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Brain MRI (brain + mri)
Selected AbstractsPolymicrogyria in monozygous twins and an elder siblingDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 7 2003Po-Cheng Hung MD Monozygous twin births have been associated with brain lesions such as hydranencephaly, multicystic encephalomalacia, and porencephaly. Prenatal circulatory injury has been considered to be the cause. Polymicrogyria is rare but has been reported in autopsied cases. The sibship in this case report, comprising monozygotic male twins and their elder sister from the same non-consanguineous parents, all had global developmental delay. Brain MRI showed polymicrogyria. We suggest that, apart from circulatory compromise, genetic etiology must be implicated as the cause of polymicrogyria. [source] CADASIL: underdiagnosed in psychiatric patients?ACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2005T. Leyhe Objective:, Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is exclusively related to symptoms of the central nervous system. Retrospectively in up to 15% the initial presentation is psychiatric disturbances. In these cases the diagnosis often is delayed or missed. Method:, Two cases of CADASIL diagnosed in a psychiatric hospital are presented. Results:, Both patients were admitted to the gerontopsychiatric department (one because of a suicidal attempt and a depressive episode, the other because of cognitive decline and progressive personal neglect). Brain magnetic resonance imaging (MRI) showed severe leukoencephalopathy in the absence of cardiovascular risk factors. In both cases, diagnosis of CADASIL was made by the identification of specific granular osmiophilic material in skin biopsies. Conclusion:, Brain MRI should be performed in all cases of late onset of severe psychiatric symptoms. CADASIL should be considered as a possible differential diagnosis whenever a marked leukoencephalopathy is detectable. Diagnosis can be verified by taking a skin biopsy or by specific genetic testing. [source] Cytologic feature by squash preparation of pineal parenchyma tumor of intermediate differentiationDIAGNOSTIC CYTOPATHOLOGY, Issue 10 2008Keiji Shimada M.D., Ph.D. Abstract Pineal parenchyma tumor of intermediate differentiation (PPTID) is a very rare intracranial tumor, and pathological investigation limited to immunohistological and ultrastructural analyses have been published to date. Although intraoperative cytology is one of the important approaches for initial diagnosis in brain tumors, no or little studies on cellular morphology of PPTID have been demonstrated due to its rarity. We report here cytological features of PPTID obtained from stereotactic surgical specimens in a case of 27-year-old female manifested by dizziness and diplopia. Brain MRI revealed an unhomogeneously enhanced, large-sized tumor (56 × 52 × 60 mm) mainly located in the pineal region expanding from the midbrain to superior portion of the cerebellum and the fourth ventricle. Squash cytology showed increased nucleocytoplasmic ratio, hyperchromatic nuclei, and small rosette-like cell cluster but cellular pleomorphism was mild to moderate and necrotic background was not observed. Histology showed high cellularity, moderate nuclear atypia, and small rosette formation but neither bizarre tumor cells nor necrosis was present. Mitotic counts were very low (less than 1 per 10 high-power fields) and the MIB-1 labeling index was relatively high (10.1%). Tumor cells were immunohistochemically positive for neural markers such as synaptophysin, neurospecific enolase but not for glial fibrillary acidic protein or S-100. In some parts, cells were strongly reactive for neurofilament protein. Taken together, we made a final diagnosis of PPTID. This is the first presentation of cytological analysis by squash preparation that gives an important clue to accurate diagnosis of pineal parenchymal tumor and to understand its malignant potential. Diagn. Cytopathol. 2008;36:749,753. © 2008 Wiley-Liss, Inc. [source] Movement-Induced Focal Motor Seizures and Choreoathetosis As- sociated with Nonketotic Hyperglycemia: A Case ReportEPILEPSIA, Issue 2000Hisashi Tanaka Case Report: We report the case of a diabetic woman who developed right-sided reflex seizures and bilateral choreoathetosis during an episode of nonketotic hyperglycemia. The patient was a 67-year-old woman with a 14-year history of HCV-related liver cirrhosis who experienced polydipsia and polyuria in January 1998. She began to have episodes of abnormal hyperkinetic movements of the right upper extremity and tonic-clonic seizures in the right arm triggered by voluntary movements of right or bilateral arms in the beginning of March 1998. The seizures increased in frequency and consequently left her disabled. She was admitted to our hospital with complaints of these abnormal motor phenomena on March 9, 1998. Neurological examinations revealed that she was alert, well-oriented, and that cranial nerve functions were normal. Slight motor weakness of the right upper limb and deep tendon hyporeflexes were observed in all extremities. Sensations and cerebellar functions were intact. Choreic or athetotic involuntary movements were seen in the bilateral upper limbs and neck. These involuntary movements were increased by voluntary movement or posturing of the upper limbs. The focal tonic-clonic seizures were easily triggered by voluntary movements such as knotting a cord. This seizure suddenly began by tonic movements in the right upper limb and gradually progressed to the right hemi-face and neck without loss of consciousness. The average duration of seizures was about one minute. The laboratory data demonstrated mild leukocytopenia, thrombocytopenia, hepatic dysfunction, and hyperglycemia without ketosis. Fasting blood glucose was 41 I mg/dl, and HbAlc was 14.5%. Blood ammonia was within normal levels. Cranial CT revealed no abnormalities. Brain MRI on T I-weighted images demonstrated bilateral high signal intensity in the putamen. An interictal