Bilateral fracture of the shoulders following epileptic seizures: a case report / Fratura bilateral de ombros após convulsões epilépticas: relato de caso

Convulsive seizures caused by hyponatremia occur when this condition is severe and develops quickly, resulting in a brain's adaptive inability to contain brain swelling. Seizures are rarely the cause of shoulder fractures. This is a case report of bilateral humerus fracture following a single epileptic seizure caused by drug hyponatremia, an unconventional event in medical practice. A 69-year-old woman was admitted to the emergency room after a single tonic-clonic seizure with spontaneously ceased sphincter relaxation, showing Glasgow 6. No falls or restraint were reported by observers. When alert, the patient reported pain and difficulty moving both arms. During examination, the movement was li- mited to the right and left. Anteroposterior radiographs revealed bilateral fracture at the neck of humerus. To complement inves- tigation for further lesions, a computed tomography confirmed bilateral fracture-dislocation with impaction of the humeral head with the glenoid. Atraumatic bilateral fracture-dislocation of the humerus after epileptic seizure is a very rare event. It is believed that some of these diagnoses have been neglected due to the difficulty of characterizing the patient's pain in a postictal state. The importance of a detailed physical examination shall be emphasized in risk groups such as the polymedicated elderly.

Convulsive seizures caused by hyponatremia occur when this condition is severe and develops quickly, resulting in a brain's adaptive inability to contain brain swelling. Seizures are rarely the cause of shoulder fractures. This is a case report of bilateral humerus fracture following a single epileptic seizure caused by drug hyponatremia, an unconventional event in medical practice. A 69-year-old woman was admitted to the emergency room after a single tonic-clonic seizure with spontaneously ceased sphincter relaxation, showing Glasgow 6. No falls or restraint were reported by observers. When alert, the patient reported pain and difficulty moving both arms. During examination, the movement was li- mited to the right and left. Anteroposterior radiographs revealed bilateral fracture at the neck of humerus. To complement inves- tigation for further lesions, a computed tomography confirmed bilateral fracture-dislocation with impaction of the humeral head with the glenoid. Atraumatic bilateral fracture-dislocation of the humerus after epileptic seizure is a very rare event. It is believed that some of these diagnoses have been neglected due to the difficulty of characterizing the patient's pain in a postictal state. The importance of a detailed physical examination shall be emphasized in risk groups such as the polymedicated elderly.

Carcinoma escamoso epicraneal metastásico con invasión parenquimatosa cerebral, a propósito de un caso / Metastatic epicranial squamous carcinoma with parenchymal brain invasion, apropos of a case

RESUMEN A nivel mundial se estiman que cada año se diagnostican aproximadamente 650 000 nuevos casos de cáncer escamoso de cabeza y cuello. Ocasionan 300 000 muertes y dos tercios de estos casos se originan en países en vías de desarrollo. Se presentó un caso de un paciente atendido en consulta a causa de crecimiento acelerado de la región frontotemporoparietal derecha, acompañado de sintomatología neurológica correspondiente a una afección funcional de los lóbulos parietal y temporal derecho. Se le realizó exámenes imagenológicos y biopsia por punción de la lesión, lo que arrojó un carcinoma escamoso como variedad histológica de la tumoración (AU).

ABSTRACT It is thought that around 650 000 new cases of head and neck squamous tumors are diagnosed in the world every year. They cause 300 000 deaths and two thirds of these cases are originated in developing countries. We presented the case of a patient who assisted the consultation due to the fast growth of the right frontotemporal parietal region, accompanied with neurological symptomatology corresponding to a functional disorder of the right parietal and temporal lobes. Imaging studies and a biopsy by lesion puncture were performed. It showed a squamous carcinoma as histological variant of the tumor (AU).

Transient Global Amnesia Developed after Zolpidem Intake

We report two patients who complained of transient anterograde amnesia and repetitive questioning, that developed after taking zolpidem and lasted for several hours. The clinical manifestations of these patients fulfill the clinical criteria for transient global amnesia (TGA). The typical clinical manifestation of TGA following the consumption of zolpidem suggests a possible relationship associated with its drug mechanism.

