Download Cranial nerve palsy

Cranial nerve palsy
Oculomotor nerve palsy
The nuclear complex of the third (IIIrd) nerve lies in
midbrain After leaving the brainstem, the nerve
enters subarachnoid space and courses forward and
laterally between posterior cerebral artery and
superior cerebellar artery. At this level the nerve is
compressed by Berry Aneurysms then the artery pass
through cavernous sinus, together with trochelear 4th
,abducent 6th ,first division (opthalmic ) and second
division (maxillary ) of the 5th cranial nerve ,after that
through superior orbital fissure to supplly somatic:
Superior rectus (SR), inferior rectus (IR), inferior
oblique (IO), medial rectus (MR).
and levator palpebrae superioris (LPS) as well as
autonomic (pupillary sphincter and ciliary) muscles of
the eye .
Oculomotor nerve lesions :
1-In nuclear lesions in the midbrain; most common
cause is stroke
2-Subarachnoid space is the most likely site of
involvement in isolated IIIrd nerve palsies.the
pathology may be compressive or infarction
secondary to microvascular involvement in diabetics
and hypertensives. Also compress by an aneurysm.
3-in cavernous sinus, one must note the associated
signs and symptoms. It may be associated with the
dysfunction of IVth and VIth nerves, first or second
division of trigeminal nerve most common cause is
thrombosis and infection especially in diabetic
4-in the superior orbital fissure together with cranial
nerves 4th ,6th and first division of trigeminal nerves
associated with proptosis.
Cavernous sinus syndrome
The cavernous sinuses are paired, venous structures
located on either side of the sella turcica, They
receive venous tributaries from the superior and
inferior orbital veins, The cavernous sinus contains
the carotid artery, its sympathetic plexus, and the
oculomovement nerves (third, fourth, and sixth
cranial nerves). In addition, the ophthalmic branch
and the maxillary branch of the fifth nerve traverse
the cavernous sinus.
Clinical manifestation : ophthalmoplegia, chemosis,
sometimes proptosis, trigeminal sensory loss in
opthalmic and maxillary branches .
Casuses
1- Cavernous sinus thrombosis is a serious condition
that can follow infection of the face, paranasal sinuses
(particularly the sphenoid sinus) or teeth most
commonly in diabetic
2- metastases and nasopharyngeal carcinoma
3- aneurysms of the intracavernous portion of the
carotid artery
Jugular foramen syndrome
The jugular foramen is a large aperture in the base of
the skull, Cranial nerves IX, X, and XI and the internal
jugular vein pass through the jugular foramen.
Clinical significance:
is characterized by the paresis of (9th,10th&11th )
cranial nerves together so patient may complain from
1- dysphagia, dysphonia/hoarseness,
2- deviation of the uvula towards the normal side
3- sternocleidomastoid and trapezius muscles paresis
Common Causes
A- Metastatic tumors
B- Infections
Bell’s palsy
Bell’s palsy is an acute peripheral facial palsy, Bell’s
palsy may occur in childhood; incidence increases
steadily with age. There is no change in incidence with
season, latitude or geography and no evidence for
familial clustering. Weak associations may exist with
diabetes and hypertension. A viral aetiology has been
postulated on the basis that detection of herpes
simplex virus type 1 (HSV-1) DNA in endoneurial fluid
in most patients. Both primary HSV-1 infection and
reactivation of latent infection have been implicated
Clinical features
Rapid onset of facial weakness progressing over 48
hours (and occasionally up to 5 days) is preceded or
accompanied by diffuse retro-auricular pain in the
region of the mastoid, Facial weakness and
asymmetry with drooling of liquids from the corner of
the mouth on the affected side often lead the patient
to suspect a stroke; most patients present promptly to
primary care physicians. Not infrequently, patients
mistakenly report that the contralateral unaffected
side is the weak side. All facial muscles are usually
equally affected., eye closure and blinking are
reduced or absent (with a visible Bell’s phenomenon
attempted eye closure).
Ectropion formation may lead to overflow of tears on
to the cheek. The angle of the mouth droops with
reduction of the nasolabial fold, smoothing of skin
wrinkles; the platysma muscle is also involved. The
extent of maximal facial weakness is variable, but is
severe in the majority, although occasionally patients
present with very mild facial weakness
Loss of taste, often described as a muddy or metallic
taste, and hyperacusis (because of paralysis of
stapedius) indicate involvement of the chorda
tympani and the branch to stapedius, Respectively
Management and outcome
Complete or almost complete recovery, without
recurrence, over 3–8 weeks is the norm in at least
85% of cases, even without any treatment.
Reassurance about the good prognosis is important.
Inability to blink in severe facial weakness may lead to
exposure keratitis and early evaluation should include
assessment of the eye. Lubricating eye drops are
often required and patients should be shown how to
tape the eye closed at night. Severe facial weakness
with complete inability to close the eye requires
urgent
ophthalmological
assessment;
lateral
tarsorrhaphy and/or temporary insertion of a gold
weight into the upper lid may be necessary. Early
treatment with oral steroids (prednisolon)and
antiviral agents(oral acylovire) is worthy .