An magnetic resonance imaging T2*‐weighted sequence at short echo time to detect putaminal hypointensity in Parkinsonisms

At 1.5 T, T2*‐weighted gradient echo (GE) sequences are more sensitive in revealing mineral deposition in the basal ganglia than standard T2 weighted sequences. T2*‐weighted GE sequences, however, may detect putaminal hypointensities either in patients affected by parkinsonian syndromes or in healthy subjects. The aim of this study was to identify the magnetic resonance imaging (MRI) T2*‐weighted sequence which more specifically detected putaminal hypointensities differentiating atypical parkinsonian syndromes from Parkinson's disease (PD) and control subjects. In a sample of 38 healthy subjects, we performed three T2*‐weighted GE sequences at increasing time echo (TE; TE = 15 millisecond, TE = 25 millisecond, and echoplanar at TE = 40 millisecond; T2* sequences study). The sequence not showing any putaminal abnormality in the healthy subjects was then used to assess putaminal signal intensity in 189 patients with PD, 20 patients with multiple system atrophy (MSA), 41 patients with progressive supranuclear palsy (PSP), and in 150 age and sex‐matched control subjects. In the T2* sequences study, the T2*‐weighted TE = 15 (T2*/15) did not show any putaminal abnormalities in the healthy subjects. This sequence detected putaminal hypointensities in a significantly higher proportion of patients with MSA (35%, P < 0.05) and PSP (24.4%, P < 0.05) than in patients with PD (5.3%), but in none of the controls. The sensitivity of putaminal hypointensity in T2*/15 sequence was 25.4% for PD, 43.9% for PSP, and 55% for MSA versus controls whereas the specificity was 93.2% for all groups. Despite the suboptimal sensitivity, the high specificity of the T2*/15 sequence performed on routine MRI suggests its usefulness in clinical practice for identifying putaminal hypointensities associated with parkinsonian disorders. © 2010 Movement Disorder Society     

低场FLAIR技术在急性脊髓炎中的诊断价值

目的 探讨快速液体衰减反转恢复(FLAIR)技术在急性脊髓炎中的应用价值. 方法 用0.5T超导磁共振(MR)机对52例健康者和33例急性脊髓炎患者行MR检查,扫描序列为TlM.T2WI,FLAIR序列,33例患者中23例作了T1WI增强扫描,比较FLAIR和TSE-T2WI两种序列对病灶的显示能力. 结果 33例患者33处病灶,FLAIR发现病灶33处,检出率100%,TSE-T2WI发现病灶23处.检出率69.7%:在显示病灶边缘情况方面,FLAIR显示清楚者32例,T2WI显示清楚者13例.在发现病灶及显示病灶边缘方面两者差异有统计学意义(P<0.01). 结论 FLAIR技术在脊髓炎的诊断中有较高的临床应用价值.应作为本病检查的常规方法.     

Diffusion-weighted MRI differentiates the Parkinson variant of multiple system atrophy from PD

OBJECTIVE AND BACKGROUND: Routine MRI as well as MR volumetry and MRS have been shown to contribute to the differential diagnosis of the Parkinson variant of multiple system atrophy (MSA-P) and PD. However, it is currently unknown whether diffusion-weighted imaging (DWI) discriminates these disorders. METHODS: Ten patients with MSA-P (mean age, 64 years) were studied, 11 with PD (mean age, 64 years), and seven healthy volunteers (mean age, 59 years) matched for age and disease duration. Regional apparent diffusion coefficients (rADC) were determined in different brain regions including basal ganglia, gray matter, white matter, substantia nigra, and pons. RESULTS: Patients with MSA-P had higher putaminal rADC (median 0.791 x 10(3)/mm(2)/s) than both patients with PD (median 0.698 x 10(3)/mm(2)/s, p < 0.001) and healthy volunteers (median 0.727 x 10(3)/mm(2)/s, p < 0.001). There were no significant differences in putaminal rADC between patients with PD and healthy volunteers. Moreover, none of the putaminal rADC values in the PD and control group surpassed the lowest value in the MSA-P group. There were no significant group differences in the rADC values in other brain regions such as pons, substantia nigra, globus pallidus, caudate nucleus, thalamus, or gray and white matter. Putaminal rADC values correlated significantly with Unified PD Rating Scale OFF scores in patients with MSA as measured by the Spearman rank test. CONCLUSION: DWI, even if measured in the slice direction only, is able to discriminate MSA-P and both patients with PD and healthy volunteers on the basis of putaminal rADC values. The increased putaminal rADC values in Parkinson variant of multiple system atrophy are likely to reflect ongoing striatal degeneration, whereas most neuropathologic studies reveal intact striatum in PD. Diffusion-weighted imaging may represent a useful diagnostic tool that can provide additional support for a diagnosis of Parkinson variant of multiple system atrophy.     

