Cause Of Neurological Symptoms Research Articles

Idiopathic Hypertrophic Spinal Pachymeningitis: A Case Report.

Idiopathic hypertrophic pachymeningitis is rare cause of neurological symptoms with myelopathy due to spinal cord compression. We report a case of pachymeningitis, which was manifested primarily by tetraparesis after low-energy trauma and recurrence the myelopathy symptoms after 5 years of surgery. The patient, a 19-year-old woman, was subjected to extensive investigation without evidence of any underlying disease. A meningeal biopsy was performed and showed an unspecific inflammatory process with extensive fibrosis of the dura mater. These findings, associated with the exclusion of other causes, suggest idiopathic hypertrophic pachymeningitis.

Disability measurement in Multiple Sclerosis patients 55 years and older: What is the Expanded Disability Status Scale really telling clinicians?

BackgroundThe Expanded Disability Status Scale (EDSS) measures disease progression in Multiple Sclerosis (MS). EDSS changes are assumed to be due to worsening MS-related disability. Strict interpretation of this premise may include some normal findings as abnormal, inflating the disability score. Further, determining the cause of neurologic symptoms can be difficult in an older population with comorbid illness and polypharmacy. ObjectiveTo examine the association between EDSS, age, comorbidities and polypharmacy. Methods106 people, 55 years and older, with and without MS were administered the EDSS and a validated comorbidity questionnaire. Polypharmacy was also assessed. ResultsMedian EDSS scores were 6.0 in people with MS and 3.0 in people without MS. No participant in our cohort had an EDSS of 0. Higher EDSS scores were associated with older age and more polypharmacy. Pyramidal and cerebellar functional systems accounted for the largest percentage of unique variance between groups. ConclusionOlder individuals with and without MS demonstrated significant disability on the EDSS. These findings indicate that EDSS scores may be partially due to factors other than MS. Our understanding of disease course and disability may benefit from the development of normative EDSS scores to correct for these factors.

Postpartum vertebral artery dissection: case report and review of the literature

BackgroundHypertensive disorders of pregnancy are associated with vascular complications, including ischemic stroke and cervical artery dissection. Vertebral artery dissection (VAD), however, is rare. We describe a 31-year-old female who presented with vertigo, nausea, and vomiting and was found to have a VAD. In addition, we discuss the presentation, differential diagnosis, and pathogenesis of this uncommon but clinically significant vascular event and summarize other cases of vertebral artery dissection described in the medical literature.Case presentationA 31-year-old Hispanic woman presented 10 days postpartum with a one-day history of vertigo, nausea, vomiting, and frontal headache. The patient’s pregnancy course had been complicated by preeclampsia, chorioamnionitis, and iron-deficiency anemia, and her delivery was complicated by acute hemorrhage. Physical examination was significant for left leg ataxia. Laboratory studies showed marked thrombocytosis. Emergent computed tomography (CT) scan of the head was obtained and revealed a left cerebellar ischemic large vessel stroke. Subsequent CT angiography of the head and neck showed a left VAD. Based on correlation of the clinical history and laboratory and imaging findings, a diagnosis of vertebral artery dissection secondary to reactive (secondary) thrombocytosis from overlapping iron-deficiency anemia and acute hemorrhage was established. The patient was started on a heparin infusion and experienced significant improvement after a four-day hospitalization.ConclusionVAD is a rare but important cause of neurologic symptoms in the postpartum period and should be considered in the differential diagnosis for women who present with headache and/or vertigo. Women aged 30 years or older and those with a history of a hypertensive disorder of pregnancy are at particularly high risk. Prompt diagnosis and management of VAD is essential to ensure favorable outcomes.

