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232 Cards in this Set

  • Front
  • Back
1. Arterial supply to the cerebral hemispheres
The arterial supply to the cerebral hemispheres is derived from the anterior circulation provided by the bilaterally paired internal carotid arteries, as well as by the posterior circulation provided by the bilateral vertebral arteries.
2. Circle of Willis
The anterior and posterior circulations meet in an anastomotic ring called the circle of Willis, from which all major cerebral vessels arise. The circle of Willis provides abundant opportunities for collateral flow; however, a complete ring in present in only approx 25% of individuals.
3. What are the terminal branches of the internal carotid arteries?
The anterior cerebral arteries and middle cerebral arteries are the terminal branches of the internal carotid arteries.
4. Where does the posterior cerebral arteries arise from?
The PCAs arise from the top of the basilar artery, which in turn is formed by the convergence of the two vertebral arteries.
5. What are the segments of the internal carotid artery?
1. Cervical segment in the neck
2. Petrous segment where it enters the temporal bone
3. Cavernous segment as the artery begins an S-shaped turn, AKA the carotid siphon, within the cavernous sinus
4. Intracranial segment, or supraclinoid, where it pierces the dura to enter the subarachnoid space.
6. What are the main branches of the supraclinoid internal carotid artery?
Remember the mnemonic OPAAM

This stands for: Ophthalmic, Posterior communicating, Anterior choroidal, Anterior cerebral, and Middle cerebral arteries.
7. Ophthalmic artery - where does it start what does it supply?
The ophthalmic artery usually arises from the bend in the internal carotid just after it enters the dura.

It enters the optic foramen with the optic nerve and provides the main blood supply to the retina.
8. Anterior cerebral artery - what does it supply?
The ACA passes forward to travel in the interhemispheric fissure as it sweeps back and over the corpus callosum. Two major branches commonly seen are the pericallosal and callosomarginal arteries.

The ACA thus supplies most of the cortex on the anterior medial surface of the brain, from the frontal to the anterior parietal lobes, usually including the medial sensorimotor cortex.
9. Middle cerebral artery
The MCA turns laterally to enter the depths of the Sylvian fissure. Within the Sylvian fissure it usually bifurcates into the superior division and the inferior division.

The branches of the MCA form loops as they pass over the insula and then around and over the operculum to exit the Sylvian fissure onto the lateral convexity.

The MCA thus supplies most of the cortex on the dorsolateral convexity of the brain.
10. Superior division of the MCA
The superior division of the MCA supplies the cortex above the Sylvian fissure, including the lateral frontal lobe and usually including the peri-Rolandic cortex.
11. Inferior division fo the MCA
The inferior division of the MCA supplies the cortex below the Sylvian fissure, including the lateral temporal lobe and a variable portion of the parietal lobe.
12. Posterior cerebral artery
The PCA curves back after raising from the top of the basilar and sends branches over the inferior and medial temporal lobes and over the medial occipital cortex.

The PCA territory therefore includes the inferior and medial temporal and occipital cortex.
13. What is the name of the most important penetrating vessels at the base of the brain?
The lenticulostriate arteries.

These small vessels arise from the initial portions of the MCA, before it enters the Sylvian fissure, and they penetrate the anterior perforated substance to supply large regions of the basal ganglia and internal capsule.

In hypertension, the lenticulostriate arteries and other similar small vessels are particularly prone to narrowing, which can lead to lacunar infarction, as well as to rupture, causing intracerebral hemorrhage.
14. Anterior choroidal artery
The anterior choroidal artery arises from the internal carotid artery.

