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Neuroleptic malignant syndrome is caused by dopamine antagonists and is characterized by slow onset, bradykinesia, lead pipe rigidity, hyperthermia and fluctuating consciousness.
MNS is characterized by generalized lead pipe rigidity and bradykinesie and normal reflexia, whereas serotonin toxicity is characterized by neuromuscular hyperactivity (e.g., clonus, hyperreflexia) and predominantly in the lower extremities.
It is indicated that the qualitative stability evolution of the system mainly depends on the effect of fluid-structure interaction (FSI), while the spinning motion will enhance the pipe rigidity and eliminate the buckling instability.
Features that are classically present in NMS, that are useful for differentiating the two, are bradykinesia and extrapyramidal "lead pipe" rigidity, whereas serotonin syndrome causes hyperkinesia and clonus.
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This hypertonia may increase against resistance and then suddenly decrease ("clasp-knife spasticity"), or it may be constant throughout the range of movement ("plastic" or "lead-pipe" rigidity).
In parkinsonism the rigidity can be uniform (lead-pipe rigidity) or ratchety (cogwheel rigidity).
Neuroleptic malignant syndrome could be ruled out from his two episodes because he had neither autonomic dysfunction nor lead-pipe rigidity of his limbs [ 9].
Typical clinical presentation of NMS is a syndrome of hyperthermia with temperatures >38°C as a key finding, altered mental status, such as delirium, somnolence, coma and mutism, 'lead pipe' skeletal muscle rigidity, and autonomic dysfunction [ 21].
This causes strong contact between the outer and inner pipes if the inner pipe has strong flexural rigidity.
The desired distribution of the flexural rigidity of the inner pipe is calculated from the outer pipe curve.
For pipes at colder temperature, the rigidity of composite increases progressively with the temperature and results in drastic decrease in the displacement at break.
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