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Cranial Nerve Disorders

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When the patient attempts to turn the eye inward, it moves slowly only to ... severe pain in the head and anesthesia in the distribution of the first division ... – PowerPoint PPT presentation

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Title: Cranial Nerve Disorders


1
Cranial Nerve Disorders
2
THIRD CRANIAL NERVE PALSIES
  • Partial to complete weakness of the muscles
    innervated by the 3rd (oculomotor) nerve,
    resulting in ptosis of the lid, mydriasis, and an
    outwardly turned eye during primary gaze.
  • When the patient attempts to turn the eye inward,
    it moves slowly only to the midline. Upward and
    downward gaze is compromised in the affected eye.
    When downward gaze is attempted, the superior
    oblique muscle causes the eye to rotate inward.

3
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4
Causes of 3rd cranial nerve palsies
  • The many causes of 3rd cranial nerve palsies
    include most major causes of CNS disease, so
    choice of diagnostic tests should be based on the
    clinical features of the palsy. Intraorbital
    structural lesions producing external
    ophthalmoplegia and ocular myopathies should be
    distinguished from cranial nerve disease.
    Exophthalmos or enophthalmos, a history of severe
    orbital trauma, or an obviously inflamed orbit
    suggests restrictive orbital disease, which may
    impair ocular motility. Myopathies are harder to
    diagnose but are suggested by a partial 3rd nerve
    palsy. The pupil is always spared in myopathy.

5
Causes of 3rd cranial nerve palsies
  • Completely nonfunctional parasympathetic fibers
    (causing fixed dilated pupils) strongly suggest
    oculomotor nerve compression. The most common
    causes are aneurysm (especially of the posterior
    communicating artery), trauma, and intracranial
    mass lesion. Oculomotor paralysis in an
    increasingly unresponsive patient suggests
    transtentorial herniation and is a major
    emergency. If the pupil is completely spared but
    all other muscles innervated by the 3rd nerve are
    affected (eg, diabetic 3rd nerve paresis), the
    cause is likely to be an ischemic process of the
    oculomotor nerve or the midbrain a demyelinating
    process is less likely. However, about 5 of
    posterior communicating artery aneurysms causing
    oculomotor paralysis spare the pupil.

6
Investigation
  • Third cranial nerve palsies are most indicative
    of serious disease when associated with severe
    headache or altered consciousness.
  • A thorough neurologic examination with CT or MRI
    is performed. Lumbar puncture is reserved for
    suspected subarachnoid hemorrhage when CT does
    not show blood. Cerebral angiography must be
    performed if aneurysm causing subarachnoid
    hemorrhage is strongly suspected or when the
    pupil is clearly affected and no head trauma
    serious enough to fracture the skull has
    occurred.

7
FOURTH CRANIAL NERVE PALSIES
  • Weakness of the muscle innervated by the 4th
    (trochlear) nerve (superior oblique muscle).
  •  
  • These palsies are often difficult to detect
    because they affect vertical eye position
    predominantly when the eye is turned inward. The
    patient sees double images, one above and
    slightly to the side of the other. However, by
    tilting the head to the side opposite the palsied
    muscle, the patient may achieve full or almost
    full ocular motility without double vision.

8
FOURTH CRANIAL NERVE PALSIES
  • There are few common identified causes of 4th
    cranial nerve palsies many are idiopathic.
    Closed head trauma without skull fracture is a
    common cause of unilateral and bilateral palsies
    the few cases that occur often follow motor cycle
    accidents. Aneurysms, tumors, and multiple
    sclerosis are rare causes.
  • Evaluation of 4th nerve palsies is similar to
    that of 3rd nerve palsies. Usually, the diagnosis
    is obvious from the history and physical
    examination. Oculomotor exercises may help.
    Sometimes surgery is necessary to restore
    concordant vision.

9
SIXTH CRANIAL NERVE PALSIES
  • Weakness of the muscles innervated by the 6th
    (abducens) nerve.
  • The eye is turned inward it moves outward
    sluggishly, reaching the midline at most.
  • Idiopathic cases are common, although many occur
    in elderly or diabetic patients in whom small
    vessel disease may be suspected. In idiopathic
    cases, no other cranial nerves are involved, and
    improvement should occur within 2 mo.

