U17 Flashcards
After bumping her forehead into a door frame, 32-year-old Jenny entirely lost her sense of smell. This anosmia persisted the following day, prompting Jenny to visit her GP. The GP referred her to her local hospital for an MRI scan which revealed a contusion to her frontal lobe and a fractured ethmoid bone.
Which cranial nerve is likely to have been damaged?
Olfactory
Lucy has abducens nerve palsy after a brain tumor. What will her symptoms be?
Looking inwards - unnopposed adduction, gets double vision when tries to look to the left.
Barry, a 68-year-old male, presents to his GP with a loss of visual acuity in his right eye. Following a head CT, a tumor was discovered to be compressing his optic nerve. Does this lesion exist anterior or posterior to the optic chiasm?
Anteiror to optic chiasm asone eye affected
Following a recent blow to the head, Jasmine has noticed that her right eye is always looking slightly upwards and towards her nose, and that she is having to tilt her head a lot to see in a straight line.
Which of Jasmine’s cranial nerves has been damaged?
Why is her right eye elevated and adducted?
Superior oblique not being innervated – trochlear
45 year-old Glynn has, over a period of several weeks, lost his lateral field of vision in both eyes. After arriving at his local hospital, he was sent for a head CT that revealed a pituitary tumor that was pressing on his optic chiasm, causing a condition known as bitemporal hemianopia.
Can you explain how this tumor is causing this specific problem?
Pressing on optic chiasm where fibres decussate so causing bilateral hemianopia
Over the last few weeks, Jake, a 23-year-old shop assistant, has noticed his right upper eyelid beginning to droop significantly. At an appointment with his GP, a light was shone into his eye and the practitioner noticed that the pupil in his right eye was dilated compared to that of his left.
Is Jake suffering from Horner’s Syndrome or Oculomotor Nerve Palsy?
With reference to the eye, compare and contrast signs/symptoms that you might expect with CNIII palsy and Horner’s syndrome.
This is Oculomotor palsy
- Horners – affected weating on one side of face and drooping of eyelid
- Oculomotor nerve palsy – down and out, miosis
Which cranial nerves have PS function
3,7,9,10
- CN I
- Where does it arise
- How does it exit the base of the cranium
- Function
- Exam
- CN I - Olfactory
- Where does it arise = Cerebrum
- How does it exit the base of the cranium = cribiform plate
- Function = Smell, sensory function.
- Exam = change in taste or sense of smell. Test each nostril and aks to identify smeell. Keep eyes closed.
- CN II
- Where does it arise
- How does it exit the base of the cranium
- Function
- Exam
- CN II - optic
- Where does it arise - cerebrum
- How does it exit the base of the cranium - optic canal
- Function - vision
- Exam - visual acuity (snellen chart), colour perception, visual fields (quadrants), accomodation reflex, pupillary light reflex, visual body reflexes, fundosocpy.
- Pituitary adenoma – Lies close proximity to optic chiasm. Compression of optic chiasm particularly affectd fibres that are crossing over from nasal half of each retina which produces visual defect affecting peripheral vision in both eyes (bitemporal hemianopia). Need surgery with transsphenoidal approach (via sphenoid sinus)
- CN III
- Where does it arise
- How does it exit the base of the cranium
- Function
- Exam
- CN III = Occulomotor Nerve
- Where does it arise = midbrain-pontine junction
- How does it exit the base of the cranium = superior orbital fissure
- Function = PS to structures in body orbit, innervate smajority of extraocular eye musces. Also symp fibres run with occoulmotor nerve to innervate superior tarsal muscle
- Exam = pupillary light reflex, pupillary accomodation, check nystagmus/ptosisis, follow H
- CN IV
- Where does it arise
- How does it exit the base of the cranium
- Function
- Exam
- CN IV = Troclear nerve
- Where does it arise = midbrian (posterior side)
- How does it exit the base of the cranium: superior orbital fissure
- Function - motor - contralateral superior oblique - depress and intort eyeball
- Exam - in conjucntion with oculomotor + abducents for movements of the eyes (follow h and check double vision)
- Plasy of trochlea nerve - vertical diplopia exacerbated when looking down + in and can develop head tilt away from affected side. Commonlyc aused by microvascular damage from DM/hypertensive disease. Also congenital malformation, thrombophlebitis of cavernous sinus and raised intracranial pressure.