Its territory includes portions of the globus pallidus, putamen, thalamus, and the posterior limb of the internal capsule extending up to the lateral ventricle.
15. Recurrent artery of Heubner
The recurrent artery of Heubner comes off the initial portion of the anterior cerebral artery to supply portions of the head of the caudate, anterior putamen, globus pallidus, and internal capsule.
16. Thalamoperforator arteries
Small penetrating arteries that arise from the proximal posterior cerebral arteries near the top of the basilar artery include the thalamoperforator arteries, which supply the thalamus and sometimes extend to a portion of the posterior limb of the internal capsule.
17. Infarcts and ischemic events are most common in which arteries supplying the brain?
Infarcts and ischemic events are more common in the MCA that in the anterior or posterior cerebral arteries, at least in part, b/c of the relatively large territory supplied by the MCA.
18. In what three general regions do MCA infarcts occur?
1. Superior division
2. Inferior division
3. Deep territory
19. MCA stem infarcts
Proximal MCA occlusions affecting all three of these regions are called MCA stem infarcts.
20. Large MCA territory infarcts
Large MCA territory infarcts often have a gaze preference towards the side of the lesion, especially in the acute period, shortly after onset.
21. Lacunes
Small deep infarcts involving penetrating branches of the MCA or other vessels are called lacunes. Certain characteristic lacunar syndromes can often be distinguished on clinical grounds from infarcts involving large blood vessel territories.
22. ACA infarcts
ACA infarcts typically produce contralateral lower extremity cortical type sensory loss and weakness of the upper motor neuron type.

There may also be a variable degree of frontal lobe dysfunction depending, in part, on the size of the infarct. Such dysfunction may include a grasp reflex, impaired judgment, flat affect, apraxia, abulia, and incontinence.
23. Alien hand syndrome
Sometimes damage to the supplementary motor area and other regions in the frontal lobe leads to an unusual "alien hand syndrome" characterized by semiautomatic movements of the contralateral arm that are not under voluntary control.
24. PCA infarcts
PCA infarcts typically cause a contralateral homonymous hemianopia. Smaller infarcts that do not involve the whole PCA territory may cause smaller homonymous visual field defects. Sometimes the small penetrating vessels that come off the proximal PCA are involved, leading to infarcts int he thalamus or posterior limb of the internal capsule.

The result can be a contralateral sensory loss, contralateral hemiparesis, or even thalamic aphasia, if the infarct is in the dominant hemisphere thereby mimicking features of MCA infarcts.
25. What type of infarction can produce alexia without agraphia?
PCA infarcts that involve the left occipital cortex and the splenium of the corpus callosum can produce alexia without agraphia.
26. Watershed zones
When a cerebral artery is occluded, ischemia or infarction occurs in the territory supplied by that vessel, with regions near other vessel relatively spared.

In contrast, when the blood supply to two adjacent cerebral arteries is compromised, the regions between the two vessels are most susceptible to ischemia and infarction. These regions between cerebral arteries are called watershed zones.
27. Bilateral watershed infarcts
Bilateral watershed infarcts in both the ACA-MCA and MCA-PCA watershed zones can occur with severe drops in systemic BP.

A sudden occlusion of an internal carotid artery or a drop in BP in a patient with carotid stenosis can cause an ACA-MCA watershed infarct, since these vessels are both fed by the carotid.
28. What are the deficits caused by a watershed infarct?
Watershed infarcts can produce proximal arm and leg weakness ("Man in the barrel" syndrome) b/c the regions of homunculus involved often include the trunk and proximal limbs.

In the dominant hemisphere, watershed infarcts can cause transcortical aphasia syndromes.

MCA-PCA watershed infarcts can cause disturbances of higher-order visual processing.

In addition to watershed infarcts between the superficial territories of different cerebral vessels, watershed infarcts can also occasionally occur between the superficial and deep territories of the MCA.
29. What are the most common causes of transient neurologic episodes?
The most common causes of transient neurologic episodes are transient ischemic attack, migraine, seizure, and other non-neurologic conditions such as cardiac arrhythmia or hypoglycemia.
30. Transient ischemic attack (TIA)
A TIA is classically defined as a neurologic deficit lasting less than 24 hours, caused by temporary brain ischemia. The more typical duration for a TIA is about 10 minutes.

