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Psychiatrists encounter patients with abnormal movements in various clinical settings. Recognizing and correctly labeling motor phenomena in each setting helps to create a differential diagnosis that serves as the basis for optimal treatment, since abnormal movements can be the first indication of an unsuspected medical or neurologic disorder in a psychiatric patient treated for psychiatric symptoms. A solid understanding of prototypical movement disorders (e.g., Huntington's disease, Parkinson's disease) and of tremors will help psychiatrists to correctly categorize abnormal movements. All movement disorders, primary or drug-induced, contribute to morbidity (with loss of independence) and mortality (e.g., secondary to falls or choking). Many are stigmatizing, as abnormal movements are immediately obvious to others.
Movement disorders caused by basal ganglia damage all create trouble starting or stopping movements. They differ from cerebellar disorders, which affect movement targeting, and from stroke-related weakness. Neuroleptic malignant syndrome and catatonia are discussed in Chapters 12 and 23 , respectively. Real patients and videos are excellent ways to learn to recognize abnormal movements. A word of caution: many of the free videos on the Internet show patients with functional movement disorders who have made videos of themselves and do not depict classic movement disorders; therefore, one should select reputable sources, such as a video atlas.
A movement disorder is a clinical diagnosis, based on history and physical examination; laboratory tests and brain imaging usually do not facilitate making the diagnosis. A family history can be informative for hereditary movement disorders. One should ask carefully about present and past medications as well as substance use, as these are the most common causes of abnormal movements.
The examination begins with unobtrusive observation, when meeting the patient in the waiting area or approaching the bedside. One should determine if the movements exist when unobserved, and if the patient shuffles or writhes when walking. A patient who lies stiffly in bed might be parkinsonian, or catatonic. The neurologic examination is focused on establishing deficits beyond their relationship to the motor strip and the basal ganglia, and includes cortical functioning and cerebellar function as well as on eliciting other motor signs. Muscle tone should be determined (e.g. rigid, spastic, or hypotonic). If you suspect catatonia, you should perform an exam for other signs of catatonia. Some patients cannot relax while their limb is being examined for muscle tone, and seem to (voluntarily) resist each passive movement. This is called gegenhalten or paratonia.
Table 21-1 summarizes common movement symptoms. Overall, it is helpful to determine if your patient moves too much (hyperkinetic) or too little (hypokinetic), or if there are rhythmic tremors or non-rhythmic twitches. Myoclonus or asterixis can appear somewhat rhythmic on first glance, so one must observe carefully. Asterixis can suggest a serious metabolic disturbance, whereas myoclonus is non-specific and may be benign. Other phenomena that mimic tremor include focal seizures and cerebellar dysmetria. Some movements defy easy categorization but should be considered in psychiatric patients (e.g., catatonic symptoms, stereotypies, mannerisms).
Action tremor —triggered by voluntary movement
Rest tremor —stops during voluntary movement
Postural tremor —seen with either action or rest tremor, not itself diagnostic
Cerebellar dysmetria (intention “tremor”)—worsens as limb approaches target
Myoclonus —involuntary non-rhythmic jerk, moves only one joint
Asterixis (negative myoclonus, “flapping tremor”)—arrhythmic lapses of sustained posture
Focal seizures —non-rhythmic trains of unilateral twitching, lasting seconds to minutes.
Fasciculations —visible contractions within a muscle that do not move a joint
Chorea and Dyskinesia are essentially synonyms—brief, unpredictable, semi-purposeful
Choreoathetosis —when you cannot decide if it is chorea or athetosis
Athetosis —slow but continuous movements
Dystonia —abnormal postures held for at least several seconds
Lead-pipe rigidity —constant resistance throughout range of passive motion
Bradykinesia —slow movements
Akinesia —sustained periods of no movement
Hemiballism —violent, unilateral repetitive but non-rhythmic jerks of proximal limbs
Stereotypies —repetitive self-soothing movements (e.g., tapping foot, biting nails)
Tics —semi-voluntary fast movement, often multi-joint, usually urge-driven
When examining a patient with a tremor the main question is whether the tremor occurs mainly at rest (resting tremor) or during action (action tremor). Postural tremors can occur with either action or rest and are not themselves diagnostic. Writing or drawing will reliably evoke an action tremor in that hand, whereas rest tremors can intensify with movement of the opposite hand. The phenomenologic description of the tremor is followed by an examination of other neurologic signs or symptoms to help refine the diagnostic possibilities. This matters, since treatment depends on the tremor's etiology, although the treatment of some tremors can be non-specific and based on its severity and the patient's tolerance of it.
Table 21-2 summarizes gait disorders. Observing a patient's gait and understanding the etiology of a gait disturbance are particularly important during a patient visit. Gait disturbances not only limit a patient's independence but can lead to dangerous falls (especially in the elderly). Hypokinetic movement disorders, including parkinsonism associated with use of antipsychotics, lead to falls because patients react too slowly when they stumble. Ataxia or hyperkinetic movement disorders lead to fewer falls. A potentially reversible cause of a gait disturbance is normal-pressure hydrocephalus (NPH) that is manifest by a triad of (parkinsonian) gait, incontinence, and dementia (the latter being a late-stage manifestation). If diagnosed early, placement of a shunt can be curative.
Parkinsonian : slow, shuffling, stooping with arms flexed, festinating (unable to stop); many falls
Choreic : posturing, writhing; fewer falls
Ataxic : wide-based, lurching; fewer falls
Neuropathic : Foot slaps, patient steps high to avoid tripping
Spastic : stiff, circumducted leg, toe-walking
Functional (astasia-abasia): wild, seemingly poor balance but no falls.
One should also ask about swallowing difficulties, which can result in aspiration pneumonia.
Idiopathic Parkinson's disease (PD) is one of the hypokinetic syndromes characterized clinically by the triad of slow movement, rigidity, and tremor. The combination of tremor plus rigidity leads to the cogwheeling on exam. Although a resting tremor is often the first sign of PD, up to one-fourth of patients have no tremor. Difficulties initiating movements, like starting to walk, are called freezing, where a patient's feet seem to be glued to the ground.
The mainstay of treatment for PD is the dopamine agonist levodopa. Bradykinesia responds better to levodopa than does tremor. Unfortunately, while levodopa is highly effective early in reversing the dopamine loss-related akinesia, its long-term administration is complicated by levodopa-induced dyskinesias due to striatal hyperresponsiveness to acute dopaminergic stimulation. In later stages of the disease, patients experience periods of immobility that alternate with good symptom control (on–off phenomenon). Some patients with PD are atypical in that their response to dopamine agonists is poor. Atypical Parkinsonian syndromes (Parkinson's-plus) refer to patients who experience not only parkinsonian symptoms but other symptoms as well. Such syndromes include Lewy body dementia (LBD) or multi-system atrophy (MSA), where, as the name implies, other brain systems are affected. We caution clinicians that one will only know if a patient is poorly responsive to levodopa if it is actually tried.
PD is, for most patients, a multi-faceted disease and more than a pure movement disorder, either due to the biological nature of the illness, the side effects of treatment, or the psychological effects of having a progressive illness. Table 21-3 summarizes its core clinical symptoms.
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