- CN V
- Where does it arise
- How does it exit the base of the cranium
- Function
- Exam
- CN V- Tirgeminal
- Where does it arise= pons
-
How does it exit the base of the cranium:
- Opthalmic - superior orbital fissure
- Maxillary - formaen rotundum
- Mandibular - foramen ovale
- Function - motor -mandibular branch only for muscles mastication (medial pterygoid, lateral pterygoid, masseter and temporalis and other 1st arch derivatives). Ps (travel with branche sof this nerve)
- Exam - Sensory (cotton wool then neurotip of areas), motor – clench jaw palpate temporalis and masseter and then move mouth right and left. Corneal reflex test.
- CN VI
- Where does it arise
- How does it exit the base of the cranium
- Function
- Exam
- CN VI = Abducens
- Where does it arise = Pontine medulla junction
- How does it exit the base of the cranium = superior orbital fissure
- Function = motor - lateral rectus muscle (abducts eyeball)
- Exam = in conj, with occulomotor and rochlea for movements of the eyes (Draw H)
- Abducens nerve palsy - anything leading to downward pressure oon brain stem and can stretch the nerve from its origin. Also diabetic neuropathy and thrombophlebitis of cavernous sinus. Diplopia, affected eye resting in adduction and inability to abduct the eye. Patient may be able to compensate by rotating head to allow eye to look sideways
- CN VII
- Where does it arise
- How does it exit the base of the cranium
- Function
- Exam
- CN VII = Facial nerve
- Where does it arise = pontine medulla junction
- How does it exit the base of the cranium = internal acoustic meatus
-
Function =
- Motor - muscles facial expression, posteiror belly igastric, stylohyoid, stapedius muscle
- Sensroy - small area aorund concha of external ear
- Special sensory- special taste to anterior 2/3 tongue via chorda tympani. Exits via petrotympanic fissure and enters infratemporal fossaand hitchhikes with lingual nerve.
- PS - supplies many of the glands of head and neck (submandibular, sublingial glands, nasal, palatine, pharyngeal mucous glands and lacrimal glands
- Exam =symmetry at rest, rase eyebrows, close eyes tightly, blow out cheeks, smile.
Damage:
- Intracranial – muscles facial expression paralysed or severely weakened. Chorda tympani (reduced slaovation + loss taste ipsilateral 2/3 tongue), nerve to stapedius (ips hyperacusis-sensitive sound), greater petrosal (ips reduced lacrimal fluid production). Mostly from infection of middle or external ear and if no cause found then bells palsy.
- Extracranial – motor function only o paralysis or severe weakness of facial expression muscles. Could be from aprotid gland patho, infection of nerve, compression in forceps delivery or idiopathic (bells palsy)
- CNVIII -
- Origin -
- Exit cranium -
- Function -
- Exam -
- CNVIII - vestibulocochlear
- Origin - pontine medulla junction
- Exit cranium - internal acoustic meatus
- Function - Hearing and equilibrum
- Exam - hearing by whispering at 2 distances and Rinnes/Webers
- Vestibular neuritis – inflammation vertigo, nystagmus, loss equilibrium, nausea and omitting.
- Labyrinthitis – inflamm labyrinth. Sensorineural eharing loss, tinnitus.
- CN IX =
- Origin =
- Exit cranium =
- Function =
- Exam =
- CN IX =glosospharyngeal
- Origin = meudlla oblongata
- Exit cranium = jugular foramen
-
Function =
- Sensory - oropharynx (pharyngeal branch), carotid body, sinus, posterior 1.3 tongue (lingual branch), middle er cavity and eustachian tube.Tonsillar branch for palatine tonsils.
- Special sensory – taste sensation to posterior 1/3 of tongue via lingual branch
- PS – PS to parotid gland.
- Motor – stylopharyngeus muscle of pharynx (Shortens + widens pharynx and elevate larynx in swallowing)
- Exam =– cough, say ‘ah’ and visualise palate ( upwards) and posterior pharyngeal wall.
- Gag reflex - GP supplies sensory to oropharync and carries afferent info for gag reflex. If absent then damage to glossopharyngeal nerve.
- CN X =
- Origin =
- Exit cranium =
- Function =
- Exam =
- CN X = Vagus nerve
- Origin = medulla oblongata
- Exit cranium = jugular foramen
-
Function =
- Sensory – skin of external acoustic meatus and internal surfaces of laryngopharynx and larynx (internal laryngeal nerve). Visceral sensation to heart (cardiac branches) and abdominal viscera.