Hippocampal Lesions of Diffusion Weighted Magnetic Resonance Image in Patients with Headache without Symptoms of Transient Global Amnesia

BACKGROUND: The dot-like hippocampal signal intensity in diffusion-weighted MR images is well-known as a characteristic imaging feature in transient global amnesia, a neurological syndrome in which sudden forward-and-backward memory loss occurs that is slowly recovered within 24 hours. We here report on patients with this dot-like hippocampal hyperintensity who did not present with anterograde amnesia except for headaches. CASE REPORT: Two women without a specific medical history presented with sudden-onset headaches on the same day. Neither had any trauma or infection history before the symptom or any sudden emotional or postural changes. Brain MRI showed tiny hippocampal high signal intensity on diffusion-weighted images (DWI). CONCLUSIONS: Dot-like hippocampal lesions seen on DWI may be present without memory impairment, and more studies are needed to determine whether there is any association with headache as in this case.

Hippocampal Hyperintensities on Diffusion-Weighted MRI without Transient Global Amnesia

Dot-like hippocampal hyperintensities on diffusion-weighted magnetic resonance imaging (MRI) have been reported as an interesting imaging finding of transient global amnesia (TGA). We report three patients with such dot-like hippocampal hyperintensities who did not present with anterograde amnesia. Episodes associated with the Valsalva maneuver such as nausea or vomiting might have produced the dot-like hippocampal hyperintensities in these patients. However, depending on the individual susceptibility to hippocampal lesions, clinical symptoms of TGA might not be present even when hippocampal lesions are present.

Human Herpes Virus 6 Encephalitis Following Bone Marrow Transplantation with Uncommon Magnetic Resonance Imaging Findings

BACKGROUND: Human Herpes Virus 6 (HHV6) is commonly associated with encephalitis following bone marrow transplantation. However, hippocampal atrophy and global hypometabolism are rare findings in HHV6 encephalitis. CASE REPORT: A 41-year-old right-handed woman with acute lymphoblastic leukemia presented with fever and mental changes 2 weeks after receiving a sibling bone marrow transplant. The patient's cerebrospinal fluid (CSF) was positive for HHV-6 deoxyribonucleic acid (DNA), but was negative for other viral DNA. Brain magnetic resonance imaging revealed atrophic changes in bilateral medial temporal lobes. Following 4 weeks of ganciclovir therapy, a CSF exam was negative for HHV-6 DNA and the patient's neurological symptoms partially improved. However, she was disoriented and had severe retrograde and anterograde amnesia. 18F-fluorodeoxyglucose-positron emission tomography indicated global hypometabolism in the medial temporal lobes and the fronto-parietal cortices. CONCLUSIONS: This is a rare and unusual case of hippocampal atrophy in the acute stage of HHV6 encephalitis. Our imaging findings may reflect the chronic indolent course of HHV6 encephalitis.

Zolpidem Induced Sleep-related Eating and Complex Behaviors in a Patient with Obstructive Sleep Apnea and Restless Legs Syndrome

Zolpidem-induced sleep-related complex behaviors (SRCB) with anterograde amnesia have been reported. We describe herein a case in which the development of zolpidem-induced sleep-related eating disorder (SRED) and SRCB was strongly suspected. A 71-year-old Korean male was admitted to the Department of Psychiatry due to his repetitive SRED and SRCB with anterograde amnesia, which he reported as having occurred since taking zolpidem. The patient also had restless legs syndrome (RLS) and obstructive sleep apnea (OSA). His baseline serum iron level was low at admission. Zolpidem discontinuation resulted in the immediate disappearance of his SRED, but did not affect his RLS symptoms. These symptoms rapidly improved after adding a single i.v. iron injection once daily, and so he was discharged to day-clinic treatment. These findings indicate that zolpidem can induce SRCB. Although the pathophysiology of zolpidem-induced SRED and other SRCB remains unclear, clinicians should carefully monitor for the potential induction of complex behaviors associated with zolpidem in patients with comorbid RLS or OSA.

