Download 2 the cranial nerves

Vertebral angiograms: arterial phase
Lateral projection
Post, lateral choroidal aa.
Sup. cerebellar aa.
Post, cerebral aa.
Thalamo\
Frontal projection
Post, pericallosal a.
|
Parietooccipital branch ^ ^
t
Post, temporal branch S> cerPebra| a
Post, cerebral aa.
I
Sup cerebellar aa
Ant. inf.
cerebellar aa
Basilar a
Inf. vermian a.
perforating aa.
\
Post, communicating aa
Basilar a
Calcarine branch I
Tonsillohemispheric
branches
Post. inf. cerebellar a.
Vertebral a.
Ant. inf. cerebellar a
Int. vermian branches
/
of
/
R. and I. post. inf. cerebellar aa.
and
L. hemispheric branch
of I. post. inf. cerebellar a.
Vertebral a.
Posterior communicating aneurysm , A - P & Lateral views ( Carotid Angiogram )
Anterior communicating aneurysm , A - P & Lateral views ( Carotid Angiogram )
Middle cerebral artery aneurysm , ( Right carotid angiogram )
Atherosclerotic stenosis at the origin of the
internal carotid artery ( Carotid
angiogram ) .
Arteriovenous malformation ( AVM ) in the
region of the basal ganglia ( Carotid
angiogram ) .
Normal peumoencephalogram ( Air Encephalogram ) Lateral & A - P ( Towne ) views .
Myelogram , A - P & Lateral views showing extradural block due
to metastasis .
Myelogram , A - P view showing
bulging .
-disk
ffe,
Myelogram , Lateral view showing L 4
disk bulging .
Myelogram , A - P view showing
intramedullary tumour . The spinal cord
shadow is widened .
Myelogram , A - P view showing
syringomyelia . The spinal cord is diffusely
enlarged in a fusiform manner .
Thoracic Myelogram , A - P view showing
intraspinal arteriovenous malformation
( AVM ) ( Multiple serpiginous filling
defects ) .
Myelogram , A - P view showing intradural
& extradural ( dumbbell ) neurofibroma .
Computed cranial tomography ( CT scan ) demonstrating infarction in territories of ( A )
internal carotid ( B ) anterior cerebral ( C ) middle cerebral ( D ) posterior cerebral arteries .
Computed cranial tomography showing hemorrhagic infarction in the distribution of the left
middle cerebral artery .
CT brain scan showing right frontal lobe
abscess .
Normal Isotope Brain Scan .
CT brain scan showing
abscess
.
right occipital lobe
Isotope brain scan , right
lateral & anterior views
showing
carcinomatous
metastases to the brain .
Normal Adult EEC
Sharp waves
Spikes
Spike & wave.
Paroxysmal Patterns
^
^
ALPHA 8 - 1 3 cycles/sec
BETA > 13 cycles/sec
THET.A 4-7 cycles/sec
DELTA <4 cycles/sec
1 second
Basic EEC Rhythms
V - ECHO - ENCEPHALOGRAPHY :
On direction of ultrasonic activity through the skull by an ultrasonic probe, it will be
reflected from the skull walls, ventricles and structures inbetween them. The reflected
echoes are recorded on an oscilloscope and photographed. Displacement of midline
structures to either side could be detected. Both false positive and false negative
echoencephalograms may occur.
VI - ELECTROMYOGRAPHY (EMG):
Recording the electrical activity of muscles, preferably by needle electrodes introduced
into the muscles and connected to a cathode ray oscillograph and to a loudspeaker. A
camera is included to photograph the oscillographic patterns. EMG helps to differentiate
between neurogenic and myogenic lesions.
Indications of EMG :
(/) Diagnosis and follow up of peripheral nerve lesions and facial palsy.
(ii) Differentiation between neurogenic and myogenic lesions.
(/// ) Diagnosis of disorders of voluntary muscles and neuromuscular junction e.g.
myositis, myotonia, muscular dystrophies and myasthenia gravis.
(j'v ) Detection of carriers of muscle dystrophy e.g. in unaffected female carriers of
Duchenne type of muscular dystrophy (pseudohypertrophic type).
(v) Localization of L.M.N.L.
N.B.: The Reaction of Degeneration (RD ):
^
Normally, faradic stimulation —> sustained contraction, while galvanic -> single
twitches on opening and closing the circuit. Denervated muscle fails to respond to
faradic stimulation and gives an abnormally slow prolonged response to galvanic
current.
VII - BIOPSY:
1 . Brain biopsy : may be indicated in some disorders e.g. tumours, dementia,
encephalitis,... etc.
2 . Peripheral nerve biopsy : to differentiate between leprosy, hypertrophic
polyneuropathy and amyloid infiltration.
3 . Muscle biopsy : e.g. in collagenoses, muscular dystrophies and myasthenia gravis.
4 . Liver, kidney, lung, skin, stomach, rectum, bone, or gland biopsy : may be
indicated to detect disorders that may be responsible for nervous system
symptomatolgy e.g. liver cirrhosis, bronchogenic carcinoma,... etc.
VIII - OTHER LABORATORY INVESTIGATIONS :
1 . Blood : RBCs, Platelets, ESR, Blood urea, Blood sugar, ....... etc.
2 . Urine : Glycosuria, Bence - Jones Protein (in myelomatosis), Porphyrins, Creatine
and creatinine (in muscular dystrophy), Phytanic acid (in Refsum's disease), .......
etc.
3 . Faeces : for occult blood, parasitic ova, fats (steatorrheas), ...... etc.
CHAPTER 2 THE
CRANIAL NERVES
I - THE OLFACTORY NERVE
Anatomy : Olfactory neurones in the nasal mucosa -> Olfactory nerve fibres, which pierce
the cribriform plates of the ethmoid bone — > Olfactory bulb -> Olfactory tract — > 2 roots:
* A lateral root — > cortical olfactory area (uncinate gyrus)
* A median root, decussates -> joins the uncrossed lateral root of the contralateral side
-> Uncinate gyrus.
oifactor, ,0.^
^ Olfactor/ Mb
The anterior commissure connects the
Olfactory tract
Orbital $ulci '
olfactory cortical regions of
the two hemispheres together.
Disturbances of the Sense of Smell :
1 . Anosmia : loss of smell.
2 . Parosmia : abnormal unpleasant
smell with or without a persistent
unpleasant olfactory hallucination.
Causes of Anosmia :
(A) Congenital or hereditary.
Optic chiasm
(B) Acquired : e.g.
Mammiliary bodies
Posterior perforated
substanca
Tuber cinereum
olfactory DCIVC (inferior view)
1 . Local infections of the nose e.g. coryza.
2 . Lesions of the olfactory tract e.g.
(/) Head injury with or without fracture base of the skull.
(ii) Olfactory groove meningiomas.
(Hi) Frontal lobe tumours, or obstructive hydrocephalus.
(iv) Basal meningitis.
(v ) Neurosyphilis.
3 . Lesions of the olfactory cortex e.g.
(/) Irritative lesions : cause uncinate fits.
(ii) Destructive lesions :
cause incomplete anosmia due to bilateral representation of olfaction.