EEG revealed a symmetrical slow background activity of 7,8 Hz. An ictal EEG recording showed a 2.5 4 Hz irregular sharp and slow wave discharge in the bilateral frontal-central regions. Treatment with carbamazepine was ineffective for the seizures. However, the seizures completely disappeared after the administration of insulin on March 17. Under good control of the hyperglycemia, the abnormal involuntary movements decreased gradually and then completely disappeared; the patient became neurologically asymptomatic by March 30. The follow-tip EEG demonstrated 9-Hz alpha background activity without any epileptic discharges. Conclusions: Nonketotic hyperglycemia has been rarely reported to cause stimulus-induced seizures or hyperkinetic involuntary movements such as hemichorea-ballism. To our knowledge, this is the first reported case of both induced seizures and involuntary movements simultaneously caused by hyperglycemia. Movement-induced seizures and choreoathetoid movements in this patient can be considered to result from transiently-increased activity in the basal ganglia and/or cerebral cortex associated with metaholic disorders. [source] Clinical Applications of Functional Brain MRIEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2009K. A. Jellinger No abstract is available for this article. [source] Brain MRI in late-onset multiple sclerosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2005J. de Seze Multiple sclerosis (MS) with clinical onset after 50 years of age is unusual (between 1 and 6%) and is frequently misdiagnosed. Furthermore, brain magnetic resonance imaging (MRI) abnormalities are frequently observed in subjects over 50 years of age. The aim of this study was to describe brain MRI in late-onset MS to evaluate the sensitivity and specificity of radiological MS criteria in patients aged over 50 years. We evaluated the brain MRI of 20 patients with onset of MS after 50 years of age. We compared these MRI with 26 controls matched for age, sex and vascular risk factors. MRI were blindly analysed by two neuroradiologists according to Paty et al.'s [Neurology38 (1988) 180] criteria, Fazekas et al.'s [Neurology38 (1988) 1822] criteria and Barkhof et al.'s [Brain120 (1997) 2059] criteria. The mean age at MRI scanning was 58 years. Sensitivity was 90% for Paty et al.'s criteria, 80% for Fazekas et al.'s criteria and 85% for Barkhof et al.'s criteria. Specificity was 54% for Paty et al.'s criteria, 69% for Fazekas et al.'s criteria and 65% for Barkhof et al.'s criteria. Barkhof et al.'s criteria are less specific in older patients than in young patients. We suggest that spinal cord MRI and cerebrospinal fluid analysis should be systematically performed in suspected late-onset MS in order to increase the specificity of the diagnosis. [source] Reversible Cytotoxic Edema in a Cirrhotic Patient Following TIPSJOURNAL OF NEUROIMAGING, Issue 4 2009James R. Babington MD ABSTRACT The authors report the magnetic resonance imaging (MRI) findings in a 52-year-old man with cirrhosis from chronic hepatitis C who developed episodic acute hepatic encephalopathy Type C following placement of transjugular intrahepatic portosystemic shunt (TIPS). Brain MRI revealed hyperintense T2 signal and restricted diffusion distributed through the cerebral cortex. The patient's mentation improved with treatment of his hyperammonemia. Brain MRI performed 5 months later revealed diffuse cerebral atrophy and new areas of hyperintense T2 signal in the cerebral white matter. The cortical signal abnormalities and low apparent diffusion coefficient values on the initial MRI resolved with exception of a mild amount of hyperintense FLAIR signal in the cingulate cortex. Acute hepatic encephalopathy following portosystemic shunting,either from placement of TIPS or from development of spontaneous shunts,is a widely recognized complication of portal hypertension and cirrhosis. We report MRI findings of reversible cytotoxic edema in a patient with acute hepatic encephalopathy following placement of TIPS. [source] Cerebral and Oculorhinal Manifestations of a Limited Form of Wegener's Granulomatosis With c-ANCA,Associated VasculitisJOURNAL OF NEUROIMAGING, Issue 1 2001Peterus Thajeb MD ABSTRACT The authors report on cerebral and oculorhinal manifestations in a patient with a cytoplasmic pattern of antineutrophil cytoplasmic autoantibody (c-ANCA),associated vasculitis. Recurrent Tolosa-Hunt syndrome, cavernous sinus syndrome, Raeder's paratrigeminal neuralgia, and seizures were the major clinical manifestations. Brain MRI showed localized enhancing lesions initially in the cavernous sinus and later in the convexity pachymeninges. The lesions disappeared following 9 months of oral prednisolone (15 mg/day) and cyclophosphamide (100 mg/day) therapy. The presence of c-ANCA, demonstration of vasculitis, and depositions of immunoglobulin G (IgG) and fibrinogen in the vessel walls of pachymeninges of the patient confirmed an immune-mediated cause of the vasculitis. Cranial pathology without renal and pulmonary involvement suggests a variant of Wegener's granulomatosis, which is called the "limited" form of Wegener's granulomatosis. