Left Inferior Quadrantanopia

Visual System

I. INTRODUCTION. The visual system is served by the optic nerve, which is a special somatic afferent nerve.

II. THE VISUAL PATHWAY (Figure 17-1) includes the following structures.

A. Ganglion cells of the retina form the optic nerve [cranial nerve (CN) II]. They project from the nasal hemiretina to the contralateral lateral geniculate body and from the temporal hemiretina to the ipsilateral lateral geniculate body.

Figure 17-1. The visual pathway from the retina to the visual cortex showing visual field defects. (1) Ipsilateral blindness. (2) Binasal hemianopia. (3) Bitemporal hemianopia. (4) Right hemianopia. (5) Ri^ht upper quad* rantanopia. (6) Right lower quadrantanopia. (7) Right hemianopia with macular sparing. (8) Left constricted field as a result of end-stage glaucoma. Bilateral constricted fields may be seen in hysteria. (9) Left central scotoma as seen in optic (retrobulbar) neuritis in multiple sclerosis. (10) Upper altitudinal hemianopia as a result of bilateral destruction of the lingual gyri. (II) Lower altitudinal hemianopia as a result of bilateral destruction of the cunei.

Optic Tract Artery

Lateral geniculate body

Temporal Nasal Nasal Temporal

Right eye

Retina Optic nerve tract loop

Visual radiation to lingual gyrus Visual radiation to cuneus

Visual cortex area 17

Left eye

B. The optic nerve projects from the lamina cribrosa of the scleral canal, through the optic canal, to the optic chiasm.

1. Transection causes ipsilateral blindness, with no direct pupillary light reflex.

2. The section of the optic nerve at the optic chiasm transects all fibers from the ipsilateral retina as well as fibers from the contralateral inferior nasal quadrant that loop into the optic nerve. This lesion causes ipsilateral blindness and a contralateral upper temporal quadrant defect (junction scotoma).

C. The optic chiasm contains decussating fibers from the two nasal hemiretinas. It contains noncrossing fibers from the two temporal hemiretinas and projects fibers to the suprachiasmatic nucleus of the hypothalamus.

1. Midsagittal transection or pressure (often from a pituitary tumor) causes bitemporal hemianopia.

2. Bilateral lateral compression causes binasal hemianopia (calcified internal carotid arteries).

D. The optic tract contains fibers from the ipsilateral temporal hemiretina and the contralateral nasal hemiretina. It projects to the ipsilateral lateral geniculate body, pretectal nuclei, and superior colliculus. Transection causes contralateral hemianopia.

E. The lateral geniculate body is a six-layered nucleus. Layers 1, 4, and 6 receive crossed fibers; layers 2, 3, and 5 receive uncrossed fibers. The lateral geniculate body receives input from layer VI of the striate cortex (Brodmann's area 17). It also receives fibers from the ipsilateral temporal hemiretina and the contralateral nasal hemiretina. It projects through the geniculocalcarine tract to layer IV of the primary visual cortex (Brodmann's area 17).

F. The geniculocalcarine tract (visual radiation) projects through two divisions to the visual cortex.

1. The upper division (Figure 17-2) projects to the upper bank of the calcarine sulcus, the cuneus. It contains input from the superior retinal quadrants, which represent the inferior visual field quadrants.

a. Transection causes a contralateral lower quadrantanopia.

b. Lesions that involve both cunei cause a lower altitudinal hemianopia (altitud inopia).

2. The lower division (see Figure 17-2) loops from the lateral geniculate body anteriorly (Meyers loop), then posteriorly, to terminate in the lower bank of the calcarine sulcus, the lingual gyrus. It contains input from the inferior retinal quadrants, which represent the superior visual field quadrants.

a. Transection causes a contralateral upper quadrantanopia ("pie in the sky")-

b. Transection of both lingual gyri causes an upper altitudinal hemianopia (al-titudinopia).

