4H Flashcards

1
Q

Describe the 4 major stages of formation of the neural tube.

A

1) transformation of the embryonic ectoderm into a thickened neural plate
2) lateral folding of the neural plate along the midline neural groove
3) apposition and fusion of the neural folds, and separation from the overlying ectoderm. Closure begins midway along the craniocaudal axis of the neural tube and extends in both directions
4) closure of the anterior and posterior neuropores, normally occurs during the 4th week.

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2
Q

Explain the importance of folate in the prevention of NTDs

A

folate is important for DNA and RNA synthesis as it donates carbons in metabolic reactions

NT formation is a period of rapid cell proliferation, therefore requiring a lot of DNA/RNA synthesis

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3
Q

Why can the SLR test elicit pain?

A

puts tension on the sciatic nerve, irritating the affected spinal nerves

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4
Q

Which spinal nerves are involved in the knee jerk reflex?

A

L3-L4

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5
Q

Which spinal nerves are involved in the ankle jerk reflex?

A

S1-S2

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6
Q

Which component of an IVD prolapses?

A

nucleus pulposus prolapses through the annulus fibrosis

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7
Q

why does a disc tend to prolapse posterolaterally?

A

the posterior longitudinal ligament attaches firmly to the posterior aspect of the IVD, so that the prolapse is forced to occur to the side of the midline

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8
Q

Which nerves contribute to the sciatic nerve?

A

L4, L5, S1, S2, S3

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9
Q

Where does the L4 spinal nerve exit from the vertebral canal?

A

at the intervertebral foramen between the pedicles of L4/L5 vertebrae

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10
Q

Which component of the nervous system is found at the level of L5/s1 IVD?

A

cauda equina

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11
Q

What is the lowest limit of CSF in the vertebral canal

A

found as far down as S2 vertebrae where the dural sac (and the lumbar cistern of CSF) terminates

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12
Q

Which nerves are responsible for the maintenance of anal tone and what are their root values?

A

left and right pudendaal nerves supply the muscle of the external anal sphincter (S2, S3 and S4)

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13
Q

Which nerves supply the detrusor muscle of the bladder? From which spinal nerves do they arise?

A

S2, S3, S4 = pelvic splanchnic nerves

T10-L2 = hypogastric nerves

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14
Q

30 year old male presents with sudden onset LBP after trying to lift a bag of cement. Pain is radiating to perineum, down the backs of both thighs and towards the calves. Complains that pain in his legs is worse than pain in his back.
Sensation of tingling down the back of the thigh and numbness around the buttocks, genitalia and anus.
Faecal incontinence and no urine passage since the injury (2 hours).

What is the most likely diagnosis?

A

central prolapse of an IVD

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15
Q

30 year old male presents with sudden onset LBP after trying to lift a bag of cement. Pain is radiating to perineum, down the backs of both thighs and towards the calves. Complains that pain in his legs is worse than pain in his back.
Sensation of tingling down the back of the thigh and numbness around the buttocks, genitalia and anus.
Faecal incontinence and no urine passage since the injury (2 hours).

Difficulty moving ankles and ankle jerk reflexes are diminshed, but knee jerk reflexes seem normal. SLR elicits pain and urinary retention is noticed.

On the basis of the motor signs, which nerve roots are most likely to have been affected?

A

sacral spinal nerve roots in general.
These roots supply muscles that flex and extend the ankle and these muscles seem weak.
The ankle jerk reflexes on both sides are weak.
anorectal and bladder dysfunction also suggest sacral nerve involvement as these organs are supplied by the sacral nerves

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16
Q

30 year old male presents with sudden onset LBP after trying to lift a bag of cement. Pain is radiating to perineum, down the backs of both thighs and towards the calves. Complains that pain in his legs is worse than pain in his back.
Sensation of tingling down the back of the thigh and numbness around the buttocks, genitalia and anus.
Faecal incontinence and no urine passage since the injury (2 hours).

Difficulty moving ankles and ankle jerk reflexes are diminshed, but knee jerk reflexes seem normal. SLR elicits pain and urinary retention is noticed.

On the basis of the sensory loss, which nerve roots are most likely to have been affected?

A

numbness on the back of the thigh and perineum are consistent with dysfunction of S2 and S4

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17
Q

What is a hernia?

A

a hernia occurs when part or all of a structure protrudes though the tissue in which it is normally contained.

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18
Q

what is the differential diagnosis of a groin lump?

A
inguinal hernia
femoral hernia
lymphadenopathy
femoral aneurysm
undescended testical
lipoma
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19
Q

On your examination, how would you distinguish a femoral hernia from an inguinal hernia?

A

Inguinal hernia: neck of an inguinal hernia lies above and medial to the pubic tubercle, above inguinal ligament

Femoral hernia: lies below and lateral to pubic tubercle, below inguinal ligament

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20
Q

What does it mean if a hernia is reducible?

A

contents can be returned to the abdominal cavity when the patient lies down or when pressure is applied

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21
Q

List three complications of an irriducible hernia

A

obstruction - loop of bowel becomes oedematous
strangulation - blood supply of the piece of bowel becomes compromised
peritonitis - due to sepsis spreading from the compromised bowel

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22
Q

How do you distinguish between direct and indirect hernias on clinical examination?

A

if possible, reduce the hernia and press over the deep ring. ask the patient to cough. a protrusion medial to the deep ring suggests a direct hernia

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23
Q

Which artery can be used as a landmark for the deep inguinal ring?

A

femoral artery. Palpable midway between ASIS and pubic symphysis (midinguinal point)

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24
Q

What is the relationship of the femoral artery to the femoral nerve and vein?

A

femoral nerve lies lateral to the artery, vein lies medial to the artery

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25
Q

What is the position of the deep inguinal ring?

A

lies above the inguinal ligament midway between ASIS and the pubic tubercle

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26
Q

What is the position of the deep inguinal ring in relation to the femoral artery?

A

lies immediately lateral and 2cm superior to femoral artery

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27
Q

What structure passes through the deep inguinal ring in males that makes it easily identifiable?

A

spermatic cord

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28
Q

Name two structures in the inguinal canal that a surgeon would take particular care to avoid damaging

A

ilioinguinal nerve

spermatic cord

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29
Q

Name 4 structures that lie within the spermatic cord

A
ductus deferens
pampiniform plexus
testicular artery
lymphatic vessels
autonomic nerves

artery of the ductus deferens
genital branch of the genitofemoral nerve

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30
Q

A hernial sac lies medial to the inferior epigastric vessels. What kind of hernia is it?

