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Stiff-Man Syndrome This is a condition of persistent spasms, particularly of the proximal lower limbs and lumbar paraspinal muscles, forcing the patient eventually to lie helplessly in bed with the feet in equinus position and the legs extended It was originally described by Moersch and Woltman in 1956 as stiff-man syndrome Since then, many examples have been reported all over the world and the term stiff-person syndrome has been used to indicate its occurrence also in women The onset is insidious, usually in middle life, and men and women are affected equally No genetic predisposition is known At rst the stiffness and spasms are intermittent; then, gradually, they become more or less continuously active in the proximal limb and axial trunk muscles and increasingly painful The spasms impart a robotic appearance to walking and an exaggerated lumbar lordosis Attempts to move an affected part passively yield an almost rock-like immobility, perceptibly different from spasticity, paratonia, or extrapyramidal rigidity Muscles of respiration and swallowing and those of the face may be involved in the more advanced cases, but trismus, a common feature of tetanus, does not occur We have observed brief periods of cyanosis and respiratory arrest during episodes of intense spasm, and one of our patients died during such an episode Eye muscles are rarely affected Any noise or other sensory stimulus or attempted passive or voluntary movement may precipitate severely painful spasms of all the involved musculature The tendon re exes are normal if they can be tested The affected muscles, particularly the lumbar paraspinals and glutei are extremely taut when palpated It is this axial spasm that is most characteristic of the disease and gives rise to a characteristic lumbar lordosis over time A similar stiffness of one limb ( stiff-limb syndrome) has been differentiated from the generalized variety by Barker and colleagues and others (see Saiz et al; Brown et al), but it seems to us to be part of the same illness, especially since most of the localized cases have antibodies to glutamic acid decarboxylase, as described below There is, however, no axial spasm or exaggerated lordosis; the condition begins in one leg and spreads to its opposite but remains isolated to the lower extremities This limited form of spasm is similar to localized tetanus A central origin of the muscle spasms is indicated by their disappearance during sleep, during general anesthesia, and with proximal nerve block The electrophysiologic features differ from those of myokymia and continuous muscle ber activity syndrome in that the EMG in stiff-man syndrome consists entirely of normal motor units, with no evidence of distal motor nerve disturbance Of interest is the nding that most of the cases of stiff-man syndrome display circulating autoantibodies that are reactive with glutamic acid decarboxylase (GAD), the synthesizing enzyme for gamma-aminobutyric acid (GABA) (Solimena et al) These ndings suggest an imbalance between the spinal inhibitory (GABAnergic) input and the excitatory input to alpha motor neurons This interpretation is supported by the fact that the spasms worsen under the in uence of drugs that enhance aminergic activity, facilitating long-latency spinal re exes, or that inhibit catecholaminergic or GABA-nergic transmitters An autoimmune mechanism is further suggested by the high incidence of insulin-dependent diabetes (present in almost all the cases under our care) with detectable.

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antibodies to islet cells; a few patients have thyroiditis, pernicious anemia, or immune-mediated vitiligo There is a rare paraneoplastic variety of stiff-man syndrome, mostly accompanying breast cancer and associated sometimes with antibodies against amphiphysin or gephyrin, proteins associated with synaptic GABA receptors Some of the cases related to the antiamphiphysin antibodies also display more conventional types of paraneoplastic neurologic disorder such as encephalopathy or opsoclonus (see Chap 31) Treatment In the stiff-man syndrome, diazepam in doses of up to 50 to 250 mg/day, increased gradually, is most effective; clonazepam, vigabatrin, or baclofen are sometimes effective as well In keeping with the presumed autoimmune mechanism, plasma exchange, high-dose corticosteroids, or intravenous gamma globulin are helpful in some patients, albeit for only several weeks or months Several of our patients have required infusions of gamma globulin for several years at intervals of 6 to 12 weeks but nevertheless became disabled if the dose of diazepam was reduced below 200 mg/day A small randomized trial of intravenous immune globulin conducted by Dalakas and colleagues had demonstrated the ef cacy of this treatment; in their study, the bene ts varied in duration from 6 weeks to 1 year Clinically, the stiff-man syndrome must be distinguished from tetanus (page 1030 and further on), the Isaacs syndrome (see earlier), and the rare syndrome of subacute myoclonic spinal neuronitis, described on page 1066 In both the stiff-man syndrome and myoclonic spinal neuronitis, the intense spasms and stiffness of muscles are due to disinhibition of interneurons (possibly via GABA-nergic Renshaw cells) in the gray matter of the spinal cord These syndromes of continuous muscle activity, except perhaps the stiff-man syndrome, are, as a rule, usually distinguishable clinically and electromyographically from extrapyramidal and corticospinal abnormalities such as dystonia, dyskinesia, and rigidity; there is only a super cial resemblance to spastic paraparesis Congenital Neonatal Rigidity A stiff-infant syndrome, observed by Dudley and colleagues in four families of mixed heritage, should probably be included in this general category The condition came to medical attention because of respiratory distress due to a generalized muscular rigidity beginning at about 2 months of age The rigidity spread slowly from cervical muscles to those of the trunk and limbs, and, as it persisted, slight hypertrophy developed The use of respiratory aid and a feeding gastrostomy enabled the infants to survive The rigidity slowly diminished in the second year of life The clinical course was unlike that of tetanus In fatal cases there were zones of ber loss, with brosis in skeletal and cardiac muscles, and a greater than normal variation in ber size Altered Z lines were observed electron microscopically in some bers.

The architecture of ILOM consists of service processor hardware, which resides on the system board, and the management software that runs within the service processor hardware The ILOM software and hardware comes preinstalled and preconfigured on a variety of Oracle Sun server platforms ILOM can be integrated with other management and monitoring tools that are already installed in your data center using the SNMP interface, such as the integration with Oracle Enterprise Manager Ops Center discussed earlier This integration will allow you to combine the provisioning and patching features of Ops Center, and extending that, to manage the system BIOS and to perform firmware updates of hardware components The service processor hardware of ILOM has a dedicated Ethernet port that you will use to connect with the management network of your data center The users will access ILOM by connecting to the Ethernet IP address using the interfaces provided here:

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