Choking,asphyxiation and the insular seizure

The insular cortex is located deep within the Sylvian fissure, and has rich connections. We describe two patients with focal epilepsy arising from this area, with symptoms of choking and strangulation during consciousness. Clinicians should be aware of this unusual presentation and that interictal electroencephalography can be normal.     

Positional cerebral ischaemia.

Four patients are described in whom recurrent, dramatic transient clinical worsening accompanied elevation from the supine toward the sitting position, though postural hypotension was not present. In each patient occlusive cerebrovascular disease was documented angiographically. During an acute stroke syndrome, some patients' compensatory capacity may be so tenuous that postural changes may produce clinical worsening. Possible mechanisms are discussed.     

Case of prolonged recovery from serotonin syndrome caused by paroxetine]

We report a case of serotonin syndrome in a patient being treated with paroxetine for depression. Despite prompt discontinuation of medication, his serotonin syndrome continued for 10 days before full consciousness was restored. The patient was a 48-year-old male with chief complaints of hypobulia and suicidal thoughts. He consulted as a psychiatric outpatient, and oral paroxetine 20 mg/day, etizolam 1.0 mg/day, and brotizolam 0.25 mg/day were immediately started. Upsurge of feeling and disinhibition state were noted the following day, then on treatment day 6 his condition deteriorated to substupor state and he was admitted for further treatment. On admission, change of mental condition (consciousness disturbance), perspiration, hyperreflexia, myoclonus and tremor were seen, and serotonin syndrome caused by paroxetine was suspected. Paroxetine was thus discontinued, and under intravenous drip his condition gradually improved. However, it was not until the 10th hospital day that he became fully alert. In examinations, no infectious, metabolic or organic diseases were detected. The patient's condition often improves with in 24 hours of discontinuation of the causative medication in serotonin syndrome. Symptoms continued for 10 days in this patient, however, perhaps because paroxetine was administered for 6 days before discontinuation. In addition, interaction with other medications may have occurred. Therefore, when serotonin syndrome is suspected, prompt discontinuation of the suspected causative medication, followed by close monitoring of the pharmacokinetics is warranted.     

Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo (BPPV) is characterized by brief recurrent episodes of vertigo triggered by changes in head position. BPPV is the most common etiology of recurrent vertigo and is caused by abnormal stimulation of the cupula by free-floating otoliths (canalolithiasis) or otoliths that have adhered to the cupula (cupulolithiasis) within any of the three semicircular canals. Typical symptoms and signs of BPPV are evoked when the head is positioned so that the plane of the affected semicircular canal is spatially vertical and thus aligned with gravity. Paroxysm of vertigo and nystagmus develops after a brief latency during the Dix-Hallpike maneuver in posterior-canal BPPV, and during the supine roll test in horizontal-canal BPPV. Positioning the head in the opposite direction usually reverses the direction of the nystagmus. The duration, frequency, and symptom intensity of BPPV vary depending on the involved canals and the location of otolithic debris. Spontaneous recovery may be expected even with conservative treatments. However, canalithrepositioning maneuvers usually provide an immediate resolution of symptoms by clearing the canaliths from the semicircular canal into the vestibule.     

变位试验结合手法复位诊治良性发作性位置性眩晕

目的:探讨变位试验诊断良性发作性位置性眩晕(BPPV)及耳石手法复位的疗效。方法:回顾性分析50例BPPV患者的资料,对所有患者进行全面病史采集,行变位试验(Roll试验和Dix-hallpike试验)判定BPPV的类型及侧别,对后半规管BPPV(PC-BPPV)患者采用Epley手法复位,对水平半规管BPPV(HC-BPPV)管石症患者采用Barbecue翻滚法复位,对水平半规管嵴顶结石症患者采用Gufoni疗法、Casani解脱法和Barbecue翻滚法复位。结果:随访3周时治愈42例(84%),有效49例(98%),无效1例(2%),且无明显不良反应。结论:根据典型病史及变位试验可判断BPPV的类型及侧别。手法复位治疗BPPV效果显著、简便、安全,适于临床推广。     

Restless legs syndrome and paroxetine

Restless legs syndrome is a frequent dyssomnia with well-known clinical features but uncertain origin and treatment. This paper describes a case of restless legs syndrome worsened by paroxetine. A possible pathogenic hypothesis related to the attributed neurochemical properties of the drug is proposed.     

