neuro #3

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neuro #3
2012-11-10 11:35:58

Jen's neuro #3
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  1. cerebral cortex- association areas
    • premotor/supplementary motor cortex (6)- involved in motor learning & planning & controlling sequential or complex movements. Controls/coordinates/sequences actions of larger groups of muscles.
    • Frontal eye fields (8)- specialized for controlling movement of eyes (rapid eye movements, directing attention)
    • broca’s area (44,45)- specialized for generating motor programs responsible for production of speech.
    • Pre-frontal cortex (9,10)- responsible for higher-order control of motor functioning (purposeful planning, organization, logic)
  2. cerebral cortex- primary motor cortex
    • directly involved in production of voluntary movement.
    • Somatotopic organization of motor control (homunculus.)
    • Each hemisphere controls contralateral side of body.
    • Beginning of pyramidal pathways to lower areas of nervous system.
    • Neurons are arranged in columns that control a small group of synergistic muscles.
    • The columns are then organized into clusters that control larger groups of muscles.
  3. subcortical nuclei of cerebrum
    before primary motor cortex sends final commands to muscles, the signals are fine-tuned thru reciprocal interactions with subcortical structures. 
  4. basal ganglia
    • receive input from primary motor & motor association areas.
    • Send output to thalamus (ventral anterior & ventral
    • lateral nuclei)
    • Pre-processing- serves to facilitate desired movements & inhibit undesired movements. 
    • Infer this function based on observations of patients with damage to these structures (parkinson’s & hunington’s disease)
    • damage associated with changes in muscle tone, irregular movement, & presence of involuntary movements. 
  5. associated structures of basal ganglia
    • substantia nigra, subthalamus
    • caudate nucleus & putamen, globus pallidus, subthalamus (diencephalon), substantia nigra (midbrain) 
  6. cerebellum
    • serves to produce smooth, synergistic, coordinated movements.
    • Associated structures (pontine nucleus & red nucleus) receive input from primary motor & motor association areas.
    • Send output to thalamus (ventral ant & ventral lat nuclei) damage produces jerky, uncoordinated movements & intentional tremor.
  7. corticospinal tract
    • bilateral primary motor corticles (add input from motor association cortex & primary somatosensory cortex).
    • Corona radiata.
    • Internal capsule, cerebral penducle of midbrain.
    • Pons.
    • Medulla (decussation of pyramids- 85-90% of fibers cross over to other side)
    • central horn motor nuclei of spinal nerve.
  8. corticonuclear tract
    • innervate cranial motor nerves (voluntary pathways for movement of all speech muscles except for respiration.)
    • begins at bilateral cortical motor cortices & terminates at motor nuclei of cranial nerves in brainstem.
    • Most bilateral innervation- diaphragm, ocular muscles, upper face, jaw, pharynx, muscles of larynx. Intermediate amount- tongue. Most unilateral innervation- lower face & trapezius. 
  9. lateral & anterior corticospinal tracts
    • lateral- crossed fibers, innervate most of muscles.
    • Anterior- uncrossed fibers, innervate trunk & thighs (midline muscles); cross at level of ventral horn motor nuclei. 
  10. Upper motor neurons & Lower motor neurons
    • UMN- neurons traveling from motor cortices to ventral horn motor nuclei in spinal cord/nerves or cranial nerve motor nuclei in brainstem/cranial nerves; 1st order neuron; synapses with lower motor neuron in motor nuclei.
    • LMN (final common pathway)- connect cranial nerve motor nuclei in brainstem/cranial or ventral horn motor nuclei in spinal cord/nerves to muscle fibers; 2nd order neuron; receive input from many pathway in add to UMN. 
  11. interneurons
    present throughout brain & spinal cord (SC); in motor system many places where there are junctions involve many connections with interneurons; in brainstem, reticular formation is comprised of interneurons; acts as filters to sensory & motor signals. 
  12. extrapyramidal system
    • Basal ganglia provides indirect control over motor movement. Pathway begins at cerebral cortex.
    • Tectospinal tract- sup colliculus to ant horn of SC. Visual & auditory info affects reflexive body postures.
    • Rubrospinal tract- red nucleus in midbrain to LMN. Cerebellar info to regulate muscle tone to support body against gravity.
    • Vestibulospinal tract- vestibular nucleus to LMN. Vestibular input to muscles to regulate reflexive adjustments of body posture.
    • Reticular descending tract- reticular formation from pons & medulla. Inhibitory & excitatory regulation of voluntary & reflexive movements (alters muscle tone & preparedness) 
  13. motor unit
    Basic element of motor system. Motor neuron (LMN), muscle fiber, neuromuscular/myoneural junction- connection b/w motor neuron & motor end plate in muscle fiber. 
  14. 3 types of muscle cells
    • cardiac (heart)
    • skeletal (arm)- striated, move thru a pull action/ contraction, work in pairs with reciprocal muscle, stimulated by a LMN.
    • Smooth (organ)
  15. skeletal muscles
    • muscle fibers contain 2 types of proteins arranged parallel to each other. Proteins contract when stimulated causing the muscle to shorten.
    • Actin (thin filament)
    • myosin (thick filament) 
  16. extrafusal & intrafusal fibers
    • extrafusal fibers- make up large mass of muscle; connected to bone by tendons; controlled by alpha motor neurons.
    • Intrafusal fibers- connected in parallel to extrafusal fibers; contain muscle spindles which detect stretch; controlled by gamma motor neurons. 
