Motor control
Motor control—the process by which the central nervous system produces purposeful, coordinated movements of the body—can be disrupted in a variety of ways by acquired brain injury:
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This can be described partially as upper motor neuron (UMN) syndrome, which is a collection of features resulting from injury to the corticospinal tracts, otherwise known as the pyramidal tracts .
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In terms of coordination, motor control is affected when damage is inflicted on the basal ganglia, cerebellum, and associated tracts—the so-called extrapyramidal system .
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Functional movement is hampered by injury to the vestibular system or the visual system.
Motor learning
The current neurorehabilitation of movement is increasingly imbued with the science of motor skill acquisition or motor learning .
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Motor learning is a complex cognitive process that involves the interaction between cortical and subcortical structures to acquire, retain, and retrieve motor plans to execute actions with speed, accuracy, coordination, and consistency to achieve task goals.
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Several pharmacologic agents are under investigation to enhance motor recovery.
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Both serotonergic and dopaminergic drugs have been suggested to possibly enhance motor outcomes particularly after stroke.
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In 2011 the results of the FLuoxetine for motor recovery After acute ischaeMic stroke (FLAME) trial suggested that fluoxetine enhanced motor recovery after stroke.
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More recently, the Fluoxetine or Control Under Supervision (FOCUS) trial demonstrated no such effect of fluoxetine on motor recovery.
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Upper motor neuron syndrome
The upper motor neuron syndrome has been described in terms of both positive signs, negative signs, and rheologic changes—referring to changes involving the physical properties of muscle and soft tissue ( Table 29.1 ).
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Although the negative features of the UMN syndrome are associated with more disability than positive features, they are also less treatable.
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The positive signs of UMN syndrome are unified by the fact that they all involve involuntary muscle overactivity.
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Spasticity, which was defined by Lance in 1980 as “velocity dependent increase in the tonic stretch reflex,” is often used in reference to all positive signs collectively, although this is not semantically correct. These various phenomena each have differing pathophysiology, different functional consequences, and different treatments.
| Negative | Positive |
|---|---|
|
|
| Rheologic | |
|
a Characteristics of the upper motor neuron syndrome are divided into negative, positive, and rheologic.
Movement disorders
Just as the motor disorders, which occur with pyramidal tract injury, can be described in terms of positive and negative signs, movement disorders can be discussed in terms of the duality of hypokinesia and hyperkinesia.
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The term dyskinesia also refers to abnormal involuntary movements.
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The label of extrapyramidal has begun to fall out of favor because the corticospinal pathways (i.e., pyramidal tracts) and basal ganglia pathways have turned out to be somewhat entangled, and disorders of movement do exist that are not associated with basal ganglia pathology.
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The classification systems of movement disorders, both as a group of disorders and as individual conditions, are now based on phenomenology as opposed to anatomical localization.
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Tremor is defined as an involuntary, rhythmic, oscillatory movement of a body part. Tremors are classified on two main axes: axis I, clinical features, and axis II, etiology ( Table 29.2 ).
TABLE 29.2
Classification of Tremor a
Axis I: Clinical Features
Historical features
Tremor Characteristics
Associated Signs
Laboratory Tests
Age at onset
Temporal evolution
Medical history
Family history
Alcohol/drug sensitivity
Body distribution
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Focal, segmental, hemi, generalized
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Activation conditions
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Rest versus action
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Action tremors: postural versus kinetic
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Postural: position dependent versus independent
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Kinetic: simple, intention, task specific
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Tremor frequency
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4 Hz, 4–8 Hz, 8–12 Hz, or >12 Hz
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Systemic signs
Neurological signs
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Isolated tremor: no other abnormal signs
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• Combined tremor: other signs present
Electrophysiological tests
Structural neuroimaging
Receptor imaging
Biomarkers
Axis II: Etiology
Acquired
Genetically defined
Idiopathic
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Familial
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Sporadic
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a The axis I classification of tremor is based in clinical features of the patient’s history and physical examination and possibly additional tests. Axis II classification is based on etiology. A syndrome in axis I may have more than one etiology, and one etiology may result in several syndrome.
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Dystonia , which is characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive movements, postures, or both, is also classified on two such axes ( Table 29.3 ).
TABLE 29.3
Classification of Dystonia a
Axis I: Clinical Features
Age at Onset
Body Distribution
Temporal Pattern
Associated Features
Infancy: birth–2 years
Childhood: 3–12 years
Adolescence: 13–20 years
Early adulthood: 21–40 years
Late adulthood: >40 years
Focal
Segmental
Multifocal
Generalized
Hemidystonia
Disease course
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Static
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Progressive
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Variability
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Persistent
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Action specific
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Diurnal
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Paroxysmal
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Isolated versus combined with another movement disorder
Presence of any cooccurring neurological or systemic manifestations
Axis II: Etiology
Nervous system pathology
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Evidence of degeneration
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Evidence of structural lesions
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No structural lesion or degeneration
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Inherited
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Autosomal dominant
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Autosomal recessive
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X-linked recessive
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Mitochondrial
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Acquired
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Perinatal brain injury
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Infection
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Drug/toxin induced
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Vascular
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Neoplastic
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Brain injury
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Psychogenic
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Idiopathic
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Familial
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Sporadic
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