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Cranial Nerve

Important Points:

Pure motor cranial nerves                 – III, IV, VI, XI, XII
Pure sensory                                         - I, II, VIII
Mixed                                                     - V, VII, IX, X.

  1. Olfactory nerve –Lesions
    Anosmia Absence of ability to smell – Kallmann syndrome (LQ 2012)
    Hyperosmia Increased sensitivity to smell – migraine, Addison’s diseases, hyperemesis gravida

    Olfactory is the only sensory modality which has no thalamic connection.Q

Extra Edge: Kallmann syndrome = Anosmia + congenital deficiency of hypothalamic gonadotrophic hormone.Q

  1. Second Cranial Nerve (Optic Nerve) –
    Localization –


Lesions in optic pathway

1. Compression of chiasma

Bitemporal hemianopia Q

2. Optic tract lesion

C/L Homonymous hemianopia Q

3. Lesions in optic radiation in temporal lobe

Superior quadrantic homonymous  hemianopia Q (Meyer’s loop)

4. Lesions in optic radiation in parietal lobe

Inferior quadrantic homo. homonymous  Q

5. Occipital cortex

1. Homonymous hemianopia with macular sparing. Q    

2. Cortical blindness

In Right optic tract lesion there is left homomymous hemianopia

IIIrd Nerve


Lesions affecting IIIrd Nerve –

Site - Midbrain                                      Clinical features

1.  Weber’s syndrome (LQ 2012)        = ipsilateral 3rd nerve palsy + contralateral hemiparesis

2.  Nothnagel syndrome                     = Ipsilateral 3rd nerve palsy + contralateral cerebellar signs

3.  Benedikt’s syndrome                     = Ipsilateral 3rd nerve palsy + Contralateral cerebellar signs

4.  Claude syndrome                          = Benedikt’s + Nothnagel syndrome

5.  Dorsal mid brain syndrome           = Parinaud’s syndrome = loss of up gaze, lid retraction, Skew deviation


Pontine syndromes

  1. Ventral pontine syndrome (Millard Gubler syndrome)
    Caused by paramedian infarction of pons
    1. Ipsilateral paresis of lateral rectus with diplopia (damage to abducent fasciculus / nucleus spared)
    2. Ipsilateral paresis of upper and lower face (damage to 7th cranial nerve)
    3. Contralateral hemiplegia with sparing of contralateral face (damage to corticospinal tract)
  2. Lower dorsal pontine syndrome (Foville's syndrome)
    Caused by lesion in dorsal tegmentum of lower pons
    1. Ipsilateral horizontal gaze palsy (damage to nucleus of abducent nerve and paramedian pontine reticular formation.)
    2. Ipsilateral paresis of whole face (damage to nucleus and fibers of 7th nerve)
    3. Contralateral hemiplegia with sparing of Contralateral face (damage to corticospinal tract)
  3. Upper dorsal pontine syndrome (Raymond Ceston syndrome)
    Caused by obstruction of long circumferential branches of basilar artery
    1. Ipsilateral ataxia and coarse intention tremor (damage to superior and middle cerebellar peduncle)
    2. Ipsilateral paralysis of muscles of mastication and sensory loss in face. (damage to sensory and motor nuclei and tracts of CNS)
    3. Contralateral loss of sensory modalities in the body (damage to spinothalamic tract and medial lemniscus)
    4. Contralateral hemiparesis of face and body (damage to corticospinal tract) may occur with ventral extension of lesion.
    5. Horizontal gaze palsy may occur (as in lower dorsal pontine syndrome)

Locked – In – syndrome: Bilateral ventral pontine lesion


Able to communicate only by vertical eye movement and blinking but otherwise is completely immobile)

  1. Occurs in patients will bilateral ventral pontine lesion
  2. Its most common cause is pontine infarction.
  3. Patient
    1. Is quadriplegic (bilateral damage to corticospinal tract in ventral pons
    2. Is unable to speak and incapable of facial movements (involvement of corticobulbar tracts)
    3. Has limited Horizontal eye movements (bilateral involvement of nuclei and fibres of 6th CN)
    4. Has intact vertical eye movements and blinking (supranuclear ocular motor pathways are spared)
    5. Has preserved consciousness (reticular formation is not damaged)

Extra Edge  Locked-in syndrome (Ref. Hari. 18th ed., Pg- 2247)

  1. Locked-in syndrome is a condition in which a patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eyes.
  2. Total locked-in syndrome is a version of locked-in syndrome where the eyes are paralyzed as well. It is the result of a brain stem lesion in which the ventral (anterior) part of the pons is damaged.
  3. Locked-in syndrome is also known as cerebromedullospinal disconnection, de-efferented state, pseudocoma, and ventral pontine syndrome.


