Symmetric T2 Research Articles

MRI Findings of Cerebral Malaria

Cerebral malaria is a protozoal disease affecting the brain caused by Plasmodium falciparum. The hallmark of cerebral malaria is progressive decline in the sensorium leading to coma and in some cases death. MR findings reported in cerebral malaria are diffuse cerebral swelling / edema, bilateral nearly symmetrical T2 hyperintense lesions in basal ganglia and similar lesions in thalamus, pons and cerebellum. The imaging findings of cerebral malaria depend on the duration of the illness and time of MR examination. We describe two patients of cerebral malaria having mixed Plasmodium falciparum and Plasmodium vivex infestation showing bilateral basal ganglia infarcts with cerebral swelling in one patient and bilateral basal ganglia and cerebellar lesions in the other.

Hippocampal involvement due to heroin inhalation—“Chasing the Dragon”

Toxic leukoencephalopathy occurs as a result of exposure to wide variety of agents. Inhalation of heroin or its vapours produces a distinct syndrome with characteristic findings on MR imaging. We report a case of heroin vapour abuse (chasing the dragon) who presented with altered sensorium. MRI of the brain showed symmetrical T2 hyperintensities over the cerebellum and hippocampi. The patient gradually improved and made good recovery but developed spasticity of all the limbs due to delayed involvement of bilateral basal ganglia. This is the first report of bilateral hippocampal involvement in a patient abusing heroin vapour.

MR Imaging of Metronidazole-Induced Encephalopathy: Lesion Distribution and Diffusion-Weighted Imaging Findings

MR imaging features of metronidazole-induced encephalopathy (MIE) have not been fully established. This study was undertaken to determine the topographic distributions and diffusion-weighted imaging (DWI) findings of MIE. We retrospectively evaluated the initial MR images (n = 7), including DWI (n = 5), and follow-up MR images (n = 4) after drug discontinuation in 7 patents with clinically diagnosed MIE. The topographic distributions of lesions were evaluated on MR images, and DWI signal intensities and apparent diffusion coefficient (ADC) values of the lesions were assessed. MR images demonstrated bilateral symmetric T2 hyperintense lesions in the cerebellar dentate nucleus (n = 7), midbrain (n = 7), dorsal pons (n = 6), medulla (n = 4), corpus callosum (n = 4), and cerebral white matter (n = 1). Brain stem lesions involved the following: tectum (n = 5), tegmentum (n = 4), red nucleus (n = 3) of the midbrain, vestibular nucleus (n = 6), and a focal tegmental lesion involving the superior olivary nucleus (n = 6) and abducens nucleus (n = 4) of the pons and vestibular nucleus (n = 4) and inferior olivary nucleus (n = 1) of the medulla. DWI (n = 5) showed isointensity or hyperintensity of lesions, and the decreased ADC value was found only in the corpus callosum lesions (n = 2). All detected lesions were completely reversible at follow-up except for the single corpus callosum lesion with an initial low ADC value. Brain lesions were typically located at the cerebellar dentate nucleus, midbrain, dorsal pons, medulla, and splenium of the corpus callosum. According to DWI, most of the lesions in MIE probably corresponded to areas of vasogenic edema, whereas only some of them, located in the corpus callosum, corresponded to cytotoxic edema.

Volumetric brain changes in females with fragile X-associated tremor/ataxia syndrome (FXTAS)

Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurodegenerative disorder occurring in male and rare female carriers of a premutation expansion (55 to 200 CGG repeats) of the fragile X mental retardation 1 (FMR1) gene. Volumetric MRI studies, clinical staging, cognitive testing, and molecular analysis were conducted in 15 female premutation carriers affected by FXTAS (age 59.5 +/- 10.3 years), 20 unaffected female carriers (43.3 +/- 11.2 years), 11 genetically normal female controls (51.0 +/- 10.3 years), 36 affected male carriers (65.0 +/- 5.6 years), 25 unaffected male carriers (53.5 +/- 12.5 years), and 39 male controls (58.0 +/- 15.0 years). Female and male carriers with FXTAS were matched on duration of disease. We found less pronounced reductions of cerebellar volume and a lower incidence of involvement (symmetric high T2 signal) of the middle cerebellar peduncles (MCP sign) in females affected by FXTAS (13%) compared with affected males (58%). We found reduced brain volumes and increased white matter disease associated with the presence of FXTAS in females compared with female controls. We also observed significant associations between reduced cerebellar volume and both increased severity of FXTAS symptoms and increased length of the CGG repeat expansion in male premutation carriers, but not in females. Females affected by fragile X-associated tremor/ataxia syndrome (FXTAS) demonstrated milder brain changes than affected males, although they showed a similar pattern of radiologic findings consistent with brain atrophy and white matter disease. FXTAS should be considered (by ordering fragile X DNA testing) in females who present with late-onset ataxia, action tremor, or neuropathy, particularly in those with a family history of mental retardation, autism, or premature ovarian failure.

