Parinaud Syndrome Artery

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Lesions of the Brain Stem

I. LESIONS OF THE MEDULLA (Figure 14-1)

A. Medial medullary syndrome (anterior spinal artery syndrome). Affected structures and resultant deficits include:

1. The corticospinal tract (medullary pyramid). Lesions result in contralateral spastic hemiparesis.

2. The medial lemniscus. Lesions result in contralateral loss of tactile and vibration sensation from the trunk and extremities.

3. The hypoglossal nucleus or intraaxial root fibers [cranial nerve (CN) XII]. Lesions result in ipsilateral flaccid hemiparalysis of the tongue. When protruded, the tongue points to the side of the lesion (i.e., the weak side). See Figure 1 3-7.

Medullary Pyramids Brain
Figure 14-1. Vascular lesions of the caudal pons at the level of the hypoglossal nucleus of cranial nerve (CN) XII and the dorsal motor nucleus of CN X. (A) Medial medullary syndrome (arterial spinal artery). (J3) Lateral medullary [posterior inferior cerebellar artery (PICA)) syndrome.

B. Lateral medullary syndrome [posterior inferior cerebellar artery (PICA) syndrome]

is characterized by dissociated sensory loss (see I B 6-7). Affected structures and resultant deficits include:

1. The vestibular nuclei. Lesions result in nystagmus, nausea, vomiting, and vertigo.

2. The inferior cerebellar peduncle. Lesions result in ipsilateral cerebellar signs [e.g., dystaxia, dysmetria (past pointing), dysdiadochokinesia].

3. The nucleus ambiguus of CN IX, CN X, and CN XI. Lesions result in ipsilateral laryngeal, pharyngeal, and palatal hemiparalysis [i.e., loss of the gag reflex (efferent limb), dysarthria, dysphagia, and dysphonia (hoarseness)].

4. The glossopharyngeal nerve roots. Lesions result in loss of the gag reflex (afferent limb).

5. The vagal nerve roots. Lesions result in the same deficits as seen in lesions involving the nucleus ambiguus (see 1 B 3).

6. The spinothalamic tracts (spinal lemniscus). Lesions result in contralateral loss of pain and temperature sensation from the trunk and extremities.

7. The spinal trigeminal nucleus and tract. Lesions result in ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia).

8. The descending sympathetic tract. Lesions result in ipsilateral Horner's syndrome (i.e., ptosis, miosis, hemianhidrosis, and apparent enophthalmos).

II. LESIONS OF THE PONS (Figure 14 2A)

A. Medial inferior pontine syndrome results from occlusion of the paramedian branches of the basilar artery. Affected structures and resultant deficits include:

1. The corticospinal tract. Lesions result in contralateral spastic hemiparesis.

2. The medial lemniscus. Lesions result in contralateral loss of tactile sensation from the trunk and extremities.

Vestibular nuclei

Abducent nucleus

Inferior cerebellar peduncle

Spinal trigeminal nucleus and tract

CN VIII (vestibular nerve) CN VII Nucleus CN VII

Lateral Inferior Pontine Syndrome

Figure 14-2. Vascular lesions of the caudal pons at the level of the abducent nucleus of cranial nerve (CN) VI and the facial nucleus of CN VII. (A) Medial inferior pontine syndrome. (B) Lateral inferior pontine syndrome (anterior inferior cerebellar artery (AICA) syndrome]. (C) Medial longitudinal fasciculus (MLF) syndrome.

Inferior cerebellar peduncle

Spinal trigeminal nucleus and tract

Vestibular nuclei

Abducent nucleus

Medial lemniscus Corticospinal tract

CN VIII (vestibular nerve) CN VII Nucleus CN VII

Figure 14-2. Vascular lesions of the caudal pons at the level of the abducent nucleus of cranial nerve (CN) VI and the facial nucleus of CN VII. (A) Medial inferior pontine syndrome. (B) Lateral inferior pontine syndrome (anterior inferior cerebellar artery (AICA) syndrome]. (C) Medial longitudinal fasciculus (MLF) syndrome.

3. The abducent nerve roots. Lesions result in ipsilateral lateral rectus paralysis.

B. Lateral inferior pontine syndrome [anterior inferior cerebellar artery (AICA) syndrome] (Figure 14-2B). Affected structures and resultant deficits include:

1. The facial nucleus and intraaxial nerve fibers. Lesions result in:

a. Ipsilateral facial nerve paralysis b. Ipsilateral loss of taste from the anterior two-thirds of the tongue C. Ipsilateral loss of lacrimation and reduced salivation d. Loss of corneal and stapedial reflexes (efferent limbs)

2. The cochlear nuclei and intraaxial nerve fibers. Lesions result in unilateral central deafness.

3. The vestibular nuclei and intraaxial nerve fibers. Lesions result in nystagmus, nausea, vomiting, and vertigo.

4. The spinal trigeminal nucleus and tract. Lesions result in ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia).

5. The middle and inferior cerebellar peduncles. Lesions result in ipsilateral limb and gait dystaxia.

6. The spinothalamic tracts (spinal lemniscus). Lesions result in contralateral loss of pain and temperature sensation from the trunk and extremities.