Use of the Putamen/Caudate Volume Ratio for Early Differentiation between Parkinsonian Variant of Multiple System Atrophy and Parkinson Disease

Background and purpose

Neuropathological studies have demonstrated that multiple system atrophy (MSA) produces selective atrophy of the putamen with sparing of the caudate nucleus, while both structures are spared in idiopathic Parkinson''s disease (PD). In this study we evaluated the clinical efficacy of using putaminal atrophy in brain MRI to differentiate MSA and PD.

Methods

We measured the putamen/caudate volume ratio on brain MRI in 24 patients with MSA and 21 patients with PD. Two clinicians who were blinded to the patients'' diagnoses and to each other''s assessments measured the volume ratio using a computer program.

Results

The measured volume ratios of the two investigators were highly correlated (r=0.72, p<0.0001). The volume ratio was significantly lower in MSA (1.29±0.28) than PD (1.91±0.29, p<0.0001). Setting an arbitrary cutoff ratio of 1.6 resulted in about 90% of patients with MSA falling into the group with a lower ratio, whereas more than 80% of patients with PD belonged to the other group.

Conclusions

The present results demonstrate that putaminal atrophy in MSA as measured on brain MRI represents an effective tool for differentiating MSA from PD.     

Retrospective case-analysis of the magnetic resonance imaging characteristics in the brain of patients with Wilson disease

BACKGROUND:Wilson disease (WD)damages liver,brain,kidney,cornea and nervous system severely.It is manifested in four ways:brain,liver,kidney and bone muscle.Whether or not magnetic resonance imagling (MRI)can clearly display the diseased region and range in brain of patient with WD,which provides imageological evidence for clinical practice,is unclear.OBJECTIVE:To observe the charactedstics of MRI of brain in patient with SD,and analyze the correlation of diseased region with clinical symptoms.DESIGN:Retrospective case-analysis.SETTING:Department of Radiology,Second Hospital Affiliated to the General Hospital of Chinese PLA.PARTICIPANTS:Thirty-one patients,including 18 males and 13 females,with WD admitted to the Department of Neurology,Second Hospital Affiliated to the General Hospital of Chinese PLA between January 1999and December 2005 were retrieved.The involved patients presented serum copper oxidase (sCP) activity decreasling and/or caruloplasmin Ievel decreasling and/or urinary copper content increasling;typical extrapyramidal symptoms and/or physical sign;abnormality showed by slit-lamp examination,Kayser-Fleischer rling positive.METHODS:①All the involved patients underwent MRI examination.A GE 1.5T imagling equipment was used.Spin-echo sequence was adopted to perform T2 and T1-weighed image at transverse axis level.Partial cases subjected to head scannling at coronal and/or sagittal level.Gd-DTPA With dosage of 0.1 mmol/kg was the strongest in 4 cases.②MRI characteristics of patients with dliferent clinical symptoms were observed.MAIN OUTCOME MEASURES:MRI detection results of patients with WD and MRI characteristics of patients with different clinical symptoms.RESULTS:Thirty-one patients with WD participated in the result analysis.①Imageological examination results:WD lnvolved many regions in the brain:dorsal caudate putamen(n=28),thalamencephalon(n=25),mesencaphalon(n=25),globus pallidus(n=23),pons(n=21),posterlor limb of intemal capsule(n=16),dentate nucleus(n=16),caudata nucleus(n=15)and cerebral cortex(n=11).MRI presented hypo-intensity signal on T2-weighted image and T1-weighted image or isointensity signal on T1-weighted image in 24 patients,characteristic hypo-intensity signal of globus pallidus in 4 patients,mixed signal of hyper-and hypo-intensity in 2 patients,hypo-intensity signal of globus pallidus,pars anterior pedunculi carebd and pontine tegmentum on T1-weighted image in 1 patient.Pathological changes distdbuted in symmetry and focus of infection mostly presented mottling,lamellar or strip.Different degrses of cerebral cortex atrophy,especially subtentodal cerebellar atrophy,ware found in 20 patients.Four patients subjected to enhancement scannling,but no clear imaqling was found.③MRI characteristics of patients with different symptoms:Abnormal signal of dorsal caudate putamen was found in 28 patients with dystonia,21 patients with dysarthda and 16 patients with bradykinesia;Abnormal signal of mesencaphalon was found in 22 patients with trepidation,among which,18 presented abnormal signal of pons;Abnormal signal of caudate nucleus and lenticular nucleus was found in 15 patients with dysphagia;Abnormal signal of dentate nucleus was found in 16 patients with carebellar ataxia;Different degrees of changes in cerebral atrophy were found in 14 patients with detedoratling memory and dementia.CONCLUSION:MRI can clearly display the characteristics of diseased regions in brain of patient with WD.Diseased regions reflected by MRI have obvious differences in patients with different clinical neurosigns.     