Reversible Posterior Leukoencephalopathy Syndrome Induced by Sunitinib

TO THE EDITOR: We would like to report the occurrence of reversible posterior leukoencephalopathy that we believe is directly attributable to sunitinib malate (Sutent; Pfizer Pharmaceuticals Group, New York, NY), a receptor tyrosine kinase inhibitor with antiangiogenic activity that is approved for the treatment of advanced renal cell carcinoma. A 70-year-old woman diagnosed with renal cell carcinoma and bone metastasis was first treated with palliative nefrectomy and interferon plus vinblastine. Afterwards, she was enrolled in a phase II clinical trial with sunitinib malate (50 mg daily for 4 weeks every 6 weeks). Two weeks after starting the treatment, she was admitted to the hospital because of partial seizures affecting her left superior extremity, headache, and vision loss in the previous 2 days. The physical examination was normal except for cortical blindness and hypertension (170/100 mmHg). Blood tests, including coagulation study and gasometry, were unremarkable. Computed tomography of the brain showed symmetric subcortical hypodense lesions in the occipital lobes, consistent with reversible posterior leukoencephalopathy syndrome (RPLS). Magnetic resonance imaging was requested to rule out brain micrometastasis and it confirmed the findings of RPLS: symmetric hyperintense T2 signal involving bilateral occipital and parietal lobes in the subcortical distribution (Fig 1). Sunitinib administration was withheld and the patient was treated with anticonvulsants and antihypertensives. She recovered completely, was discharged in a few days and had a normal brain computed tomography performed 1 month later. The RPLS was initially reported by Hinchey et al. It is a clinical condition characterized by headache, seizures, impaired vision, acute hypertension, and typical magnetic resonance imaging and computed tomography imaging findings (symmetric and reversible). This syndrome has been described related to different circumstances: hypertensive encephalopathy, eclampsia, collagen vascular disorders (systemic lupus erythematosus, polyarteritis nodose, Behcet), trombotic thrombocytopenic purpura, acute porphyria, postcarotid endarterectomy, and Guillain-Barre syndrome. However, it is most commonly caused by immunosuppressive agents and cytotoxic drugs as cyclosporine A, tacrolimus, interferon alfa, cisplatin, cytarabine, IV immunoglobulins, L-asparaginase, and more recently by bevacizumab (antiangiogenic agent) and sorafenib (tyrosine kinase inhibitor). Its pathogenesis is not precisely known. It is postulated that the alterations can be related with the appearance of vasogenic edema because of elevation in the blood pressure (vasospasm) or because of toxic damage to blood-brain barrier or vascular endothelium. Sunitinib has a dual activity: extracellular action against vascular endothelial growth factor receptor (antiangiogenic) and intracellular action against tyrosine kinase domains, which can produce hypertension. In our case, the set of symptoms could be caused through both mechanisms.

PRIMARY SPINAL CORD NEURODEGENERATION IN LEBER HEREDITARY OPTIC NEUROPATHY

Leber hereditary optic neuropathy (LHON) is a subacute bilateral optic neuropathy that typically presents in young adult men due to one of three point mutations of mitochondrial DNA (mtDNA, m.11778G→A, m.3460G→A, or m.14484T→C) affecting genes coding for complex I of the mitochondrial respiratory chain. Most patients only develop visual failure, but some develop additional neurologic features, including a multiple sclerosis (MS)–like illness.1 ### Case report. A 39-year-old woman developed a progressive gait and sensory disturbance 5 years after subacute bilateral visual failure. She smoked cigarettes and took regular alcohol, multivitamins, and folic acid. In addition to the reduced visual acuity (counting fingers), central scotomata, and optic atrophy, she had horizontal gaze-evoked nystagmus and symmetric pyramidal-pattern lower limb weakness. Tendon reflexes were brisk, ankle jerks absent, and plantar responses extensor. Vibration sensation was absent below the hips and elbows. She had a macrocytosis (110 fL), vitamin B12 level of 769 ng/L (normal = 160 to 600 ng/L), red cell folate level of 342 μg/L (normal = 95 to 570 μg/L), and alanine transaminase level of 198 μ/L (normal <45 μ/L), with a normal serum creatine kinase. Urine toxicology, HIV, VDRL, and hepatitis serology were all negative. Vitamin E, very long chain fatty acids, autoantibodies, and immunoglobulins were normal. The CSF was acellular, with a normal protein, glucose, and no oligoclonal bands. Her 12-lead EKG was normal. Brain MRI revealed symmetric high T2 signal in the substantia nigra, pontine tegmentum, inferior olives, and dorsal columns of the spinal …

