Intermittent Ocular Microflutter in a Patient with Acute-Onset Oscillopsia.

Saccadic intrusions are small involuntary saccadic movements that disrupt visual fixation. Among saccadic intrusions without intersaccadic intervals, ocular flutter and opsoclonus are prominent. The saccade amplitude can occasionally be very small, which is referred to as ocular microflutter. The authors present a patient with acute-onset oscillopsia following a non-specific viral condition. An ocular microflutter was subsequently detected using video-oculography. After extensive investigation, a diagnosis of isolated idiopathic or post-viral ocular microflutter was made. The evolution of the condition was favourable, and the progressive improvement of oscillopsia occurred during the following months; however, complete resolution was not achieved. Ocular microflutter is a saccadic intrusion that is rarely described in the literature and is likely go clinically unnoticed because of its small amplitude and the rare use of video-oculography in daily practice. In patients in whom this condition is suspected, the use of video-oculography is essential for a correct diagnosis.

Brain oscillatory activity during sleep shows unknown dysfunctions in early encephalopathy

Electroencephalographic recordings in cirrhotic patients without overt hepatic encephalopathy (HE) have mainly been performed during wakefulness. Our aim was to quantify their alterations in nocturnal sleep electroencephalogram (EEG). In 20 patients and 20 healthy volunteers, we recorded a nocturnal digital polysomnography. Different sleep parameters were measured. Besides, we performed quantitative analysis of EEG (qEEG) as follows: spectral power in the different sleep stages was calculated in the frequency bands low δ, δ, θ, α, and σ. Also, the mean dominant frequency and Sleep Indexes were obtained. In comparison with controls, the group of patients showed (1) different alterations in both the microstructure and the macrostructure of sleep; (2) an increase in, both, θ band power and the average mean dominant frequency during rapid eye movement (REM); (3) in all sleep stages, a decrease of sleep electroencephalogram spectral power in low δ band and an increase in δ band: and (4) in stages N3 and REM, significant increases in the minimum of mean dominant frequency and in the respective sleep indexes. Therefore, in cirrhotic patients without overt HE, and likely having minimal hepatic encephalopathy, we found different alterations in both the microstructure and the macrostructure of nocturnal sleep. Also, sleep qEEG showed a brain dysfunction in slow oscillatory mechanisms intrinsic of sleep stages, with an increase in the frequency of its maximal electroencephalogram synchronization, from low δ to δ band. These alterations may reflect the onset of encephalopathy; sleep qEEG may, thus, be an adequate tool for its brain functional evaluation and follow-up

Brain oscillatory activity during sleep shows unknown dysfunctions in early encephalopathy.

Electroencephalographic recordings in cirrhotic patients without overt hepatic encephalopathy (HE) have mainly been performed during wakefulness. Our aim was to quantify their alterations in nocturnal sleep electroencephalogram (EEG). In 20 patients and 20 healthy volunteers, we recorded a nocturnal digital polysomnography. Different sleep parameters were measured. Besides, we performed quantitative analysis of EEG (qEEG) as follows: spectral power in the different sleep stages was calculated in the frequency bands low δ, δ, θ, α, and σ. Also, the mean dominant frequency and Sleep Indexes were obtained. In comparison with controls, the group of patients showed (1) different alterations in both the microstructure and the macrostructure of sleep; (2) an increase in, both, θ band power and the average mean dominant frequency during rapid eye movement (REM); (3) in all sleep stages, a decrease of sleep electroencephalogram spectral power in low δ band and an increase in δ band: and (4) in stages N3 and REM, significant increases in the minimum of mean dominant frequency and in the respective sleep indexes. Therefore, in cirrhotic patients without overt HE, and likely having minimal hepatic encephalopathy, we found different alterations in both the microstructure and the macrostructure of nocturnal sleep. Also, sleep qEEG showed a brain dysfunction in slow oscillatory mechanisms intrinsic of sleep stages, with an increase in the frequency of its maximal electroencephalogram synchronization, from low δ to δ band. These alterations may reflect the onset of encephalopathy; sleep qEEG may, thus, be an adequate tool for its brain functional evaluation and follow-up.

[Critical illness myopathy. Neurophysiological and muscular biopsy assessment in 33 patients]. / Miopatia del enfermo crítico. Valoracion neurofisiológica y biopsia muscular en 33 pacientes.