Nontraumatic intracerebral hemorrhage in young adults

We reviewed our experience with 72 patients, aged 15 to 45 years, who were hospitalized for nontraumatic intracerebral hemorrhages (ICHs) between 1978 and 1985. Evaluation included arteriography in 61 patients. Computed tomography demonstrated 41 lobar, 11 putaminal, four thalamic, four pontine, four intraventricular, two caudate, two midbrain, two cerebellar, one globus pallidum, and one corpus callosum hemorrhage. Forty-three patients, with either progressive neurologic deterioration, arteriovenous malformations (AVMs), or saccular aneurysms underwent surgery. The overall in-hospital survival, including those patients treated medically, was 87.5%. A presumed cause for the ICH was found in 55 (76.4%) patients. The main causes were ruptured arteriovenous malformations (21), hypertension (11), ruptured saccular aneurysms (seven), and sympathomimetic drug abuse (five). Surgical explorations demonstrated a necrotizing angiitis in one patient and arteriovenous malformations in two patients who had negative arteriograms. Young patients with nontraumatic ICHs represent a heterogeneous group. A cause can be established in most patients. Arteriovenous malformations account for less than one third of the hemorrhages in young adults, and other causes should be sought.     

Magnetic resonance imaging and brain-stem auditory evoked potentials in neuro-Behcet's disease

We studied central nervous system lesions in patients with neuro-Behcet's disease using magnetic resonance imaging (MRI) of the brain and recording of brain-stem auditory evoked potentials (BAEPs). MRI revealed abnormal findings in seven of eight patients. MRI studies demonstrated extensive regions with high intensity signal in the brain stem and/or basal ganglia on T2-weighted images obtained during the acute stage of the disease in three patients. One of these patients had a strongly gadolinum-enhanced round lesion in the lower pons. In four of the other five patients with chronic disease, brain-stem atrophy was observed on T1-weighted images. Atrophic changes were more severe in the brain stem than in the cerebellum. Abnormal BAEPs were observed in three patients and consisted of prolongation of interpeak latency of waves III-V and defects of wave III or V. Abnormal BAEPs were recorded in patients with severe inflammatory changes or progression of atrophic changes in the brain stem. Our findings show that MRI and BAEPs are useful in detecting the presence and assessing the degree of neurological involvement in patients with neuro-Behcet's disease.     

