The accuracy of MRI for the diagnosis of ramp lesions.

OBJECTIVES: To assess the diagnostic accuracy of MRI in diagnosing ramp lesions in patients with an acute lesion of the anterior cruciate ligament (ACL). MATERIALS AND METHODS: All consecutive patients over 15 years of age who underwent surgical repair of the ACL at a single hospital between January and May 2019, with MRI data available, were included in this retrospective study, except patients who had previous knee surgery. The gold standard was arthroscopic evaluation. Two trained radiologists with 5 and 14 years of experience did a blinded review of the MRIs. The following pathological signs were studied: complete fluid filling between the capsule and the posterior horn of the medial meniscus, irregular appearance of the posterior wall of the medial meniscus, oedema of the capsule, fluid hyperintensity in contact with the medial meniscus and anterior subluxation of the medial meniscus. Logistic regressions in univariate then multivariate analysis were carried out and measures of diagnostic accuracy and interobserver agreement were calculated with R software (version 3.6). RESULTS: Fifty-seven patients were included. Twelve had a ramp lesion diagnosed by arthroscopy (21%). Only complete fluid hyperintensity between the posterior horn of the medial meniscus and the capsule was significantly associated with ramp lesions (P value < 0.01). The diagnostic accuracy of this specific sign was moderate, with a specificity of 84%, sensitivity of 75%, PPV of 56%, NPV of 93% and a good level of inter-observer agreement (k = 0.79). CONCLUSION: The complete fluid filling is the only significant pathological MRI sign for ramp lesions, with moderate accuracy.

Significant response to immune therapies in a case of subacute necrotizing myopathy and FKRP mutations.

Necrotizing myopathies can be encountered in various conditions as acquired myopathies (toxic or autoimmune) or muscular dystrophies. We report a twenty-year-old Caucasian woman who presented with clinical findings suggestive of an inflammatory myopathy: subacute onset of lower limb muscle weakness, myalgia, weight loss and absence of family history. The serum creatine kinase level was elevated at 4738 IU/L (normal range, 25-175 IU/L). Muscle biopsy was consistent with necrotizing myopathy. The patient showed significant clinical improvement following corticosteroid, azathioprine and intravenous immunoglobulin treatments. Biological tests revealed no specific autoantibodies associated with necrotizing autoimmune myopathies. Immunohistochemical staining for sarcolemmal proteins in muscle biopsy samples finally led to a diagnosis of limb-girdle muscular dystrophy 2I (fukutin-related protein gene mutations). The response to immune therapies suggested a possible inflammatory component associated with the muscular dystrophy and highlighted the potential benefit of corticosteroid treatment in patients with LGMD2I and subacute onset.

[Ma2 antibody and multiple mononeuropathies]. / Mononeuropathie multiple et anticorps anti-Ma2.

Anti-Ma2 antibodies belong to a family of onconeuronal antibodies that target proteins expressed in brain, testis and several tumors. Previously observed in patients presenting with limbic encephalitis, they seem to be associated with several other paraneoplastic syndromes. We report the case of a 73-year-old woman presenting sensory and motor neuropathy associated with non-small-cell lung cancer who had Ma2-antibodies.

Asymmetric metabolic profile in mesial temporal lobes: localized H-1 MR spectroscopy in healthy right-handed and non-right-handed subjects.

PURPOSE: To determine a possible asymmetric metabolic profile in right- handed and non-right-handed healthy subjects by comparing proton spectra from temporal lobes. MATERIALS AND METHODS: Twenty-eight healthy adults (17 right-handers, 11 non-right-handers) underwent magnetic resonance (MR) imaging and single-voxel MR spectroscopy. N-acetylaspartate (NAA), choline (Cho), and creatine (Cr) peak areas were measured. RESULTS: Volume of hippocampal formations was larger on the right in right-handers (right volume: 4.04 cm3 +/- 0.67 vs left volume: 3.84 cm3 +/- 0.62; P = .00004) and in non-right-handers (right volume: 4.22 cm3 +/- 0.78 vs left volume: 4.05 cm3 +/- 0.80; P = .004). NAA/Cho was significantly higher in the left temporal lobe of right-handers (right lobe: 1.53 +/- 0.18 vs left lobe: 1.89 +/- 0.18; P=.00004) as was NAA/Cr (right lobe: 1.79 +/- 0.36 vs left lobe: 2.45 +/- 0.45; P=.0001). No statistically significant difference was noted for these ratios in non-right-handers: NAA/Cho (right lobe: 1.49 +/- 0.18 vs left lobe: 1.61 +/- 0.35) and NAA/Cr (right lobe: 1.93 +/- 0.45 vs left lobe: 2.40 +/- 0.70). CONCLUSION: A clear metabolic asymmetry observed in right-handers is less clear-cut in non-right-handers. Both tendencies should be considered when assessing the brain metabolism of patients with uni- or bilateral disorders, such as temporal lobe epilepsy.