7. The descending sympathetic tract. Lesions result in ipsilateral Horner's syndrome.

C. Medial longitudinal fasciculus (MLF) syndrome (internuclear ophthalmoplegia)

[see Figure 14-20] interrupts fibers from the contralateral abducent nucleus that project, through the MLF, to the ipsilateral medial rectus subnucleus of CN III. It causes medial rectus palsy on attempted lateral conjugate gaze and nystagmus in the abducting eye. Convergence remains intact. This syndrome is often seen in patients with multiple sclerosis.

D. Facial colliculus syndrome usually results from a pontine glioma or a vascular accident. The internal genu of CN VI1 and the nucleus of CN VI underlie the facial colliculus.

1. Lesions of the internal genu of the facial nerve cause:

a. Ipsilateral facial paralysis b. Ipsilateral loss of the corneal reflex

2. Lesions of the abducent nucleus cause:

a. Lateral rectus paralysis b. Medial (convergent) strabismus C. Horizontal diplopia

III. LESIONS OF THE MIDBRAIN (Figure 14-3)

A. Dorsal midbrain (Parinaud's) syndrome (see Figure 14-3A) is often the result of a pinealoma or germinoma of the pineal region. Affected structures and resultant deficits include:

1. The superior colliculus and pretectal area. Lesions cause paralysis of upward and downward gaze, pupillary disturbances, and absence of convergence.

2. The cerebral aqueduct. Compression causes noncommunicating hydrocephalus.

B. Paramedian midbrain (Benedikt) syndrome (see Figure 14-3B). Affected structures and resultant deficits include:

Medial geniculate body

Substantia nigra

Corticospinal tract

Posterior commissure and center for vertical conjugate gaze Superior colliculus Nucleus of CN III

Spinothalamic tract

Medial lemniscus

Dentatothalamic tract

Corticobulbar tract

Medial geniculate body

Substantia nigra

Corticospinal tract

Corticobulbar tract

Medial Lemniscus

Medial lemniscus

Dentatothalamic tract

Red nucleus

Figure 14-3. Lesions of the rostral midbrain at the level of the superior colliculus and oculomotor nucleus of cranial nerve (CN) III. (A) Dorsal midbrain (Parinaud's) syndrome. (B) Paramedian midbrain (Bcncdikt) syndrome. (C) Medial midbrain (Weber) syndrome.

Red nucleus

Figure 14-3. Lesions of the rostral midbrain at the level of the superior colliculus and oculomotor nucleus of cranial nerve (CN) III. (A) Dorsal midbrain (Parinaud's) syndrome. (B) Paramedian midbrain (Bcncdikt) syndrome. (C) Medial midbrain (Weber) syndrome.

1. The oculomotor nerve roots (intraaxial fibers). Lesions cause complete ipsilateral oculomotor paralysis. Eye abduction and depression is caused by the intact lateral rectus (CN VI) and superior oblique (CN IV) muscles. Ptosis (paralysis of the levator palpebra muscle) and fixation and dilation of the ipsilateral pupil (complete internal ophthalmoplegia) also occur.

2. The dentatothalamic fibers. Lesions cause contralateral cerebellar dystaxia with intention tremor.

3. The medial lemniscus. Lesions result in contralateral loss of tactile sensation from the trunk and extremities.

C. Medial midbrain (Weber) syndrome (see Figure 14-3C). Affected structures and resultant deficits include:

1. The oculomotor nerve roots (intraaxial fibers). Lesions cause complete ipsilateral oculomotor paralysis. Eye abduction and depression is caused by intact lateral rectus (CN VI) and superior oblique (CN IV) muscles. Ptosis and fixation and dilation of the ipsilateral pupil also occur.

2. The corticospinal tracts. Lesions result in contralateral spastic hemiparesis.

3. The corticobulbar fibers. Lesions cause contralateral weakness of the lower face (CN VII), tongue (CN XII), and palate (CN X). The upper face division of the facial nucleus receives bilateral corticobulbar input. The uvula and pharyngeal wall are pulled toward the normal side (CN X), and the protruded tongue points to the weak sidet

IV. ACOUSTIC NEUROMA (SCHWANNOMA) [Figure 14-4] is a benign tumor of Schwann cells that affects the vestibulocochlear nerve (CN VIII). It accounts for 8% of all intracranial tumors. It is a posterior fossa tumor of the internal auditory meatus and cerebellopontine angle. The neuroma often compresses the facial nerve (CN VII), which accompanies CN VIII in the cerebellopontine angle and internal auditory meatus. It may impinge on the pons and affect the spinal trigeminal tract (CN V). Schwannomas occur twice as often in females as in males. Affected structures and resultant deficits include:

Cochlear Neuroma

Figure 14-4. Magnetic resonance image of an acoustic neuroma. This coronal section shows dilation of the ventricles. The vestibulocochlear nerve is visible in the left internal auditory meatus. The tumor indents the lateral pons. Cranial nerve (CN) palsies include CN V, VII, and VIII. Symptoms include unilateral deafness, facial anesthesia and weakness, and an absent coronal reflex. This is a T1-weighted image.

