• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/183

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

183 Cards in this Set

  • Front
  • Back
1. What are the three major categories of cerebrovascular diseases?
1. Thrombosis
2. Embolism
3. Hemorrhage
2. What are the most common cerebrovascular disorders?
Thrombosis secondary to atherosclerosis, embolism, hypertensive parenchymal hemorrhage, and ruptured aneurysm
3. In what ways may the brain be deprived of oxygen?
1. Functional hypoxia in a setting of a low partial pressure of oxygen
2. Impaired oxygen carrying capacity of the blood, or inhibition of oxygen use by tissue
3. Ischemia, either transient or permanent, after interruption of the normal circulatory flow.

Cessation of blood flow can result from a reduction in perfusion pressure, as in hypotension, or secondary to large or small vessel obstruction, or both.
4. The survival of the tissue at risk depends on what factors?
1. The availability of collateral circulation
2. Duration of ischemia
3. Magnitude and rapidity of the reduction of flow
5. What are the two principal types of acute ischemic injury?
1. Global cerebral ischemia occurs when there is a generalized reduction of cerebral perfusion

2. Focal cerebral ischemia fools reduction or cessation of blood flow to a localized area of the brain due to large vessel disease (thrombosis or embolus) or to small vessel disease (vasculitis)
6. What are the symptoms of global cerebral ischemia?
In mild cases, there may be only a transient postischemic confusional state, w/eventual complete recovery and no irreversible tissue damage. On the other hand, irreversible damage to CNS tissue does occur in some pts who suffer mild or transient global ischemic insults.

In severe global cerebral ischemia, widespread neuronal death occurs. Pts who survive in this state often remain severely impaired neurologically and deeply comatose.
7. What is the hierarchy of CNS cells that show preferential susceptibility to global cerebral ischemia?
Neurons are the most sensitive cells, although glial cells (oligodendrocytes and astrocytes) are also vulnerable.
8. What is the morphology of the brain in global cerebral ischemia?
The brain is swollen, the gyri are widened, and the sulci are narrowed. The cut surface shows poor demarcation between gray and white matter.

There are three categories of changes:
1. Early changes
2. Subacute changes
3. Repair
9. What is the morphology of the brain in the early changes (12-24 hrs after insult)?
Early changes include acute neuronal cell change (red neurons) characterized at first by microvacuolization, then eosinophilia of the neuronal cytoplasm, and later nuclear pyknosis and karyorhexis. Similar changes occur in astrocytes and oligodendroglia.
10. What cells are the most susceptible to global ischemia of short duration?
***Pyramidal cells of the Sommer sector of the hippocampus, Purkinje cells of the cerebellum, and the pyramidal neurons in the neocortex are the msot susceptible to global ischemia of short duration.
11. What is the morphology of the brain in the subacute changes (24 hrs - 1 week after insult)?
Subacute changes (24 hrs - 1 week after insult) include necrosis of tissue, influx of macrophages, vascular proliferation, and reactive gliosis.
12. What is the morphology of the brain in the repair (after 2 weeks)?
The repair stage is characterized by eventual removal of all necrotic tissue, loss of normally organized CNS structure, and gliosis.

In the cerebral cortex, the neuronal loss and gliosis produce and uneven destruction of the neocortex, w/preservation of some layers and involvement of others, a pattern called pseudolaminar necrosis.
13. What are border zone (watershed) infarcts?
These are wedge shaped areas of infarction that occur in the regions of the brain and spinal cord that lie at the most distal fields of arterial irrigation.

In the cerebral hemispheres, the border zone between the ACA and MCA is at greatest risk.

Damage to this region produces a sickle-shaped band of necrosis over the cerebral convexity a few cm lateral to the interhemispheric fissure. Border zone infarcts are usually seen after hypotensive episodes.
14. What about focal cerebral ischemia?
Cerebral arterial occlusion may lead to focal ischemia and ultimately to infarction of a specific region of CNS tissue w/in the territory of distribution of the compromised vessel.

Note the most important factor is the adequacy of collateral flow. *The major source of collateral flow is the circle of Willis. Thus, there is reinforcement over the surface of the brain for the distal branches of the ACA, MCA, and PCA arteries.
15. Where is there little collateral flow?
The deep penetrating vessels supplying structures such as the thalamus, basal ganglia, and deep white matter have little to no collateral flow.
16. What neurotransmitters are released during ischemia?
Excitatory AA neurotransmitters, such as glutamate, are released during ischemia and may cause damage by overstimulation and persistent opening of specific membrane channels including N-methy-D-aspartate and kainate receptors.

This may cause cell death thru an uncontrolled influx of calcium ions or through the neurotransmitter and potential toxin NO.
17. Occlusive vascular disease of severity sufficient to lead to an infarction is most likely due to?
Due to in situ thrombosis or embolization from a distant source.

There is a frequent association with systemic diseases such as hypertension and diabetes.
18. What are the most common sites of primary thrombosis?
The majority of thrombotic occlusions are due to atherosclerosis.

*The most common sites of primary thrombosis causing cerebral infarction are the carotid bifurcation, the origin of the MCA, and either end of the basilar artery.
19. What are some things that cause arteritis of small and large vessels?
Infectious vasculitis is now more commonly seen in the setting of immunosuppression and opportunistic infection such as toxoplasmosis, aspergillosis, and CMV encephalitis.

It is also seen in polyarteritis nodosa and other collagen vascular diseases.
20. What is primary angiitis of the CNS?
Primary angiitis of the CNS is an inflammatory disorder that involves multiple small to medium sized parenchymal and subarachnoid vessels and is characterized by chronic inflammation, multinucleated giant cells, and destruction of the vessel wall.

There is granuloma formation associated with the giant cells.

Affected individuals manifest a diffuse encephalopathic or multifocal clinical picture, often w/cognitive dysfunction; pts improve w/steroid and immunosuppressive treatment.
21. What is cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)?
CADASIL is a rare hereditary form of stroke caused by mutations in the Notch3 gene. The disease is characterized clinically by recurrent strokes (usually infarcts) and dentia.

Histopathologic study has shown abnormalities of white matter and leptomeningeal arteries consisting of concentric thickening of the media and adventitia.

*Basophilic, PAS positive granules have been consistently detected in the walls of affected vessels, w/loss of smooth muscle cells.
22. How do the Notch3 mutations cause vessel problems?
Many of the Notch3 mutations add or remove Cys residues from the EGF repeats of the extracellular domain of the protein.
23. What is cerebral amyloid angiopathy (CAA)?
CAA is a condition in which amyloidogenic peptides, nearly always the same one found in Alzheimer disease, Aβ₄₀, deposit in the walls of medium and small caliber meningeal and cortical vessels.

