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Neurological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Clonus is a series of repeated involuntary contractions of the stretched muscle and is a consequence of spasticity and hyper-reflexia. Ankle clonus is demonstrated by flexing the knee slightly then rapidly dorsiflexing the foot.
Evaluation of the Spine in a Child
Published in Nirmal Raj Gopinathan, Clinical Orthopedic Examination of a Child, 2021
Ashish Dagar, Sarvdeep Singh Dhatt, Deepak Neradi, Vijay G Goni
The clonus is present in cases of exaggerated DTR where a single stimulus causes repetitive contraction of the muscle. Ankle clonus: With the hip and knee flexed to 90°, a sudden but gentle dorsiflexion of the ankle is carried out. If present, there will be alternating contraction and relaxation of the gastrocnemius and soleus. Sustained clonus (more than six beats) is a sign of an upper motor neuron lesion.11Patellar clonus: With the patient supine and knee extended, a sudden distally directed push is given to the patella.
Genetically Epilepsy-Prone Rats
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Phillip C. Jobe, Pravin K. Mishra, John W. Dailey
Third, the actual determination of convulsive pattern resulting from brainstem seizures appears to occur within the spinal cord.20 Rather than establishing convulsive pattern per se, the brain determines the number of seizure impulses being delivered to the spinal cord per unit time. According to this line of reasoning, impulses delivered at a low rate result in running activity. A somewhat higher rate causes generalized clonus. Further increases cause the appearance of tonic seizure involvement in a progressive manner identical to that set forth for class 5 through 9 audiogenic convulsions. These observations have been made in several species of artificially respired animals in which the brain has been severed from the spinal cord at the atlanto-occipital junction. Under these conditions and as described above in this paragraph, direct electrical stimulation of the proximal spinal cord produces convulsions that duplicate all of the motor patterns observed during generalized brainstem seizures in intact animals. Running, clonic, or tonic responses which outlast the duration of the stimulus are obtained predictably by varying one parameter, i.e., the square wave pulse frequency. Experimental evidence indicates that with such massive input into the spinal cord, the origins or functions of the tracts carrying the descending impulses from the brain become irrelevant.20
Transcutaneous spinal cord stimulation effects on spasticity in patients with spinal cord injury: A systematic review
Published in The Journal of Spinal Cord Medicine, 2023
Anas R. Alashram, Elvira Padua, Manikandan Raju, Cristian Romagnoli, Giuseppe Annino
The MAS49 and the pendulum tests were used in the selected studies to assess spasticity in patients with SCI. The pendulum test correlates with the MAS in patients with SCI.50 These measures were complemented by the assessments of other presentations of spasticity, such as clonus and muscle spasms.9 The latter being pathophysiologically distinct from exaggerated stretch reflexes.9 Except for the study of Sayenko et al. (2018),40 the selected studies showed positive effects of the tSCS intervention on spasticity in patients with chronic SCI.38,39,41,42 The patients in the selected studies were chronic (>6 months) with various ASIA scale grades and injury levels. The session duration and frequency for the selected studies were 30–120 minutes per session, with sessions range 1–12 sessions. The treatment dosage, including the electrode site, intensity, frequency, pulse width, and electrode size was varied between the selected studies. It makes determining the population who most likely would benefit from the intervention, long-term effects, and the optimal treatment dosage is difficult.
Safety of treating acute liver injury and failure
Published in Expert Opinion on Drug Safety, 2022
Miren García-Cortés, Aida Ortega-Alonso, Raúl J. Andrade
Development of HE brain edema and intracranial hypertension (ICH) may occur in one-third of cases who progress to grade 3 or 4 HE [145]. More commonly encountered clinical signs are sustained clonus, pupillary abnormalities and increase in muscular tone. Late signs of this complication are arterial hypertension, bradicardia, and mydriasis. Trans-cranial Doppler in combination with arterial Ammonia levels, is a useful noninvasive monitoring tool in less severe cases of neurologic impairment, in order to decide which patients need ICP monitor insertion. However, invasive intracranial pressure monitoring should be considered in more severe cases with high risk of ICH [1]. Mannitol or hypertonic saline should be administered when ICH is detected to increase serum osmolarity, and therefore reduce intracraneal pressure [146,147]. A prospective ramdomized clinical trial showed that mannitol and hypertonic saline have similar reduction in ICP and short‐term survival with significantly reduced rebound cerebral edema with the later. Besides, mannitol has shown an increased risk of kidney injury, thus 3% hypertonic saline seems to be a better modality for management of raised ICP in ALF patients [148].
The impact of early spasticity on the intensive functional rehabilitation phase and community reintegration following traumatic spinal cord injury
Published in The Journal of Spinal Cord Medicine, 2020
Andréane Richard-Denis, Bich-Han Nguyen, Jean-Marc Mac-Thiong
Our cohort was subdivided into two groups based on the development of spasticity during the acute care hospitalization. Group 1 included 55 (36.7%) individuals with a TSCI (“no early spasticity group”) who did not develop spasticity during the acute care hospitalization, while Group 2 (“early spasticity group”) included 95 individuals (63.3%) who developed spasticity during the acute care hospitalization. The development of spasticity was noted based on physical findings assessed by the attending treating team and symptoms reported by the patient. The diagnosis of spasticity required one of the following three criteria: 1) presence of increased velocity-dependant muscle tone at physical examination (Modified Ashworth scale score of >1); 2) spasm and/or clonus noted at physical examination, and 3) spasms and/or clonus reported by the patient.