Causes of Parosmia :
(/) Head injury.
(ii) Depressive illness.
II - THE OPTIC NERVE
Anatomy of visual pathways :
1 . The Optic Nerves : are the axons of the ganglion cells of the retina. They pass
through the optic foramina and terminate posteriorly at the optic chiasma.
2 . The Optic Chiasma : lies a little behind the sella turcica, with the third ventricle
above and the internal carotid arteries lateral to it. Fibres from the nasal halves of the
retinae decussate in the optic chiasma, while those from the temporal halves do not
decussate, but pass backwards in the ipsilateral optic tract.
3 . The Optic Tracts : Each is composed of uncrossed fibres from the temporal half of
the retina of the same side and crossed fibres from the nasal half of the opposite retina. The
optic tracts bend around the midbrain and end in the superior colliculus , lateral geniculate
body and the pulvinar of the thalamus.
4 . The Optic Radiations ( Geniculocalcarine Pathway ) : Fibres arise from the lateral
geniculate body, enter the posterior limb of the internal capsule, behind the somatic sensory
fibres and medial to the auditory radiations. The upper or dorsal fibres derived from the
upper half of the retina pass directly to the visual cortex, above the calcarine fissure, while
those derived from the lower half of the retina run in the temporal lobe, turn round the tip of
the descending horn of the lateral ventricle, to the visual cortex below the calcarine fissure.
38
5 . The Visual Cortex (area striata ): is located above and below the calcarine fissure
and in adjacent portions of the cuneus and lingual gyrus of the occipital lobe. The upper
quadrants of the retina are represented in the upper part of the visual cortex, above the
calcarine fissure and the lower quadrants below. The main arterial supply of the visual
cortex is the posterior cerebral artery. The macula receives additional supply from the
middle cerebral artery. LESIONS OF THE VISUAL PATHWAYS :
1. Optic Nerve Lesions :
(/) Complete lesion of the one optic nerve produces blindness in the ipsilateral eye.
(ii) Neuritis and compressive lesions lead to a central scotoma. (iii) Papilloedema
produces an enlargement of the blind spot and a peripheral concentric
constriction.
2. Lesions of the Optic Chiasma :
(i) Compression e.g. by a pituitary tumour, suprasellar craniopharyngioma,
meningiomas or cysts, third ventricular tumour or dilatation in hydrocephalus,
I.C. aneurysm or a glioma of the chiasma itself.
(ii) Inflammatory e.g. chronic arachnoiditis or syphilitic meningitis.
(iii) Demyelinating e.g. multiple sclerosis (M.S.) and neuromyelitis optica.
(iv) Vascular and traumatic lesions are rare.
The resultant field defects vary according to the site of pressure :
(a) Midline Pressure of the chiasma results in bitemporal hemianopia (due to
compression of the decussating fibres derived from the nasal halves of both
retinae, which receive images from the temporal halves of the visual fields).
Pressure from below e.g. by a pituitary tumour porduces bitemporal upper
quadrantanopia white pressure from above e.g. by a craniopharyngioma produces
bitemporal lower quadrantanopia.
(b) Compression of the lateral angles of the chiasma is rare e.g. in atheroma of the
internal carotid arteries, produces binasal hemianopia.
3 . Lesions of the Optic Tract: e.g.
A pituitary tumour, temporal lobe tumour, internal carotid aneurysm, posterior
communicating aneurysm and basal syphilitic meningitis. The resultant field defect is
a crossed homonymous hemianopia with loss of the pupillary light reflex if light is
thrown on the cor responding halves of the retinae.
4 . Lesions of the Optic Radiation :
(a) Complete destruction of one optic radiation results in a crossed homonymous
hemianopia with macular sparing.
:(b) Temporal lobe lesions e.g.vascular lesions, tumors or abscess, produce a crossed
homonymous inferior quadrantanopia.
(c) Parietal lobe lesions produce a crossed homonymous inferior quadrantanopia
(d) Irritative lesion produces visual hallucinations.
5. Lesions of the Visual Cortex: e.g. vascular lesions, tumours and gun-shot wounds.
(a) Unilateral destruction of the visual cortex produces a crossed homonymous
hemianopia.
(b) Destruction of the upper half (i.e. the area above the calcarine fissure) produces a
crossed homonymous inferior quadrantanopia.
(c) Destruction of the lower half(\.Q. the area below the calcarine fissure) produces a
crossed homonymous superior quadrantanopia.
(d) Thrombosis of one posterior cerebral artery produces a crossed homonymous
hemianopia sometimes with macular sparing.
(e) Thrombosis of both posterior cerebral arteries produces complete blindness
except for central vision (due to additional supply by middle cerebral artery).
(0 Irritative lesions produce flashes of light.
39
PAPILOEDEMA (Choked Disc): oedema of the optic disc or papilla.
Causes:
1.
2.
3.
4.
Increased intracranial pressure, due to combined venous and lymphatic obstru ction.
Optic neuritis and retrobulbar neuritis.
Malignant hypertension and giant cell arteritis.
Obstructed retinal venous drainage due to orbital tumours, gumma, central retinal
vein thrombosis, cavernous sinus thrombosis, carotid -cavernous aneurysm and
intrathoracic venous obstruction.
5. Some cases of Guillain-Barre syndrome, due to increased protein in the CSF.
6. Other causes e.g. Disseminated lupus erythematosis, reticulosis, infective
endocarditis, carcinomatous neuropathy, hypercapnia, exophthalmos,
hypoparathyroidism, Vit. A poisoning, lead poisoning, profound anaemia,
polycythemia, & emphysema.
Causes of increased intracranial tension:
(i) Brain tumour.
(//) Brain abscess.
(iii) Hydrocephalus.
(iv) Meningitis.
(v) Intracranial sinus thrombosis.
(vi) Subarachnoid haemorrhage.
(vii) Rare causes e.g. emphysema, parathyroid tetany, hypervitaminosis A, & oral
contraceptives.
(viii) Benign increased ICT : the cause is unknown.
(ix) Hypertensive encephalopathy. OPTIC
NEURITIS & RETROBULBAR NEURITIS :
Inflammation of the optic nerve (infective or toxi-infective)
Causes:
1. Demyelinating diseases:
(i) Multiple sclerosis (M.S.). ^ ~
(ii) Schilder's disease.
(iii) Neuromyelitis Optica (Devic's disease).
2. Infective :
(i) Syphilis, toxoplasmosis,
(ii) Ophthalmic herpes zoster.
(Hi) Orbital infections & retinitis, typhoid fever, mumps.
(iv) Meningitis and encephalitis.
3. Toxic causes: e.g. Tobacco, lead, arsenic, methyl alcohol, thalium, quinine, I.N.H.,
carbon bisulphide and some insecticides.
4. Metabolic causes:
(i) Diabetes mellitus.
(//) B12 deficiency.
(iii) Intestinal or uterine haemorrhage.
5. Hereditary degenerations :
(i) Marie's ataxia.
(ii) Friedreich's ataxia.
(///) Leber's optic atrophy.
