+Model NEURAD-515; No. of Pages 13
ARTICLE IN PRESS
Journal of Neuroradiology (2015) xxx, xxx—xxx
Available online at
ScienceDirect www.sciencedirect.com
ORIGINAL ARTICLE
Brain MRI findings in aspartylglucosaminuria Anna M. Tokola a,∗, Laura E. Åberg b, Taina H. Autti a a
HUS Medical Imaging Center, Radiology, University of Helsinki and Helsinki University Hospital, P.O. Box 340, FI-00029 HUS, Helsinki, Finland b Department of Psychiatry, Jorvi Hospital, P.O. Box 827, FI-00029 HUS, Finland
KEYWORDS Aspartylglucosaminuria; Lysosomal storage disorder; Inborn errors of metabolism; Magnetic resonance imaging; Intellectual disability
Summary Background and purpose: The aim of this study was to identify characteristic 3.0 T brain MRI findings in patients with aspartylglucosaminuria (AGU), a rare lysosomal storage disorder. Previous AGU patient material imaged at 1.0 and 1.5 T was also re-evaluated. Materials and methods: Twenty-five brain MRI examinations from 20 AGU patients were included in the study. Thirteen patients underwent a prospective 3.0 T MRI (5 male, 8 female, aged 9—45 years). Twelve examinations from nine patients (4 male, 5 female, aged 8—33 years) previously imaged at 1.0 or 1.5 T were re-evaluated. Two patients were included in both the prospective and the retrospective groups. Visual analysis of the T1- and T2-weighted images was performed by two radiologists. Results: The previously reported signal intensity changes in T2-weighted images were visible at all field strengths, but they were more distinct at 3.0 T than at 1.0 or 1.5 T. These included signal intensity decrease in the thalami and especially in the pulvinar nuclei, periventricular signal intensity increase and juxtacortical high signal foci. Poor differentiation between gray and white matter was found in all patients. Some degree of cerebral and/or cerebellar atrophy and mild ventricular dilatation were found in nearly all patients. This study also disclosed various unspecific findings, including a higher than normal incidence of dilated perivascular spaces, arachnoid cysts, pineal cysts and mildly dilated cavum veli interpositi. Conclusion: This study revealed particular brain MRI findings in AGU, which can raise the suspicion of this rare disease in clinical practice. © 2015 Elsevier Masson SAS. All rights reserved.
Abbreviations: MRI, magnetic resonance imaging; AGU, aspartylglucosaminuria; T, Tesla; AGA, aspartylglucosaminidase; SI, signal intensity; WM, white matter; GM, grey matter; T2 TSE, T2-weighted turbo spin echo; T1 3D TFE, T1-weighted three-dimensional turbo field echo; TR, repetition time; TE, echo time; SE, spin echo; T1 3D MP-RAGE, T1-weighted three-dimensional magnetization-prepared rapid acquisition gradient echo; FLAIR, fluid-attenuated inversion recovery; PVS, perivascular space; MCM, mega cisterna magna; CJD, Creutzfeldt—Jakob disease; CSF, cerebrospinal fluid; CVI, cavum veli interpositi. ∗ Corresponding author. Tel.: +358 9 4711. E-mail addresses: anna.tokola@hus.fi (A.M. Tokola), laura.aberg@fimnet.fi (L.E. Åberg), taina.autti@hus.fi (T.H. Autti). http://dx.doi.org/10.1016/j.neurad.2015.03.003 0150-9861/© 2015 Elsevier Masson SAS. All rights reserved.
Please cite this article in press as: Tokola AM, et al. Brain MRI findings in aspartylglucosaminuria. J Neuroradiol (2015), http://dx.doi.org/10.1016/j.neurad.2015.03.003
+Model NEURAD-515; No. of Pages 13
ARTICLE IN PRESS
2
A.M. Tokola et al.
