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Flashcards in Motor System Deck (27)
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Posterior Limb of Internal Capsule

Corticospinal tract


Pyramidal decussation

-at level of foramen magnum
-where medulla becomes SC


Bell's Cruciate Paralysis

-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


Corticobulbar fibers

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


Direct corticobulbar fibers

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


Lesions of corticobulbar fibers

-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)


Indirect corticobulbar fibers

-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


Aberrant corticobulbar fibers

-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


Supra nuclear Facial Palsy

-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


Extrapyramidal System

-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


Principal Subcortical Loop

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


Dorsal division of ansa lenticularis

-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


Ventral division of ansa lenticularis

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


Nigro-thalamic fibers or Striatonigral

-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


Nigro-Striatal Fiber

-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


Pallidal and Subtantia Nigra Loops

-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


Lesions of extrapyramidal system

-unilateral lesions exhibit contralateral deficits
-bilateral lesions are common and are due to NT imbalances or neuronal dysfunction


Parkinson's Disease

-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


Postencephalic syndrome

-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


Arteriosclerotic Parkinsonism

-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


Sequelae of certain tranquilizer or antipsychotic drugs

-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


S/S of Parkinson's Disease

-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


Huntington's Chorea

-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


S/S of Huntington's Dz

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


S/S and degenerating structure of Parkinson's Dz

-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


S/S and generating structure of Huntington's Chorea

-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


Genu of internal capsule

corticobulbar fibers