Upper and Lower Motor Syndromes

What is the root cause of upper motor neuron syndromes?

1) Damage either to the motor cortex or the lateral reticulospinal tract results in a disinhibition of extensor muscle tone by inhibitng the deep tendon reflex 2) Damage to the motor cortex also results in a loss of voluntary motor control due to a disruption of the corticospinal tract connection with the LMNs

What signs are present in a cortical upper motor neuron lesion, but not in a medulla levels lesion knocking out just the reticular inhibitory fibers?

1) No muscle atrophy 2) No babinski sign (as this is not related to hyperreflexia) 3) No voluntary paralysis

What would be the consequences of a lesion at the level of the medulla, knocking out the reticular inhibitory neurons?

1) Spasticity 2) Hyperreflexia of deep tendon reflexes 3) Clonus

When would a babinski sign be present?

1) Upper motor neuron lesion 2) Lesion to the corticospinal tract

What are the consequences of a lesion at the level of the primary motor cortex?

1) Voluntary paralysis 2) Decorticate posture 3) Hyperreflexia of the deep tendon reflexes 4) Clonus 5) Babinski sign 6) Neurogenic bladder

Function of reticulospinal projections from the medulla

A group of upper motor neurons inhibit extensor muscle tone and the deep tendon reflexes

What is the clinical "glove and stocking" (A) peripheral neuropathy typically indicative of?

A metabolic or infectious process - neurons innervating the distal appendages tend to have the longest more fragile axons that are susceptible to injury

Spasticity

A velocity dependent increased resistance to passive stretch - As you try to passively move a patients arm, you will feel resistance opposing you equal to the amount of velocity you move the arm

What is the cause of fibrillations?

ACh receptors begin to spread out along the endplate - ACh from neighboring axons stimulate receptors that aren't in the right place. These are subthreshold potentials. ***Only detectable on EMG

Babinski sign

Activation of the toe extensors indicating an upper motor neuron lesion - NOT related to hyperreflexia

Why is their no muscle atrophy in an upper motor neuron lesion?

Although you have removed voluntary movement, the lower motor neuron can still stimulate the effector muscle via reflex pathways etc...therefore the muscle can retain tone

If their is a lesion at T2, where would you see the lower motor neuron syndrome and why?

At T2 the motor neurons going out to the muscle have been damaged, so those motor neurons are no longer activating their muscles

How is tone of the muscles influenced if injury is to motor neurons inferior to the red nucleus?

Both the upper and lower extremity extensors will be activated

Flaccid paralysis or paresis

Due to destruction of the lower motor neuron, the muscles do not respond to voluntary or reflex activation. There is decreased muscle tone and the muscles are flaccid.

What fiber type if responsible for clonus?

Fiber type 1a

When is the only time that an upper motor neuron will run directly to the motor neuron, bypassing all interneurons?

If the motor neuron is innervating fingers and toes

Why is their a loss of RIFMs in central cord syndrome but no Babinski sign?

In the lateral corticospinal tract at the high cervical level, is a topography of neuron projections - mot medially the neurons will go to the brachial regions and laterally, those neurons will innervate the lumbar region

Where are the reticulospinal tract cells located?

In the medulla

Neurogenic bladder

Incontinence and incomplete voiding due to hyperreflexia of the bladder

Decorticate posture

Increased tone in anti-gravity muscles results in flexion at the arm and extension at the lower extremity

***FLIP*** Above - the demyelination is occurring in the descending corticospinal tracts

Is the lesion above or below this spinal cord level?

What is the cause of muscle atrophy?

Loss of the trophic influence (due to damage of peripheral nerve), which has a much greater effect than the disuse alone

What will damage to the peripheral nerve cause?

Lower Motor Neuron Syndrome: 1) Flaccid paralysis - muscle loses tone 2) Paresis - 3) Atrophy 4) Areflexia or hyporeflexia of deep tendon reflexes 5) Fasciculations

If neurons of an individual have been damaged due to a pathologic process, and a lesion superior to the corresponding level of the spinal cord occurs, will the patient experience upper motor neuron syndrome?

No - the lower motor neurons will have already been damaged, and therefore not be intact; a necessary criteria for upper motor neuron syndrome

What is the cause of Areflexia/Hyporeflexia of deep tendon reflexes in LMN syndrome?

Reflex activity depends on the integrity of both the afferent and efferent limbs of the reflex arc. In the LMN syndrome, damage to the efferent limb of the reflex arc decreases activity of the reflex

How is tone of the muscles influenced if injury is to motor neurons superior to the red nucleus?

The arm will be flex and the lower extremity extended

What spinal tract is responsible for RIFMs?

The corticospinal tract

Hyperreflexia of Deep Tendon Reflexes

The muscle stretch reflexes become more sensitive due to a loss of tonic descending inhibitory influences. The degree of hyperreflexia is usually expressed on a graded scale of + to ++++. Hyperreflexia = > ++

What defines a lower motor neuron?

The neuron that projects to the effector muscle

Voluntary paralysis

The patient cannot voluntarily move the muscle, but it can be contracted by other means because of the hyperreflexia - the reflex arc is intact and functioning

Why is the arm flexed in a cortical upper motor neuron lesion?

The red nucleus drives flexion in the arm without the extensors being activated (I don't really get this)

If a patient comes in with aflexia/hypoflexia, but has a normal strength test, what would that indicate?

There has been a lesion to the dorsal root of the nerve, or the CNS, but the motor neurons have not been injured

Fasciculations

These are muscle twitches that are grossly observable beneath the skin. The appearance of these muscle contractions has been likened to "worms crawling under the skin"

Fibrillations

These are spontaneous contractions of individual muscle fibers due to denervation hypersensitivity

What is the cause of fasciculations?

This activity is due to the agonal discharges of lower motor neurons as they are dying. The dying neurons fire in a random, uncoordinated fashion

Muscle Atrophy

This phenomenon is due to the loss of trophic influence that neurons normally exert on skeletal muscle. The atrophy is much more pronounced than that caused by inactivity. Disuse atrophy accounts for a loss of not more than 20-30% of the muscle mass.

When does central cord syndrome occur?

When the patient has a lesion at the high mid-cervical level - typically injuries such as whip lash, resulting in a contusion at the central cord, resulting in swelling that damages the medial side of the lateral corticospinal tract

***FLIP*** Lesions A and B: If you cut the sensory neuron you will get aflexia or hyporeflexia, but *not LMN Syndrome*

Which lesion(s) results in LMN Syndrome?

Clonus

With hyperexcitability, passive initiation of the stretch reflex may produce self-perpetuating reflex activity. Clonus is manifest as the rhythmic oscillation of reflexive muscle contraction and relaxation

What results from a isolated lesion to the corticospinal tract?

You get only the components related to loss of the corticospinal tract: 1) Loss of rapid independent finger movements (fine motor skills) 2) Babinski sign - dependent on the corticospinal tract