Frank On Motor Lesions

Front 1

Name and describe the differences between the two areas of the nervous system (as categorised by clinicians)?

Back 1

Upper motor neurons (UMN) - injury = strengthening of muscle stretch reflex

Lower motor neurons (LMN) - injury = weakening of muscle stretch reflex

Front 2

Why does injury of the UMN area of the nervous system cause the response that it does?

Back 2

It causes an increase in the muscle stretch reflex as the stronger muscle will be in control. The UMN acts as a break to the LMN and so damage there will cause control to be lost.

Front 3

What make up the LMNs?

Back 3

Peripheral nerves, spinal roots and alpha motor neurons.

Front 4

What do alpha motor neurons do?

Back 4

Directly responsible for generation of force by muscle

Front 5

What makes up a motor unit?

Back 5

alpha motor neurons + muscle fibres

Front 6

What do alpha motor units do?

Back 6

They innervate extrafusal fibres (surface fibres).

Front 7

What do gamma motor neurons do?

Back 7

They innervate the intrafusal fibres.

Front 8

What are 2 generalised signs of LMN lesions?

Back 8

Flaccid weakness or paralysis. Decreased MSR's (hyporeflexia)

Front 9

What are the signs/stages of muscle denervation due to LMN lesions?

Back 9

Fasciculations, fibrillations, atrophy

Front 10

What causes fasciculations that are originally brought on by LMN lesions?

Back 10

Injury. Depolarisation at the site of injury, releasing injury potentials. Action potentials fire along the distal part of the axon to the muscle units and cause visible contractions.

Front 11

What causes fibrillations that are originally brought on by LMN lesions?

Back 11

After fasciculations the axon degenerates more. The individual muscle units respond, no longer blocks of them. Small contractions occur though not visible - need to be detected using an electromyogram (EMG)

Front 12

What causes atrophy that are originally brought on by LMN lesions?

Back 12

After fibrillations the axon is now completely degenerated. No more potentials. Lack of trophic support as you need tone to keep muscles healthy. Muscles involved individually, not in groups. Often also sensory loss of pattern.

Front 13

Why is there often a sensory loss pattern that is associated with atrophy brought on by LMN lesions?

Back 13

The atrophy follows dermatomes or fragments of dermatomes (area of skin supplied by an axon from a single dorsal root)

Front 14

Name 6 potential causes of LMN lesions?

Back 14

Infections. Diabetic neuropathy. Toxins. Inherited. Indirect. Muscular dystrophies.

Front 15

Describe an example of how an infection might cause a lesion to the LMN?

Back 15

e.g. poliomyelitis: enterovirus kills some whilst sparing other motor neurons in the spinal cord and brainstem (originally a CNS infection) = paralysis or absent reflexes.

Front 16

Describe how diabetic neuropathy might cause a lesion to the LMN?

Back 16

High glucose in blood stream leads to damage due to metabolic disturbance such that the patient gets accumulation of sugars in axons and Schwann cells leading to death or can be occlusion of nutrient vessels to the nerves

Front 17

Describe an example of how toxins might cause a lesion to the LMN?

Back 17

led = axonal degeneration and demyelination. Causes can be from alcohol, vitamin B12deficiency, botulin

Front 18

Describe an example of how the cause of lesions to the LMN might be inherited?

Back 18

Charcot-Marie-Tooth– numerous genes are involved/effected resulting in a loss of myelin and thus a loss of neuronal function. Sometimes called the inverted champagne bottle disease – thighs are still strong and healthy but there is calf muscle wastage and so the leg tapers down until it’s very skinny.

Front 19

How can a cause of lesions to the LMN be indirect?

Back 19

i.e.affects muscles directly. Myathenia gravis, autoimmune disorder: is a result of a decrease in the number of functional acetylcholine receptors in neuromusclular junctions. Causes fatigue and progressive muscular weakness, affecting the most active muscles first, e.g. Ptosis

Front 20

What is Ptosis?

Back 20

drooping/falling of upper eye lid due to lesions of the LMN

Front 21

What is diplopia?

Back 21

double vision, caused by both eyes not being able to look in the same direction at the same time due to lesions of the LMN.

Front 22

Describe muscular dystrophy and give an example

Back 22

- Usually inherited, degeneration of skeletal muscle which gets replaced by connective tissue. Caused by genetic faults. Duchenne’s, X-lined recessive, usually males. Seen in children (3y). As leg muscles atrophy = shorted = immobility of joints = scoliosis. Death by inability to breathe.

Front 23

Name some signs of UMN lesions

Back 23

Weakness. Clumsiness and imprecise motor control. Increased MSR's (hyperactive reflexes). Reflexes = jerky/spastic movements.

If damage = extensive = multiple firings (oscillations, clonus). Apparent reversal of some reflexes

Front 24

Describe how apparent reversal of some reflexes can be a sign of UMN lesions?