  17. muscle fibers
    muscle activity- individual fibers are either contracted or not. Muscle tone is dependent on the number of fibers that are contracted. The more motor units active, the greater the muscle tone (contraction). The fewer motor units active, the less the muscle tone. 
  18. motor speech disorders
    • Disturbance of the speech production system of neurologic origin that results in being imperfectly understood or creating the impression that speech is bizarre or unusual (not a disorder of speech perception or a disorder of lang processing).
    • Usual result is impaired production of speech segments (discrete sounds) & suprasegments (rate, stress, intonation). Can co-exist with other cognitive disturbances (aphasia).
    • Caused by the same neuropathologies as other neurogenic disorders (stroke, disease, accidents, poisons, tumors). 
  19. apraxia
    • Inability to perform a learned motor skill in the absence of paralysis. Muscle tone, strength, range of movement (ROM) are all normal.
    • Characterized by loss of ability to voluntarily execute learned purposeful movements despite having the desire & the physical ability to perform.
    • Not caused by incoordination, sensory loss, or failure to comprehend commands.
    • Considered to be a disorder of motor planning. 
  20. apraxia of speech
    • Clinical signs- groping, inconsistent errors, increasing errors with length & complexity of utterance, patient aware of deficit, normal muscle tone, strength, range of movement.
    • Neurological areas involved- premotor area, supplementary motor area, insular lobe. 
  21. dysarthria
    • Inability to speak because of a lack of coordination, spasticity, or weakness of the muscles of speech. Muscle tone is impaired (hypo/hypertonia), strength & ROM are reduced.
    • Components of neural motor system- UMN, LMN, basal ganglia, cerebellum. 
  22. oral/ buccofacial apraxia
    inability to perform nonspeech movements with muscles of larynx, pharync, tongue, & cheeks
  23. spastic (UMN) dysarthria
    • lesion results in increased tone & resistance to movement (hypertonia, spastic paralysis, hyperreflexia, clonus, babinski sign.
    • Spastic- unilateral UMN damage- produces symptoms similar to bilateral, but less severe & temporary, cased by stroke or tumor; bilateral UMN damage- pyramidal (corticobulbar) & extrapyramidal pathways (from cortex to brainstem/spinal cord) run close to one another & both are damaged, caused by wide variety of neuropathologies.
    • General characteristics- hypertonia (increased muscle tone, but weak muscles), hyperreflexia (stretch reflexes), limited range of motion, slowed rate of movement.
    • Speech characteristics- harsh, monolound, monopitch, hypernasal w/o emission, imprecise artic. 
  24. flaccid (LMN) dysarthria
    • damage may be caused by infections, tumors, trauma, stroke, myasthenia gravis. Lesion in cranial/spinal nerve, ant horn of spinal cord, or cranila nerve axons in brainstem (hypotonia, flaccid paralysis, atrophy, fibrillations & fasciculations, hypo/areflexia.
    • General characteristics- hypotonicity, hyporeflexia, weak muscles/muscle atrophy, fasciculations (tiny spontaneous muscle contractions).
    • Speech characteristics- breathy, audible inhalation, hypernasal w/nasal emission, imprecise artic w/plosives & fricatives. 
  25. hypokinetic (basal ganglia) dysarthria
    • parkinson’s disease.
    • Symptoms- tremor, rigidity, bradykinesia, masked fascies.
    • Speech aracteristics- monopitch/loudness, decreased intensity, inconsistent rate (rushes of speech, inappropriate silence, repetition) 
  26. hyperkinetic (caudate & putamen) dysarthria
    • huntington’s disease.
    • Symptoms- rapid, jerky involuntary movements.
    • Speech characteristics- tremor, variable loudness, involuntary phonation, irregular artic, prosodic breaks, variable rate. 
  27. ataxic (cerebellum) dysarthria
    • associated with cerebelar involvement.
    • Lack of coordination.
    • Fluctuations in phonation, loudness, pitch, & resonance.
    • Imprecise artic including vowel distortions.
    • Poor coordination of breathing with speech. 
  28. mixed (multiple levels) dysarthria
    • both UMN & LMN damage.
    • Mixed signs of both spastic & flaccid. 
  29. spasmodic dysphonia
    • Adductor- sudden involuntary muscle movements cause vocal folds to slam together & stiffen, making it difficult for the vocal folds to vibrate & produce voice. Words are often cut off or difficult to start. Speech may be choopy & sound similar to stuttering. Described as strained so strangled & full of effort. Stress makes muscle spasms more severe.
    • Abductor- sudden involuntary muscle movements or spasms cause the vocal folds to open, so vocal folds cannot vibrate. Allows air to escape from lungs during speech. Voice sounds weak, quiet & breathy or whispery.
    • Similar to hyperkinetic dysarthira except that resonance & artic not affected. Prosody may be affected due to changes in phonation. 
  30. 5 aspects of speech quality
    • phonation- related to oscillation of vocal folds within the larynx. Caused by passage of air from lungs thru glottis. Related to voice quality, pitch & loudness.
    • Resonance- related to size & shape of oral-pharyngeal cavity, influenced by closed of velopharyngeal gap. Reflected in nasality of speech
    • Artic- determined by juxtaposition & movement of jaw, tongue, & lips
    • Prosody- rate, rhythm, intonation of speech. Suprasement aspects of speech
    • Respiration- inhalation & expiration of air. Powered by movement of muscles affecting shape of lung cavity. Limited by glottal opening.