MR of the brain in mitochondrial myopathy.

PURPOSETo determine the spectrum of MR findings in patients with mitochondrial myopathy and correlate them with central nervous system symptoms and signs.METHODSWe performed a prospective evaluation of the MR findings of eight patients with mitochondrial myopathy (three with Kearns-Sayre syndrome and five with chronic progressive external ophthalmoplegia), six of whom had central nervous system symptoms or signs (ataxia, sensorineural hearing loss, or cognitive dysfunction).RESULTSAll six patients with neurologic symptoms or signs had multiple abnormal MR findings, whereas patients without neurologic symptoms had either normal MR findings (one patient) or the solitary finding of cortical atrophy (one patient). Abnormal MR findings consisted of cerebral cortical atrophy (seven patients), cerebellar atrophy (six patients), and hyperintense signal abnormalities on T2-weighted images within the cerebral white matter (three patients), cerebellar white matter (one patient), basal ganglia (three patients), brain stem (one patient), and thalamus (one patient). In two patients, the cerebral white matter signal abnormalities were primarily peripheral and involved the arcuate fibers. All patients with ataxia had abnormal cerebellar findings on MR imaging, but there was poor correlation between other neurologic features and MR findings.CONCLUSIONSCerebral and cerebellar atrophy are the most common MR findings in Kearns-Sayre syndrome and chronic progressive external ophthalmoplegia. White matter and deep gray nuclei abnormalities, presumed to result from the diffuse spongiform encephalopathy reported in these patients, can also be seen. Patients with abnormal neurologic findings typically have multiple abnormalities on MR imaging, which frequently do not correlate with specific symptoms.     

Effects of gadopentetate dimeglumine administration after osmotic blood-brain barrier disruption: toxicity and MR imaging findings

Osmotic blood-brain barrier disruption with intraarterial chemotherapy has been shown to be beneficial in the treatment of malignant brain tumors. Imaging blood-brain barrier disruption is necessary to document the extent and degree of disruption and to correlate disruption with drug delivery. The present study evaluated blood-brain barrier disruption with gadopentetate dimeglumine-enhanced MR imaging and the associated toxicity of gadopentetate dimeglumine administration. Blood-brain barrier disruption was performed in seven dogs for imaging analysis and 17 dogs for toxicity evaluation. In the absence of gadopentetate dimeglumine administration, blood-brain barrier disruption could not be imaged. Enhanced MR imaging with a gadopentetate dimeglumine dose of 0.1 mmol/kg provided good images of disruption at an imaging time of 3 hr after disruption. However, when gadopentetate dimeglumine was given intravenously in conjunction with osmotic blood-brain barrier disruption, there was a statistically significant (p = .02) dose-dependent increase in the frequency of seizures, with 50% of the animals who received 0.1 mmol/kg and 75% who received 0.2 mmol/kg developing delayed seizures. Our findings show that, as with ionized iodinated CT contrast agents, gadopentetate dimeglumine is associated with toxicity when used in conjunction with osmotic blood-brain barrier disruption in dogs. Such toxicity may be a contraindication to the use of gadopentetate dimeglumine for monitoring patients with osmotically induced disruption of the blood-brain barrier.     

MR of vasculitis-induced optic neuropathy.

PURPOSETo describe the MR characteristics of optic neuropathy caused by vasculitis.METHODSNine cases of optic neuropathy with diagnosis of vasculitis (six with systemic lupus erythematosis and one each with rheumatoid arthritis, Sjögren disease, and radiation vasculitis) were reviewed retrospectively. Patients were 31 to 62 years old, and all but one were women. All patients had MR imaging through the orbits and anterior visual pathways, five with fat suppression, with and without gadopentetate dimeglumine. Five patients also had MR imaging of the entire brain. The size and enhancement of various segments of the optic nerve and anterior visual pathways were studied.RESULTSMR imaging with contrast material showed enhancement and enlargement of segments of the optic nerves and/or chiasm in six of the nine patients (all but three with systemic lupus erythematosis). Enlargement of a segment of the anterior visual pathway never occurred without enhancement, but enhancement alone did occur in three cases. Of the five patients who had MR imaging of the whole brain, abnormalities were seen in three: periventricular hyperintensity in two and a lacunar infarct in one; none had vessel abnormalities.CONCLUSIONBecause the MR enhancement seen represents disruption of the blood-brain barrier within the optic nerve, MR imaging with gadopentetate dimeglumine and fat suppression should be performed to detect increased permeability of the blood-brain barrier in acute optic neuropathy.     

