Muscle twitching

Isaacs syndrome (an acquired neuromyotonia) is caused by autoantibodies directed against 4-aminopyr-idine or a-dendrotoxin-sensitive K+ channels (Kvl.l and Kvl.6) in motor and sensory neurons. The syndromes include muscle twitching during rest, cramps during muscle contraction, impaired muscle relaxation, and muscle weakness due to hyperexcitability of peripheral motor nerves. 

Neurotoxicity (damage to the nervous system by a toxic substance) may also be seen with the administration of the aminoglycosides. Signs and symptoms of neurotoxicity include numbness, skin tingling, circum-oral (around the mouth) paresthesia, peripheral paresthesia, tremors, muscle twitching, convulsions, muscle weakness, and neuromuscular blockade (acute muscular paralysis and apnea). 

MONITORING FOR NEUROTOXICITY. The nurse should be alert for symptoms such as numbness or tingling of the skin, circumoral paresthesia, peripheral paresthesia (numbness or tingling in the extremities), tremors, and muscle twitching or weakness. The nurse reports any... 

An abstinence syndrome after long-term, low-dose treatment has also been described (Busto et al. 1986a Covi et al. 1973 Petursson and Lader 1981b Tyrer et al. 1981). Reported symptoms include muscle twitching, abnormal perception of movement, depersonalization or derealization, anxiety, headache, insomnia, diaphoresis, difficulty concentrating, tremor, fear, fatigue, lowered threshold to perception of sensory stimuh, and dysphoria. 

Sodium nitroprusside 0.25-10 mcg/kg/minute as IV infusion11 Immediate 1-2 minutes Nausea, vomiting, muscle twitching, sweating, thiocyanate and cyanide intoxication Most hypertensive emergencies use with caution with high intracranial pressure or azotemia... 

A muscle twitch is a brief, weak contraction produced in a muscle fiber in response to a single action potential. While the action potential lasts 1 to 2 msec, the resulting muscle twitch lasts approximately 100 msec. However, a muscle twitch in a single muscle fiber is too brief and too weak to be useful or to perform any meaningful work. In fact, hundreds or thousands of muscle fibers are organized into whole muscles. In this way, the fibers may work... 

As mentioned previously, a single action potential lasting only 2 msec causes a muscle twitch that lasts approximately 100 msec. If the muscle fiber has adequate time to completely relax before it is stimulated by another action potential, the subsequent muscle twitch will be of the same magnitude as the first. However, if the muscle fiber is restimulated before it has completely relaxed, then the tension generated during the second muscle twitch is added to that of the first (see Figure 11.3). In fact, the frequency of nerve impulses to a muscle fiber may be so rapid that there is no time for relaxation in between stimuli. In this case, the muscle fiber attains a state of smooth, sustained maximal contraction referred to as tetanus. 

The amount of tension developed by a muscle fiber during tetanic contraction can be as much as three to four times greater than that of a single muscle twitch. The mechanism involved with this increased strength of contraction involves the concentration of cytosolic calcium. Each time muscle fiber is stimulated by an action potential, Ca++ ions are released from the sarcoplasmic reticulum. However, as soon as the these ions are released, a... 

Figure 11.3 Muscle twitch summation and tetanus. A single action potential (represented by A) generates a muscle twitch. Because duration of the action potential is so short, subsequent action potentials may restimulate the muscle fiber before it has completely relaxed, leading to muscle twitch summation and greater tension development. When the frequency of stimulation becomes so rapid that no relaxation occurs between stimuli, tetanus occurs. Tetanus is a smooth, sustained, maximal contraction.

The answer is b. (Hardmanr p 1158.) Isoniazid inhibits cell-wall synthesis in mycobacteria. Increasing vitamin B6 levels prevents complications associated with this inhibition, including peripheral neuritis, insomnia, restlessness, muscle twitching, urinary retention, convulsions, and psychosis, without affecting the antimycobacterial activity of INH. 

The answer is e. (Hardman, p 1563 ) The toxicity of INI I is mainly on the peripheral and central nervous systems (PNS, CNS). This is attributable to competition of 1NH with pyridoxal phosphate for apotryp-tophanase. This results in a relative deficiency of pyridoxine, which causes peripheral neuritis, insomnia, and muscle twitching among other effects. 

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