ABSTRACT
n-Hexane gives cause to one of the most common toxic polyneuropathies seen in poorly ventilated factories. It is a sensory-motor polyneuropathy ending up with axonal degeneration. Nerve biopsy reveals paranodal axonal swelling and secondary myelin retraction in early stages. Myelin retraction imitates demyelination causing focal conduction block and failure before axonal degeneration emerges. This brings to mind the new category of nodo-paranodopathy described first for anti-ganglioside antibody-mediated neuropathies, which can be proved by electrophysiological re-evaluations. We, herein, discuss the clinical and electrophysiological follow-up of three patients with n-hexane neuropathy and remark overlaps with new concept nodo-paranodopathy.
Subject(s)
Action Potentials/drug effects , Hexanes/toxicity , Neural Conduction/drug effects , Occupational Exposure/adverse effects , Polyneuropathies/chemically induced , Polyneuropathies/diagnosis , Action Potentials/physiology , Adolescent , Adult , Humans , Male , Neural Conduction/physiology , Polyneuropathies/physiopathologyABSTRACT
Anti-N-methyl-D-aspartate receptor NMDA-R encephalitis is caused by antibodies against the NMDA-R and characterized by a severe encephalopathy with psychosis, epileptic seizures and autonomic disturbances. This disorder is often accompanied with malignancies, especially ovarian teratoma. Some patients' EEGs show a different pattern similar to the waveforms of premature infants and this pattern is specifically named as extreme delta brush (EDB). We report a 24-year-old female having anti-NMDA receptor encephalitis and EDB patern.
Subject(s)
Anti-N-Methyl-D-Aspartate Receptor Encephalitis/diagnosis , Anti-N-Methyl-D-Aspartate Receptor Encephalitis/physiopathology , Autoantibodies/blood , Delta Rhythm , Receptors, N-Methyl-D-Aspartate/immunology , Acute Disease , Adult , Anti-N-Methyl-D-Aspartate Receptor Encephalitis/complications , Anti-N-Methyl-D-Aspartate Receptor Encephalitis/pathology , Biomarkers/blood , Diagnosis, Differential , Fatal Outcome , Female , Humans , Magnetic Resonance Imaging , Psychotic Disorders/etiology , Status Epilepticus/etiology , Status Epilepticus/physiopathologyABSTRACT
AIM: The aim of carotid endarterectomy (CEA) is the successful removal of the atherosclerotic plaque and meticulous anatomical and physiological reconstruction of the carotid artery without any perioperative complications. Endarterectomy can also be carried out with regional anesthesia, which allows monitoring of the neurological status. This study reviews patients who underwent CEA with regional anesthesia. MATERIAL AND METHODS: A total of 71 consecutive patients were planned to undergo carotid endarterectomy under regional anesthesia between 2000 and 2006. All of these patients, assessed by our neurovascular team, were recruited prospectively and the data was analyzed retrospectively. RESULTS: The study group consisted of 23 women and 48 men with a mean age of 62 (range 37-79). 67 patients (94,4%) had symptomatic, and 4 (5,6%) had asymptomatic (5.6%) carotid stenosis. Six patients (8.45%) were intolerant to carotid clamping (8,45%). The stroke morbidity rate was 1.4% and the mortality rate was 1.4%. The mean hospitalization time was 2.07 (range 1-10) days. CONCLUSION: Carotid endarterectomy performed under regional anesthesia can be a safe method which may lead to better neurological outcome. This method offers several advantages including monitorization of the cerebral ischemia during surgery, usage of selective shunting, decreased need for intensive care and shorter hospitalization time.
Subject(s)
Anesthesia, Conduction/mortality , Carotid Stenosis/mortality , Carotid Stenosis/surgery , Endarterectomy, Carotid/mortality , Medical Audit , Adult , Aged , Comorbidity , Critical Care/statistics & numerical data , Female , Humans , Length of Stay/statistics & numerical data , Male , Middle Aged , Postoperative Complications/mortality , Retrospective StudiesABSTRACT
In this study, we aimed to evaluate motor cortical excitability changes in patients with juvenile myoclonic epilepsy (JME) and their asymptomatic siblings (AS) using single-pulse transcranial magnetic stimulation (spTMS). 21 patients with JME and their 21 AS were compared to 20 healthy controls. All of JME patients were receiving antiepileptic therapy and their seizures were well controlled. Firstly, standard EEG examinations and then TMS studies were performed. Resting motor threshold (RMT), motor evoked potential (MEP) amplitudes, the durations of central motor conduction time (CMCT) and cortical silent period (CSP) were measured. After TMS studies, EEG recordings were repeated in an hour to evaluate any effect of TMS study on EEG. There were no significant differences between the first and second EEG recordings. No seizures were recorded during and after the TMS study. RMT was found higher in JME patients than AS and normal controls. There were no significant differences between cortical MEP amplitudes and MEP amplitude/CMAP (compound muscle action potential) amplitude ratio in all three groups. CMCT duration was shorter in JME patients than AS. CSP durations of JME patients were found to be longer than controls. In AS, CSP durations were also found to be longer than controls but this difference was not found statistically significant. Our results suggested that although high MT may be related to antiepileptic therapy, the prolongation of CSP duration may reflect impairment of supraspinal and/or intracortical inhibitory mechanism in JME. To eliminate the drug effect, further studies are needed in newly diagnosed JME patients without medication and large series of their asymptomatic siblings.
