Neuroscience Week 8, Lesions and study helps

Upper motor neurons (UMN) origin

Precentral gyrus

UMN decussate in the

medulla

Lower motor neurons (LMN) location

Ventral horn of the spinal cord

LMNs innervate

skeletal muscles of the face and head through cranial nerves, and skeletal muscles of the limb and trunk through spinal nerves

Dorsal column-medial lemniscal system (DCML) function

Discriminative touch, vibration, and position information

DCML originates from

mechano-receptors (sensory receptors sensitive to mechanical deformation) located in the body wall and projects to the contralateral cerebral

DCML how may neurons

3

Fasciculus gracilis vs. Fasciculus cuneatus level

Gracilis is below T6 (leg/lower trunk); cuneatus is above T6 (arm/upper trunk).

First-order neuron cell body in DCML

Dorsal root ganglion (DRG)

Second-order neuron cell body in DCML

Nucleus gracilis or nucleus cuneatus in the medulla

Third-order neuron cell body in DCML

Ventral posterior lateral nucleus (VPL) of the thalamus

Lateral spinothalamic tract (LSTT) function

Conveys pain and temperature sensation

LSTT originates from

nociceptors (free nerve endings and chemo-receptors) and projects to the opposite (contralateral) cerebral hemisphere via a three neuron projection system.

LSTT decussation point

At or about the level of entry in the spinal cord

LSTT first order neuron

-Cell body: dorsal root ganglion (DRG)

-Distal axon: innervates nociceptors via peripheral nerves

-Proximal axon: enter the spinal cord, diverge 1-3 levels and terminate on second-order neurons in the dorsal horn

LSTT 2nd order neuron

-Cell body: dorsal horn

-Axon: decussates at or about the level of entry and projects to the contralateral thalamus (ventral posterior lateral nucleus, VPL) via the lateral spinothalamic tract

Right dorsal column lesion at L1 symptom

Ipsilateral (right leg) loss of light touch, vibration, and position sense

dorsal column lesion

Common causes include

MS, penetrating injuries, and compression from tumors.

DCML Lesion

Ipsilateral loss of light touch, vibration, and position sense generalized below the lesion level

Lesion of the left fasciculus gracilis 

Sensory impairment: absence of light touch, vibration, and position sensation in the left leg and lower left trunk.

Lesion of the right fasciculus cuneatus at C3 produces what impairment?

Damage to the right fasciculus cuneatus at C3 causes the  absence of light touch, vibration, and position sensation in the right arm and upper trunk. 

Fasciculus Cuneatus Lesion

Ipsilateral loss of light touch, vibration, and position sense In the right arm and upper trunk

Right lateral corticospinal tract lesion at L1 symptom

Ipsilateral (right leg) UMN signs (weakness, hyperreflexia, hypertonia)

Lateral Corticospinal Tract Lesion below the medulla

Ipsilateral upper motor neurons signs generalized below the lesion level

causes of corticospinal tract lesions

penetrating injuries, lateral compression from tumors, and MS

Right lateral spinothalamic tract lesion at L1 symptom

Contralateral (left leg) loss of pain and temperature sensation

Lesion of the anterior gray and white commissures (central cord syndrome) at C5-C6  produces what impairment?

Bilateral loss of pain and temperature sensation in C5-C6 dermatomes

Central Cord Syndrome

occurs with hyperextension of the cervical area. Symptoms include weakness or paresthesia in the upper extremities but normal strength in lower.

central cord syndrome symptoms

-loss of motor function more severe in upper extremities than in lower

-varying degrees and patterns of sensory loss

-bladder function may be affected

-usually urinary retention

causes of central cord syndrome

- Anterior and/or posterior cord compression

- Acute hyperextension injury

- Damage from microvascular compromise of the center of the cord

- Spinal stenosis

posttraumatic contusion and syringomyelia, and intrinsic spinal cord tumors.

Complete transection of the right half the spinal cord (Hemicord or Brown-Sequard syndrome) at L1 produces what impairments?

-Damage to the right dorsal columns at L1 causes the absence of light touch, vibration, and position sense in the right leg.

