In the absence of depression, crying spells associated with neurological disease usually result from pseudobulbar palsy or, more rarely, from crying seizures. To our knowledge, there are no prior reports of crying spells heralding or signifying a transient ischaemic attack. We report on a patient with prominent cerebrovascular risk factors who had a transient episode of intractable crying and focal neurological findings.
The patient was a 55 year old right handed man who presented with acute, uncontrolled crying spells followed by left sided paraesthesias. Around 6 00 am he awoke with a diffuse, pressure headache and suddenly started crying for no apparent reason. There was no accompanying feeling of sadness. This crying, which involved lacrimation and “sobbing,” abruptly ceased after 5 minutes. Within 30 minutes of his initial crying spell, his headache had resolved but he became aware of numbness over his left face and numbness and pain in his left neck and arm. The numbness was not progressive, and the patient did not complain of …
Abstract We compared epilepsy phenotypes with genotypes of Angelman syndrome (AS), including chromosome 15q11‐13 deletions (class I), uniparental disomy (class II), methylation imprinting abnormalities (class III), and mutation in the UBE3A gene (class IV). Twenty patients were prospectively selected based on clinical cytogenetic and molecular diagnosis of AS. All patients had 6 to 72 hours of closed‐circuit television videotaping and digitized electroencephalographic (EEG) telemetry. Patients from all genotypic classes had characteristic EEGs with diffuse bifrontally dominant high‐amplitude 1‐ to 3‐Hz notched or triphasic or polyphasic slow waves, or slow and sharp waves. Class I patients had severe intractable epilepsy, most frequently with atypical absences and myoclonias and less frequently with generalized extensor tonic seizures or flexor spasms. Epileptic spasms were recorded in AS patients as old as 41 years. Aged‐matched class II, III, and IV patients had either no epilepsy or drug‐responsive mild epilepsy with relatively infrequent atypical absences, myoclonias, or atonic seizures. In conclusion, maternally inherited chromosome 15q11‐13 deletions produce severe epilepsy. Loss‐of‐function UBE3A mutations, uniparental disomy, or methylation imprint abnormalities in AS are associated with relatively mild epilepsy. Involvement of other genes in the chromosome 15q11‐13 deletion, such as GABRB3, may explain severe epilepsy in AS.
Minassian, Berge A.; Bronstein, Yuri; DeLorey, Timothy M.; Olsen, Richard W.; Philippart, Michel; Zhang, Quanwei; Guerrini, Renzo; Van Ness, Paul; Livet, Marie O.; Delgado-Escueta, Antonio V.Editor(s): Nuwer, Marc R. Author Information
Abstract This chapter describes the neuroanatomy and neurotransmitters of frontal-subcortical circuits and the clinical behavioral syndromes associated with the specific focal lesions within the circuits. It reviews the neuropsychological and behavioral consequences of posterior pallidotomy and of deep-brain stimulation in the pallidum and subthalamic nucleus in patients with Parkinson's disease. Thus, both “naturally occurring” and intentional lesions or interruption of the circuit are considered.
Background: Telestroke systems have offered expert stroke care to underserved communities across the United States. Usually, the telestroke service is provided by external consultants, from other institutions with limited access to patients’ medical charts and prior imaging. Here, we report on our one-year experience of an internal telestroke system at a community Primary Stroke Center. Methodology: Prior to August 2013, assessment of thrombolytics was provided by in-house neurologists through bedside consultation during the day and telephone consultation after hours. However, starting August 2013 acute stroke care is provided by neurologists using a telemedicine device via an integrated internal telestroke program. Given the integrated nature of our hospital system, these physicians have immediate access to medical charts, history, laboratory, and prior as well as current imaging. In order to prove the viability of this program, we compared outcomes between the two acute stroke care processes. We determined thrombolytic utilization rate, door-to-needle time (DNT), rate of stroke mimics, and discharge destination of those patients who received thrombolytics 12 month before and after telestroke implementation. Results: We noted improvement in the percentage of eligible stroke patients receiving thrombolytics (8% vs 18.2%). Our DNT decreased by 23 minutes (mean 93.4 vs 69.7 minutes, P<0.005). Thrombolytics administered to stroke mimics was reduced from 16.7% to 8.6%. Patients discharged to a non-home facility (acute rehabilitation or skilled nursing facilities) decreased from 16.6% to 8.6%. Conclusion: Compared to our previous local acute stroke management, stroke care was not inferior. In fact, as a result of an internal telestroke system implementation, our thrombolytic utilization rate increased, our DNT improved, our stroke mimic rate decreased, and non-home discharge disposition decreased. Although not specifically assessed in our study, we suspect that internal telestroke systems also offer obvious advantages for patient care compared to external systems. Further studies evaluating stroke outcomes in these distinct systems are needed.
Background: Telestroke systems have offered expert stroke care to underserved communities across the United States. Usually, the telestroke service is provided by external consultants, from other institutions with limited access to patients’ medical charts and prior imaging. Here, we report on our one-year experience of an internal telestroke system at a community Primary Stroke Center. Methodology: Prior to August 2013, assessment of thrombolytics was provided by in-house neurologists through bedside consultation during the day and telephone consultation after hours. However, starting August 2013 acute stroke care is provided by neurologists using a telemedicine device via an integrated internal telestroke program. Given the integrated nature of our hospital system, these physicians have immediate access to medical charts, history, laboratory, and prior as well as current imaging. In order to prove the viability of this program, we compared outcomes between the two acute stroke care processes. We determined thrombolytic utilization rate, door-to-needle time (DNT), rate of stroke mimics, and discharge destination of those patients who received thrombolytics 12 month before and after telestroke implementation. Results: We noted improvement in the percentage of eligible stroke patients receiving thrombolytics (8% vs 18.2%). Our DNT decreased by 23 minutes (mean 93.4 vs 69.7 minutes, P<0.005). Thrombolytics administered to stroke mimics was reduced from 16.7% to 8.6%. Patients discharged to a non-home facility (acute rehabilitation or skilled nursing facilities) decreased from 16.6% to 8.6%. Conclusion: Compared to our previous local acute stroke management, stroke care was not inferior. In fact, as a result of an internal telestroke system implementation, our thrombolytic utilization rate increased, our DNT improved, our stroke mimic rate decreased, and non-home discharge disposition decreased. Although not specifically assessed in our study, we suspect that internal telestroke systems also offer obvious advantages for patient care compared to external systems. Further studies evaluating stroke outcomes in these distinct systems are needed.