Extra Edge: Blink reflex is used for mid pontine lesion.(AIIMS Nov 2012)

Lesion affecting VI nerve –


Site Clinical features

Pons  Millard – Gubler synd =  ipsilateral VI, VII palsy +  C/L hemiparesis                                                                                          

Foville’s syndrome = lat. gaze palsy, ipsilateral VI, VII, palsy,  C/L hemiparesis


Extra Edge (Ref. Hari. 18th ed., Pg- 3434) 

  1. Headache and earache are the most frequent symptoms of transverse sinus thrombosis.
  2. A transverse sinus thrombosis may also present with otitis media, sixth nerve palsy, and retroorbital or facial pain (Gradenigo's syndrome).
  3. Sigmoid sinus and internal jugular vein thrombosis may present with neck pain.

V Cranial Nerve (Trigeminal Nerve) –

Anatomy –

  1. Sensory system – Ophthalmic div – forehead, nose.
    1. Maxillary div – Malar region, upper lip
    2. Mandibular div – Chin. lower lip
  2. Motor system – Masseter ms.Q Temporalis ms.Q  Pterygoid ms.Q
  3. Reflexes –
  1. Corneal reflex – Receptor Free nerve ending (pain)
                          Aff Trigeminal nerveQ  Eff Facial nerveQ
    This reflex lost in any lesion involving this reflex arc. Also lost in lesion of parietal lobe.
  2. Jaw Jerk – Exaggerated in pseudobulbar palsy.Q
  3. Blink reflex/glabellar reflex/orbicularis oculi reflex.
    Aff – Trigeminal nerveQ     Eff – Facial nerveQ

Clinical Features-

  1. Nuclear lesion
    1. This occur due to diseases affecting pons, medulla and upper cervical cord upto C2

      Causes -
  2. Tumour, Demyelination, Vascular lesion, Syringomyelia, Syringobulbia.
  3. Pontine lesion – Ipsilateral atrophy and weakness of the muscles of mastication along with ipsilateral facial sensory loss with C/L hemiplegia.
  4. Lower medulla & upper cervical cord
    1. Ipsilateral loss of pain and temp. over the face and C/L hemiplegia   
    2. Causes – Tumour, abscess, Herpes zoster.
    3. It is associated with a number of complications like pain, uveitis, keratitis and corneal perforation.

Reader’s paratrigeminal syndrome –

  1. This results due to lesion close to the Gasserian ganglion.
  2. It is characterized by unilateral Horner’s syndrome without facial anhidrosis (as the pseudomotor fibres to the face are not involved) and ipsilateral loss of facial sensation.

Post ganglionic lesions –


Causes – cavernous sinus lesion (III, IV, VI also)
              Gradenigo’s syndrome (ophth + Max div. + VI + Retrobulbar pain)

Petrous apex Mastoiditis - Gradenigo’s syndrome = Deafness, diplopia, headache, Ipsilateral VI palsy

Cavernous sinus Thrombus       III, IV, V, VI, N lesion  

Trigeminal Neuralgia  
(Ref. Hari. 18th ed., Pg- 3361)

  1. Paroxysm of intense pain in the distribution of fifth nerve usually Unilateral, mainly in the mandibular and maxillary area due to anomalous intracranial vessel and compressing trigeminal root.
  2. Face screw up with pain (Dic douloureux) triggering factors are face wash, eating, shaving.
  3. Patient are usually above 50 years
  4. Secondary causes are aneurysm, tumor, multiple sclerosis
  5. Treatment –
    1. Drugs therapy
      1. Carbamazepine
      2. Gabapentin (LQ 2012)
    2. Surgical therapy. (Ref. Hari. 18th ed., Pg- 3361)
      1. The most widely used method currently is microvascular decompression to relieve pressure on the trigeminal nerve as it exits the pons.
      2. Gamma knife radiosurgery is also utilized for treatment and results in complete pain relief in more than two-thirds of patients.
      3. Another procedure, radiofrequency thermal rhizotomy, creates a heat lesion of the trigeminal (gasserian) ganglion or nerve.

VII cranial nerve (Facial nerve) –


Anatomy – Upper half of the face has a B/L representation whereas the lower half of face has a unilateral representation.

Table: Functional components of the facial nerve




Somatic motor

VII nucleus in pons: facial nerve

Muscles of facial expression + stapedius

Visceral efferent parasympathetic

Superior salivary nucleus: nervus intermedius

Lacrimal gland, submandibular and sublingual salivary glands

Special afferent (taste)

Lingual nerve, chorda tympani, geniculate ganglion, nervus intermedius, tractus solitarius

Taste sensation on anterior 2/3 of tongue

Somatic afferent

Geniculate ganglion

Cutaneous sensation to external ear


Localisation of Lesion –




Clinical features

1. Cortex (supranuclear)

cerebral infract-

C/L facial weakness (upper part of face spared)

2. Pons

Infract- /Hemg.