[Value of gadolinium magnetic resonance imaging of the lumbosacral roots in acute polyradiculoneuritis]. / Intérêt de l'imagerie en résonance magnétique avec gadolinium des racines lombo-sacrées dans les polyradiculonévrites aiguës.

Four patients with acute inflammatory polyradiculoneuropathy were evaluated with MRI. In 3 of 4 cases, gadolinium enhancement was observed in the nerve roots of cauda equina, on frontal and horizontal slices. This enhancement was correlated with the severity of the clinical picture and the cerebrospinal-fluid inflammatory protein concentration and supports the inflammatory nature of this forms of acute polyradiculoneuropathy.

Late thalamic atrophy in infarction of the middle cerebral artery territory in neonates. A prospective clinical and radiological study in four children.

We report four cases of progressive thalamic atrophy following ipsilateral cerebral infarction in the territory of the middle cerebral artery in neonates, with prospective radiological and clinical follow-up. This type of atrophy appears within 6 months after the onset of cerebral infarction. In the short term, this atrophy has no action on sensory and memory function and/or on sensory evoked potentials. This atrophy is not the result of secondary ischemic neuronal damage. Judging from several other experimental studies, thalamic atrophy may primarily result from retrograde degeneration. It would be interesting to observe the consequences of this atrophy on sensory and memory function over a long period.

Risk factors for primary cerebral hemorrhage: a population-based study--the Stroke Registry of Dijon.

Risk factors for primary cerebral hemorrhage remain uncertain. The population-based Stroke Registry of Dijon provides data on the risk factors. Among residents of Dijon (France), 130 cases of primary cerebral hemorrhage hospitalized from 1985 to 1992 were matched with 130 controls by age and sex. The following data were collected: history of hypertension, alcohol consumption, tobacco consumption, history of coagulation disorder, diabetes mellitus, dyslipidemia, and infectious disease in the 7 days before admission. The following parameters were measured on admission: blood pressure, blood glucose, cholesterol, triglycerides, hematocrit, fibrinogen, prothrombin levels, platelet counts, prothrombin time, bilirubin, transaminases, gamma-glutamyltransferase, and alkaline phosphatase. Electrocardiogram and Doppler ultrasound examination of cervical arteries were performed. Statistical analysis was performed by means of relative risk ratio for paired samples when dealing with proportions, and Student's t test for quantitative variables. A stepwise discriminant analysis was carried out to establish the relative weight of the different risk factors and their discriminant values. Among the qualitative data, the significant factors were history of hypertension, alcohol consumption, cardiac arrhythmia, atherosclerosis of carotid arteries and a previous infectious disease in the 7 days before admission. Among the quantitative data, the significant factors were early hypertension, high blood glucose levels, high hematocrit, and low cholesterol levels, in the acute stage of the stroke. After multifactorial analysis, only two factors were significant: hypertension and low cholesterol levels. Our population-based case-control study showed that hypertension and low cholesterol levels are the two discriminant risk factors for both lobar and basal ganglia primary cerebral hemorrhage. Therefore, treatment of hypercholesterolemia may increase risk of cerebral hemorrhage.

[Prevalence and prognostic value of transient ischemic complication preceding cerebral infarction]. / Prévalence et valeur pronostique d'un accident ischémique transitoire précédant un infarctus cérébral.

To evaluate the prevalence, the aetiological profile and the neurological consequences at day 15 of a transient ischaemic attack (TIA) before a cerebral infarction, we undertook survey from 1985 to 1991, on 1,149 cases with cerebral infarction observed on the population of Dijon. On 1,149 cases, 275 (24%) were preceded by a TIA. Fifty seven cases were lacunar infarcts (20.7%) and 218 were cortical infarcts (79.3%). On the aetiological point of view, the group with 275 infarctions preceded by a TIA was statistically different from the group of 874 infarctions without any TIA, with higher blood pressure, cardiac arrhythmia, tobacco abuse and ischaemic cardiac disease history. Only 65 out of 275 infarctions preceded by one TIA (23.6%) had a perfect territorial relationship between the 2 attacks, and 210 out of 275 (76.4%) had no territorial relationship. While the Barthel score at day 15 was similar within the 2 groups, inversely, pseudo-bulbar syndrome was significantly more frequent in the first group. Former TIA does not increase the general handicap resulting from a cerebral infarct, nevertheless it gives rise to a pseudo-bulbar syndrome.

Preliminary observations of metabolic characterization of bilateral temporal epileptic focus, using proton magnetic resonance spectroscopy. Three cases.