CD8 encephalitis with CSF EBV viraemia and HIV drug resistance, a case series

IntroductionCD8 encephalitis is a relatively recently described condition in the setting of HIV infection. It is becoming increasingly recognised in recent years though is still likely underdiagnosed. MethodsWe present three cases of encephalitis in HIV-positive black African females initially presenting with neurological pathology. Two cases concern recent presentations of patients attending HIV services at a large tertiary referral hospital and the third case involves a retrospective analysis of an archived case. Results and discussionMRI brain demonstrated periventricular white matter changes in 2 cases and a cerebellar lesion in the third case. CSF examination revealed lymphocytosis and elevated protein levels. CSF HIV viral load analysis showed viral escape along with new antiretroviral drug resistance mutations. CSF flow cytometry studies demonstrated a reversed CD4:CD8 ratio with a high CD8+ cells percentage. All patients had EBV DNA detected in their CSF. Brain biopsy in two patients confirmed CD8 encephalitis and also revealed isolated cells demonstrating EBV positivity by in-situ hybridization using EBER (Epstein–Barr virus-encoded small RNAs). Treatment with steroids and ART optimisation led to significant clinical and radiological improvements in all cases. DiscussionCD8 encephalitis should be considered as a cause of neurological symptoms and confusion in the HIV-positive patient, particularly if poor ART adherence or viral resistance are suspected. Brain biopsy should be considered in HIV-positive patients with encephalopathy of uncertain cause. Early treatment with high-dose corticosteroids when suspecting this diagnosis is essential for a favourable outcome. The prognosis is variable but can be favourable even following severe encephalopathy. The presence of new INSTI mutations in the CSF but absent peripherally in two INSTI-era patients is a novel finding for this case series in the context of CD8 encephalitis. The role played by EBV in this disease remains unclear and warrants further investigation.

An Uncommon Hyperosmolar Nonketotic Condition

Hyperglycemia may present with neurological symptoms. This rare condition is called non-ketotic hemichorea-hemiballismus (HCHB). When investigating the causes of neurological symptoms in these cases, magnetic resonance imaging (MRI) imaging typically has a hyperintense appearance in T1 sections and a variable intense appearance in T2. A 68-year-old female patient was admitted to the emergency department with speech disorder. Blood sugar elevation and cranial tomography revealed hyperdense appearance in the left caudate nucleus and lentiform nucleus. The patient was hospitalized with a preliminary diagnosis of HCHB. Magnetic resonance in hyperintense T1W sequences in the nucleus caudatus hood and corpus on the left, putamen, globus pallidus, Significant hypointense signal changes were observed in T2W sequences. The patient was admitted to the hospital for treatment and his blood sugar regulation was restored. HCHB is a rare condition in emergency. After the regulation of blood sugar, neurological picture regression is observed. Blood sugar levels should be checked and appropriate treatment should be given in patients presenting with neurological symptoms.

Larger screw on the concave side of apex pedicle: Friend or foe? Report on a rare cause of neurological deficit in scoliosis surgery

Pedicle screw instrumentation is currently the “gold standard” in scoliosis surgery. However, placement of pedicle screws in thoracic spine is considered challenging. Previous studies have described morphometric changes in the pedicle when a larger screw is inserted, with pedicle expansion preceding screw cutout and pedicle fracture. We report an unusual case of neurological deficit due to cord compression by an expanded pedicle following pedicle screw insertion on the concave side of the apical vertebra in a 14-year-old patient with Lenke Type 3C(-) adolescent idiopathic scoliosis. Identification of the expanded pedicle as the cause of neurological symptoms, prompt action, and deferring the corrective surgery while accepting less correction helped us in negotiating the problem without causing permanent neurological deficit. Pedicle expansion in an immature spine can cause neurological complications. The screw diameter at the apical vertebrae on the concave side should be carefully selected.