Figure 14-4. Magnetic resonance image of an acoustic neuroma. This coronal section shows dilation of the ventricles. The vestibulocochlear nerve is visible in the left internal auditory meatus. The tumor indents the lateral pons. Cranial nerve (CN) palsies include CN V, VII, and VIII. Symptoms include unilateral deafness, facial anesthesia and weakness, and an absent coronal reflex. This is a T1-weighted image.

A. The cochlear nerve of CN VIII. Damage results in tinnitus and unilateral nerve deafness.

B. The vestibular nerve of CN VIII. Damage results in vertigo, nystagmus, nausea, vomiting, and unsteadiness of gait.

C. The facial nerve (CN VII). Damage results in facial weakness and loss of the corneal reflex (efferent limb).

D. The spinal trigeminal tract (CN V). Damage results in paresthesia, anesthesia of the ipsilateral face, and loss of the corneal reflex (afferent limb).

E. Neurofibromatosis type 2 often occurs with bilateral acoustic neuromas.

V. JUGULAR FORAMEN SYNDROME usually results from a posterior fossa tumor (e.g., glomus jugulare tumor, the most common inner ear tumor) that compresses CN IX, X, and XI. Affected structures and resultant deficits include:

A. The glossopharyngeal nerve (CN IX). Damage results in:

1. Ipsilateral loss of the gag reflex

2. Ipsilateral loss of pain, temperature, and taste in the tongue

B. The vagal nerve (CN X). Damage results in:

1. Ipsilateral paralysis of the soft palate and larynx

2. Ipsilateral loss of the gag reflex

C. The accessory nerve (CN XI). Damage results in:

1. Paralysis of the sternocleidomastoid muscle, which results in the inability to turn the head to the opposite side

2. Paralysis of the trapezius muscle, which causes shoulder droop and inability to shrug the shoulder

VI. "LOCKED-IN" SYNDROME is a lesion of the base of the pons as the result of infarction, trauma, tumor, or demyelination. The corticospinal and corticobulbar tracts are af

Gag Reflex AnatomyGag Reflex Anatomy

Figure 14-5. Anatomy of tbe subclavian steal syndrome. Thrombosis of the proximal part of the subclavian artery (left) results in retrograde blood flow through the ipsilateral vertebral artery and into the left subclavian artery. Blood can be shunted from the right vertebral artery and down the left vertebral artery (A). Blood may also reach the left vertebral artery through the carotid circulation (J3). ACA = anterior cerebellar artery; ACOM = anterior communicating artery; AICA = anterior interior cerebellar artery; ASA = anterior spinal artery; J3A = basilar artery; BCT = brachiocephalic trunk; CCA = common carotid artery; ECA = external carotid artery; 1CA = internal carotid artery; MCA = middle cerebral artery; PCA = posterior cerebral artery; PCOM = posterior communicating artery; PICA = posterior inferior cerebellar artery; SCA = superior communicating artery; SCLA = subclavian artery; VA = vertebral artery.

fected bilaterally. The oculomotor and trochlear nerves are not injured. Patients are conscious and may communicate through vertical eye movements.

VII. CENTRAL PONTINE MYELINOLYSIS is a lesion of the base of the pons that affects the corticospinal and corticobulbar tracts. More than 75% of cases are associated with alcoholism or rapid correction of hyponatremia. Symptoms include spastic quadriparesis, pseudobulbar palsy, and mental changes. This condition may become the locked-in syndrome.

VIII. "TOP OF THE BASILAR" SYNDROME results from embolic occlusion of the rostral basilar artery. Neurologic signs include optic ataxia and psychic paralysis of fixation of gaze (Balint's syndrome), ectopic pupils, somnolence, and cortical blindness, with or without visual anosognosia (Anton's syndrome).

IX. SUBCLAVIAN STEAL SYNDROME (Figure 14-5) results from thrombosis of the left subclavian artery proximal to the vertebral artery. Blood is shunted retrograde down the left vertebral artery and into the left subclavian artery. Clinical signs include transient weakness and claudication of the left arm on exercise and vertebrobasilar insufficiency (i.e., vertigo, dizziness).

X. THE CEREBELLOPONTINE ANGLE is the junction of the medulla, pons, and cerebellum. CN VII and VIII are found there. Five brain tumors, including a cyst, are often located in the cerebellopontine angle cistern. Remember the acronym SAME: schwannoma (75%), arachnoid cyst (1%), meningioma (10%), ependymoma (1%), and epidermoid (5%). The percentages refer to cerebellopontine angle tumors.

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Responses

  • Fatimah
    What cerebral artery affects the vestibulochoclear nerve?
    6 years ago

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