Introduction Aspartylglucosaminuria (AGU) is an inherited, autosomal recessive, progressive neurodegenerative disease. It is a lysosomal storage disorder and manifests with progressive decline in cognitive and motor functions, leading to premature death [1]. The disease is caused by a mutation of the AGA gene, located on 4q34.3 [2], resulting in deficient activity of aspartylglucosaminidase, a lysosomal hydrolase enzyme. As a result, there is excessive accumulation of uncleaved glycoasparagines in lysosomes and elevated metabolite levels in urine. In Finland, the estimated incidence of the disease is 1:18,000, while in other countries, the incidence is unknown [3,4]. Sporadic cases are found in many countries and at least 27 different mutations of the gene exist [5]. Children with AGU appear healthy at birth. Delayed speech and clumsiness are typically the first symptoms noticed around the age of 2 to 3 years. Later on, progressive intellectual impairment becomes evident [6]. Typical facial features (a broad lower jaw, a short, broad nose, periorbital puffiness and round cheeks) become more pronounced during the teens [7]. Epilepsy may develop in adulthood and life expectancy is typically less than 45 years [1,6]. Lysosomal storage disorders that primarily affect the central nervous system have no known treatment available to cure or slow down the progression of the disease. Mouse model studies investigating virus-mediated gene therapy and enzyme replacement therapy in AGU have shown some metabolic correction and decreased storage in the brain [8—10]. Previous brain MRI studies at 1.0 and 1.5 T have shown thalamic T2 SI decrease, delayed myelination and increased T2 SI in the periventricular WM in AGU [1,11,12]. Furthermore, slow progressive brain atrophy has been reported. No specific SI alterations in T1-weighted images have been reported in AGU. A histopathologic study has revealed that the cortical and deep GM neurons contain vacuoles, and there is diffuse pallor of myelin staining and gliosis in the WM [1]. The aim of this study was to identify characteristic 3.0 T brain MRI findings in patients with AGU. Also, previous AGU patient material imaged at 1.0 and 1.5 T was re-evaluated to assess the impact of field strength on the findings.
Materials and methods In total, 25 brain MRI examinations from 20 AGU patients were included in the study. Thirteen patients (5 male, 8 female, age between 9 and 45 years, mean 25.5 years, SD 9.8) were recruited for this study, and underwent prospective 3.0 T MRI. In addition, retrospective MRI material from nine AGU patients (4 male, 5 female, age between 8 and 33 years, mean 15.6, SD 7.3) consisting of 12 examinations imaged at 1.0 T and/or 1.5 T was re-evaluated. Mean age was calculated using age at the first examination. One patient was imaged four times (twice at 1.0, once at 1.5 and 3.0 T) and two patients twice (one at 1.0 and 1.5 T, and the other at 1.5 and 3.0 T). In all cases, the AGU diagnosis was confirmed with a urine test showing elevated levels of aspartylglucosamin and a blood test showing deficiency in the AGA
enzyme. The patients imaged at 3.0 T are presented in Table 1, and the patients imaged at 1.0 and 1.5 T in Table 2. The patients imaged at 3.0 T were recruited with assistance from Suomen AGU Ry patient association and Rinnekoti Foundation. Informed consent was obtained from the parents of the patients prior to inclusion in the study. A clinical neurological examination was performed on all patients and data on their medical history were collected from parents and medical records. No sedation was used during the scanning and all patients were in good physical condition at the time of the examination. All patients were intellectually disabled and four of the patients had epilepsy. The study was approved by the ethics committee of the Hospital for Children and Adolescents, University of Helsinki.
MRI acquisition For the new patient material, the MR imaging was performed using a 3.0 T Achieva device (Philips, Best, Netherlands). The examination included a T2 TSE axial series (TR 4000, TE 80, slice thickness 4 mm, flip angle 90◦ , matrix 512 × 512) and a T1 3D TFE series (TR 8.19, TE 3.79, slice thickness 1 mm, flip angle 8◦ , matrix 256 × 256). From the previous patient material, five examinations were performed using a 1.0 T Magnetom Harmony device (Siemens, Erlangen, Germany) including T2 dual SE axial and coronal images (TR 2500, TE 90, slice thickness 5 mm, gap 1 mm, matrix 256 × 256) and T1 axial images (TR 600, TE 15, slice thickness 4 mm, gap 0.8 mm, matrix 256 × 256). Four examinations were performed using a 1.5 T Magnetom Vision device (Siemens, Erlangen, Germany) including a T2 TSE axial series (TR 3500 or 3000, TE 90 or 85, slice thickness 5 mm, gap 1 mm, flip angle 180◦ , matrix 256 × 256), a T1 3D MP-RAGE series (TR 1900, TE 3.68, TI 1100, flip angle 15◦ , matrix 512 × 512) and a FLAIR axial series (TR 9000, TE 105, TI 2500, flip angle 180◦ , slice thickness 5 mm, gap 1 mm, matrix 256 × 256). The remaining three examinations were performed using a 1.5 T Sonata device (Siemens, Erlangen, Germany) including a T2 TSE axial series (TR 6000, TE 125, slice thickness 5 mm, gap 1 mm, flip angle 150◦ and matrix 512 × 384) and a T1 3D MP-RAGE series (TR 1900, TE 3.68, TI 1100, flip angle 15◦ , matrix 512 × 512). The patients imaged at 1.0 and 1.5 T had participated in previous studies [11,12]. Their images were subsequently re-evaluated using the same parameters as in the 3.0 T group.