Ischemic deficits lasting more than about 10 minutes probably produce at least some permanent cell death in the involved region of the brain. TIAs lasting more than an hour, in fact, are usually small infarcts. On the other hand, despite the appearance of a small infarct on an MRI scan, complete functional recovery can sometimes occur within one day.
31. Mechanisms for transient ischemic attack
ne possibility is that an embolus temporarily occludes the blood vessel but then dissolves, allowing return of blood flow before permanent damage occurs.

Other possibilities include in situ thrombus formation on the blood vessel wall and/or vasospasm leading to temporary narrowing of the blood vessel lumen.
32. What are some other diagnoses that can commonly mimic TIAs?
Focal seizures and migraines; also - episodes of hypoglycemia can sometimes produce transient focal neurologic deficits, especially in the elderly.
33. What can cause a transient loss of consciousness without other focal features?
This is a special case of transient neurologic dysfunction. The most common cause by far is cardiogenic syncope including vasovagal transient episodes of hypotension ("fainting"), arrhthmias, and other non-neurologic causes.

Neurological causes are responsible for less than 5-10% of cases of syncope, and include seizures, and rarely, TIA of the posterior circulation affecting the brainstem reticular activating systems.
34. Stroke
Stroke is the third leading cause of death in the US and a major cause of permanent disability.

Stroke refers to both hemorrhagic events, such as intracerebral or subarachnoid hemorrhage, and to ischemic infarction of the brain.
35. Hemorrhagic conversion
Sometimes ischemic strokes can cause blood vessels to become fragile and rupture, leading to secondary hemorrhagic conversion.
36. Mechanisms of ischemic stroke
Ischemic stroke occurs when there is inadequate blood supply to a region of the brain for enough time to cause infarction (death) of brain tissue.

In clinical practice, a distinction is often made between embolic and thrombotic infarcts.
37. Embolic infarcts
A piece of material (usually a blood clot) is formed in one place and then travels through the bloodstream to suddenly lodge in and occlude a blood vessel supplying the brain.
38. Thrombotic infarct
In thrombotic infarcts, a blood clot is formed locally on the blood vessel wall, ususally at the site of an underlying atherosclerotic plaque, causing the vessel to occlude.

Embolic infarcts are considered to occur suddenly with maximal deficits at onset, while thrombotic infarcts may have a more stuttering course.
49. Large-vessel infarcts
Large-vessel infarcts involve the major blood vessels on the surface of the brain, such as the MCA and its main branches.

Large-vessel infarcts are most often caused by emboli, although thrombosis can also occasionally occur, esp in large proximal vessels such as the vertebral, basilar, and carotid arteries.
40. Small-vessel infarcts
Small vessel infarcts involve the small penetrating vessels that supply deep structures.

In the cerebral hemispheres these include the basal ganglia, thalamus, and internal capsule, while in the brainstem these include the medial portions of the midbrain, pons, and medulla.

Small-vessel infarcts are sometimes also called lacunar infarcts b/c they resemble small lakes or cavities when the brain is examined on pathologic section.
41. Dissection of the carotid or vertebral arteries often results in...?
Often results in thrombus formation, which can embolize to the brain.
42. Patent foramen ovale and embolus
Sometimes, a patent foramen ovale can allow a thromboembolus formed in the venous system to bypass the lungs and pass directly from the right to the left side of the heart, reaching the brain.
43. Lypohalinosis
In hypertension, the small penetrating vessels become occluded by a pathologic process known as lipohyalinosis.
44. Ataxic hemiparesis
In ataxic hemiparesis, the ataxia is caused by damage to proprioceptive or cerebellar circuitry rather than by damage to the cerebellum itself.
45. Thalamic lacunes vs. basal ganglia lacunes
Thalamic lacunes can cause contralateral somatosensory deficits, sometimes followed by a thalamic pain syndrome.

Basal ganglia lacunes can occasionally cause movement disorders such as hemibalismus.
46. Cortical lesions
Corical lesions can be differentiated from subcortical lesions by the presence of cortical signs.