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 84JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003V Donadio The aim of the study is to determine the site of autonomic lesion in a patient with Holmes-Adie Syndrome (HAS) who subsequently developed generalized anhydrosis. We describe a 38-year-old woman who from age 33 showed a right pupil larger than the left and from age 34 complained of focal and, a year later, generalized anhydrosis. Neurological examination showed absent tendon reflexes and right mydriatic pupil. Brain MRI, EEG, motor and sensory conduction studies were normal. Serologic screening for autoimmune disease was negative. To determine the site of the autonomic lesion the patient underwent the following investigations: pupillary tests with a diluted solution of pilocarpine (0.062%) and adrenaline (0.1%); cardiovascular reflexes; thermoregulatory sweat test (TST); circadian rhythm of body core temperature (CRT°); sympathetic skin response (SSR); microneurography recording of skin sympathetic activity (SSA) from median and peroneal nerves, and muscle sympathetic activity (MSA) from peroneal nerve; skin biopsy to evaluated the eccrine glands. Pupillary tests showed postganglionic parasympathetic and sympathetic denervation only of the right pupil. TST showed complete anhydrosis, SSR and SSA were absent and skin biopsy revealed normal morphology of the eccrine glands with hypotrophy of their structures. These results indicated a lesion of the postganglionic skin sympathetic fibers. Mechanisms for heat loss and conservation, cardiovascular reflexes and MSA were normal excluding a hypothalamic dysfunction or a more diffuse involvement of the autonomic nervous system. In conclusion, our patient showed a HAS associated with generalized anhydrosis and the autonomic investigations suggested underlying postganglionic parasympathetic and sympathetic autonomic lesions. [source] AUTOMIC FAILURE AND NORMAL PRESSURE HYDROCEPHALUS IN A PATIENT WITH CHRONIC DEMYELINATING INFLAMMATORY NEUROPATHYJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002M. Laurà A 75-year-old man with HCV hepatitis developed at the age of 70 presented with rest and action tremor localized at both hands and progressive cognitive impairment with memory loss. Four years later he begun to complain of progressive fatigue, occasional falls, numbness at the extremities and orthostatic hypotension. One month after admission, he rapidly worsened with inability to walk, mainly because of autonomic failure. Neurological examination revealed gait disturbances, including a wide base of support and short stride, slurred speech, reduction of upward gaze, rest and action tremor at both hands, intrinsic hand muscle and anterior tibialis muscle wasting and weakness on both sides, absent deep tendon reflexes, loss of vibration sense at lower limbs, and bilateral pes cavus. Routine laboratory studies, autoantibodies, thyroid function, neoplastic markers and immunoelectrophoresis were normal. Cryoglobulins were absent, whereas CSF protein content was increased (142 mg/dl). Autonomic nervous system investigation detected severe orthostatic hypotension. Nerve conduction studies showed absent sensory potentials and a marked reduction of compound motor action potential amplitudes and of motor conduction velocities. A sural nerve biopsy revealed remarkable onion bulb-like changes, endoneurial and perivascular infiltrations of inflammatory cells. Psychometric tests showed mild cognitive impairment. Brain MRI was consistent with normotensive hydrocephalus. The findings indicated the presence of chronic inflammatory demyelinating polyneuropathy, autonomic nervous system involvement and normal pressure hydrocephalus. A condition of multiple system atrophy (MSA) might be taken into account, even if somatic peripheral nerve involvement may rarely occur in MSA. Moreover the normal pressure hydrocephalus could be due to the high protein content in CSF (Fukatsu R et al., 1997). [source] ATP13A2 mutations (PARK9) cause neurodegeneration with brain iron accumulation,MOVEMENT DISORDERS, Issue 8 2010Susanne A. Schneider MD Abstract Kufor Rakeb disease (KRD, PARK9) is an autosomal recessive extrapyramidal-pyramidal syndrome with generalized brain atrophy due to ATP13A2 gene mutations. We report clinical details and investigational results focusing on radiological findings of a genetically-proven KRD case. Clinically, there was early onset levodopa-responsive dystonia-parkinsonism with pyramidal signs and eye movement abnormalities. Brain MRI revealed generalized atrophy and putaminal and caudate iron accumulation bilaterally. Our findings add KRD to the group of syndromes of neurodegeneration with brain iron accumulation (NBIA). KRD should be considered in patients with dystonia-parkinsonism with iron on brain imaging and we suggest classifying as NBIA type 3. © 2010 Movement Disorder Society [source] Adult T-cell lymphoma involving the leptomeninges associated with a spinal cord schwannomaNEUROPATHOLOGY, Issue 3 2001Toshiko Nagashima Adult T-cell lymphoma (ATL-L) developing initially in the meninges is rare. An autopsy case of ATL-L with an acute onset of meningitis and generalized lymphadenopathy in association with a cervical cord schwannoma is reported here. A 78-year-old woman with sensori-motor weakness of both arms over a 1-year period, developed febrile episodes and drowsiness with neck stiffness. Lumbar puncture revealed an increased protein content (161 mg/dL) and increased cell count (463/3) consisting of 99% of lymphocytes which contained atypical lymphocytes with multilobulated nuclei (,flower cells'), which are characteristic of ATL-L. Viral titers were positive only for HTLV-I antibodies (serum 3 640: CSF 3 16). Biopsy of an enlarged retroperitoneal lymph node revealed malignant lymphoma of the T-cell type. Brain MRI was negative, whereas an intradural extramedullary mass was found at the C4 level. With a diagnosis of ATL-L stage IV, chemotherapy was commenced, which was effective in reducing the generalized lymphadenopathy as well as the cervical mass and restoring the CSF findings to normality. The cervical cord mass was verified to be a solitary schwannoma, and ATL-L involvement was found not only in the leptomeninges, but also within the cervical cord schwannoma. [source] Etiologic yield of autistic spectrum disorders: A prospective studyAMERICAN JOURNAL OF MEDICAL GENETICS, Issue 1 2006Agatino Battaglia Abstract Studies addressing etiologic yield in childhood developmental disabilities have mainly looked at individuals with developmental delay/mental retardation. The few studies addressing the question of etiologic yield in patients with pervasive developmental disorders (PDDs) had a major drawback, in that the enrolled subjects were diagnosed as having the autistic spectrum disorders based only on history and clinical examination, and/or on unspecified instruments. In