Visual analysis The T1 and T2-weighted images were evaluated by two radiologists. A FLAIR series was also available from four patients imaged at 1.5 T. The consensus of opinion was used as the final assessment. From the MR examinations, twelve parameters were evaluated. These included thalamic (1) and pulvinar nuclei SI changes (2), periventricular (3) and other white matter SI abnormalities (4), GM/WM differentiation (5), PVS dilatation (6), widening of cerebral sulci (7) and cerebellar fissures (8), enlargement of ventricles (9), abnormalities of the corpus callosum (10), cystic changes (11) and the presence of cavum variations (12).
Please cite this article in press as: Tokola AM, et al. Brain MRI findings in aspartylglucosaminuria. J Neuroradiol (2015), http://dx.doi.org/10.1016/j.neurad.2015.03.003
Sex
Thalamus T2 SI
Pulvinar T2 SI
Periventricular Juxtacortical GM/WM T2 SI T2 foci differentiation
Cerebral and cerebellar atrophy
CC atrophy
PVS dilatation
Other
1
12.0
F
Decreased
Decreased
Increased
None
Poor
Some prominent sulci
Atrophy
Normal
2
17.3
F
Decreased
Decreased
Normal
None
Poor
Atrophy
Normal
3
26.6
F
Decreased
Decreased
Mildly increased
Several
Poor
Mild cerebral and cerebellar atrophy Mild cerebral and cerebellar atrophy
Pineal cyst 8 mm, mild CVI dilatation 13 mm, lateral ventricles borderline normal Lateral ventricle dilatation
Atrophy
Dilatation ≤ 2 mm
4
30.4
F
Decreased
Decreased
Increased
Several
Poor
Mild cerebral and evident cerebellar atrophy
Atrophy
Dilatation > 2 mm
5
32.4
F
Decreased
Decreased
Increased
Several
Poor
Mild cerebral atrophy
Atrophy
Dilatation > 2 mm
6
33.5
F
Heterogenous/ Heterogenous/ Increased increased increased
Several
Poor
Mild cerebral and evident cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
Pineal cyst 6 mm, CVI dilatation 12 mm, lateral and 3rd ventricle dilatation Pineal cyst 6 mm, choroid plexus cysts 10 mm and 13 mm, CSP, mild lateral and 3rd ventricle dilatation Pineal cyst 5 mm, small retrocerebellar arachnoid cyst or MCM, CVI dilatation 11 mm, mild lateral ventricle dilatation Multilocular pineal cyst 14 mm, mild lateral and 3rd ventricle dilatation
ARTICLE IN PRESS
Age
+Model
Patient
NEURAD-515; No. of Pages 13
Patients imaged with 3.0 T and their findings.