LMN type of face weakness often VI nerve also affected C/L hemiparesis Millar Gubler syndrome  

3. Cerebellopontine angle neuroma


LMN type of I/L facial weakness tinnitus.
Ophth div of V nerve also affected

4. Facial conal (Petrous bone)

Bell’s palsy
Herpes zoster
(Ramsay Hunt synd)

LMN type of weakness loss of taste, salivation & Lacrimation (proximal to chordee)
Hyperacusis (Proxi to n. to stapedius)

Common causes of VII nerve palsy




1. UMN type

1. UMN type

a. Vascular

a. Multi infract dementia

b. Cerebral tumour

b. Motor neuron disease

c. Multiple sclerosis


2. LMN type

2. LMN type

a. Bell’s palsy

a. Guillain – Barre syndrome

b. Parotid tumour

b. Sarcoidosis        

c. Diabetes

c. Leprosy



B/L UMN palsy

B/L LMN palsy

a. Bell’s phenomenon –



b. Emotional fibres –



c. Long track Signs –



d. Jaw jerk –



e. Corneal reflex –



Bell’s Palsy – 
(Ref. Hari. 18th ed., Pg- 3363)

  1. Acute onset non – suppurative inflammation of the facial nerve with in the facial canal above the stylomastoid foramen.
  2. Pathophysiology (Ref. Hari. 18th ed., Pg- 3362)
    1. In acute Bell's palsy there is inflammation of the facial nerve with mononuclear cells, consistent with an infectious or immune cause.
    2. Herpes simplex virus (HSV) type 1 DNA was frequently detected in endoneurial fluid and posterior auricular muscle, suggesting that a reactivation of this virus in the geniculate ganglion may be responsible for most cases.
  3. Risk factors – Diabetes, Hypertension, herpesvirus type 1

Poor prognostic factors –

  1. Age > 60yrs.                       
  2. Decrease Lacrimation                 
  3. Hyperacusis                
  4. Diabetes, Hypertension
  5. Total paralysis at the onset

Complications –

  1. Incomplete recovery
  2. Contracture
  3. Crocodile tears
  4. Cross innervation

Treatment  (Ref. Hari. 18th ed., Pg- 3363)

  1. Artificial tears (osmoles drops)
  2. Recovery spontaneous in 70 – 80% pt with in 2 – 12 weeks
  3. A course of glucocorticoids, given as prednisone 60–80 mg daily during the first 5 days and then tapered over the next 5 days, appears to shorten the recovery period and modestly improve the functional outcome.
  4. Physiotherapy
Important Points: Bell's Palsy: (AIIMS May 2010)

No added benefit of acyclovir (400 mg five times daily for 10 days) compared to prednisolone alone for treatment of acute Bell's palsy.


Extra Edge: Möbius syndrome (LQ 2012)

  1. It is an extremely rare congenital neurological disorder
  2. It is characterized by facial paralysis and the inability to move the eyes from side to side.
  3. Most people with Möbius syndrome are born with complete facial paralysisand cannot close their eyes or form facial expressions.
  4. People with Möbius syndrome have normal intelligence, although their lack of facial expression is sometimes incorrectly taken to be due to dullness or unfriendliness.

Melkersson–Rosenthal syndrome (LQ 2012)

  1. It is characterized by recurring facial paralysis, swelling of the face and lips (usually the upper lip), and the development of folds and furrows in the tongue. 
  2. Onset is in childhood or early adolescence. After recurrent attacks, swelling may persist and increase, eventually becoming permanent.
  3. The lip may become hard, cracked, and fissured with a reddish-brown discoloration.
  4. The cause of this is unknown, but there may be a genetic predisposition.
  5. It can be symptomatic of Crohn's disease or sarcoidosis.
Important Points:-  Ramsay – Hunt Syndrome

This is due to affection of the geniculate ganglion by Herpes zoster. Q (LQ 2012)

  1. Vesicular lesions over ext. auditory meatus & pharynx.
  2. LMN type of facial nerve palsy
  3. Loss of taste, salivation & lacrimation
  4. Hyperacusis     
  5. Often VIII nerve also affected

Mimic Paralysis


It is due to frontal or thalamic lesions Q, which abolish the C/L emotional movements of the face, leaving the voluntary movement unimpaired


