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This is now a relatively uncommon spinal cord disorder that was introduced in relation to the subject of low back pain (page 180) It is characterized clinically by a combination of painful root and spinal cord symptoms that may mimic intraspinal tumor Pathologically there is opaci cation and thickening of the arachnoidal membranes and adhesions between the arachnoid and dura the result of proliferation of connective tissue The subarachnoid space is unevenly obliterated In this sense, the term arachnoiditis is not entirely appropriate, although it seems likely that the connective tissue overgrowth is a reaction to an antecedent arachnoidal in ammation Some forms of arachnoiditis can be traced to syphilis or to a subacute, therapeutically resistant meningitis of another type Most others have followed the introduction of a variety of substances, most no longer used, into the subarachnoid space for diagnostic or therapeutic purposes These included penicillin and other antibiotics, methylene blue, iophendylate (Pantopaque), and other contrast media and corticosteroids At one time, many examples of adhesive arachnoiditis were observed following spinal anesthesia, occurring soon afterward or after an interval of weeks, months, or even years Our colleagues observed more than 40 such cases This complication was eventually traced to a detergent that had contaminated vials of procaine If enough of the contaminant

Subacute Combined Degeneration of the Spinal Cord (SCD; see also Chap 41, page 992)

This classic form of nutritional spinal cord disease is due to vitamin B12 de ciency and is fully described on pages 992 to 996 Almost invariably it begins with bilateral symptoms and signs of posterior column involvement in the hands (paresthesias and reduced touch, pressure and joint sensibility), which, if untreated, is followed within a matter of several weeks or months by progressive spastic

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some extent, but this property is most characteristic of paramyotonia and it is in this condition that cold-induced weakness persists for up to several hours once started, even after the body is rewarmed Percussion myotonia can be evoked in the tongue and thenar eminence According to Haass and colleagues, myotonia that is constantly present in a warm environment diminishes with repeated contraction, whereas myotonia induced by cold increases with repeated contraction (paradoxical myotonia) Like hyperkalemic periodic paralysis, paramyotonia congenita is transmitted in an autosomal dominant manner, and both diseases have been linked to the same gene (SCN4A), which encodes the alpha subunit of the muscle membrane sodium channel; the two diseases are caused by allelic mutations Laboratory Findings In both hyperkalemic periodic paralysis and paramyotonia congenita, the serum K is usually above the normal range during bouts of weakness, but paralysis has been observed at levels of 5 meq/L or even lower Each patient appears to have a critical level of serum K, which, if exceeded, will be associated with weakness (This has led some authors to term the periodic paralysis as potassium dependent) The administration of KCl, raising serum K to above 7 meq/L, a level that has no effect on normal individuals, invariably induces an attack As mentioned earlier, the ECG must be monitored during such provocative testing The EMG shows myotonic discharge in all muscles, even at normal temperatures The CK may be elevated In vitro studies of muscle from patients with cold-induced stiffness and weakness have shown that as temperature is reduced, the muscle membrane is progressively depolarized to the point where the bers are inexcitable (Lehmann-Horn et al) A sodium channel blocker (tetrodotoxin) prevents the cold-induced depolarization In patients with paramyotonia but not in those with hyperkalemic periodic paralysis Subramony and colleagues have observed a diminution of the compound muscle action potential in response to the cooling of muscle, settling the argument as to whether the two syndromes (hyperkalemic paralysis and paramyotonia) are the same or different Some patients with paramyotonia, like those with certain other forms of periodic paralysis, may in later life slowly develop a myopathy that causes persistent weakness In some cases this is suf ciently severe that it mimics the pattern of late-onset limb girdle muscular dystrophy However, in the case of paramyotonia there are relatively few histologic changes, primarily vacuoles in some of the muscle bers and minimal evidence of myo ber degeneration Treatment Most patients with hyperkalemic periodic paralysis and its variants bene t from prophylactic use of the carbonic anhydrase inhibitor acetazolamide, 125 to 250 mg two or three times a day Acetazolamide reduces the frequency of attacks and may provide some relief from myotonia There are no controlled studies of acetazolamide in these disorders, but a rigorous trial of the related carbonic anhydrase inhibitor dichlorphenamide demonstrated a reduced frequency of paralytic spells in both hyper- and hypokalemic forms of periodic paralysis (Tawil et al) In contrast, many attacks of primary hyperkalemic paralysis and of paramyotonia congenita are too infrequent, too brief, or too mild to require continuous treatment The continuous use of conventional diuretics such as hydrochlorothiazide (about 05 g daily), keeping the serum K below 5 meq/L, also prevents attacks but risks inducing dangerous degrees.

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