Pre-placement

Question 1

Which questions do you ask in a neurology systems review?

Answer 1

• Headaches
• Visual problems
• Fits, faints and funny turns.
• Memory problems
• Numbness, tingling
• Incontinence or erectile dysfunction
• Balance or coordination difficulties
• Weakness
• Speech and swallowing difficulties
• Activities of daily living

Question 2

What are headache red flags?

Answer 2

Sudden onset high severity headache
Headache with fever
New onset neurological deficit
New onset cognitive dysfunction
Change in personality
Impaired level of consciousness
Recent head trauma (within past three months)
Headache triggered by cough, sneeze, exercise, or changes in posture.
Headache associated with halos around lights or headaches that get worse in the dark.
Headache associated with jaw claudication and scalp tenderness.

Question 3

What are the causes of fits, faints and funny turns?

Answer 3

Syncope such as vasovagal and cardiogenic (dangerous)
Seizures (provoked and unprovoked)
Psychogenic non-epileptic attacks
Rarer causes such as migraines, sleep disorders, cerebrovascular events and vestibular disorders.

Question 4

How do you assess loss of consciousness?

Answer 4

Pre-syncopal symptoms such as light headedness, dizziness
Eyewitness history
Epileptic symptoms- pre, during and post episodes.
Previous LoC
Video recordings

Question 5

What is syncope?

Answer 5

Syncope is LoC caused by lack of cerebral blood supply

Question 6

What is seen in syncope?

Answer 6

Motor activity such as twitching of the limbs, stiffening and jerking.

Presyncopal symptoms can distinguish vasovagal and cardiogenic syncope.

Cardiogenic syncope is usually sudden syncope

• May be brought on exercise
• Young men (risk factor)

Question 7

What is the MRC grading scale?

Answer 7

The MRC grading scale can be used to quantify the power assessment:

0) No power
1) Twitching but no movement
2) Movement, but cannot overcome gravity
3) Can overcome gravity
4) Movement against gravity and resistance
5) Normal muscle strength

Question 8

What is UMN?

Answer 8

The general definition of an UMN is a neuron whose cell body originates in the cerebral cortex or brainstem and terminates within the brainstem or spinal cord.

Therefore neurons which give rise to the various descending motor tracts are all UMNs. In addition, neurons which input to the nuclei of the extrapyramidal tracts (such as the rubrospinal tract) are also UMNs.

All UMNs exert their effects via LMNs, which may be one singular LMN or several LMNs.

Question 9

What would damage to the UMN cause?

Answer 9

As expected, damage to an UMN would cause weakness (-paresis) or paralysis (-plegia) of movement for the group of muscles it innervates. This paresis or paralysis is typically widespread in the form of either a mono/hemiparesis or mono/hemiplegia.

Question 10

What are the signs of UMN damage?

Answer 10

Hypertonia 
Hyperreflexia 
Spasticity 
Positive babinski sign 
Clonus 

Long term disuse of a muscle due to paralysis may cause disuse atrophy.

It is also important to note that although hypertonia and hyperreflexia are long term consequences of UMN damage, there is often an initial hypotonia and hyporeflexia immediately following damage.

This is often seen in strokes of the cerebral cortex or within the internal capsule and occurs contralateral to the side of the lesion.

Question 11

Why does hypertonia occur in UMN damage?

Answer 11

UMNs are believed to have a modulatory role in governing muscle tone through what is known as descending inhibition, althought this is not fully understood.

It is thought that UMNs regulate inhibitory interneurons and their effect on alpha and gamma motor neurons. Loss of UMN input, and thus descending inhibition, means firing of alpha and gamma motor neurons is favoured, causing hypertonia.

Furthermore, damage to cortical inputs to other descending tract nuclei, especially the medullary reticulospinal tract, known to inhibit spinal reflexes, may also be implicated.

Question 12

Why does hyperreflexia occur in UMN damage?