A

direct hernia because it has passed directly through the posterior wall of the inguinal canal

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31
Q

What is the conjoint tendon and where does it lie in relation to the inguinal canal

A
conjoint tendon (inguinal falx) is the common aponeurosis of the transversus abdominis and internal oblique muscles. 
Lies in the posterior wall of the inguinal canal
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32
Q

Which muscle is the principal flexor of the hip?

A

psoas major

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33
Q

Which muscle are the principal flexors of the knee

A

biceps femoris, semitendinous and semimembranous muscles

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34
Q

What is motor neuron disease?

A

degenerative neurological disease

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35
Q

Which CNS component is affected in MND?

A

neurons in the motor cortex, cranial nerve nuclei and corticospinal tracts

clinical manifestations are primarily in skeletal muscles rather than smooth/cardiac

often no involvement of the extraocular muscles - very late feature of the disease

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36
Q

In which pathways from the motor cortex do most motor impulses descend?

A

lateral and anterior corticospinal tracts and the corticobulbar tracts

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37
Q

what is a motor unit?

A

a single lower motor neuron and all the muscle fibres it stimulates

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38
Q

What do fasciculations indicate?

A

lower motor neuron injury

Fasciculations are small involuntary contractions of a motor unit. Can only be seen if the muscle is relaxed

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39
Q

List the six muscles responsible for moving the eyeball and the nerve supply of each

A

1) superior rectus - CN III
2) inferior rectus - CN III
3) medial rectus - CN III
4) lateral rectus - CN VI
5) superior oblique - CN IV
6) inferior oblique - CN III

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40
Q

Which muscle moves the eyelid and what is its nerve supply

A

levator palpebrae superioris - CN III

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41
Q

What is a PEG tube?

A

percutaneous endoscopic gastrostomy tube

allows nutrient solution to be passed directly into the stomach alleviating the need to chew or swallow food

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42
Q

What is the innervation of the muscles of mastication?

A

mandibular branch of the trigeminal nerve

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43
Q

Which muscle is responsible for raising the eyebrows?

A

occipitofrontalis muscle

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44
Q

Which muscle is responsible for closing the eyes tightly?

A

orbicularis oculi

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45
Q

Which muscle is used with blowing out the cheek?

A

orbicularis oris (relies upon the pursing of the lips to create an airtight seal)

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46
Q

What are the sensory and autonomic functions of the facial nerve?

A

sensory - anterior 2/3 of the tongue (taste) = chorda tympani

autonomic - innervation of submandibular and sublingual salivary glands, lacrimal glands (saliva and tears)

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47
Q

Which CN innervates the parotid gland?

A

glossopharyngeal nerve

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48
Q

Which CN is responsible for shrugging of the shoulders?

A

CN XI - spinal accessory

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49
Q

What is amaurosis fugaux?

A

transient loss of vision in one eye
common painless symptom and implies transient retinal ischaemia
associated with emboli or stenosis of ipsilateral ICA

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50
Q

What is a transient ischaemic attack?

A

episode where there is a temporary loss of brain function due to vascular insufficiency
usually lasts about 30 minutes with a complete recovery within 24 hours

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51
Q

What symptoms are typical of a transient ischaemic attack in the anterior (internal carotid) circulation?

A

dysphasia
one-sided motor weakness in the upper and/or lower limb
hemisensory deficit
visual disturbance

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52
Q

What symptoms are typical of a transient ischaemic attack in the posterior (vertebral artery) circulation?

A

diplopia
ataxia
amnesia
vertigo

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53
Q

what is xanthelasma and what is its clinical significance?

A

adipose deposit at the eyelids

associated with hyperlipidaemia or hypercholesterolaemia

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54
Q

Describe the mechanism of action of aspirin

A

antiplatelet drug

inhibits thromboxane A2 in platelets and prostacyclin in endothelial cell walls

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55
Q

Describe the mechanism of action of statins

A

lipid modulating drugs
inhibit HMG-CoA reductase, an enzyme involved in cholesterol biosynthesis
results in decreased plasma cholesterol and increased LDL receptors

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56
Q

Describe the mechanism of action of thiazide diuretics

A

inhibit sodium reabsorption in the PCT, reducing water reabsorption and thereby BP

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57
Q

What arteries arise from the ICA at the cranial cavity?

A

anterior cerebral artery
middle cerebral artery
posterior communicating arteru
opthalmic artery

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58
Q

In neuroanatomy, what is meant by the term somatotopic localisation?

A

concept that certain regions of the nervous system mediate neurological function in certain parts of the body

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59
Q

61 year old man has two episodes:

1) vision in left eye went foggy for about two minutes
2) vision ‘went funny’ again and became weak down his right side (right hand and lower limb). Visual disturbance affected right side of field of vision in both eyes

What is the most likely diagnosis of the first episode?

A

amaurosis fugax - transient loss of vision in one eye

suggests ischaemia of left retina or left optic nerve

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60
Q

61 year old man has two episodes:

1) vision in left eye went foggy for about two minutes
2) vision ‘went funny’ again and became weak down his right side (right hand and lower limb). Visual disturbance affected right side of field of vision in both eyes

What is the most likely diagnosis of the second episode?

A

Ischaemia in the left internal capsule

ischaemia in the cerebral hemisphere.
visual and motor pathways both decussate, therefore the problem must be in the left hemisphere
the motor and visual pathways run close together in the region of the internal capsule

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61
Q

What will cause left hemiplegia (weakness of face, upper limb and lower limb)

A

infarction of the right internal capsule

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62
Q

what motor loss is associated with occlusion of the anterior cerebral artery?

A

lower limb region

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63
Q

what motor loss is associated with occlusion of the middle cerebral artery?

A

upper limb/head and neck

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64
Q

Which cells are responsible for myelin production?

A

CNS - oligodendrocytes

PNS - schwann cells

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65
Q

Give 3 ways in which a LMN differs from a sensory neuron

A

Motor neuron:

  • all myelinated
  • transmission from CNS to muscle fibres
  • multipolar
  • cell body in ventral grey horn

Sensory neuron:

  • some myelinated
  • transmission to CNS from surroundings
  • unipolar
  • cell body in DRG
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66
Q

patient’s right pupil constricts further when light is shone into left eye than when light is shone into right eye directly. what is the name of this phenomenon?