PB1964 ROLE OF HOMOCYSTEINE AND METHILMALONIC ACID IN NEUROLOGICAL PATHOLOGY

Background:Vitamin B12 (B12) deficiency causes hematological and non‐hematological disorders. The latter include neurological syndromes such as polyneuropathies, subacute combined degeneration, basal ganglia lesions, dementia or ischemic stroke. These symptoms can be present even in the absence of anemia or macrocytosis, and the lack of these hematologic changes cannot exclude B12 deficiency as a cause of neurological symptoms..There may be deficiency of B12 with normal or borderline serum levels, hence the relevance of assessing its metabolites homocysteine (HCY) and methylmalonic acid (MMA), that increase in case of B12 deficiency.Aims:To determine the value of HCY and MMA in the diagnosis of B12 deficiency in patients with neurological symptoms.Methods:A retrospective analysis of the cases in which evaluation of B12 and folic acid was requested from the Neurology department during a period of thirteen months was performed.Analytical (complete blood count –CBC–, serum B12, serum folate, erythrocyte folate –when serum folate was low–, HCY, MMA, serum creatinine and estimated glomerular filtration rate –eGFR–) and demographic parameters were evaluated. B12 levels under 150 pg/L were considered low (LB12); between 150 and 200 pmol/L, borderline (BB12); and higher than 200 pmol/L, normal (NB12).Results:One thousand thirty nine (7.8%) of the 14644 requests came from the Neurology department. LB12 was found in 101 (9%) of these cases, BB12 in 177 (15.5%) and NB12 in 861 (75.6%). Folate deficiency was found in 11 (1%) patients.Regarding to patients with LB12, 62% had no alterations in the CBC, 25% had non‐macrocytic anemia and 8% had macrocytic anemia or macrocitosis. These results were similar in the group with BB12. Considering the patients with NB12, 72% of them had a normal CBC, 11,5% had non‐macrocytic anemia, and macrocytic anemia or macrocytosis was observed in 6%. Hematological alterations in these three groups were mild or moderate in 90% of cases; in none was severe (considered if hemoglobin <7 gr/dL, platelets <50x10e9/L, neutrophils <0.5x10e9/L).The metabolite levels were available in 162 cases of the NB12 group. In these patients, high HCY (>14.5 umol/L) was found in 18.8%. Folate levels were normal for all of them, although 32% had an abnormal eGFR that may contribute to the increase in HCY. Mutational status of the MTHFR gene is unknown in these patients. MMA was measured in 7.8% of the patients with NB12; increased levels (>0.4 umol/L) were found in 23.5%. In the NB12 group, 10 patients showed an increase in both metabolites (table 1), suggesting an actual B12 deficiency despite the normal B12 levels. Sensory polyneuropathy was the neurological finding in 9 of these patients and B12 deficiency was assumed the cause in 4 of them, who were given supplementary treatment.Summary/Conclusion:The incidence of B12 deficiency in patients with neurological symptoms is high. Most of these B12‐deficient patients did not show hematological changes or these were mild, and some of them presented with normal serum B12. Assessment of the metabolites is essential in these patients with normal serum B12 and neurological symptoms. This situation represents a true diagnostic and therapeutic challenge.imageTherefore, in the context of a high clinical suspicion, a normal or borderline B12 does not rule out a functional deficiency and metabolites should be assessed.

Intracranial ependymal cyst with unusual presentation: Case report and review of literature

Abstract Background Ependymal cysts remain a very rare cause of neurological symptoms among intracranial cystic lesions. It differs from an arachnoid cyst, as it does not communicate with subarachnoid space. Case description A 33-year-old woman was admitted in our neurosurgery department with history of headache, vomiting and right unilateral blindness. Neuroimaging studies showed an intraparenchymal cystic lesion in the right frontal lobe with radiologic characteristic as seen in the ependymal cyst or hydatic cyst. She underwent the neurosurgical procedure of marsupialization and was discharged on day 6 post op. At one month follow up, the patient presented with a decrease vision acuity on the left eye, and head CT scan showed a recurrence of the cyst hence, we performed a second surgery with shunt procedure. Histological examination of the resected tissue demonstrated that, it was an ependymal cyst. Conclusion Since there is often times a clinico-radiological discordance they are generally incidental findings in majority of cases. While complete surgical excision is the treatment of choice for the symptomatic cysts, cystic fluid diversion presents a better compromise nevertheless in cases where this may not be achieved.

Case Report: Brachial Neuritis in a Patient with Epstein Barr Virus

A 41 year-old man, recently returned from Thailand, presented with bilateral shoulder pain and weakness, fever greater than 38 degrees and coryzal symptoms. He had no significant past medical history. He had abnormal liver function tests and an abnormal electromyogram of his right upper limb. He was diagnosed with acute Epstein Barr virus infection, however cerebrospinal fluid was negative for the virus. At follow up after three months, the patient had persistent weakness of his right upper limb. The literature suggests neurological features present in up to 7.5% of patients with Epstein Barr virus, although argues this is underestimated with the virus often being overlooked as a cause of neurological symptoms.

Neuroimaging Applications in Functional Movement Disorders.