addition, only some of these patients underwent a complete laboratory evaluation. To investigate the etiologic yield of PDDs, we undertook a large prospective study on subjects selected according to very strict criteria and diagnosed as having PDD based on the present "gold standard" (ADI-R and ADOS-G), and a clinical diagnosis made by a child psychiatrist. Eighty-five (85) patients with PDD and their first degree relatives participated in this study. These patients were selected from a sample of 236 subjects who had received a clinical diagnosis of PDD at the Stella Maris Institute between March 2002 and 2005. Selection criteria for entering the study were: (1) a diagnosis of PDD (with exclusion of the Rett syndrome) confirmed after the administration of the ADI-R (autism diagnostic interview-revised) and the ADOS-G (autism diagnostic observation schedule-generic). In addition, a clinical diagnosis was made by the child psychiatrist, on the basis of presence or absence of DSM-IV symptoms of autism; (2) chronological age between 4 and 18 years; (3) IQ>30; (4) availability of both biologic parents. Patients, 65/85 (76.5%), had autism, 18/85 (21.2%) had PDD-NOS, and the remaining 2/85 (2.3%) had Asperger syndrome. Ages varied between 4 years 2 months and 12 years 5 months (mean 7.6 years), and there was a marked male preponderance (68/85). All subjects underwent various laboratory studies and neuroimaging. With respect to possible etiologic determination, a detailed history and physical examination in this group of patients with PDD was informative in 10.5% (9/85). HRB karyotype was diagnostic in one, and molecular fragile X studies in one child. Brain MRI was informative in two children (2.3%) with relative macrocrania but no neurological features; and EEG was helpful in one child, identifying a Landau,Kleffner disorder. Audiometry and brainstem auditory evoked potentials (BAEPs) showed a bilateral sensorineural loss in another child. Metabolic evaluation gave normal results in all subjects. The results suggest an evaluation paradigm with reference to etiologic determination for individuals with PDDs that does not presently justify metabolic or neuroimaging on a screening basis. Recurrence risk, treatment implications, and significant and long-lasting emotional relief for the parents suggest that serious consideration be given to clinical genetic examination, genetic testing, EEG study (during wakefulness and sleep), and audiometry, despite a relatively low yield. © 2006 Wiley-Liss, Inc. [source] Visual fields and optic disc morphology in very low birthweight adolescents examined with magnetic resonance imaging of the brainACTA OPHTHALMOLOGICA, Issue 8 2009Kerstin Hellgren Abstract. Purpose:, We aimed to evaluate visual fields (VFs) and optic disc morphology in very low birthweight (VLBW) adolescents compared with age- and gender-matched controls, and to relate the findings to magnetic resonance imaging (MRI) results. Methods:, Fifty-nine VLBW adolescents and 55 age- and gender-matched controls with normal birthweight were examined. Visual fields were tested using computerized rarebit perimetry (RB). Optic nerve and retinal vessel morphology were evaluated by digital image analysis of fundus photographs. Brain MRI was conducted in the VLBW subjects. Results:, Ten of the 57 VLBW subjects (p = 0.022) had subnormal VF results defined as a mean hit rate below the fifth percentile of the controls (i.e. < 89%). All of these also had significantly lower mean hit rates (p = 0.039) in the inferior hemifield. Sixteen of 57 (28%) VLBW subjects had white matter damage of immaturity (WMDI) on MRI. Six of 15 subjects with WMDI (who underwent VF testing) also had subnormal RB results, compared with four of 39 with normal MRI findings (p = 0.02). The mean neural retinal rim area was 9% smaller (p = 0.018) in the VLBW group than in the control group. The VLBW adolescents had a significantly higher index for tortuosity of arterioles than the controls (p < 0.001). Conclusions:, In the present study, 18% of all VLBW adolescents and 40% of those with WMDI had subnormal RB VF findings. The VLBW group had increased arterial tortuosity and a somewhat smaller (9%) mean neural retinal rim area than the control group. Thus sequels to VLBW appear to persist in adolescence. [source] Brain Abscess in an Adult With Atrial Septal DefectCLINICAL CARDIOLOGY, Issue 4 2010Chong Won Sung MD Brain abscess is a serious complication of congenital heart disease in children and adolescents. This association is rarely observed in adults. This article describes the case of a 41-year-old man who presented with altered mental status. Brain MRI showed a brain abscess at the left frontal lobe. The patient was successfully treated with surgical removal and appropriate antibiotics. Echocardiographic examination showed atrial septal defect (ASD) with bidirectional shunt. Transcatheter closure of ASD was carried out 6 months after neurosurgical treatment. We discuss the association of brain abscess and ASD. Copyright © 2010 Wiley Periodicals, Inc. [source] Magnetic resonance imaging at term and neuromotor outcome in preterm infantsACTA PAEDIATRICA, Issue 3 2000AM Valkama In order to evaluate the value of neonatal brain magnetic resonance imaging (MRI) for predicting neuromotor outcome in very low birthweight (VLBW) preterm infants, 51 such infants with gestational age <34 wk underwent brain MRI at term age. Myelination, parenchymal lesions (haemorrhage, leukomalacia, infarction, reduction of white matter), parenchymal lesions without subependymal haemorrhage, ventricular/brain ratios and widths of the extracerebral spaces were assessed. The MRI findings were compared with cranial ultrasound (US) performed at term. Infants' neuromotor development was followed up until 18 mo corrected age. Parenchymal lesions seen in MRI at term predicted cerebral palsy (CP) with 100% sensitivity and 79% specificity, the corresponding figures for US being 67% and 85%, respectively. Parenchymal lesions in MRI, excluding subependymal