A

relative afferent pupillary defect (RAPD)

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67
Q

Describe the steps of a normal pupillary light reflex

A

Light shone into the eye activates retinal ganglion cells. This triggers an action potential in the optic nerve, which carries the impulse to the pretectal nucleus of the midbrain, where it synapses. The impulse is passed to the Edinger-Westphal (parasympathetic) nucleus of CN III.

Oculomotor parasympathetic nerve fibres synapse in the ciliary ganglion. ciliary ganglion. Ciliary ganglion neurons innervate the constrictor muscle of the iris, causing pupillary constriction

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68
Q

Name the ridges on the surface of the cerebellum

A

folia

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69
Q

Name the principal nucleus that lies within the cerebellar hemisphere

A

dentate nucleus

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70
Q

Name the bundles that connect the cerebellum to the midbrain, pons and medulla

A

midbrain - superior peduncle
pons - middle peduncle
medulla - inferior peduncle

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71
Q

Give 6 signs of cerebellar dysfunction

A

1) ataxia
2) dysdiadochokinesis
3) nystagmus
4) intention tremor
5) scanning speech
6) past pointing
7) hypotonia

Remember: DANISH Pastry
D = dysdiadochokinesis
A = ataxia
N = nystagmus
I = intention tremor
S = scanning speech
H = hypotonia
P = past pointing
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72
Q

What are the clinical features of an UMN lesion?

A
hyperreflexia
hypertonia (spastic paralysis)
Clonus
weakness (decreased power)
positive babinski
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73
Q

Through which opening in the base of the skull is the spinal cord continuous with the brainstem?

A

foramen magnum

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74
Q

At what vertebral level does the spinal cord end?

A

L1/L2

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75
Q

Loss of vibration sensation below the level of the umbilicus indicates spinal cord compression at what level?

A

T10

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76
Q

spinocerebellar tract

A

ascending tract

conveys proprioceptive information from muscle and joint receptors to the cerebellum

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77
Q

How do you routinely measure systolic and diastolic BP using a stethoscope?

A

take arm measurements using a sphymomanometer. Place the inflatable cuff around the arm and inflate until pressure is greater than that expected. slowly deflate the cuff with the stethoscope over the brachial artery. systolic BP is when korotkoff sounds are first heard, diastolic is when the sounds become muffled

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78
Q

What do you do with BP results?

A

record them reading in the notes and arrange for two repeat measurements at separate times. Give lifestyle advice if required.

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79
Q

What is the calculation for determining MAP?

A

MAP = diastolic + 1/3(systolic-diastolic)

MAP is a time-weighted average of arterial BP over the whole of the cardiac cycle

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80
Q

How is BMI calculated?

A

BMI = weight (kg)/height (m)^2

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81
Q

What are the BMI categories?

A
<18.5kg/m2 = underweight
18.5-24.9 = healthy weight
25-29.9 = overweight
>30 = obese
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82
Q

Explain the physiological mechanism by which postural hypotension occurs

A

whenba person stands up quickly, there is a sudden fall in venous return to the heart from veins of the lower limbs. This leads to a fall in stroke volume, cardiac output and therefore decreases BP

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83
Q

What are two specific areas of the brain associated with speech, and what language problems can result from damage to these areas?

A

Brocas area - coordinates speech production. damage gives expressive aphasia

Wernicke’s area - centre for comprehension of speech. Damage gives receptive aphasia

Both supplied by the middle cerebral artery. Usually found in the dominant hemisphere (left in most)

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84
Q

Patient with trouble comprehending spoken and written language, producing coherent speech, paralysis on right side in upper limb and face.

Blockage of which artery most likely explains these symptoms?

A

Left middle cerebral artery

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85
Q

Which artery supplies the region of the motor cortex that controls the lower limb?

A

anterior cerebral artery

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86
Q

How can AF lead to stroke?

A

AF is a complication of hypertension.
AF means blood is not pumped effectively through the atria and can clot, leading to an embolism, which can lodge in the brain

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87
Q

What could be the underlying problem in a patient who wakes up one morning with:
o Right-sided weakness (hemiparesis) affecting most of the body, but sparing the leg
o aphasia

A

a stroke (cerebrovascular accident) affecting the left middle cerebral artery

Supplies motor cortex as well as broca’s/wernicke’s areas
Movement in the leg was spared because the area of the motor cortex controlling the leg is supplied by
the anterior cerebral artery

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88
Q

Multiple sclerosis

A

Inflammatory disease affecting white matter; caused by discrete lesions affecting myelin that surrounds many CNS axons.
– seen as plaques in white matter of brain and spinal cord
pattern of symptoms/signs cannot be explained by one focal lesion
In MS, lesions occur in several different regions of CNS white matter

may have:
o partial loss of vision
o double vision (altered eye movements)
o sensory changes (e.g. numbness)
o motor symptoms (e.g. weakness, ataxia)
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89
Q

Alar plate

A

forms dorsal horn

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90
Q

Basal plate

A

forms ventral horn

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91
Q

Spina bifida

A

failure of closure of the neural tube

occulta
meningocoele
myelomeningocoele

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92
Q

What is the relationship between spinal nerves and the meninges

A

As spinal nerves and their roots pass laterally, they are surrounded by tubular sleeves of dura mater, which
merge with and become part of the epineurium

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93
Q

Blood Supply of the Spinal Cord

A

The vertebral arteries are the main source of blood to the spinal cord. Branches from the vertebral arteries directly supply the spinal cord itself:

1) one anterior spinal artery
2) two posterior spinal arteries
3) anterior and posterior radicular (segmental) arteries – small vessels which enter via the nerve roots. The largest anterior segmental medullary artery is the artery of Adamkiewicz. It arises from the inferior intercostal or upper lumbar arteries, and supplies the inferior 2/3 of the spinal cord.

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94
Q

Venous drainage of the Spinal Cord

A

three anterior and three posterior spinal veins.

valveless, and form an anastamosing network along the surface of the spinal cord. They also receive venous blood from the radicular veins.