- Special sensory – taste sensation to epiglottis and root tongue
- Motor – mot muscles pharynx, soft palate + larynx
- PS – smooth muscle trachea, bronchi, GIT and heart rhythm regulator.
- Exam = Gag reflex, open mouth say “ah”
- CV disorders - vasovagal syncope, hoarse voice…
- Gi lesions - dysphagia, palatoglossal arch drop, ulnar deviates away form affecing side
- RLNS lesions 0 dysphonia, aphonia, stridor
- CN XI =
- Origin =
- Exit cranium =
- Function =
- Exam =
- CN XI = Accessory nerve
- Origin = Medulla oblongata
- Exit cranium = jugular foramen
- Function = Moto - SCM, trapexius, retract scapula, pull scapula inferiorly.
- Exam = Rotae ehad, shrug shoulder nromal and against reistsance
- Palsy of accessory nerve – iatrogenic mostly like cervical lymph node excision. Muscle wasting and partial paralysis o SCM so cant rotate head or weakness in shrugging shoulders and asymmetrical neckline.
- CN XII =
- Origin =
- Exit cranium =
- Function =
- Exam =
- CN XII = Hypoglossal nerve
- Origin = Medulla oblongata (anteiror to olive)
- Exit cranium = Hypoglossal canal
- Function = Motor = Extrinsic muscles (genioglossus, hypoglossus, styloglgossus – all bar palatoglossus which is vagus) and intrinsic (superior longitudinal, inferior longitudinal, transverse, vertical)
- Exam =protrude tongue, push tongue against cheek, feel for pressure
- Hypoglossal nerve palsy – could be from head and neck malignancy an penetrating traumatic injuries. Acute pain can suggest internal carotid artery dissection. Deviation tongue to damaged side on protrusion and muscle wasting and fasciculations on affected side.
What are the descending tracts of the CNS
Motor signals -> LMN. Neurones synapse with LMN as termination. Cell bodies in cerebral cortex or brain stem and axons in CNS as UMN.
- Pyramidal – cerebral cortex -> spinal cord -> brain stem. Voluntary control of musculature of body and face
- Extrapyramidal tracts – Brain stem -> spinal cord. Involuntary + autonomic control musculature (including muscle tone, balance, posture and location)
Pyramidal tarcts
Pass through medulalr pyramid
- Voluntary control of musculature of the body and face
- Corticospinal tracts = musculature of the body
- Corticobulbar tracts = musculature of head and neck.
Describe the path of the corticospinal tract
- Begin in cerebral cortex.
- Inputs = Primary motor cortex, premotor cortex, supplementary motor area (also somatosensory area to regulate activity ascending tracts).
- Descends through internal capsule (susceptible to compression from haemorrhagic bleeds- capsular stroke, leading to lesion of descending tracts).
- Neurones pass through crus cerebri of midbrain, pons and into medulla
- In most inferior (caudal) part of medulla, tract divides into two:
- Lateral corticospinal tract fibres decussate + descending into spinal cord, terminating in ventral horn then LMN -> muscles of body.
- Anterior corticospinal tract remains ipsilateral, descending into spinal cord. Then decussate and terminate in ventral horn of cervical and upper thoracic segmental levels.
WHta happens if you damage the corticospinal tract
If only unilateral lesion of R/L CS tract symptoms appear on contralateral side of body.
Hypertonia, Hyperreflexia, Clonus (invol, rhythmic muscle contractions), Babinskis sign (extension of hallux in response to blunt stimulation of sole of foot), muscle weakness.
Corticobulbar tract - the pathway
- Begin in lateral aspect of the primary motor cortex.
- Inputs - Primary motor cortex, premotor cortex, supplementary motor area (also somatosensory area to regulate activity ascending tracts).
- Converge + pass through internal capsule -> brainstem
- Neurones terminate on motor nucleus of cranial nerves + synapse with LMN which carry motor signals to muscles of face and neck
- Many of the fibres innervate motor neurones bilaterally but some exceptions:
- UMN for facial nerve have contralateral innervation – only affects muscles in lower quadrant of face
- UMN for hypoglossal nerve only provide contralateral innervate.