haemorrhages, predicted CP with a sensitivity of 82% and a specificity of 97%, the corresponding figures for US being 58% and 100%, respectively. Delayed myelination, ventricular/brain ratios and widths of the extracerebral spaces failed to predict CP. Term age is a good time for neuroradiological examinations in prematurely born high-risk infants. Parenchymal lesions seen in MRI are reliable predictors for CP. [source] Cognitive visual dysfunctions in preterm children with periventricular leukomalaciaDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 12 2009ELISA FAZZI MD PHD Aim, Cognitive visual dysfunctions (CVDs) reflect an impairment of the capacity to process visual information. The question of whether CVDs might be classifiable according to the nature and distribution of the underlying brain damage is an intriguing one in child neuropsychology. Method, We studied 22 children born preterm (12 males, 10 females; mean age at examination 8y, range 6,15y; mean gestational age 30wks, range 28,36wks) with periventricular leukomalacia, spastic diplegia, normal intelligence (mean Full-scale IQ 84; mean Verbal IQ 97; mean Performance IQ 74), and normal visual acuity, focusing on higher visual functions. Brain magnetic resonance images (MRI) were analysed to establish the presence of lesions along the primary optic pathway, in the occipitoparietal and occipitotemporal regions. Results, Most children displayed an uneven cognitive profile, with deficits in visual object recognition, visual imagery, visual,spatial skills, and visual memory, and sparing of visual associative abilities, non-verbal intelligence, and face and letter recognition. Conventional brain MRI did not document major alterations of parietal and temporal white matter, or cortical alteration of areas involved in visual associative functions. Interpretation, We suggest a widespread involvement of higher visual processing systems, involving both the ventral and dorsal streams, in preterm children with periventricular leukomalacia. The lack of major alterations on conventional MRI does not exclude the possibility of malfunctioning of higher visual processing systems, expressing itself through discrete CVDs. Possible mechanisms underlying these neuropsychological deficits are discussed. [source] Visual Function in Infants with West Syndrome: Correlation with EEG PatternsEPILEPSIA, Issue 7 2004Teresa Randò Summary:,Purpose: Several studies have reported behavioral and electrophysiological evidence of visual impairment during the active stage of West syndrome. The underlying mechanisms are, however, poorly understood, and little has been reported about the correlation between visual impairment, EEG patterns, and brain lesions. The aim of the study was to assess visual function at the onset of spasm and 2 months thereafter and relate visual findings to brain lesions and EEG features. Methods: Twenty-five infants with West syndrome were enrolled and studied with (a) a full clinical assessment including a battery of tests specifically designed to assess visual function, (b) a video-polygraphic study, and (c) brain magnetic resonance imaging (MRI). Besides brain neuroimaging and EEG comparison with visual function, an intra-EEG analysis was performed to investigate the possible relation of EEG patterns to fluctuating visual behavior (fixation and following). Results: Twenty-two children had at least one abnormal result on one or more of the tests assessing visual function at T0. Visual impairment at the spasm onset was related to the sleep disorganization rather than to the hypsarrhythmic pattern in awake EEG. After 2 months, both EEG features become significantly linked to visual function. Visual function improved in several cases after 2 months, in parallel with the seizure regression. No relation was found between EEG patterns and fluctuating visual behavior. Conclusions: The study supplies new evidence of the involvement of visual function in West syndrome. The presence of abnormal visual findings in infants without lesions on brain MRI suggests that visual abnormalities are due not only to brain injury but also to epileptic disorder per se. New insight is also provided into the possible mechanisms underlying clinical and EEG abnormalities. [source] Vasoconstriction as the Etiology of Hypercalcemia-induced SeizuresEPILEPSIA, Issue 5 2004Tsung-Hua Chen Summary: Purpose: Reversible cerebral vasoconstriction has been hypothesized to be the etiology of seizures due to hypercalcemia, but angiographic studies documenting vasoconstriction have not previously been available. Methods: We present a 43-year-old woman who had frequent seizures that later evolved to status epilepticus with marked hypercalcemia at the time of the seizures. Results: Magnetic resonance imaging (MRI) of the patient's brain revealed high signal changes in T2 -weighted imaging, fluorescence-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) over the bilateral occipital and thalamic areas. Cerebral angiography showed blood vessels narrowing, disappearing altogether over the right posterior cerebral artery (PCA) branch, which is compatible with vasoconstriction. Vasoconstriction caused the MRI high signal in the occipital area, which was associated with subsequent periodic lateralized epileptic discharges. The patient's clinical condition improved with management of seizures and hypercalcemia. A second brain MRI 2 weeks later revealed complete resolution of the high-signal lesions. Follow-up cerebral angiography study also showed total recovery of vasoconstriction. Conclusions: The sequence of events suggests the hypothesis that reversible cerebral vasoconstriction may play a role in hypercalcemia-induced seizures. [source] Differences in grey and white matter atrophy in amnestic mild cognitive impairment and mild Alzheimer's diseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2009M. L. F. Balthazar Background:, Grey matter (GM) atrophy has been demonstrated in amnestic mild cognitive impairment (aMCI) and mild Alzheimer's disease (AD), but the