In epidural space

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95
Q

Lidocaine mechanism

A

local anaesthetic

Block voltage-gated sodium channel
Sodium cannot enter the neuron and threshold is not reached, and impulses cannot be
transmitted

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96
Q

Propagation of the action potential

A

 Generated in the axon hillock
 When the sodium channels are opened, sodium ions rush in; once inside they cause nearby regions of the
neuron to become depolarized by moving laterally through the axon.
 This, in turn, causes the opening of more voltage-gated sodium channels in those regions.

i.e. the currents flowing inwards at a point on the axon during anaction potentialspread out along the axon,
and depolarize the adjacent sections of its membrane

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97
Q

Somatotopy

A

the point-for- point correspondence of an area of the body to a specific point on the central
nervous system.

98
Q

Distal to the cavernous sinus, each ICA gives rise to:

A

Ophthalmic artery – Supplies the structures of the orbit.
Posterior communicating artery
Anterior cerebral artery – Supplies part of the cerebrum.

99
Q

What vertebral levels is the trachea associated with?

A

C6 - T4 (sternal angle)

100
Q

major structures contained in thecarotid sheath

A

o commoncarotidartery (medial)
o internal jugular vein (lateral)
o Vagus nerve (CN X) (posterior)

101
Q

Which nerves emerge from behind the SCM muscle?

A

great auricular nerve - sensory nerve, runs up to supply sensation to the area of the mandible

Transverse cervical nerve - supplies sensation to the skin on the front of the neck

102
Q

Which nerve Lies on the surface of the scalenes anterior

muscle?

A

phrenic nerve`

103
Q

What is the relationship of the brachial plexus and subclavian artery in the posterior triangle?

A

both structures run between scalenus medius and scalenes anterior muscles

subclavian artery runs behind brachial plexus

104
Q

Where does the stellate ganglion lie?

A

in the neck of the first rib

stellate ganglion is a combination of the inferior cervical and the first thoracic sympathetic ganglia

105
Q

How can you differentiate between the Internal and external carotid arteries?

A

o Internal carotid has a large bulge (sinus)

o Internal carotid has no branches in the neck

106
Q

Referred Pain

A

occurs when visceral pain is felt as cutaneous pain

107
Q

Retropharyngeal space

A

Potential space between the pharynx and vertebral column/associated muscles

If bacterial infection occurs here, the pus will track all the way to the diaphragm (T12) under the fascial planes

108
Q

White ramus communicans

A

pathway by which preganglionic sympathetic fibres reach the sympathetic trunk from spinal nerves

109
Q

Grey ramus communicans

A

pathway by which postganglionic sympathetic fibres travel to the spinal nerves from the sympathetic trunk

110
Q

Central cord syndrome

A

Hyperextension injury
Compression of the cord anteriorly by osteophytes (degenerative change) and
posteriorly by ligamentum flavum

Centre of the spinal cord is affected:
o Light touch/proprioception may be unaffected (DCML)
o Some impairment of sharp/blunt discrimination and temperature sensation
o Nerves coming from more proximal muscles are closer to the centre of the cord
o patients therefore often have strong legs and weak upper limbs

111
Q

Brown – Sequard Syndrome

A

Hemisection of the cord

  • loss of pain/temperature sensation on contralateral side
  • ipsilateral paralysis
  • ipsilateral loss of fine touch discrimination/proprioception
112
Q

Neurogenic Shock

A

 Occurs in people who have SCI above T6 (> 50% loss of sympathetic innervation)
 The body’s response to the sudden loss of sympathetic control -> Loss of vascular tone

Clinical Triad:
o Hypotension
o Bradycardia
o Hypothermia – vasodilation & loss of body heat

Patients need inotropic support, not volume repletion

113
Q

upper motor neuron lesion

A

lesion of the neural pathway above the ventral horn cell of the spinal cord or motor nuclei of the cranial nerves (brain or spinal cord).

114
Q

Lower motor neuron lesion

A

affects nerve fibres travelling from the ventral horn of the spinal cord or the cranial motor nuclei to the relevant muscle

115
Q

Spinal Cord Injury between C1 and C5

A

UMN signs are present in both upper and lower limbs

Tetraplegic

116
Q

Spinal Cord Injury between T3 and T12

A

paraplegic

UMN signs are present in the lower limbs and upper limbs are normal

117
Q

Spinal Cord Injury between T12 and S2

A

LMN signs are present in the lower limbs

upper limbs are normal

118
Q

Spinal shock

A

loss of sympathetic activity
immediate loss of function below the level of injury
Temporary suppression of all reflex activity below the level of injury

Clinical findings
 Flaccid paralysis
 Areflexia
 Loss of sensation
 Bladder - urine retention and overflow incontinence
 Bowel
119
Q

Spinal shock vs neurogenic shock vs autonomic dysreflexia

A

Neurogenic shock = loss of vasomotor tone:
o Hypotension
o Bradycardia
o Hypothermia – vasodilation & loss of body heat;
spinal cord injury at or above t6

Spinal shock = loss of all reflex activity below level of injury:
 Flaccid paralysis
 Areflexia
 Loss of sensation
 Bladder 
 Bowel 

autonomic dysreflexia:

  • occurs after resolution of spinal shock and in patients with spinal cord injury at or above t6
  • causes an imbalanced reflex sympathetic discharge, leading to potentially life-threatening hypertension
120
Q

autonomic dysreflexia

A

A strong sensory input (not necessarily noxious) is carried into the spinal cord via intact peripheral nerves. The most common origins are bladder and bowel. (B)

Input travels up the spinal cord and evokes a massive reflex sympathetic surge from the thoracolumbar sympathetic nerves, causing widespread vasoconstriction = peripheral hypertension occurs.

The brain detects this hypertensive crisis through intact baroreceptors in the neck and attempts to shut down the sympathetic surge by sending descending inhibitory impulses. These impulses are unable to travel to most sympathetic outflow levels because of the spinal cord injury at T6 or above. Inhibitory impulses are blocked in the injured spinal cord.

brain attempts to bring down peripheral blood pressure nerve; however, this compensatory bradycardia is inadequate and hypertension continues.

