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by rippling waves of muscle contraction Percussion of muscles yields a pronounced and painful local mounding Similar familial and sporadic cases have been traced to a defect in caveolin, a protein otherwise implicated in one of the muscular dystrophies (Vorgerd) An autoimmune process has been implicated in some other cases (Muley and Day) The EMG discloses neither myotonic discharges nor the action potentials of cramp, indicating that the basic abnormality is in the muscle membrane Schwartz-Jampel Syndrome A syndrome characterized by continuous muscle ber activity with stiffness and blepharospasm, accompanied by obvious dysmorphic features (dwar sm, pinched face with low-set ears, blepharophimosis, high-arched palate, receding chin, diffuse metaphyseal and epiphyseal bone dysplasia with attened vertebrae), was crystallized by Schwartz and Jampel in 1962 It has also been reported under other names including myotonic chondrodystrophy Intelligence is usually preserved There may be percussion myotonia The stiff muscles disturb gait The muscle stiffness is the result of frequent, almost continuous muscle activity with a combination of normal motor units as well as high-frequency discharges and afterdischarges similar to those seen in Isaacs syndrome The discharges can be demonstrated to arise from muscle bers themselves since the activity is not obliterated by curare Agents such as procainamide, which block sodium channels in muscle, inhibit the discharges, just as they do in some other myotonic disorders However, Spaans and associates, who have reviewed the clinical, EMG, and histologic features of 30 cases of this syndrome, report a diminished chloride conductance by the sarcolemma, which can be suppressed by procainamide or even better by mexiletine The disorder is usually inherited as an autosomal recessive trait that is caused by mutations in perlecan, a heparin-sulfate proteoglycan that is bound to the basement membranes of skeletal muscle and cartilage Loss of function of the protein perturbs the organization of the basement membrane leading to an altered clustering of ACh esterase and abnormal expression of ion channels Electron microscopic studies of muscle have yielded inconsistent ndings: dilated T system, Z-band streaming, and dilatation of mitochondria; in addition, in the patient reported by Fariello and colleagues, muscle biopsy disclosed signs of denervation (group atrophy) In the latter case, treatment with procainamide, phenytoin, diazepam, and barbiturates was ineffective The condition described by Aberfeld and coworkers, of two siblings in whom myotonia was combined with dwar sm, diffuse bone disease, and unusual ocular and facial abnormalities and thought by them to represent a unique disorder, is probably a variant of the Schwartz-Jampel syndrome.

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continuous muscular activity syndromes, or myotonia and other involuntary spasms no longer use energy During contracture, the muscles are almost silent electrically in the EMG This condition is spoken of as pharmacologic or physiologic contracture McArdle and Tarui diseases are discussed more fully beginning on page 1232 Pseudomyotonia This phenomenon is observed in hypothyroidism, where the muscle bers contract and relax slowly This response is readily demonstrated in eliciting tendon re exes, particularly the Achilles re ex The muscles are large and subject to myoedema; when used, they may show waves of slow contraction The basis of this disorder appears to be a slowness in the reaccumulation of calcium ions in the endoplasmic reticulum and in the disengagement of thin actin and thick myosin laments The EMG may show afterpotentials following voluntary contraction, but they do not resemble the typical waning discharges ( myotonic runs ) of true myotonia A closely related syndrome, wherein painless contracture is induced by exercise, has been described by Lambert and Goldstein, and by Brody Whereas muscle contraction is normal, the relaxation phase becomes increasingly slow during exercise Lambert and coworkers referred to it as an unusual type of myotonia, and Brody, as a decrease of relaxing factor The slow relaxation of muscles has also been attributed to a decreased uptake of calcium by the sarcoplasmic reticulum In some cases, the disease is transmitted as a recessive trait; the gene defects are mutations that impair the function of a sarcoplasmic reticular calcium adenosine triphosphatase (ATPase; Odermatt et al) In other instances, the disease is transmitted as a dominant trait that is not genetically linked to the calcium ATPase Tetanus (See page 1030) This disorder is characterized by persistent spasms of skeletal muscles, owing to the effect of the tetanus toxin on spinal neurons (Renshaw and other cells), the natural function of which is to inhibit the motor neurons As the condition develops, activities that normally excite the neurons (ie, voluntary contraction and startle from visual and auditory stimulation) all evoke involuntary spasms Sleep tends to quiet them, and they are suppressed by spinal anesthesia and curare The EMG shows the expected interference pattern of action potentials Once the muscle is involved in persistent contraction, it is said that the shortened state is not abolished by procaine block or severance of nerve (in animals), but this so-called myostatic contracture has not been demonstrated in humans The effect on the inhibitory neurons is analogous to that of strychnine There is also an action of the tetanus toxin at the neuromuscular junction, which has been more dif cult to evaluate in the face of its powerful central action Having injected this toxin locally in animals, Price and associates have demonstrated its localization at motor end plates It binds with ganglioside in the axon membrane and is transported by retrograde ow to the spinal cord, where it induces local tetanus effects Neurons that innervate slowtwitch type 1 muscle bers are more sensitive than those supplying fast-twitch type 2 bers Presynaptic vesicles increase, ACh is blocked, and terminal axon injury may paralyze muscle bers Fibrillation potentials and axonal sprouting follow The similarities to stiff-man syndrome have already been mentioned Black Widow Spider Bite The toxin produced by this spider, within a few minutes of the bite, leads to a striking syndrome of.

Web-based interface You can use the industry-standard web browser to log in to the web interface of ILOM and perform management and monitoring functions The service processor hardware runs an embedded web server that is able to service requests coming from the web browser With this capability, you can redirect the server KVM to the web browser running on a remote system You can also share the remote system s disk drive or CDROM with the server as if it was locally connected to the server that is being managed by ILOM

Physiologic Contracture Due to Phosphorylase De ciency (McArdle) and Phosphofructokinase De ciency (Tarui) These are examples of an entirely different type of painful shortening and hardness of muscle In both these diseases, an otherwise healthy child, adolescent, or adult begins to complain of weakness and stiffness and sometimes pain on using the limbs Muscle contraction and relaxation are normal when the patient is in repose, but strenuous activity, especially under conditions of ischemia, causes the muscles to shorten gradually, due to a failure of relaxation The contracted muscles in these disorders unlike muscles in cramp,

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