Etifoxine for Pain Patients with Anxiety

Etifoxine (etafenoxine, Stresam(R)) is a non-benzodiazepine anxiolytic with an anticonvulsant effect. It was developed in the 1960s for anxiety disorders and is currently being studied for its ability to promote peripheral nerve healing and to treat chemotherapy-induced pain. In addition to being mediated by GABA(A)alpha2 receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to beta2 or beta3 subunits of the GABA(A) receptor complex. It also modulates GABA(A) receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (TSPO) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral benzodiazepine receptor (PBR). Therefore, the effects of etifoxine are not completely reversed by the benzodiazepine antagonist flumazenil. Etifoxine is used for various emotional and bodily reactions followed by anxiety. It is contraindicated in situations such as shock, severely impaired liver or kidney function, and severe respiratory failure. The average dosage is 150 mg per day for no more than 12 weeks. The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines. It potentiates GABA(A) receptor-function by a direct allosteric effect and by an indirect mechanism involving the activation of TSPO. It seems promising that non-benzodiazepine anxiolytics including etifoxine will replenish shortcomings of benzodiazepines and selective serotonin reuptake inhibitors according to animated studies related to TSPO.

Paraneoplastic Limbic Encephalitis in a Male with Squamous Cell Carcinoma of the Lung

BACKGROUND: Paraneoplastic limbic encephalitis (PLE) is a rare syndrome characterized by memory impairment, symptoms of hypothalamic dysfunction, and seizures. It commonly precedes the diagnosis of cancer. Small-cell lung cancer is the neoplasm that is most frequently reported as the etiology underlying PLE. CASE REPORT: This report describes a male patient who presented with neurologic symptoms consistent with anterograde amnesia, apathy, and disorientation. MRI revealed diffuse hyperintensities located predominantly in the medial bitemporal lobes, basal ganglia, frontal lobes, and leptomeninges on fluid attenuated inversion recovery images, suggesting PLE. Study of the primary tumor revealed squamous cell carcinoma of the lung. The patient was treated with neoadjuvant chemotherapy followed by surgery and adjuvant chemoradiotherapy, which resulted in his neurologic symptoms gradually improving. CONCLUSIONS: PLE might be a rare debut of squamous cell carcinoma of the lung. Treatment of the primary tumor may improve the neurologic symptoms.

A Case of Anterograde Amnesia with Bilateral Hippocampus Involvement After Acute Glufosinate Ammonium Intoxication

A 51-year-old man developed anterograde amnesia following the ingestion of glufosinate ammonium. Brain MRI revealed hyperintense lesions involving the bilateral hippocampus and parahippocampal gyrus, and the right occipital lobe. The mechanism underlying acute glufosinate ammonium intoxication and the differential diagnosis of hippocampal lesions are discussed.

Isoflurane Induces Transient Anterograde Amnesia through Suppression of Brain-Derived Neurotrophic Factor in Hippocampus

OBJECTIVE: Transient anterograde amnesia is occasionally observed in a number of conditions, including migraine, focal ischemia, venous flow abnormalities, and after general anesthesia. The inhalation anesthetic, isoflurane, is known to induce transient anterograde amnesia. We examined the involvement of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) in the underlying mechanisms of the isoflurane-induced transient anterograde amnesia. METHODS: Adult male Sprague-Dawley rats were divided into three groups : the control group, the 10 minutes after recovery from isoflurane anesthesia group, and the 2 hours after recovery from isoflurane anesthesia group (n=8 in each group). The rats in the isoflurane-exposed groups were anesthetized with 1.2% isoflurane in 75% nitrous oxide and 25% oxygen for 2 hours in a Plexiglas anesthetizing chamber. Short-term memory was determined using the step-down avoidance task. BDNF and TrkB expressions in the hippocampus were evaluated by immunofluorescence staining and western blot analysis. RESULTS: Latency in the step-down avoidance task was decreased 10 minutes after recovery from isoflurane anesthesia, whereas it recovered to the control level 2 hours after isoflurane anesthesia. The expressions of BDNF and TrkB in the hippocampus were decreased immediately after isoflurane anesthesia but were increased 2 hours after isoflurane anesthesia. CONCLUSION: In this study, isoflurane anesthesia induced transient anterograde amnesia, and the expressions of BDNF and TrkB in the hippocampus might be involved in the underlying mechanisms of this transient anterograde amnesia.

