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Less invasive direct anterior approach (DAA) and dual mobility cup (DMC) are increasingly adopted in practice over the last decade. Their use aims to reduce, as much as possible, soft tissue dissection and dislocation rate. This study aims to present a novel surgical technique to reduce a DMC prosthesis during a DAA easily. A mildly modified version of the direct anterior approach is proposed. When leg lengths, stability, impingement, and tension have been checked, the trial stem is disassembled in situ, dislocated, and removed, leaving the space to exchange the trial double mobility head with the definitive one. When the definitive stem is inserted, the surgeon guides and helps the assistant to match the trunnion in the double mobility head. As soon as the components are matched, the traction is released, and the unit is impacted by an alternation of axial traction and release. Of 164 patients who underwent primary total hip arthroplasty (December 2016–May 2017) by a single surgeon, a double mobility cup through DAA and the “head-first” technique was performed in 26 patients (15.8%). The mean operative time was 130 min (85–220 min; SD 34.28). No significant complications occurred during the mean follow-up of 23.6 months. Specific difficulties can be anticipated when pairing dual mobility cup and direct anterior approach. The “head-first” technique is a useful technique in reducing the possible difficulties related to the reduction of double mobility cup through a less invasive direct anterior approach.

Objective Cerebral amyloid angiopathy–related inflammation (CAA-ri) is characterized by vasogenic edema and multiple cortical/subcortical microbleeds, sharing several aspects with the recently defined amyloid-related imaging abnormalities (ARIA) reported in Alzheimer's disease (AD) passive immunization therapies. Herein, we investigated the role of anti–amyloid β (Aβ) autoantibodies in the acute and remission phases of CAA-ri. Methods We used a novel ultrasensitive technique on patients from a retrospective multicenter case–control study, and evaluated the anti-Aβ autoantibody concentration in the cerebrospinal fluid (CSF) of 10 CAA-ri, 8 CAA, 14 multiple sclerosis, and 25 control subjects. Levels of soluble Aβ40, Aβ42, tau, P-181 tau, and APOE genotype were also investigated. Results During the acute phase of CAA-ri, anti-Aβ autoantibodies were specifically increased and directly correlated with Aβ mobilization, together with augmented tau and P-181 tau. Following clinical and radiological remission, autoantibodies progressively returned to control levels, and both soluble Aβ and axonal degeneration markers decreased in parallel. Interpretation Our data support the hypothesis that the pathogenesis of CAA-ri may be mediated by a selective autoimmune reaction against cerebrovascular Aβ, directly related to autoantibody concentration and soluble Aβ. The CSF dosage of anti-Aβ autoantibodies with the technique here described can thus be proposed as a valid alternative tool for the diagnosis of CAA-ri. Moreover, given the similarities between ARIA developing spontaneously and those observed during immunization trials, anti-Aβ autoantibodies can be considered as novel potential biomarkers in future amyloid-modifying therapies for the treatment of AD and CAA. Ann Neurol 2013;73:449–458

Primary or spontaneous intracranial hypotension (SIH) is a rare syndrome which causes postural headache associated with spinal fluid hypotension. We report three cases of SIH, characterised on magnetic resonance imaging (MRI) by pachymeningeal enhancement not only at cerebral level, but also in the cervical spinal cord, which subsequently resolved completely and spontaneously. We discuss the possible pathogenetic mechanisms of the dural alterations and underline the radiological aspects.

A 68-year-old man presented with a 4-month history of progressive memory loss and mood disorders. Neurologic examination revealed severe impairment of attention and verbal skills, without motor and sensory deficits. His medical history included mild arterial hypertension, idiopathic partial epilepsy, and obsessive compulsive disorder. Brain MRI showed the presence of bilateral, asymmetric, swollen white matter lesions in the cerebral hemispheres, hyperintense in T2-weighted images, that partially involved the left frontal cortex (figure). On diffusion-weighted sequences, the white matter abnormalities were consistent with vasogenic edema. No pathologic contrast enhancement was present. Figure MRI of cerebral amyloid angiopathy–related inflammation (CAA-ri) and levels of anti-Aβ 1-40 and 1-42 autoantibodies in the CSF Axial fluid-attenuated inversion recovery brain MRI shows bilateral hyperintense lesions of the subcortical white matter (A), which are reduced after 20 days of steroid treatment (B). Axial T2*-weighted gradient-echo MRI (C) obtained 33 days later shows further reduction of white matter lesions and multiple, scattered, hypointense cortical lesions due to microhemorrhages (arrows). (D) Reiber's graph. X- and y-axes show, respectively, albumin (QAlb) and immunoglobulin G quotient (QIgG), obtained by the ratio between the level of the protein in the CSF from the first lumbar puncture and in the plasma. The QAlb indicates the permeability of the blood–brain barrier (BBB) to water-soluble molecules. The QIgG (total IgG including specific anti-Aβ autoantibodies) plotted into the graph discriminates between intrathecal production of IgG and …

