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Two cases of patients with paraneoplastic limbic encephalitis, difficult to control seizures, and unilateral hippocampal hypermetabolism on positron emission tomography (PET) are described. Two women aged 33 and 61 presented with uncontrolled complex partial seizures, profound memory loss and cognitive decline. One was later diagnosed with breast cancer and the other with lung cancer. Video-EEG on the first patient recorded multifocal sharp waves and bilateral independent seizure onsets. The second patient had no epileptiform discharges and bitemporal ictal onset, even though the clinical seizures suggested a right temporal onset. Magnetic resonance imaging (MRI) was normal in both patients. PET scans obtained in the interictal state showed right hippocampal hypermetabolism in both patients. In the second patient, the lung cancer was irradiated with resolution of seizures and improvement of memory function. A PET scan six months later was normal. Subsequent seizure recurrence and worsening of memory led to the discovery of widespread metastases. Limbic encephalitis should be considered in the differential diagnosis of intractable partial epilepsy, particularly if accompanied by severe memory loss and cognitive decline. Treatment of the underlying cancer may be lead to improved seizure control. Hippocampal hypermetabolism may be a common feature on PET, and may indicate subclinical seizure activity.
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PMID:Limbic encephalitis and hyperactive foci on PET scan. 1060 May 85

Paraneoplastic limbic encephalitis (PLE) is a rare disorder characterized by personality changes, irritability, depression, seizures, memory loss and sometimes dementia. The diagnosis is difficult because clinical markers are often lacking, and symptoms usually precede the diagnosis of cancer or mimic other complications. The frequency of antineuronal antibodies in patients with PLE has not been investigated. We examined the neurological symptoms and the causal tumours in 50 patients with PLE to determine the utility of paraneoplastic antibodies and other tests. The diagnosis of PLE required neuropathological examination or the presence of the four following criteria: (i) a compatible clinical picture; (ii) an interval of <4 years between the development of neurological symptoms and tumour diagnosis; (iii) exclusion of other neuro-oncological complications; and (iv) at least one of the following: CSF with inflammatory changes but negative cytology; MRI demonstrating temporal lobe abnormalities; EEG showing epileptic activity in the temporal lobes. Of 1047 patients with neurological symptoms, whose sera or CSF were examined for paraneoplastic antibodies, 79 had the presumptive diagnosis of limbic encephalitis, dementia, cognitive dysfunction, or confusion. Fifty of these patients fulfilled our criteria for PLE. Pathological confirmation was obtained in 12 patients. The commonly associated neoplasms were of the lung (50%), testis (20%) and breast (8%). Neurological symptoms preceded the cancer diagnosis in 60% of patients (by a median of 3.5 months). Twenty-five of 44 (57%) patients with MRI studies had signal abnormalities in the limbic system. Thirty (60%) patients had antineuronal antibodies (18 anti-Hu, 10 anti-Ta, 2 anti-Ma), and 20 were antibody-negative or had uncharacterized antibodies (n = 4). The combination of symptoms, MRI findings and paraneoplastic antibodies established the diagnosis of PLE in 78% of the patients. Patients with anti-Hu antibodies usually had small-cell lung cancer (94%), multifocal neurological symptoms (78%) and a poor neurological outcome. Patients with anti-Ta (also called anti-Ma2) antibodies were young men with testicular tumours (100%), frequent hypothalamic involvement (70%) and a poor neurological outcome. In the group of patients without anti-Hu or anti-Ta antibodies, the tumour distribution was diverse, with cancer of the lung the most common (36%); 57% had positive MRI. Fifteen of 34 (44%) patients with a median follow-up of 8 months showed neurological improvement. Treatment of the tumour appeared to have more effect on the neurological outcome than the use of immune modulation. Improvement was observed in 38% of anti-Hu patients, 30% of anti-Ta patients and 64% of patients without these antibodies.
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PMID:Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients. 1086 59