This deposition can result in weakening of the vessel wall and risk of hemorrhage.
24. What is the interaction of apoE genotype with Alzhemier disease, and how does it relate to CAA?
There is an effect of apoE genotype on the risk of recurrence of hemorrhage from sporadic CAA, the presence of either an ε2 or ε4 allele increasing the risk of rebleeding.
25. What causes a familial form of CAA called hereditary cerebral hemorrhage with amyloidosis, Dutch type?
A mutation in the precursor protein for the Aβ₄₀ peptide (amyloid precursor protein, APP) causes a familial form of CAA called hereditary cerebral hemorrhage with amyloidosis, Dutch type.
26. What causes hereditary cerebral hemorrhage with amyloidosis, Icelandic type?
Another peptide that can be found in a similar disorder is derived from cystatin C (a secreted inhibitor of cysteine proteins), which causes the syndrome of hereditary cerebral hemorrhage with amyloidosis, Icelandic type.
27. What are the most common sources of emboli to the brain?
Cardiac mural thrombi are among the most common sources; MI, valvular disease, and Afib are important predisposing factors. Next in importance are thromboemboli arising in arteries, most often originating over atheromatous plaques w/in the carotid arteries.
28. Where do most emboli tend to lodge themselves?
The territory of distribution of the MCA - the direct extension of the internal carotid artery - is most freq affected by embolic infarction.

Emboli tend to lodge where blood vessels branch or in ares of pre-existing luminal stenosis.
29. What is an indication that the bone marrow has embolized to the brain?
Widespread hemorrhagic lesions involving the white matter are characteristic of embolization of bone marrow after trauma.
30. What are hemorrhagic (red) infarctions?
Hemorrhagic infarctions are characterized macroscopically by multiple, sometimes confluent, petechial hemorrhages, and is typically associated with embolic events.

The hemorrhage is presumed to be secondary to reperfusion of damaged vessels and tissue, either thru collaterals or directly after dissolution of intravascular occlusive material.
31. What are nonhemorrhagic (pale, bland, anemic) infarcts?
Nonhemorrhagic infarcts are usually associated with thrombosis.

They are evident at 48 hours as pale, soft regions of edematous brain.
32. What is the macroscopic appearance of a nonhemorrhagic infarct?
Change w/time. During first 6 hrs of injury, little is observed. By 48 hrs, the tissue becomes pale, soft, and swollen, and the corticomedullary junction becomes indistinct. From 2-10 days, the brain becomes gelatinous and friable, and the previously ill-defined boundary btwn normal and abnormal tissue becomes more distinct as edema resolves in the adjacent tissue that has survived.

From 10 days to 3 weeks, the tissue liquefies, eventually leaving a fluid-filled cavity lined by dark gray tissue, which gradually expands as dead tissue is removed.
33. What is the microscopic appearance of a nonhemorrhagic infarct?
After the first 12 hrs, ischemic neuronal change (red neurons) and both cytotoxic and vasogenic edema predominate. There is loss of the usual tinctorial characteristics of the white and gray matter structures.

Up to 48 hrs, neutrophilic emigration progressively increases and then falls off. Phagocytic cells derived from circulating monocytes and activated microglia are evident at 48 hours and become the predominant cell type in the ensuing 2-3 weeks.

After several months, the striking astrocytic nuclear and cytoplasmic enlargement recedes. The pia and arachnoid are not affected and do not contribute to the healing process.
34. What is the morphology of hemorrhagic infarcts?
The microscopic picture and evolution of hemorrhagic infarction parallel ischemic infarction, with the addition of blood extravasation and resorption.

Venous infarcts are often hemorrhagic, and may occur after thrombotic occlusion of the superior sagittal sinus or other sinuses or occlusion of the deep cerebral veins.

Carcinoma, localized infections, and other conditions leading to a hypercoagulable state place pts at risk for venous thrombosis.
35. What is incomplete infarction?
Incomplete infarction occurs in focal cerebral ischemia when there is selective necrosis of neurons w/relative preservation of glia and supporting tissues.
36. What about spinal cord infarction?
Spinal cord infarction may be seen in the setting of hypoperfusion or as a consequence of interruption of the feeding tributaries derived from the aorta. Occlusion of the anterior spinal artery is rarer and may occur as a result of embolism or vasculitis.
37. What causes primary hemorrhages w/in the epidural or subdural space?

What about in the brain parenchyma and subarachnoid space?
Primary hemorrhages w/in the epidural or subdural space are typically related to trauma.

Hemorrhages w/in the brain parenchyma and subarachnoid space, in contrast, are often a manifestation of underlying cerebrovascular disease.
38. What are spontaneous (nontraumatic) intraparenchymal hemorrhages?
Spontaneous intraparenchyml hemorrhages occur most commonly in middle to late adult life, w/a peak incidence at about 60 years.

Most are caused by the rupture of a small intraparenchymal vessel.

***Hypertension is the most common underlying cause of primary brain parenchymal hemorrhage, accounting for more than 50% of clinically significant hemorrhages.
39. Hypertension and hemorrhages...
Hypertension causes a number of abnormalities in vessel walls, including accelerated atherosclerosis in larger arteries; hyaline arteriolosclerosis in small vessels, and in severe cases, proliferative changes and frank necrosis of arterioles.

Arteriolar walls affected by hyaline changes are presumably weaker and more vulnerable to rupture.
40. What are Charcot-Bouchard microaneurysms?
In some instances, chronic hypertension is associated w/the development of minute aneurysms, termed Charcot-Bouchard microaneurysms, which may be the site of rupture.

These aneurysms occur in vessels that are less than 300 um in diameter, most commonly w/in the basal ganglia.
41. Where do hypertensive intraparenchymal hemorrhages originate?
They may originate in the putamen (50-60% of cases), thalamus, pons, cerebellar hemispheres (rarely), and other regions of the brain.
42. What are ganglionic hemorrhages?

Lobar hemorrhages?
When the hemorrhages occur in the basal ganglia and thalamus, they are designated ganglionic hemorrhages to distinguish them from those that occur in the lobes of the cerebral hemispheres, which are called lobar hemorrhages.
43. What is the morphology of intracerebral (intraparenchymal) hemorrhages?
Acute hemorrhages are characterized by extravasation of blood w/compression of teh adjacent parenchyma.