Back 24

(e.g. Babinski and Bing reflexes) No signs of muscle denervation. Alpha motor neurons of the brain and spinal cord unaffected inUMN lesions, therefore muscles remain innervated.Muscles affected in groups, an entire half of the body. Sensory loss pattern similar to motor i.e. quadrants or halves of the body

Front 25

What determines how much damage a UMN lesion will cause?

Back 25

the site of the leasion

Front 26

What symptoms does damage to the basal ganglia (UMN) cause?

Back 26

affect of initiation and cessation of movement (Parkinson's)

Front 27

Cerebellum lesions (UMN) cause what symptoms?

Back 27

affects gait, balance, stability (ataxia)

Front 28

What are the different types of symptoms that can be seen after a complete transection of the spinal cord?

Back 28

1) loss of voluntary movement but not reflexes

2) total anesthesia (sensory gone too)

3) temporary period of areflexia followed by permanent hyperreflexia.

Front 29

Describe in more detail what occurs after the temporary period of areflexia that occurs after complete transection of the spinal cord?

Back 29

after 1-6 weeks it's followed by permanent hyperreflexia - spontaneous reflexes come back. Some patients can seem paralysed and over time get better. This is due to an influx of astrocytes around the damaged region (immune response) - the time is required for this to all settle down.

Front 30

How does the position of complete spinal transection affect the type of damage occurring?

Back 30

Cervical transection = quadriplegia. Below cervical transection = paraplegia

Front 31

Where do deficits occur after brainstem lesions and why?

Back 31

Deficits occur contralateral to the lesion (sensory and cortical spinal tracts cross below the level of the middle medulla). Nuclei for the cranial nerves situated here so lesions here also can affect LMN because motor neurons are here as well. Therefore, can also get an ipsilateral effect

Front 32

How can you tell if an unconscious patient has vestibular lesions?

Back 32

Pour water that is warmer than blood into the patient's ear = nystagmus (eyes flick side-to-side)

Front 33

FACIAL MOTOR NUCLEUS OR SOMETHING

Back 33

DON'T FORGET TO LOOK IT UP

Front 34

Describe amyotrophic lateral sclerosis (motor neurone disease)

Back 34

Affects both LMN and UMN, destroying the motor neurons but also the cortex neurons which innervate them. Starts with hyperreflexia, weakness and atrophy, next 3-5 years all voluntary movement is lost, walk, speak, swallow, breathing. Unknown cause.

Front 35

Describe multiple sclerosis

Back 35

Autoimmune inflammatory disease which affects CNS neurons, loss of myelin (produced by oligodendrocytes) -> loss of conduction. Formation of plaques (regions of no myelin), variable in size and time. Clinical diagnosis implies different forms: relapsing and remitting, primary progressive. Manifests depending on the region of the brain affected. Causes unknown but genetics and environment probably.

Front 36

What is the most common form of UMN lesion and why do they occur?

Back 36

Strokes. Interruption of blood flow to a part of the brain resulting in ischaemia and infarction. Thrombosis, embolism, haemorrhage.

Front 37

How are strokes (or cerebrovascular accidents) diagnosed?

Back 37

1. time course (few secs to a few hours) i.e. nothing else is as rapid (e.g. tumours, tend to be much slower)


2. distribution of symptoms, because vascular in origin only those regions of the brain close to blood supply are affected.

Front 38

How is thrombosis developed?

Back 38

development of a blood clot, formed from an atherosclerotic plaque (necrotic cells, lipids and cholesterol -> degeneration of vessel wall -> attracts platelets and fibrin thrombus grows, decrease in blood pressure = blood flow stops

Front 39

What are the symptoms of a stroke via thrombosis?

Back 39

- tends to occur during sleep. Patient awakes paralysed, but initially may be unaware until tries to walk

- can appear in a stepwise manner with first neurological signs and then no worse and then further deterioration

Front 40

What causes an embolism? When do they occur?

Back 40

Formed by a foreign substance e.g., could be a thrombus formed in a different part of the body e.g. a mass of bacteria. Heart, especially valves, diseased or artificial, area good source for embolisms. “rough edges” attract platelets. 


Tends to occur in periods of activity and can be very quick

Front 41

Describe a haemorrhage

Back 41

Commonly associated with headaches. Patient will not be conscious; can cause stupor and coma which may progress. Causes can be aneurysms: idiopathic probably congenital, increase risk with age

Front 42

What increases the chances of someone getting a stroke?

Back 42

hypertension, damages arteriole walls hyperlipidaemia, cigarette use, diabetes mellitus and heart disease increase atherosclerosis 


Front 43

What determines the area of the brain affected by a stroke?

Back 43

The blood vessel that is affected.