Another interesting approach has been to inject botulinum toxin in muscles affected by prominent focal tics, including the vocal ones as described by Scott and colleagues; curiously, this treatment is said to relieve the premonitory sensory urge. Deep brain stimulation of thalamic and other nuclei has shown promise in a few small series of drug resistant cases.
Using the model of Sydenham chorea, a recent line of investigation has implicated streptococcal infection in the genesis of abruptly appearing Tourette syndrome and of less-generalized tics in children. This association has been extended by some authors to explain obsessive-compulsive behavior of sudden and unexplained onset. These putative poststreptococcal disorders were summarized by Swedo and colleagues under the acronym PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection). In a few cases there has been a relapsing course that is similar to that seen in Sydenham chorea. Two health database studies have suggested a modest association between tic disorder, obsessive-compulsive disorder, and streptococcal infection. These observations taken together are intriguing but not confirmed and several groups have been unable to differentiate patients with PANDAS and Gilles de la Tourette syndrome from controls on the basis of epidemiologic factors or serum autoantibodies to streptococcus (Singer et al, 2005; Schrag and coworkers).
This term was coined by Haskovec in 1904 to describe an inner feeling of restlessness, an inability to sit still, and a compulsion to move about. When sitting, the patient constantly shifts his body and legs, crosses and uncrosses his legs, and swings the free leg. Running in place and persistent pacing are also characteristic. This abnormality of movement is most prominent in the lower extremities and may not be accompanied, at least in mild forms of akathisia, by perceptible rigidity or other neurologic abnormalities. In its advanced form, patients complain of difficulty in concentration, distracted, no doubt, by the constant urge to move.
First noted in patients with Parkinson disease and Alzheimer disease, akathisia is now observed most often in patients receiving neuroleptic drugs as a component of tardive dyskinesia or independently. However, this disorder may be observed in psychiatric patients who are receiving no medication. It occurs in both medicated and unmedicated patients with Parkinson disease.
The main diagnostic considerations are an agitated depression, particularly in patients already on neuroleptic medications, and the “restless legs” syndrome—a sleep disorder that may be evident during wakefulness in severe cases (see Chap. 18). Patients with the restless leg syndrome describe a crawling or drawing sensation in the legs rather than an inner restlessness, although both disorders create an irresistible desire for movement. At times these distinctions are blurred.
Many of the medications used for the restless legs syndrome, such as clonazepam, may be tried for akathisia or, if the symptom is a component tardive dyskinesia, selecting a less potent neuroleptic, an anticholinergic medication, amantadine, or a beta-adrenergic–blocking drug.
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