Effect of dexamethasone on tumorous brain edema--changes in regional cerebral blood flow and glucose utilization

An experimental brain tumor was produced by implanting a piece of A.A. ascites tumor into the parietal brain of rat. Local cerebral blood flow (LCBF) and glucose utilization (LCGU) were determined in this model with 14C-iodoantipyrine and 14C-deoxyglucose quantitative autoradiographic methods, respectively, to investigate the change of blood flow and glucose metabolism and the effect of dexamethasone in the brain with tumor. LCBF and LCGU in the peritumoral brain tissue were reduced 75% and 60%, respectively, compared with the values of the control. In the ipsilateral frontal and occipital cortical areas far from the tumor, 50% and 45% reduction of LCBF, respectively, was observed. More than 30% reduction of LCGU was seen in the same areas. In the caudate and corpus callosum ipsilateral to the tumor, LCBF was diminished 25% and 40%, respectively. LCGU was not significantly changed in these areas. No significant changes of LCBF and LCGU were observed in the contralateral hemisphere. In the dexamethasone-treated animal, the reduction of LCBF was less in all areas where it was reduced in the untreated animal. In the peritumoral brain tissue, LCBF was significantly higher compared to that of the untreated group, and 80% of the normal level. In the ipsilateral frontal and occipital cortical areas, caudate and corpus callosum, LCBF was about the same as that of the control group. In the animal treated with dexamethasone, quantitative analysis of LCGU could not be made because of high glucose levels in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of the pathology of cerebral white matter with post-mortem magnetic resonance imaging (MRI) in the elderly brain

White matter lesions (WML) on magnetic resonance imaging (MRI) brain scans are associated with ageing. They are unrelated to specific disorders, and their impact on cognitive and other brain functions is poorly characterized. Pathological studies often omit systematic survey of WML because of the need to study multiple full coronal tissue blocks, and uncertainty over the significance of lesions identified in periventricular and deep subcortical regions. Post-mortem MRI provides a means of mapping WML but the sensitivity and specificity of the method are unresolved. In this study post-mortem MRI of WML in fixed brain slices was compared with pathology in 33 brains donated to the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). This study shows that MRI detection of WML was less sensitive than pathology: periventricaular lesions (PVL) sensitivity = 95% (87-99%), specificity = 71% (44-90%); deep subcortical lesions (DSCL) sensitivity = 86% (79-93%), specificity = 80% (72-88%). False negative MRI was associated with milder pathology, but lesions detected by myelin attenuation alone showed both microglial and endothelial activation. Therefore post-mortem MRI of formalin-fixed brain slices is a reliable method to obtain systematic data on the severity and distribution of cerebral white matter disease, and appears to detect those WML most likely to have clinical impact.     

The anatomy of aphasia revisited

OBJECTIVE: To determine lesion locations associated with the various types of aphasic disorders in patients with stroke. BACKGROUND: The anatomy of aphasia has been challenged by several recent studies. Discrepancies are likely to be due to methodologic issues. METHODS: We examined 107 patients with a standardized aphasia battery and MRI. Three examiners blinded to the clinical data rated signal abnormalities in 69 predetermined regions of interest. The statistical procedure used classification tree testing, which selected regions associated with each aphasic disorder. RESULTS: 1) Nonfluent aphasia depended on the presence of frontal or putaminal lesions; 2) repetition disorder on insula-external capsule lesions; 3) comprehension disorder on posterior lesions of the temporal gyri; 4) phonemic paraphasia on external capsule lesions extending either to the posterior part of the temporal lobe or to the internal capsule; 5) verbal paraphasia on temporal or caudate lesions; and 6) perseveration on caudate lesions. These analyses correctly classified 67% to 94% of patients. CONCLUSIONS: Lesion location is the main determinant of aphasic disorders at the acute stage. Most clinical-radiologic correlations supported the classic anatomy of aphasia.     