Imaging changes and cognitive outcome in primary CNS lymphoma after enhanced chemotherapy delivery

BACKGROUND AND PURPOSE: In children, MR imaging abnormalities consistent with leukoencephalopathy after treatment for hematologic malignancy do not correlate with neurologic dysfunction and are often overinterpreted with regard to clinical significance. We hypothesized that this would also be true in primary CNS lymphoma (PCNSL) patients who attained a complete response (CR) after treatment with chemotherapy and osmotic blood-brain barrier disruption (BBBD). We hypothesized that cognitive function loss measured after tissue diagnosis but before BBBD-enhanced chemotherapy could be correlated with brain changes visualized by imaging, whereas a correlation would not be present after therapy if the patient attained a complete tumor response, analogous to the findings in children. METHODS: Sixteen primary CNS lymphoma patients were followed after CR (no enhancing tumor) by using a methotrexate-based regimen. Neuropsychological (NP) cognitive testing and MR imaging or CT (when MR imaging was not available) were performed before treatment and at completion of the 12-month treatment for each patient. Thereafter, the same studies were available for nine of these 16 CR patients, who were followed for a median of 55 months. Zone I was defined as enhancing tumor, and zone II as surrounding abnormal MR T2 signal intensity or low-attenuation CT. The cognitive scores were converted to Z scores and the MR T2 signal intensity or CT low-attenuated changes were converted to a summary zone II abnormality score. RESULTS: A significant association between neurocognitive data and zone II abnormality was found at baseline after tissue diagnosis but before chemotherapy (r = -.55; P < .028), but no correlation existed at end of treatment. Imaging studies showed that seven patients developed a new T2 or low-attenuation abnormality by the end of treatment, whereas 15 patients showed a decrease, stable appearance, or complete resolution of their baseline zone II abnormality by end of treatment. Although cognitive loss compared with age-matched control subjects was common before starting therapy, by the end of treatment all patients' cognitive function improved significantly (P < .005). CONCLUSION: The current data suggest that neither enhanced chemotherapy delivery nor changes in MR imaging T2 signal intensity or CT low attenuation, in PCNSL patients who attained a CR, were associated with a decrease in cognitive function.     

Infantile-onset spinocerebellar ataxia: MR and CT findings.

PURPOSETo report the MR and CT findings in a hereditary disease, infantile-onset spinocerebellar ataxia (IOSCA).METHODSWe studied the brains of 17 patients with infantile-onset spinocerebellar ataxia with CT and/or MR to determine the presence of cerebellar and brain stem atrophy and parenchymal lesions.RESULTSCerebellar cortical atrophy was seen in 13 patients. The degree of atrophy correlated with increasing age and clinical deterioration. Brain stem atrophy was seen in 8 patients. It was never severe, and the basis pontis was not flattened even in the most severe cases. Hyperintense lesions were noted within the white matter of cerebellum, in the dentate nuclei, and in the middle cerebellar peduncles in 3 patients. The upper cervical cord was seen in 9 patients and showed mild to moderate atrophy in 4. The basal ganglia and cerebral hemispheres were normal, except in 2 patients transient cortical and subcortical lesions developed during episodes of status epilepticus; mild cortical brain atrophy subsequently developed.CONCLUSIONThe brain MR and CT findings of patients with infantile-onset spinocerebellar ataxia correspond to the neuropathologic entities of cerebellar cortical atrophy, olivopontocerebellar atrophy, and spinocerebellar atrophy. The appearance of the findings followed a uniform time sequence from cerebellar cortical atrophy in the early stage of the disease to olivopontocerebellar atrophy and spinocerebellar atrophy in the later stage. The severity of atrophy correlated with clinical deterioration.     

Subacute sclerosing panencephalitis: evaluation with CT and MR.