121
Q

Concussion

A

A (temporary) disturbance in brain function as a result of trauma

122
Q

Main factors causing cerebral ischaemia

A

1) increased ICP
2) systemic hypoxaemia
3) decreased CPP

123
Q

Breakdown of global attention

A

results in delirium/acute confusional state
o impaired arousal: ‘drowsiness’, coma
o impaired vigilance: ‘impersistence’
o impaired divided and selective attention: ‘distractible’

124
Q

Breakdown of domain-specific attention

A

focal impariment of attention, e.g. following CVA

o visual inattention - inattention confined to the visual sensory modality
o sensory inattention
o neglect e.g. Hemispatial neglect

125
Q

Hemispatial neglect

A

inability of a person to process and perceive stimuli on one side of the body or environment, where that inability is not due to a lack of sensation

126
Q

Observed effects with damage to ARAS

A

global loss of attention, causing drowsiness, delirium, coma

Lots of different neurotransmitters involved in ARAS

metabolic/drug-induced disturbances can easily
disrupt the function of ARAS

This may explain why so many metabolic causes of delirium exist

127
Q

Observed effects with damage to cortical structures controlling attention

A

focal attention deficit, causing inattention and neglect

128
Q

Nociception

A

the neural processes of encoding and processing noxious stimuli

129
Q

Components of nociception

A

1) Transduction of peripheral stimulus into an AP

2 Transmission – AP is transmitted along neural network

3) Modulation – often occurs in the spinal cord dorsal horn/higher centres
4) Perception - pain is a conscious perception

130
Q

Peripheral sensitisation

A

Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields

Repetitive exposure to noxious stimuli as neurons are bathed in “inflammatory soup”

131
Q

Red flags in lower back pain

A
 Weight loss, PMH of Malignancy
 Fever
 Signs of systemic inflammatory disease
 Anatomical change
 history of trauma
 Cauda equina syndrome - saddle anaesthesia, bowel/bladder dysfunction
 Neurological signs (radiculopathy)
132
Q

What is the embryonic origin of the muscles of facial expression?

A

2ndpharyngeal arch

133
Q

Neural crest cells

A

group of embryonic cells that are pinched off during the formation of the neural tube

migrate to numerous locations and contribute to the formation of diverse structures, including:
melanocytes, craniofacial skeleton, dorsal root ganglia, Schwann cells, Adrenal Medulla cells

134
Q

Differentiation of the spinal cord

A

Neural tube consists of neuroepithelial cells.

Give rise to neuroblasts (primitive nerve cells), which form the mantle layer. Later becomes gray matter

processes grow out, forming the marginal layer. This becomes myelinated, and gives rise to white matter

Proliferation of cells causes formation of thickenings:
Alar plate (dorsal) and basal plate (ventral), separated by the SULCUS LIMITANS
135
Q

Formation of spinal nerves

A

Motor cell bodies form from basal plate

Sensory cell bodies (DRG) arise from neural crest cells, and axons grow into dorsal horn

136
Q

Which brain vesicle does the cerebellum arise from?

A

metencephalon gives rise to cerebellum and pons

137
Q

What is the key regulatory molecule in eye development?

A

PAX 6, restricted to the optic cup and lens

PAX 2 in optic stalk

138
Q

Which artery supplies blood to the lower third of the spinal cord?

A

Major anterior medullary (segmental) artery

139
Q

Between which vertebrae is the inferior end of the adult human spinal cord (i.e. the caudal tip of the conus medullaris) typically located?

A

L1 and L2

140
Q

Damage to which specific part of the brain results in Broca’s (expressive) aphasia in most patients?

A

Left inferior frontal gyrus

141
Q

A disorder in which of the main dopaminergic pathways in the CNS is implicated in schizophrenia?

A

Mesolimbic/mesocortical

142
Q

In which part of the brainstem is the cerebral crus located?

A

Cerebral peduncle of midbrain

143
Q

The facial muscle most responsible for moving the lips both upward and laterally to produce a smile is:

A

Zygomaticus major

144
Q

Which congenital defect of the eyes would result from a loss-of-function mutation in the SHH gene?

A

Cyclopia

145
Q

Which artery supplies the inferior temporal gyrus?

A

posterior cerebral artery

146
Q

Which spinal nerve(s) are responsible for anal sensation?

A

S4-5

147
Q

Which structure first receives cerebrospinal fluid into the venous blood system?

A

superior sagittal sinus

148
Q

Why do scalp wounds bleed profusely?

A

Walls of the blood vessels in the scalp are firmly attached to the tissue of the superficial fibrous layer

Cut ends of the vessels therefore do not readily retract, and are held open if they are injured

149
Q

Why is the base of the skull particularly important in relation to head injuries?

A

site of important vessels and exit of cranial nerves

There has to be a high index of clinical suspicion for base of skull fractures, as clinical signs take several hours to appear

These fractures are typically associated with more complex intracranial injuries, such as damage to
cranial nerves and intracranial haematomas because of the amount of important structures that travel along the base of the skull

150
Q

Clinical signs of base of skull fractures:

A

Bruising over the mastoid process
Panda/raccoon eyes – significant bruising around both eyes

In both cases, bleeding from the fracture site tracks along the soft tissue planes until it reaches the surface, where it can be seen

151
Q

Monroe-Kellie Principle

A

Intracranial Volume is constant
 In addition to brain parenchyma, the skull contains blood and CSF
 Expansion in volume of any of these components must be offset by an equal decrease in volume of the other components, or the ICP will increase
 The compensatory capacity within the skull is very limited

152
Q

Describe the effect of a Mass lesions in the brain on ICP

A

Mass lesions in the brain exceeding 100-120ml will cause the ICP to increase very rapidly

Increasing volume created by a mass lesion inside the brain is initially compensated for by the displacement of
a small amount of venous blood and CSF into the circulation and space around the spinal cord. The brain itself is incompressible, so it has to remain about the same volume, and the arterial volume also doesn’t change because it’s important to provide a continual blood supply to the brain.

As the intracranial mass expands further, the maximal compensatory state is achieved (no more than about 75ml of venous blood and CSF can be displaced).Critical point = point at which the limit of compensation has been achieved

As the mass expands, the pressure within the skull starts to increase exponentially

153
Q

Describe the effect of elevated ICP on CPP

A

CPP = MAP – ICP

The rising ICP after a head injury has an adverse effect on the CPP.

Raised ICP decreases the pressure gradient for blood flow to the brain, resulting in reduced blood flow (CPP decreases with increased ICP)

After a head injury, homeostatic mechanisms fail, so a rising ICP leads to reduced CPP and ischaemic damage

Cerebral vascular resistance normally increases with head injury, making the brain even more susceptible to injury

Reduced CPP results in decreased oxygen and metabolite delivery, resulting in ischaemic injury to brain cells

154
Q

How is increasing ICP detected?

A

ICP can be monitored but this is an invasive procedure. Neurological observations are used instead.