6. Giant-cell arteritis.
Differential Diagnosis Between Papilloedema and Optic Neuritis
Features
(i) Pain in the eye :
(ii) Visual acuity :
(iii) Visual field:
(iv) Oedema of the disc:
_
Papilloedema
- Absent
- Slight impairment
- Concentric constriction
- Marked.
Optic Neuritis
- Present
- Markedly impaired
- Central Scotoma
- Slight
Retina
Optic nerve
Meyer's loop
Optic
radiation
Commonly encountered visual field defects and
the loci of their corresponding lesions.
A. Right anopsia
B. Bitemporal hemianopsia
C. Bin as ai hemianopsia
D. Left homonymous hemianopsia
E. Left homonymous hemianopsia
F. Left homonymous superior quadrantanopsia
G. Left homonymous inferior or superior quadrantanopsia
H. Left homonymous hemianopsia
Moderate papilloedema
Temporal pallor of optic disc in multiple sclerosis
Unilateral primary optic atrophy
Unilateral optic neuritis
Secondary optic atrophy
Components and Functions of Cranial Nerves
Cranial \erve
Olfactory (I)
SVA
Optic (II)
SSA
Oculomotor (III)
GSE
GVE
Trochlear (IV).
GSE
Trigeminal (V)
GSA
GSA
SVE
Abducens (VI)
GSE
Facial (VII)
SVA
GVA
CSA
GVE
SVE
Component* and Location
Neurosensory cells of sup. nasal
concha and upper i of nasal
septum — » bipolar cells of olfactory epithelium — » olfactory
bulb
Bipolar cells of retina — » ganglion cell layer of retina — » lateral geniculate — * visual cortex
Oculomotor nucleus — >• levator
palpebrae; medial, sup., inf.
recti; inf. oblique
Edinger-Westphal nucleus — *
ciliary and episcleral ganglia to
sphincter pupillae and ciliary
muscle
Trochlear nucleus — » superior
oblique
Sensory endings of skin of face,
mucous membranes, teeth, orbital contents, supratentorial meninges — » trigeminal ganglion
-* spinal trigeminal and chief
sensory nucleus
Muscles of mastication and ext.
ocular muscles — » mesencephalic nucleus
Motor nucleus — » masseters,
temporalis, pterygoids, mylohyoid, tensor tympani, ant. belly
digastric
Abducens nucleus — » lateral
rectus
Taste buds of ant. jf tongue — »
chorda tympani — * geniculate
ganglion — » rostral tractus solitarius
Sensory receptors of tonsil, soft
palate and middle ear to geniculate ganglion — » caudal tractus
solitarius
Sensory receptors of ext. auditory meatus and ext. ear — >• geniculate ganglion — » spinal trigeminal nucleus
Sup. salivatory nucleus — >
greater petrosal n. — » pterygopalatine ganglion — * maxillary
n. — » lacrimal gland, nasal and
palatal mucosa: chorda tympani
to lingual — » submandibular
post. gang, to submandibular
and sublingual glands
Motor nucleus —» facial muscles,
stylohyoid, and post, belly digastric
Function
Smell
Clinical Findings
with Lesion
Anosmia
Vision
Amaurosis, anopia
Eye movements
Diplopia, ptosis
Pupillary constriction, accommodation
Mydriasis, loss of
accommodation
Eye movement
Diplopia
General
sensation
Numbness of face
Proprioccption
Mastication
Weakness, wasting
Eye movement
Diplopia
Taste
Loss of taste ant. $
tongue
General
sensation
General
sensation
Secretion
Dry mouth, loss o*
lacrimation
Facial expression
Paralysis of upper
and lower facial
muscles
Continued
Cranial \crvc
V'estihulocochlear
•VIII)
SSA
SS^ ( «lossophar\ ugeal
S\'A
i IX)
c;v,\
CSA
CVE
Vagus (X)
CVA
GSA SVE
CVE
Spinal accessory
Coinjunicnt* and Location
Hair cc'lls of organ of Corti — *
bipolar cells of spiral ganglion
— * dorsal and ventral cochlear
nucleus
Function
Hearing
Hair cells of crivt.i ampullae,
semicircular canals and maculae of
Equilibrium
saccule anil utricle — * vestib-ular
nuclei and cerebellum
Taste
Taste buds post, i tongue -» inf.
petrosal ganglion — * rostral tractus soliturius
Sensory receptors of ant. surface
epiglottis, root of tongue, border
of soft palate, uvula, tonsil,
pharynx, auditory tube, carotid
sinus and body — » caudal tractus
solitarius
Sensory receptors of middle and
external ear — * geniculate ganglion — » spinal trigeminal nucleus
Nucleus ambiguus — * stylopharyngeus
Inf. salivatory nucleus — » tympani nerve to — » lesser petrosal
nerve — » otic ganglion — >• auricSVA ulotemporal n. — * parotid gland
Taste buds in region of epiglottis
— * inf. (nodose) ganglion — >
SVK
Sensory receptors post, surface
epiglottis, larynx, trachea, bronchi, esophagus, stomach, small
intestine, ascending and transverse colon — *• inf. (nodose) ganglion -* caudal tractus solitarius
Sensor)' receptors in ext. ear and
meatus — » sup (jugular) ganglion
SVE — » spinal trigeminal nucleus
Nucleus ambiguus — * pharyu-geal
constrictor and intrinsic muscles
of larynx, palatal muscles
General
sensation
Hypoglossal (XII)
Ant. horn cells Cl-5 —»
sternocleidomastoid and
trapezius
GSE
Hypoglossal nucleus — * muscles
of tongue
Loss taste post, i
tongur
Anesthesia of
pharynx
General sensation
Elevates pharynx
Partial dry mouth
Secretion
Taste
General sensation
General
sensation
Deglutition,
phonation
Cardiac depress., \
isceral movement,
secretion
Phonation
Dysphagia, hoarseness, palatal
paralysis
Doisal motor nucleus — *• thoracic and abdominal viscera
Caudal nucleus ambiguus — »
vagus — * muscles of larvnx
GSE
Clinical Findings
with Lcxion
Deafness, tinnitus
Vertigo, dysecjuilibrium, nystagmus
Hoarseness
Head and
shoulder
movement
Tongue
movements
Weakness, wasting
Weakness, wasting
TVA—special visceral afferent, SSA — special somatic afferent, SVE — special visceral efferent, GVA— general vis.MrnMii. v . v t
i > f i i « - i . t i ^iscerai ciirirni, v^Sil—genera! soni.iti' "0»T«'nt
!s.I ulTiivui, C3.\—{^tMU.-iai MMuuii
Seventh Nerve Paralysis
Site
Supranuclear lesions
Nuclear or pontine lesion
Extracranial in cerebellopontine angle
Characteristics
Etiology
Weakness of contraiateral,
lower face
Sparing of upper portion of face
Widening of palpebrul fissure
Mouth pulled toward side of
lesion
Total facial paralysis on side of
lesion
Impaired salivary secretion
Taste intact
Impaired lacrimation same side
Associated paralysis of sixth or
fifth nerve on same side
Eyes may be conjugately
deviated toward side of
lesion
Possible intemuclear ophthalmoplegia
Possible contraiateral hemiparesis
Total facial paralysis on side of
lesion
Hearing loss on side of lesion
Episodic vertigo
Corneal re Hex depressed on
side of lesion
Impaired salivary secretion
Impaired lacrimation on side of
lesion ^
Lesion involving corticobulbar
tract above pons
Congenital: Mnbius syndrome
Infectious: < •:<., < phalitis, rabies,
meningitis
alopath\
Neoplastic pontine giioina
Vascular: infarction, hemorrhage
Degenerative: multiple
sclerosis, svringobulbia.