PURPOSETo evaluate the progression of CT and MR changes of the brain in subacute sclerosing panencephalitis (SSPE) as a basis for assessing the effects of different types of therapy.METHODSFifty-two patients with SSPE were examined, 44 with MR imaging and 42 with CT of the brain on one or more occasions. A total of 92 MR and 67 CT studies were performed.RESULTSCorrelation between the clinical status and the MR findings in admission was poor. Of 20 patients with clinically advanced disease, only 8 had marked MR abnormalities; 6 had normal or almost normal findings on MR examinations. Two of 4 patients with clinically mild disease had advanced MR changes. The progression of the MR findings appeared to follow a constant pattern. The earliest pathologic finding was focal, high-T2-intensity white matter changes; later atrophic changes followed. The atrophy lagged behind the white matter changes and was thus mild when white matter changes were moderate or severe. In the most advanced stage, when the patient was in a neurovegetative state, an almost total loss of white matter had usually taken place. At this stage, the corpus callosum was also thin. Basal ganglia changes, usually involving the putamina, were seen in one third of patients and cortical gray matter changes were seen in one fourth of patients examined with MR imaging. In 2 of 20 patients, MR changes regressed in parallel with clinical improvement following therapy, but in 5 patients clinical improvement was accompanied by progression of MR changes.CONCLUSIONThe progress of MR abnormalities seen in patients with SSPE seems to follow a constant pattern, but the severity of MR changes does not always correlate well with the clinical findings. Caution must therefore be used when evaluating the effects of therapy.     

MR of carcinoma-specific monoclonal antibody conjugated to monocrystalline iron oxide nanoparticles: the potential for noninvasive diagnosis.

PURPOSETo determine if tumor-specific monoclonal antibodies conjugated to superparamagnetic monocrystalline iron oxide nanoparticles can be used to yield specific diagnoses with the use of MR imaging.METHODSMonoclonal antibodies conjugated to monocrystalline iron oxide nanoparticles were given to nude rats with intracranial tumors either by intravenous injection, intraarterial injection with osmotic blood-brain barrier disruption, or direct intratumoral inoculation. Either L6, a tumor-specific antibody, or P-1.17, a control isotype-matched antibody, was used. Coronal T1-weighted, T2-weighted, and spoiled gradient-recalled acquisition in the steady state images were obtained before, 30 minutes after, 6 hours after, and 24 hours after injection.RESULTSIntravenous injection of greater than 2 mg of the tumor-specific antibody showed a specific pattern of enhancement of the tumors with the largest concentration of antibody in the area with the greatest density of tumor cells. The control antibody showed nonspecific changes. After intraarterial injection with barrier disruption to increase delivery globally or direct inoculation to increase delivery focally, no specific enhancement pattern was seen.CONCLUSIONMonoclonal antibodies conjugated with monocrystalline iron oxide particles may provide a method to obtain specific diagnoses with the use of MR imaging.     

Cerebrotendinous xanthomatosis (van Bogaert-Scherer-Epstein disease): CT and MR findings.

PURPOSETo describe the CT and MR findings in the brain and spinal cord of patients with cerebrotendinous xanthomatosis and to seek possible correlations between clinical, biochemical (cholestanol levels), and neuroimaging findings.METHODSTen patients with well-defined clinical and biochemical diagnoses of cerebrotendinous xanthomatosis were examined. Brain CT was performed in eight cases. In all patients MR was obtained using spin-echo and gradient-echo sequences. In eight patients spine MR was also performed.RESULTSNeuroradiologic findings included diffuse cerebral and cerebellar atrophy. In half the cases, atrophy of the brain stem and corpus callosum was also found. In the majority of patients cerebellar bilateral focal lesions and mild white matter signal alterations were present. Spinal cord MR did not show signal abnormalities or atrophy.CONCLUSIONSWe found cranial alterations in patients with severe neurologic impairment, but there was no correlation with cholestanol plasma levels. No spinal cord abnormalities were present.     

Cerebral visual impairment in periventricular leukomalacia: MR correlation.

PURPOSETo evaluate the involvement of central visual pathways in cases of periventricular leukomalacia, and to correlate the neuroradiologic findings with the degree of visual acuity.METHODSThe MR brain examinations of 27 preterm children affected by cerebral palsy resulting from periventricular leukomalacia and without significant ophthalmologic lesions were reviewed retrospectively to search for possible involvement of the optic radiations and/or of the calcarine cortex. The data were compared with the degree of visual acuity estimated by means of the Teller Acuity Cards test.RESULTSSeventeen (63%) of the 27 patients had cerebral visual impairment, which correlated strongly with MR lesions. Quantitative reduction and signal hyperintensity of the peritrigonal white matter and atrophy of the calcarine cortex were present in the more severe cases. In two blind patients, an altered MR signal was detected in the lateral geniculate bodies.CONCLUSIONThis study clearly establishes a relationship between specific MR findings and visual impairment in children with periventricular leukomalacia. The finding of hyperintensity in the lateral geniculate bodies was interpreted as an axonal reaction. MR imaging is useful for detecting potential visual impairment and for improving clinical diagnosis.     