Type-2 Fuzzistics for Symmetric Interval Type-2 Fuzzy Sets: Part 1, Forward Problems

Interval type-2 fuzzy sets (T2 FS) play a central role in fuzzy sets as models for words and in engineering applications of T2 FSs. These fuzzy sets are characterized by their footprints of uncertainty (FOU), which in turn are characterized by their boundaries-upper and lower membership functions (MF). In this two-part paper, we focus on symmetric interval T2 FSs for which the centroid (which is an interval type-1 FS) provides a measure of its uncertainty. Intuitively, we anticipate that geometric properties about the FOU, such as its area and the center of gravities (centroids) of its upper and lower MFs, will be associated with the amount of uncertainty in such a T2 FS. The main purpose of this paper (Part 1) is to demonstrate that our intuition is correct and to quantify the centroid of a symmetric interval T2 FS, and consequently its uncertainty, with respect to such geometric properties. It is then possible, for the first time, to formulate and solve forward problems, i.e., to go from parametric interval T2 FS models to data with associated uncertainty bounds. We provide some solutions to such problems. These solutions are used in Part 2 to solve some inverse problems, i.e., to go from uncertain data to parametric interval T2 FS models (T2 fuzzistics)

Wilson's disease tremor is associated with magnetic resonance imaging lesions in basal ganglia structures

Wilson's disease (WD) is an inherited disorder of copper metabolism yielding marked motor deficits, including a severely disabling tremor. As a structural correlate of the disease, a variety of cerebral abnormalities has been revealed. However, the relationship between motor deficits and cerebral lesions has remained largely unknown. Here, we investigated correlation between WD tremor and cerebral magnetic resonance imaging (MRI) findings. Cerebral MRI abnormalities in 6 symptomatic WD patients were compared to findings in 6 asymptomatic WD patients and 10 healthy controls. All patients were treated with long-term copper chelating therapy. Motor symptoms including tremor were determined by Unified Parkinson's Disease Rating Scale Part III (UPDRS-III). MRI findings in symptomatic WD patients revealed significant symmetric T2*-weighted hypointense signal alterations of globus pallidus, head of the caudate nucleus, and substantia nigra. In contrast, MRI of asymptomatic WD patients did not differ from healthy controls. Correlation analysis revealed a significant positive correlation between MRI basal ganglia lesions and UPDRS action tremor score. Our results demonstrate for the first time that Wilson's disease tremor is associated with lesions of the globus pallidus, the head of the caudate nucleus, and the substantia nigra.

Bilateral wallerian degeneration of the middle cerebellar peduncles due to unilateral pontine infarction: A morphologic and spectroscopic study

We report the case of a patient with bilateral and symmetrical T2 hyperintensities of the middle cerebellar peduncles. She had a history of left pontine infarction 8 months before. This was attributed to bilateral Wallerian degeneration. MR Spectroscopy showed decreased N-acetyl aspartate/Creatine (NAA/Cr) ratio in the cerebellar peduncles as well as in the whole cerebellum. We hypothesize that this could reflect neuronal degeneration following a stroke.

Facial Dysmorphism in Leigh Syndrome With SURF-1 Mutation and COX Deficiency

Leigh syndrome is an inherited, progressive neurodegenerative disorder of infancy and childhood. Mutations in the nuclear SURF-1 gene are specifically associated with cytochrome C oxidase-deficient Leigh syndrome. This report describes two patients with similar facial features. One of them was a 2(1/2)-year-old male, and the other was a 3-year-old male with a mutation in SURF-1 gene and facial dysmorphism including frontal bossing, brachycephaly, hypertrichosis, lateral displacement of inner canthi, esotropia, maxillary hypoplasia, hypertrophic gums, irregularly placed teeth, upturned nostril, low-set big ears, and retrognathi. The first patient's magnetic resonance imaging at 15 months of age indicated mild symmetric T2 prolongation involving the subthalamic nuclei. His second magnetic resonance imaging at 2 years old revealed a symmetric T2 prolongation involving the subthalamic nuclei, substantia nigra, and medulla lesions. In the second child, at the age of 2 the first magnetic resonance imaging documented heavy brainstem and subthalamic nuclei involvement. A second magnetic resonance imaging, performed when he was 3 years old, revealed diffuse involvement of the substantia nigra and hyperintense lesions of the central tegmental tract in addition to previous lesions. Facial dysmorphism and magnetic resonance imaging findings, observed in these cases, can be specific findings in Leigh syndrome patients with cytochrome C oxidase deficiency. SURF-1 gene mutations must be particularly reviewed in such patients.