MR序列优化组合在创伤性脑损伤的诊断价值

目的分析MR诊断创伤性脑损伤(TBI)的价值,探讨TBI患者MR一站式诊断的可行性。方法对260例TBI病例进行MR序列组合扫描,包括小角度激发快速梯度回波序列(FLASH)、流动衰减反转恢复序列(FLAIR)、自旋回波(SE)T1WI、快速自旋回波(TSE)T2WI,比较MR序列组合和CT对各种类型TBI诊断的差异。结果脑实质内出血61例,MR显示61例,CT显示53例;硬膜下出血55例,MR显示55例,CT显示49例;硬膜外出血45例,MR显示45例,CT显示40例;脑挫(裂)伤35例,MR显示35例,CT显示25例;蛛网膜下腔出血35例,MR显示31例,CT显示33例;弥漫性轴索损伤29例,MR显示29例,CT显示5例。MR序列组合准确显示病变256例,CT为209例,两者差异有极显著统计学意义(P0.01),MR序列组合总体诊断敏感性高于CT。结论 MR序列组合(FLASH\FLAIR\T1WI\T2WI)诊断创伤性脑损伤明显优于CT,可列为TBI常规检查方法,实行TBI一站式诊断。     

MRI T2 shortening ('black T2') in multiple sclerosis: frequency, location, and clinical correlation

Abnormal iron deposition occurs in the brains of patients with multiple sclerosis (MS) and may cause MRI T2 shortening ('black T2'; BT2). The frequency, distribution and clinical significance of BT2 in MS is unknown. Analysis of brain MRI scans of 114 MS patients showed BT2 in thalamus (n = 65; 57%), putamen (n = 48; 42%), caudate (n = 27; 24%) and Rolandic cortex (n = 9; 8%). BT2 was significantly related to longer disease duration and advancing neurological disability. Wheelchair-bound patients had worse BT2 in thalamus (p < 0.05), putamen (p < 0.001) and Rolandic cortex (p < 0.05). Patients with secondary progressive disease (n = 34) had worse BT2 in thalamus, putamen and caudate (all p < 0.05) than those with relapsing remitting disease (n = 80). BT2 is proposed as a clinically relevant finding relating to neuronal degeneration in MS.     

ATP13A2 mutations (PARK9) cause neurodegeneration with brain iron accumulation

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     

Putaminal magnetic resonance imaging features at various magnetic field strengths in multiple system atrophy

We delineated the effects of magnetic field strength on signal intensities to facilitate the specific findings of multiple system atrophy (MSA). Fifteen patients with probable MSA were imaged by 0.35T fast spin‐echo (FSE), 1.5T FSE, and 3.0T FSE using a consistent protocol, testing all field strengths on the same day. Sixty patients with probable Parkinson's disease (PD) also underwent imaging. Moderate or marked hyperintensity at the dorsolateral outer putaminal margin, hyperintensity of the putaminal body, hypointensity relative to the globus pallidus at the dorsolateral putaminal margin, and infratentorial signal changes were evaluated as specific findings for MSA. As the field strength increased, the occurrence of hyperintensity both at the dorsolateral outer putaminal margin and of the putaminal body decreased, while the occurrence of hypointensity at the dorsolateral putaminal margin increased in MSA. The occurrence of uniform mild hyperintensity of the outer putaminal margin was evident in 7% at 0.35T, 40% at 1.5T, and 47% at 3.0T in MSA and in 5% at 0.35T, 60% at 1.5T, and 75% at 3.0T in PD. However, no PD patients showed hyperintensity at the dorsolateral outer putaminal margin and that of the putaminal body. Putaminal magnetic resonance imaging (MRI) findings in MSA were altered considerably by magnetic field strength. The severity and distribution of signal changes are important for assessing putaminal MRI findings in MSA. © 2010 Movement Disorders Society     

Role of dopaminergic treatment in dopamine receptor down-regulation in advanced Parkinson disease: a positron emission tomographic study