Signs of increasing ICP:
 Decreasing GCS
 Diminished pupil response to light
 Lateralising signs – e.g. one-sided weakness

155
Q

Describe the process of brain herniation in the case of an expanding extradural haematoma,

A

1) displacement of the cingulate gyrus from one hemisphere to the other, underneath the falx cerebri
2) uncal herniation - compresses the oculomotor nerve
3) central herniation of brain stem

156
Q

uncal herniation

A

herniation of the medial temporal lobe from the middle into the posterior cranial fossa, across the tentorial opening

The uncus becomes squashed against the midbrain, compressing the oculomotor nerve on the same side
o This causes a fixed and dilated pupil

157
Q

Which layer contains nerves and vessels of the scalp?

A

Dense connective tissue layer

158
Q

Which strategies does the nervous system use for controlling movement?

A

Ballistic (pre-programmed) movements - Rapid but at expense of accuracy, e.g. swatting a fly. Cannto be interrupted/corrected

Pursuit or visual feedback movements - Motor command continually updated according to sensory feedback (e.g. visual). Highly accurate (can be modified while in progress) but slow

159
Q

Proprioception

A

feedback from peripheral sensory receptors on the positions and movement of limbs to the somatic sensory cortex

Loss of proprioception results in inability to create movements, not due to paralysis but due to lack of control

160
Q

Central pattern generators

A

intrinsic circuits of the spinal cord can produce rhythmic motorneuron activity which drives stepping

Two sets of pattern-generating neurones project to flexor and extensor motorneuron pools

Reciprocal inhibitory connections between the two sets of pattern-generating neurones help to co-ordinate
their activity, so that there is alternating excitation of flexors and extensors

161
Q

spinocerebellar tract

A

conveys proprioceptive information from the body to the cerebellum.

162
Q

Ora serrata

A

serrated junction between the retina and the ciliary body

163
Q

Fundus Fluorescein Angiogram

A

Investigation for AMD

Inject fluorescein intravenously. Fluorescein is bound to albumin - remains within normal capillaries because of blood-retinal barrier.

o In a normal situation there is no leakage into the retina
o With retinal problems the dye becomes visible as it leaks into the retina

164
Q

Pain

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage

165
Q

Triple response

A

 Red reaction - a red line immediately at the site of mild injury due to direct vasodilation, mediated by
histamine.

 Wheal - slight oedema at the site of injury, also mediated by histamine (increased capillary permeability and exudation of fluid).

 Flare - surrounding ill-defined erythema, due to an axon reflex

Nociceptive afferent neuron releases neuropeptides
CGRP and Sub P. These activate mast cells
o Mast cells release histamine -> further sensitises the nociceptor

o CGRP causes vasodilation - gives rise to flare region and redness
o Substance P causes plasma extravasation - causes oedematous wheal region

166
Q

Thrombosis in the anterior cerebral artery (beyond the anterior communicating artery)

A

paralysis or weakness of muscles of the leg and foot of the opposite side

This means, the effects of the arterial occlusion is on the upper part of the “Motor area – area corresponding to area 4 of Brodmann”.

upper parts of the “Sensory area” corresponding to area 1,2,3 of Brodmann is also affected, leading to loss or dulling of sensations from the leg and foot of the opposite side.

personality changes occur, by involvement of the frontal lobe.

167
Q

Thrombosis in the middle cerebral artery

A

hemiplegia and loss of sensations on the opposite half of the body, affecting the face and arms the most.

Also because the middle cerebral artery is the supply to the Broca’s area and Wernicke’s area, aphasia results, especially if the thrombosis is in the dominant hemisphere (left hemisphere in a right handed person)

168
Q

Thrombosis in the posterior cerebral artery

A

leads mainly to visual effects causing contralateral homonymous hemianopia

macular area is often spared (this is referred to as “macular sparing”).

169
Q

Which structures pass through the cavernous sinuses?

A

internal carotid artery
abducent nerve [VI]

Structures in the lateral wall of each cavernous sinus are, from superior to inferior:
 oculomotor nerve [III]
 trochlear nerve [IV]
 ophthalmic nerve [V 1 ]
 maxillary nerve [V 2 ]
170
Q

cavernous sinus thrombosis

A

Patient will have fever and a swollen eye

passageways within the cavernous sinus form a meshwork of fine channels

 This makes the blood flow very slow
 Ophthalmic veins communicate with veins on the face
 This means that infection can spread intracranially
 The slow flow through the cavernous sinuses means that bacteria has time to multiply,
 Give off toxins, which can cause the blood to clot resulting in a cavernous sinus thrombosis

171
Q

stellate ganglion

A

sympathetic ganglia on either side of the root of the neck.

combination of the inferior cervical and the first thoracic sympathetic ganglia

172
Q

pancoast tumour

A

a malignant tumour of the superior sulcus of the lung, with destructive lesions of the thoracic inlet.

invade the brachial plexus causing C8/T1 palsy with small muscle wasting in the hand and weakness as well as pain radiating down the arm.

173
Q

Horner’s syndrome

A

combination of symptoms that arises from a sympathetic trunk lesion (and thereby an interruption of the sympathetic nerve supply to the head and neck).

May be central, preganglionic or postganglionic depending on the site of the lesion

174
Q

Clinical features of Horner’s syndrome

A

1) unilateral miosis (constricted pupil) - loss of sympathetic innervation to the iris dilator muscle
2) partial ptosis (drooping eyelid) - loss of sympathetic tone to Müller’s muscle
3) Anhydrosis (loss of sweating) on same side -
4) apparent enopthalmus

175
Q

Explain how these symptoms might be part of the same disease process:
 Ptosis, anhidrosis and miosis
 Weakness of hand
 Discolouration and swelling of arm

A

Ptosis, anhidrosis and miosis → compression of stellate ganglion

Weakness of hand → compression or invasion of the brachial plexus

Discolouration and swelling of arm → occlusion of the subclavian vein

Loss of sympathetic innervation also leads to loss of vascular tone. Tenderness, erythema and warmth may present.

176
Q

spinal segment

A

area of the spinal cord that gives rise to the dorsal and ventral rootlets, which will form a single pair of spinal nerves.

177
Q

IVD Prolapse

A

repeated compression-relaxation cycle of IVD can lead to peripheral tears of the anulus fibrosus. Causes extrusion and herniation of the nucleus pulposus.

This often occurs with age:
o NP becomes more dehydrated, transferring more of the compression forces to the AF
o This added stress may cause AF thickening and tears.