MRI features of neurodegenerative Langerhans cell histiocytosis

CNS complications of LCH include "space occupying" lesions corresponding to histiocytic granulomas and "neurodegenerative" presentation (ND-LCH) characterized by a progressive cerebellar ataxia. Studies analyzing specifically the MRI presentation of ND-LCH are scarce. We present here the MRIs of 13 patients registered as isolated ND-LCH. Posterior fossa was involved in 12 patients (92%), showing a symmetrical T2 hyperintensity of the cerebellar white matter areas in seven cases with a circumscribed T1 hyperintensity of the dentate nuclei in five cases, definite hyperintense T2 areas in the adjacent pontine tegmentum white matter in nine cases associated with a hyperintensity of the pontine pyramidal tracts in four cases. A cerebellar atrophy was noted in eight cases. The supratentorial region was involved in 11 patients, showing T2 hyperintense lesions in the cerebral white matter in eight cases and a discrete symmetrical T1 hyperintense signal in the globus pallidus in eight patients. A diffuse cortical atrophy was present in three cases and a marked focal atrophy of the corpus callosum in three cases. This series allows us to establish a not previously reported evocative semeiologic MR presentation to precisely orientate to the diagnosis of the pure neurodegenerative form of LCH.

Neurobrucellosis presenting as leukoencephalopathy: the role of cytotoxic T lymphocytes.

A 65-year-old man developed a leukoencephalopathy associated with neurobrucellosis. The disease followed a 15-month progressive course with neurologic symptoms, and magnetic resonance imaging revealed bilateral symmetrical T2 signal hyperintensities in the white matter. Biopsy of the cerebral cortex and white matter was significant for nongranulomatous meningoencephalitis with reactive microgliosis and astrogliosis. The inflammatory infiltrate was predominantly composed of T lymphocytes, including numerous cytotoxic T cells. There was no evidence of significant myelin destruction. No organisms were detected microscopically, but elevated immunoglobulin G titers to Brucella were found in the cerebrospinal fluid. An abscess formed at the biopsy site, and Brucella melitensis was cultured from abscess contents. Neurobrucellosis is difficult to diagnose outside endemic regions and is associated with leukoencephalopathy-like pathology. Cytotoxic T lymphocytes and microglia activation play an immunopathogenic role in this rare disease.

Neurobrucellosis Presenting as Leukoencephalopathy: The Role of Cytotoxic T Lymphocytes

A 65-year-old man developed a leukoencephalopathy associated with neurobrucellosis. The disease followed a 15-month progressive course with neurologic symptoms, and magnetic resonance imaging revealed bilateral symmetrical T2 signal hyperintensities in the white matter. Biopsy of the cerebral cortex and white matter was significant for nongranulomatous meningoencephalitis with reactive microgliosis and astrogliosis. The inflammatory infiltrate was predominantly composed of T lymphocytes, including numerous cytotoxic T cells. There was no evidence of significant myelin destruction. No organisms were detected microscopically, but elevated immunoglobulin G titers to Brucella were found in the cerebrospinal fluid. An abscess formed at the biopsy site, and Brucella melitensis was cultured from abscess contents. Neurobrucellosis is difficult to diagnose outside endemic regions and is associated with leukoencephalopathy-like pathology. Cytotoxic T lymphocytes and microglia activation play an immunopathogenic role in this rare disease.

DENSEST CIRCLE PACKING ON THE FLAT TORUS

Melissen [1] considered packings of k congruent circles in the symmetric flat torus T 2 = [0, 1)2 and determined the largest possible radius for k ≤ 4. In the present paper the analogous problem is studied for an arbitrary asymmetric torus T′2 = [0,b) × [0,a), 0 < a ≤ b and the maximal radius is found again for k ≤ 4.

Recovering a centred convex body from the areas of its shadows: a stability estimate

The main result of this paper is an estimate of the Hausdorff distance between two centrally symmetric bodies T1 and T2 of R3 by the L2 -norm of A(T1; z) — A(T2; z). Here A(Ti; z), i=1, 2, is the area of the orthogonal projection of Ti in the direction z.