role of white matter (WM) atrophy has not been well characterized. Despite these findings, the validity of aMCI concept as prodromal AD has been questioned. Methods:, We performed brain MRI with voxel-based morphometry analysis in 48 subjects, aiming to evaluate the patterns of GM and WM atrophy amongst mild AD, aMCI and age-matched normal controls. Results:, Amnestic mild cognitive impairment GM atrophy was similarly distributed but less intense than that of mild AD group, mainly in thalami and parahippocampal gyri. There were no difference between aMCI and controls concerning WM atrophy. In the mild AD group, we found WM atrophy in periventricular areas, corpus callosum and WM adjacent to associative cortices. Discussion:, We demonstrated that aMCI might be considered a valid concept to detect very early AD pathology, since we found a close proximity in the pattern of atrophy. Also, we showed the involvement of WM in mild AD, but not in aMCI, suggesting a combination of Wallerian degeneration and microvascular ischaemic disease as a plausible additional pathological mechanism for the discrimination between MCI and AD. [source] Brain MRI in late-onset multiple sclerosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2005J. de Seze Multiple sclerosis (MS) with clinical onset after 50 years of age is unusual (between 1 and 6%) and is frequently misdiagnosed. Furthermore, brain magnetic resonance imaging (MRI) abnormalities are frequently observed in subjects over 50 years of age. The aim of this study was to describe brain MRI in late-onset MS to evaluate the sensitivity and specificity of radiological MS criteria in patients aged over 50 years. We evaluated the brain MRI of 20 patients with onset of MS after 50 years of age. We compared these MRI with 26 controls matched for age, sex and vascular risk factors. MRI were blindly analysed by two neuroradiologists according to Paty et al.'s [Neurology38 (1988) 180] criteria, Fazekas et al.'s [Neurology38 (1988) 1822] criteria and Barkhof et al.'s [Brain120 (1997) 2059] criteria. The mean age at MRI scanning was 58 years. Sensitivity was 90% for Paty et al.'s criteria, 80% for Fazekas et al.'s criteria and 85% for Barkhof et al.'s criteria. Specificity was 54% for Paty et al.'s criteria, 69% for Fazekas et al.'s criteria and 65% for Barkhof et al.'s criteria. Barkhof et al.'s criteria are less specific in older patients than in young patients. We suggest that spinal cord MRI and cerebrospinal fluid analysis should be systematically performed in suspected late-onset MS in order to increase the specificity of the diagnosis. [source] Brain Apparent Water Diffusion Coefficient Magnetic Resonance Image During a Prolonged Visual AuraHEADACHE, Issue 6 2010Robert Belvís MD (Headache 2010;50:1045-1049) Background., Reversible changes in brain magnetic resonance imaging (MRI) weighted in diffusion-weighted images (DWI) and apparent water diffusion coefficient (ADC) maps have been reported in acute stroke, epilepsy, eclampsia, and hypoglycemia, but they are contradictory regarding to migraine aura. Objective., A 41-year-old woman with known basilar migraine for 5 years consulted about a persistent visual aura (visual snow phenomenon) plus bilateral paresthesias in the extremities for 4 days. The headache was treated with success with 10 mg of wafer rizatriptan and 600 mg of ibuprophen. Methods., The neurologic and ophthalmologic examination were normal. An urgent brain MRI detected no lesions in T1, T2, fluid-attenuated inversion recovery, and DWI, but an abnormal signal appeared in the left occipital lobe in ADC and (r)ADC maps. The brain MRI angiography, carotid ultrasound study, transesophageal echocardiography, 24-hour cardiac Holter monitoring, and thrombophilia study were normal. Results., A new brain MRI 8 days after did not show any previous lesion in the same sequences. Conclusions., We present a patient with migraine and transitory abnormal signals in the ADC map of an occipital region during persistent visual aura. The clinical-radiological relationship is congruent. Some similar cases have showed these MRI signals during the aura, suggesting cytotoxic edema, without ischemic lesions in the MRI controls. Theses ADC images probably appear in complex auras. [source] Red Ear Syndrome and Migraine: Report of Eight CasesHEADACHE, Issue 2 2002Vincenzo Raieli MD We describe eight idiopathic cases of red ear syndrome in seven children and one adult. All were migraineurs with a history of paroxysmally painful and red ear, unilateral or alternating, in isolation or associated with migraine attacks. The reported duration of these episodes varied from 30 minutes to 1 hour. Neurologic examination, brain MRI and CT scans, and x-rays of the cervical spine were normal. The close temporal relationship between the "red ear episodes" and migraine attacks suggests an association between the two conditions. [source] Impact of cerebrovascular pathology on behavioural and neuropsychiatric symptoms in patients with Alzheimer's dementia: findings from a retrospective, naturalistic studyINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 7 2009A. Klugman Summary Aim:, Cerebrovascular disease (CVD) has been associated with depression and a host of neuropsychiatric conditions including dementia. This study assessed the relationship between cerebrovascular findings reported on MRI brain scans and neuropsychiatric symptoms (NPS) and behavioural problems in patients with Alzheimer's disease (AD). Methods:, Medical notes were retrospectively reviewed in patients undergoing brain MRI following referral for cognitive impairment to a memory clinic between January 2004 and June 2008. Patients with AD were graded into four categories of CVD severity based on neuroradiology reports and assessed for behavioural and NPS and activities of daily living using Neuropsychiatric Inventory (NPI), Geriatric Depression Scale (GDS) and Bristol Activities of Daily Living (BADL). Frontal lobe symptoms and parkinsonian features were also evaluated. Results:, Of the