Brain MRI findings in aspartylglucosaminuria
Please cite this article in press as: Tokola AM, et al. Brain MRI findings in aspartylglucosaminuria. J Neuroradiol (2015), http://dx.doi.org/10.1016/j.neurad.2015.03.003
Table 1
3
Thalamus T2 SI
Pulvinar T2 SI
Periventricular Juxtacortical GM/WM T2 SI T2 foci differentiation
Cerebral and cerebellar atrophy
CC atrophy
PVS dilatation
Other
7
34.7
F
Decreased
Decreased
Mildly increased
Several
Poor
Mild cedebral and evident cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
8
45.3
F
Heterogenous/ Decreased decreased
Increased
Several
Poor
Evident cerebral and cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
9
9.9
M
Decreased
Decreased
Increased
None
Poor
Mild cerebral and cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
10
19.5
M
Decreased
Heterogenous/ Mildly decreased increased
ARTICLE IN PRESS
Journal of Neuroradiology (2015) xxx, xxx—xxx
Available online at
ScienceDirect www.sciencedirect.com
ORIGINAL ARTICLE
Brain MRI findings in aspartylglucosaminuria Anna M. Tokola a,∗, Laura E. Åberg b, Taina H. Autti a a
HUS Medical Imaging Center, Radiology, University of Helsinki and Helsinki University Hospital, P.O. Box 340, FI-00029 HUS, Helsinki, Finland b Department of Psychiatry, Jorvi Hospital, P.O. Box 827, FI-00029 HUS, Finland
KEYWORDS Aspartylglucosaminuria; Lysosomal storage disorder; Inborn errors of metabolism; Magnetic resonance imaging; Intellectual disability
Summary Background and purpose: The aim of this study was to identify characteristic 3.0 T brain MRI findings in patients with aspartylglucosaminuria (AGU), a rare lysosomal storage disorder. Previous AGU patient material imaged at 1.0 and 1.5 T was also re-evaluated. Materials and methods: Twenty-five brain MRI examinations from 20 AGU patients were included in the study. Thirteen patients underwent a prospective 3.0 T MRI (5 male, 8 female, aged 9—45 years). Twelve examinations from nine patients (4 male, 5 female, aged 8—33 years) previously imaged at 1.0 or 1.5 T were re-evaluated. Two patients were included in both the prospective and the retrospective groups. Visual analysis of the T1- and T2-weighted images was performed by two radiologists. Results: The previously reported signal intensity changes in T2-weighted images were visible at all field strengths, but they were more distinct at 3.0 T than at 1.0 or 1.5 T. These included signal intensity decrease in the thalami and especially in the pulvinar nuclei, periventricular signal intensity increase and juxtacortical high signal foci. Poor differentiation between gray and white matter was found in all patients. Some degree of cerebral and/or cerebellar atrophy and mild ventricular dilatation were found in nearly all patients. This study also disclosed various unspecific findings, including a higher than normal incidence of dilated perivascular spaces, arachnoid cysts, pineal cysts and mildly dilated cavum veli interpositi. Conclusion: This study revealed particular brain MRI findings in AGU, which can raise the suspicion of this rare disease in clinical practice. © 2015 Elsevier Masson SAS. All rights reserved.
Abbreviations: MRI, magnetic resonance imaging; AGU, aspartylglucosaminuria; T, Tesla; AGA, aspartylglucosaminidase; SI, signal intensity; WM, white matter; GM, grey matter; T2 TSE, T2-weighted turbo spin echo; T1 3D TFE, T1-weighted three-dimensional turbo field echo; TR, repetition time; TE, echo time; SE, spin echo; T1 3D MP-RAGE, T1-weighted three-dimensional magnetization-prepared rapid acquisition gradient echo; FLAIR, fluid-attenuated inversion recovery; PVS, perivascular space; MCM, mega cisterna magna; CJD, Creutzfeldt—Jakob disease; CSF, cerebrospinal fluid; CVI, cavum veli interpositi. ∗ Corresponding author. Tel.: +358 9 4711. E-mail addresses: anna.tokola@hus.fi (A.M. Tokola), laura.aberg@fimnet.fi (L.E. Åberg), taina.autti@hus.fi (T.H. Autti). http://dx.doi.org/10.1016/j.neurad.2015.03.003 0150-9861/© 2015 Elsevier Masson SAS. All rights reserved.
Please cite this article in press as: Tokola AM, et al. Brain MRI findings in aspartylglucosaminuria. J Neuroradiol (2015), http://dx.doi.org/10.1016/j.neurad.2015.03.003
+Model NEURAD-515; No. of Pages 13
ARTICLE IN PRESS
2
A.M. Tokola et al.
