Neuroscience Week 3: Spastic Paralysis, Spinal Motor Organization and Brain Stem Supraspinal Paths Flashcards
Upper Motor Neurons
brain and brain stem supraspinal pathways (use gluatamate to excite LMNs, entire cell body axons and cell bodies reside in the CNS, myelinated by oligodendrocytes
UMNs Activity affects muscle contraction indirectly via connections with LMNs Does NOT include sensory neurons (e.g. DRG neurons) Use glutamate as a neurotransmitter Axons never leave the CNS Lesion: typically contralateral to functional deficit(s)
Lower Motor Neurons
brainstem as cranial nerves and spinal cord ventral neurons, myelinated by Schwann cells
LMNs Innervate skeletal (and visceral) muscle directly via axons that leave the CNS; final common path from CNS to muscle Use ACh as neurotransmitter Lesion: typically ipsi lateral to functional deficit(s)
LMN lesions typically cause ipsilateral/contralateral functional deficits
Typically cause ipsilateral functional deficits
UMN lesions typically cause ipsilateral/contralateral functional deficits
Typically cause contralateral
EXCEPT in the spinal cord they will cause ipsilateral functional deficits
Primary Motor Cortex neuron type
First order UMNs in the precentral gyrus
First-order UMN innervate what?
Can directly innervate some LMNs but typically innervate interneurons to indirectly affect LMN activity
Homunculus
the number of neurons that regulate particular body regions is proportional to its size. More UMNs are needed to control the fingers and lips Fewer are required to control the trunk
Stimulation of a homunculus with an electrode in an area will cause
individual muscle contraction
Activity controls speed, force and direction
Corticospinal Tract
- Grey matter of precentral gyrus gives rise to axonal fibers which descend through the posterior limb of the internal capsule and run through some of the basal ganglia and the thalamus
- then will partially create and travel through the cerebral peduncles
- axons dive internally into the pons then become external at the pontomedullary junction creating the pyramids
- decussate at the cervico-medullary junction (caudal medulla) and become an internal fiber pathway in the spinal cord
CST path through the brainstem
- Grey matter of precentral gyrus gives rise to axonal fibers which descend through the posterior limb of the internal capsule and run through some of the basal ganglia and the thalamus
- then will partially create and travel through the cerebral peduncles
- axons dive internally into the pons then become external at the pontomedullary junction creating the pyramids
- decussate at the cervico-medullary junction (caudal medulla) and become an internal fiber pathway in the spinal cord
Pre and post olivary sulcus
by the pyramids
Lateral corticospinal tract
Corticospinal Homunculus
in cervical cord lost face because they will have already synapsed
the fibers that are closest medially are the ones that will synapse in the ventral horns at every level so arm fibers will be most medial in the cervical spine
Identify CST Homunculus
Identify CST Homunculus
Identify CST Homunculus
Premotor cortex
Premotor Cortex (PMC)
- Some fibers project directly to spinal cord, striatum, thalamus (part of CST)
- Primarily innervate MNs that control
- paraxial (trunk) muscles during reaching
- Integrates sensory information from
- objects close to the body
- also mirror neurons to mimic other people’s behavior such as smiling at a child and the child smiles back
Supplementary motor (SMA)
- Extensive connections with pre frontal cortex, cerebellum
- Involved in the planning & execution of complex movements
- Stimulation causes coordinated movements
- mouse wanted to go left
Primary sensory cortex
- modulates movement via changes to sensory
- pathways in the dorsal
- horns (feedback mechanism); intimately connected with M1
Posterior Parietal cortex (PPC)
modulates CST activity during the planning and execution of movements (hands/eyes) apraxia (inability to perform actions when asked
Damage to this area causes apraxia
Posterior parietal cortex
Identify
of fibers in peduncles and the pyramids
Corticobulbar tract CBT
the homunculus on this figure is not correct!!!