High-Speed Spiral-Scan Echo Planar NMR Imaging-I

An improved echo planar high-speed imaging technique using spiral scan is presented and experimental advantages are discussed. This proposed spiral-scan echo planar imaging (SEPI) technique employs two linearly increasing sinusoidal gradient fields, which results in a spiral trajectory in the spatial frequency domain (k-domain) that covers the entire frequency domain uniformly. The advantages of the method are: 1) circularly symmetric T2 weighting, resulting in a circularly symmetric point spread function in the image domain; 2) elimination of discontinuities in gradient waveforms which in turn will reduce initial transient as well as steady-state distortions; and 3) effective rapid spiral-scan from dc to high frequency in a continuous fashion, which ensures multiple pulsing with interlacing for further resolution improvement without T2 decay image degradation. Some preliminary experimental results will be presented and further possible improvements suggested.

Method for measuring vibrational temperatures in CO2gasdynamic lasers

A method is developed for measuring the vibrational temperatures of the asymmetric vibration mode T3 and both symmetric modes T2 of the CO2 molecules under gasdynamic laser resonator conditions. The method involves simultaneous measurement of the gain at the wavelength 10.6μ and the spontaneous emission intensity in the 4.3μ band of carbon dioxide using the vibrational-rotational band theory in the calculations. The results of measurements of the vibrational temperatures T3 and T2 in a supersonic stream of 0.05CO2 + O.O5N2 + 0.2CO + 0.7He laser active mixture are presented and the errors of the method are analyzed.

Spectra of tetrahedral complexes of transition metals. Jahn–Teller effect in the tetrabromoferrate(III) ion

The single-crystal spectra of RFeBr4(R = 4-ethylpyridinium, Me4N+, Me3NH+, Me2NH2+, and MeNH3+) have been recorded at room temperature and ca.80 K. The fine structure resolvable in one transition has been analysed as vibrational progressions of non-totally symmetric t2 modes. The consequences of this observation are discussed in terms of a Jahn–Teller distortion of the excited electronic state. It is shown that a consistent assignment of the excited states is possible with the aid of a crystal field energy calculation. The spin–orbit splittings of the lowest-lying excited quartet and doublet states are calculated from the Tanabe–Sugano–Schroeder–Tree matrices. It is suggested that the Jahn–Teller effect is responsible for a quenching of the expected spin–orbit splittings. Finally, the spectral differences between the isoelectronic MnBr42– and FeBr4– complexes are discussed.

Breast-feeding

<b>BACKGROUND AND PURPOSE:</b> MR imaging features of metronidazole-induced encephalopathy (MIE) have not been fully established. This study was undertaken to determine the topographic distributions and diffusion-weighted imaging (DWI) findings of MIE. <b>MATERIALS AND METHODS:</b> We retrospectively evaluated the initial MR images (<i>n</i> = 7), including DWI (<i>n</i> = 5), and follow-up MR images (<i>n</i> = 4) after drug discontinuation in 7 patents with clinically diagnosed MIE. The topographic distributions of lesions were evaluated on MR images, and DWI signal intensities and apparent diffusion coefficient (ADC) values of the lesions were assessed. <b>RESULTS:</b> MR images demonstrated bilateral symmetric T2 hyperintense lesions in the cerebellar dentate nucleus (<i>n</i> = 7), midbrain (<i>n</i> = 7), dorsal pons (<i>n</i> = 6), medulla (<i>n</i> = 4), corpus callosum (<i>n</i> = 4), and cerebral white matter (<i>n</i> = 1). Brain stem lesions involved the following: tectum (<i>n</i> = 5), tegmentum (<i>n</i> = 4), red nucleus (<i>n</i> = 3) of the midbrain, vestibular nucleus (<i>n</i> = 6), and a focal tegmental lesion involving the superior olivary nucleus (<i>n</i> = 6) and abducens nucleus (<i>n</i> = 4) of the pons and vestibular nucleus (<i>n</i> = 4) and inferior olivary nucleus (<i>n</i> = 1) of the medulla. DWI (<i>n</i> = 5) showed isointensity or hyperintensity of lesions, and the decreased ADC value was found only in the corpus callosum lesions (<i>n</i> = 2). All detected lesions were completely reversible at follow-up except for the single corpus callosum lesion with an initial low ADC value. <b>CONCLUSION:</b> Brain lesions were typically located at the cerebellar dentate nucleus, midbrain, dorsal pons, medulla, and splenium of the corpus callosum. According to DWI, most of the lesions in MIE probably corresponded to areas of vasogenic edema, whereas only some of them, located in the corpus callosum, corresponded to cytotoxic edema.