Introduction Aspartylglucosaminuria (AGU) is an inherited, autosomal recessive, progressive neurodegenerative disease. It is a lysosomal storage disorder and manifests with progressive decline in cognitive and motor functions, leading to premature death [1]. The disease is caused by a mutation of the AGA gene, located on 4q34.3 [2], resulting in deficient activity of aspartylglucosaminidase, a lysosomal hydrolase enzyme. As a result, there is excessive accumulation of uncleaved glycoasparagines in lysosomes and elevated metabolite levels in urine. In Finland, the estimated incidence of the disease is 1:18,000, while in other countries, the incidence is unknown [3,4]. Sporadic cases are found in many countries and at least 27 different mutations of the gene exist [5]. Children with AGU appear healthy at birth. Delayed speech and clumsiness are typically the first symptoms noticed around the age of 2 to 3 years. Later on, progressive intellectual impairment becomes evident [6]. Typical facial features (a broad lower jaw, a short, broad nose, periorbital puffiness and round cheeks) become more pronounced during the teens [7]. Epilepsy may develop in adulthood and life expectancy is typically less than 45 years [1,6]. Lysosomal storage disorders that primarily affect the central nervous system have no known treatment available to cure or slow down the progression of the disease. Mouse model studies investigating virus-mediated gene therapy and enzyme replacement therapy in AGU have shown some metabolic correction and decreased storage in the brain [8—10]. Previous brain MRI studies at 1.0 and 1.5 T have shown thalamic T2 SI decrease, delayed myelination and increased T2 SI in the periventricular WM in AGU [1,11,12]. Furthermore, slow progressive brain atrophy has been reported. No specific SI alterations in T1-weighted images have been reported in AGU. A histopathologic study has revealed that the cortical and deep GM neurons contain vacuoles, and there is diffuse pallor of myelin staining and gliosis in the WM [1]. The aim of this study was to identify characteristic 3.0 T brain MRI findings in patients with AGU. Also, previous AGU patient material imaged at 1.0 and 1.5 T was re-evaluated to assess the impact of field strength on the findings.
Materials and methods In total, 25 brain MRI examinations from 20 AGU patients were included in the study. Thirteen patients (5 male, 8 female, age between 9 and 45 years, mean 25.5 years, SD 9.8) were recruited for this study, and underwent prospective 3.0 T MRI. In addition, retrospective MRI material from nine AGU patients (4 male, 5 female, age between 8 and 33 years, mean 15.6, SD 7.3) consisting of 12 examinations imaged at 1.0 T and/or 1.5 T was re-evaluated. Mean age was calculated using age at the first examination. One patient was imaged four times (twice at 1.0, once at 1.5 and 3.0 T) and two patients twice (one at 1.0 and 1.5 T, and the other at 1.5 and 3.0 T). In all cases, the AGU diagnosis was confirmed with a urine test showing elevated levels of aspartylglucosamin and a blood test showing deficiency in the AGA
enzyme. The patients imaged at 3.0 T are presented in Table 1, and the patients imaged at 1.0 and 1.5 T in Table 2. The patients imaged at 3.0 T were recruited with assistance from Suomen AGU Ry patient association and Rinnekoti Foundation. Informed consent was obtained from the parents of the patients prior to inclusion in the study. A clinical neurological examination was performed on all patients and data on their medical history were collected from parents and medical records. No sedation was used during the scanning and all patients were in good physical condition at the time of the examination. All patients were intellectually disabled and four of the patients had epilepsy. The study was approved by the ethics committee of the Hospital for Children and Adolescents, University of Helsinki.
MRI acquisition For the new patient material, the MR imaging was performed using a 3.0 T Achieva device (Philips, Best, Netherlands). The examination included a T2 TSE axial series (TR 4000, TE 80, slice thickness 4 mm, flip angle 90◦ , matrix 512 × 512) and a T1 3D TFE series (TR 8.19, TE 3.79, slice thickness 1 mm, flip angle 8◦ , matrix 256 × 256). From the previous patient material, five examinations were performed using a 1.0 T Magnetom Harmony device (Siemens, Erlangen, Germany) including T2 dual SE axial and coronal images (TR 2500, TE 90, slice thickness 5 mm, gap 1 mm, matrix 256 × 256) and T1 axial images (TR 600, TE 15, slice thickness 4 mm, gap 0.8 mm, matrix 256 × 256). Four examinations were performed using a 1.5 T Magnetom Vision device (Siemens, Erlangen, Germany) including a T2 TSE axial series (TR 3500 or 3000, TE 90 or 85, slice thickness 5 mm, gap 1 mm, flip angle 180◦ , matrix 256 × 256), a T1 3D MP-RAGE series (TR 1900, TE 3.68, TI 1100, flip angle 15◦ , matrix 512 × 512) and a FLAIR axial series (TR 9000, TE 105, TI 2500, flip angle 180◦ , slice thickness 5 mm, gap 1 mm, matrix 256 × 256). The remaining three examinations were performed using a 1.5 T Sonata device (Siemens, Erlangen, Germany) including a T2 TSE axial series (TR 6000, TE 125, slice thickness 5 mm, gap 1 mm, flip angle 150◦ and matrix 512 × 384) and a T1 3D MP-RAGE series (TR 1900, TE 3.68, TI 1100, flip angle 15◦ , matrix 512 × 512). The patients imaged at 1.0 and 1.5 T had participated in previous studies [11,12]. Their images were subsequently re-evaluated using the same parameters as in the 3.0 T group.