LMNs that are inervated by corticbulbar fibers are innervated bilaterally (EXCEPTION the face)
LMNs that are inervated by corticbulbar fibers are innervated
Bilaterally except for CN VII on the lower face
CN VII lesion UMN vs LMN lesions
Alternating Hemiplegia
- ophthalmoplegia ipsilateral to the lesion
- with contralateral hemiplegia
- Can have deficits that are contralateral in the body and ipsilateral ophthalmoplegia because corticospinal and corticobulbar
- if contralateral hemiplegia with no ocular symptoms you might think the lesion is solely in the brain or in the cord but not the brainstem
Alternating Hemiplegia AKA
Weber Syndrome
UMN Syndrome Symptoms
Tests for UMN disease
- Hyperreflexia
- clonus
- Babinski +
Babinski test
Spasticity vs. Rigidity
and clasp-knife spasticity
- Spasticity is characteristic of a UNM lesion
- Rigidity is not characteristic of UMN lesion
- in UMN lesions the clasp-knife spasticity will give way to transient flaccid paralysis
Rigidity is characteristic of?
basal ganglia pathology (parkinsons, huntingtons)
UMN and LMN
Cases 1 and 2
Cases 3 and 4
Cases 5 and 6
Vitamin B12 Deficiency First AID
FIRST AID:
Subacute combined degeneration (
SCD
)
demyelination of
S
spinocerebellar tracts, lateral
C
corticospinal tracts, and
D
dorsal Columns.
Vitamin B12 Deficiency Etiology
Severe chronic B 12 deficiency (B12 is required for red blood cell
production)
Vitamin B12 Deficiency Pathogenesis
Cause: absorption deficiency due to lack of Gastric Intrinsic Factor (GIF) caused by autoimmunity, genetic or surgical (resection of stomach/small intestine); others include vegan diet, celiac disease, tapeworm infection.
Vitamin B12 Deficiency Early Symptoms
Early Symptoms (slowly progressing): weakness and fatigue, breathlessness and dizziness, pale or jaundiced skin, sensations of pins and needles, vision changes, numbness (hands and feet), memory/mood disturbances, fevers
Vitamin B12 Deficiency Late Symptoms
Late Symptoms: absent ankle reflex, patellar hyperreflexia, Babinski sign, changes to mobility/balance, distal anesthesia}Treatment: supplementation if caught early (pills, nasal spray, injections)
Vitamin B12 Deficiency Treatment
Treatment: supplementation if caught early (pills, nasal spray, injections
Anterior Spinal Artery Syndrome FIRST AID
FIRST AID: Spares dorsal columns. Mid-thoracic ASA territory is watershed area, as artery of Adamkiewicz supplies ASA below T8.
Anterior Spinal Artery Syndrome Common causes
Can be caused by aortic aneurysm repair.
Anterior Spinal Artery Syndrome Clinical Presentation
Presents with ipsilateral UMN deficit below level of lesion (CST), LMN deficit at the level of the lesions (anterior horn), and contralateral loss of pain and temperature sensation below the lesion (spinothalamic tract)
Brown-Séquard Syndrome FIRST AID
Ipsilateral UMN signs below the level of the lesion (CST damage)
Brown-Séquard Syndrome Clinical Presentation
Ipsilateral LMN signs at the level of the lesion
sensory stuff on other lectures i guess
Brown-Séquard Syndrome Supplementary Complications and Considerations
If lesion occurs above T1 patient may present with ipsilateral Horner’s syndrome
Supraspinal Tracts
UMNs in the brainstem involved in unconscious movements and posture
Vitamin B12 Deficiency Overview
Anterior Spinal Artery Syndrome Overview
Brown-Séquard Syndrome Overview
majority of spinal cord is supplied by the anterior Spinal Artery
the ver
Anterior Spinal Artery Syndrome
LMN at the level of the lesion but UMN ipsilateral to the lesion anywhere below the lesion because degeneration of the fiber pathways in the corticospinal pathway below T8
contralateral loss of temperature and pain sensation
Reticular formation
series of interconnected nuclei and pathways not anatomically well-defined
Ascending Reticular Activating System communication with this system and the cortex is believed to cause consciousness
What systems cause consciousness?