MELAS syndrome: imaging and proton MR spectroscopic findings.

PURPOSETo evaluate imaging findings in MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, strokes) syndrome for the presence and location of infarctions and the presence of lactate.METHODSEight patients were studied with MR (n = 8) and CT (n = 2). One patient underwent single-photon emission CT with technetium 99m hexamethyl-propyleneamine oxime and one patient had conventional catheter angiography. One fixed brain was studied with MR imaging. Five patients underwent single volume proton MR spectroscopy. Imaging studies were evaluated for atrophy, edema, and infarctions. Proton MR spectroscopy was visually analyzed for presence or absence of lactate.RESULTSOne patient showed a cerebral infarction, and later a second distant infarction developed. One patient showed a transient area of cortical edema. Two patients had small nonspecific periventricular white matter abnormalities and one patient had diffuse white matter hyperintensities. Two patients had nonspecific MR abnormalities (probably age-related changes), and two had normal MR findings. None had basal ganglia involvement. Proton MR spectroscopy showed presence of lactate in one case with transient cortical edema; in two cases with nonspecific (probably age-related) brain findings; and in two patients with normal MR findings.CONCLUSIONSPatients with MELAS have a variety of MR findings. The fact that proton MR spectroscopy showed lactate in all five cases studied, regardless of MR findings, indicates that proton MR spectroscopy may be more sensitive in the detection of MELAS-associated abnormalities than MR imaging.     

Cerebral MR and CT imaging in Creutzfeldt-Jakob disease

Magnetic resonance (MR) imaging and CT of three patients with Creutzfeldt-Jakob disease (CJD) showed bilateral cortical atrophy and no apparent white matter changes. Serial examinations revealed the progressive nature of the atrophy, findings compatible with the patients' clinical deterioration. At autopsy some white matter abnormalities were detected in one patient 6 months after MR imaging. The available data suggest that the white matter abnormalities, if present, develop during the final stage of CJD.     

老年人血脑屏障通透性、缺血性脑白质高信号严重程度与认知功能的关系

 目的 探讨老年血脑屏障通透性、缺血性脑白质高信号(white matter hyperintensity,WMH)严重程度与认知功能的关系。方法 选择120例老年缺血性WMH患者为观察组,120例老年健康体检者为对照组。行MRI检查,比较两组血脑屏障通透性指标。根据Fazekas评分法将老年缺血性WMH患者分为三组:轻度(Fazekas评分为0~2分)、中度(Fazekas评分为3~4分)、重度(Fazekas评分为5~6分),比较不同WMH严重程度患者的血脑屏障通透性指标和认知功能水平,分析老年缺血性WMH患者血脑屏障通透性与WMH严重程度、认知功能的相关性。结果 观察组脑白质正常区的渗透转运速率、渗透曲线下面积均显著高于对照组(P<0.05)。轻、中、重度WMH组的渗透转运速率、渗透曲线下面积比较,差异均有统计学意义(P<0.05),从高至低依次为重度WMH组、中度WMH组、轻度WMH组。轻、中、重度WMH组的MMSE评分、MoCA评分比较,差异均有统计学意义(P<0.05),从高至低依次为轻度WMH组、中度WMH组、重度WMH组。老年缺血性WMH患者渗透转运速率、渗透曲线下面积与其WMH严重程度均呈正相关(P<0.05),与其MMSE评分、MoCA评分均呈负相关(P<0.05)。结论 老年缺血性WMH患者血脑屏障通透性随着WMH严重程度加重而增强,而血脑屏障通透性越强,认知功能损伤越严重。     

Neuroradiologic findings in children with mitochondrial disorders.