On microscopic exam, the early lesion consists of a central core of clotted blood surrounded by a rim of brain tissue showing anoxic neuronal and glial changes as well as edema. Eventually, teh edema resolves, pigment- and lipid laden macrophages appear, and proliferation of reactive astrocytes is seen at the periphery of the lesion.
44. What are some causes of lobar hemorrhages?
Lobar hemorrhages may arise in the setting of hemorrhagic diathesis, neoplasms, drug abuse, infectious and noninfectious vasculitis, and cerebral amyloid angiopathy.
45. What are the most frequent cause of clinically significant subarachnoid hemorrhage?

What else can cause a subarachnoid hemorrhage?
Rupture of a saccular (berry) aneurysm (most common type of aneurysm in the cranial vault).

Subarachnoid hemorrhage may also result from extension of a traumatic hematoma, rupture of a hypertensive intracerebral hemorrhage into the ventricular system, vascular malformation, hematologic disturbances, and tumors.
46. Where are mycotic, traumatic, and dissecting aneurysms found?
These three, like saccular aneurysms, are most often found int eh anterior circulation. They usually present with cerebral infarction rather than subarachnoid hemorrhage.
47. In which disorders is there an increased risk of saccular aneurysms?
1. Autosomal dominant polycystic kidney disease
2. Vascular type Ehlers-Danlos syndrome (type 4)
3. NF1
4. Marfan syndrome
5. Fibromuscular dysplasia of extracranial arteries
6. Coarctation of the aorta
48. What is the morphology of a saccular aneurysm?
An unruptured saccular aneurysm is a thin-walled outpouching at an arterial branch point along the circle of Willis or a major vessel just beyond. Saccular aneurysms measure a few mm to 2 or 3 cm in diameter and have a bright red, shiny surface and a thin, translucent wall.

Brownish discoloration of the adjacent brain and meninges is evidence of prior hemorrhage. The neck of the aneurysm may be either wide or narrow.
49. Where does a rupture of a berry aneurysm typically occur?
Rupture usually occurs at the apex of the sac w/extravasation of blood into the subarachnoid space, the substance of the brain, or both.

*At the neck fo the aneurysm, the muscular wall and intimal elastic lamina stop short and are absent from the aneurysm sac itself. The sac is made up of thickened hyalinized intima.
50. When is rupture of an aneurysm most common?
Rupture with clinically significant subarachnoid hemorrhage is most freq in the 5th decade and is slightly more freq in females.

Those greater than 1 mm in diameter have a roughly 50% risk of re-bleeding per year. Rupture may occur at any time but in about 1/3 of cases it is associated w/acute increases in intracranial pressure, such as with straining at stool or sexual orgasm.
51. What is important to know about the early post-subarachnoid hemorrhage period?
There is an increased risk of injury from vasospasm involving vessels other than those originally injured. This vasospasm can lead to additional ischemic injury.

*This problem is of greatest significance in cases of basal subarachnoid hemorrhage, in which vasospasm can involve major vessels of the circle of Willis.
52. What are the 4 classes of vascular malformations of the brain?
1. AVMs
2. Cavernous angiomas
3. Capillary telangiectasias
4. Venous angiomas
53. What are AVMs?
AVMs involve vessels in the subarachnoid space extending into the brain parenchyma or may occur exclusively w/in the brain.

In macroscopic appearance, they resemble a tangled network of wormlike vascular channels and have a prominent pulsatile AV shunt w/high blood flow thru the malformation.

On microscopic exam, they are composed of greatly enlarged blood vessels separated by gliotic tissue, often w/evidence of prior hemorrhage.
54. What are cavernous hemangiomas?
Cavernous hemangiomas consist of greatly distended, loosely organized vascular channels w/thin, collagenized wallls and are devoid of intervening nervous tissue (thus distinguishing them from capillary telangiectasias).

They have a low flow w/o AV shunting
55. What are the most freq places for cavernous hemangiomas?
They occur most often in the cerebellum, pons, and subcortical regions, in decreasing order of frequency.
56. What are capillary telangiectasias?

What are venous angiomas (varices)?
Capillary telangiectasias are microscopic foci of dilated, thin walled vascular channels separated by relatively normal brain parenchyma and occurring most freq in the pons.

Venous angiomas (varices) consist of aggregates of ectatic venous channels.
57. What is Foix-Alajouanine disease?
Foix-Alajouanine disease (angiodysgenetic necrotizing myelopathy) is a venous angiomatous malformation of the spinal cord and overlying meninges associated with ischemic myelomalacia and slowly progressive neurologic symptoms most often referable to the lumbosacral cord.
58. What are the clinical features of vascular malformations in the brain?
AVMs are the most common type; males are affected 2x as females and the lesion is often recognized clinically btwn the ages of 10 and 30 years presenting as a seizure disorder, an intracerebral hemorrhage, or a subarachnoid hemorrhage.

*The most common site is the territory of the MCA, particularly is posterior branches.
59. What are slit hemorrhages?
Hypertension gives rise to rupture of the small caliber penetrating vessels and the development of small hemorrhages.

In time, these hemorrhages resorb, leaving behind a slitlike cavity (slit hemorrhage) surrounded by brownish discoloration.

On microscopic exam, these hemorrhages show focal tissue destruction, pigment laden macrophages, and gliosis.
60. What is acute hypertensive encephalopathy?
Acute hypertensive encephalopathy is a clinicopathologic syndrome arising in a hypertensive pt characterized by diffuse cerebral dysfunction, including headaches, confusion, vomiting, and convulsions, sometimes leading to coma.

*Petechiae and fibrinoid necrosis of arterioles in the gray and white matter may be seen microscopically.
61. What is vascular (multi-infarct) dementia?
Patients who, over the course of many months and years, suffer multiple, bilateral, gray matter and white matter infarcts may develop a syndrome characterized by dementia, gait abnormalities, and pseudobulbar signs, often w/superimposed focal neurologic deficits.
62. What are the three causes of vascular (multi-infarct) dementia?
1. Cerebral atherosclerosis
2. Vessel thrombosis or embolization from carotid vessels or heart
3. Cerebral arteriolar sclerosis from chronic hypertension
63. What is Binswanger disease?
When the pattern of injury preferentially involves large areas of the subcortical white matter w/myelin and axon loss, the disorder is referred to as Binswanger disease.