BACKGROUND: In patients with advanced Parkinson disease (PD) who are undergoing long-term treatment with a dopaminergic medication, a down-regulation of striatal dopamine D2 receptor expression has been demonstrated and interpreted as a consequence of either the disease itself or dopaminergic drug administration. OBJECTIVE: To compare, using positron emission tomography, the striatal binding of raclopride carbon C 11, a dopamine D2 receptor ligand, in PD patients who completely discontinued dopaminergic therapy (off drug) with that in PD patients who continued receiving dopaminergic therapy (on drug) after undergoing subthalamic nucleus stimulation. MAIN OUTCOME MEASURES: The positron emission tomographic data were acquired in off-stimulation and, for 12 hours, off-medication conditions. Five off-drug PD patients, 7 on-drug PD patients, and 8 healthy subjects participated. RESULTS: In off-drug PD patients, the putaminal raclopride C 11 binding was 24% higher than in on-drug PD patients. The same tendency was noted for the caudate nucleus, but was not significant (P=.07). Compared with control subjects, the putaminal raclopride C 11 binding was increased by 21% in off-drug and was normal in on-drug PD patients. Compared with controls, the caudate raclopride C 11 binding was reduced by 23% in on-drug and was normal in off-drug PD patients. Further analysis using statistical parametric mapping showed a significant increase of binding bilaterally in the caudate nucleus and putamen in off-drug compared with on-drug PD patients (P=.002 at cluster level). CONCLUSIONS: The down-regulation of dopamine D2 receptors probably relates to the long-term and intermittent administration of dopaminergic treatments rather than to disease progression. This phenomenon is reversed by the complete withdrawal of dopaminergic drugs. Furthermore, an up-regulation of putaminal dopamine D2 receptors is demonstrated in late-stage PD after dopaminergic drug withdrawal.     

Early post-operative seizures after burr-hole drainage for chronic subdural hematoma: correlation with brain CT findings.

The incidence of seizures in patients undergoing burr-hole crainiostomy with closed-system drainage for chronic subdural hematoma (CSDH) is low. The post-operative use of anticonvulsants is, thus, controversial. In this study, we tried to correlate pre-operative computed tomographic (CT) appearance of the CSDH with the need for post-operative seizure prophylaxis. From April 1998 to November 2001, 128 cases of CSDH surgically treated at our hospital were studied. All patients underwent burr-hole craniostomy with closed system drainage. All CSDHs were classified as low-density, isodense, and mixed-density lesions according to CT findings. The incidence of early post-operative seizures (within 3 weeks of surgery) among all patients was 5.4% (7/128). In the subgroups by lesion density, the incidences were 6.2% (1/16) in the low-density group, 2.4% (2/83) in the isodense group, and 13.7% (4/29) in the mixed-density group (all p < 0.05). The mean age among the seven patients (five males and two females) who had seizures was 71 years. The locations of the CSDHs among the 128 patients were the left side of the brain in 53 (41.4%) patients, right side in 45 (35.2%), and bilateral in 30 (23.4%) patients. Among the seven patients who suffered from post-operative seizures, five (71.4%) had left side CSDHs, one (14.2%) had a right side CSDH, and one (14.2%) had bilateral CSDHs. We concluded that the post-operative seizure rate appeared high in the group with mixed-density type lesions on CT, and in those with left unilateral CSDH. We suggest the use of prophylactic anticonvulsants for patients with mixed-density lesions on pre-operative CT.     

Deficits of neuronal glutamatergic markers in the caudate nucleus in schizophrenia