Damage to the Corticobulbar tract
(UMN)
Unilateral lesions usually results in mild muscle weakness due to bilateral nature. Few exceptions:
- Hypoglossal nerve – Lesion to UMN for CNXIII -> spastic paralysis of contralateral genioglossus so deviation of tongue.
- Facial Nerve – Lesion to UMN for CNVII -> spastic paralysis of muscles in contralateral lower quadrant of the face.
Extrapyramidal
- Originate in brianstem, carryig motor fibres to spinal cord
- involuntary and automatic control of all musculature including muscle tone, balance, posture + locomotion
- Damage - common in degenerative diseases, encephalitis, tumours. Various types dyskinesias or disorders of involuntary movement.
- 4 tracts: vestibulospinal + reticulospinal (don’t decussate, ipsilateral innervation) and rubospinal + tectospinal (decussate, contralateral innervation).
Vestibulospinal tract
- Medial/lateral pathways. Arise from vestibular nuclei (input from organs of balance) -> spinal cord. Remains ipsilaterally.
- Control balance and posture by innervating ‘anti-gravity’ muscles via LMN.
Reticulospinal tract
Medial reticulospinal tract – from pons. Vol movements, increases muscle tone. Ipsilateral innervation
Lateral reticulospinal tract – from medulla. Inhibits vol movements, reduces muscle tone.
Rubrispinal tract
- Originates from red nucleus (midbrain structure). Fibres emerge and decussate and descend to spinal cord. Contralateral innervation
- Thought to play role in fine control of hand movements.
Tectospinal tract
- Begins at superior colliculus of midbrain (receives input from optic nerves). Neurons quickly decussate and enter spinal cord and terminate at cervical levels spinal cord. Contralateral innervation.
- Coordinates movements of head in relation to vision stimuli.
Describe the tectum of the midbrain
- Located posterior to the cerebral aqueduct.
- Houses 4 colliculi
- Inferior to collicul, trochlear nerve emerges
What never exists between cerebral peduncles
Occulomotor nerve exits between peduncles
What nerve tract runs aorund the supeiror border of the midbrain
Optic tract
WHat level is this image
Midbrain - level of inferior colliculus
What level is this image
Midbrain - level of usperior colliculus
What arteries supply the midbrain?
Basilar artery and branches
What is the pons?
Group of nerves that function as connection between cerebrum adn cerebellum.
What nerves arise from the pons and where abouts?
- CNV – trigeminal – from lateral aspect mid pons
- CN VI – abducent – pontomedullary junction, close to midline
- CN VII- facial – cerebellopontine angle (more lateral aspect pontomedullary junction)
- CN VIII – vestibulocochlear – lateral to facial nerve
The difference in functiion between ventral pons and tegmentum
- Ventral pons - coordinate movement
- Tegmentum. form spart of reticular ofmraiton which is responsible for arpusal and attentiveness. Damage may result in anosognosia for hemiplegia (patients unaware paralysis)
Ascending spinothalamic tracts
Responsible for pain and temp sensation
Ascending medial lemniscus tracts
Fine touch, vibration, proprioception
Descending corticobulbar tracts
Voluntary motor control of face, head, neck
Descending corticospinal tarct
Voluntary motor contorl of body
Where is the main sensory nucleus
Main sensory nucleus (somatosensory from face) + trigeminal motor nucleus = in midpons at level where fibres originate form lateral aspect of pons. 2 nuclei that receive sensory from trigeminal nerve:
Spinal trigeminal nucleus and mesencephalic nucleus
Where is abducens nucleus
controls abducens nerve (innervates ipsilateral lateral rectus muscle). Located on caudal pons.
Where is acial nucleus
Facial nucleus more anterior + lateral at same level to abducens nucleus. Controls muscles facial expression and fibres unusually loop around abducens nucleus before exiting brainstem
Cochlear and vestibular nuclei
– dorsolaterally from inferior pons to superior medulla.
Vasculature to the pons
Most pons – pontine arteries (branches of basilar artery), smaller part from anterior inferior cerebellar artery and superior cerebellar artery (AICA and SCA)
here is cerebello pontien angle syndrome
Often place of intracranial growths which can lead to impairment of nearby structures. Symptoms start with mild impairment of cranial nerve in area (CNVIII).