PURPOSEWe report the neuroradiologic findings in 25 children with various mitochondrial diseases.METHODSTwenty-two children with a mitochondrial disorder had MR imaging of the brain and three children had CT studies. In all cases, the diagnosis was based on examination of muscle morphology, analysis of oxygen consumption and respiratory chain enzyme activity in isolated muscle mitochondria, and analysis of rearrangements of the mitochondrial DNA.RESULTSFifteen patients were found to have the classical syndromes of mitochondrial diseases. Four children had Kearns-Sayre syndrome, but only one had the typical neuroradiologic findings of basal ganglia and brain stem lesions, T2 hyperintensity of the cerebral white matter, and cerebellar atrophy; the others had nonspecific or normal findings. Eight patients had Leigh syndrome, and all showed changes in the putamina. Involvement of the caudate nuclei, globus pallidi, thalami, and brain stem was common, and diffuse supratentorial white matter T2 hyperintensity was seen in two of these patients. Three patients had mitochondrial encephalopathy with lactic acidosis and strokelike episodes (MELAS), with infarctlike lesions that did not correspond to the vascular territories. Ten children with complex I or IV deficiencies and abnormal muscle morphology had nonspecific imaging findings, such as atrophy and abnormal or delayed myelination. One patient with combined complex I and IV deficiency had extensive white matter changes. None of the patients with clinical encephalopathy had normal findings.CONCLUSIONMR imaging is helpful in the diagnosis of the classical mitochondrial diseases; however, nonspecific findings are common.     

MR imaging findings in children with merosin-deficient congenital muscular dystrophy

BACKGROUND AND PURPOSE: Our purpose was to determine the brain MR imaging characteristics of merosin-deficient congenital muscular dystrophy in children. METHODS: We reviewed the MR imaging findings of the brain in three children with known merosin-deficient congenital muscular dystrophy to determine the presence of any cerebral or cerebellar abnormalities of development or abnormalities of the white matter. RESULTS: In all three patients, there was normal formation of the cerebrum, the cerebellum, and no evidence of neuronal migration anomalies. All three patients had abnormal white matter in the cerebrum, with sparing of the corpus callosum, internal capsule, cerebellum, and brain stem. CONCLUSION: MR imaging of the brain in children with merosin-deficient congenital muscular dystrophy reveals a consistent pattern of white matter abnormality. We postulate that disruption of the blood-brain barrier associated with merosin deficiency leads to increased water content, resulting in abnormal white matter signal intensity.     

Transient partial amnesia complicating cardiac and peripheral arteriography with nonionic contrast medium

The aim of this study was to present a case of disruption of the blood-brain barrier during the coronary and lower extremity angiographies with radiological and clinical findings. This condition was secondary to intraarterial use of a nonionic, monomeric contrast medium. A total of 450 cc contrast media was used. Computed tomography examination showed contrast enhancement of the right occipital and frontoparietal cortical regions, which returned to normal one day after. The patient also fully recovered from the neurological symptoms within 24 h. We discussed the possible mechanism for blood-brain barrier disruption in this case.

     

Cerebral MR in ophthalmoplegia plus.

PURPOSETo evaluate MR patterns in ophthalmoplegia plus and correlate them with clinical symptoms.METHODSMR was performed on a 1.5-T whole-body scanner with T2-weighted gradient-echo and spin-echo images. The retrospective analysis included 19 patients with clinically established diagnoses of ophthalmoplegia plus.RESULTSTwo types of cerebral MR abnormalities were found in ophthalmoplegia plus: brain atrophy and hyperintensities restricted to the white matter and basal ganglia, which appeared as either focal or diffuse areas of high signal intensity and were of strictly supratentorial location. No specific distribution was found. These findings differ markedly from infarction-like lesions found in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes.CONCLUSIONSMR is sensitive for the detection of central nervous system involvement in ophthalmoplegia plus, but findings are nonspecific. However, cerebral MR in ophthalmoplegia plus is different from other mitochondrial encephalomyopathies and underlines the clinical differentiation of mitochondrial encephalomyopathies.     

