RESUMO
Effectiveness of antiepileptic drugs (AEDs) has been traditionally monitored by patient-reported seizures. A 31-year-old male patient was treated with a responsive neurostimulation system (RNS). The ambulatory electrocorticographic data were used to guide AED choice and dosing in achieving subsidence of disabling seizures and minimization of the adverse effects of polypharmacy.
RESUMO
An otherwise healthy 30-year-old male acquired gastrointestinal beriberi and subsequent Wernicke's encephalopathy after 1 session of heavy drinking. Nausea, vomiting, and anorexia relentlessly progressed. The patient developed external ophthalmoplegia after 2 months. Intravenous 1,000 mg thiamine reversed both neurologic and gastrointestinal symptoms within hours. It is hard to diagnose gastrointestinal beriberi since the symptoms are nonspecific. The patient underwent 11 emergency room visits, 3 hospital admissions, and laparoscopic cystectomy within 2 months, but the gastrointestinal symptoms continued to progress. Two months after the onset of gastrointestinal symptoms, external ophthalmoplegia appeared, and, therefore, intravenous thiamine was given. The simultaneous resolution of the debilitating gastrointestinal symptoms and external ophthalmoplegia was unique. Thiamine deficiency remains underdiagnosed and should be considered in patients who develop unexplained gastroparesis or autonomic nervous failure of the digestive system, even in the nonalcoholic population.
RESUMO
We report a case of a 60-year-old woman with a history of intractable seizures and isolated delusional psychosis who was later diagnosed with steroid-responsive encephalopathy associated with autoimmune thyroiditis. The patient underwent right temporal lobectomy (epilepsy surgery) 15 years before coming to this clinic, but continued to have focal seizures, resulting in frequent emergency room visits thereafter. After admission for intensive inpatient video electroencephalogram monitoring and subsequent 7 months of close follow-up, both the electroencephalogram abnormalities and isolated delusional psychosis were found to be responsive to immunotherapy. This suggests that her epilepsy may be autoimmune in nature. Steroid-responsive encephalopathy associated with autoimmune thyroiditis was diagnosed after 26 years since the onset of seizures. Performing invasive epilepsy surgery in patients with autoimmune epilepsy cannot reverse the inflammatory process; therefore, it is reasonable to test for autoimmune etiologies before excision surgery on patients with medically intractable epilepsy. This case demonstrates the clinical use of quantitative electroencephalogram in assisting with the diagnosis of steroid-responsive encephalopathy associated with autoimmune thyroiditis and supports that it is a spectrum disorder with protean manifestations.
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Patients with nontoxic lithium levels can still develop hand tremors, downbeat nystagmus, and an unsteady gait.
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We report a case of Hashimoto's encephalopathy (HE), who presented with epilepsia partialis continua (EPC) and a frontal lobe lesion. The diagnosis of HE remained elusive until the serum thyroid antibodies became positive 7 months after the onset of EPC. The histopathology of this frontal lesion showed nonvasculitic inflammation.
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Limbic encephalitis (LE) can present as a nonspecific manifestation preceding neoplastic disease. Having high clinical suspicion and using newer onconeural antibodies, like antiglial nuclear antibody (AGNA), can lead to an earlier diagnosis. We report a patient with AGNA-positive LE who is later diagnosed and treated for small-cell lung carcinoma.
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We report a case of early-onset dementia with subclinical seizures. Aggressive seizure control improved the patient's cognition. Commonly, an EEG is only performed following overt behavioral seizures. Therefore, subclinical seizures tend to be underdiagnosed. Serial or extended EEG should be seriously considered in patients with early-onset dementia.
RESUMO
With the increased availability of laboratory tests, glutamic acid decarboxylase (GAD) antibody-positive limbic encephalitis has become an emerging diagnosis. The myriad symptoms of limbic encephalitis make the diagnosis challenging. Symptoms range from seizures, memory loss, dementia, confusion, to psychosis. We present a case of a 21-year-old female with GAD65 antibody-positive limbic encephalitis. The case is unique because the clinical course suggests that non-convulsive seizures are the major cause of this patient's clinical manifestations. The following is the thesis: systemic autoimmune disease, associated with the GAD65 antibody, gives rise to seizures, in particular, non-convulsive seizures. Temporal lobes happen to be the most susceptible sites to develop seizures. The greater part of these seizures can be non-convulsive and hard to recognize without electroencephalogram (EEG) monitoring. The variable symptoms mirror the severity and locations of these seizures. The magnetic resonance imaging (MRI) signal abnormities in the bilateral hippocampus, fornix, and mammillary body correlate with the density of these seizures in the similar manner, which suggests it is secondary to post-ictal edema.
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BACKGROUND: Abnormality in diffusion-weighted magnetic resonance imaging representing early changes of acute ischemic lesions in human and animal models of focal status epilepticus has been reported to correlate with clinical outcome. CASE REPORT: We reported a 35 year-old woman with initial status epilepticus, probably related to previous head injury with traumatic intracerebral hemorrhage. The presenting MRI showed reversible hyperintensity lesions on DWI, which is probably corresponding to the epileptogenic lesion. Similar abnormalities in the splenium as a remote effect were demonstrated in this case. CONCLUSION: The atrophic changes in the splenium and right parietal lobe in the follow-up MRI scans were supposed to correlate with the following neurological sequelae.