Motor System

Question 1

Posterior Limb of Internal Capsule

Answer 1

Corticospinal tract

Question 2

Pyramidal decussation

Answer 2

• at level of foramen magnum

- where medulla becomes SC

Question 3

Bell’s Cruciate Paralysis

Answer 3

• characterized by midline involvement of the upper portion of pyramidal decussation resulting in paralysis of upper extremity W/O lower extremity involvement
  
  • upper extremity motor fibers in medulla decussation more superior and medial compared to the more inferior and lateral decussation of lower extremity motor fibers
  • upper extremity CST fibers are medial in LCST while lower extremity CST fibers assume a more lateral position
    
    • so this palsy may be caused by damage to Odontoid process b/c its proximity of medial decussating arm fibers

Question 4

Corticobulbar fibers

Answer 4

Descend from cortex thru the genu of internal capsule

• decussation in lower pons b/w level of trigeminal and Abducens N
• brainstem LMNs receive some degree of bilateral Innervation from direct or indirect corticobulbar fibers

Question 5

Direct corticobulbar fibers

Answer 5

• terminate upon LMNs of trigeminal, facial, And Hypoglossal motor nuclei
• exert a predominant influence on the fcn of nuclei

Question 6

Lesions of corticobulbar fibers

Answer 6

• lesions of CBF above decussation may result in some contralateral cranial N palsies
• lesions of CBF below decussation may result in some ipsilateral cranial N palsies
• in the first year post stroke, some of these deficits are ameliorated due to varying degree of bilateral Innervation of these nuclei and contributions from corticoreticulobulbar fibers (indirect CBF)

Question 7

Indirect corticobulbar fibers

Answer 7

• referred to corticoreticulobulbar fibers b/c of bilateral course and termination in reticular formation surrounding brainstem motor nuclei
• descending influences are relayed on to respective LMNs
• fibers do not affect the LMNs as strongly as the direct corticobulbar fibers, but they may play a role in recovery from infarction involving the direct corticobulbar fibers

Question 8

Aberrant corticobulbar fibers

Answer 8

• these originate in frontal and occipital eye fields and descend in the dorsal aspect of midbrain adjacent to central gray
• separation of these fibers from corticospinal and corticobulbar fibers makes it difficult to destroy all 3 in same lesion
• terminate in superior colliculus and PPRF as part of Oculomotor system
• drive volitional and nonvolitional eye movements

Question 9

Supra nuclear Facial Palsy

Answer 9

• caused by unilateral lesions of corticobulbar fibers above the level of facial nucleus
• result in paralysis of contralateral lower quadrant of face
• upper quadrant of face is unaffected by unilateral lesions of corticobulbar fibers due to the bilateral Innervation from the facial nucleus

Question 10

Extrapyramidal System

Answer 10

• involved in crude, stereotyped, associative movements of axial and proximal limb musculature such as swinging arms while walking
• initiates movement patterns thru its complex sub cortical loops
• plays a role in facilitation of motor centers and activation of reflex arcs
• primary influence is on the primary and pre motor cortices

Question 11

Principal Subcortical Loop

Answer 11

All areas of cortex–>striatum made up of caudate and putamen–>globus pallidus and substantia nigra–>ventral lateral and ventral anterior

Question 12

Dorsal division of ansa lenticularis

Answer 12

• called lenticular fasciculus
• pallido-thalamus fibers join with fibers from ventral division to form the thalamic fasciculus
• projections are shared in common with those fibers from dentato-thalamic and dentato-rubro-thalamic pathways

Question 13

Ventral division of ansa lenticularis

Answer 13

-most of fibers in the ansa lenticularis are pallido-thalamic fibers which join with the lenticular fasciculus to form the thalamic fasciculus

Question 14

Nigro-thalamic fibers or Striatonigral

Answer 14

• connections of substantia nigra
• non dopaminergic fibers that originate from pars reticularis substantia nigra
  
  • terminate in VA and VL thalamic nuclei
• fibers from globus pallidus and substantia nigra DO NOT terminate in same areas of VL and VA thalamic nuclei
  
  • important in stereotaxic surgery for Parkinson’s Dz

Question 15

Nigro-Striatal Fiber

Answer 15

• connection of substantia nigra
• dopaminergic fibers that originate in pars compacta of substantia nigra
  
  • terminate in caudate and putamen–striatum
• neurons in this area of the substantia nigra are destroyed in Parkinson’s Dz
• destruction of inhibitory, GABA nergic fibers in these fibers are in Huntington’s Dz