amyotrophic lateral s<. lernsis
Inflammation: meningitis,
tuberculosis, syphilis, fungi
Nroplastic: neurilemoma,
meningioma, dermoid, chordoma, meningeal carcinomatosis
Vascular: aneurysni of basilar
artery
Degenerative: multiple
sclerosis
Paralysis of one or more of the
following cranial nerves:
fifth, sixth, seventh, eighth,
ninth, tenth, twelfth
Extracranial in facial canal
a. Between internal auditory meatus and geniculate ganglion
I). Between geniculate
ganglion and origin of
nerve to stapedius
c. Between origin of
nerve to stapedius and
origin of chorda
tympani
d. Distal to origin of
chorda tympani
Total facial paralysis same side
Hearing loss same side
Impaired lacrimation same side
Impaired salivary secretion
Taste lost anterior two-thirds
tongue same side
Total facial paralysis same side
Impaired salivary secretion Taste
lost anterior two-thirds tongue
same side Hyperacusis
Total facial paralysis same side
Impaired salivary secretion
Taste loss anterior two-thirds
tongue same side
Total facial paralysis same side
only
Traumatic: fractures involving
petrous temporal bone
Infectious: otitis media, mastoiditis, Bell's palsy (see
below), Hei~pes zoster of
geniculate ganglion (Ramsey
Hunt ssndrome) (see below),
sarcoidosis, postinfei-tious
polyneuritis (bilateral)
Metabolic: diabetes mellitus
Neoplastic: cholestearoma,
epidermoid, temporal bone
tumors, parotid gland tumors,
leukemic deposits in facial
canal
seal p.face, eye,
fron & eth. sinuses,
nasal cav.
chief sensory nuc.
cochlear. vestibular nuc
face.sphen. &
max. sinuses,
palate,teeth, gums,
nasal cavity
mastication mm..cheek.
teeth,gums, tongue.
face.ext. ear
facial mm..ext. ear-ant. 2/X
tongue cochlea semicirc.
canals.utr.sac.
post. J^ tongue
pharynx,tongue.ext. & mid.ear
esoph.,thoracic & abd. organs
ext ear -
Ci.uii.il nerve sensory nuclei.
tongue mm
ciliary m.
sph. pupillae
all ocular mm.
except sup. obi.
& lat. rectus
V N. motor nuc.
\ 1 !
mastication mm.,
tens, tympani. ant.
belly digastric,
mylohyoid
VI N. nuc.
VH N. nuc Q\
lacnmal nuc
C1.2.3
Criiruai nerve motor riucl
OPTIC ATROPHY: (Primary and Secondary)
Causes:
1. Familial Disorders e.g.
(/) Cerebromacular Degeneration (Amaurotic family idiocy or Tay-Sachs diseases):
Two forms:
* Infantile form with cherry - red spot in the retina .
* Juvenile form with macular pigmentation, but no cherry-red spot.
It presents with progressive diplegia, mental deterioration, optic atrophy and
convulsions .
(/i) Hereditary Ataxia.
(Hi) Retinitis Pigmentosa.
(iv) Leber's Hereditary Optic Atrophy.
(v ) Congenital optic atrophy.
2. Consecutive Optic atrophy : e.g. in retinitis, choroidoretinitis and central retinal
artery thrombosis.
3. Post papilloedemic optic atrophy.
4. Post neuritic optic atrophy.
5. Syphilitic optic atrophy.
6. Toxic optic atrophy : e.g. tobacco, lead, arsenic, methyl alcohol, quinine, isoniazid,
carbon bisulphide, thalium, diabetes, severe anaemia and some insecticides.
7. Pressure : e.g.
* glaucoma.
* osteitis dcformans (Paget's disease).
* optic nerve glioma, or meningioma of the optic sheath.
* Pituitary tumour or craniopharyngioma.
* suprascllar meningioma, or olfactory groove meningioma.
* glioma of the optic chiasma, or localized arachnoiditis.
* dilated third ventricle in obstructive hydrocephalus.
* arteriosclerotic internal carotid, or intracranial aneurysms.
8. Trauma : e.g. head injury, or surgical division of optic nerve.
Differential Diagnosis Between Papilloedema, Secondary
Optic Atrophy and Primary Optic atrophy
Features
1 . Visual Acuity :
2. Visual field :
3. Ophthalmoscopy :
(i) Optic Disc :
* Colour
* Edges
* Physiological cup
* Swelling
(ii) Retina :
* Haemorrhages
* Exudates
* Retinal veins
* Retinal arteries
4. Signs of increased
ICT:
Papilloedema
Seconday Optic atrophy
Primary optic
atroph;
Early impairment
Central scotoma
Mild impairment
Concentric constriction
Late impairment
Concentric constriction
and enlargement of the
blind spot
Dark pink
Blurred
Filled
Marked oedema
Pale
Blurred
Filled
Flat disc
Whitish or gray
Well defined
Preserved
Absent
Ptesent (flame-shaped)
Present
Congested (Engorged)
Normal
Present
may be present
may be present
Congested
Constricted
Present
Absent
Absent
Normal
Normal
Absoni
CAUSES OF SUDDEN BLINDNESS : 1.
Trauma : Ocular or post-head injury. 3. 2. Vitreous haemorrhage e.g. in diabetics.
Retinal detachment. 5. Embolism of
4. Acute glaucoma.
retinal artery. 7. Cranial arteritis. 9.
6. Thrombosis of retinal vein.
Retrobulbar neuritis. 11. Migraine.
8. Toxins e.g. methyl alcohol.
10. Cerebrovascular accidents.
12. Hysteria.
HI. THE OCULOMOTOR NERVE
Anatomy:
Its nucleus lies in the midbrain anterior to the cerebral aqueduct at the level of the
superior colliculus. The oculomotor nucleus is composed of:
(i) The median single nucleus ofPerlia for convergence and accomodation.
(ii) The lateral paired nucleus ofEdinger Westphal for constrictor pupillae.
(iii) The paired, large-celled, lateral nucleus for levator palpebrae, superior rectus,
inferior oblique, medial rectus and inferior rectus, in this order from above
downwards. Decussating fibres connect the lower parts of the nuclei together.
The third nerve fibres leave the nucleus and pass through the medial longitudinal
bundle, the red nucleus and the medial margin of the substantia nigra to emerge from the
Ed in. West. n.
brain - stem on the
N. Pcrlia
medial side of the crus
cerebri. The nerve
'
passes
forwards
—V- Lev.
between the posterior cerebral
and superior cerebellar arteries along the
posterior communicating artery to enter
through the lateral wall of the cavernous
sinus where it lies close to the fourth, 6th
and ophthalmic division of the fifth nerves.