Ascending Reticular Activating System (ARAS) communication with this system and the cortex is believed to cause consciousness
Decorticate posturing
lesion closer to cortex
Decerebrate Posturing
Lower brainstem lesion
Vestibular System function
- Detection of head orientation, acceleration
- Maintain balance
Vestibular System dysfunction
- False sense of motion; vertigo
- causes: idiopathic, trauma, infection or intentional
Vestibular System Overview
How does the Vestibular System interact with the limbs
Vestibular System Test
Romberg Test
remove shoes
stand feet together arms folded 30 seconds eyes open and then eyes closed
the test is positive if the patient cannot maintain balance with eyes closed or if they open eyes or take a step
Rubrospinal Tract Origin
Red Nucleus (Thalamus) w/cerebellar input
Rubrospinal Tract Descends
lateral column
Rubrospinal Tract Terminates
LMNs in the cervical cord
Rubrospinal Tract Function
- Primarily facilitates flexors of upper limbs (elbow/forearm)
- Cortical input largely inhibitory (loss causes (flexion);
- In Decorticate posturing only not in Decerebrate
- the cortex inhibits this but when the person is unconscious the cortex is no longer being inhibited and it is allowed to be activated
Pontine/Medial Reticulospinal Tract Origin/Pathway
Medial longitudinal fasciculus
Ventral funiculus
Pontine/Medial Reticulospinal Tract Function
Function
Facilitate extensors (anti-gravity), inhibited by cortical centers Influences posture and locomotion
Medullary/lateral(LRST)◦Origin/Pathway
Throughout spinal column (lateral funiculus)
Medullary/Lateral Reticulo Spinal Tract (LRST) Function
Function
Facilitates upper limb flexors; facilitated by cortical centers
Strong enough to Inhibit reflexes
Influences posture and locomotion, + autonomic functions (respiration, shivering, GI function)
Medullary/Lateral Reticulo Spinal Tract (LRST) Origin/Pathway
Throughout the spinal column (lateral funiculus)
Summary of Supraspinal pathways
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Decorticate vs Decerebrate posturing
If a patient is Decorticate than showing Decerebrate
means the lesion is probably descending towards the respiratory centers of the medulla
Can go from Decerebrate to Decorticate
could be getting better
Recovery from capsular stroke
lesion destroying the posterior limb
down in the spinal cord the lateral corticospinal tract strong innervation of digit function while proximal muscles are innervated more by multiple pathways while digit muscles are innervated solely by CST
Relatively more contribution of supraspinal pathways of proximal muscles
Acute Phase of capsular stroke
Complete contralateral motor hemiparesis (contralateral) including face, arm and leg
sometimes tongue and soft palate are affected due to predominant contralateral innervation by CBT
Volitional movements are absent
May include UMN signs (Babinski, hypertonia, hyperreflexia)
Tongue and soft palate are innervated how
predominantly contralateral innvervation
The Reticulospinal tract is comprised of
the medial (pontine) tract and the lateral (medullary) tract.
Chronic Recovery from capsular stroke
Contralateral Spastic Hemiplegia
Contralateral Spastic Hemiplegia
- Postural control recovers, some proximal control recovers
- Antigravity muscles (ventromedial supraspinal pathways)
- Tongue and soft palate deficits disappear; ipsilateral CBT inputs compensate for the loss of contralateral inputs
- Can walk because proximal muscles and can have flexed arms and curled fingers but extended arms and legs much like Decorticate posture
- Almost never regain fine control of distal muscles (digits) because these are controlled solely by the CST
- Face won’t be able to smile contralateral to lesion but can raise eyebrows
UMN signs remain or become exaggerated (hypertonia, hyperreflexia)
Supraspinal innervation is?
Bilateral
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