Clinical Aspects of Motor Systems Donald Allen, Ph.D.

What do we affect with injury to motor systems Muscle strength and bulk Muscle contraction Muscle tone Muscle stiffness Reflexes

Muscle strength and bulk Paralysis Paresis Also described by regions of body affected –Hemiplegia –Paraplegia –Tetraplegia

Atrophy –Disuse atrophy –Neurogenic atrophy

Involuntary muscle contractions Ones that can occur occasionally in intact Nervous System Spasms Cramps Fasciculations

Involuntary movements that always indicate a pathological condition Fibrillations Abnormal movements caused by dysfunction in basal ganglia

Muscle tone Tension in resting muscles Damage to nervous system can frequently affect tone Hypotonia –Flaccidity Hypertonia

Hypotonia What can cause hypotonia? –Transection of Ventral root Peripheral nerve Dorsal root Rhizotomy –Injury to cerebellum

Hypertonia Chronic injury to UMN or some basal ganglia disorders Spasticity – velocity-dependent hypertonia –Accompanied by hyperreflexia of DTR –Clasp knife phenomenon –Clonus

Rigidity – velocity-independent hypertonia –Lead-pipe rigidity –Cog-wheel rigidity

Two types of rigidity seen after severe lesions to the brain Decorticate rigidity –Superior to midbrain –UE F, LE Ext Decerebrate rigidity –Midbrain level –Ext, UE IR, PF

Spinal or Cerebral Shock Descending motor commands interrupted by injury to upper motor neurons Lower motor neurons become temporarily inactivated Spinal or cerebral shock depending on location of injury Hypotonia Hyporeflexia Resolves with time

Disorders of LMNs Many different causes –Trauma –Infectious diseases (poliomyelitis) –Degenerative diseases –Vascular diseases –Tumors Where does the injury occur in the nervous system?

Signs of LMN injury Loss of reflexes to muscle Atrophy Flaccid paralysis –Hypotonicity Fibrillations

Post-polio Syndrome

UMN injury Where does the injury occur in the nervous system?

Signs and Symptoms of UMN Injury Abnormal cutaneous reflexes Abnormal timing of muscle activation Paresis Muscle hyperstiffness Clasp-knife response and clonus

Abnormal Cutaneous Reflexes Babinski’s sign –Normal until 6 months of age –Occurs after injury to corticospinal tract Muscle spasms in response to normally innocuous stimuli

Babinski’s sign

Abnormal timing of muscle activation Can contribute to movement problems –Delayed initiation of movement –Rate of force development is delayed –Muscle contraction time is prolonged –Relationship of timing of activation of agonists and antagonists is altered

Paresis Weakness Inability to activate LMN Loss of ability to fractionate movements –Lateral corticospinal tracts –Fine movements of hands

Myoplastic Hyperstiffness Post Stroke Hyperstiffness – excessive resistance to muscle stretch Due to changes in muscles –Loss of sarcomeres –Increased weak binding of actin and myosin –Atrophy of muscle fibers

Changes in muscle fibers Muscle fiber diameter decreased Selective atrophy of Type II fibers –Slow twitch muscle more resistant to stretch

Hyperactive Stretch Reflexes After stroke, most patients DO NOT have hyperactive stretch reflexes Hyperreflexia seen only in people with hemiplegia and severe contractures Evidence suggests that hyperreflexia may result from contractures, not the other way around Shortened muscles have an amplified stretch of muscle spindles during a stretch, producing a greater stretch reflex

Changes after incomplete spinal cord injury Contractures Hypertonicity Predominance of Type IIB muscle fibers and a decrease in Type I muscle fibers –Different from after a stroke

Reflexes after SCI Hypertonia Tonic stretch reflex (# of synapses) – Phasic stretch reflex (# of synapses) –

Other signs more often seen after chronic SCI Clasp-knife response Clonus

Types of Upper Motor Neuron Lesions Spinal cord injury Stroke Congenital lesions

Complete Spinal Cord Injury All descending motor control lost below the level of the lesion Spinal Shock –At and below level of lesion Muscle toneDecreased Reflexes Lost Voluntary Control of Movement