Limbic encephalitis was identified as a clinicopathological entity in 1968. Up to a few years ago, 200 cases were described, most associated with lung cancer and more infrequently with other tumors. The recent identification of patients with this syndrome, idiopathic limbic encephalitis, who never develop cancer and have high titers of antibodies to voltage-gated potassium channels (VGKC) and an excellent response to immunosuppressive therapy, has extended the etiological spectrum and suggests that the syndrome may be under-recognized. The disorder, which develops in a few days or weeks, is characterized by the development of short-term memory loss, seizures, confusion and psychiatric features. The presence of symptoms beyond the limbic system is highly suggestive of a paraneoplastic origin. When limbic encephalitis is suspected, the following tests should be performed in order to demonstrate: a) involvement of the temporal lobes (EEG and brain MRI); b) presence of inflammatory abnormalities in the CSF, and c) the presence of onconeural antibodies or anti-VGKC. Once the diagnosis is confirmed by the clinical picture and MRI findings, treatment must be initiated without waiting for the antibody results because its negativity does not exclude the diagnosis. Detection of an onconeural antibody will confirm that the limbic syndrome is paraneoplastic and will help us to search for an underlying tumor and to predict possible response to the treatment. The recommended treatment is cycles of methylprednisolone (1 g/day for 3 to 5 days). Therapeutic response in the idiopathic limbic encephalitis is excellent and may be good in limbic encephalitis with anti-Ma2 or without onconeural antibodies. On the contrary, immunosuppressant treatment is not usually effective in limbic encephalitis associated to anti-Hu antibodies.
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PMID:[Limbic encephalitis: a probably under-recognized syndrome]. 1570 18

A quota sample of 3272 people from the Australian population was surveyed by telephone about the health risks of marijuana use. Three-fifths of the sample (62%) believed that there were health problems caused by marijuana use and one in four (27%) were uncertain. The most commonly cited health effects were: lung cancer, mental problems, memory loss and respiratory disease. The health risks of marijuana use were perceived to increase with increasing frequency of use, and to be greater when the user was a teenager rather than an adult. The perceived health risks of marijuana increased with age, were higher among women than men, decreased with increasing education and frequency and quantity of alcohol and were substantially lower among those who had used marijuana, and those who knew someone who had used marijuana.
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PMID:Correlates of the perceived health risks of marijuana use among Australian adults. 1620 64

Memory loss can be a symptom of paraneoplastic limbic encephalitis (PLE) a neuropsychiatric disorder associated mostly with small-cell lung cancer and anti-Hu antibodies or with testicular tumors and anti-Ma2 antibodies. We present the case of a patient with temporal coincidence of beginning cognitive decline and diagnosis of a carcinoma of the prostate in whom we diagnosed anti-Ma1/Ma2-positive PLE. The tumor had been completely resected but memory impairment further deteriorated. As the effective treatment of the cancer is considered as the most efficient treatment of a paraneoplastic neurological syndrome (PNS) a second neoplasia was suspected in the patient. By the aid of whole body positron emission tomography with 18-fluorine fluoro-2-deoxy-glucose (FDG-PET) an adenocarcinoma of the cecum could be detected. Two months after surgery anti-Ma antibodies were negative. We conclude that a second neoplasia should be considered, if effective cancer treatment does not lead to improvement or stabilisation of a PNS. Tumor search should be exhaustive and include PET when conventional imaging fails to show a malignancy.
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PMID:Second primary tumor in anti-Ma1/2-positive paraneoplastic limbic encephalitis. 1631 42

Fifty consecutive new cardiology clinic patients who were on statin drug therapy (for an average of 28 months) on their initial visit were evaluated for possible adverse statin effects (myalgia, fatigue, dyspnea, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental CoQ(10) at an average of 240 mg/day upon initial visit. Patients have been followed for an average of 22 months with 84% of the patients followed now for more than 12 months. The prevalence of patient symptoms on initial visit and on most recent follow-up demonstrated a decrease in fatigue from 84% to 16%, myalgia from 64% to 6%, dyspnea from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy from 10% to 2%. There were two deaths from lung cancer and one death from aortic stenosis with no strokes or myocardial infarctions. Measurements of heart function either improved or remained stable in the majority of patients. We conclude that statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental CoQ(10). We saw no adverse consequences from statin discontinuation.
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PMID:Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation. 1687 39