178
Q

Most common site of prolapsed intervertebral disc

A

L4/L5 and L5/S1 (mass being supported and bending of vertebral column are greatest)

Protrusion of the nucleus pulposus usually occurs posteriorly and towards the intervertebral foramen, compressing the spinal nerve root below (L5 or S1).

pain and sensory loss will be dermatomal in distribution. Sensory changes usually precede motor loss.

179
Q

L5 nerve compression symptoms

A

Pain: over hip, SI joint, and down side of leg. Numbness of lateral leg and first 3 toes. Weak dorsiflexion of hallux, potential foot drop. Reflexes not altered

180
Q

S1 nerve compression symptoms

A

Pain down back of thigh and leg to foot. Numbness back of calf and sole of foot
Weak plantarflexion of foot/hallux. Difficulty walking on toes.
Diminished/absent ankle jerk reflex

181
Q

Briefly describe Descending pain modulation

A

spinothalamic tract has projections to the periaqueductal gray. PAG activates neurons in the nucleus raphe magnus, which release 5-HT/NA. This directly inhibits dorsal horn cells, and also activates inhibitory interneurons, which release enkephalin onto dorsal horn cells, inhibiting pain transmission.

182
Q

Referred pain

A

pain experienced at a site distant from source of the pain.
branches of visceral pain fibres synapse on the same second-order neurons in the dorsal horn that receive pain signals from the skin.

Pain signals from the viscera are conducted through the same neurons that conduct pain signals from the skin, and the person has the feeling that the sensations
originate in the skin.

183
Q

Red flags of LBP

A
urine retention
saddle anaesthesia
weight loss
PMH of malignancy
signs of systemic infection e.g. fever
trauma
sciatica/radiation of pain
Immunocompromised patients
age >50 (increased fracture risk)
bilateral leg numbness
184
Q

Which nerve exits the posterior aspect of the midbrain?

A

trochlear

185
Q

Which nerve marks the midbrain/pons junction?

A

oculomotor

186
Q

Which CN exit at the pontine medulla junction?

A

abducens (VI), facial(VII), and vestibulocochlear (VIII) nerves

187
Q

foramina of Luschka (lateral apertures)

A

Connect 4th ventricle to subarachnoid space

188
Q

foramen of Magendie (median aperture)

A

Connects 4th ventricle to central canal of spinal cord

189
Q

Vestibulo-ocular reflex

A

stabilizes the position of the retina in space, during movements of the head, by rotating the eyeball in the
opposite direction.

produces movements of the eyes that are equal and
opposite the movement of the head.

This reflex can be tested by the rapid head impulse test test, in which the head is rapidly moved to the side with force, and is controlled if the eyes succeed to remain looking in the same direction.

190
Q

Nystagmus

A

Nystagmus is a rhythmical, repetitive and involuntary movement of the eyes. It is usually from side to side, but sometimes up and down or in a circular motion.

to see nystagmus is to spin a person around for 30 seconds, stop and then have them try to stare at an object. If they have nystagmus, their eyes will first move slowly in one direction, then move rapidly in the opposite direction

191
Q

saccades

A

eye movements used to rapidly refixate from one object to another.

test saccades by holding two widely spaced targets in front of the patient and asking the patient to look back and forth between the targets

192
Q

Reflex

A

predictable, involuntary, and stereotyped response to an eliciting stimulus.

 Spinal reflex: a reflex mediated by a nerve pathway with a sensory afferent to the spinal cord, linkages within
the cord, and an efferent to muscle from the cord.

193
Q

Which nerve provides somatosensory innervation to the nasal cavity?

A

Trigeminal Nerve (ophthalmic and maxillary divisions)

194
Q

Which intrinsic eye muscles are innervated by the oculomotor nerve?

A

sphincter pupillae (pupil constriction) and the ciliary muscle (accommodation).

195
Q

Where is the trigeminal ganglion localized and what is its functions?

A

Sensory ganglion of the trigeminal nerve (CN V)

 occupies a cavity (Meckel’s cave) in the dura mater
This is in the middle cranial fossa

 contains the sensory cell bodies of the 3 branches of the trigeminal nerve

196
Q

How to differentiate between CSF and nasal secretions

A

CSF should have glucose in it, but nasal secretions do not

“halo sign” on tissue of blood-stained fluid beta-2-transferrin level

197
Q

Association cortices

A

Are adjacent to the particular primary sensory cortex

Integrate the sensory input, relate it to past experience, recognise what it is and its significance

198
Q

Explain why vibrating tendons leads to errors in the perception of joint angles

A

vibration distorts the perceptions of static joint angle and movement

199
Q

How does transcranial magnetic stimulation work?

A

Magnetic stimuli applied over the motor cortex activate the corticospinal tract.

action potentials are produced in pyramidal neurons, which cause activation of motorneurons and therefore
twitch contractions are elicited in skeletal muscles.

200
Q

What would be the effect of absent stretch reflex on muscle tone?

A

Stretch reflex is absent therefore there is no feedback, resulting in hypotonia

201
Q

Which type of axon would be affected first with nerve compression – motor or pain fibres?

A

 The larger the fibre, the earlier it is affected by compression

 Motor axons are affected first with compression( Aalpha and Abeta)
 This is because these fibres are larger

Sensory loss but intact pain sensation

202
Q

Phases of Spinal Shock

A

1) areflexia - loss of descending excitatory input (days 0-1)
2) initial reflex return - upregulation of NT receptors after denervation makes muscles more excitable (days 1-3)
3) initial hyperreflexia - formation of new synapses with interneurons (1-4 weeks)
4) spastic hyperreflexia - cell bodies send out projections to form new synapses (1-12 months)

203
Q

Pattern of reflex return

A

1) plantar response (Babinski)
2) bulbocavernosus reflex
3) tendon jerks (flexors before extensors)

204
Q

Superior colliculi

A

coordinate movements of the eyeballs in response to visual and other stimuli

205
Q

Inferior colliculi

A

coordinate movements of the head and trunk and response to auditory stimuli

206
Q

PRIMARY AND SECONDARY BRAIN INJURY

A

Primary: brain injury that occurs as an immediate consequence of the causative trauma

Secondary: injury to the brain can occur subsequently as a result of hypoxia and/or raised intracranial pressure

207
Q

Neural Plasticity

A

potential for brain to change its structure and function.

