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guanethidine into the affected limb (with the venous return blocked for several minutes) may alleviate the pain for days or longer. Epidural infusions, particularly of analgesics or ketamine; intravenous infusion of bisphosphonates; and spinal cord stimulators are other forms of treatment (see Kemler). The roles of the central and sympathetic nervous systems in causalgic pain have been critically reviewed by Schott and by Schwartzman and McLellan. Recent investigations have begun to de ne the molecular changes that occur in sensory neurons and the spinal cord in cases of chronic pain of this type. Alterations in N-methyl-D-aspartate (NMDA) receptors, induction of cyclooxygenase and prostaglandin synthesis, and changes in GABA-nergic inhibition in the dorsal horns are all implicated (Woolf). The term causalgia is best reserved for the syndrome described above i.e., persistent burning pain and abnormalities of sympathetic innervation consequent upon trauma to a major nerve in an extremity. Others have applied the term to a wide range of conditions that are characterized by persistent burning pain but have only an inconstant association with sudomotor, vasomotor, and trophic changes and an unpredictable response to sympathetic blockade. These latter states, which have been described under a plethora of terms (e.g., Sudeck atrophy of bone, minor causalgia, shoulder-hand syndrome, algoneurodystrophy), may follow nontraumatic lesions of the peripheral nerves or even lesions of the CNS ( mimocausalgia ). We have no explanation for the so-called causalgia-dystonia syndrome (Bhatia et al) in which a xed dystonic posture is engrafted on a site of causalgic pain. The clinical features of both the causalgic and dystonic elements of the syndrome were somewhat unusual in the cases reported. The degree of injury was often trivial or nonexistent and no signs of a neuropathic lesion were evident. Remarkably, both the causalgia and dystonia spread from their initial sites to widely disparate parts of the limbs and body. The syndrome did not respond to any form of treatment, although some patients recovered spontaneously. Its origin is not explained. The treatment of re ex sympathetic dystrophy is largely unsatisfactory, although a certain degree of improvement can be expected if treatment is started early and the limb is mobilized. The alternatives for treatment are discussed further on.
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The sensor board works by producing modulated infrared radiation with an infrared LED and using the PNA4602 module to detect any radiation reflected from the surface of solid objects. The PNA4602 sensor is designed to respond only to infrared that is modulated at a frequency somewhere between 38 42 kHz. The circuit is tuned to modulate the infrared LED at this frequency. Depending on the proximity of the sensor to the object, a greater or lesser number of infrared pulses will be reflected back. The number of reflected hits that the sensor receives in a given time frame allows the robot to determine how close it is to objects. The higher the number of reflected pulses, the closer the sensor is to the object. The output pin from the PNA4602 is connected to a microcontroller input pin, and a software routine is used to monitor the sensor.
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of the horizontally acting recti (a small vertical disparity should be disregarded); if the separation is mainly vertical, the paresis will be found in the vertically acting muscles, and a small horizontal deviation should be disregarded. In the position of maximal separation, the image projected farther from the center is attributable to the paretic muscle of the implicated pair that is identi ed in the rst step above. The patient may be aided in identifying which image is diverted most by having her several times momentarily uncover one eye and observe which image is most peripheral.
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