Important Points:
  1. IX Cranial Nerve (Glossopharyngeal nerve)
    It supplies taste sensation to post. third of tongue. It also supplies stylopharyngeus muscleQ.
  2. X Cranial nerve – (Vagus nerve)
    1. It is the longest cranial nerve. It supplies ms. of soft palate except tensor palatiQ, pharynx, larynx. It also supplies resp. tract, heart and abdominal viscera.
    2. Dysphagia
      1. To solid food – UMN type               
      2. To liquid – LMN type
  3. Tests –
    Usually both IX and X cranial nerves are tested simultaneously
    1. Taste from post. 1/3 of tongue.
    2. Palatal reflex – Elevation of soft palate on both sides and position of uvula is noted.
      1. Unilateral palatal palsy – The palatal arch on that side is at a lower level than on the healthy side. On saying ‘ah’ the uvula is pulled to the healthy side by normal palate.
      2. B/L palatal palsy – The palate remains immobile on both sides.
    3. Palatal myoclonus – Seen in autosomal dominant cerebellar ataxia or olivopontocerebellarQ atrophy. This movement is present even during sleep.
      Site of lesion - Triangle of Guillain and Mollaret (Triangle formed b/w Red nucleus, Dentate nucleus and olivary nucleus)
    4. Gag reflex –
      1. Absent – LMN type of palsy                
      2. Exaggerated – UMN (Pseudobulbar palsy)

XI Cranial nerve (Accessory nerve)


Two parts:

  1. Cranial
  2. Spinal
  1. The spinal part arise from lat. column of spinal cord foramen magnum Joins cranial part Emerge through Jugular foramen.
  2. It supplies trapezius and sternocleidomastoid.

Lesion of IX, X, XI




Clinical features

Jugular foramen (Vernet syndrome)

Glomus tumour Meningioma

IX, X + weakness of trapezius & sternocleidomastoid

Lateral sinus thrombosis (LST) (LQ 2012)

  1. It is usually occurs as a complication of middle ear infection.
  2. Griesinger's sign: Erythema and edema over the mastoid process due to septic thrombosis of the mastoid emissary vein and thrombophlebitis of the sigmoid sinus
  3. The most frequent presenting symptoms were headache, otalgia, fever, otorrhoea & vomiting and pain in the neck.
  4. Severe headache, otalgia, “picket-fence” fever, and papilloedema are regarded as specific symptoms and signs for LST.
  5. Extension of thrombophlebitis in to the jugular bulb and internal jugular vein may present as tender mass in the neck along or across stenocleidomastoid muscle. 9th, 10th, 11th cranial nerve may be paralyzed by the presence and pressure of clot in the jugular bulb

XII cranial nerve

Hypoglossal nucleus (in the floor of 4th ventricle) Hypoglossal canal of the skull Neck Tongue

                                               LMN palsy           UMN palsy

1. Tongue Wasting                 Present                      Absent

2. Tongue Fibrillation            Present                     Absent

3. Tongue Protrusion             Possiblex                   Difficult

4. Tongue muscle                 Flaccid                      Spastic

5. Jaw jerk                             Normal                    Exaggerated

Lateral Medullary Syndrome


It is due to occlusion of:

  1. V4 segment of vertebral artery (Ref. Hari. 18th ed., Pg- 3288)
  2. Post. inf. cerebellar artery (PICA) (VA > PICA)

It is also known as Wallenberg’s syndrome.


A. On the side of lesion

Symptoms & signs

Structures involved

1. Pain, numbness over half of face

 Descending tract and V nerve nucleus.

2. Ataxia of limb

Cerebellar hemisphere, fibre
spinocerebellar tract.

3. Nystagmus, diplopia, vertigo,

Vestibular nucleus.

4. Horner’s syndrome

Descending sympathetic tract

5. Dysphagia, hoarseness, gag reflex negative

IX, X nerve.

6. Loss of taste

Nucleus & tractus solitarius

7. Numbness of arm, trunk, leg

Cuneate & gracile nuclei.

B. On the opposite side
• Impaired pain and thermal sense  
  Over half of body  → Spinothalamic tract.

Medial Medullary Syndrome


Symptoms & signs

Structures involved

1. Paralysis with atrophy of half the tongue

Ipsilat. XII nerve nucleus

2. Paralysis of arm, leg sparing face

Contralateral pyramidal tract.

3. Impaired proprioception

Contralateral Medial lemniscus


Total unilateral medullary syndrome (occlusion of vertebral artery) combination of lateral + medial medullary syndrome
  1. Lateral medullary syndrome = Ipsilateral 10th,   8th , 5th, Horner syndrome, Contra lateral loss of pain touch and temperature.
  2. Medial medullary syndrome = Ipsilateral 12th nerve palsy, C/L loss of position and vibration sense.
    (In Right side 12th nerve LMN palsy, on protruding tongue, it deviates to same side ( Right Side)
    If lesion occur at jugular foramen (Just outside the skull)  9th , 10th , 11th , 12th nerve palsy occur.

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