In other words, it's a form of multi-infarct dementia caused by damage to the white brain matter.
64. Nuclear and infranuclear pathways
Nuclear and infranuclear pathways involve the brainstem nuclei of CN III, IV, and VI; the peripheral nerves arising from these nuclei; and the eye movement muscles
65. Supranuclear pathways
Supranuclear pathways involve brainstem and forebrain circuits that control eye moments thru connections w/the nuclei of CN III, IV, and VI.
66. What are the six extraocular muscles?
1. Lateral rectus CN VI
2. Media rectus CN III
3. Superior rectus CN III
4. Inferior rectus CN III
5. Superior oblique CN IV
6. Inferior oblique CN III
67. Contraction of the superior rectus
Causes elevation and intorsion of eye
68 .Contraction of the inferior rectus
Causes depression and extorsion of eye
69. Contraction of the inferior oblique
Elevation and extorsion; elevation increases w/adduction and extorsion increases with abduction
70. Contraction of the superior oblique
Depression and intorsion; depression increases with adduction; intorsion increases w/abduction
71. What are the eye muscles that are not extraocular muscles?
1. Levator palpebrae superior
2. Pupillary constrictor
3. Dilator muscles
4. Ciliary muscle
72. Divisions of CN III
Superior: superior rectus and levator palpebrae superioris

Inferior: Medial rectus, inferior rectus, and inferior oblique

*Also carries preganglionic parasympathetic fibers to the pupillary constrictor muscles of the eye and ciliary muscles of the lens.
73. Occulomotor nuclei
Located in the upper midbrian at the level of the superior colliculi and red nuclei, just ventral to the periaqueductal gray matter.

Fascicles of the occulomotor nerve exit the brainstem as CN III in the interpeduncular fossa between the posterior cerebral and superior cerebellar arteries.
74. Edinger-Westphal nuclei
Contain preganglionic parasympathetic fibers, form a V shape as they curve over the dorsal aspect of the oculomotor nuclei and fuse anteriorly in the midline.

The parasympathetic fibers controlling pupil constriction run in the superficial portion of the oculomotor nerve as it travels in the subarachnoid space, and they are susceptible to compression from aneurysms, particularly arising from the nearby posterior communicating artery.
75. Clinical significances of oculomotor subnuclei
1. Unilateral weakness of the levator palpebrae superior, or unilateral pupillary dilation, cannot arise from unilateral lesions of the oculomotor nucleus.

2. Lesions of the oculomotor nucleus affect the contralateral superior rectus.

Lesions of the oculomotor nucleus will actually affect the ipsilateral superior rectus since the crossing fibers traverse the oculomotor nucleus before exiting the third nerve fascicles.
76. Trochlear nuclei
Located in the lower midbrain at the level of the inferior colliculi and the decussation of the superior cerebellar peduncle.

Like the oculomotor nuclei, they lie just ventral to the periaqueductal gray matter and are bounded ventrally by the fibers of the medial longitudinal fasciculus.

The trochlear nerves are the only cranial nerves to exit the brain dorsally. Also, unlike any other cranial nerve, the trochlear nerves exit the brainstem in a completely crossed fashion.
77. Course of the trochlear nerves
The are very thin and are relatively easily damaged by shear injury from head trauma.

They travel through the subarachnoid space along the underside of the tentorium cerebelli and then enter the cavernous sinus to reach the orbit via the superior orbital fissure, and they innervate the superior oblique muscles.
78. Abducens nuclei
Lie on the floor of the fourth ventricle under the facial colliculi in the mid to lower pons.

Abducens fibers travel ventrallly to exit at the pontomedullary junction. The abducens nerve must then follow a long course in the subarachnoid space, ascending between the pons and clivus
79. What is Dorello's canal?
The abducens nerve then exits the dura to enter Dorello's canal, running between the dura and skull, under the petroclinoid ligament.
80. Course of the abducen's nerve
It next makes a sharp bend as it passes over the petrous tip of the temporal bone to reach the cavernous sinus.

This long vertical course may explain why the abduncens nerve is highly susceptible to downward traction injury produced by elevated intracranial pressure.

After traversing the cavernous sinus, the abducens nerve enters the orbit via the superior orbital fissure to innervate the lateral rectus muscle.
81. Causes of diplopia (5)
1. Mechanical problems such as orbital fracture with muscle entrapment
2. Disorders of the extraocular muscles such as thyroid disease, or orbital myositis
3. Disorders of the neuromuscular junction such as myastenia gravis
4. Disorders of CN III, IV, VI, and their central pathways.
5. Disorders involving the supranuclear oculomotor pathways such as internuclear opthalmoplegia, skew deviation, and ingestion of toxins such as EtOH or anticonvulsants
82. Two things to ask the patient that presents w/diplopia
1. Did the diplopia go away when the patient closed or covered one eye?
-suggests it was caused by an eye movement abnormality

2. Did the diplopia get worse with near or far objects, when looking up or down or to the left or right?
-This info can help localize the cause
83. Dysconjugate gaze
When an extraocular muscle is not working properly, dysconjugate gaze results, causing diplopia.

A helpful rule of thumb is that the image farther toward the direction of gaze is always the one seen in the abnormal eye.

For example, when looking at an object to the right, if one eye does not move to the right then it will form a second image that appears displaced to the right.
84. Exotropia and esotropia
Exotropia: Abnormal lateral deviation of one eye

Esotropia: Abnormal medial deviation
85. Hypertropia
Vertical deviation is usually described only with respect to the eye that is higher, and it is called hypertropia.
86. Phoria
Mild weakness present only with an eye covered is called a phoria, in contrast to a tropia.
87. Young children and strabismus
In young children, b/c the visual pathways are still developing, congenital eye muscle weakness can produce strabismus (dysconjugate gaze) that over time causes suppression of one of the images, resulting in amblyopia (decreased vision in one eye). For this reason, early intervention is essential.
88. Complete disruption of the oculomotor nerve (oculomotor palsy)
Causes paralysis of all extraocular muscles except for the lateral rectus and superior oblique.

Therefore, the only remaining movements of the eye are some abduction and some depression and intorsion.

B/c of decreased tone in all muscles except the lateral rectus and superior oblique, the eye may come to lie in a "down and out" position at rest. In addition, paralysis of the levator palpebrae superior causes the eye to be closed (complete ptosis) unless the upper lid is raised with a finger.

Also, the pupil is dilated and unresponsive to light b/c of involvement of the parasympathetic fibers that run w/the oculomotor nerve.
89. Diagonal diplopia
Someone with oculomotor palsy, the patient may report that the diplopia is worse when looking at near objects and better when looking at distant objects, since convergence is impaired.

Red glass testing in the third-nerve palsy generally reveals diagonal diplopia that is most severe when looking up and medially with the affected eye.
90. Common causes of oculomotor nerve palsy
Diabetic neuropathy or head trauma in which shearing forces damage the nerve.

Another important cause is compression of the nerve by intracranial aneurysms, most often arising from the junction of the Pcomm with the internal carotid artery.

Can also be damaged by other abnormalities in the subarachnoid space, cavernous sinus, or orbit.

Herniation of the medial temporal lobe can compress the nerve.

