Project description:Saccadic intrusions such as opsoclonus and ocular flutter are often due to a paraneoplastic or a parainfectious condition. Toxins/drugs may rarely cause them. Herein, we report a rare case of ocular flutter/opsoclonus due to phencyclidine (PCP) toxicity. Our patient is a 21-year-old male who presented with a 3-day history of headache, generalized ill health, and aggressive behavior. He was admitted with reduced level of consciousness following generalized seizures. He had features of sympathetic overactivity with ocular flutter and opsoclonus. Urine toxicology was positive for PCP. Despite supportive care, he succumbed to complications of rhabdomyolysis. Several drugs including cocaine, phenytoin, lithium, and amitriptyline are known to cause ocular flutter/opsoclonus rarely. It is poorly described with PCP. This case highlights PCP as a rare cause of toxin-induced saccadic intrusions and attempts to postulate its pathogenesis. Moreover, our report is the first case of PCP intoxication in Sri Lanka and one of the few documented reports in the South Asian region. Therefore, it represents a significant worrisome alarm about the spread of this substance in this region.
Project description:When we explore a static visual scene, our eyes move in a sequence of fast eye movements called saccades, which are separated by fixation periods of relative eye stability. Based on uncertain sensory and cognitive inputs, the oculomotor system must decide, at every moment, whether to initiate a saccade or to remain in the fixation state. Even when we attempt to maintain our gaze on a small spot, small saccades, called microsaccades, intrude on fixation once or twice per second. Because microsaccades occur at the boundary of the decision to maintain fixation versus starting a saccade, they offer a unique opportunity to study the mechanisms that control saccadic triggering. Abnormal saccadic intrusions can occur during attempted fixation in patients with neurodegenerative disorders. We have implemented a model of the triggering mechanism of saccades, based on known anatomy and physiology, that successfully simulates the generation of saccades of any size-including microsaccades in healthy observers, and the saccadic intrusions that interrupt attempted fixation in parkinsonian patients. The model suggests that noisy neuronal activity in the superior colliculus controls the state of a mutually inhibitory network in the brain stem formed by burst neurons and omnipause neurons. When the neuronal activity is centered at the rostral pole, the system remains at a state of fixation. When activity is perturbed away from this center, a saccade is triggered. This perturbation can be produced either by the intent to move one's gaze or by random fluctuations in activity.
Project description:The eyes do not stay perfectly still during attempted fixation; fixational eye movements and saccadic intrusions (SIs) continuously change the position of gaze. The most common type of SI, square-wave jerks (SWJs), consists of saccade pairs that appear purely horizontal on clinical inspection: the first saccade moves the eye away from the fixation target, and after a short interval, the second saccade brings it back toward the target. SWJs are prevalent in certain neurological disorders, including progressive supranuclear palsy (PSP). Here, we developed an objective method to identify SWJs. We found that SWJs are more frequent, larger, and more markedly horizontal in PSP patients than in healthy human subjects. Furthermore, the loss of a vertical component in fixational saccades and SWJs was the eye movement feature that best distinguished PSP patients from controls. We moreover determined that, in PSP patients and controls, the larger the saccade the more likely it was part of a SWJ. Furthermore, saccades produced by PSP patients had equivalent properties whether they were part of a SWJ or not, suggesting that normal fixational saccades (microsaccades) are rare in PSP. We propose that fixational saccades and SIs are generated by the same neural circuit and that, both in PSP patients and in controls, SWJs result from a coupling mechanism that generates a second corrective saccade shortly after a large fixation saccade. Because of brainstem and/or cerebellum impairment, fixational saccades in PSP are abnormally large and thus more likely to trigger a corrective saccade, giving rise to SWJs.
Project description:We describe a case of maxillofacial trauma in a paediatric patient in which the left mandibular condyle was superolaterally displaced into the temporal fossa, medial to the zygomatic arch which was intact and the right condyle was also displaced similarly but the zygomatic arch was also fractured on this side. Also, there was an associated mandibular symphyseal fracture.
Project description:Bilateral involvement of the breast with tuberculosis is extremely rare. It most commonly affects young lactating multiparous females, although rarely it may be reported in prepubescent males also. We present a case of a 27-year-old nulliparous female who presented with a history of multiple pus discharging sinuses around both areolae and was diagnosed as a case of bilateral tubercular mastitis. Tubercular mastitis being a paucibacillary disease, diagnosis is often difficult. Treatment consists of antitubercular therapy with or without surgery..
Project description:Radiation-induced sarcoma of the breast is an iatrogenic malignancy that occurs secondary to radiotherapy, which is most commonly given following breast conservation surgery. It has an incidence of 3.2 per 1,000 patients at 15 years and is associated with a poor prognosis. We report a 62-year-old female with a history of bilateral breast conservation surgery and radiotherapy 5 years ago presenting with bilateral angiosarcoma. This case report highlights the importance of considering radiation-induced angiosarcoma of the breast as a differential diagnosis in a patient with recurrent breast neoplasms. The challenges in the management with recent evidence on new treatment modalities are discussed.