Functional (psychogenic) movement disorders are a subtype of functional neurological disorder, a common and disabling cause of neurological symptoms. Abnormal movement in people with functional movement disorders has specific characteristics (e.g., distractibility, variability, incongruence with deficits caused by neurological disease), allowing positive diagnosis and differentiation from other causes of movement disorder. Attempts to understand the pathophysiology of this disorder have previously focused mainly on the psychological level, emphasizing the importance of psychological trauma and adverse life events. However, the last two decades has seen a broadening of this approach to consider the neurobiological level, and brain imaging has formed a key part of this work. Here we review the available imaging evidence in functional movement disorders and explain how this evidence can help us understand more about the underlying pathophysiology of this common cause of abnormal movement control.

Chapter 46 - Multiple sclerosis

Multiple sclerosis is a potentially progressive, autoimmune neurologic disorder of the central nervous system, resulting from an autoimmune attack on central nervous system white matter. It is a leading cause of neurologic symptoms in young adults, with no known cure. Emerging disease-modifying therapies aim to control symptoms, with increasingly sophisticated immune function modulation. Though several environmental exposures increase the risk of developing the disease, a large fraction of overall risk is heritable and can be attributed to hundreds of common genetic variants influencing gene regulation in specific immune subsets. Here, we review the history of the disease, the realization that risk is heritable, and the recent revelation of hundreds of genetic variants driving this risk by international consortia studying tens of thousands of patients. Finally, we discuss how these results are revealing the specific pathobiology of multiple sclerosis and how this knowledge is transforming drug discovery.

Chapter 17 - Acute and chronic viral infections

A large number of viruses belonging to various families are able to cause central nervous system (CNS) infections and contribute significantly to burden of disease in humans globally. Most viral CNS infections are benign and self-limiting, and most remain undiagnosed. However, some viruses can cause severe inflammation, leading to morbidity and mortality, and result in severe long-term residual damage and neurologic dysfunction in patients. The potential of viruses to cause CNS inflammation greatly varies depending on host factors, such as age, sex, and genetic background, as well as viral factors. Despite the need for protection against viral invasion and replication, the extent of the immune response in the CNS is carefully regulated to prevent excessive inflammation and tissue destruction leading to irretrievable loss of neurons. Direct cytopathology is for many virus infections a major cause of neurologic symptoms; however, the antiviral immune response can in some instances contribute substantially to pathology. This chapter highlights a selection of clinically important neurotropic viruses that infect the CNS and cause neurologic diseases such as meningitis, encephalitis, and myelitis in humans, with a focus on neuropathologic findings.

Ankylosing spondylitis and spinal trauma – with an emphasis on the role of radiology

Diagnosis of spinal injury in a patient with chronic ankylosing spondylitis can be challenging. Minor insult can result in an unstable three-column injury which may be subtle. Spinal deformity, osteoporosis and limited mobility are associated with difficulty in positioning patients for imaging studies, including radiography and both computed tomography and magnetic resonance imaging. It is important to maintain a high index of suspicion of fracture, avoid forced neck extension during radiological imaging, and to consider whole spine imaging in these patients. Other causes of neurological symptoms simulating potential spinal injury are also briefly addressed.

Platinum-induced neurotoxicity: A review of possible mechanisms.

Patients treated with platinum-based chemotherapy frequently experience neurotoxic symptoms, which may lead to premature discontinuation of therapy. Despite discontinuation of platinum drugs, these symptoms can persist over a long period of time. Cisplatin and oxaliplatin, among all platinum drugs, have significant neurotoxic potential. A distal dose-dependent symmetrical sensory neuropathy is the most common presentation of platinum neurotoxicity. DNA damage-induced apoptosis of dorsal root ganglion (DRG) neurons seems to be the principal cause of neurological symptoms. However, DRG injury alone cannot explain some unique symptoms such as cold-aggravated burning pain affecting distal extremities that is observed with oxaliplatin administration. In this article, we briefly reviewed potential mechanisms for the development of platinum drugs-associated neurological manifestations.

Prostate cancer, Hu antibodies and paraneoplastic neurological syndromes.

