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Anatomy

Cranial Nerve Lesions

Question 174 of 180

Oculomotor (CN III) palsy with sparing of the pupillary reflex is most likely caused by which of the following:

Answer:

Compressive causes of CN III palsy cause early pupillary dilatation because the parasympathetic fibres run peripherally in the nerve and are easily compressed. In diabetes mellitus the lesions are ischaemic rather than compressive and therefore typically affect the central fibres resulting in pupillary sparing.

Cranial Nerve III: Oculomotor Nerve

The oculomotor nerve (CN III) is responsible for movements of the eyeball and eyelid.

Cranial Nerve Oculomotor Nerve (CN III)
Key anatomy Arises from midbrain, passes through lateral aspect of cavernous sinus, exits skull through superior orbital fissure
Function Motor: innervates four extraocular muscles (inferior oblique, superior, inferior and medial rectus muscles), levator palpebrae superioris muscle (elevation of upper eyelid), sphincter pupillae muscle (pupillary constriction), ciliary muscle (accommodation), efferent pathway of pupillary light reflex
Assessment Eye movements, accommodation, pupillary light reflex
Clinical effects of injury Depressed and abducted (down and out) eye, diplopia, ptosis, fixed and dilated pupil with loss of accommodation and abnormal pupillary light reflex
Causes of injury Tumours, aneurysms (posterior communicating), subdural or epidural haematoma, diabetes mellitus

Function

The oculomotor nerve is a motor nerve innervating all of the extraocular muscles responsible for eyeball movements (except for the superior oblique and lateral rectus muscles) and the levator palpebrae superioris muscle responsible for elevation of the upper eyelid. It also provides the parasympathetic supply to the sphincter pupillae (pupillary constriction) and ciliary muscle (accommodation).

Anatomical Course

The oculomotor nerve arises from the anterior aspect of the midbrain and then passes forwards between the posterior cerebral and superior cerebellar arteries, very close to the posterior communicating artery. It pierces the dura near the edge of the tentorium cerebelli, and passes through the lateral part of the cavernous sinus (together with CN IV and VI nerves and the ophthalmic division of CN V) to enter the orbit through the superior orbital fissure.

Oblique Section through the Right Cavernous Sinus. (Image by Henry Vandyke Carter [Public domain], via Wikimedia Commons)

At this point it divides into a superior branch innervating the superior rectus and levator palpebrae superioris muscles and an inferior branch innervating the inferior rectus, medial rectus and inferior oblique muscles and supplying parasympathetic innervation to the sphincter pupillae and ciliary muscles. The parasympathetic fibres pass on the periphery of the oculomotor nerve.

Oculomotor Nerve. (Image by Henry Vandyke Carter [Public domain], via Wikimedia Commons)

Assessment

The oculomotor nerve should be assessed by testing:

  • Ocular movements (which also tests the trochlear nerve (CN IV) and the abducens nerve (CN VI))
  • Pupillary accommodation
  • Pupillary light reflex (which also tests the afferent optic nerve (CN II)).

Likely Causes of Disease or Injury

Causes of CN III palsy:

  • Compressive aetiology
    • Tumours (commonly by compression against the fixed edge of the tentorium as the medial part of the temporal lobe herniates down)
    • Aneurysms (carotid or posterior communicating artery)
    • Subdural or epidural haematoma
    • Trauma
    • Cavernous sinus disease
  • Ischaemic aetiology
    • Diabetes mellitus
    • Hypertension

Compressive causes of CN III palsy cause early pupillary dilatation because the parasympathetic fibres run peripherally in the nerve and are easily compressed. In diabetes mellitus the lesions are ischaemic rather than compressive and therefore typically affect the central fibres resulting in pupillary sparing.

Common Clinical Effects

CN III palsy results in:

  • A depressed and abducted eye (down and out pupil) due to unopposed action of the lateral rectus and superior oblique muscles
  • Diplopia on looking up and in
  • Ptosis
  • Fixed pupillary dilatation
  • Loss of accommodation (cycloplegia)
  • Abnormal pupillary light reflex
    • Ipsilateral direct reflex lost
    • Contralateral consensual reflex intact
    • Contralateral direct reflex intact
    • Ipsilateral consensual reflex lost

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  • Biochemistry
  • Blood Gases
  • Haematology
Biochemistry Normal Value
Sodium 135 – 145 mmol/l
Potassium 3.0 – 4.5 mmol/l
Urea 2.5 – 7.5 mmol/l
Glucose 3.5 – 5.0 mmol/l
Creatinine 35 – 135 μmol/l
Alanine Aminotransferase (ALT) 5 – 35 U/l
Gamma-glutamyl Transferase (GGT) < 65 U/l
Alkaline Phosphatase (ALP) 30 – 135 U/l
Aspartate Aminotransferase (AST) < 40 U/l
Total Protein 60 – 80 g/l
Albumin 35 – 50 g/l
Globulin 2.4 – 3.5 g/dl
Amylase < 70 U/l
Total Bilirubin 3 – 17 μmol/l
Calcium 2.1 – 2.5 mmol/l
Chloride 95 – 105 mmol/l
Phosphate 0.8 – 1.4 mmol/l
Haematology Normal Value
Haemoglobin 11.5 – 16.6 g/dl
White Blood Cells 4.0 – 11.0 x 109/l
Platelets 150 – 450 x 109/l
MCV 80 – 96 fl
MCHC 32 – 36 g/dl
Neutrophils 2.0 – 7.5 x 109/l
Lymphocytes 1.5 – 4.0 x 109/l
Monocytes 0.3 – 1.0 x 109/l
Eosinophils 0.1 – 0.5 x 109/l
Basophils < 0.2 x 109/l
Reticulocytes < 2%
Haematocrit 0.35 – 0.49
Red Cell Distribution Width 11 – 15%
Blood Gases Normal Value
pH 7.35 – 7.45
pO2 11 – 14 kPa
pCO2 4.5 – 6.0 kPa
Base Excess -2 – +2 mmol/l
Bicarbonate 24 – 30 mmol/l
Lactate < 2 mmol/l

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