Opthalmoplegic migraine is a condition usually seen in children that causes reversible oculomotor nerve palsy.
91. How would the eyes appear for a patient with a complete left oculomotor nerve palsy?
Left eye would be down and out, and the left eye would be closed unless the upper lid is raised with a finger.

The left pupil would be dilated and unresponsive to light.
92. Aneurysms and third-nerve palsy
Since aneurysms can cause life-threatening intracranial hemorrhage, there should be a high index of suspicion for aneurysms in patients presenting w/third nerve palsy.

Aneurysms classically cause a painful oculomotor palsy that involves the pupil.

***These patients should be considered to have a PComm aneurysm unless proven otherwise.***
93. What causes a complete oculomotor palsy that spares the pupil...?
Complete oculomotor palsy that spares the pupil is not caused by aneurysms; it is usually caused by diabetes.

The reason is though to be that the parasympathetic fibers are located near the surface of the nerve, and if the nerve compression is severe enough to cause complete paralysis of the muscles innervated by CN III, then the pupillary fibers should be involved as well.
94. What causes a partial oculomotor palsy that spares the pupil?
Could be caused by partial compression of CN III by an aneurysm, so an angiogram is usually necessary.
95. Lesions of the oculomotor nerve within the orbit can cause...?
Can sometimes affect the superior division or inferior division in isolation.

A lesion of the superior division causes weakness of the superior rectus and levator palpebrae superior, production so-called double elevator palsy.
96. Function of trochlear nerve

What happens in trochlear palsy?
The trochlear nerve produces depression and intorsion of the eye.

Therefore, in trochlear nerve palsy there is vertical diplopia.

If the weakness is severe, the affected eye may show hypertropia.

There may also be extorsion of the eye, which is not usually visible to the examiner.
97. Appearance of a patient with trochlear nerve palsy
Patients w/ CN IV palsy often report that they can improve the diplopia by looking up (chin tuck) and by tilting the head away from the affected eye b/c these maneuvers compensate for the hypertropia and extorsion, respectively.

The vertical diplopia is most severe when the affected eye is looking downward and toward the nose, which can be confirmed w/red glass testing.
98. In order to Dx a fourth nerve palsy, what are the four typical findings?
1. The affected eye has hypertropia

2. Vertical diplopia worsens when the affected eye looks nasally

3. Vertical diplopia improves with head tilt away from the affected eye

4. Vertical diplopia worsens with downgaze
99. What is another test used to Dx fourth nerve palsy?
Have the patients look at a horizontal line.

In a trochlear nerve palsy, the patient will see two lines, with the lower line tilted.

These two lines form an arrowhead with the "point" directed toward the affected side.
100. Relationship between compensatory head positions and eye movements
The head movement is always in the direction of action normally served by the affected muscle.

For example, in a right trochlear palsy the head is held down and tilted to the left; the normal action of the right trochlear nerve is depression and intorsion of the eye.
101. How would the eyes appear and what head position would be seen in a patient with a complete left trochlear nerve palsy?
The head would be tilted to the right, chin tucked and looking up, and the affected eye would show hypertropia.
102. What is the most commonly injured cranial nerve in head trauma?
The trochlear nerve is the most commonly injured cranial nerve in head trauma, probably b/c of its long course and thin caliber, making it susceptible to shear injury.
103.How does the trochlear nerve get damaged?
Head trauma, and other causes, such as CN IV pathology in the subarachnoid space, cavernous sinus, or orbit include neoplasm, infection and aneurysms.

In many cases the cause remains unknown, and these cases may be caused by microvascular damage to the nerve, esp in diabetic patients.

Vascular or neoplastic disorders within the midbrain or near the tectum can also affect the trochlear nuclei or nerve fascicles.
104. What are four other causes of vertical diplopia?
1. Disorders of extraoxcular muscles
2. Myasthenia gravis
3. Lesions of the superior division of the oculomotor nerve affecting the superior rectus
4. Skew deviation
105. Skew deviation
Defined as vertical disparity in the position of the eyes of supranuclear origin.

Unlike trochlear palsy, in skew deviation the vertical disparity is typically (but not always) relatively constant in all positions of gaze.

Skew deviation can be caused by lesions of the cerebellum, brainstem, or even the inner ear.
106. What are other causes of head tilt?
1. Cerebellar lesions
2. Meningitis
3. Incipient tonsillar herniation
4. Torticollis
107. Lesions of the abducens nerve produce...?
Horizontal diplopia.

In some cases esotropia of the affected eye may be present as well.

In contrast to third-nerve palsy, patients report that the diplopia is better when they are viewing near objects and worse when they are viewing far objects.
108. Appearance of a patient with CN VI palsy
On examination, the affected eye does not abduct normally. In milder abducens nerve palsy these may simply be incomplete "burial of the sclera" on lateral gaze.

Diplopia worsens when the patient tries to abduct the affected eye, which can be confirmed by red glass testing.

Some patients may tend to turn the head toward the affected eye in an effect to compensate for the diplopia.
109. Vulnerability of the abducens nerve to injury
B/c of its long course along the clivus and over the sharp ridge of the petrous temporal bone, the abducens nerve is particularly susceptible to injury from downward traction caused by elevated ICP.

Abducens palsy is therefore an important early sign of supratentorial or infratentorial tumors, pseudotumor cerebri, hydrocephalus, and other intracranial lesions.
110. What are other causes of aducens palsy?
Damage to CN VI can occur in the subarachnoid space, sinus, or orbit.

Common disorders include head trauma, infection, neoplasm, inflammation, aneurysms, and cavernous sinus thrombosis.

Can also result from microvascular neuropathy like that seen in diabetes.
111. Pontine infarcts or other disorders affecting the exiting abducens fascicles in the pons
Cause weakness of ipsilateral eye abduction resembling a peripheral abducens nerve lesion.

However, lesions of the abducens nucleus in the pons produce not a simple abducens palsy, but instead a horizontal gaze palsy in the direction of the lesion.

Additionally, lesions of the abducens nucleus often affect the nearby fibers of CN VII in the facial colliculus, resulting in a ipsilateral facial weakness.
112. Gaze palsy
Movements of BOTH eyes in one direction are decreased.
113. Other causes of horizontal diplopia
Myasthenia gravis and disorders of the extraocular muscles caused by thyroid disease, tumors, inflammation, or orbital trauma.
114. Parasympathetic pathways involved in pupillary constriction

(From the eye to the Edinger-Westphal nuclei)
Light entering one eye activates retinal ganglion cells, which project to both optic tracts b/c of fibers crossing over in the optic chiasm.