Greater exposure to a particular stimulus prompts the brain to dedicate more neurones to that stimulus (and a
lack of stimulation allows the brain to reassign neurones to a different function).

208
Q

Tinnitus

A

sensation of a sound when there is no auditory stimulus.

results from heightened awareness of neural activity in the auditory pathways.

209
Q

Vertigo

A

sensation of motion without any actual motion, or an exaggerated sense of motion.

210
Q

The facial muscle most responsible for moving the lips both upward and laterally to produce a smile is:

A

Zygomaticus major

211
Q

crus cerebri

A

anterior portion of the cerebral peduncle (midbrain)

212
Q

Drainage of the Frontal Sinuses

A

drain into the nasal cavity at the semilunar hiatus on the lateral wall.

213
Q

Drainage of the Sphenoid Sinuses

A

Drain into roof of nasal cavity

214
Q

Drainage of the Ethmoidal Sinuses

A

o Anterior – semilunar hiatus
o Middle – Ethmoid bulla
o Posterior – Superior meatus

215
Q

Drainage of the Maxillary Sinuses

A

drains into the nasal cavity at the semilunar hiatus, underneath the frontal sinus opening.

potential pathway for spread of infection – fluid draining from the frontal sinus can enter the maxillary sinus.

216
Q

Which sinuses drain into the semilunar hiatus?

A

FAM

F- frontal
A - anterior ethmoidal
M - maxillary

217
Q

Regions of the pharynx

A

1) nasopharynx = end of nasal septum to lower border of soft palate
2) oropharynx = soft palate to tip of epiglottis. Palatoglossal fold is anterior border
3) laryngopharynx = tip of epiglottis to lower border of cricoid cartilage (C6)

218
Q

piriform fossae

A

Shallow recess in the laryngopharynx, lateral to laryngeal inlet

219
Q

PHARYNGEAL RECESS

A

fossa of rosenmuller
Deep recess in the area behind the auditory tube
Much deeper than the piriform fossa
Goes as far as the area where the internal carotid artery ascends into the skull

220
Q

VALLECULA

A

small groove between the epiglottis and the tongue just behind the root of the tongue between the folds in the throat

221
Q

Fenestra Cochlea

A

round window

222
Q

Fenestra vestibule

A

Oval window

223
Q

Glue ear

A

Chronic otitis media with effusion

condition of the middle ear that is characterised by a non purulent effusion of the middle ear due to eustachian tube dysfunction

Tubular tonsil growth blocks the auditory tube, new air can’t get in to the middle ear

Respiratory epithelium lining the middle ear produces mucus, which cannot be drained and builds up in middle ear cavity

Goblet cells may increase in number with glue ear

Build up of mucus impairs the mechanism of the ossicles → less able to conduct sound

224
Q

Most common cause of deafness

A

Wax in external auditory meatus

225
Q

Why is a lumbar puncture dangerous in a patient with raised intracranial pressure?

A

When lumbar puncture is performed in these patients, a low-pressure shunt is formed at the site of LP where CSF can escape.

As the CSF pressure drops in the spinal column, CSF and brain mass may then shift towards the low-pressure outlet (the LP site).

I.e. The pressure drives the fluid out, pushing the cerebellum with it

This can lead to SPINAL CONING

226
Q

positive Rinne’s test

A

air conduction is heard louder than bone conduction

Indicates normal hearing

227
Q

Negative Rinne’s test

A

bone conduction is louder than air conduction. Indicates conductive hearing loss in that ear

228
Q

Normal Weber’s

A

midline weber’s. Sound should be detected equally in both ears

229
Q

Weber’s heard louder in left ear

A

Weber’s lateralises towards a conductive hearing loss and away from a sensorineural hearing loss

Either:
1) conductive hearing loss in left ear (If they have a conduction defect, then ambient noise will seem less so the sound being transmitted through the skull to the ossciles/etc will seem relatively louder)

or

2) sensorineural hearing loss in right ear (tone referred to better ear)

230
Q

sensory innervation of palatine tonsils?

A

mandibular branch of trigeminal nerve

231
Q

Which named lymph node drains the palatine tonsil?

A

Jugulodigastric node

232
Q

To which lymph nodes does the posterior part of the tongue drain?

A

deep cervical nodes

233
Q

Define what is meant by the “glottis”

A

Area of the airway between the vocal folds

234
Q

What is the “sinus or ventricle of the larynx”?

A

a recess, situated between the vestibular and vocal folds on either side, and extending nearly their entire length.

235
Q

Where do the ducts of the major salivary glands open into the mouth?

A

Parotid – near the second upper molar

Submandibular – next to the frenulum

Sublingual – big ducts open into the sublingual papilla on the floor of the mouth, but smaller ducts drain into
the submandibular duct

236
Q

Which cranial nerve is sensory to the mucosa of the larynx and which local nerves are involved?

A

The vagus nerve, superior and recurrent laryngeal nerves

237
Q

Accommodation reflex

A

Three components:

  1. Convergence of eyes due to contraction of medial rectus muscles
  2. Miosis - constriction of pupils due to constrictor pupillae muscle contraction.
  3. Accommodation to increase refractive power of the lens. This is due to the contraction of ciliaris muscle.
238
Q

Explain how the accommodation reflex occurs

A

Visual input reaches the occipital cortex, which sends signals via the oculomotor nerve to:

1) constrictor pupillae - miosis
2) ciliaris muscle - lens fattens to increase refractive power
3) medial rectus muscles - eyes converge

NB: fibres do not pass through the pretectal nuclei

239
Q

Pancoast tumour symptoms

A

superior sulcus tumour

Horner syndrome
severe shoulder pain + radicular nerve pain C8/T1
muscle wasting in the hand
paraesthesia + paresis (muscle wasting)

240
Q

Horner’s syndrome

A

combination of symptoms that arises from a sympathetic trunk lesion (and thereby an interruption of the sympathetic nerve supply to the head and neck).

241
Q

Clinical features of horner’s syndrome

A
  • unilateral miosis (loss of sympathetic innervation to dilator pupillae)
  • partial ptosis (loss of innervation to the superior tarsal muscle)
  • unilateral anhidrosis (depends on level of injury - seen in 1st/2nd order lesions)
  • apparent enopthalmus

pancoast tumour causes compression of the second order neuron, which travels over the apex of the lung, causing a second order lesion

242
Q

emissary veins

A

connect the extracranial venous system with the intracranial venous sinuses