It enters the orbit through the superior
orbital fissure supplying the above
mentioned muscles.
Features of Third Nerve Palsy :
1. Ptosis : due to paralysis of the levator
palpebrae superioris.
2. External ophthalmoplegia with
divergent squint.
3. Internal ophthalmoplegia : with dilated,
fixed pupil and paralysis of
accomodation.
4. Diplopia is masked by the ptosis of the
upper lid.
•
.
^^
The Oculomotor Nucleus
IV. -THE TROCHLEAR NERVE
Anatomy:
Its nucleus lies below the third nerve nucleus in the midbrain at the level of the inferior
colliculus. The fourth nerve fibres leave the nucleus and turn backwards, then downwards
and medially to decussate before emerging from the dorsal aspect of the midbrain. The
nerve passes between the cerebral peduncle and the temporal lobe, to enter the lateral wall
of the cavernous sinus. It enters the orbit through the superior orbital fissure to innervate
the supericr olbique muscle.
42
Features of Fourth Nerve Palsy :
1. Paralysis of the superior oblique with weakness of movement of the eye downwards
and inwards.
2. Diplopia occurs on looking downwards resulting in difficulty on walking downstairs.
N.B. Lesions in the extracerebral course of the fourth nerve produce ipsilateral paralysis,
while those involving the nucleus or the nerve fibres before their decussation in the
midbrain lead to paralysis of the opposite superior oblique.
VI.- THE ABDUCENT NERVE
Anatomy :
Its nucleus lies in thepons, encircled by the looping fibres of the facial nerve. The nerve
passes forwards through the pons to emerge at its inferior border. It follows a long
extracerebral course along the base of the brain to enter the lateral wall of the cavernous
sinus, then passes through the superior orbital fissure to innervate the lateral rectus muscle.
Features of Sixth Nerve Plasy :
1 . Paralysis of the lateral rectus.
2 . Convergent squint.
3 . Diplopia : apparent on abduction .
THE SUPRANUCLEAR & INTERNUCLEAR PATHS
FOR OCULAR MOVEMENT
(A) Centres For Conjugate Lateral Deviation :
1 . Area 8 in the posterior part of the middle frontal gyrus is concerned with voluntary
conjugate lateral deviation of the eyes (spontaneous or on command). Fibres from
area 8 descend through the corona radiata,and internal capsule to the midbrain,
where they decussate and enter the pons, where they divide, some fibres go to the
nucleus of the sixth nerve, while others cross the midline, ascend in the medial
longitudinal bundle and end in the part of the third nerve nucleus which innervates
the opposite medial rectus.
2 . Cortical area in the visual cortex in the occipital lobe : is concerned with reflex
conjugate deviation.
(B) The Centre For Conjugate Vertical Deviation :
Probably fibres arise in the middle frontal gyrus, pass through the internal capsule,
decussate in the midbrain and end in the parts of the third and fourth nerve nuclei
innervating the elevators and depressors of the eye.
(C) Conjugate Convergence :
Probably, fibres run through the visual cortex, to the middle frontal gyrus,descend with
the pyramidal fibres to the midbrain, where they decussate to end in the nuclei of the
medial recti.
(D) Reflex Conjugate Ocular Fixation : may occur in response to :
(/) Retinal stimulation e.g. by moving an object in front of the patient's eyes.
(//) Auditory stimulation e.g. by a sound.
(Hi) Labyrinthine stimulation e.g. by caloric a«u! rotatory tests.
(zV) Passive movement of the head. (E ) The
Medial Longitudinal Bundle (M.L.B.)
It extends from the midbrain to the pons, connecting the nuclei of the third, fourth and
sixth nerves togther with cochlcar and vestibular parts of the 8th nerve, trigeminal nerve
and spinal accessory nucleus. It associates the lateral rectus with the opposite medial rectus
in conjugate latcro! deviation of tbf P.V
43
EXTERNAL OCULAR MOVEMENTS
Clinical Actions of Extraocular Muscles
Muscle
Cranial Nerve
Medial rectus
ffl
Adduction
Superior rectus
Inferior oblique
Inferior rectus
Superior oblique
Lateral rectus
m
m
m
Elevates when eye abducted
Elevates when eye adducted
Depresses when eye abducted
Depresses when eye adducted
Abduction
Levator palpebrae
Mtiller's muscle
Orbicularis oculi
IV
VI
m
Sympathetic
vn .
Action
Elevates upper lid
Elevates upper lid
Closure of eyelids
Clinical actions of the extraocular muscles
I.O.
= Inferior oblique
S.O. = Superior oblique
S.R.
= Superior rectus
I.R. = Inferior rectus
M.R.
= Medial rectus
L.R. = Lateral rectus
Paralysis of Individual Ocular Muscles : presents with :
1. Defective ocular movement.
2 . Squint (Strabismus).
3 . Erroneous projection of the visual field .
4 . Diplopia (double vision).
OPHTHALMOPLEGIA
Definition: Paralysis of the ocular muscles supplied by the oculomotor nerves III, IV & VI.
CAUSES :
I - SUPRANUCLEAR & INTERNUCLEAR LESIONS :
They cause paralysis of conjugate movements and not of individual muscles.
1 . Lesions of the frontal centres produce loss of voluntary conjugate lateral movement
of the eyes, with preservation of the ability to follow a moving object.
2 . Lesions of the occipital centres produce loss of reflex fixation of a moving objec t,
while voluntary ocular movements are preserved.
1 Pontine lesions abolish both reflex conjugate lateral deviation (loss of the ability to
follow a moving object) and the voluntary conjugate lateral movement (on
command), suggesting the presence of a pontinc centre, common for both voluntary
and R !Vx nuHvmcniN
44
Eye Findings in Cases of Individual Muscle Paralysis
Paralyzed
Upper Lid
Muscle
Superior
Ptosis
rectus
Inferior
oblique
Normal
Normal position
Limited elevation
when eye
adducted
Medial
rectus
Normal
Abducted
Limited adduction
Inferior
rectus
Normal
Normal position
Limited depression particularly
on abduction
Superior
oblique
Normal
Normal position
Limited depres-
Images
Oblique, false above
true — diplopia increases on attempted
elevation and abduction
Oblique, false above
and lateral to true —
diplopia increases on
attempted elevation and
adduction
Crossed, parallel,
diplopia increasing on
attempted adduction
Oblique, false image
below and medial to
true image — diplopia
increases on attempted
depression and
abduction
Oblirjue, false image
sion when eye
below and lateral to
adducted
true — diplopia
increases on attempted
depression and
adduction
Parallel, uncrossed —
diplopia increases on
attempted abduction
and distance vision
Lateral
rectus
Normal
Eye at Rest
Normal position
Movements
Limited elevation
particularly on
abduction
Add ucted
Limited abduction
Paralysis of the Third Cranial Nerve (Oculomotor)
Head
1 lead
tilted
toward
sound
side
Head
turned
toward
arfected
side
Paralysis ol the Sixth Cranial Nerve (Abducens)
tntemuclear Ophthaimoptegta
4 . Spasmodic lateral deviation : may occur in :
(/) Focal epileptic fits due to frontal or occipital lesions.