Visual analysis The T1 and T2-weighted images were evaluated by two radiologists. A FLAIR series was also available from four patients imaged at 1.5 T. The consensus of opinion was used as the final assessment. From the MR examinations, twelve parameters were evaluated. These included thalamic (1) and pulvinar nuclei SI changes (2), periventricular (3) and other white matter SI abnormalities (4), GM/WM differentiation (5), PVS dilatation (6), widening of cerebral sulci (7) and cerebellar fissures (8), enlargement of ventricles (9), abnormalities of the corpus callosum (10), cystic changes (11) and the presence of cavum variations (12).
Please cite this article in press as: Tokola AM, et al. Brain MRI findings in aspartylglucosaminuria. J Neuroradiol (2015), http://dx.doi.org/10.1016/j.neurad.2015.03.003
Sex
Thalamus T2 SI
Pulvinar T2 SI
Periventricular Juxtacortical GM/WM T2 SI T2 foci differentiation
Cerebral and cerebellar atrophy
CC atrophy
PVS dilatation
Other
1
12.0
F
Decreased
Decreased
Increased
None
Poor
Some prominent sulci
Atrophy
Normal
2
17.3
F
Decreased
Decreased
Normal
None
Poor
Atrophy
Normal
3
26.6
F
Decreased
Decreased
Mildly increased
Several
Poor
Mild cerebral and cerebellar atrophy Mild cerebral and cerebellar atrophy
Pineal cyst 8 mm, mild CVI dilatation 13 mm, lateral ventricles borderline normal Lateral ventricle dilatation
Atrophy
Dilatation ≤ 2 mm
4
30.4
F
Decreased
Decreased
Increased
Several
Poor
Mild cerebral and evident cerebellar atrophy
Atrophy
Dilatation > 2 mm
5
32.4
F
Decreased
Decreased
Increased
Several
Poor
Mild cerebral atrophy
Atrophy
Dilatation > 2 mm
6
33.5
F
Heterogenous/ Heterogenous/ Increased increased increased
Several
Poor
Mild cerebral and evident cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
Pineal cyst 6 mm, CVI dilatation 12 mm, lateral and 3rd ventricle dilatation Pineal cyst 6 mm, choroid plexus cysts 10 mm and 13 mm, CSP, mild lateral and 3rd ventricle dilatation Pineal cyst 5 mm, small retrocerebellar arachnoid cyst or MCM, CVI dilatation 11 mm, mild lateral ventricle dilatation Multilocular pineal cyst 14 mm, mild lateral and 3rd ventricle dilatation
ARTICLE IN PRESS
Age
+Model
Patient
NEURAD-515; No. of Pages 13
Patients imaged with 3.0 T and their findings.
Brain MRI findings in aspartylglucosaminuria
Please cite this article in press as: Tokola AM, et al. Brain MRI findings in aspartylglucosaminuria. J Neuroradiol (2015), http://dx.doi.org/10.1016/j.neurad.2015.03.003
Table 1
3
Thalamus T2 SI
Pulvinar T2 SI
Periventricular Juxtacortical GM/WM T2 SI T2 foci differentiation
Cerebral and cerebellar atrophy
CC atrophy
PVS dilatation
Other
7
34.7
F
Decreased
Decreased
Mildly increased
Several
Poor
Mild cedebral and evident cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
8
45.3
F
Heterogenous/ Decreased decreased
Increased
Several
Poor
Evident cerebral and cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
9
9.9
M
Decreased
Decreased
Increased
None
Poor
Mild cerebral and cerebellar atrophy
Atrophy
Dilatation ≤ 2 mm
10
19.5
M
Decreased
Heterogenous/ Mildly decreased increased