Fibers in the extrageniculate pathway continue in the brachium of the superior colliculus past the lateral geniculate nuclear to reach the pretectal area just rostral to the midbrain.

After synapsing, axons then continue bilaterally to the Edinger-Westphal nuclei, which contain preganglionic parasympathetic neurons.
115. Parasympathetic pathways involved in pupillary constriction

(From the Edinger-Westphal nuclei to the pupillary constrictor muscles)
Some of the crossing fibers travel in the posterior commissure. The Edinger-Westphal nuclei lie just dorsal and anterior to the oculomotor nuclei near the midline. Preganglionic parasympathetic fibers travel bilaterally from the Edinger-Westphal nuclei via the oculomotor nerves to reach the ciliary ganglia in the orbit.

From there, postganglionic parasympathetics continue to the pupillary constrictor muscles to cause the pupils to become smaller.
116. Direct response vs. consensual response
Note that a light shown in one eye causes a direct response in the same eye and a consensual response in the other eye b/c information crosses bilaterally at multiple levels.
117. What are the three components of the accommodation response?

When does this response occur?
Occurs when a visual object moves from far to near.

Three components:
1. Pupillary constriction
2. Accommodation of the lens ciliary muscle
3. Convergence of the eyes.
118. Activation of the accommodation response
Activated by visual signals relayed to the visual cortex. From there, thru pathways still unknown, the pretectal nuclei are again activated, causing bilateral pupillary constriction mediated by the parasympathetic pathways.
119. Activation of contraction of the ciliary muscle
Contraction of the ciliary muscle of the lens is parasympathetically mediated by the same pathway.

Note that the lens is normally under tension from the suspensory ligament. The ciliary muscle acts as a sphincter (like the pupillary constructor), so when it contracts it causes the suspensory ligament to relax, producing a rounder, more convex lens shape.
120. Sympathetic pathway for pupillary dilation
A descending sympathetic pathway from the hypothalamus travels in the lateral brainstem and cervical spinal cord to reach thoracic spinal cord levels T1 and T2.

This descending pathways activates preganglionic sympathetic neurons in the IML of the upper thoracic cord.

Axons of the preganglionic sympathetic neurons exit the spinal cord via ventral roots T1 and T2, and join the paravertebral sympathetic chain via white rami communicantes.

The axons synapse in the superior cervical ganglion. From there, postganglionic sympathetic fibers ascend thru the carotid plexus along the walls of the internal carotid artery, ultimately reaching the pupillary dilatory muscle.
121. Sympathetic pathway and its importance in the wide eye stare
Sympathetic pathway is also important in controlling the smooth muscle of the superior tarsal muscle which elevates the upper lid, causing a wide-eyed stare in conditions of increased sympathetic outflow.

These pathways also innervate the smooth muscle orbitalis, which prevents the eye from sinking back in the orbit, as well as the cutaneous arteries and sweat glands of the face and neck.
122. Three classic signs in Horner's syndrome
1. Ptosis
2. Miosis
3. Anhidrosis
123. Possible locations for lesions causing Horner's syndrome
1. Lateral brainstem (infarct or hemorrhage)
2. Spinal cord trauma
3. First and second thoracic roots (pancoast's tumor or trauma)
4. Sympathetic chain trauma or tumor
5. Carotid plexus dissection
6. Cavernous sinus problems
7. Orbit infection or neoplasm
124. Why are postganglionic lesions not usually associated with anhidrosis?
The sympathetics for sudomotor innervation diverge from the oculosympathetic pathway before the superior cervical ganglion.
125. What are pontine pupils?
Large bilateral lesions of the pons are sometimes associated with pontine pupils, in which both pupils are small but reactive to light.

This small pupillary size is probably caused by bilateral disruption of the descending sympathetic pathways.
126. What is a Marcus Gunn pupil?
An afferent pupillary defect.

In this condition the direct response to light in the affected eye is decreased or absent, while the consensual response of the affected eye to light in the opposite eye is normal.

This defect is caused by decreased sensitivity of the affected eye to light, resulting from lesions of the optic nerve, retina, or eye.
127. Test for Marcus Gunn pupil
A useful way to detect an afferent pupillary defect is with the swinging flashlight test. The flashlight is moved back and forth between the eyes every 2-3s.

The afferent pupillary defect becomes obvious when the flashlight is moved from the normal to the affected eye, and the affected pupil dilates in response to light.

*This abnormal dilation should be distinguished from hippus, which is a normal brief oscillation of the pupil size that sometimes occurs in response to light.
128. Pharmacological miosis and mydriasis
Opiates cause bilateral pinpoint pupils, and barbiturate overdose can also cause bilateral small pupils, mimicking pontine lesions.

Anticholinergic agents affecting muscarinic receptors, such as scopolamine or atropine, can cause dilated pupal.
129. Benign (essential, physiologcal) anisocoria
A slight pupillary asymmetry of less than 0.6 mm is seen in 20% of the general population.

This can vary from one examination to the next. There are no association abnormal findings, such as dilation lag, changes in the asymmetry with lighting conditions, or eye movement abnormalities.
130. Light-near dissociation
In light-near dissociation, the pupils constrict much less in response to light than to accommodation.

The mechanism for this disparity is not known for certain, and the mechanism may not be the same in different disorders.
131. Argyll Robertson pupil
A classic example of light-near dissociation associated w/neurosyphilis, in which, in addition to light-near dissociation, the pupils are small and irregular.
132. Adie's myotonic pupil
This disorder is characterized by degeneration of the ciliary ganglion or postganglionic parasympathetic neurons, resulting in a mid-dilated pupil that reacts poorly to light.

Some pupillary constriction can be elicited with the accommodation response, but the pupil then remains constricted and dilates very slowly. The cause is not known.
133. Midbrain corectopia
In this relatively rare condition, lesions of the midbrain can sometimes cause an unusual pupillary abnormality in which the pupil assumes an irregular, off-center shape.
134. Eye opening and eye closure
Eye opening is performed by striated skeletal muscle of the levator palpebrae superioris together with Muller's smooth muscle in the upper lid. The frontalis muscle of the forehead (CN VII) performs an accessory role.

Eye closure is performed by the orbicularis oculi muscle (CN VII)
135. Ptosis
Drooping of the upper eyelid.

Can be seen in Horner's syndrome. Other causes of unilateral or bilateral ptosis include oculomotor nerve palsy affecting the levator palpebrae superior, myasthenia gravis, and redundant skin folds associated with aging.