(ii) Major fits.
(iii) Postencephalitic Parkinsonism.
(iv ) Labyrinthine lesions.
5 . Paralysis of conjugate lateral movement to one side : results from a lesion of the
supranuclear fibres e.g.
(i) Tumours affecting the pontine centre.
(ii) Encephalitis.
(iii) Multiple sclerosis (M.S.)
(iv) Vascular lesions.
Features : (a ) Lesions in the midbrain above the decussation of the supranuclear
fibres cause
paralysis of conjugate lateral movement to the opposite side. (b ) Lesions in the
pons below the decussation produce paralysis of conjugate lateral
movement to the same side.
(c) Lesions of the decussation or bilateral pontine lesions produce bilateral paralysi
(d) Convergence is preserved.
(e) No diplopia, as the ocular axes remain parallel.
6 . Dissociation of conjugate lateral movement (Ophthalmoplegia internuclearis
anterior of Lhermitte) e.g. in multiple sclerosis involving the ascending fibres of
the medial longitudinal bundle linking the lateral rectus on one side with the
opposite medial rectus.
Features:
(i) On conjugate lateral movement, the lateral rectus contracts normally, but the
opposite medial rectus is weak or paralysed. (ii) Convergence is normal i.e.
the affected medial rectus contracts normally on
convergence.
7 . Spasm of conjugate vertical movement upwards : is met with in :
(i) Petit mal fit
(//') Major fit.
(///) Postencephalitic Parkinsonism (oculogyric crisis).
8 . Paralysis of coniugate vertical movement:
The upper midbrain contains a centre for
vertical movement upwards, another for
downward movement and a third one for
convergence. Paralysis of conjugate
vertical movement may be:
(a) Congenital.
(b) Acquired : e.g. encephalitis,
third ventricular tumours midbrain
tumour, pinealoma and vascular
lesions of the midbrain.
Gaze Paralysis
9 . Paralysis of Convergence : may occur in :
(/) Postencephalitic Parkinsonism.
(ii) Midbrain lesions involving the convergence centre.
(iii) Head injury.
(iv) Hysterical.
Features:
(a) Loss of convergence alone or together with loss of vertical conjugate movement
with or without loss of the pupillary light reflex.
(b) Diplopia may occur.
45
II - NUCLEAR OPHTHALMOPLEGIA :
Paralysis of ocular muscles due to a lesion of the nuclei of the oculomotor nerves.
Types :
1. External Ophthalmoplegia.2. Internal Ophthalmoplegia.3 . Total Ophthalmoplegia.
Causes:
1 . Congenital defects of ocular movements e.g. congenital aplasia of the oculomotor
nuclei.
2 . Traumatic : e.g. Head injury (brain - stem contusion).
3 . Inflammatory : e.g. syphilis, disseminated encephalomyelitis (D.E.M.), and
encephalitis lethargica.
4 . Vascular lesions of the brain - stem : e.g. haemorrhage, thrombosis, embolism and
aneurysm.
5 . Neoplastic : e.g. tumours of the midbrain, pons, third ventricle and pineal body.
6 . Degenerative and demyelinating : e.g. Progressive nuclear ophthalmoplegia,
syringobulbia, M.S. and D.E.M.
7 . Deficiency : e.g. Avitaminosis.
8 . Toxic : e.g. Alcoholism.
III - INFRANUCLEAR LESIONS :
Sites:
(i) Brain - stem : e.g. trauma, tumour, encephalitis, haemorrhage, infarction,
aneurysm, M.S. and syringobulbia. (ii) Base of the brain : e.g. Fracture base of
the skull, basal meningitis (syphilitic,
tuberculous, or pyogenic), or meningeal metastases. (iii) Wall of cavernous sinus :
e.g. sinus thrombophlebitis, parasellar meningioma,
internal carotid or posterior communicating aneurysm. (iv)
Superior orbital fissure : e.g. periostitis, (v) Nerves themselves :
e.g. polyneuritis. Causes:
1 . Traumatic : e.g. fracture base of the skull.
2 . Inflammatory : e.g.
(a) Basal meningitis (syphilitic, tuberculous, or pyogenic).
(b) Encephalitis.
(c) Poliomyelitis.
(d) Polyneuritis cranialis : diabetic, diphtheritic, alcoholic, rheumatic, or syphilitic
polyneuritis.
(e) Periostitis of the superior orbital fissure.
(f) Petrositis secondary to otitis media with sixth nerve palsy, trigeminal neuritis and
mastoiditis (Gradenigo's syndrome).
3 . Vascular : e.g.
(a) Subarachnoid haemorrhage.
(b) Cavernous sinus thrombosis.
(c) Infarction of the oculomotor nerves.
(d) Aneurysm of the internal carotid or posterior communicating arteries.
4 . Neoplastic : e.g. Brain tumour, either through direct compression of the nerves, or as
a false localizing sign of increased ICT.
5 . Demyelinating & Degenerative : e.g. M.S. & syringobulbia.
6 . Ophthalmoplegic migraine.
7 . Myasthenia gravis.
8 . Spinal anaesthesia may be followed by 6th. nerve palsy. The cause is unknown.
9 . Meningeal metastases at the base of the skull compressing the III, IV, and / or VI
nerves.
10 . Carcinoma of a nasal sinus invading the orbit, or encroachment upon the orbit by a
mucocele of the ethmoid sinus.
46
OPHTHALMOPLEGIA
NYSTAGMUS
Definition :
Nystagmus means rhythmical oscillation of the eyes. In many instances it possesses a
quick and a slow phases. The quick phase indicates the direction of nystagmus. So we say
nystagmus to the right when the quick phase is to the right. Nystagmus may be horizontal,
vertical, or rotary.
Nystagmus
47
CAUSES OF NYSTAGMUS :
I - Hysterical Nystagmus may be associated with spasm of convergence.
II-Organic:
(A) Congenital and Familial Nystagmus :
A fine pendular oscillation of the eyes, with or without oscillation of the head,
present at rest, affects males more than females (3 :1 ) and may be associated with
albinism, astigmatism or amblyopia.
(B) Acquired Nystagmus:
1 . Nystagmus of Retinal Origin :
(a) Amblyopia : poor vision, defective ocular fixation and pendular nystagmus.
(b) Miner's nystagmus : due to diminished macular vision.
(c) Optokinetic nystagmus : in a person looking out of the window of a moving
train. It is a brain - stem reflex, the cortical centre of which lies in the
supramarginal and angular gyri. It could be tested by the Barany drum (a
reveling striped cylinder).
2 . Labyrinthine Nystagmus : could be induced by the caloric test and positional
tests, or occurs spontaneously in labyrinthine lesions whether primary or
secondary to otitis media. It is usually rotary.
3 . Nystagmus due to weakness of the ocular muscles or lesion of cranial nerves 3,4,
or 6 e.g. in alcoholic polyneuritis, myasthenia gravis and botulism.
4 . Nystagmus due to central lesions : e.g.