Question 16

Pallidal and Subtantia Nigra Loops

Answer 16

• cortical and Subcortical feedback loops play important roles in initiating motor movement patterns and integrating them with cerebellum, cerebral cortex, and limbic system
• fibers are inhibitory upon these specific motor thalamic nuclei

Question 17

Lesions of extrapyramidal system

Answer 17

• unilateral lesions exhibit contralateral deficits

- bilateral lesions are common and are due to NT imbalances or neuronal dysfunction

Question 18

Parkinson’s Disease

Answer 18

• Subcortical degeneration disorder involving substantia nigra, globus pallidus, upper brainstem nuclei, and postganglionic sympathetic neurons
• dz may be brought on by:
  
  1. Post encephalitic syndrome
  2. Arteriosclerotic Parkinsonism
  3. Sequelae of certain tranquilizer or antipsychotic drugs

Question 19

Postencephalic syndrome

Answer 19

• one of the causes of Parkinson’s
• involves substantia nigra and reticular formation
• affects younger ppl
• likely to produce mental changes
• often seen on one side
• pt may have oculogyric crisis of eyes and head in which they appear to be forced upward for minutes w/o loss of consciousness

Question 20

Arteriosclerotic Parkinsonism

Answer 20

• cause of Parkinson’s Dz
• pts usually present with history of TIA and abrupt onset of ischemic episodes
  
  • in older individuals, dementia may occur
• infarction may affect the substantia nigra, nigrostriatal pathways, basal ganglia
• prognosis is poor with a high risk of additional cerebral and myocardial infarction

Question 21

Sequelae of certain tranquilizer or antipsychotic drugs

Answer 21

• cause of Parkinson’s
• over titration of certain neuroleptic drugs may result in tardive dyskinesia
  
  • this is a repetitive involuntary licking and smacking movements of lips
  • always a result of drugs and may be present in other motor disorders
  • may be reversible
  • if medication is not adjusted, effects are irreversible

Question 22

S/S of Parkinson’s Disease

Answer 22

-dyskinesia, tremor, and rigidity are major symptoms

1. Bradykinesia–difficulty initiating movement
   
   • difficulty initiating motor movement patterns especially gait patterns
2. Tremor during rest–may be in jaw and upper extremity
   
   • slow tremor that is absent or reduced during movement
3. Rigidity–most disabling, inc resistance of extremities to passive movement in all directions
   
   • may be initially unilateral and progress to other side
   • limbs may exhibit cogwheel, knife clasp, or lead pipe rigidity
4. Absence of facial expression–masked face
   
   • may stare with infrequent blinking–reptilian gaze
   • positive glabellar reflex–tapping on pt’s forehead with finger results in no attenuation of pt’s repetitive blinking
5. Postural embarrassment
6. Cognitive changes–deterioration of memory, obsessions

Question 23

Huntington’s Chorea

Answer 23

• autosomal dominant motor disorder which has localized on chromosome 4
• common features include dementia, chorea, and behavioral disturbances
• deteriorates and dies 10-15 yrs after onset

Question 24

S/S of Huntington’s Dz

Answer 24

1. Choreiform movements–sudden, irregular, involuntary, jerky, purposeless movements
   
   • pt may develop severe dementia–choreiform movements are debilitating but the dementia is more limiting
   • principal areas of degeneration are corpus striatum and cerebral cortex–symptoms due to excessive dopaminergic influence in degenerated striatum or loss of inhibition from GABAnergic neurons

Question 25

S/S and degenerating structure of Parkinson’s Dz

Answer 25

• S/S: bradykinesia, tremor during rest, rigidity, masked face, glabellar reflex, postural embarrassment, autonomic effect, cognitive changes
• degeneration of: substantia nigra, globus pallidus, brainstem reticular formation and postganglionic sympathetic neurons

Question 26

S/S and generating structure of Huntington’s Chorea

Answer 26

• S/S: Onset age 30-40 yo
  
  • choreiform movements, severe dementia, choreoathetosis, behavioral disturbances
• autosomal dominant disorder–chromosome 4
• denigrating structure: corpus striatum, cerebral cortex results in excessive dopaminergic influence in degenerated striatum or loss of inhibition from GABAnergic neurons of STRIATONIGRAL pathway

Question 27

Genu of internal capsule

Answer 27

corticobulbar fibers