The authors report the case of 3 patients with bilateral temporal lobe epilepsy demonstrated by EEG and sphenoïdal electrodes. Two out of the 3 patients presented with childhood febrile convulsions. Their neurological and mental examination was normal. EEG showed spikes within the anterior part of the 2 temporal lobes. CT scan and MRI showed no atrophic lesion within the 2 temporal lobes. Proton magnetic resonance spectroscopy, performed within a cube of 8 cube-centimetres localized in the anterior part of the 2 temporal lobes showed a significant decrease of N-acetyl-aspartate in the 2 temporal lobes of the 3 cases, compared with controls matched with age, sex and laterality. Because N-acetyl-aspartate is a marker of the neuronal cells, the decreased level of NAA in the temporal area with spikes, may be related to a decreased number of neuronal cells, developing an abnormal tendency to seizures.

Early seizures after acute stroke: a study of 1,640 cases.

We evaluated prospectively the occurrence of seizures within 15 days of a first stroke or transient ischemic episode in 1,640 patients to study relation between seizures and type of stroke. Seizures occurred in 90 patients (5.4%), including 36 (4.4%) of 814 with infarct owing to atheroma, 21 (16.6%) of 126 with infarct owing to cardiogenic embolus, 3 (1%) of 273 owing to lacunar infarct, 5 (1.9%) of 259 owing to transient ischemic attack (TIA), 21 (16.2%) of 129 owing to supratentorial hematoma, and 4 (16.6%) of 24 owing to subarachnoid hemorrhage. Thirteen (14.6%) of 89 subcortical infarcts were associated with seizures. Seizures were the initial sign of stroke in 80 (89%) of 90 cases and were usually single and partial. Seizure symptoms were most often motor, sensory, or visual.

[Gyratory epileptic seizures. Radioclinical correlations]. / Les crises épileptiques giratoires. Corrélations radio-cliniques.

The authors report 3 cases of gyratory seizures whose epileptic nature was demonstrated on the following features. They appeared with a loss of consciousness. In 2 cases, they ended with a tonic-clonic generalized fit and in the 3 cases, they were mixed with other generalized seizures. From an etiological point of view, in 2 cases, a deep lesion was discovered, the first one near the paracentral lobule, the second in the para-thalamic area. The third one was an idiopathic generalized epilepsy on clinical and electroencephalographic grounds. These 3 cases focus on the difficulties to classify gyratory seizures that may appear in 2 opposite situations, namely in symptomatic partial epilepsy and in idiopathic generalized epilepsy.

Homolateral ataxia and crural paresis: a crossed cerebral-cerebellar diaschisis.

A patient developed weakness of the right leg and homolateral ataxia of the arm, caused by a subcortical infarct in the area supplied by the anterior cerebral artery in the left paracentral region, demonstrated by CT and MRI. Cerebral blood flow studied by technetium-labelled hexamethyl-propylene-amine oxime using single photon emission computed tomography showed decreased blood flow in the left lateral frontal cortex and in the right cerebellar hemisphere ("crossed cerebral-cerebellar diaschisis"). The homolateral ataxia of the arm may be caused by decreased function of the right cerebellar hemisphere, because of a lesion of the corticopontine-cerebellar tracts, whereas crural hemiparesis is caused by a lesion of the upper part of the corona radiata.

So-called generalized epilepsy in children leading to frontal epilepsy with a frontal syndrome in adulthood: a clinical, EEG and radiological study of 10 cases.

The authors report 10 cases of epileptic patients with the onset in childhood of the clinical and EEG features of cryptogenic generalized epilepsy which evolved into frontal epilepsy, confirmed by the clinical and EEG features and was associated with a frontal syndrome. CT-scan and MRI showed mild atrophy in the frontal area, while SPECT showed a decrease in the frontal blood flow in 70% of the cases. The authors consider that frontal epilepsy may mimic generalized epilepsy.

[Transient neurologic deficit preceding intracerebral hemorrhage. Physiopathological hypotheses]. / Déficits neurologiques transitoires précédant les hémorragies intraparenchymateuses. Hypothèses physiopathologiques.

Seventeen out of 238 cases (7%) of intracerebral hemorrhage were preceded by transient neurological deficit. In two cases, intracerebral hemorrhage and transient neurological deficit were thought to be due to amyloid angiopathy, this diagnosis was confirmed at autopsy in one case. In one case, intracerebral hemorrhage and transient neurological deficit were due to a cavernoma. In the other 14 cases, hypertension was the major risk factor. In 3 of them, CT-scans made after the transient neurological deficit but before the intracerebral hemorrhage showed deep small hypodensities suggestive of lacunas. The mechanisms of transient neurological deficit preceding intracerebral hemorrhage are reviewed.