Causes of bilateral ptosis or closed eyes without loss of consciousness include non-dominant parietal lobe lesions, dorsal lesions of the oculomotor nuclei affecting the central caudal nucleus, and voluntary eye closure associated with phototopia in migraine or meningeal irritation.
136. Differentiation of weakness of the orbicularis oculi caused by CN VII lesions vs. ptosis
Careful exam of the lids using the irises as a reference point can usually resolve this dilemma; in ptosis the upper lid comes down farther over the iris in the affected eye, while in facial weakness the palpebral fissure is widened mainly b/c of sagging of the lower lid in the affected eye.
137. Cavernous sinus
Consists of a collection of venous sinusoids located on either sides of the pituitary that receives venous blood from the eye and superficial cortex and ultimately drains via several pathways into the internal jugular vein.

It lies between the periosteal and dural layers of the dura mater.

It contains:
1. CN VI
2. CN III
3. CN IV
4. CN V1 (ophthalmic division of trigeminal)
5. CN V2 (maxillary division of trigeminal)
6. Internal carotid a.
138. Orbital apex
This is the region where nearly all nerves, arteries, and veins of the orbit converge before communicating with the intracranial cavity via the optic canal and superior orbital fissure.
139. Complete lesions of the cavernous sinus
Disrupts CN III, IV, an VI, causing total opthalmoplegia, usually accompanied by a fixed, dilated pupil.

Can also causes sensory loss due to involvement of CN V1 and V2.
140. Orbital apex syndrome
Produces the same deficits as cavernous sinus syndrome, but they are more likely to involve CN II also, causing visual loss, and often are associated with proptosis, or bulging of the eye, due to mass effect in the orbit.
141. Causes of cavernous sinus syndrome
1. Metastatic tumores
2. Direct extension of nasopharyngeal tumors
3. Meningioma
4. Pituitary tumors
5. Aneurysms of the intracavernous carotid
6. Cavernous carotid arteriovenous fistula
7. Bacterial infection causing vacernous sinus thrombosis
8. Idiopathic granulomatous disease (Tolosa-Hunt syndrome)
9. Fungal infections such as aspergillosis or murcomycosis.
142. Causes of orbital apex syndrome
1. Metastatic tumors
2. Orbital cellulitis (bacterial infection)
3. Idiopathic granulomatous disease (orbital myositis or pseudotumor)
4. Fungal infections such as aspergillosis
143. Saccades
These are rapid eye movements reaching velocities of up to 700 degrees per second. They function to bring targets of interest into the field of view.

Vision is transiently suppressed during saccadic eye movements.

Saccades are the only type of eye movements that can easily be performed voluntarily, although they can be elicited by reflexes as well.
144. Smooth pursuit eye movements
These eye movements are not under voluntary control; they reach velocities of only 100 degrees per second.

They allow stable viewing of moving objects.
145. Vergence eye movements
These eye movements maintain fused fixation by both eyes as target move toward or away from the viewer. The velocity is about 20 degrees per second.
146. Reflex eye movements
These eye movements include optokinetic nystagmus and the vestibulo-ocular reflex.
147. What is nystagmus?
It is a rhythmic form of reflex eye movements composed of slow eye movements in one direction interrupted repeatedly by fast saccade like eye movements in the opposite direction
148. What are the 3 important horizontal gaze centers?
1. Medial longitudinal fasciculus (MLF)
2. Abducens nucleus
3. Paramedian pontine reticular formation (PPRF)
149. Medial longitudinal fasciculus (MLF)
This interconnects the oculomotor, trochlear, abducens, and vestibular nuclei.

Through connections in the MLF, eye movements are normally yoked together, resulting in conjugate gaze in all directions. For example, during horizontal eye movements the actions of the aducens and oculomotor nuclei are coordinated thru connections in the MLF.
150. Abducens nucleus
Through this circuit in the MLF, the abducens nucleus does more than just control abduction of the ipsilateral eye. In reality, the abducens nucleus is a horizontal gaze center, controlling horizontal movements of both eyes in the direction ipsilateral to the side of the nucleus.
151. Paramedian pontine reticualr formation (PPRF)
In the pontine tegmentum near the abducens nucleus is an additional important horizontal gaze center called the PPRF that provides inputs from the cortex and other pathways to the abducens nucleus, resulting in lateral horizontal gaze.
152. Lesions of the abducens nerve vs. abducens nucleus
Lesions of the abducens nerve cause impaired abduction of the ipsilateral eye.

Lesions of the abducens nucleus produces an ipsilateral lateral gaze palsy involving both eyes b/c of the connections through the MLF.

Similarly, lesions of the PPRF cause an ipsilateral lateral gaze palsy.
153. Lesions of the MLF
Lesions of the MLF interrupt the input to the medial rectus. Therefore the eye ipsialteral to the lesion does not adduct fully on attemted horizontal gaze.

In addition, for uncertain reasons there is also nystagmus of the opposite eye, possibly b/c of mechanisms trying to bring the eyes back into alignment.
154. Internuclear opthalmoplegia (INO)
This is the classic neurologic syndrome produced by an MLF lesion. In an INO, eye adduction on the affected side is impaired with horizontal gaze but is often spared during convergence b/c the inputs to the oculomotor nucleus mediating convergence arise from the pretectal region and hence do not travel in the caudal MLF.
155. Causes of INO
Include MS plaques, pontine infarcts, or neoplasms involving the MLF.

A subtle INO can sometimes be detected only by testing of horizontal saccades in both directions and observation of a slight lag in the adduction of the eye on the affected side.
156. Lesions involving both the MLF and the adjacent abducens nucleus or PPRF
There is a combination of an ipsilateral INO and an ipsilateral lateral gaze palsy.

***Results in "one-and-a-half syndrome"
157. "One-and-a-half syndrome"
The ipsilateral eye cannot move at all horizontally, and the contralateral eye loses half of its movements, preserving only its ability to abduct, resulting in the quaint name "one-and-a-half syndrome"
158. What are the brainstem areas that control vertical eye movements?
The rostral midbrain reticular formation and pretectal area.

The ventral portion of this region is thought to mediate downgaze, while the more dorsal region mediates upgaze.
159. What region mediates downgaze?
An important nucleus that is thought to mediate downgaze is the rostral interstitial nucleus of the MLF.
160. What muscles produce convergence?

What muscles produce divergence?
Convergence of the eyes is produced by the medial recti.

Divergence is produced by the lateral recti.

Vergence movements are under the control of descending inputs from the visual pathways in the occipital and parietal cortex and constitute part of the accommodation response.
161. Parinaud's syndrome

What are the 4 components?
1. Impairment of vertical gaze, especially upgaze. This may be due to compression of the dorsal part of the vertical gaze center.