Prostate cancer is the most common cancer among American and European men. Nervous system affection caused by local tumor growth or osseous metastases are the main causes of neurological symptoms in prostate cancer patients. Prostate cancer is rarely reported in association with paraneoplastic neurological syndromes (PNS). We have, therefore, studied clinical and paraclinical findings of a series of patients with prostate cancer and PNS, and reviewed cases reported in the literature. Case histories of 14 patients with definite PNS from the PNS Euronetwork database and from the authors' databases were reviewed. A PubMed literature search identified 23 patients with prostate cancer and PNS. Thus, a total of 37 case histories were reviewed with respect to syndrome type, cancer evolution, paraclinical investigations, antibody status, treatment and outcome. The three most frequent isolated PNS were paraneoplastic cerebellar degeneration, paraneoplastic encephalomyelitis (PEM)/limbic encephalitis and subacute sensory neuronopathy (SSN). Onconeural antibodies were detected in 23 patients, in most cases the Hu antibody (17 patients, 74% of all antibody-positive cases). Other well-characterized onconeural antibodies (Yo, CV2/CRMP5, amphiphysin, VGCC antibodies) were found in a minority. PNS was diagnosed prior to prostate cancer diagnosis in 50% of the cases. The association of PNS with prostate cancer is quite infrequent, but clinically important. PNS often heralds prostate cancer diagnosis. Syndromes associated with Hu antibodies predominate. Another tumor more prone to associate with PNS should always be excluded.

Ischemic Stroke in Critically Ill Patients with Malignancy.

BackgroundCerebrovascular diseases are a frequent cause of neurological symptoms in patients with cancer. The clinical characteristics of ischemic stroke (IS) in patients with cancer have been reported in several studies; however, limited data are available regarding critically ill patients with cancer who develop IS during their stay in the intensive care unit (ICU).MethodsAll consecutive patients who underwent brain magnetic resonance imaging (MRI) for suspicion of IS with acute abnormal neurologic symptoms or who developed signs of IS while in the ICU were retrospectively evaluated. We compared the clinical characteristics and diffusion-weighted imaging (DWI) lesion patterns between patients finally diagnosed as having or not having IS.ResultsOver the study period, a total of 88 patients underwent brain MRI for suspicion of IS, with altered mental status in 55 (63%), hemiparesis in 28 (32%), and seizure in 20 (23%). A total of 43 (49%) patients were ultimately diagnosed with IS. Multiple DWI lesions (41%) were more common than single lesions (8%). The etiologies of IS were not determined in the majority of patients (n = 27, 63%). In the remaining 16 (37%) patients, the most common aetiology of IS was cardioembolism (n = 8), followed by large-vessel atherosclerosis (n = 3) and small-vessel occlusion (n = 2). However, brain metastases were newly diagnosed in only 7 (8%) patients. Univariate comparison of the baseline characteristics between patients with or without IS did not reveal any significant differences in sex, malignancy type, recent chemotherapy, vascular risk factors, or serum D-dimer levels at the time of suspicion of IS. Thrombotic events were more common in the IS group than in the non-IS group (P = 0.028). However, patients who were ultimately diagnosed with IS had more hemiparesis symptoms at the time of suspicion of IS (P = 0.001). This association was significant even after adjusting for potentially confounding factors (adjusted odds ratio 5.339; 95% confidence interval, 1.521–19.163).ConclusionsIS developed during ICU stays in critically ill patients with cancer have particular features that may be associated with cancer-related mechanism.

Two Cases of Legionella pneumophila Pneumonia with Prolonged Neurologic Symptoms and Brain Hypoperfusion on Single-Photon Emission Computed Tomography.

Cerebral and cerebellar symptoms are frequently associated with Legionnaires' disease. However, corresponding brain lesions are difficult to demonstrate using either computed tomography (CT) or magnetic resonance imaging (MRI). We report here two patients with Legionella pneumophila pneumonia accompanied by prolonged neurologic symptoms. In contrast to brain CT and MRI, which failed to detect any abnormalities, single-photon emission computed tomography (SPECT) showed multiple sites of hypoperfusion within the brains of both patients. These cases suggest that vasculopathy, which is detectable by SPECT, might be one of the causes of neurologic symptoms in patients with Legionnaires' disease.