G. The visual cortex (Brodmann's area 17) is located on the banks of the calcarine fissure. The cuneus is the upper bank. The lingual gyrus is the lower bank. Lesions cause contralateral hemianopia with macular sparing. The visual cortex has a retinotopic organization:

1. The posterior area receives macular input (central vision).

2. The intermediate area receives paramacular input (peripheral input).

3. The anterior area receives monocular input.

Bilateral Homonymous Quadrantanopia

Lower r. homonymous quadrantanopia

Field defects

Lat. geniculate

Lesion A of visual radiations to sup. bank of calcarine sulcus

Calcarine sulcus

Upper r. homonymous quadrantanopia

Lesion B of visual radiations to inf. bank of calcarine sulcus

Figure 17-2. Relations of the left upper and left lower divisions of the geniculocalcarine tract to the lateral ventricle and calcarine sulcus. Transection of the upper division (A) results in right lower homonymous quadrantanopia. Transection of the lower division (B) results in right upper homonymous quadrantanopia. (Reprinted with permission from Fix JD: BRS Neuroanatomy. Baltimore, Williams &. Wilkins, 1997, p 261.)

III. THE PUPILLARY LIGHT REFLEX PATHWAY (Figure 17-3) has an afferent limb

(CN II) and an efferent limb (CN III). It includes the following structures:

A. Ganglion cells of the retina, which project bilaterally to the pretectal nuclei

B. The pretectal nucleus of the midbrain, which projects (through the posterior commissure) crossed and uncrossed fibers to the Edinger-Westphal nucleus

C. The Edinger-Westphal nucleus of CN III, which gives rise to preganglionic parasympathetic fibers. These fibers exit the midbrain with CN III and synapse with postganglionic parasympathetic neurons of the ciliary ganglion.

D. The ciliary ganglion, which gives rise to postganglionic parasympathetic fibers. These fibers innervate the sphincter muscle of the iris.

IV. THE PUPILLARY DILATION PATHWAY (Figure 17 4) is mediated by the sympathetic division of the autonomic nervous system. Interruption of this pathway at any level causes ipsilateral Horner's syndrome. It includes the following structures:

A. The hypothalamus. Hypothalamic neurons of the paraventricular nucleus project directly to the ciliospinal center (T1-T2) of the intermediolateral cell column of the spinal cord.

B. The ciliospinal center of Budge (T1-T2) projects preganglionic sympathetic fibers through the sympathetic trunk to the superior cervical ganglion.

C. The superior cervical ganglion projects postganglionic sympathetic fibers through rhe perivascular plexus of the carotid system to the dilator muscle of the iris. Postganglionic sympathetic fibers pass through the tympanic cavity and cavernous sinus and enter the orbit through the superior orbital fissure.

Posterior commissure

Posterior commissure

Pretectal nucleus

Cerebral aqueduct

Edinger-Westphal nucleus of CN III

Red nucleus

Red Nucleus

Retinal ganglionic cell

Sphincter muscle of iris

Medial geniculate nucleus

Lateral geniculate nucleus

Crus cerebri

Figure 17-3. The pupillary light pathway. Light shincd into one eye causes both pupils to constrict. The response in the stimulated eye is called the direct pupillary light reflex. The response in the opposite eye is called the consensual pupillary light reflex. CN = cranial nerve.

Retinal ganglionic cell

Sphincter muscle of iris

Medial geniculate nucleus

Optic tract CN III Ciliary ganglion CN II

Pretectal nucleus

Brachium of superior colliculus

Cerebral aqueduct

Edinger-Westphal nucleus of CN III

Red nucleus

Lateral geniculate nucleus

Crus cerebri

Figure 17-3. The pupillary light pathway. Light shincd into one eye causes both pupils to constrict. The response in the stimulated eye is called the direct pupillary light reflex. The response in the opposite eye is called the consensual pupillary light reflex. CN = cranial nerve.

V. THE NEAR REFLEX AND ACCOMMODATION PATHWAY

A. The cortical visual pathway projects from the primary visual cortex (Brodmann's area 17) to the visual association cortex (Brodmann's area 19).

B. The visual association cortex (Brodmann's area 19) projects through the cortico-tectal tract to the superior colliculus and pretectal nucleus.

C. The superior colliculus and pretectal nucleus project to the oculomotor complex of the midbrain. This complex includes the following structures:

1. The rostral Edinger-Westphal nucleus, which mediates pupillary constriction through the ciliary ganglion

2. The caudal Edinger-Westphal nucleus, which mediates contraction of the ciliary muscle. This contraction increases the refractive power of the lens.

3. The medial rectus subnucleus of CN III, which mediates convergence

VI. CORTICAL AND SUBCORTICAL CENTERS FOR OCULAR MOTILITY

A. The frontal eye field is located in the posterior part of the middle frontal gyrus (Brodmann's area 8). It regulates voluntary (saccadic) eye movements.