Positional moulding in premature hydrocephalics

Seven premature hydrocephalics presenting with lambdoid positional moulding (LPM) were reviewed. All were treated for hydrocephalus secondary to aqueductal stenosis, Dandy Walker Syndrome and infection. Parenchymal hemorrhage, intraventricular bleed, cortical atrophy, septal agenesis, cortical anomalies and subdural hygroma were the other common associations. These children did not show expected improvement in their higher mental functions at 6 months to 5.4 years of follow-up, following the management of hydrocephalus. It was not the LPM but associated intracranial anomalies, which were most probably responsible for their poor outcome. The differentiation from posterior plagiocephaly is also highlighted.     

Brain metabolic changes in major depressive disorder from pre- to post-treatment with paroxetine

Functional brain imaging studies of subjects with Major Depressive Disorder (MDD) have suggested that decreased dorsolateral (DLPFC) and increased ventrolateral (VLPFC) prefrontal cortical activity mediate the depressed state. Pre- to post-treatment studies indicate that these abnormalities normalize with successful treatment. We performed [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) scans on 16 outpatients with MDD before and after treatment with paroxetine (target dose = 40 mg/day). Regions of interest (ROIs) for this analysis were drawn by a rater blind to subject identity on the magnetic resonance image of each subject and transferred onto their coregistered PET scans. We hypothesized that DLPFC metabolism would increase, while ventral frontal metabolism [in the VLPFC, the orbitofrontal cortex (OFC), and the inferior frontal gyrus (IFG)] would decrease with successful treatment. Treatment response was defined as a decrease in the Hamilton Depression Rating Scale of > 50% and a Clinical Global Improvement Scale rating of 'much' or 'very much' improved. By these criteria, nine of the subjects were classified as treatment responders. These responders had significantly greater decreases in normalized VLPFC and OFC metabolism than did non-responders. There were no significant effects of treatment response on change in the DLPFC or IFG in this sample. However, there was a positive correlation between change in HAM-D scores and change in normalized IFG and VLPFC metabolism. There were no significant interactions with laterality. On pre-treatment scans, lower metabolism in the left ventral anterior cingulate gyrus was associated with better treatment response. These findings implicate ventral prefrontal-subcortical brain circuitry in the mediation of response to serotonin reuptake inhibitors in MDD.     

Positional nystagmus reversing from geotropic to apogeotropic: a new central vestibular syndrome

Journal of Neurology -     

Predictors of asphyxiation risk in adults with intellectual disabilities and dysphagia

Background Adults with learning disabilities referred for assessment of their eating and drinking are frequently reported to cough and choke when eating and drinking. The research literature investigating dysphagia has often overlooked asphyxiation risk, highlighting coughing and choking as indicators of aspiration only. This is a notable oversight due to the prevalence of asphyxia as a cause of mortality in this population. Aim This study aims to identify the physiological and environmental factors that predict asphyxiation risk in adults with intellectual disabilities and dysphagia. Method Data were collected from dysphagia‐trained speech and language therapists (SLTs) working with the participant adults with intellectual disabilities and dysphagia. The SLTs used case notes, clinical assessment and videofluoroscopic assessment reports to gather the data. Results Speed of eating, cramming food and premature loss of the bolus into the pharynx were identified as significant predictors of asphyxiation risk in this population. Conclusions The findings highlight the importance of maladaptive eating strategies in exacerbating the risk of asphyxiation and choking. These factors should be considered in the assessment of asphyxiation and choking risk and management. Finally, the need for joint assessment and management with other members of the multidisciplinary team is advocated.     

Positional and positioning vertigo and nystagmus

Positional and positioning vertigo and nystagmus syndromes can be attributed to either peripheral or central vestibular dysfunction. The most common form is benign paroxysmal positioning vertigo which is caused by cupulolithiasis into the posterior semicircular canal. Other labyrinthine manifestations such as positional alcohol nystagmus, positional nystagmus with macroglobulinaemia and "heavy water" or glycerol ingestion occur because of a specific gravity differential between the cupula and the endolymph (buoyancy mechanism). Neurovascular compression of the vestibular nerve may be a causative factor for "disabling positional vertigo" which is an insufficiently described entity. Hesitation is highly justifiable since retromastoid craniectomy for microvascular decompression is the recommended management. Central positional vertigo is either induced by head movements which result in a transient ischaemia of the ponto-medullary brainstem, or by a change in head position relative to the gravitational vector. The latter is comprised of at least three forms: positional downbeat nystagmus (nodulus), positional nystagmus without concurrent vertigo, and positional vertigo with nystagmus. The site of the lesion is always near the fourth ventricle and the vestibular nuclei. The most probable explanation for the positional response is a vestibular tone imbalance caused by disinhibition of the vestibular reflexes on perception, eye, head and body position.