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Disorders of movement in children often cause semiological and diagnostic difficulties to the paediatricians concerned. Based on personal experience, the author analyzes aspects which are particularly useful in overcoming these problems. Epidemiology, rules for history taking, indications as to the interpretation of clinical signs and use of complementary studies are considered.
A procedure is proposed for comprehensive rehabilitation of children with mental and somatic abnormalities. The rehabilitation programme contains three sections: expert diagnostic, corrective-reparative, and professional orientational ones. The results of testing the procedure in health care facilities are given.
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Poststreptococcal disorders exhibit a remarkable comorbidity of neurologic and psychiatric features. A similar combination of symptoms is also described in other conditions, such as connective tissue or paraneoplastic disorders, albeit less frequently. A better understanding of the underlying mechanisms associated with autoaggressive immune-mediated attack on the basal ganglia is required. This understanding will ideally aid clinicians in diagnosing these conditions and lead to appropriate clinical trials, for example, of chemoprophylaxis strategies to prevent recurrent streptococcal infection and of the use of immunosuppressive treatments.
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OBJECTIVE: To increase awareness of the possibility of opioid induced movement disorders. SETTING: A university-affiliated Veterans Affairs Hospital. PATIENT: A patient with upper extremity pain due to complex regional pain syndrome type I (reflex sympathetic dystrophy). INTERVENTIONS: Attempted pain control with methadone. RESULTS AND CONCLUSIONS: After failing many attempts at control, the authors were able to provide their patient significant pain relief from her complex regional pain syndrome type I using methadone. Unfortunately, the patient eventually developed a movement disorder, characterized by tremor, choreiform movements, and a gait abnormality, probably related to this opioid. The authors conclude that, while this type of movement disorder is uncommon, clinicians need to be aware of opioid-induced movement disorders, because they are disturbing to patients and often easily treated.
BACKGROUND: The selective D2 antagonist tiapride is administered in various movement disorders. Furthermore, there are indications that tiapride increases platelet counts. AIM: To characterize tiapride's potential to increase platelet counts in healthy subjects and patients with movement disorders. METHODS: In Part A, 10 healthy volunteers received tiapride (300 mg/day) for 21 days in a longitudinal, prospective, open trial. One hundred healthy subjects served as controls. Part B was a retrospective analysis of 15 patients with movement disorders on tiapride [Huntington's disease (n=6), Morbus Little (n=3), hyperkinetic syndromes of undetermined etiology (n=3), blepharospasm (n=1), cervical dystonia (n=1), perioral dyskinesia (n=1)] and 15 age- and sex-matched controls. RESULTS: Part A: Although serum prolactin levels increased by 526+/-14%, confirming good drug compliance, tiapride elicited only minor changes in platelet counts. Part B: Platelet counts correlated positively with the dose of tiapride (100-800 mg/day; r=.67; P=.007). Platelet counts were significantly higher in patients on tiapride compared to healthy age-matched controls (P<.001). Four patients responded to an increase in the tiapride dosage with an increase in platelet count by 97-173 cells/nl. CONCLUSION: Three weeks of treatment with tiapride (300 mg/day) is insufficient to elevate platelet counts to a clinically relevant extent in young healthy volunteers. However, in elderly patients with movement disorders tiapride treatment is associated with markedly increased platelet counts.
There is little information on the frequency of movement disorders seen by physicians in the continent of Africa. We performed a medical record review of all patients seen in a university-based neurology clinic in Addis Ababa, Ethiopia, over 1 year to determine the frequency of movement disorders seen, disease characteristics, diagnostic evaluations, and treatment. A total of 15.1% of the neurological patients were seen for movement disorders. Of these, most were for parkinsonism (47.7%), followed by ataxia (16.5%), dystonia (8.3%), essential tremor (8.3%), chorea (7.3%), and miscellaneous (11.9%). Diagnostic evaluations were limited, but treatment was available, although expensive. In spite of the limitations, patients with movement disorders require and seek care in Ethiopia in proportions comparable to developed nations. This finding underlines the need for adequate training in movement disorders for physicians and neurologists in Africa.