Abnormal glutamate neurotransmission has been implicated in the pathophysiology of schizophrenia. In the present study we investigated two potential neuronal glutamatergic markers, the Excitatory Amino Acid Transporter 3 (EAAT3) and the Vesicular Glutamate Transporter 1 (VGluT1), in post-mortem striatal tissue from control subjects and from subjects with schizophrenia (n = 15 per group). We also investigated the possible influence of chronic antipsychotic administration (typical and atypical) on striatal VGluT1 expression in the rat brain. We found deficits in EAAT3 in all striatal regions examined in schizophrenia when compared to controls. Following correction for confounding factors (post-mortem interval), these deficits only remained significant in the caudate nucleus (p = 0.019). We also found significant deficits in VGluT1 in the caudate nucleus (p = 0.009) in schizophrenia. There were no significant differences in VGluT1 in the striatum of antipsychotic treated rats when compared to their vehicle treated controls. The data provides additional evidence for a glutamatergic synaptic pathology in the caudate nucleus in schizophrenia and may reflect a loss of glutamatergic cortico-striatal pathways. The absence of an effect of antipsychotic administration on VGluT1 indicates that the deficits in schizophrenia are unlikely to be a consequence of pharmacotherapy and thus likely to be a correlate of the disease process.     

Basal ganglia alterations and brain atrophy in Huntington's disease depicted by transcranial real time sonography

OBJECTIVES AND METHODS: Transcranial real time sonography (TCS) was applied to 49 patients with Huntington's disease and 39 control subjects to visualise alterations in the echotexture of the basal ganglia. For comparison T1 weighted, T2 weighted, and fast spin echo MRI was performed in 12 patients with Huntington's disease with and in nine patients without alterations of the basal ganglia echotexture as detected by TCS and T1 weighted, T2 weighted, and fast spin echo MRI. Furthermore, the widths of the frontal horns, third ventricle, and the lateral ventricles were depicted in TCS examinations and correlations examined with corresponding CT slices. RESULTS: Eighteen out of 45 (40%) of the patients with Huntington's disease with adequate insonation conditions showed hyperechogenic lesions of at least one basal ganglia region. In 12 patients TCS depicted hyperechogenic lesions of the substantia nigra; in six patients the head of the caudate nucleus was affected. The lentiform nucleus (n=3) and the thalamus (n=0) were less often affected or spared. Hyperechogenic lesions were significantly more frequent in patients with Huntington's disease than in 39 control subjects, who had alterations of the echotexture in 12.8% (4/39) of the examinations. The number of CAG repeats and the clinical status correlated with the identification of hyperechogenic lesions of the substantia nigra (p<0.01). Hyperechogenic lesions of the caudate nucleus were associated with an increased signal intensity in T2 weighted MR images (p<0.05). All TCS parameters indicating brain atrophy correlated with CT findings (p<0.0001). CONCLUSIONS: TCS detects primarily abnormalities of the caudate nucleus and substantia nigra in Huntington's disease. These changes in the echotexture may represent degenerative changes in the basal ganglia matrix and are partially associated with CAG repeat expansion and the severity of clinical findings.     

Magnetic resonance imaging in partial epilepsy: additional abnormalities shown with the fluid attenuated inversion recovery (FLAIR) pulse sequence.

Thirty six patients with a history of partial epilepsy had MRI of the brain performed with conventional T1 and T2 weighted pulse sequences as well as the fluid attenuated inversion recovery (FLAIR) sequence. Abnormalities were found in 20 cases (56%), in whom there were 25 lesions or groups of lesions. Twenty four of these lesions were more conspicuous with the FLAIR sequence than with any of the conventional sequences. In 11 of these 20 cases, lesions thought to be of aetiological importance were only seen with the FLAIR sequence. In eight this was a solitary lesion. In the other three, an additional and apparently significant lesion (or lesions) was only seen with the FLAIR sequence when another lesion had been identified with both conventional and FLAIR sequences. The 11 additional lesions or groups of lesions were seen in the hippocampus, amygdala, cortex, or subcortical and periventricular regions. No lesion was found with any pulse sequence in 16 (44%) of the original group of 36 patients. In the eight cases where a lesion was seen only with the FLAIR sequence, localisation was concordant with the electroclinical features. Two of the eight patients with solitary lesions seen only on the FLAIR sequence underwent surgery, after which there was pathological confirmation of the abnormality identified with imaging. In one patient with a congenital cavernoma, the primary lesion was best seen with a contrast enhanced T1 weighted spin echo sequence. In this selected series, the FLAIR sequence increased the yield of MRI examinations of the brain by 30%.