levetiracetam and Brain-Edema

This review provides management recommendations for medical and neurologic problems in patients with brain tumors, including vasogenic edema, infections, seizures, prophylaxis and treatment of venous thromboembolism, drug interactions, cognitive and emotional problems, palliative symptom management, and long-term sequelae of brain tumors and their therapy.. Non-enzyme-inducing antiepileptic drugs are the preferred category of seizure medication for patients with brain tumors, and levetiracetam is emerging as the drug of choice. Select groups of patients, such as those with cortically based hemorrhagic melanoma metastases, may benefit from prophylactic antiepileptic drug use. Antiangiogenic agents can reduce the steroid requirement of patients with vasogenic edema. Patients with brain tumors remain at risk for infections from the perioperative period through many months after treatment, and steroids may mask signs of infection. Few studies have been done on management of common cognitive issues such as short-term memory deficits and fatigue, but memantine may help delay cognitive deficits in patients receiving whole-brain radiation therapy. Palliative care conversations should begin early in the course of treatment.. Meticulous medical management begins at diagnosis of brain tumors and continues through the active treatment course and into either palliative care strategies or management of long-term sequelae of treatment. During the active treatment phase, problems such as vasogenic edema, seizures, and venous thromboembolism predominate, whereas late complications include the continuing risk of infections; sequelae of radiation such as vascular disease, cavernous angiomas, and cognitive decline; and secondary tumors. Attention to symptom palliation is an important part of the neurologist's role throughout the course of a brain tumor patient's illness.

Topics: Angiogenesis Inhibitors; Anticonvulsants; Brain Edema; Brain Neoplasms; Cognition Disorders; Dopamine Agents; Humans; Levetiracetam; Memantine; Palliative Care; Piracetam; Seizures

Symptoms of COVID-19, as reported during the SARS-CoV-2 pandemic in 2019-2020, are primarily respiratory and gastrointestinal, with sparse reports on neurological manifestations. We describe the case of a 17-year old female with Cornelia de Lange syndrome and well controlled epilepsy, who sustained significant cortical injury during a COVID-19 associated multi-inflammatory syndrome.

Topics: Acute Kidney Injury; Adolescent; Airway Extubation; Anticonvulsants; Blood Coagulation Disorders; Bone Marrow Failure Disorders; Brain Diseases; Brain Edema; C-Reactive Protein; COVID-19; De Lange Syndrome; Disease Progression; Electroencephalography; Epilepsy; Female; Ferritins; Humans; Influenza B virus; Influenza, Human; Levetiracetam; Magnetic Resonance Imaging; Midazolam; Necrosis; Phenobarbital; Pseudomonas Infections; Respiration, Artificial; Rhabdomyolysis; SARS-CoV-2; Seizures; Sepsis; Systemic Inflammatory Response Syndrome; Tachycardia, Ventricular

BACKGROUND This study was designed to investigate the effects of different doses of levetiracetam on aquaporin 4 (AQP4) expression in rats after fluid percussion injury. MATERIAL AND METHODS Sprague-Dawley rats were randomly divided into 4 groups: sham operation group, traumatic brain injury group, low-dose levetiracetam group, and high-dose levetiracetam group. Brain edema models were established by fluid percussion injury, and intervened by the administration of levetiracetam. Samples from the 4 groups were collected at 2, 6, 12, and 24 h, and at 3 and 7 days after injury. Histological observation was performed using hematoxylin-eosin staining and immunohistochemical staining. AQP4 and AQP4 mRNA expression was detected using Western blot assay and RT-PCR. Brain water content was measured by the dry-wet method. RESULTS Compared with the traumatic brain injury group, brain water content, AQP4 expression, and AQP4 mRNA expression were lower in the levetiracetam groups at each time point and the differences were statistically significant (P<0.05). The intervention effects of high-dose levetiracetam were more apparent. CONCLUSIONS Levetiracetam can lessen brain edema from fluid percussion injury by down-regulating AQP4 and AQP4 mRNA expression. There is a dose-effect relationship in the preventive effect of levetiracetam within a certain extent.

