The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform

S. Kristensen - One of the best experts on this subject based on the ideXlab platform.

  • the aetiology and pathogenesis of trismus
    Clinical Otolaryngology, 2009
    Co-Authors: K Tveteras, S. Kristensen
    Abstract:

    Review: The aetiology and pathogenesis of trismus The word trismus, from the Greek ‘trismos’, is defined as a prolonged, Tetanic Spasm of the jaw muscles by which the normal opening of the mouth is restricted (locked jaw). The designation was originally used only in tetanus, but as inability to open the mouth may be seen in a variety of conditions, the term is currently used in restricted jaw movement regardless of aetiology.1 As the literature on the subject mainly consists of case reports, the authors have reviewed the pathogenesis, aetiology and management of trismus

K Tveteras - One of the best experts on this subject based on the ideXlab platform.

  • the aetiology and pathogenesis of trismus
    Clinical Otolaryngology, 2009
    Co-Authors: K Tveteras, S. Kristensen
    Abstract:

    Review: The aetiology and pathogenesis of trismus The word trismus, from the Greek ‘trismos’, is defined as a prolonged, Tetanic Spasm of the jaw muscles by which the normal opening of the mouth is restricted (locked jaw). The designation was originally used only in tetanus, but as inability to open the mouth may be seen in a variety of conditions, the term is currently used in restricted jaw movement regardless of aetiology.1 As the literature on the subject mainly consists of case reports, the authors have reviewed the pathogenesis, aetiology and management of trismus

Kristian Barlinn - One of the best experts on this subject based on the ideXlab platform.

  • Strychnine poisoning causing generalized Tetanic Spasm
    Neurology: Clinical Practice, 2020
    Co-Authors: Simon Winzer, Kristian Barlinn
    Abstract:

    A 55-year old male presented with spontaneous and stimulus-triggered Tetanic-like activity of the whole body without losing consciousness or orientation (video, http://links.lww.com/CPJ/A196). There was no history of trauma, and clinical examination did not reveal any tetanus-prone wound. Electroencephalography showed no significant alteration in brain activity. Serial intravenous benzodiazepines showed limited effect. Frequency and duration of muscle contractions increased over time and led to severe hypoxemia requiring intubation and sedation with propofol for almost 24 hours followed by continuous infusion of midazolam. Daily sedation pauses revealed ongoing generalized muscle Spasm triggered by tactile and auditory stimuli and severe vegetative dysregulation. Tetanus antibody level suggested long-term protection. On day 6, toxicology revealed toxic levels of strychnine in serum (180 ng/ml [toxicity > 75 ng/ml]) and urine (514 ng/ml [no toxicity level defined]). Repeated testing showed markedly declined strychnine levels in serum (2.8 ng/ml) and urine (1.1 ng/ml) on day 11. Sedation was ultimately stopped on day 10. Subsequently, the patient recovered completely and was discharged on day 25. Strychnine ingestion mode remained unclear. Generalized Tetanic Spasm with sustained alertness, presumably caused by selective inhibition of post-synaptic glycine receptors in the spinal cord, should trigger testing for strychnine poisoning.1,2 High-dose intravenous benzodiazepines are considered first-line therapy for controlling muscle Spasms; however, in patients whose muscle contractions are refractory to benzodiazepines, sedation with propofol or barbiturates is deemed necessary.1

Simon Winzer - One of the best experts on this subject based on the ideXlab platform.

  • Strychnine poisoning causing generalized Tetanic Spasm
    Neurology: Clinical Practice, 2020
    Co-Authors: Simon Winzer, Kristian Barlinn
    Abstract:

    A 55-year old male presented with spontaneous and stimulus-triggered Tetanic-like activity of the whole body without losing consciousness or orientation (video, http://links.lww.com/CPJ/A196). There was no history of trauma, and clinical examination did not reveal any tetanus-prone wound. Electroencephalography showed no significant alteration in brain activity. Serial intravenous benzodiazepines showed limited effect. Frequency and duration of muscle contractions increased over time and led to severe hypoxemia requiring intubation and sedation with propofol for almost 24 hours followed by continuous infusion of midazolam. Daily sedation pauses revealed ongoing generalized muscle Spasm triggered by tactile and auditory stimuli and severe vegetative dysregulation. Tetanus antibody level suggested long-term protection. On day 6, toxicology revealed toxic levels of strychnine in serum (180 ng/ml [toxicity > 75 ng/ml]) and urine (514 ng/ml [no toxicity level defined]). Repeated testing showed markedly declined strychnine levels in serum (2.8 ng/ml) and urine (1.1 ng/ml) on day 11. Sedation was ultimately stopped on day 10. Subsequently, the patient recovered completely and was discharged on day 25. Strychnine ingestion mode remained unclear. Generalized Tetanic Spasm with sustained alertness, presumably caused by selective inhibition of post-synaptic glycine receptors in the spinal cord, should trigger testing for strychnine poisoning.1,2 High-dose intravenous benzodiazepines are considered first-line therapy for controlling muscle Spasms; however, in patients whose muscle contractions are refractory to benzodiazepines, sedation with propofol or barbiturates is deemed necessary.1

Baburam Pokharel - One of the best experts on this subject based on the ideXlab platform.

  • seizure Tetanic Spasm and primary hypoparathyroidism
    Journal of Kathmandu Medical College, 2014
    Co-Authors: Arun Dhungana, J N Singh, A R Singh, Saroj Sapkota, Baburam Pokharel
    Abstract:

    Primary hypoparathyroidism is not a common disease, and it is not a common cause of seizures. Here we present a 21-year-old female with hypoparathyroidism who presented with Tetanic Spasm and seizure. Her parathyroid hormone level was low, Calcium level was low and Phosphorus was increased. Electroencephalogram showed sharp spike and Computed Tomography scan showed multiple symmetrical calcification in the basal ganglia, thalamus, cerebellum, cerebral hemisphere and periventricular region. With these features, our provisional diagnosis was Fahrs syndrome. Patient was treated with calcium gluconate and anticonvulsant. Patient improved and was discharged on medication. DOI: http://dx.doi.org/10.3126/jkmc.v2i2.10633 Journal of Kathmandu Medical College, Vol. 2, No. 2, Issue 4, Apr.-Jun., 2013, Page: 94-96