Ä Ä 0 —fj

ä

Looking straight ahead

c iO iD

Looking right Looking left Eyes converged

Looking straight ahead

Looking right

Looking up Eyes converged

Looking left and down

No reaction to light Eyes converged

Eyes of a comatose patient

Looking straight ahead

Figure 17-4. Ocular motor palsies and pupillary syndromes. (A) Relative afferent (Marcus Gunn) pupil, left eye. (B) Horner's syndrome, left eye. (C) Internuclear ophthalmoplegia, right eye. (D) Third-nerve palsy, left eye. (E) Sixth-nerve palsy, right eye. (F) Paralysis of upward gaze and convergence (Parinauds syndrome). (G) Fourth-nerve palsy, right eye. (J J) Argyll Robertson pupil. (/) Destructive lesion of the right frontal eye field. (J) Third-nerve palsy with ptosis, right eye.

Figure 17-4. Ocular motor palsies and pupillary syndromes. (A) Relative afferent (Marcus Gunn) pupil, left eye. (B) Horner's syndrome, left eye. (C) Internuclear ophthalmoplegia, right eye. (D) Third-nerve palsy, left eye. (E) Sixth-nerve palsy, right eye. (F) Paralysis of upward gaze and convergence (Parinauds syndrome). (G) Fourth-nerve palsy, right eye. (J J) Argyll Robertson pupil. (/) Destructive lesion of the right frontal eye field. (J) Third-nerve palsy with ptosis, right eye.

1. Stimulation (e.g., from an irritative lesion) causes contralateral deviation of the eyes (i.e., away from the lesion).

2. Destruction causes transient ipsilateral conjugate deviation of the eyes (i.e., toward the lesion).

B. Occipital eye fields are located in Brodmann's areas 18 and 19 of the occipital lobes. These fields are cortical centers for involuntary (smooth) pursuit and tracking movements. Stimulation causes contralateral conjugate deviation of the eyes.

C. The subcortical center for lateral conjugate gaze is located in the abducent nucleus of the pons (Figure 17-5). Some authorities place the "center" in the paramedian pontine reticular formation.

1. It receives input from the contralateral frontal eye field.

2. It projects to the ipsilateral lateral rectus muscle and, through the medial longitudinal fasciculus (MLF), to the contralateral medial rectus subnucleus of the oculomotor complex.

D. The subcortical center for vertical conjugate gaze is located in the midbrain at the level of the posterior commissure. It is called the rostral interstitial nucleus of the MLF and is associated with Parinaud's syndrome (see Figures 14-3A and 17-4F).

Inferior Quadrantanopia

Medial rectus subnucleus of CN III

Medial rectus muscle

Medial rectus subnucleus of CN III

Medial rectus muscle

Midbrain

Left MLF

Right MLF

Pons

Nucleus of CN VI

Bilateral MLF syndrome

Left

Left

Conjugate Gaze Palsies

Patient with MLF syndrome cannot adduct the eye on attempted lateral conjugate gaze, and has nystagmus in abducting eye. The nystagmus is in the direction of the large arrowhead. Convergence remains intact.

Figure 17-5. Connections of the pontine center tor lateral conjugate gaze. Lesions of the medial longitudinal fasciculus (MLF) between the abducent and oculomotor nuclei result in medial rectus palsy on attempted lateral conjugate gaze and horizontal nystagmus in the abducting eye. Convergence remains intact (inset). A unilateral MLF lesion would affect only the ipsilateral medial rectus. CN = cranial nerve.

VII. CLINICAL CORRELATION

A. In MLF syndrome, or internuclear ophthalmoplegia (see Figure 17-4), there is damage (demyelination) to the MLF between the abducent and oculomotor nuclei. It causes medial rectus palsy on attempted lateral conjugate gaze and monocular horizontal nystagmus in the abducting eye. (Convergence is normal.) This syndrome is most commonly seen in multiple sclerosis.

B. One-and-a-half syndrome consists of bilateral lesions of the MLF and a unilateral le* sion of the abducent nucleus. On attempted lateral conjugate gaze, the only muscle that functions is the intact lateral rectus.

C. Argyll Robertson pupil (pupillary light-near dissociation) is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation-convergence). It occurs in syphilis and diabetes.