A 59-year-old man who was diagnosed with small cell lung cancer (SCLC), achieved a complete response to the induction chemoradiotherapy and received prophylactic cranial irradiation (PCI) (25 Gy at 250 cGy per fraction) in October 2008. Three months later, he complained of anorexia, weight loss, fatigue, and short-term memory loss and developed dementia and systemic muscle weakness. Magnetic resonance imaging in April and July 2009 revealed the progression of the diffuse brain atrophy without evidence of the metastasis of SCLC. Paraneoplastic neurological syndrome was suspected because anti-Hu antibody was detected in his serum and cerebrospinal fluid, but the adverse effects of chemotherapy and/or radiotherapy were also suspected as the cause of his neurological disorder.
Lung Cancer 2011 Mar
PMID:Acute onset of brain atrophy and dementia in a patient with small cell lung cancer: a case report. 2121 22

The term "paraneoplastic neurologic disorders" refers to a group of syndromes mediated by immune responses triggered by tumors that express neuronal proteins or by immunological disturbances caused by the tumor. In most cases, limbic encephalitis is a disorder of adulthood, particularly in association with small-cell lung cancer or a testicular germ-cell tumor. The clinical picture of this disorder includes anxiety, depression, confusion, delirium, hallucinations, short-term memory loss and sometimes seizures. We report on 2 new pediatric cases from a single hospital: in the first case, limbic encephalitis revealed Hodgkin lymphoma; it heralded meningeal relapse of acute lymphoblastic leukemia in the other. Despite its extreme rarity, this syndrome is a possible diagnosis in childhood.
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PMID:[Paraneoplastic limbic encephalitis: 2 pediatric cases]. 2347 34

Limbic encephalitis is a syndrome characterised by irritability, depression, sleeping disturbance, convulsion, hallucination and short-period memory loss that is commonly associated with a malignancy even if there is no evidence of it by the time of presentation. Most reported cases of limbic encephalitis as a paraneoplastic syndrome are associated with small-cell lung cancer and lymphoma. This article is a case report of a patient with limbic encephalitis associated with an oesophageal adenocarcinoma. The patient is a middle-aged man who presented apathy and unstable mood. After months, developed diplopia, reduced visual acuity and involuntary movements. Later, gait disability, disorientation, memory loss and aggressive behaviour were detected, associated with seizures. After investigation, limbic encephalitis was diagnosed and, as the patient developed dysphagia, oesophageal adenocarcinoma was detected. Oesophageal carcinoma usually does not have neurological symptoms associated.
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PMID:Limbic encephalitis as the presenting symptom of oesophageal adenocarcinoma: another cancer to search? 2359 72

Paraneoplastic limbic encephalitis is a rare neurological disorder that frequently precedes the detection of malignancy. We report the case of a 68-year-old male with small-cell lung cancer who developed paraneoplastic limbic encephalitis associated with presence of the anti-Hu antibody, after achieving complete remission of the tumor by chemotherapy. The patient visited our hospital because of progressive sensory disturbance of the distal extremities at 65 years of age. Though paraneoplastic sensory neuropathy was suspected, we could not find any tumor and he did not improve with steroids or immunoglobulin therapy. Chest computed tomography (CT) revealed large mediastinal lymphadenopathy. He was subsequently diagnosed with small cell lung cancer at one year and three months after the neurological symptoms occurred. As his serum analysis was positive for the anti-Hu antibody, we diagnosed paraneoplastic sensory neuropathy. The lung cancer disappeared with chemotherapy, but he had developed short-term memory loss six months later. Brain fluid attenuated inversion recovery (FLAIR) imaging showed an abnormal high-intensity lesion in the left medial temporal lobe including the hippocampus. We therefore made the diagnosis of paraneoplastic limbic encephalitis following subacute sensory neuropathy associated with the anti-Hu antibody. To our knowledge, this is the first report of a patient presenting with paraneoplastic neurological syndrome in which limbic encephalitis developed after tumor disappearance. So we must recognize the possibility of neurological symptoms occurring during remission. As the mechanism of pathogenesis, delayed neuronal cell damage due to immune responses against the tumor is implicated.
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PMID:[Following sensory neuropathy, anti-Hu antibody-positive paraneoplastic neurological syndrome presenting with limbic encephalitis occurs after complete remission]. 2360 43


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