initial 232 patients who underwent MRI 72% were diagnosed with AD. 89% of AD patients had CVD findings reported on MRI. Moderate-to-severe CVD was present in 47% of patients. None of the AD patients satisfied a diagnosis of vascular dementia. There was no significant relationship observed between level of MRI CVD findings and scores on NPI (p = 0.57), GDS (p = 0.26) and BADL (p = 0.46). The level of CVD severity did not appear to influence frontal lobe and parkinsonian assessments (p = 0.60). Conclusion:, The contribution of CVD to the pathogenesis of various NPS is still debated. Our study, based on patients diagnosed with AD in a memory clinic setting, suggests that there is no relationship between the extent of CVD pathology and neuropsychiatric and behavioural measures in AD patients. Further prospective quantitative studies are needed to assess the role of CVD, if any, in neuropsychiatric and behavioural symptoms in AD. It is possible that the relatively small pathological contribution of CVD to the development of these symptoms is obscured by the effect of the wider neurodegeneration encountered in AD. [source] The Nutrition, Aging, and Memory in Elders (NAME) study: design and methods for a study of micronutrients and cognitive function in a homebound elderly populationINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 6 2006Tammy M. Scott Abstract Background Micronutrient status can affect cognitive function in the elderly; however, there is much to learn about the precise effects. Understanding mediating factors by which micronutrient status affects cognitive function would contribute to elders' quality of life and their ability to remain in the home. Objectives The Nutrition, Aging, and Memory in Elders (NAME) Study is designed to advance the current level of knowledge by investigating potential mediating factors by which micronutrient status contributes to cognitive impairment and central nervous system abnormalities in the elderly. NAME targets homebound elders because they are understudied and particularly at risk for poor nutritional status. Methods Subjects are community-based elders aged 60 and older, recruited through area Aging Services Access Points. The NAME core data include demographics; neuropsychological testing and activities of daily living measures; food frequency, health and behavioral questionnaires; anthropometrics; gene status; plasma micronutrients, homocysteine, and other blood determinants. A neurological examination, psychiatric examination, and brain MRI and volumetric measurements are obtained from a sub-sample. Results Preliminary data from first 300 subjects are reported. These data show that the NAME protocol is feasible and that the enrolled subjects are racially diverse, at-risk, and had similar basic demographics to the population from which they were drawn. Conclusion The goal of the NAME study is to evaluate novel relationships between nutritional factors and cognitive impairment. These data may provide important information on potential new therapeutic strategies and supplementation standards for the elderly to maintain cognitive function and potentially reduce the public health costs of dementia. Copyright © 2006 John Wiley & Sons, Ltd. [source] MRI white matter hyperintensities, 1H-MR spectroscopy and cognitive function in geriatric depression: a comparison of early- and late-onset casesINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 12 2001Tetsuhito Murata Abstract Background and Objectives Geriatric depression is often thought to differ from that at other times of adulthood. Recently, several studies have shown that the incidence of white matter hyperintense lessions identified by brain MRI is higher in patients with geriatric depression than in healthy elderly subjects, but a consensus has not yet been reached on the relationship between the severity of white matter lesions and either cognitive impairment or depressive symptoms. Method Forty-seven patients aged 50 to 75 years with major depression were divided into two groups based on age at onset of depression: early-onset (<,50 years) group (20 patients; mean age, 62.7,±,6.7) and late-onset (,50 years) group (27 patients; mean age, 65.6,±,5.4). The severity of hyperintense white matter lesions on MRI was classified by region, then a proton magnetic resonance spectroscopy (1H-MRS) focusing on the white matter of the frontal lobes, multidimensional neuropsychological tests and evaluation of depressive symptoms were conducted. Results The severity of the deep white matter lesions, the deterioration of cognitive function related to subcortical/frontal brain system and clinician-rated depressive symptoms were all more pronounced in the late-onset group compared with those in the early-onset group. It was further observed that the more severe the deep white matter lesions, the lower the levels of N-acetylaspartate/creatine. With the age of onset as the covariate, the patients with moderate deep white matter lesions had more pronounced cognitive impairment and clinician-rated depressive symptoms than those with none and/or mild lesions. Conclusion These results suggest that subcortical/frontal type cognitive impairment and the persistence of depressive symptoms in geriatric depression is related to moderate deep white matter lesions more often complicated in the late-onset group. The 1H-MRS findings were suggested to be a useful indicator of neuronal/axonal loss in the white matter of the frontal lobes which precedes cognitive impairment. Copyright © 2001 John Wiley & Sons, Ltd. [source] Magnetic resonance images of the globus pallidus in patients with idiopathic portal hypertension: A quantitative analysis of the relationship between signal intensity and the grade of portosystemic shuntJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2006Takeshi Fukuzawa Abstract Background and Aim:, To elucidate a quantitative relationship between hyperintensity of the globus pallidus on T1-weighted magnetic resonance images (MRI) and portosystemic shunt (PSS) in portal