Answer 12

Descending inhibition from the UMNs also regulates the extent to which the myotatic stretch reflex is elicited. Therefore, loss of the UMN causes brisk reflexes.

Question 13

Why does spasticity occur in UMN damage?

Answer 13

This describes the phenomenon where a muscle is tight and stiff on passive movement in a velocity dependent manner. In spasticity, the amount of resistance is directly proportional to the speed of passive movement.

For example, on rapid passive movement of a limb there will be a point where the muscle becomes suddenly resistant to further stretch.

Furthermore, a ‘clasp knife reflex’ may also be present.

Question 14

What is a clasp knife reflex?

Answer 14

This phenomenon describes how following a sudden increase in resistance there is a swift decrease in tone of a muscle, allowing the muscle to easily be stretched.

Question 15

What is the babinski test?

Answer 15

The Babinski test is a fundamental component of a neurological examination used to assess UMNs. The clinician will stroke a blunt object along the lateral border of the plantar surface of the foot.

A normal response is flexion of the large toe and adduction of the other toes – this a negative Babinski sign.

However, in patients who have an UMN syndrome an abnormal planar reflex is elicited whereby the large toe extends and there is abduction of the other toes – this is a positive Babinski sign.

In infants below the age of two, a positive Babinski sign is normal. This is because the corticospinal tracts are not yet fully developed.

Question 16

Why does clonus occur in UMN damage?

Answer 16

this is a series of contractions which occur in a muscle when it is suddenly stretched and held in that position. This is thought to arise due to an exaggerated stretch reflex.

Question 17

What is LMN?

Answer 17

The cell body of a LMN lies within the ventral horn of the spinal cord or the brainstem motor nuclei of the cranial nerves which have motor modalities. Therefore, the cell body of a LMN lies within the central nervous system (CNS).

The axon of a LMN exits the CNS and forms the somatic motor part of the peripheral nervous system (PNS). Finally, the LMN terminates on the muscle fibres which it innervates.

The combination of the LMN and these fibres is known as a motor unit. It is important to note that although one LMN will innervate several muscle fibres, a single muscle fibre is innervated by only one LMN.

Question 18

What is the neuromuscular junction?

Answer 18

The bridging gap between the LMN’s axon terminal and the muscle fibre it supplies is known as the neuromuscular junction (NMJ).

It is here that the motor neuron releases the neurotransmitter acetylcholine, which causes firing of an action potential in the receiving muscle fibre.

Question 19

What is LMN syndrome?

Answer 19

A LMN syndrome is the term used by clinicians to describe the collection of signs and symptoms present when a patient damages α-motor neurons.

This damage can occur anywhere between the origins of the LMN in the ventral horn or brainstem nuclei and its termination on a muscle.

Question 20

What are the signs and symptoms of LMN syndrome?

Answer 20

Hyporeflexia
Hypotonia 
Flaccid muscle weakness
Fasciculations 
Muscle atrophy

Question 21

Why does hyporeflexia occur in LMN damage?

Answer 21

Since the efferent portion of the reflex arc is damaged, eliciting the myotatic stretch reflex will produce decreased or absent reflexes depending on the extent of that damage.

Question 22

Why does hypotonia occur in LMN damage?

Answer 22

Tone is a product of the contraction of the extrafusal fibres in response to the stretch of a muscle. Therefore, loss of α-motor neurons leads to reduced or absent muscle tone.

Question 23

Why does fasciculations occur in LMN damage?

Answer 23

When α-motor neurons are damaged, they can fire spontaneous action potentials, causing contractions in the fibres of the motor unit. This can be seen as small involuntary muscle twitches, often compared to having ‘a bag of worms under the skin’.

Question 24

Why does muscle atrophy occur in LMN damage?

Answer 24

The loss of neurotrophic factors from the α-motor neuron nerve terminal, which typically support the muscle, causes atrophy. This is different to the disuse atrophy which may been observed in an UMN syndrome.