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is often related to the A3243G mutation of the mitochondrial DNA, accounting for about 80% of typical cases, with a relevant phenotypic variability. Hemorrhagic strokes are quite unusual in these patients. A case of recurrent brain hematomas has been reported in a MELAS patient carrying the G13513A mutation, with clinical onset at age 31 [1]. Another fatal case of intracerebral hemorrhage was reported in a MERRF/MELAS overlap syndrome due to a T8356C mutation [2]. Finally, a putaminal hemorrhagic stroke was described in a MERRF patient carrying the A8344G mutation, with clinical onset at age 26 [3]. Here, we report the case of a 37-year-old male arriving to our attention because of a two-week history of headache associated with nausea, vomiting, and dizziness. A brain MRI scan showed a left hemispheric cerebellar hemorrhage at a stage compatible with the onset of the symptoms. The patient neither had history of arterial hypertension, any hemorrhagic risk-factor, diabetes, nor was taking any medication. A few years before, he was found to be asymptomatic carrier of the A3243G mitochondrial DNA mutation (heteroplasmy confirmed on a blood sample), since a MELAS diagnosis was made on his younger brother expressing a typical phenotype. On current examination, our patient presented slight left ataxic hemiparesis and hypoesthesia. A cerebral angiography failed to show any vascular abnormality. Since our patient was carrier of a MELAS mutation, we decided to assess its putative clinical burden. An EEG showed generalized electrogenetic dysfunction with a single generalized epileptic spike discharge; EMG suggested slight myopathic signs; mild perceptive bilateral deafness was also present. A venous lactic acid test with compression of the right arm was significant (baseline values 2.9 mmol/L; increase up to 7.5 mmol/L after 3 min; NV 0.44–2.22 mmol/L). No hearth conduction defects were present. A week later, on a control CT scan, progressive blood reabsorption was noted and basal ganglia calcifications were not observed; the headache had improved and the neurological examination was normal. Iizuka et al. [4] demonstrated cortical laminar necrosis and focal HMPAO SPET hyperperfusion during subacute stages of stroke-like episodes; moreover, they reported several cases of microhemorrhages and at least one case of intracortical gyral hemorrhage, suggesting that stroke-like episodes are characterized by increased capillary permeability and focal hyperemia [5]. Consistently, vasogenic edema has been reported during stroke-like episodes [6]. Anyhow, in our case, the aspect of the lesion does not suggest the hemorrhagic transformation of a stroke-like episode; this also considering that the hematoma was confined in a specific vascular territory, which is not a characteristic of stroke-like episodes [4]. Conversely, we cannot exclude a hemorrhagic coincidental event in a patient carrying the A3243G mutation with a subclinical MELAS phenotype. However, mitochondrial angiopathy in E. Saracchi L. Tremolizzo J. C. DiFrancesco L. Brighina G. Costantino B. Frigeni M. Brioschi M. L. Piatti L. Fumagalli L. Marzorati N. A. Curto C. Ferrarese Department of Neurology, S. Gerardo Hospital, Monza, Italy

PURPOSE:We compared [11C]choline-positron emission tomography (PET) with [18F]fluorodeoxyglucose-PET for re-staging prostate cancer in a group of 100 patients.MATERIALS AND METHODS:A total of 100 consecutive patients referred for whole body [18F]fluorodeoxyglucose-PET for clinical prostate re-staging after radical treatment for prostate cancer were retrospectively included in the study. Mean prostate specific antigen (PSA) was 6.57 ng./ml. In all cases [11C]choline-PET was also performed. PET studies were done with a multiring device 5 minutes after intravenous injection of approximately 370 MBq. [11C]choline and 60 minutes after injection of approximately 370 MBq. [18F]fluorodeoxyglucose. PET findings were compared with those obtained with different conventional imaging and with PSA assessed at the time of PET and 1 year later.RESULTS:Areas of abnormal focal increases were noted in 47% of patients on [11C]choline-PET and in 27% on [18F]fluorodeoxyglucose-PET. Of the 100 patients 49 had positive conventional imaging findings. All except 14 [11C]choline-PET findings were concordant with conventional imaging, including 6 negative and 8 positive conventional imaging results. All except 1 [11C]choline-PET negative cases also had negative conventional imaging after 1 year. PSA at 1 year remained stable or decreased in 80% and 62% of [11C]choline-PET negative and positive cases, respectively.CONCLUSIONS:[11C]choline-PET seems to be useful for re-staging prostatectomy cases with increasing serum PSA levels. It is superior to [18F]fluorodeoxyglucose-PET and complementary to conventional imaging but with the advantage of staging disease at a single step

We report a series of four patients in whom the onset of systemic cancer was heralded by dysautonomic symptoms and a neurological non-metastatic complication mediated by immunological and endocrine factors. The series includes: a patient with acute leukaemia and autonomic sensory-motor polyradiculoneuropathy, a patient affected by colon carcinoma and autonomic neuropathy and limbic encephalitis, a patient with lung cancer and autonomic neuropathy and hypercalcaemic encephalopathy, a patient with small cell lung cancer associated with autonomic neuropathy in Lambert-Eaton Myasthenic Syndrome (LEMS) and syndrome of inappropriate ADH secretion (SIADH). We underline the prognostic importance and discuss the possible etiopathogenetic role of autonomic dysfunction, which is frequently associated with paraneoplastic neurologic syndromes of autoimmune and/or dysendocrine origin.

Three elderly patients with, respectively: mild cognitive impairment, severe and progressive neurologic involvement, and focal neurologic deficit, were observed. MRI showed multiple areas of white matter edema, at times partially involving the cortex, in the first two patients, and a single area in the third. Treatment with steroids determined the disappearance of the lesions and clinical amelioration. The key to the diagnosis of cerebral amyloid angiopathy-related inflammation (CAA-ri) was the demonstration, with appropriate MRI sequences, of microbleeds consistent with cerebral amyloid angiopathy (CAA). This diagnosis was supported by genetic analysis of APOE with demonstration of ε4/ε4 genotype, found in about 80% of CAA patients who develop inflammatory changes. In the appropriate clinical setting, MRI demonstration of microbleeds supported by results of genetic analysis of APOE may strongly support the diagnosis of CAA-ri thus avoiding cerebral biopsy.