Chronic neuroleptic therapy may be associated with the development of diverse movement disorders including Tardive dyskinesia (TD), Parkinsonism, dystonia, and akathisia in a subset of schizophrenic patients. It is presently unknown why only a proportion of neuroleptic-treated patients develop these movement disorders. In the following communication, we present a series of studies which demonstrate that the development of these movement disorders may be facilitated by certain risk factors including disturbances in pineal melatonin functions, diabetes mellitus, cognitive deficits, suicidal behavior, and disturbances in the functions of the choroid plexus. Recognition of these biological factors may prove useful in: (a) further understanding of the pathophysiology of these disorders, and (b) identifying patients at risk for these movement disorders.
Recent investigations of childhood-onset obsessive compulsive disorder (OCD) and pediatric movement disorders such as tics, Tourette's syndrome (TS), and Sydenham's chorea suggest that these disorders may be related. Although comorbid obsessive-compulsive symptoms have long been recognized in individuals with TS, more recent studies have demonstrated that tics and TS are surprisingly common in children with primary OCD, and further, that the two disorders seem to have a common genetic vulnerability. Obsessive-compulsive symptoms are also manifest in Sydenham's chorea, a neurologic variant of rheumatic fever in which antistreptococcal antibodies are thought to cross-react with neuronal tissue, particularly within the basal ganglia, and cause inflammatory changes resulting in neuropsychiatric symptomatology. The frequent comorbidity of OCD and Sydenham's chorea and similar postulates of basal ganglia dysfunction for both disorders suggest that Sydenham's chorea may serve as a medical model for OCD. Of note, however, is that the medications (e.g., neuroleptics) that are effective in treating this and other movement disorders are distinctly different from those that are efficacious for OCD (e.g., serotonin reuptake blockers). Examinations of the similarities and differences among these various neuropsychiatric conditions may lead to greater understanding of the pathophysiology of OCD and offer further insights into the etiology and treatment of this troubling disorder.
STUDY OBJECTIVES: To evaluate the type, duration, and distribution of rhythmic movements in sleep stages in school-aged children and young adults; to find out if cases of rhythmic movement disorder persisting beyond infancy are associated with any daytime symptoms or psychopathology. DESIGN: All participants underwent neurologic examination, biochemical screening, electroencephalography, neuroimaging, overnight videopolysomnography, and psychologic examination. SETTING: Department of Neurology and Sleep Laboratory, 1st Medical Faculty, Charles University, Prague. PATIENTS OR PARTICIPANTS: Ten subjects referred to the sleep disorders center because of rhythmic movement disorder. Five males, 5 females; age range, 7-24 years; mean age 14.7 +/- 5.69 years. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Biochemical screening, electroencephalogram, and neuroimaging were unremarkable in all cases. According to duration, 2 types of rhythmic movements were observed on polysomnography: longer episodes appeared in wakefulness and in non-rapid eye movement stage 1 sleep, while shorter episodes (2-80 seconds) occurred during non-rapid eye movement stage 2, non-rapid eye movement stage 3-4, and rapid eye movement sleep. According to sleep-stage distribution, we defined (a) rhythmic movements prevailing in the first half of the night and in the morning hours, usually associated with wakefulness or superficial sleep; (b) rhythmic movements occurring throughout the night in all sleep stages; (c) rhythmic movements prevailing in the second half of the night and mainly associated with rapid eye movement sleep. Psychologic examination showed symptoms of the attention-deficit/hyperactivity disorder in 6 cases. CONCLUSIONS: According to our study, rhythmic movement disorder persisting beyond infancy may be connected with various daytime symptoms; a strong association between rhythmic movement disorder and attention-deficit/hyperactivity disorder was found in school-aged children. We speculate that pathogenetic mechanisms similar to those in attention-deficit/hyperactivity disorder are involved in rhythmic movement disorder or that symptoms of attention-deficit/hyperactivity disorder may be secondary to rhythmic movement disorder.
