Unit 7: Tutoring Flashcards
Primary Motor Cortex
Efferent
-Cause contralateral motor deficits & facial anomalies
Motor Association Cortex
- Made up of premotor cortex and supplementary motor area
- Cause deficit in motor: Apraxia
Sensory Cortex
Afferent (parietal lobe)
-Sensory deficit on contralateral side of body and face pain/temp loss, neglect
Somatosensory Association Cortex
Lesions here would cause high-order sensory analysis
Homunculus
- Legs medial in brain (affected by ACA)
- Hand, face, & tongue lateral (affected by MCA)
Anatomy of SC
- Cervical &. Lumbrosacral Enlargements
- Gray matter on inside (butterfly shape)
- Ex, of GTO (Sensory receptor for stretch)
- Somatotopic SC organization
Cervical and Lumbosacral Englargemtents (Anatomy of SC)
- Much more motor neurons in anterior horn
- Most white. matter in cervical segments> makes it the biggest of all
Example of GTO (anatomy of SC)
- Sensory receptor for stretch
- GTO sends info to dorsal root ganglion, sends signal through dorsal rootlets, enter SC through dorsal horn, and synapses w/ ascending tract or direct w/ alpha motor neuron (which control muscles), AMN then sends signal back to muscle to contract (bc GTO senses stretch)
- Alpha motor neuron sends signal out through Rexed laminae IX (motor nuclei for innervation of skeletal muscle)
Somatotopic SC Organization (anatomy of SC)
-Descending motor pathways are divided into lateral and medial system based on location in the SC
-Lateral Motor System: for distal limb movements and
favoring flexors
-Medial Motor System: for proximal limb/ trunk
movements, favoring extensors
-Flexors tend to be more superior/ dorsal, and extensors tend to be more inferior/ ventral
ACA and PCA’s (SC Blood Supply)
ASA (SC Blood Supply) -Causes motor problems if cut off -Ventral ⅔ of SC -Branches off of Vertebral Artery PSA's (SC Blood Supply) -Syphilis> Sensory loss> Posterior cord syndrome -Dorsal 1/3 of SC -Braches off the vertebral or PICA Both. combine to form artery plexus around spinal cor
Radicular Arteries
Great Radicular Artery of Adamkiewics
-Lumbar and Sacral region (T9-12)
Vulnerable Zone
-Mid-thoracic area (T4-8) there are no radicular arteries> sole supply from either ASA or PSA
-Area is susceptibe to infarct (especially of ASA) during surgery
-Blood cut off> ASA cut off> motor loss
Lateral Motor System
- Lateral Corticospinal Tract
- Rubrospinal tract
- Flexor and distal masculature to a skilled movement
Medial Motor System (AVTR)
- Anterior Corticospinal Tract
- Vestibulospinal Tract (2)
- Reticulospinal Tract (2)
- Tectospinal Tract: Posture, balance
Lateral Corticospinal Tract
Most important descending motor pathway in SNA
LCST & ACST have neurons referred to as…
Corticospinal fibers as they originate in the brain
- Synapse at the Ventral Horn (SC)
- Have Corticobulbar fibers that directly control the CN in the brainstem (bulb) to move face, jaws, tongue, and eyelid
- These fibers can influence the brainstem tracts, but NOT directly control them
Rubro, tecto, vestibulo, and reticulospinal tracts all originate in the…
Brain stem
- Descend to the ventral horn of the spinal cord.
- The brain itself does send corticobulbar fibers onto these tracts but does not fully control them nor considered the origination of these tracts.
ANS Review
ANS neurons have additional synapses before terminating on target
-Motor nerves have direct pathway to skeletal muscle
Sympathetic (ANS Review)
- Short PREganglionic fibers that originate at Rexed Lamina VII
- Terminate onto either: Paravertebral Ganglia or Prevertebral Ganglia
- Paravertebral Ganglia (outside vertebrae) running from C4-S4 (AKA: Sympathetic Trunk) ~or~
- Prevertebral Ganglia of celiac ganglia (liver, stomach, pancreas) or at inferior mesenteric ganglia
Parasympathetic (ANS Review)
Long preganglionic fibers that terminate close or near the target end organ
-No thoracic involvement
Preganglionic Neurons (Pharmacology)
-In BOTH SYMPATHETIC & PARASYMPATHETIC → release acetylcholine to activate Nicotinic cholinergic receptors
POSTganglionic Neurons -
-SYMPATHETIC → release epinephrine/ norepinephrine onto target end organ w/ adrenergic/Noradrenergic receptors
-PARASYMPATHETIC → release mostly acetylcholine on to Muscarinic receptors of end organs
-End organ control is done through these rules w/ the exception of sweat glands,
actually receiving sympathetic postganglionic releasing UMN vs. L
Fasciculations
Rapid twitching motion
- Indicative of a muscle dying when the alpha motot neurons (ex. LMN) to the muscle that is lesioned
- Appears as a twitching of the muscle at rest and/or with movements, can occur w/ injury or overuse of a muscle as well
- Spasticity
- Weakness patterns and localization
Spacicity (Fasciculations)
Velocity dependent & assesses resistance (rididity) to PROM. Often the modified ashworth scale is used
Weakness Patterns & Localization
- Can result from lesion to anywhere
- Lesion to BA 4 = severe deficits
- While association cortices like 3, 1, 2, 5, & 7 and Limbic Structures can lead to apraxia and other forms of ‘weakness’ with movements.
- Association cortices lead to Apraxia & weakness with movements
- Although weakness occurs at LMN & UMN, it can also occur anywhere else such as Thalamus, Cerebellum, Basal Ganglia —> anywhere. Not just the motor neurons
Unilateral Face (droop), arm, and leg weakness or paralysis (hemiparesis) with sensory deficits
- Rule out: likely not medulla/SC or muscles since the face is involved
- (CN VII facial N. above pons so it’s probably not lesion in medulla/SC)
- We are left with everything above the medulla
- Entire B4, internal capsule (IC), cerebral peduncle or basis pontis (corticospinals of LCST, and corticobulbars to face)
- Lesion will be contralateral to the deficits as any of these structures are above pyramidal decussation
- Common causes: CVA, hemorrhage, tumor, trauma, or brain herniation results in an infarct (dead brain tissue) in addition it can appear briefly in a postictal state (post seizure state) but generally resolves.
Multiple Sclerosis
-Autoimmune of CNS Myelin
-No known cause
-Onset 20-40 y/o
Diagnosis:
-Symptoms: Spasticity, pain, impaired
B&B, sexual dysfunction, dysphagia, and
psychiatric findings
-MRI→ can see plaques where myelin has
been destroyed
-Lumbar puncture of CSF
-Evoked potentials (slow conduction
velocity)
Characteristics: MS affects people in one of
these ways, and may progress from RRMS-SPMS:
-Relapsing remitting MS: Multiple symptoms, Remitting phase to complete recovery
-Secondary progressive MS: Progressive symptoms, Never remit to normal over time
-Primary progressive MS: Onset digress- no remitting
-Relapse: exacerbation, attack, flare-up