Complete SCI When spinal shock resolves –Tone –Monosynaptic Reflexes –Polysynaptic Reflexes –Voluntary muscle control

Incomplete SCI Some ascending and/or descending fibers intact We will cover more in the chapter on the spinal cord

Stroke Occlusion or hemorrhage of a blood vessel in the CNS Most common site is the middle cerebral artery

Middle Cerebral Artery

MCA Stroke

Disrupts connections between the cerebral cortex and the brainstem, spinal cord and cerebellum Damages adult upper motor neurons (corticospinal tracts) –Paresis –Loss of fractionation of movement Sensory and communication systems may also be damaged

Effect on motor systems Abnormal muscle inactivation Corticospinal Lat. Reticulospinal Med. Reticulospinal Vestibulospinal

Standing Posture Hemiparetic upper extremity –Contracture –Weak actin-myosin bonds –Atrophy of type II muscle fibers Lower extremity –Excessive extension in standing and walking Changes in activation of different pathways Paresis Myoplastic hyperstiffness in specific muscles

Gandevia (1993) Muscle weakness in one group of muscles on paretic side associated with weakness in antagonist muscle group Distal muscles weaker than proximal muscles on both limbs In general, muscles on the non-paretic side were weaker than muscles in matched healthy subjects

Congenital Disorders of Upper Motor Neurons Spastic cerebral palsy –Motor disorders Abnormal tonic stretch reflexes at rest and while moving Reflex irradiation Abnormal co-contraction of antagonist muscles Lack of postural preparation prior to movement

Common Characteristics of Upper Motor Neuron Lesions Paresis Abnormal cutaneous reflexes Abnormal timing of muscle activation Myoplastic stiffness

Signs more common with SCI Hyperreflexia of phasic stretch reflexes Clonus Clasp-knife phenomenon

Signs more common with congenital disorders Abnormal co-contraction of antagonist muscles Reflex irradiation

Interventions Constraint-induced movement Botulinum toxin

Constraint-induced movement Taub Correct learned non-use –Non-use leads to secondary consequences Atrophy Contractures –Used at least 1 year post-stroke –Constrain non-paretic limb –Specific exercises for paretic limb

Constraint-induced movement Improves upper limb function Forced movement immediately following a lesion may increase the lesion –Animal studies –Neuronal excitotoxicity –Section 4: Neuroplasticity

Other techniques Movement against resistance Bicycling with high workloads Walking with partial weight supported –More symmetrical gait –More normal muscle activation patterns

Botulinum Toxin Used to decrease muscle stiffness –Stroke –Spastic cerebral palsy Also inhibits active muscle contraction Injected into muscle and blocks release of Ach from presynaptic nerve terminal

Treatment of Hyperreflexia post SCI Baclofen –Stimulates presynaptic release of GABA which activates GABA-B receptors –Methods of administration Oral Pump into subarachnoid or subdural space

Actions of Baclofen Inhibits stretch reflex pathways –Decreases calcium intake into presynaptic terminal of primary sensory afferent fibers –Stabilizes postsynaptic membrane Does not alter myoplastic hyperstiffness

Efficacy of Baclofen Positive effects –Decreases spasms, pain and sleep disturbances –Improves bladder function –Increased mobility Negative effects –Can reduce function if reflexive muscle contraction is used functionally Stability Mobility

Degeneration of Voluntary Motor System Amyotrophic lateral sclerosis (ALS) –Lou Gehrig’s Disease Systems damaged –Lateral activating systems –Anterior horn neurons Signs & Symptoms –Both upper and lower motor neuron –Sensory and autonomic usually normal

ALS 90% idiopathic For familial type, the gene has been identified Death results from respiratory complications

Upper motor neuron S & S Paresis Fasciculations Spasticity Hyperreflexia Babinski’s sign Clonus

Lower motor neurons S & S Fibrillations Atrophy Paralysis