Topics: Animals; Aquaporin 4; Blotting, Western; Brain; Brain Edema; Brain Injuries; Dose-Response Relationship, Drug; Gene Expression Regulation; Immunohistochemistry; Levetiracetam; Male; Percussion; Piracetam; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; RNA, Messenger; Water

Our previous study showed that treatment with levetiracetam (LEV) after status epilepticus (SE) termination by diazepam might prevent the development of spontaneous recurrent seizures via the inhibition of neurotoxicity induced by brain edema events. In the present study, we determined the possible molecular and cellular mechanisms of LEV treatment after termination of SE. To assess the effect of LEV against the brain alterations after SE, we focused on blood-brain barrier (BBB) dysfunction associated with angiogenesis and brain inflammation. The consecutive treatment of LEV inhibited the temporarily increased BBB leakage in the hippocampus two days after SE. At the same time point, the LEV treatment significantly inhibited the increase in the number of CD31-positive endothelial immature cells and in the expression of angiogenic factors. These findings suggested that the increase in neovascularization led to an increase in BBB permeability by SE-induced BBB failure, and these brain alterations were prevented by LEV treatment. Furthermore, in the acute phase of the latent period, pro-inflammatory responses for epileptogenic targets in microglia and astrocytes of the hippocampus activated, and these upregulations of pro-inflammatory-related molecules were inhibited by LEV treatment. These findings suggest that LEV is likely involved in neuroprotection via anti-angiogenesis and anti-inflammatory activities against BBB dysfunction in the acute phase of epileptogenesis after SE.

Topics: Acute Disease; Animals; Anticonvulsants; Astrocytes; Blood-Brain Barrier; Brain Edema; Capillary Permeability; Cytokines; Disease Models, Animal; Endothelial Cells; Gliosis; Hippocampus; Levetiracetam; Male; Mice, Inbred ICR; Microglia; Neovascularization, Pathologic; Piracetam; Status Epilepticus

The management of status epilepticus (SE) is important to prevent mortality and the development of post-SE symptomatic epilepsy. Acquired epilepsy after an initial brain insult by SE can be experimentally reproduced in the murine model of SE induced by pilocarpine. In the present study, we evaluated the possibility of treatment with a high-dose of levetiracetam in this model. Repeated treatment with high-dose levetiracetam after termination of SE by diazepam significantly prevented the incidence of spontaneous recurrent seizures and mortality for at least 28 days. To determine the brain alterations after SE, magnetic resonance imaging was performed. Both T2-weighted imaging and diffusion-weighted imaging showed changes in the limbic regions. These changes in the limbic regions demonstrated the development of cytotoxic edema three hours after SE, followed by the development of vasogenic edema two days after SE. In the pilocarpine-SE model, the incidence of spontaneous recurrent seizures after SE was strongly associated with neuronal damage within a few hours to days after SE by the development of vasogenic edema via the breakdown of the blood-brain barrier in the limbic regions. High-dose levetiracetam significantly suppressed the parameters in the limbic areas. These data indicate that repeated treatment with high-dose levetiracetam for at least two days after SE termination by diazepam is important for controlling the neuronal damage by preventing brain edema. Therefore, these findings suggest that early treatment with high-dose levetiracetam after SE termination by diazepam may protect against adverse sequelae via the inhibition of neurotoxicity induced by brain edema events.

Topics: Animals; Anticonvulsants; Brain Edema; Cell Death; Disease Models, Animal; Levetiracetam; Magnetic Resonance Imaging; Male; Mice; Mice, Inbred ICR; Muscarinic Agonists; Neurons; Pilocarpine; Piracetam; Status Epilepticus; Time Factors

Cerebral amyloid angiopathy is a major cause of lobar hemorrhage in older adults, and of microvascular ischemic disease. The rarest form of this disease is an inflammatory form causing seizures. It is important to recognize because the patients usually respond to a brief course of immunosuppression.. Case report.. A 66-year-old man developed gradual cognitive decline, insidiously increasing headaches, and then had a likely seizure. MRI showed diffuse white matter edema, and innumerable superficial microhemorrhages characteristic of amyloid angiopathy. He was empirically treated with oral prednisone and an anticonvulsant. His symptoms improved and the white matter edema resolved over several months. ApoE genotype was 4/4, which is commonly found in inflammatory amyloid angiopathy.. Inflammatory cerebral amyloid angiopathy can be clinically diagnosed and treated without brain biopsy. Clinical diagnosis is important because of the good response to a brief course of steroids in most cases.

Topics: Aged; Anticonvulsants; Apolipoprotein E4; Brain Edema; Cerebral Amyloid Angiopathy, Familial; Diffusion Magnetic Resonance Imaging; Drug Therapy, Combination; Genotype; Humans; Image Processing, Computer-Assisted; Immunosuppressive Agents; Levetiracetam; Magnetic Resonance Imaging; Male; Neurologic Examination; Neuropsychological Tests; Occipital Lobe; Piracetam; Prednisone; Temporal Lobe