Clinical History

There are several symptoms that are suggestive of hypokinesia. Patients report difficulty getting out of chairs, especially car seats and sofas; trouble turning over in bed; and an overall reduced speed of activities of daily living. Patients and families might interpret slowness as a sign of old age or early arthritis and not suspect a neurological disorder. Some patients may misinterpret hypokinesia as weakness. Slowness and fatigue, although they are particularly prominent in hypokinesia, can be features of depression, catatonia, or hypothyroidism.

Trouble starting and stopping can also be seen with hypokinesia. Parkinsonian patients may complain of start-hesitation or freezing [2 during turning, when they are trying to reach a target, or when they are passing through a doorway. Difficulty stopping is the complaint of patients who have festination as part of hypokinesia, and these patients have a tendency to build up speed as they walk, even to the point of running. They cannot stop until coming to a barrier, such as a wall. The mechanism is considered to be a combination of the loss of postural reflexes and the flexed posture, which brings the center of gravity in front of the feet.

Falling is an important historical feature of movement disorders, and all adults who fall without ready explanation should be evaluated neurologically. In parkinsonian disorders, patients eventually develop loss of postural reflexes, which can lead to poor balance and falling. This problem is particularly apparent to patients with freezing. Falling occurs in other movement disorders as well, especially in patients with Huntington's disease, in whom loss of postural reflexes occurs in association with a stuttering, dancing gait. Truncal ataxia due to cerebellar or proprioceptive impairment may cause a wide-based staggering stance and gait, which patients interpret as "walking like a drunk."

Falling is also a common feature of hyperekplexia or excessive startle syndrome. In this disorder, often inherited with a defect in the gene for the glycine receptor, y a sudden noise or threat can trigger the patient to lose muscle tone and then fall. In this disorder, the patient has an exaggerated startle reflex, y which can be measured electrophysiologically. If patients have a delayed reaction to sudden noise or threat, a psychogenic problem should be considered. y , [6

Another cause of falling is positive and negative myoclonus. The positive myoclonic jerk can result in a patient being thrown off balance. Negative myoclonus, especially of the thigh muscles when the patient is standing or walking, produces a bouncing stance, and the sudden inhibitions of the muscles leads to a fall. Posthypoxic myoclonus is the most common cause of this type of negative myoclonus,y and in these cases, patients complain of sudden body jerks that cause them to lose balance control without warning.

Not knowing what to call the various forms of hyperkinesias, patients may use terms such as muscle jerks and shaking movements to describe their disorder. Only the examination can definitively differentiate the type of dyskinesia, but the history can suggest the most likely categories. Sudden muscle jerks are usually myoclonus or tics. Rhythmical movements are usually tremors, rhythmical (segmental) myoclonus, or the repetitive movements of tardive dyskinesia, such as oral-lingual-buccal dyskinesias, body rocking, and marching in place. In dystonia, movements may occur or increase with volitional activity such as writing, pouring liquids, buttoning, and walking. The timing of abnormal movements is important to document, especially with tremors. Parkinsonian tremor occurs during rest while the patient is watching television or lying in bed. Postural tremor, associated with many drugs, hyperthyroidism, or familial tremor, is seen during activity and affects handwriting, and the patient often complains of large, sloppy handwriting. Cerebellar end-point kinetic tremor is seen when patients extend their arms maximally to complete a task,

and the dyssynergia that accompanies the tremor causes extreme sloppiness, spilling, and soiling of clothes.

In most movement disorders, the onset of symptoms is insidious, although frequently patients date them to an incident such as a frightening event or trauma. An exception to this rule is hemiballismus, which often is sudden in onset and related to a cerebrovascular accident.

Sudden movement induces some special forms of dyskinesia. A history of intermittent attacks of dyskinesias that arise just as a person stands up or starts to run immediately raises the suspicion of a paroxysmal dyskinesia, [8 such as paroxysmal kinesigenic dyskinesia. In addition to sudden movement, startle and hyperventilation can also be the precipitating factor. y Prolonged exercise can induce attacks of hyperkinesia as well and leads to the diagnosis of paroxysmal exertional dyskinesia. y Other types of paroxysmal dyskinesias are more commonly induced by fatigue, stress, or ingestion of caffeine and alcohol. Nonkinesigenic paroxysmal dyskinesias, however, especially those without a family history, are often psychogenic in etiology. y Most psychogenic movement disorders are continual rather than intermittent and can present as any type of hyperkinesiay and even hypokinesia^! and gait disorders. There are many historical clues to suspect the psychogenic etiology of a movement disorder,[5 including their frequent distractability, inconsistency of signs, and abrupt, strokelike onset. y

Medication exposure requires a special place in the clinical history of a movement disorder. The most important drugs that induce movement disorders are those that are dopamine D2 -receptor antagonists, the so-called dopamine receptor blocking agents. These drugs can cause acute dystonic reactions, acute akathisia, drug-induced parkinsonism, neuroleptic malignant syndrome, and the tardive dyskinesia syndromes. The last entity presents a wide variety of dyskinesias, y which are characterized by their frequent persistence even after drug withdrawal. Drugs, and certain endocrine compounds such as thyroxine, epinephrine, and insulin that alter noradrenergic tone, can exaggerate physiological tremor. Anticonvulsants can induce chorea, and valproate may even induce hypokinesia. Cocaine can induce chorea,y tics,y and opsoclonus-myoclonus.y

Although movement disorders are primary motor conditions, a number of sensory phenomena can occur. Painful muscle cramps are most often due to neuromuscular disease^ but can occur with severe rigidity or stiff-person syndrome. y Dystonia can sometimes be painful, particularly drug-induced forms. Painful foot cramping due to dystonic spasms can be an early sign of parkinsonism. y Also in parkinsonism, pain may be focal in the oral and genital areas y and have a burning quality or numbness and itching. In patients with akathisia, a movement disorder associated with a primary subjective restlessness, patients frequently describe a vague but intense discomfort in their body that is relieved by movement.

In addition to these historical elements, a careful medical and family history is important in evaluating hypokinesia and hyperkinesia. The medical history should include an evaluation of all body systems, including the mind, because dementia, psychosis, depression, and various personality traits like attention deficit disorder and hyperactivity, and obsessive-compulsive disorder can help in diagnosis and co-morbidity analyses. Several primary movement disorders are hereditary, and therefore the creation of a family tree focusing on the type of movement disorder the patient has along with other neurological and psychiatric disorders may prove pivotal to the final neurological diagnosis.


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