Ácido domoico e intoxicación amnésica por moluscos en salud pública: [revisión] / Domoic acid and amnesic shellfish poisoning in public health: [review]

El ácido domoico es una biotoxina marina que por primera vez produjo una intoxicación alimentaria en más de cienpersonas en 1987 en Canadá, con muerte en algunos de ellos después de la ingesta de mejillones contaminados. Dentro de las manifestaciones clínicas destacó la amnesia anterógrada, no vista con ninguna biotoxina ni fármaco conocido, pudiendo llegar a ser permanente, por lo cual el síndrome fue denominado intoxicación amnésica por moluscos. En el examen histopatológico del cerebro de los fallecidos, se encontró que el hipocampo fue una de las estructuras más afectadas, con necrosis celular en algunas áreas, lo que explicó el deterioro irreversible de la memoria. Se ha encontrado que muchas especies de mariscos, peces filtradores, krill y animales marinos, pueden contaminarse con dicha biotoxinaque es producida por algunas algas microscópicas y que muchas veces son responsables de las denominadas mareas rojas. La biotoxina puede llegar al humano por la cadena alimenticia. En este artículo, se revisa los brotes tóxicos en mamíferos y aves marinas con posterior muerte debido al ácido domoico, el mecanismo en la producción de toxicidad, su agonismo en los receptores glutamatérgicos, la importancia en la salud pública, sus riesgos por evaluar en la salud humana, así como la difusión de la biotoxina por el mundo, incluyendo el Océano Pacífico y las posibles razones de tal difusión, así como su importancia ecológica y económica que ha obligado a la vigilancia mundial.

Domoic acid is a sea biotoxin that was first identified to produce food poisoning in more than a hundred people inCanada, in 1987, with some deaths reported, after intake of contaminated mussels. As part of the clinical presentation, anterograde amnesia is highlighted. As it had not been seen before with any know biotoxin or drug, and could be permanent, the syndrome was called amnesic poisoning due to shellfish. In the histopathological examination of the brain of the dead patients, the hippocampus was one of the most affected, showing cellular necrosis in some areas, which explains the irreversible deterioration of the memory. Many shellfish species, filtrating fish, krill and marine animalscan get contaminated by the biotoxin , which is produced by microscopic algae, which are often responsible of the redtides. The biotoxin can reach the human being through the food chain. In this article, we revise the toxic outbreaks inmammals and marine birds, causing death due to domoic acid, the mechanism of toxicity production, its agonism in the glutamatergic receptors, its importance in public health, the risk they pose to human health and ought to be evaluated, and the diffusion of the biotoxin throughout the world, including the Pacific Ocean and the possible reasons of this diffusion, as well as its ecologic and economic importance, which has made it surveillance compulsory in all the world.

Aprendizaje de nombres en una paciente con amnesia anterógrada / Names learning in an anterograde amnesic patient

En este trabajo se describe la aplicación de algunas técnicas empleadas para la rehabilitación de la memoria en personas con daño cerebral, con el fin de facilitar el aprendizaje de nombres de personas cercanas y conocidas en una paciente de 55 años, universitaria, diestra y quien como secuela de una encefalitis herpética presentó lesión isquémica en territorio frontotemporal izquierdo y severas alteraciones cognoscitivas y funcionales. Aunque la aplicación combinada de técnicas favorece los procesos de aprendizaje, éstos suelen ser lentos y desgastantes en personas con amnesia severa. No obstante, los resultados apoyan la propuesta de la conservación de la memoria implícita en esta población y favorecen el planteamiento de perspectivas de intervención.