10
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11
Causes
  • One identifiable cause is compression of the 6th
    nerve in the cavernous sinus by a tumor
    originating in the nasopharynx. Typically, severe
    pain in the head and anesthesia in the
    distribution of the first division of the 5th
    nerve also occur. Anything that causes the brain
    to shift may stretch the 6th nerve because of the
    acute angle it makes before entering Dorello's
    canal. Thus 6th nerve palsies may be due to large
    brain tumors remote from the nerve, to increased
    intracranial pressure, or to lumbar puncture.

12
Causes
  • Diabetic infarction is one of the more common
    causes. Other causes include trauma of
    insufficient force to cause a basilar skull
    fracture, infections or tumors affecting the
    meninges, Wernicke's encephalopathy, aneurysm,
    and multiple sclerosis. In children without
    evidence of increased intracranial pressure,
    these palsies can result from respiratory
    infection and thus may be recurrent.

13
SIXTH CRANIAL NERVE PALSIES
  • Diagnosing complete 6th cranial nerve palsies is
    easy, but determining their etiology can be more
    challenging. Excluding increased intracranial
    pressure and papilledema (by looking for retinal
    venous pulsations during funduscopy) is
    important. MRI or CT can help exclude
    intracranial mass lesions, hydrocephalus, and
    direct nerve compression by lesions in the orbit,
    cavernous sinus, and base of the skull. Lumbar
    puncture determines the CSF opening pressure and
    can detect leptomeningeal inflammatory,
    infectious, or neoplastic infiltrates entrapping
    the 6th nerve. A collagen vascular screen helps
    exclude a vasculopathic process. In many cases,
    6th nerve palsies resolve once the primary
    disorder is treated.

14
TRIGEMINAL NEURALGIA(Tic Douloureux)
  • A disorder of the trigeminal nerve producing
    bouts of excruciating, lancinating pain, lasting
    between seconds and 2 min, along the distribution
    of one or more of its sensory divisions, most
    often the maxillary.
  • At surgery or autopsy, intracranial arterial and,
    less often, venous loops compressing the
    trigeminal nerve root where it enters the brain
    stem have been found, suggesting that the tic is
    a compressive neuropathy. The disorder usually
    affects adults, especially the elderly. Pain is
    often set off by touching a trigger point or by
    activity (eg, chewing or brushing the teeth).
    Although each bout of intense pain is brief,
    successive bouts may be incapacitating.

15
TRIGEMINAL NEURALGIA(Tic Douloureux)
  • Differential diagnosis includes neoplasm,
    vascular malformation of the brain stem, a
    vascular insult, and multiple sclerosis
    (especially in a younger patient). Postherpetic
    pain is differentiated by its typical antecedent
    rash, scarring, and predilection for the
    ophthalmic division. Trigeminal neuropathy may
    occur in Sjögren's syndrome or RA, but with a
    sensory deficit that is often perioral and nasal.
    Migraine may produce atypical facial pain, with
    normal examination results, but the pain is more
    prolonged and is burning or throbbing.

16
FACIAL NERVE DISORDERS
  • Unilateral facial weakness is a common neurologic
    sign.

17
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18
Bell's Palsy
  • Unilateral facial paralysis of sudden onset and
    unknown cause.
  • The mechanism presumably involves swelling of the
    nerve due to immune or viral disease, with
    ischemia and compression of the facial nerve in
    the narrow confines of its course through the
    temporal bone.
  • Pain behind the ear may precede facial weakness.
    Weakness develops within hours, sometimes to
    complete paralysis. The affected side becomes
    flat and expressionless, but patients may
    complain instead about the seemingly twisted
    intact side. In severe cases, the palpebral
    fissure widens, and the eye does not close. The
    patient may complain of a numb or heavy feeling
    in the face, but no sensory loss is demonstrable.
    A proximal lesion may affect salivation, taste,
    and lacrimation and may cause hyperacusis.

