Cranial Neraves-Final MBBS MCQ Medicine /Anatomy

3. Bi temporal hemianopia
Causes
• Pituitary tumor – mainly upper outer quadronopia
• Craniopharyngioma-mainly lower outer quadronopia
• Suprasellar meningioma
• Gliomas
• Vascular lesions – aneurysms

4. Also 3rd Nerve supplies to
Levator palpebrae superior –Upper eye lid

5. Sphincter Pupillae Muscle – Cause pupillary constriction

6. General clinical features of 3rd
nerve palsy
• Complete Ptosis
• Dilated pupil
• Opthalmoplegia

7. • Unilateral ptosis
Drooping of upper eyelid due to paralysis of levator palpebrae superior
muscle
• Divergent strabismus
Due to MR palsy and unopposed action of LR supplied by VI nerve. In fact the
eye will be “Down & out” because the SO (IV nerve) is unatagonised by the
paralysis SR ,IR,IO muscles
• Opthalmoplegia
Impaired adduction of eye due to paralysis MR
• Mydriasis (Dilated pupils)
Due to involvement of parasympathetic nerve supply from “Edinger-
westphal nucleus”. These fibers are located superiorly , thus in external
compression they are affected first making pupil dilated.
• Loss of accomadation feflex
Due to involvement of cillary muscle

8. Types of strabismus

9. Opthalmoplegia
• Ophthalmoparesis refers to weakness (-paresis) or paralysis (-plegia)
of one or more extraocular muscles which are responsible for eye
movements.
• It is a physical finding in certain neurologic, ophthalmologic, and
endocrine disease.
• 2 types
o Internal ophthalmoplegia means involvement limited to the pupillary sphincter and
ciliary muscle.
o External ophthalmoplegia refers to involvement of only the extraocular muscles.
Complete ophthalmoplegia indicates involvement of both.

10. Causes for opthalmoplegia
Ophthalmoparesis can result from disorders of various parts of the eye and nervous system:
• Infection around the eye. Ophthalmoplegia is an important finding in orbital cellulitis.
• The orbit of the eye, including mechanical restrictions of eye movement, as in Graves' disease.
• The muscle, as in progressive external ophthalmoplegia or Kearns–Sayre syndrome.
• The neuromuscular junction, as in myasthenia gravis.
• The relevant cranial nerves (specifically the oculomotor, trochlear, and abducens), as in cavernous
sinus syndrome or raised intracranial pressure.
• The brainstem nuclei of these nerves, as in certain patterns of brainstem stroke such as Foville's
syndrome.
• White matter tracts connecting these nuclei, as in internuclear ophthalmoplegia, an occasional
finding in multiple sclerosis.
• Dorsal midbrain structures, as in Parinaud's syndrome.
• Certain parts of the cerebral cortex (including the frontal eye fields), as in stroke.
• Toxic envenomation by kraits.
• Thiamine deficiency can cause ophthalmoparesis in susceptible persons; this is part of the
syndrome called Wernicke encephalopathy. The causal pathway by which this occurs is unknown.
Intoxication with certain substances, such as phenytoin, can also cause ophthalmoparesis.

11. 3rd Nerve Palsy
Where is the lesion?
• The classification of 3rd nerve palsy is as follows
1) Surgical 3rd nerve palsy
• Here the pupillomotor fibers of the 3rd nerve are affected causing
dilation of the pupil
• Seen in lesions of the midbrain and compression of the 3rd nerve
along its course. Due to external compression of the occulomotor
nerve somewhere along it cause.
2) Medical 3rd nerve palsy
Here the pupil is unaffected

12. Anatomy of 3rd
Nerve
Anatomical pathway
Originates at the midbrain at the level of superior colliculus……………passes
between superior cerebellar and posterior cerebellar
arteries…………pierces the dura matter anterior and lateral to posterior
clinoid process……..transverses the cavernous sinus………divides in to two
branches (superior and inferior) at the orbit.
From where it originate
• Oculomotor nucleus- originates at the
level of superior nuclei
• Edinger-westphal nucleus-Supplies
parasympathetic fibers via the ciliary
ganglion.
Superior
colliculus

13. Surgical 3rd nerve palsy-The lesion can be localized
based on the pathway of the 3rd cranial nerve
Form of stoke
characterized by
presence of an
ipsilateral 3rd nerve
palsy.

15. Ptosis

16. Horner syndrome

18. 6th nerve palsy

19. 7th nerve palsy
Where is the lesion?
What is the pathology?
• Both upper and lower parts of the face would be
affected in a LMN lesion
• while only the lower part of the face would be affected in an UMN
lesion
• Bilateral LMN Facial nerve palsy- GBS, Leprosy, B/L Bell’s palsy,
sarcoidosis

24. What are the treatment options available for Bell’s palsy?
• Most patients recover spontaneously
• Physiotherapy
• Electrical stimulation of the facial nerve
• Steroids
• Acyclovir
Lesions of the lower cranial nerves
• This involves lesions of the CN 9, 10 and 12
• Try to identify the clinical pattern of the lesion. These are given below

25. Bulbar palsy and pseudobulbar palsy

28. Nystagmus and cerebellar signs
• There are clinical types of nystagmus.
• These are jerky nystagmus and pendular nystagmus
Pendular nystagmus
Oscillations are equal in speed and amplitude in both directions. Seen in
patients with severe refractory error and macular disease.
Jerky nystagmus
Has a fast phase and a slow phase. Seen in patients with cerebellar disease,
vestibular disease and disorders of their central connections

29. Cerebellar signs
• Scanning dysarthria
• Past pointing
• Rebound phenomenon
• Dysdiadochokinesia
• Pendular knee jerk
• Heel shin test