-Damage to the lateral corticospinal tract causes upper motor neuron signs in the right leg (Monoplegia)

-and damage to the lateral spinothalamic tract causes the absence of pain and temperature sensation in the left leg.

Brown-Sequard Syndrome (Hemicord lesion) symptoms

Ipsilateral touch/vibration/UMN loss, contralateral pain/temperature loss below lesion

Complete transection of the spinal cord (Transverse cord lesion) at L1 would produce what impairments?

-Damage to the dorsal columns, bilaterally, causes the absence of light touch, vibration, and position sense in the both legs. 

-Damage to the lateral corticospinal tracts, bilaterally,  cause upper motor neuron signs in the both legs (Paraplegia), and damage to the lateral spinothalamic tracts, bilaterally, cause the absence of pain and temperature sensation in the both legs 

Transverse cord lesion at L1 symptoms

Bilateral paraplegia, bilateral loss of touch, and pain/temp sensation below L1

Complete transection of the dorsal columns, bilaterally, (posterior cord syndrome) in the cervical region would produce what impairments?

bsence of light touch, vibration, and position sense, bilaterally, from the neck down (below the lesion level).

Posterior Cord Syndrome

Loss of dorsal columns bilaterally, bilateral loss of proprioception, vibration, pressure, stereognosis, 2 point discrimination; preservation of motor function, pain and light touch; very rare!

Anterior Cord Syndrome symptoms

Bilateral UMN signs and pain/temp loss; light touch and proprioception spared

Positive Babinski sign

Outward fanning of toes, indicating an upper motor neuron lesion (UMNL)

Babinski is normal in

infants up to around 2 years

Cerebellar lesion signs (DANISH)

Disdiadochokinesia/Dysmetria, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia

intention tremor

involuntary trembling when an individual attempts a voluntary movement

Common in cerebellar lesions and alcoholism

resting tremor

a tremor that is apparent when the client is at rest and diminishes with activity

Common in Parkinson's disease

Basal ganglia input nuclei

Caudate and putamen (striatum)

Basal ganglia output nuclei

Globus pallidus and substantia nigra

CN1 test

Cover one nostril, close eyes and smell an object

CN 2 test

-Snellen chart

-Visual field test: Cover 1 eye, move object around until pt views object in the field of sight

CN 3, 4, and 6 testing method

H-test (tracking pen with eyes) and accommodation reflex

Pupillary light reflex

pupil constricts due to light stimulus; CNs 2 and 3

CN 5 test

Trigeminal

-Sharp vs dull for face sensation

-Masseter (clench jaw) and pterygoids (open mouth)

CN 7 (Facial) testing method

Facial muscle expressions (smile, raise eyebrows, pucker) and sweet/salty taste

CN 8 test

Finger rubbing next to ears

Uvula deviation in CN 9/10 lesion

Deviates away from the side of the lesion

Tongue deviation in CN 12 lesion

Deviates toward the side of the lesion

CN 11 test

Shoulder shrug test

SCM test

Primary headache types

migraine, tension, cluster, hormonal, sinus

Migraine headache characteristics

Unilateral, gradual onset, crescendo pattern, lasts 4-72 hours, with photo/phonophobia

The most common headache!

tension

tension headache characteristics

Most common type of headache

Vice-like, squeezing, tight

Generalized

Intense around bilateral around the forehead

NO focal neurological symptoms

Duration: several hours

Cluster headache characteristics

-Unilateral, orbital, excruciating pain, with Horner's syndrome symptoms (ptosis, miosis)

-Characteristic: pain begins quickly, deep, and continuous, excruciating and explosive

-Duration: 30min-3 hours

Sinus headache

a headache resulting from congestion or infection in the paranasal sinuses

Hormonal headache

Hormonal headaches are related to oestrogen. The produce a generic, non-specific, tension-like headache. They tend to be related to low oestrogen:

Two days before and first three days of the menstrual period

Around the menopause

Pregnancy. It is worse in the first few weeks and improves in the last 6 months. Headaches in the second half of pregnancy should prompt investigation for pre-eclampsia.

The oral contraceptive pill can improve hormonal headaches.