19
Diagnosis 
  • Weakness of the entire half of the face
    distinguishes Bell's palsy from supranuclear
    lesions (eg, stroke, cerebral tumor), in which
    the weakness is partial, affecting the frontalis
    and orbicularis oculi less than the muscles in
    the lower part of the face. Bell's palsy must be
    differentiated from unilateral facial weakness
    due to other disorders of the facial nerve or its
    nucleus, chiefly geniculate herpes (Ramsay Hunt's
    syndrome), middle ear or mastoid infections,
    sarcoidosis, Lyme disease, petrous bone
    fractures, carcinomatous or leukemic nerve
    invasion, chronic meningeal infections, and
    cerebellopontine angle or glomus jugulare tumors.
    Skull x-rays and CT and MRI scans are obtained
    when the diagnosis is in doubt. MRI may show
    contrast enhancement of the facial nerve, but CT
    and skull x-rays are typically negative. However,
    they may show a fracture line, bony erosion due
    to infection or neoplasm, or internal auditory
    canal expansion due to a cerebellopontine angle
    tumor. CT and MRI scans may show the
    contrast-enhancing mass of angle or glomus
    tumors. Blood tests for Lyme disease help
    diagnose it. A chest x-ray and serum ACE are used
    to detect sarcoidosis, a common cause of facial
    nerve paralysis in blacks.

20
Prognosis and Treatment
  • The extent of nerve damage determines outcome
    nerve conduction studies and electromyography are
    useful. Complete recovery within several months
    invariably follows acute partial paralysis. The
    likelihood of complete recovery after total
    paralysis is 90 if the nerve branches in the
    face retain normal excitability to supramaximal
    electrical stimulation but is only about 20 if
    electrical excitability is absent.
  • Misdirected regrowth of nerve fibers may
    innervate lower facial muscles with periocular
    fibers and vice versa, resulting in contraction
    of unexpected muscles during voluntary facial
    movements (synkinesia) or "crocodile tears"
    during salivation. Facial muscle contractures may
    follow chronic weakness.
  • Measures must be taken to prevent corneal drying.
    They include frequent use of natural tears,
    isotonic saline and methylcellulose drops, and
    strips of skin tape to help close the eye.
    Supportive measures, such as temporary patching,
    may suffice to protect the exposed eye
    tarsorrhaphy may be needed when palpebral fissure
    persists.

21
Corticosteroids
  • Some studies suggest that corticosteroids (eg,
    prednisone 60 to 80 mg/day po begun 24 to 48 h
    after onset and given for 1 wk, then decreased
    gradually over the 2nd wk) help modestly reduce
    residual paralysis and expedite recovery. Mild
    electrical stimulation of the nerve and massage
    of the facial muscles have no proven benefit.
    Hypoglossal-facial nerve anastomosis may
    partially restore facial function if none has
    returned in 6 to 12 mo but results in difficulty
    in eating and speaking, so its role is limited.

22
GLOSSOPHARYNGEAL NEURALGIA
  • A rare syndrome characterized by recurrent
    attacks of severe pain in the posterior pharynx,
    tonsils, back of the tongue, and middle ear.
  • The cause is unknown, and no pathologic change
    can be found (except rarely, when due to a tumor
    in the cerebellopontine angle or the neck). Men
    are more commonly affected, usually after age 40.
  •  
  • As in trigeminal neuralgia, intermittent attacks
    of brief, severe, excruciating pain occur
    paroxysmally, either spontaneously or
    precipitated by movement (eg, chewing,
    swallowing, talking, sneezing). The pain, lasting
    seconds to a few minutes, usually begins in the
    tonsillar region or at the base of the tongue and
    may radiate to the ipsilateral ear. The pain is
    strictly unilateral. In 1 to 2 of patients,
    increased vagus nerve activity causes cardiac
    sinus arrest with syncope. Attacks may be
    separated by long intervals.

23
Diagnosis and Treatment
  • Location of the pain, precipitation of an attack
    by swallowing or by touching the tonsils with an
    applicator, and temporary elimination of pain
    with lidocaine applied locally to the throat
    (after which the pain cannot be evoked by
    stimulation) distinguish glossopharyngeal
    neuralgia from trigeminal neuralgia of the
    mandibular division. Tonsillar, pharyngeal, and
    cerebellopontine angle tumors and metastatic
    lesions in the anterior cervical triangle must be
    ruled out by brain imaging.
  • Carbamazepine is the drug of choice. Phenytoin,
    baclofen, or amitriptyline in doses as for
    trigeminal neuralgia (see above ) or trazodone
    150 to 400 mg/day in 3 divided doses may be added
    if necessary. If they are ineffective,
    cocainization of the pharynx may provide
    temporary relief, and surgery may be necessary.
    When pain is restricted to the pharynx, the nerve
    in the neck may be avulsed it must be sectioned
    intracranially if pain is widespread.
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