Symptoms of bladder dysfunction, including hesitancy, urgency, frequency, and incontinence, occur commonly with interruption of descending fibers from cerebral areas controlling micturition, especially in cases of spinal cord involvement. Urinary retention, as a result of damage to sacral segments of the cord is less frequent (see Fig. 25-4). These symptoms are often associated with erectile dysfunction, a symptom that the patient may not report unless specifically questioned in this regard.
Paroxysmal attacks of neurologic deficit, lasting a few seconds or minutes and sometimes recurring many times daily, are a relatively infrequent but well-recognized feature of MS (see Mathews and also Osterman and
Westerberg). Usually the attacks occur during the course of relapsing and remitting phase of the illness, rarely as an initial manifestation. These clinical phenomena are referable to any part of the CNS but tend to be stereotyped in an individual patient. The most common phenomena are dysarthria and ataxia, paroxysmal pain and dysesthesia in a limb, flashing lights, paroxysmal itching, or tonic “seizures,” taking the form of flexion (dystonic) spasm of the hand, wrist, and elbow with extension of the lower limb. The paroxysmal symptoms, particularly the tonic spasms, may be triggered by sensory stimuli or can be elicited by hyperventilation. On a few occasions we have seen dystonic hand and arm spasms as the first symptoms; an acute plaque was detected in the opposite internal capsule. In advanced cases, the spasms may involve all 4 limbs and even a degree of opisthotonos. The cause of paroxysmal phenomena is uncertain. They have been attributed by Halliday and McDonald to ephaptic transmission (“cross-talk”) between adjacent demyelinated axons within a lesion.
These transitory symptoms appear suddenly, may recur frequently for several days or weeks, sometimes longer, and then remit completely, that is, they exhibit the temporal profile of a relapse or an exacerbation. It is sometimes difficult to determine whether they represent an exacerbation or a new lesion. Years ago, Thygessen pointed out in an analysis of 105 exacerbations in 60 patients that there were new symptoms in only 19 percent; in the remainder the episodes were only a recurrence of old symptoms. Another problem is that the original lesion may have been asymptomatic and emerges only with fever or a medical stress. This is most obviously reflected in the many patients who are found to have impaired visual evoked responses but have never had symptomatic visual changes. Thus, new symptoms and signs may be manifestations of previously formed but asymptomatic plaques. However, the observations of Prineas and Connell indicate that symptoms and signs may progress without the appearance of new plaques. These and other factors need to be taken into consideration in evaluating the clinical course of the illness and the effects of a therapeutic program (see Poser, 1980). Carbamazepine is usually effective in controlling such spontaneous attacks, and acetazolamide blocks the painful tonic spasms that are elicited by hyperventilation.
Unusually severe fatigue is another peculiar symptom of MS; it is often transient and more likely to occur when there is fever or other evidence of disease activity but it can be a persistent complaint and a source of considerable distress. Depression may play a role in these recalcitrant cases, although the response to pharmacologic agents suggests that these 2 aspects of the disease are dissociable. Thus, antidepressants often do not improve fatigue, whereas drugs that alleviate fatigue, such as modafinil and amantadine, do not function as antidepressants.