Multiple Sclerosis and Related Disorders

Multiple sclerosis (MS) is a relatively common cause of neurologic symptoms and disability in young adults. The distinguishing pathologic features of MS are loss of myelin and inflammation in the central nervous system (CNS). The myelin sheath is essential for rapid conduction of nerve signals along large-diameter axons. Oligodendrocytes produce and maintain myelin in the CNS, and Schwann cells produce and maintain myelin in the peripheral nerves. In addition to MS, there are a number of related disorders causing demyelination, inflammation, or both in the CNS. This chapter discusses MS and related disorders, including neuromyelitis optica, optic neuritis, acute disseminated encephalomyelitis, transverse myelitis, Behçet syndrome, neurosarcoidosis, inherited demyelinating diseases (leukodystrophies, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and virus-induced demyelination (progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis). The section on MS covers epidemiology, etiology/genetics, pathogenesis, diagnosis, differential diagnosis, management, and prognosis. Figures include organization of the microenvironment of larger-diameter axons, typical magnetic resonance imaging findings in MS and neuromyelitis optica, postgadolinium images of the cervical spine in MS, and an approach to treatment of relapsing-remitting MS. Tables list MS and related disorders, distribution of neurologic deficits at the onset of MS, differential diagnosis of MS, disease-modifying therapies for relapsing-remitting MS, and selected leukodystrophies, as well as diagnostic criteria and selected symptomatic therapies for MS. This chapter contains 3 highly rendered figures, 7 tables, 82 references, 1 teaching slide set, and 5 MCQs.

Multiple Sclerosis and Related Disorders

Multiple sclerosis (MS) is a relatively common cause of neurologic symptoms and disability in young adults. The distinguishing pathologic features of MS are loss of myelin and inflammation in the central nervous system (CNS). The myelin sheath is essential for rapid conduction of nerve signals along large-diameter axons. Oligodendrocytes produce and maintain myelin in the CNS, and Schwann cells produce and maintain myelin in the peripheral nerves. In addition to MS, there are a number of related disorders causing demyelination, inflammation, or both in the CNS. This chapter discusses MS and related disorders, including neuromyelitis optica, optic neuritis, acute disseminated encephalomyelitis, transverse myelitis, Behçet syndrome, neurosarcoidosis, inherited demyelinating diseases (leukodystrophies, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and virus-induced demyelination (progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis). The section on MS covers epidemiology, etiology/genetics, pathogenesis, diagnosis, differential diagnosis, management, and prognosis. Figures include organization of the microenvironment of larger-diameter axons, typical magnetic resonance imaging findings in MS and neuromyelitis optica, postgadolinium images of the cervical spine in MS, and an approach to treatment of relapsing-remitting MS. Tables list MS and related disorders, distribution of neurologic deficits at the onset of MS, differential diagnosis of MS, disease-modifying therapies for relapsing-remitting MS, and selected leukodystrophies, as well as diagnostic criteria and selected symptomatic therapies for MS. This chapter contains 3 highly rendered figures, 7 tables, 82 references, 1 teaching slide set, and 5 MCQs.

254-POS

Objectives Between 0.5% and 5% of all pregnancies are complicated by preeclampsia (PE), a multi-organ disease and the most significant cause of neurological symptoms during the peripartum period. Although numerous clinical studies assess neurocognitive outcome of children born to mothers with PE and various animal models of PE dealing with mechanisms and symptoms of this disease exist, there is a lack of basic and clinical research analyzing cognitive performance of mothers after PE. The aim was to critical review available literature regarding the effects of pregnancies complicated by preeclampsia on maternal cognitive functioning. Methods Analysis of current evidence from database PubMed with keywords “Preeclampsia AND cognition/memory”, “Preeclampsia AND dementia”, “Hypertensive pregnancy AND cognition/memory”, “Placental ischemia-induced hypertension AND cognition/memory”, “Transgenic preeclampsia rat model AND cognition/memory” and “Reduced uterine perfusion pressure AND cognition/memory” was performed. Publication years 1994–2014 were included in this analysis. Results Search revealed only n = 5 clinical studies dealing with the effect of PE/hypertensive pregnancies on cognitive outcome in mothers, whereas not a single report from basic research was available. Results from clinical research were rather conflicting with n = 2 reporting no effect of a former preeclamptic pregnancy on cognition and n = 3 showing impairments in cognitive functioning later in life. Conclusions Despite the fact that neurological symptoms are a well-known consequence of pregnancies complicated by PE, basic and clinical studies assessing cognitive abilities in formerly preeclamptic mothers are rare, conflicting, or even nonexistent. Given the fact that decrements in cognition and memory can not only lead to psychosocial problems but could moreover affect the interaction between mother and child, thus tremendously impacting the quality of life of both, more research relating to the origin and management of these issues is highly required. Disclosures K.M. Hillerer: None. V.R. Jacobs: None. L. Aigner: None. T. Fischer: None.