INTRODUCTION: Critical illness patients may show marked weakness acquired in the Intensive Care Unit (ICU). There are some disagreements about the myopathic versus neuropathic damage in this condition, presumably due to the lack of reliable diagnostic criteria. AIMS: To report the neurophysiological findings in critical patients, to classify them in groups according to the electro-physiological data of myopathy, and to ascertain the rapport between the neurophysiological classification of myopathy and the muscle biopsy results. PATIENTS AND METHODS: A prospective assessment of 33 ICU patients with marked weakness by means of needle electro-myography, electroneurography, and percutaneous muscle biopsy was carried out. Direct muscle stimulation was performed in 9 patients and repetitive nerve stimulation in 14 cases. RESULTS. According to neurophysiological criteria, patients were classified in 3 groups: definite (33%), probable (46%), and uncertain (21%) myopathy. The most conspicuous myopathic pathological findings including fibrillar atrophy and necrosis, vacuoles, and myosin and mitochondrial anomalies, were observed in both, definite and probable groups (26 patients). In 17 of these cases, low amplitude of the compound motor action potentials and normal sensory nerve action potentials were found. Axonal sensory-motor neuropathy was present in 11 patients, concomitant with neurophysiological data of myopathy in 7 cases. CONCLUSIONS: Based on the neurophysiological criteria for the assessment and classification of acquired weakness in critically ill patients, myopathy is highly predominant over the neuropathic impairment. Histopathological findings are closely related to the electrophysiological diagnosis of myopathy. Neither neurophysiological nor pathological data support a hypothetic motor axonal neuropathy in this series.

Miopatía del enfermo crítico. Valoración neurofisiológica y biopsia muscular en 33 pacientes / Critical illness myopathy. Neurophysiological and muscular biopsy assessment in 33 patients

Introducción. Los enfermos críticos pueden desarrollar cuadros de debilidad importante en la Unidad de Cuidados Intensivos (UCI). Debido a la diversidad de criterios diagnósticos utilizados, existe desacuerdo sobre el origen miopático o neuropático de este cuadro. Objetivos. Describir las alteraciones neurofisiológicas de enfermos críticos, establecer grupos de pacientes según los datos electrofisiológicos de miopatía y determinar su correspondencia con los resultados de la biopsia muscular. Pacientes y métodos. Se estudiaron prospectivamente 33 pacientes en UCI con debilidad importante, mediante electromiografía, electroneurografía y biopsia muscular percutánea. En nueve casos se amplió el estudio con estimulación muscular directa y en 14 con estimulación repetitiva. Resultados. Aplicando criterios neurofisiológicos de miopatía, se describieron tres grupos de pacientes: miopatía definida (33%), miopatía probable (46%) y miopatía incierta (21%). En la biopsia muscular, las alteraciones miopáticas más intensas, con atrofia y necrosis fibrilar, vacuolas y alteraciones miosínicas y mitocondriales, se observaron en los grupos con miopatía definida y probable (26 casos). En 17 de ellos, los potenciales de acción muscular compuestos fueron de baja amplitud y los potenciales de acción del nervio sensitivo normales. Once pacientes mostraron polineuropatía axonal sensitivomotora, que en siete de ellos se asociaba con datos de miopatía. Conclusiones. En enfermos críticos con debilidad intensa, las alteraciones miopáticas en el estudio neurofisiológico son mucho más frecuentes que la afectación neuropática. En concordancia con estos hallazgos, las alteraciones miopáticas en la biopsia muscular son manifiestas y abundantes. Los datos histopatológicos y neurofisiológicos de esta serie no sustentan una hipotética neuropatía axonal motora pura (AU)

Introduction. Critical illness patients may show marked weakness acquired in the Intensive Care Unit (ICU). There are some disagreements about the myopathic versus neuropathic damage in this condition, presumably due to the lack of reliable diagnostic criteria. Aims. To report the neurophysiological findings in critical patients, to classify them in groups according to the electrophysiological data of myopathy, and to ascertain the rapport between the neurophysiological classification of myopathy and the muscle biopsy results. Patients and methods. A prospective assessment of 33 ICU patients with marked weakness by means of needle electromyography, electroneurography, and percutaneous muscle biopsy was carried out. Direct muscle stimulation was performed in 9 patients and repetitive nerve stimulation in 14 cases. Results. According to neurophysiological criteria, patients were classified in 3 groups: definite (33%), probable (46%), and uncertain (21%) myopathy. The most conspicuous myopathic pathological findings including fibrillar atrophy and necrosis,vacuoles, and myosin and mitochondrial anomalies, were observed in both, definite and probable groups (26 patients). In 17 of these cases, low amplitude of the compound motor action potentials and normal sensory nerve action potentials were found. Axonal sensory-motor neuropathy was present in 11 patients, concomitant with neurophysiological data of myopathy in 7 cases. Conclusions. Based on the neurophysiological criteria for the assessment and classification of acquired weakness in critically ill patients, myopathy is highly predominant over the neuropathic impairment. Histopathological findings are closely related to the electrophysiological diagnosis of myopathy. Neither neurophysiological nor pathological data support a hypothetic motor axonal neuropathy in this series (AU)