Cerebellar lesions and lesions of the cerebellar connections in the brain - stem,
the vestibular nucleus and the posterior longitudinal bundle. Causes : M.S.,
hereditary ataxias (e.g. Friedreich's ataxia), encephalitis,syringpmyelia, tumours
and vascular lesions of the brain stem and cerebellum. Syphilis is a rare cause.
Nystagmus is usually positional.
5 . Nystagmus due to spinal cord lesions: is rare e.g. in lesions of the cervical region
of the cord.
6 . Errors of refraction & macular lesions.
THE PUPILS
ANATOMY
1. The Iridodilator Fibres ;
Start from the frontal cortex -> hypothalamus -> cerebral peduncle -> tegmentum of the
pons —> medulla —» cervical cord -> lateral horn cells of C8, Th 1&2 segments —>
preganglionic fibres —> ventral roots of the spinal nerves --> white rami communicantes of
the sympathetic -» cervical sympathetic trunk -> superior cervical ganglion -> post ganglionic fibres —> join the internal carotid plexus to enter the skull with it —> pass with the
ophthalmic division of the 5th nerve to the nasociliary and long ciliary nerves —> pupil.
2. The Iridoconstrictor Fibres:
Arise from the Edinger-Westphal nuclei -» third nerve -» ciliary ganglion -»
postganglionic fibres —> short ciliary nerves —» sphincter pupillae muscle.
3. The Ciliary Fibres :
Arise from the median nucleus ofPerlia and follow the same course to end in the-ciliary
muscle which is responsible for accomodation of the eye for near vision.
4. The Light Reflex :
Exposure of one eye to light produces constriction of both pupils (direct and consensual
reaction).
(a) Afferent path : Retina -» optic nerve -» optic chiasma -> optic tracts -> anterior
colliculus -> pretectal region -» oculomotor nuclei.
(b) Efferent path : Nuclei of Edinger-Westphal -> Third nerve -> ciliary ganglia -»
sphincter pupilae. 5. The Reaction on
Accomodation - Convergence:
Shifting the gaze from a distant to a near object results in convergence (by contraction
48
of the medial recti), accomodation (by contraction of the ciliary muscle)and pupillary
contraction (brought about by impulses starting in the visual cortex and descending either
directly or to end in the nuclei of Edinger-Westphal, then go along the third nerve to the
ciliary ganglion then to the pupils).
Reflex Iridoplegia: A failure of the pupil to react to light.
Argyll Robertson pupil: is a form of reflex iridoplegia characterized by :
(i) The pupil is small in size and usually irregular.
(ii) It does not react to light but reacts to accomodation.
(iii) It dilates slowly and incompletely to mydriatics.
Commonest causes are syphilis (Tabes dorsalis) & diabetes mellitus. Rarely :
alcoholism, encephalitis, M.S., vascular or neoplastic lesions of midbrain.
Causes of Reflex Iridoplegia:
1. Lesions of the Optic Nerve : Produce blindness and loss of light reflex. The reaction
on accomodation is preserved.
2 . Lesions of the Optic Tract: Produce crossed homonymous hemianopia and loss of
light reflex .
3 . Central Lesions : Upper midbrain lesions e.g. trauma, tumour, vascular lesions,
encephalitis lethargica, M.S., syringomyelia, syphilis and diabetes.
Diabetes may cause Argyll Robertson pupils and absent ankle jerks (due to
peripheral neuritis) simulating tabes dorsalis and is therefore called diabetic
pseudotabes.
4 . Lesions of the Motor Path (Third Nerve Lesions): usually unilateral.
The Holmes - Adie Syndrome : (Tonic Pupils and absent Tendon Reflexes)
It is a rare syndrome, the aetiology of which is unknown, usually affects females during
the third decade of life and is characterized by loss of reaction on accomodation, as well as
hyporeflexia or areflexia of the ankle jerks, knee-jerks and arm jerks.
Features
(/) Bilaterality
(//) Size
(iii) Regularity
(iv) Light Reflex
(v) Reaction on accomodation
(vi) Response to Mydriatics
Argyll Robertson pupil
Usually bilateral
Myotic (small)
Usually irregular
Lost
Normal
Incomplete
Tonic pupil
Unilateral in 80 %
Wide
Regular
Lost
Sluggish
Complete
Causes of Myosis : (Constriction of the pupil)
1 . Homer's syndrome : Ocular sympathetic paralysis.
2 . Argyll Robertson pupil :due to interruption of the iridodilator fibres in the midbrain.
Commonly seen in syphilis.
3 . Lesions ofthepons e.g. pontine haemorrhage.
4 . Lateral medullary syndrome (Wallenberg syndrome) due to thrombosis of the
posterior inferior cerebellar artery.
5 . Lesions of the spinal cord involving the lateral horns of the upper thoracic region.
6 . Klumpke type of birth palsy of the brachial plexus.
7 . Lesions of the cervical sympathetic e.g. trauma or compression .
8 . Retro-orbital tumour or aneurysm.
9 . Drugs, e.g. Pilocarpine, eserine and morphine.
10 . Bright light focussed on the eye.
49
Causes of Mydriasis : (Dilatation of the pupil)
1. Third nerve palsy : paralysis of the sphincter pupilae.
2 . Atropine and belladonna.
3 . Cocaine .
4 . Darkness.
Causes of Irregularity of the pupils:
1. Syphilis.
2 . Encephalitis lethargica.
3 . Iritis.
THE EYELIDS
The upper eyelid is elevated by 2 muscles:
1 . Levator palpebrae superioris : innervated by the third nerve.
2 . Midler's palpebral muscle : innervated by the cervical sympathetic.
The eye is closed by the orbicularis oculi muscle which is innervated by the facial nerve.
Causes of Ptosis (Drooping of the upper eyelid):
1 . Third nerve palsy : Nuclear or intranuclear lesion.
2 . Horner's syndrome : ptosis, myosis, enophthalmos and anhydrosis.
3 . My asthenia gravis.
4 . Congenital ptosis.
5 . Myopathy.
6 . Tabes dorsalis.
1. Hysteria.
Causes of exophthalmos:
1 . Exophthalmic goitre.
2. Exophthalmic ophthalmoplegia.
3 . Pseudotumour of the orbit.
4 . Retro - orbital space-occupying lesions e.g. meningiomas, or aneurysms.
5 . Optic nerve glioma, or meningioma of the optic sheath.
6. Empyema, mucocele, or carcinoma of the nasal sinuses.
7 . Rare causes : e.g. craniostenosis, carotid-cavernous sinus aneurysm, chloroma,
xanthomatosis and metastases.
Ptosis
50
Horner's Syndrome
V.- THE TRIGEMINAL NERVE
ANATOMY:
(A) Central Connections:
1. Motor nuclei:
(a) The motor nucleus is located in the lateral part of the tegmentum of the ports.
(b) The mesencephalic root originating in the nddbrain is probably motor.
2 . Sensory nuclei:
(a) The principal sensory nucleus is located in the substantia gelatinosa in the
lateral part of the tegmentum of the pons. It is concerned with touch and deep
sensations. Fibres from this nucleus cross the midline forming the
trigeminothalamic tract or trigeminal lemniscus .