What is a vestibular schwannoma and the effects
Vestibular schwannomas (Acoustic Neuromas) are the most common growth in the area (lead to cerebllpontine angle syndrome) . They are benign and complications are from compression of structures. Slow growing and related to progressive ipsilateral hearing loss.
- Ipsilateral hearing loss and tinnitus – due to compression of cochlear component of CN VIII
- Disequilibrium. And more rarely vertigo – due to compression of vestibular component of CN VIII
- Nystagmus – due compression of cerebella flocculus
Untreated leads to compression:
- Facial paralysis – due to compression of CN VIII
- Reduced corneal reflex – due to involvement of both CN V and CN VII
- Trigeminal palsy – due to compression of CN V
- Ipsilaterally cerebellar signs
Surgical resection guarantees a very good outcome mostly.
*
Where is this?
Medulla - decussation of pyramids
What level is this
Medulla - decussation medial lemniscus
What level is this
Medulla - level of olives
Vasculature of medulla
Where is this cross section?
Midbrain die to inferior colliculu, cerebral aqueduct and micky mouse
Where is this?
Pons - fourth ventricle, corticospinal tracts
Where is this?
Pons
Where is this?
Medulla - pyramids
Where is this?
Medulla
Where does the nuclei arise from?
- Abducens - caudal pons
- Trigeminal motor - mid pons
- Facial motor - caudal pontine tegmentu
What happens in a Lumbosacral lesion?
Lumbosacral spinal cord lesion: Weakness, wasting, fasciculation of muscles, areflexia of the lower limbs (LMN lesion), incontinence, sensory loss below level of lesion and ‘sensory’ ataxia.
Thoracic spinal cord lesion
Thoracic spinal cord lesion: Spastic paraparesis, hyperreflexia, and extensor plantar responses (UMN lesion), incontinence, sensory loss below level of lesion and ‘sensory’ ataxia.
Lower cervical soinal cord leison - what it involves
Lower cervical spinal cord lesion: Weakness, wasting, fasciculation of muscles, and areflexia of upper limn (LMN lesion) . In addition, there is spastic paraparesis, hyperreflexia and extensor plantar responses(UMN lesion) in lower limbs, incontinence, sensory loss below level lesion and ‘ sensory’ ataxia.
Upper cervical spinal cord lesion -
High cervical cord lesion causes spastic tetraplegia with hyperreflexia, extensor plantar responses (UMN lesion), incontinence, sensory loss below level of lesion and ‘sensory’ ataxia.
Unilateral VS brainstem lesion courses
- Unilateral brainstem lesion = can be caused by stroke, tumour or multiple sclerosis. Causes ipsilateral cranial nerve dysfunction, contralateral spastic hemiparesis, hyperreflexia and an extensor plantar response (UMN lesion), contralateral hemisensory loss and ipsilateral incoordination
- Bilateral lesions = destroys the ‘vital centres; that control breathing and the circulation, leading to coma and death. This usually follows a massive stroke of the brainstem and is the end result of raised intracranial pressure, due to a space occupying lesion, which displaces the cerebellar hemispheres down through the foramen magnum to compress the upper brainstem .
What are the 3 kinds of symptoms caused by focal cerebral lesions
- Focal epileptic seizures
- Sensory/motor deficits
- Psychological deficits eg, language, memory etc.
Where is the brainstem lesion?
Weakness of the left upper and lower limb, deviation of tongue towards the right, loss of vibration and proprioception in the limbs on the left hand side. Where is the lesion:
The right medial medulla
What lesion of braintem is this?
Weakness of the ace, upper and lower limbs on the right hanf side. Left eye turned down and out and pupil dilated
Left medial midbrain
Where is this brianstem lesion:
Altered sensation of pain and temperature on left side of face. Left sided horner’s syndrome, altered sensation of pain and temperature in right arm and leg. An inability to speak (dysarthria), altered gag reflex and an elevated palate on the right. Vertigo.
Left lateral medulla.
Where is this brianstem lesion
Right sided deafness, right sided facial numbness, right sided loss of corneal reflex and right sided hemi-facial spasms.
Right lateral pons
Spinal cord lesions
What tract is this?
- Posterior column- medial lemniscal pathwaydorsal columns
- Somatosensory pathways conveying modalities of conscious proprioception, vibrtion and discriminative touch
Describe the Anterolateral/spinothalamic tract
- Somatosensory pathway converying modalities of pain, temperature and crude touch
- Deccusate at ventral white commissure.