Leukoaraiosis: correlation of MR and CT findings with blood flow, atrophy, and cognition

Hypodense periventricular white-matter lesions detected by CT (leukoaraiosis) and high-intensity T2 signals detected by MR imaging were correlated with measurements of local cerebral blood flow (LCBF), cerebral atrophy, and cognitive performance. Subjects studied included elderly volunteers who were neurologically normal (n = 6), patients with chronic cerebral infarctions and intact cognition (n = 2), patients with multiinfarct dementia (n = 14), and patients with Alzheimer dementia (n = 9). Leukoaraiosis correlated with periventricular high-intensity lesions detected by MR, LCBF reductions, cognitive impairments, and cerebral atrophy. Moderate to severe leukoaraiosis was associated with LCBF reductions in the cortex, basal ganglia, and frontal white matter. Periventricular MR lesions correlated with cerebral atrophy but not with cognitive impairments or reductions in LCBF. The exquisite sensitivity of MR revealed small lesions that did not correlate with LCBF reductions and cognitive impairments. Remote subcortical white-matter lesions detected by MR did not correlate with periventricular MR lesions, leukoaraiosis, LCBF, cerebral atrophy, or cognitive performance, indicating little clinical relevance. We concluded that diffuse cerebral hypoperfusion, particularly in combination with the poor collateral circulation of white matter surrounding the lateral ventricles, is responsible for leukoaraiosis.     

Osmotic blood-brain barrier disruption: CT and radionuclide imaging.

PURPOSETo compare CT and radionuclide imaging of osmotic blood-brain barrier disruption. To develop a quantitative method for imaging osmotic blood-brain barrier disruption and to see if iopamidol could be safely given intravenously in conjunction with blood-brain barrier disruption.METHODSForty-five blood-brain barrier disruption procedures were imaged with CT and radionuclide scans. The scans were evaluated with visual and quantitative scales. Patients were observed for adverse effects after blood-brain barrier disruption.RESULTSThere was a 4% rate of seizures in this study. There was good agreement between visual CT and radionuclide grading systems. Quantitative methods to grade disruption did not add useful information to visual interpretations.CONCLUSIONSNonionic iodine-based contrast medium has a lower incidence of seizures when injected intravenously in conjunction with osmotic blood-brain barrier disruption than ionic contrast material. Contrast-enhanced CT is the preferred method to image disruption because it has better spatial resolution than radionuclide techniques.     

Brain MRI in neurodegeneration with brain iron accumulation with and without PANK2 mutations

BACKGROUND AND OBJECTIVE: Patients with a clinical diagnosis of neurodegeneration with brain iron accumulation (NBIA, formerly called Hallervorden-Spatz syndrome) often have mutations in PANK2, the gene encoding pantothenate kinase 2. We investigated correlations between brain MR imaging changes, mutation status, and clinical disease features. METHODS: Brain MRIs from patients with NBIA were reviewed by 2 neuroradiologists for technical factors, including signal intensity abnormalities in specific brain regions, presence and location of atrophy, presence of white matter abnormality, contrast enhancement, and other comments. PANK2 genotyping was performed by polymerase chain reaction amplification of patient genomic DNA followed by automated nucleotide sequencing. RESULTS: Sixty-six MR imaging examinations from 49 NBIA patients were analyzed, including those from 29 patients with mutations in PANK2. All patients with mutations had the specific pattern of globus pallidus central hyperintensity with surrounding hypointensity on T2-weighted images, known as the eye-of-the-tiger sign. This sign was not seen in any studies from patients without mutations. Even before the globus pallidus hypointensity developed, patients with mutations could be distinguished by the presence of isolated globus pallidus hyperintensity on T2-weighted images. Radiographic evidence for iron deposition in the substantia nigra was absent early in disease associated with PANK2 mutations. MR imaging abnormalities outside the globus pallidus, including cerebral or cerebellar atrophy, were more common and more severe in mutation-negative patients. No specific MR imaging changes could be distinguished among the mutation-negative patients. CONCLUSION: MR imaging signal intensity abnormalities in the globus pallidus can distinguish patients with mutations in PANK2 from those lacking a mutation, even in the early stages of disease.     

海马硬化的MRI诊断

目的 探讨海马硬化的ＭＲＩ表现和病理特征。方法 对１６例海马硬化患者进行ＭＲ横断面和垂直于海马长轴的段斜冠状面ＳＥＴ１ＷＩ、Ｔ２ＷＩ和液体衰减恢复序列（ＦＬＡＩＲ）扫描。结果 １６例患者中,１例为双侧海马硬化,１５例为单侧海马硬化（左侧９例,右侧６例）,１５例经手术病理证实,１６例１７个患侧ＭＲＩ表现为患侧海马萎缩变小;Ｔ２ＷＩ（１５侧）和ＦＬＡＩＲ成像（１７例）呈高信号;１１个患侧海马头部浅沟消