In this work, we describe the application of some techniques used for the memory rehabilitation in people with brain damage, in order to facilitate learning the names of close and known persons in a 55 year old patient, college graduate, right handed, with herpetic encephalitis who presented injury in left frontotemporal region and severe cognitive and functional alterations. As show in the results, of the six names selected for the intervention, it was possible to work with three of them and to obtain significant results in two. Although the mix of techniques favors the learning processes, this process is usually slow in people with severe amnesia. However, these results support the proposal of the implicit memory conservation and favor the intervention from this perspective.

Amnesia global transitoria: estudio de 260 pacientes / Transitory global amnesia. I study of 260 patients

La amnesia global transitoria (AGT) es un trastorno de memoria que aparece en personas de edad madura y ancianas, el cuadro clínico está dado por episodios de amnesia anterógrada y confusión de varias horas de duración con recuperación total y patogenia no bien reconocida. Se desarrolló esta investigación para tratar de establecer las características clínicas, factores de riesgo (FR) y evolución de los pacientes atendidos en este medio. Se realizó un estudio prospectivo de 260 enfermos con AGT atendidos en el Servicio de Neurología entre los años 1988 y 2002, incluyendo ambos. Los datos se obtuvieron mediante entrevistas a los pacientes y familiares y se analizaron las características clínicas, FR, exámenes complementarios y evolución. Se observó que 226 (86,9 por ciento) se hallaban por encima de los 60 años. El promedio de edad fue de 68,3 años. La hipertensión arterial (HTA) fue factor precipitante en 144 enfermos (55,4 por ciento), en tanto el estrés lo fue en 138 (53,1 por ciento). El promedio de duración de los episodios fue de 3,5 h. Entre los factores de riesgo vascular (FRV), la hipertensión arterial estuvo presente en 160 enfermos (61,5 por ciento), seguida por el hábito de fumar, en 92 (35,4 por ciento). Hubo 188 personas (72,4 por ciento) que tuvieron entre 1 y 3 episodios. El promedio fue de 2,3 ataques. El tiempo de seguimiento promedio en nuestra casuística es de 8,1 años. Se comprobó que 217 enfermos (83,5 por ciento) se encontraban asintomáticos, mientras 21(8,1 por ciento) habían fallecido y 12, habían sufrido un ictus. Se concluyó que la AGT es un síndrome que suele aparecer con mayor frecuencia por encima de los 60 años, la patogenia continúa sin dilucidar y existen diversos factores de riesgo cuyo papel no se ha podido precisar. La evolución de los enfermos no ayuda a determinar la etiología y todo parece indicar, según lo observado por nosotros, que se trata de un proceso benigno.

study of postictal sleep architecture in epileptic patients

The relationship between sleep and epilepsy is complicated and reciprocal; an understanding of the influences of each on the other has important clinical implications. The post-ictal state precisely could produce profound changes in the sleep-wake cycle, and it frequently causes disruption in sleep architecture. To assess sleep architecture postictally, within a maximum period of 48 hours in epileptic patients. Post-ictal assessment of sleep architecture using polysomnographic recording and long-term video EEG monitoring was applied for twenty epileptic patients with non-symptomatic generalized or localization-related epilepsies as well as for 10 age and gender matched controls. All patients were submitted to full clinical, laboratory and radiological assessment. Epileptic patients had significantly less number of awakenings, higher percentages of S2, lower percentages of SWS from total sleep time and shorter latency to SWS as compared to the control. Patients with generalized epilepsies had significantly higher periods of sleep latency to S2 as compared to patients with focal seizures and those on polytherapy had significant shorter sleep latency to S2, with significant higher apnea index in NREM sleep compared to those on monotherapy. Post-ictal state appears to disrupt the regulation of sleep architecture, which mainly recognized in the NREM sleep

A Case of Neuro-Behcet's Disease Presenting as Anterograde Amnesia

Anterograde amnesia in Behcet's disease is a rare occurrence. A 50-year-old man presented with anterograde amnesia. He had been suffering multiple oral aphthous ulcers and genital ulcers with erythema nodosum. A neurological examination revealed prominent anterograde memory disturbance. Brain MRI revealed high signal intensity lesions involving the anterior thalamus, posterior part of the basal ganglia and the mesial temporal lobe. We report a rare case of Behcet's disease manifesting severe anterograde amnesia resulting from thalamic and mesial temporal lesions.