hypertension. Methods:, Fifteen patients with idiopathic portal hypertension (IPH) and 44 patients with liver cirrhosis (LC) underwent brain MRI to asses signal intensity at the globus pallidus and Doppler sonography to examine the blood flow volume of PSS. Blood manganese (Mn) levels were examined in 36 patients and neuropsychological tests were performed in 15 patients without overt hepatic encephalopathy. Results:, Pallidal hyperintensity on MRI was more prominent in patients with IPH than in patients with LC. There was no correlation between MRI pallidal hyperintensity and the severity of liver dysfunction or hepatic encephalopathy. The grade of hyperintensity correlated well with the grade of PSS. The correlation was stronger in patients with IPH than in patients with LC. The plasma ammonia level and whole blood Mn level significantly correlated with MRI pallidal hyperintensity, but blood Mn level showed a stronger correlation than plasma ammonia. Conclusion:, Hyperintensity of the globus pallidus on T1-weighted MRI correlated with the development of PSS independent of liver cell function. This brain image should be an index of the grade of PSS rather than a landmark of chronic liver failure. [source] Progressive Cerebral Disease in Lymphomatoid Granulomatosis Causes Anterograde Amnesia and Neuropsychiatric DisorderJOURNAL OF NEUROIMAGING, Issue 2 2006Dominic A. Carone PhD ABSTRACT The authors report neuropsychological (NP) and serial quantitative magnetic resonance imaging (MRI) findings of a 29-year-old woman with lymphomatoid granulomatosis (LG). Disease course was characterized by acute psychosis, tremor, fever, seizures, and progressive cognitive impairment. At the time of symptom onset, brain MRI revealed mild lesion volume and normal parenchymal volume. This was followed by dramatic progression of brain lesions and atrophy over 2 years, at which point the patient expired. Atrophy was most prominent in the mesial temporal lobes. NP testing revealed marked amnesia and mild impairments in other cognitive domains. To our knowledge, this is the first recorded case of LG in which bilateral temporal lobe atrophy is evident and accompanied by anterograde amnesia. We speculate that temporal lobe atrophy was influenced by the established susceptibility of this region in various neurological diseases. [source] Computer-Assisted Magnetic Resonance Imaging Brain Morphometry in American Staffordshire Terriers with Cerebellar Cortical DegenerationJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2008D. Henke Background: Cerebellar cortical degeneration exists in American Staffordshire Terriers. Magnetic resonance imaging (MRI) can be suggestive, but a definitive diagnosis requires histopathology. Hypothesis: Computer-assisted MRI morphometry can be used to distinguish between American Staffordshire Terriers with or without cerebellar cortical degeneration. Animals: Normal American Staffordshire Terriers (n = 17) and those with clinical signs of cerebellar cortical degeneration (n = 14). Methods: This was a partly retrospective and partly prospective study. Causes of cerebellar disease were ruled out with brain MRI, cerebrospinal fluid (CSF) analysis, CBC, blood biochemistry, and clinical follow-up. On T2-weighted midsagittal MR images, the following parameters were calculated: size of the cerebellum relative to the entire brain, size of the CSF space surrounding the cerebellum relative to the cerebellum, and 2 threshold-dependent cerebellar CSF indices (with and without surrounding CSF). Results: Statistical analyses indicated a significantly lower relative cerebellar size (P < .001) and a larger relative cerebellar CSF space (P < .001) in dogs with cerebellar cortical degeneration. The measurement of relative cerebellar size could distinguish between affected and nonaffected dogs with a sensitivity and a specificity of 93 and 94%, respectively, using a cut-off of 13.3%. Using a cut-off of 12.8%, the measurement of relative CSF space could distinguish between both groups with a sensitivity of 93% and a specificity of 100%. There was a significant difference in 1 of the 2 CSF indices between affected and normal dogs. Conclusions and Clinical Importance: Relative cerebellar size and relative CSF space calculated from MRI are effective in American Staffordshire Terriers to differentiate between normal animals and those with cerebellar cortical degeneration. [source] Prospective real-time correction for arbitrary head motion using active markersMAGNETIC RESONANCE IN MEDICINE, Issue 4 2009Melvyn B. Ooi Abstract Patient motion during an MRI exam can result in major degradation of image quality, and is of increasing concern due to the aging population and its associated diseases. This work presents a general strategy for real-time, intraimage compensation of rigid-body motion that is compatible with multiple imaging sequences. Image quality improvements are established for structural brain MRI acquired during volunteer motion. A headband integrated with three active markers is secured to the forehead. Prospective correction is achieved by interleaving a rapid track-and-update module into the imaging sequence. For every repetition of this module, a short tracking pulse-sequence remeasures the marker positions; during head motion, the rigid-body transformation that realigns the markers to their initial positions is fed back to adaptively update the image-plane,maintaining it at a fixed orientation relative to the head,before the next imaging segment of k -space is acquired. In cases of extreme motion, corrupted lines of k -space are rejected and reacquired with the updated geometry. High-precision tracking measurements (0.01 mm) and corrections are accomplished in a temporal resolution (37 ms) suitable for real-time application. The correction package requires minimal additional hardware and is fully integrated into the standard user interface, promoting transferability to clinical practice. Magn Reson Med, 2009. © 2009 Wiley-Liss, Inc. [source] | |||||||||||||||||||||||||||||||