SNOOP mnemonic for secondary headaches

Systemic, Neurologic, Onset sudden, Older age (>40), Previous headache change

Examples of secondary headache

temporal arteritis, malignant hypertension, brain tumor, SAH, infectious, glaucoma, medicines, internal carotid dissection

tone consists of

-Active (neural) component

-Passive (viscoelastic) component

tone is necessary for

Postural control

Movement preparation

Efficient motor control

hypertonia types

Spasticity

Rigidity

Dystonia

Paratonia

postural tone

-Found mainly in axial muscles

-Maintains upright posture

-Influenced heavily by gravity

-Sustained contractions

phasic tone

-Rapid stretch responses

-Primarily assessed clinically

-Seen in extremities with DTRs

Spasticity vs. Rigidity

Spasticity is velocity-dependent; rigidity is velocity-independent resistance in agonist/antagonist

Type Ia vs. Type II sensory afferents

Ia detects velocity of stretch (reflexes); II detects static muscle length (posture)

GTO Function

Monitor tension

GTO produces the

Inverse stretch reflex

Dynamic Stretch Reflex

- Strong signal from primary sensory ending

- Caused by rapid stretch or rapid "slack"

-Nuclear bag fibers activated

-Ia afferents fire

-Alpha motor neuron stimulated

-Muscle contracts

Static Stretch Reflex

-Sustained stretch

-Nuclear chain fibers activated

-Type II afferents fire

-Alpha motor neuron activation

-Mild sustained contraction

Alpha-Gamma Coactivation purpose

Maintains muscle spindle sensitivity during extrafusal muscle contraction

Corticospinal Tract (CST) function

Voluntary movement, Tone inhibition

Dorsal Reticulospinal Tract (Medullary RST) function

Strong inhibition of tone, Inhibits gamma motor neurons

loss of the Dorsal Reticulospinal Tract (Medullary RST)

major cause of spasticity.

Tone fascilitory pathways

-Vestibulospinal Tract

-Medial Reticulospinal Tract (Pontine RST)

Vestibulospinal Tract function

Medial VST: positioning of head and neck, extensor tone

Lateral VST: balance

Medial Reticulospinal Tract (Pontine RST) function

Facilitates tone

Cerebellar Functions

-Coordination of movement

-Motor planning

-Cognitive functions, including rapid shifts of attention

cerebellar lesion results in

Loss of muscle tone, clumsy and uncertain movement:

Ataxia

Tremor

Hypotonia

Balance and gait dysfunction

Speech impairments

Cognitive and psychiatric impairment

Clasp-knife phenomenon

Initial high resistance to passive stretch followed by sudden release

DYSTONIA

Sustained or intermittent contractions causing abnormal postures and movements.

Dystonia mechanism

Loss of Inhibition

Abnormal Sensory Integration

Abnormal Plasticity

Network Disorder

Dystonia results in

Co-contraction

Overflow movement

Poor motor control

Paratonia

Increased resistance proportional to examiner's applied force, seen in dementia

Paratonia commonly seen in

Dementia and Frontal lobe dysfunction

Corticobulbar

-direct control of movements in head and neck

-UMN control of cranial nerve motor nuclei — relevant for facial asymmetry/localization.

Reticulospinal

posture/locomotion, stepping pattern generators, alpha-gamma co-activation. TONE

Vestibulospinal:

axial/head/trunk posture/balance; protective head/neck reactions. EXTENSORS

Rubrospinal

extrapyramidal, crosses in midbrain, modulates corticospinal. FLEXORS

DCML lesion in brain/cerebrum

contralateral loss.

DCML lesion below medulla

ipsilateral loss

Cuneocerebellar:

Head/neck unconscious proprioception C1-C8

Posterior spinocerebellar:

ipsilateral unconscious proprioception of LE C8-L2; does NOT cross.

Anterior spinocerebellar:

crosses twice, carries unconscious proprioception below L2/3.

Brown-Séquard (hemisection):

Ipsilateral motor deficits (UMN) and ipsilateral DCML loss; contralateral pain & temperature loss (a few levels below).

Anterior cord syndrome:

Loss of corticospinal and spinothalamic bilaterally; DCML spared.