Voluntary movement requires complex interaction of the corticospinal (pyramidal) tracts, basal ganglia, and cerebellum (the center for motor coordination) to ensure smooth, purposeful movement without extraneous muscular contractions.
The pyramidal tracts pass through the medullary pyramids to connect the cerebral cortex to lower motor centers of the brain stem and spinal cord.
The basal ganglia (caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra) form the extrapyramidal system. They are located deep in the forebrain and rostral midbrain. The basal ganglia direct their output mainly through the thalamus to the cerebral cortex (see figure Basal ganglia).
Most neural lesions that cause movement disorders occur in the extrapyramidal system; thus, movement disorders are sometimes called extrapyramidal disorders.
Classification of Movement and Cerebellar Disorders
Movement disorders are commonly classified as those with
The classic and most common hypokinetic disorder is
Hyperkinetic disorders refer to
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Chorea (including hemiballismus [rapid chorea] and athetosis [slow chorea])
However, this classification does not account for overlap between categories (eg, tremors that occur in Parkinson disease).
Cerebellar disorders are sometimes considered hyperkinetic disorders.
Hyperkinetic disorders
Hyperkinetic disorders (see figure Classification of common hyperkinetic disorders and table Hyperkinetic Disorders) can be
Rhythmic disorders are primarily tremors—regular alternating or oscillatory movements, which can occur mainly at rest, while maintaining a position, and/or during attempted movement. However, in some cases, a tremor, though rhythmic, is irregular, as occurs when tremor is associated with dystonic disorders.
Nonrhythmic hyperkinetic disorders can be
Rapid nonrhythmic hyperkinetic disorders may be
Athetosis and chorea may occur together as choreoathetosis. Chorea is the most characteristic movement disorder in Huntington disease.
Multiple motor and phonatory tics are the defining feature of Tourette syndrome.
Hyperkinetic Disorders
Abnormal Movement |
Causes |
Description |
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Drugs (eg, cocaine, amphetamines, antipsychotics) |
Movements are nonrhythmic, slow, writhing, and sinuous (snakelike), primarily in distal muscles; alternating postures of the proximal limbs often blend continuously to produce a flowing stream of movement. Athetosis has features of dystonia and chorea and often occurs with chorea as choreoathetosis. |
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Huntington disease, hyperthyroidism, hypoparathyroidism, paraneoplastic syndromes, systemic lupus erythematosus (SLE) affecting the CNS, other autoimmune disorders, rheumatic fever, tumors or infarcts of the caudate nucleus or putamen Pregnancy, often in women who had rheumatic fever Drugs that can cause chorea (eg, levodopa, phenytoin, cocaine, oral contraceptives) Drugs that can cause tardive dyskinesia (eg, antipsychotics) |
Movements are nonrhythmic, jerky, rapid, and nonsuppressible, primarily in distal muscles or the face. Sometimes abnormal movements are incorporated into semipurposeful acts that mask the involuntary movements. Chorea often occurs with athetosis as choreoathetosis. |
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Dystonias |
Primary (idiopathic) Degenerative or metabolic disorders (eg, Wilson disease, neurodegeneration with brain iron accumulation [NBIA] such as PKAN due to a PANK2 mutation [previously, Hallervorden-Spatz disease], various lipidoses, multiple sclerosis, cerebral palsy, stroke, brain hypoxia) Drugs that block dopamine receptors, most often antipsychotics (eg, phenothiazines, thioxanthenes, butyrophenones) or antiemetics |
Sustained or intermittent muscle contractions often distort body posture or cause twisting, repetitive movements. |
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Lesions (most often due to stroke) in the contralateral subthalamic nucleus or in connecting afferent or efferent pathways |
Movements are nonrhythmic, rapid, nonsuppressible, violent, and flinging. |
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Various causes (eg, degeneration of the basal ganglia, dementias, epileptic syndromes, metabolic disturbances, physical and hypoxic encephalopathies, toxic encephalopathies, viral encephalopathies, certain drugs such as levodopa, lithium, and MAO inhibitors) |
Very rapid and jerky, nonsuppressible, shocklike twitches occur; they may be focal, segmental, or generalized. |
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Tics |
Primary:Tourette syndrome Secondary: Huntington disease, neuroacanthocytosis, PKAN, infections, stroke, drugs (eg, methylphenidate, cocaine, amphetamines, dopamine antagonists [which can cause tardive dyskinesias]) |
Movements are nonrhythmic, stereotypical, rapid, and repetitive; characteristically, patients have an urge to do them and feel brief relief after doing them. Tics can be suppressed only for brief periods and with conscious effort. Tics may be motor or phonatory; they may be simple (eg, eye blinking, growling, clearing the throat) or complex (eg, shoulder shrugging, arm swinging, shouting words or sentences, including obscenities). |
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Essential tremor Wilson disease Certain drugs (eg, lithium, valproate, olanzapine, other typical and atypical antipsychotics—see table Some Causes of Parkinsonism) Endocrine, metabolic, and toxic disorders (eg, anoxic encephalopathy, hepatic encephalopathy,, hypoglycemia, hyperparathyroidism, hyperglycemia, hyperthyroidism, hypocalcemia, uremia, heavy metal toxicity) Physiologic |
Movements are regular, mostly rhythmic, and oscillatory. |
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CNS = central nervous system; MAO = monoamine oxidase; PKAN = pantothenate kinase‒associated neurodegeneration. |
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Drugs Mentioned In This Article
| Drug Name | Select Trade |
|---|---|
methylphenidate |
CONCERTA, RITALIN |
olanzapine |
ZYPREXA |
phenytoin |
DILANTIN |
levodopa |
Levodopa |
dopamine |
No US brand name |
lithium |
LITHOBID |
