1/5. Inhibition of forearm EMG by palatal myoclonus.The forearm electromyogram (EMG), pharyngeal EMG, and wrist tremor were recorded simultaneously from a 74-year-old woman with the syndrome of palatal myoclonus and progressive ataxia. Her wrist tremor had the characteristics of enhanced physiologic tremor. The enhancement of her tremor was attributable to 50- to 80-ms silent periods in the forearm EMG that followed the 1.9-Hz bursts of palatal myoclonus by 50 to 60 ms. This observation and those of previous authors support the notion that rhythmic olivocerebellar discharges can cause tremorogenic excitation and inhibition of postural EMG activity in the upper extremities.- - - - - - - - - - ranking = 1keywords = upper (Clic here for more details about this article) |
2/5. spinal cord seizures: a possible cause of isolated myoclonic activity in traumatic spinal cord injury: case report.spinal cord seizures are infrequently reported. They have been associated with intravenous dye placement, transverse myelitis and multiple sclerosis, but never with traumatic spinal cord injury (SCI). We report the case of a 48-year-old SCI male with complete C6 quadriplegia, and apparent spinal cord seizures. These seizures were characterised by myoclonus simplex activity involving the upper extremities only. The lower extremities were spared. The patient was conscious throughout the myoclonic activity and an electroencephalogram of the brain obtained during an event revealed no cortical epiliptiform activity. The seizures lasted approximately 30 seconds to a few minutes, and an acute increase in blood pressure and a decrease in pulse generally occurred 30 to 60 seconds prior to the event. Previously reported spinal cord seizures in multiple sclerosis were frequently treated with carbamazepine. In this case successful treatment was with diazepam. spinal cord seizures may present in those with traumatic SCI. benzodiazepines may be useful in the treatment of spinal cord seizures.- - - - - - - - - - ranking = 1keywords = upper (Clic here for more details about this article) |
3/5. Single case study. Contact epilepsy: a rare form of reflex epilepsy.An 80-year-old male is presented who had violent myoclonic seizures with occasional brief loss of consciousness, triggered by tactile stimuli directed to the upper extremities and upper part of the trunk which evolved over a 10-year period. physical examination revealed very few neurological abnormalities. His resting electroencephalograms were normal, but generalized spikes, polyspikes, and slow wave discharges were precipitated by tactile stimuli with the patient sitting up. He showed no significant response to standard anticonvulsant therapy. The relevant literature is reviewed briefly.- - - - - - - - - - ranking = 2keywords = upper (Clic here for more details about this article) |
4/5. A distinct form of adult polyglucosan body disease with massive involvement of central and peripheral neuronal processes and astrocytes: a report of four cases and a review of the occurrence of polyglucosan bodies in other conditions such as Lafora's disease and normal ageing.We have described 4 patients with progressive lower and upper motor neuron deficits, marked sensory loss in the legs, 'neurogenic bladder', and, in 2 of the 4, dementia. autopsy of two revealed a profusion of microscopic bodies resembling corpora amylacea or Lafora bodies, but restricted to processes of neurons and astrocytes. Similar (but especially large) bodies were seen within axons of sural nerves taken at biopsy from the other two patients. A general term--'polyglucosan body'--is introduced to refer to these structures in all the circumstances in which they may occur, such as in Lafora's disease, in a syndrome of longstanding double athetosis, in some cases of amyotrophic lateral sclerosis, in type IV glycogenosis, in diabetic rats, and in the normal course of ageing. Except in type IV glycogenosis, the causes for accumulation of polyglucosan bodies are unknown. They may damage tissue by more than one mechanism--probably by impeding axonal flow and impairing perivascular diffusion of metabolites.- - - - - - - - - - ranking = 1keywords = upper (Clic here for more details about this article) |
5/5. Cortical hyperexcitability in progressive myoclonus epilepsy: a study with transcranial magnetic stimulation.In progressive myoclonus epilepsy (PME), responses to afferent input are frequently abnormal. It is unclear whether the abnormality lies at the cortical, subcortical, or segmental level. To obtain evidence for an exaggerated effect on motor cortical excitability, we used peripheral nerve and transcranial magnetic stimulation in controls and subjects with idiopathic generalized epilepsy and PME. Mean threshold intensity was higher in those with idiopathic generalized epilepsy and PME than in controls, probably as a result of anticonvulsant treatment. A long-latency response to peripheral stimulation and an exaggerated facilitatory effect of peripheral stimulation on the motor evoked potential was present in subjects with PME. Latency differences between the late responses in the upper and lower limbs provided evidence against a segmental reflex and implicated rapidly conducting fibers in the spinal cord. Both the late response and the facilitatory effect had onset latencies consistent with a transcortical pathway, suggesting an exaggerated effect of afferent input on motor cortical excitability in PME.- - - - - - - - - - ranking = 1keywords = upper (Clic here for more details about this article) |