Changes of Regional Cerebral Blood Flow in Left Anterior Thalamic Infarction: Analysis of 99mTc-Ethyl Cysteinate Dimer (ECD) SPECT by using Statistical Parametric Mapping

BACKGROUND: The thalamus has multiple connections with areas of the cerebral cortex involved in arousal and cognition. Thalamic damage has been reported to be associated with variable neuropsychological dysfunctions and dementia. This study investigates the changes of regional cerebral blood flow (rCBF) by using SPM analysis of 99mTc-ECD SPECT and examining the neuropsychological abnormalities of 4 patients with anterior thalamic infarctions. METHODS: Four patients with left anterior thalamic infarctions and eleven normal controls were evaluated. K-MMSE and the Seoul Neuropsychological Screening Battery were performed within 2 days after stroke. The normalized SPECT data of 4 patients were compared to those of 11 controls for the detection of areas with decreased rCBF by SPM analysis. RESULTS: All 4 patients showed anterograde amnesia in their verbal memory, which was not improved by recognition. Dysexecutive features were occasionally present, such as decreased word fluency and impaired Stroop test results. SPM analysis revealed decreased rCBF in the left supramarginal gyrus, the superior temporal gyrus, the middle and inferior frontal gyrus, the medial dorsal and anterior nucleus of the left thalamus. CONCLUSIONS: The changes of rCBF in patients with left anterior thalamic infarctions may be due to the remote suppression on metabolism by the interruption of the cortico-subcortial circuit, which connects the anterior thalamic nucleus and various cortical areas. The executive dysfunction and dysnomia may be caused by the left dorsolateral frontal dysfunction of the thalamocortical circuit. Anterograde amnesia with storage deficit may be caused by the disruption of mamillothalamic tract.

The evaluation of conscious sedation for dental surgery with various intravenous agents

Effect of Flumazenil on the Anterograde and Retrograde Amnesia Caused by Midazolam / 대한마취과학회지

We report a case of profound amnesia, anterograde and retrograde, in a patient, who had been premedicated with midazolam and underwent a posterior fusion of the cervical spine under inhalation anesthesia. The patient's memory was restored immediately after intravenous injections of the benzodiazepine antagonist flumazenil.

Retrograde Amnesia Following Anterior Thalamic Infarction

BACKGROUND: Retrograde amnesia (RA) refers to the failure to recall events that occurred before a brain injury. RA is known to be associated with brain lesions involving the hippocampus, entorhinal cortex and the frontal lobe. Anterior thalamic lesion often causes anterograde amnesia but rarely causes RA. The aim of the present study is in two parts . First, we discuss the neuroanatomical perspectives of RA based on our case with severe RA after a right anterior thalamic infarction. Second, we introduce a test for RA termed the "Korean Public Events Recall Test (K-PERT)", which was developed based on famous Korean public events from 1966 to 1997. METHODS: A 62-year-old woman with transient RA after a left anterior thalamic infarction 4 years ago presented severe and persistent RA following a right anterior thalamic infarction. We followed up the patient with neuropsychological tests. We also performed the K-PERT on the patient as well as on 14 women of the same age and education. RESULTS: Neuropsychological tests showed severe impairment in autobiographical memory with frontal lobe dysfunction. On K-PERT, the normal controls scored 13.7 +/- 3.7 in recall and 21.2 +/- 3.1 in recognition out of a maximum score of 30, whereas the patient obtained only 3/30 and 4/30, respectively. CONCLUSIONS: In our case, RA might have resulted from damage to the pathway that retrieves old memories, which are stored in the frontal lobe. Thus, anterior thalamus might be viewed as the gate of memory engram. Further studies are needed to elaborate the usefulness of K-PERT as an objective tool for investigating remote memory.