2. Large, irregular pupils that do not react to light but sometimes may react to near-far accommodation.

3. Eyelid abnormalities ranging from bilateral lid retraction or "tucking" to bilateral ptosis.

4. Impaired convergence, and sometimes convergence-retraction nostagmus, especially on attempted upgaze (the eyes rhythmically converge and retract in the orbits).
162. Causes of Parinaud's syndrome
The most common causes are pineal region tumors and hydrocephalus.

Hydrocephalus can cause dilation of the suprapineal recess of the third ventricle which pushes downward onto the collicular plate of the mibrain.

Thus, hydrocephalus, especially in children, can produce the bilateral setting-sun sign, in which the eyes are deviated inward b/c of bilateral sixth nerve palsies and downward b/c of a Parinaud's syndrome.
163. Superior colliculi
Descending cortical pathways travel either directly to the brainstem centers for horizontal, vertical, or convergence eye movements or via relays in the midbrian superior colliculi.
164. Frontal eye fields
The best-known cortical area that controls eye movements consists of the frontal eye fields.

The frontal eye fields generate saccades in the contralateral direction via connections to the contralateral PPRF.
165. Parieto-occipito-temporal cortex
More posterior cortical regions of the parieto-occipito-temporal cortex are primarly responsible for smooth pursuit movements in the ipsilateral direction, via connections with the vestibular nuclei, cerebellum, and PPRF.

The parieto-occipito-temporal cortex may make some contribution to contralateral eye movements as well.
166. What role does the basal ganglia have in vision?
The basal ganglia also play a role in modulatory control of eye movements, and characteristic disorders of eye movements can be seen in basal ganglia dysfunction.
167. Lesions of the cerebral hemispheres
Normally impair eye movements in the contralateral direction, often resulting in a gaze preference toward the side of the lesion.

This gaze preference is typically accompanied by weakness contralateral to the cortical lesion (if the corticospinal pathways are involved), so that the eyes look away from the side of the weakness.
168. Wrong-way eyes
Certain situations can cause the eyes to look toward the side of the weakness. This condition is called wrong-way eyes.

Causes include seizure activity in the cortex, which can drive the eyes in the contralateral direction b/c of activatino of the frontal eye fields, while also causes abnormal or decreased movements of the contralateral side of the body b/c of involvement of motor association cortex and other structures.
169. What other things can cause wrong way eyes?
Large lesions such as thalamic hemorrhage can disrupt the corticospinal pathways of the internal capsule, casing contralateral weakness, yet may also cause the eyes to deviate toward the side of the weakness.

Lesions of the pontine basis and tegmentum can cause wrong-way eyes b/c disruption of the corticospinal fibers causes contralateral hemiplegia, while involvement of the abducens nucleus or PPRF causes ipsilateral gaze weakness.
170. Optokinetic nystagmus (OKN)
The examiner can elicit OKN in the horizontal direction by moving a thick ribbon with vertical stripes horizontally in front of the eyes.

The eyes alternate between smooth pursuit movements in the direction of stripe movement and backup saccades opposite the direction of stripe movement in an attempt to stabilize the image.

OKN is sometimes called train nystagmus b/c it can be observed in the eyes of fellow passengers as they watch the passing visual scene thru an open window.
171. Slow phase, or smooth pursuit phase of OKN
The slow phase, or smooth pursuit phase of OKN, is mediated by the ipsilateral posterior cortex, with connections to the vestibular nuclei and flocculonodular lobe of the cerebellum projecting to the PPRF and abducens nuclei.
172. Fast phase, or saccadic phage of OKN
The fast phase, or saccadic phage of OKN is mediated by the frontal eye fields projecting ultimately to the contralateral PPRF.
173. OKN lesion summary
Therefore, lesions of the frontal cortex or anywhere in the saccadic pathways disrupt the fast phases of OKN, while the slow phases are disrupted by lesions in the smooth pursuit pathways.
174.236. Symptoms:
1. Left frontal and retro-orbital headaches
2. History of left eye drifting to the left, and diplopia with image from left eye above and to the right of image from right eye, with diplopia worse when looking to the right.
3. Left eye with limited but not absent upgaze, downgaze, and adduction, left ptosis, and a fixed dilated left pupil.
Compatible with an oculomotor nerve palsy in the left oculomotor nerve commonly caused by aneurysm where the PComm branches off from the internal carotid.
175. Horizontal diplopia, worse on left gaze, with incomplete abduction of the left eye
This patient has dysfunction of the left lateral rectus muscles causing dysconjugate horizontal gaze, and diplopia.

Most likely Dx is an isolated left abducens nerve palsy.
176. Right hypertropia, and vertical diplopia worse w/downward and leftward gaze and worse with rightward head tilt
These findings are compatible with a right trochlear palsy.

Most likely cause is an idiopathic neuropathy of presumed microvascular origin.
177. On right gaze: left eye pain, limited adduction, and horizontal diplopia, w/right image vanishing when left eye was covered.

On left gaze: mild horizontal diplopia, with the left image vanishing when the left eye was covered.

Pain and erythema of the left orbital conjunctiva
Possible cause is from a lesion that restricts movements of the left lateral rectus muscle due to orbital trauma.
178. Initial left abducens palsy, evolving to ophthalmoplegia, ptosis, and a fixed dilated pupil.

Pain, paresthesia, and decreased sensation to pinprick in the left forehead, eyelid, bridge of nose, and upper cheek.
This patient has dysfunction of the left CN III, IV, VI, and V1, constituting a left cavernous sinus syndrome.
179. Left ptosis, small reactive left pupil, with decreased ciliospinal reflex, and decreased left facial sweating
Dx: Horner's syndrome due to lesion in left sympathetic chain.
180. Lethargy, rightward gaze preference, w/inability to move either eye past the midline toward the left

Right face, arm, and leg weakness, w/upgoing plantar response on the right.
This patient has a combo of a left horizontal gaze palsy and right hemisparesis constituting so called wrong way eyes.

Most likely Dx is an infarct in the left pons involving the left corticospinal and corticobulbar fibers as well as the left abducens nucleus (or PPRF).

Could also be due to seizures in left hemisphere.
181. Left eye did not adduct past the midline and right eye had sustained end gaze nystagmus on abduction.
These findings constitute a left INO localized to the left MLF.
182. Inability of either eye to move past the midline when looking to the left

No adduction of the left eye

End gaze nystagmus on right eye abduction
These finding constitute a left INO plus a left horizontal gaze palsy, also called one and a half syndrome.
183. Headaches, large pupils w/minimal reaction to light but preserved reaction to accommodation (light-near dissociation)

Inability to look upward and lid retraction and convergence-retraction nystagmus.
This patient has a classic Parinaud's syndrome due to compression of or lesions in the dorsal midbrain.