NSCS 730

621 - Subconscious motor

NSCS 730

Subconscious Motor Control

Dr. Mark Kindy503 - STB; 792-0559; [email protected]

621 - Voluntary motor

Descending regulation of motor activity

• Simplest control is by reflex connections

• Voluntary motor control is by direct cortical pathways

• Subconscious motor control is carried out by several pathways with connections in brainstem

• All descending pathways use reflex interneurons

• All descending activity converges on -motor neuron pools

Reflexconnections

Voluntary motor

Subconscious motor


Descending systems to regulate posture & tone• Pathways arising in

brainstem influence muscle tone and posture– operate at subconscious

level

• Pathways: (more medial projections than corticospinal)– Reticulospinal– Vestibulospinal– Cerebellum influences

tone & posture indirectly through these other systems


Upper vs Lower Motor neuron lesions• All motor neuron lesions include

paralysis• Lower motor neuron lesions: injury to

segmental () motor neurons– Dysfunction may involve single muscle– Muscle atrophy, wasting– Tone and reflexes absent, flaccidity– Fasciculation of muscle cells

• Upper motor neuron lesions: injury to higher order neurons or descending tracts– Usually all muscles of a part of the

homunculus– Spasticity: especially in extensors

(antigravity muscles)– Lack atrophy & fasciculation

• Spasticity: increased tone and stretch reflexes– Resistance to passive movement– Clasp-knife, clonus– Babinski’s sign

Upper

Lower

2/9/09 621 - Subconscious motor



Reticular formation of brainstem affects tone• Reticulospinal

tracts (from brainstem reticular formation) important for regulating tone

• Strong influence on -motor neurons

• Two systems have opposite effects which are normally in balance• Medial reticular formation inhibits extensors

– Receives strong excitation from motor cortex

• lateral reticular formation facilitates extensors• Lesions of corticospinal tracts leaves reticular influences unbalanced

– Extensor fascilitation, spasticity



Spasticity - hypertonia, hyperreflexia• Spasticity

– Results from abnormally high -motor input

• Resistance to passive movement, increased tone– Especially for extensors– Velocity dependent: rapid

stretch - more resistance– Hyperactive stretch reflexes– Clasp-knife , clonus • Altered plantar reflex:

• Normal adult – toes ventroflex

• After upper MN injury – toes dorsiflex and fan– Babinski’s sign


Vestibular system• Vestibular portions of

inner ear:• 3 semicircular canals

– Respond to angular acceleration

• Utricle & Saccule– Respond to linear

acceleration & gravity

• Membrane-lined fluid filled cavities in temporal bone

• Receptors are hair cells– Depolarize when stereocilia are bent– Specializations allow head movement to stimulate them


Semicircular canals• Respond to angular acceleration

• 3 on each side– Filled with fluid– Perpendicular to each other– Pairs of canals in same plane


Semicircular canals• Mechanism of stimulation:

• Hair cells located in ampulla - Gelatinous Cupula covers stereocilia

• During rotation of head in the plane of a canal:– Fluid moves around canal– Tilts the cupula; Stereocilia

bent– Afferents excited on one

side & inhibited on the other










Utricle and Saccule• Respond to linear

acceleration & gravity• One of each on each side

– Utricle - macular surface horizontal

– Saccule - macular surface vertical

• Mechanism of stimulation:– hair cells in macular surface– Stereocilia covered by

gelatinous matrix– Otoliths embedded in gelatin

• Otoliths more dense than water

– Linear acceleration or gravity forces otoliths to move gelatin and bend stereocilia– Utrical signals horizontal forces– Saccule signals vertical forces










Central vestibular connections

• Afferent fibers relay through 4 vestibular nuclei

• 2 vestibulospinal tracts• Lateral:

– receives much input from utricle and saccule

– Changes muscle tone in response to gravity

• Medial:– receives much input from

semicircular canals– Causes movement of head and

shoulders to coordinate head and eye movements

• Other vestibular pathways ascend to oculomotor nuclei- CN-III, IV, VI

• Cause eye movement in response to head rotation: Nystagmus

• Strong input to cerebellum


Vestibulo-occular control• Subject seated on stool and rotated to left• Initial response (hard to visualize)

– Slow tracking eye movements to right– Fast eye movements back to left

• Nystagmus: alternate slow and fast eye movement

• Response to stopping turning (post-rotatory)– Head stops but fluid continues moving left– Eyes track slowly left, quick movement to right

• Nystagmus normal for head rotation and repetitive moving object (optokinetic)– Nystagmus without movement = sign of lesion

Post-rotatory nystagmus


Cerebellum

• attached to brainstem

• Elaborate cortex & deep nuclei

Compares sensory inputs with motor programs to correct and fine-tune movements

Deep nuclei

Cortex


Cerebellar Input / Output• Sensory inputs:

– Somatic - tactile, proprioceptors– Vestibular– Visual, auditory

• Motor input:– From motor and premotor cortex– Signals about the intended

movement

• All inputs converge on cerebellar cortex

• Complex cortical processing• All output is from purkinje cell

axons to deep nuclei • Deep nuclei compare cerebellar inputs with cortical output pattern, and relay error signals back to cerebral motor centers


Cerebellar Outputs• No direct

connections to -motor neurons

• Output from cerebellum returns to motor areas of cortex to fine-tune motor programs

Red nucleus

thalamus


Function of cerebellum• Compares sensory

inputs with motor programs to correct and fine-tune movements

• Signs of Cerebellar damage:– Ataxia, unsteady gait

and stance– Intention tremor– Dysmetria– Asynergy– Reduced muscle tone


Basal ganglia• Large nuclei of

forebrain below cerebral cortex

• Striatum– Caudate nucleus– putamen

• Globus pallidus• Substantia nigra

(dopamine cells)

• Receive wide cortical inputs

• Send output up to premotor areas to help organize stereotypic motor sequences


Basal ganglia diseases• Dysfunctions:• Excess movements

– Resting tremor – Choreoform– Athetoid– ballistic

• Bradykinesia– Absent or difficult initiation

• Rigidity– Leadpipe or cogwheel

• Examples:• Parkinson’s disease

– Loss of dopamine-containing cells of substantia nigra

– Resting tremor, leadpipe rigidity, bradykinesis

• Huntington’s disease– X-linked genetic– Degeneration of gaba-ergic &

cholinergic cells of striatum– Choreoform movements– Mental deterioration

Cerebral palsy• About 10 percent of children with cerebral palsy have athetoid

cerebral palsy. Athetoid cerebral palsy is caused by damage to the cerebellum or basal ganglia. These areas of the brain are responsible for processing the signals that enable smooth, coordinated movements as well as maintaining body posture. Damage to these areas may cause a child to develop involuntary, purposeless movements, especially in the face, arms, and trunk. These involuntary movements often interfere with speaking, feeding, reaching, grasping, and other skills requiring coordinated movements. For example, involuntary grimacing and tongue thrusting may lead to swallowing problems, drooling and slurred speech. The movements often increase during periods of emotional stress and disappear during sleep. In addition, children with athetoid cerebral palsy often have low muscle tone and have problems maintaining posture for sitting and walking.


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