(b) The nucleus of the spinal tract or descending nucleus is located in the lateral part
of the medulla and ends at the level of C2 segment. It is concerned with pain
and temperature sensations. The ophthalmic division ends in the lowest part of
the spinal nucleus, the mandibular division ends in the uppermost part, and the
maxillary division inbetween. Also fibres of the butterfly (central) part of the
face end in its lateral half , while those of the outer face end in its medial
half. Fibres from the spinal nucleus cross the midline and ascend to join the
spinothalamic tract in the pons, from the thalamus, fibres ascend in the internal
capsule to the sensory cortex.
(B) Peripheral Distribution :It has a large sensory root and a small motor one.
The two roots pass forwards in the posterior fossa. The sensory root expands to form
the trigeminal ganglion (Gasserian or semilunar ganglion). This ganglion gives rise to
the 3 divisions of the fifth nerve; ophthalmic, maxillary and mandibular divisions. 1.
The Sensory Root:
(a) The Ophthalmic Division : lies in the lateral wall of the cavernous sinus, then
enters the orbit through the superior orbital fissure, to supply sensory fibers to
the eye, skin of the nose, forehead and anterior half of the scalp and to the
mucous membrane of the frontal sinuses and the upper part of the nose.
(b) The Maxillary Division : passes through the foramen rotundum into the
pterygopalatine fossa. It enters the orbit through the inferior orbital fissure as
the infraorbital nerve, which reaches the face via the infraorbital foramen to
supply the skin of the upper lip, the skin over the maxilla, the mucous
membrane of the maxillary sinus, nose, upper lip, palate, anterior part of soft
palate, together with the teeth of the upper jaw.
(c) The Mandibular Division : fuses with the motor root and passes out of the skull
through \he foramen ovale to the infra-temporal fossa. It supplies the skin of the lower
lip and chin, the tympanic membrane, the external acoustic meatus, the skin of the
temple, the mucous membrane of the cheek, lower jaw, floor of the mouth and
anterior 2/3 of the tongue and the teeth of the lower jaw. It carries fibres of taste
sensation from the anterior 2/3 of the tongue which separates as the chorda tympani
that joins the facial nerve. The fifth nerve gives meningeal branches to supply the
tentorium and most of the dura mater above it. 2 . The Motor Root: joins the
mandibular division and supplies the folowing muscles: temporal, masseter, medial and
lateral pterygoids, anterior belly of the digastric, mylohyoid, tensor tympani and
tensor veli palatini.
LESIONS OF THE TRIGEMINAL NERVE (A)
Peripheral Lesions: Causes:
Syphilitic meningitis, tumour, aneurysm, tabes, pituitary tumour,meningioma,
fracture of the base of the skull, Gradenigo's syndrome, trigeminal herpes zoster or
fracture of the bones of the face. Features:
1. Pain with or without cutaneous anaesthesia and analgesia.
51
2 . Weakness and wasting of the masticatory muscles and deviation of the jaw to the
paralysed side when the mouth is opened.
— Ophthalmic division
Second cervical
segment -
-Maxillary division
Third cervical segment —
--• Mandibular division
Cutaneous distribution of the trigeminal nerve.
A. Peripheral distribution.
B. Segmental distribution
Diagram of Trigeminal Nerve
1 . Gasserian ganglion 4
. Main sensory nucleus
7. Medial lemniscus Th.
= Thalamus M. =
2. Mesencephalic nucleus
5. Spinal nucleus
8. Spino-thalamic tract
M. B. = Midbrain.
Cl,2,3 : Upper 3 cervical segments of the cord
Medulla.
P. = Pons.
52
3 . Main motor nucleus
6. Trigemino-thalamic tract
9. Pyramidal fibres
(B) Central Lesions:
Causes:
Tumours, syringobulbia and vascular lesions of the pons, medulla and Cl-2 segments of
the cord. Features:
1. Ponline lesions: as Millard-Gublar and Foville's syndromes result in weakness of
the muscles of mastication and anaesthesia to light touch over the face with
preservation of pain and temperature sensations.
2 . Lesions of the medulla and the upper cervical segments of the cord produce
dissociated sensory loss (loss of pain and temperature sensations with
preservation of light touch) e.g. in syringobulbia and posterior inferior cerebellar
artery occlusive syndrome.
3 . Lesions of the lowest part of the medulla and the upper part of the spinal cord
result in dissociated anaesthesia in the distribution of the ophthalmic division on
the same side.
4 . Syringobulbia produces dissociated sensory loss starting from the outer part of
the face and gradually spreading towards the nose.
5 . Tabes dorsalis : produces complete anaesthesia starting in the central (butterfly)
area of the face and spreading later on to the periphery of the face.
TRIGEMINAL NEURALGIA
(Tic Douloureux) Definition : Paroxysmal brief
attacks of pain in the distribution of one or more of the
sensory divisions of the fifth nerve.
Aetiology:
(i) The cause is unknown. Alcoholism, diabetes or herpes zoster might be responsible, (ii)
Females are affected more than males (3 : 2) (iii) Usually starts at the age of 50, but any age
may be affected, (iv) Exposure to cold, emotions, or a blow on the face may precipitate the
first attack. (v) It is rarely a symptom of organic disease e.g. M .S. or acoustic neuroma.
Clinical Picture:
1. Brief severe paroxysms of pain (1 or 2 minutes) in the distribution of one division of
the nerve, usually the 2nd and / or 3rd divisions.
2 . Pain is burning or stabbing in character, usually unilateral and rarely bilateral.
Remissions may occur in the course.
3 . Characteristically, the attacks are precipitated by chills, touching the face, washing,
shaving, talking, mastication and swallowing.
4 . Trigger zones may be present from which the attack can be excited by touching.
5 . Reflex spasm of the facial muscles fflushiugf lacrimation and salivation may occur.
6 . No sensory loss, nor corneal areflexia.
Differential Diagnosis:
1 . Multiple sclerosis or acoustic neuroma may cause trigeminal pain and are
distinguished from trigeminal neuralgia by the presence of the appropriate features
of these disorders.
2 . Compression of the 5th nerve e.g. by a tumour : Pain is more persistent + sensory loss
+ paresis of the muscles supplied by the nerve.
3 . Posterior inferior cerebellar artery thrombosis : Signs of brain - stem lesion are
present.
4 . Post - herpetic trigeminal pain : Persistent pain, sensory impairment & history of
herpes zoster eruption.
5 . Tabes dorsalis: is distinguished by its characteristic signs & positive W.R.
53
6. Referred pain :
* Frontal or maxillary sinusitis.
* Dental caries, unerupted tooth, peri-apical abscess.
7 . Psycho genie facial pain .
* Glaucoma.
* Heart and lung lesions.
8 . Migrainous neuralgia.
Treatment:
(A) Medical:
1. Carbamazepine (Tegretol), 200 mg 3 or 4 times daily, is the most effective remedy.
2 . Phenytoin sodium (Epanutin), 100 mg t.d.s. is helpful in some cases.
3 . Aspirin, bromides, etc.
(B) Surgical:
1. Alcoholic injections of the nerve .
2 . Division of the sensory root or tractotomy (division of the spinal tract of the 5th nerve in the medulla).