Many drugs have been known to cause movement disorders with different mechanisms of action. Most of these drugs interfere with dopaminergic transmission within the basal ganglia. However, numerous other drugs are capable of producing movement disorders, whose mechanism is not at all clearly understood. Neuroleptic drugs-induced extrapyramidal symptoms such as dystonia, akathisia, parkinsonism have been related to sudden imbalance between the striatal dopamine and cholinergic systems, causing a relative preponderance of acetylcholine. Some calcium channel blockers and H2 blockers induced or aggravated parkinsonism and other extrapyramidal symptoms. It has been suggested that calcium channel blockers-induced extrapyramidal symptoms are much more common in elderly patients. In H2 blockers induced movement disorders, renal and liver dysfunction is the risk factor of them, but the mechanism is not clearly understood.
This review covers recent advances in a variety of dyskinesias. Introduction of new drugs for the treatment of myoclonus and sensory biofeedback therapy for focal dystonia are expanding our concepts of these types of movement disorders. Progress in the treatment of action myoclonus is especially noteworthy and has led to the implication of serotonin deficit in the pathophysiology of this syndrome. Knowledge of the biochemical pathology of Huntington's chorea has outpaced therapy for this disorder, but new forms of therapy have been proposed based on the chemical findings. Basic pharmacologic studies suggest pathophysiologic mechanisms for the syndrome known as tardive dyskinesia, but treatment is still far from ideal for this disorder. Other movement disorders with recent therapeutic advances include essential tremor and hemiballism. This review will cover only those dyskinesias in which new therapies have been advanced in the last few years. Aside from parkinsonism, which will not be discussed here, progress in the treatment of movement disorders has been slow, but steady. New drugs are being tested constantly, and the purpose of this review is to call attention to the ongoing evaluation in this field. Descriptions and etiologies for these dyskinesias are covered elsewhere (Fahn, 1976a) and therefore are not repeated here.
Toxins can be cited as a cause of several movement disorders, but this association is rare and the resultant syndromes usually include additional signs that are not typical for the idiopathic movement disorders. Most instances of confirmed toxin-induced movement disorders show lesions on CT and MRI scans of cortical or subcortical structures. A common underlying element in these toxin-induced syndromes is the development of lesions primarily in the pallidum and striatum. Because many toxins result in lesions affecting these structures, a selective vulnerability to hypoxic or metabolic insults has long been postulated. The susceptibility of these structures may relate to a number of factors, including the pattern of oxidative metabolism, heavy metal concentration, vascular perfusion, and neuronal innervation. Finally, in addition to causing disability, certain neurotoxins have led to a better understanding of human disease through the development of research models. As an example, the MPTP model has not only provided an animal model to study therapeutic strategies in PD but has also contributed important insights into the mechanism of neuronal degeneration.
Impaired hand function is a frequent finding in movement disorders. The skilled control of prehensile finger forces is an essential feature of tool use in daily life. In healthy subjects, grip force is precisely adjusted to the mechanical object properties, such as weight and surface friction. Grip force is accurately scaled to be only a small amount higher than the minimum necessary to prevent a hand-held object from slipping. When an object is lifted and moved around in space, grip force is modulated in parallel with the movement-induced fluctuations in load. The absence of a temporal delay between grip and load force profiles implies that the central nervous system is able to predict the load variations before the intended manipulation. Sensory information is used to adjust the level of applied finger forces efficiently to the requirements of the mechanical object properties and the task at hand. The characteristics of impaired finger force control include inefficient grip force scaling and imprecision of the temporal coupling between grip and load force profiles. Here, we review the characteristics of deficient grip force behavior in movement disorders, e.g. Parkinson's disease, task-specific dystonia, Gille de la Tourette's syndrome and cerebellar disease. Grip force analysis is a highly sensitive method to document even subtle impairments of finger force control and may be used both as a diagnostic tool and for the objective evaluation of treatment in neurological movement disorders.