D. Horner's syndrome is caused by transection of the oculosyuipatheik; pathway at any level (see IV). This syndrome consists of miosis, ptosis, apparent enophthalmos, and hemianhidrosis.

E. Relative afferent (Marcus Gunn) pupil results from a lesion of the optic nerve, the afferent limb of the pupillary light reflex (e.g., retrobulbar neuritis seen in multiple sclerosis). The diagnosis can be made with the swinging flashlight test (see Figure 17-4A).

F. Transtentorial (uncal) herniation occurs as a result of increased supra tentorial pressure, which is commonly caused by a brain tumor or hematoma (subdural or epidural).

1. The pressure cone forces the parahippocampal uncus through the tentorial incisure.

2. The impacted uncus forces the contralateral crus cerebri against the tentorial edge (Kernohans notch) and puts pressure on the ipsilateral CN III and posterior cerebral artery. As a result, the following neurologic defects occur.

a. Ipsilateral hemiparesis occurs as a result of pressure on the corticospinal tract, which is located in the contralateral crus cerebri.

b. A fixed and dilated pupil, ptosis, and a "down-and-out" eye are caused by pressure on the ipsilateral oculomotor nerve.

C. Contralateral homonymous hemianopia is caused by compression of the posterior cerebral artery, which irrigates the visual cortex.

G. Papilledema (choked disk) is noninflammatory congestion of the optic disk as a result of increased intracranial pressure. It is most commonly caused by brain tumors, subdural hematoma, or hydrocephalus. It usually does not alter visual acuity, but it may cause bilateral enlarged blind spots. It is often asymmetric and is greater on the side of the supratentorial lesion.

H. Adie's pupil is a large tonic pupil that reacts slowly to light but does react to near (light-near dissociation). Frequently seen in females with absent knee or or ankle jerks.

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Responses

  • Aatifa
    Why Lateral Geniculate Nucleus quadrant blindness?
    6 years ago
  • danait mewael
    Is the lateral geniculate ganglion the same as pretectal nucleus?
    6 years ago
  • carlos
    What artery causes superior quad hemianopia?
    6 years ago
  • Gorbulas
    What causes inferior quadrantanopia?
    6 years ago
  • pedro
    Where would damage occur along the visual pathway to cause upper or lower quadrantanopia?
    6 years ago
  • DIAMOND
    Which brain tumor cause left lateral rectus palsy?
    5 years ago
  • awet
    What causes superior binasal homonymous quadrantanopia?
    5 years ago
  • WOLFGANG
    Can a brain tumor cause left superior quadrantanopia?
    5 years ago
  • BEATA TREVISANO
    What causes left inferior quadrantanopia?
    5 years ago
  • Danielle
    Is quadrantanopia progressive?
    5 years ago
  • berhane
    What causes and left inferior homonymous quadrantanopia?
    5 years ago
  • annunziata
    How get left inferior quadrantanopsia?
    4 years ago
  • gianetto
    Where is the contralateral right lateral crus?
    4 years ago
  • amilcare
    What causes monocular quadrantanopia visual field defect?
    4 years ago
  • goldilocks longhole
    What is left medial lower quadrant defect?
    4 years ago
  • melvin
    What causes a left inferior quadranopia?
    4 years ago
  • amanuel
    What causes an inferior, left. quadrant visual field defect?
    4 years ago
  • matthias abt
    What give a homonymous inferior quadrantanopia visual neglect?
    3 years ago
  • glen
    What is lower quandrinopsia?
    3 years ago
  • taimi
    What is left medial eye quadrant lesion?
    3 years ago
  • Dodinas
    Does quadrantonopia improve?
    3 years ago
  • FLORIAN
    Does mca stroke cause inferior or superior quadranopia?
    3 years ago
  • anna
    What causes am inferior homoymous quadrantanopia?
    2 years ago
  • Karin
    What causes left inferior quadrantopia in both eyes?
    2 years ago
  • Lloyd
    Is it possible to has a bitemporal quadrantanopia?
    2 years ago
  • Maxwell
    Can you have just unilateral quadrantonopia?
    2 years ago
  • Joona
    How to draw left homonymous quadrantanopia?
    1 year ago
  • goldilocks
    What is the right inferrior quandrant in the eye?
    4 months ago
  • michael petros
    Can you have a monocular inferior quadrantaopia?
    4 months ago
  • LEIGHA
    How does bilateral inferior quadrantanopia effect vision?
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