The motor (corticospinal, pyramidal) system
Blood supply to the brain
Stroke related to the carotid artery and its cerebral branches are associated with focal epilepsy, a contralateral sensory/motor deficit and a psychological deficit (eg, aphasa)
Recovery of function can occur, but it may take up to 2years and can be incomplete.
• The internal carotid artery terminates lateral to the optic chiasm, giving rise to the anterior and middle cerebral arteries.
- The anterior cerebral artery passes into the great longitudinal fissure and supplies the medial aspect of the cerebral hemisphere.
- The middle cerebral artery passes into the lateral fissure and supplies the lateral aspect of the cerebral hemisphere.
- The principal terminal branch of the basilar artery is the posterior cerebral artery, which supplies the occipital lobe of the cerebral hemisphere.
Right: Occlusion of the posterior choroidal artery, producing necrosis in part of the thalamus.
Left: Multiple hemorrhages within the brain secondary to head trauma.
Head computed tomography showing two epidural hematomas in a 23-yr-old involved in a motor vehicle accident.
Note air bubbles that are a result of linear fracture in the left temporal bone
EDH between the outer layer of the dura mater and the inner table of the skull. The middle meningeal artery supplies most of the dura mater and the bones of the cranial vault. It is this artery or vein that is usually ruptured in an epidural hemorrhage.
- CT appearance: Variable white to gray on brain windows
- Location: Peripheral to brain, temporal region
- Shape: Biconvex disc or lens
- White swirl sign means active bleeding
- Significance: May cause mass effect and herniation
- Look for midline shift
- Surgery to remove the blood clot and stop the bleeding/Release the pressure by craniotomy
The swirl sign refers to the non-contrast CT appearance of acute extravasation of blood into a haematoma. The most important treatment when a midline shift is present is relieving the pressure that is pushing the brain off-center. If a collection of blood is the cause, such as a subdural hematoma, surgery will be needed to remove the blood clot and stop the bleeding
Epidural hematoma on magnetic resonance image. Brain MRI: More sensitive. Indicated in situations in which there is a strong clinical suspicion but no evidence of EDH on head CT.
Coronal T2-weighted images show hypointense biconvex extraaxial collection in the left temporal region.
• Note : Lumbar puncture (LP) is contraindicated in EDH due to risk of brain stem herniation.
Chronic subdural haematoma. (arrows) . A large haematoma causing mass effect with ventricular shift to the opposite side visualized with MRI. The accumulated subdural blood typically has a crescent shape, as it can flow freely in the subdural space. Larger SDHs, or those causing neurological dysfunction, require surgical drainage; smaller, asymptomatic SDHs can sometimes be followed expectantly.
Different types haematoma and Findings
What is herniation
Uncal herniation occurs when a space-occupying lesion in the temporal lobe displaces the uncus medially, forcing the uncus into the opening of the tentorium cerebelli. In turn, this compresses the midbrain, interfering with the function of the oculomotor nerve and consciousness (effect on ascending reticular activating system).
What is this
A large subdural hematoma displaced the right cerebral hemisphere, causing uncal herniation.
Note the distortion of the shape of the lateral ventricles, and that both lateral ventricles and the third ventricle are to the left of the midline. An infarct of the posterior cerebral artery occurred secondary to uncal herniation.
Sagittal MRI:
Left: Normal – Label it yourself
Right: Pituitary tumor.
Sagittal T1 magnetic resonance imaging (MRI) with contrast.
Pituitary tumors account for approximately 10% of all intracranial neoplasms. Most are benign and slow growing. Symptoms result from the mass pushing on surrounding structures or hormonal hyposecretion or hypersecretion. Symptoms include headaches, nausea and vomiting, irregular menses and lactation, and sexual dysfunction. In addition, the person may have high blood pressure, increased blood glucose level, acromegaly (growth hormone disorder that begins in adulthood, causing gigantism with enlargement of the head, hands, feet), or Cushing’s disease (excessive ACTH, causing fatigue, hypertension, osteoporosis, and abnormal deposits of facial and trunk fat). Because the tumor may compress cranial nerve 3, 4, or 6, the person may experience double vision. Bitemporal hemianopia (loss of both temporal visual fields is common with larger pituitary lesions because the axons cross in the optic chiasm directly above the pituitary gland.
