generally allow differential diagnosis of these entities in which no reversal of 1H-MRS changes are expected. Acknowledgments The support of the National Ataxia Foundation, Minneapolis is acknowledged.
5. Discussion Cerebellitis is associated with several infectious illnesses, usually viral, and vaccinations [1–3]. However, in many cases, despite extensive serological tests, the causative agent of acute cerebellitis remains unknown [1,2]. The mechanisms underlying the damage to the cerebellum in acute cerebellitis are not established. In some cases a direct role of the infective agent is supported by its demonstration in the CSF [1], in other cases, an immunological alteration similar to that of acute disseminated encephalomyelitis is assumed [5]. The clinical presentation of acute cerebellitis usually entails a variable combination of tremor, ataxia, dysarthria, ophthalmoparesis, headache, altered mental status and fever. Hydrocephalus due to cerebellar swelling may require CSF shunting [3]. Although the course of the acute cerebellitis is usually benign with resolution of symptoms in few days/weeks, it may be fatal [6] or leave residual cerebellar ataxia. Since the clinical features of acute cerebellitis are nonspecific, demonstration with MRI of areas of signal changes in the cerebellar folia in T2 weighted images which can be symmetric or restricted to one cerebellar hemisphere and show contrast enhancement is important for the differential diagnosis of this condition with other causes of acute ataxia [1–3]. However, as confirmed by our observations, the areas
References [1] Sawaishi Y, Takahashi I, Hirayama Y, Abe T, Mizutani M, Hirai K, Takada G. Acute cerebellitis by Coxiella burnetii. Ann Neurol 1999; 45:124 –7. [2] Connolly AM, Dodson WE, Prensky AL, Rust RS. Course and outcome of acute cerebellar ataxia. Ann Neurol 1994;35:673–9. [3] Bakshi R, Bates VE, Kinkel PR, Mechtler LL, Kinkel WR. Magnetic resonance imaging findings in acute cerebellitis. Clin Imaging 1998; 22:79 – 85. [4] Keevil SF, Topp S, Leach MO, Ring P, Henriksen O, Barbiroli B, Cady EB, Carlier P, Gobbi B, Hennig J, Kugel H, Moser E, Mlynarik V, Podo F. A multicentre trial of protocols and test objects for metabolite quantification by in vivo localised proton magnetic resonance spectroscopy. In: Podo F, Bovee´ WMMJ, de Certaines JD, Henriksen O, Leach MO, Leibfritz D, editors. Eurospin Annual 1995–1996. Rome: Istituto Superiore di Sanita`, 1996. p. 229 – 41. [5] Komatsu H, Kuroki S, Shimizu Y, Takada H, Takeuchi Y. Mycoplasma pneumoniae meningoencephalitis and cerebellitis with antiganglioside antibodies. Pediatr Neurol 1998;18:160 – 4. [6] Levy EI, Harris AE, Omalu BI, Hamilton RL, Branstetter BF 4th, Pollack IF. Sudden death from fulminant acute cerebellitis. Pediatr Neurosurg 2001;35:24 – 8. [7] Nagamisu S, Matsuishi T, Ishibashi M, Yamashita Y, Nishimi T, Ichikawa K, Yamanishi K, Kato H. Decreased cerebellar blood flow in postinfection acute cerebellar ataxia. J Neurol Neurosurg Psychiatry 1999;67:109 –12. [8] Wang Z, Sutton LN, Cnaan A, Haselgrove JC, Rorke LB, Zhao H, Bilaniuk LT, Zimmerman RA. Proton MR spectroscopy of pediatric cerebellar tumors. AJNR Am J Neuroradial 1995;16:1821–33.
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L. Guerrini et al. / Magnetic Resonance Imaging 20 (2002) 619 – 622
[9] Davie CA, Barker GJ, Webb S, Tofts PS, Thompson AJ, Harding AE, McDonald WI, Miller DH. Persistent functional deficit in multiple sclerosis and autosomal dominant cerebellar ataxia is associated with axonal loss. Brain 1995;118:1583–92.
[10] Klisch J, Juengling F, Speer J, Koch D, Thiel T, Buchert M, Arnold S, Feuerhake F, Schumacher M. Lhermitte-Duclos disease: assessment with MR imaging, positron emission tomography, single-photon emission CT, and MR spectroscopy. AJNR Am J Neuroradiol 2001;22:824–30.