These signs include aphasia, neglect, homonymous visual field defects, and cortical sensory loss.
47. Headaches in ischemic strokes
Headache occurs in 25-30% of ischemic strokes. When the headache is unilateral, it is more commonly on the side of the infarct, although exceptions do occur.

Headache may be more common for posterior than for anterior circulation infarcts, and is often seen in dissection of the carotid or vertebral arteries.
48. Summary of emboli, lacunes, and thrombosis...
1. Emboli usually cause large-vessel infarcts involving cerebral or (less commonly) cerebellar cortex, with sudden onset of maximal deficits.

2. Lacunes are small-vessel infarcts usually seen in chronic hypertension, commonly affecting the deep white matter and nuclei of the cerebral hemispheres and brainstem.

3. Thrombosis occasionally occurs in large proximal vessels such as vertebral, basilar, and carotid arteries and may also contribute to lacunar infarction.
49. Common stroke risk factors
1. Hypertension
2. Diabetes
3. Hypercholesterolemia
4. Cigarette smoking
5. Positive family history
6. Cardiac disease (valvular disease, atrial fibrillation, patent foramen ovale, low ejection fraction)
7. Prior history of stroke or other vascular disease
50. Hypercoagulation and strokes
Less commonly, several other systemic medical conditions may affect the coagulation pathways or work through other mechanisms to increase both thrombotic and embolic infarcts.

These hypercoagulate states also increase the risk for venous thrombosis.
51. Ischemic strokes in young patients
Ischemic stroke is relatively uncommon in young individuals b/c the cumulative effects of the major stroke risk factors tend to worsen with age.

When stroke does occur in a young patient, conditions such as arterial dissection, patent foramen ovale, or the hypercoagulable states should be considered.
52. Diagnostic workup of ischemic stroke and TIA
Prompt medical attention allows early therapeutic interventions that improve outcome.

When the history and exam suggest a possible ischemic event, an imaging study of the brain should be done immediately to rule out hemorrhage.

Remember that an infarct will often not be visible on the CT scan, especially if it is done within a few hours of symptoms onset; however, a hemorrhage will almost always be visible.

Meanwhile, routine blood chemistries, cell counts, and coagulation studies should be sent.
53. Treatment of ischemic stroke
Once a hemorrhage has been ruled out by CT, many physicians treat patients with thrombolytic agents, such as t-PA in acute ischemic stroke.

This treatment has been demonstrated to be effective and it improves the chances of a good functional outcome if given within 3 hours of stroke onset; however, it does carry increased risk of intracranial hemorrhage.
54. What do you give patients that are not eligible for t-PA treatment, or those patients who have had a TIA?
Heparin anticoagulation is often used while further diagnostic studies are being performed.

As with t-PA, it is essential to rule out the presence of intracranial hemorrhage before administering this treatment.
55. Intra-arterial thrombolysis
This is performed by catheterization of the occluded vessel, which allows direct administration of the thrombolytic agent to the thrombus.
56. Should hyperglycemia be corrected in an acute stroke?
Hyperglycemia should be corrected in acute stroke b/c it can worsen infarctions, possibly by increasing local tissue acidosis and blood-brain barrier permeability.
57. How does one assess blood flow in the major cranial and neck vessels?
Blood flow in the major cranial and neck vessels should be assessed with Doppler ultrasound and/or magnetic resonance angiography.

This is aprticularly important in suspected internal carotid artery stenosis, since carotid enarterectomy may be required.

Conventional angiography may be needed in cases where the degree of stenosis is uncertain based on these invasive tests.
58. Patients with atrial fibrillation and stroke
Patients with atrial fibrillation are at increased risk of embolic stroke, and that this risk is significantly reduced when they are treated with Coumadin oral anticoagulation.
59. Hemicraniectomy
In patients with large MCA infarcts, there may be substantial edema and mass effect, which can sometimes lead to herniation and death.

One therapeutic measure that is being investigated for such patients in hemicraniectomy, in which a portion of skull is temporarily removed over the region of swelling and is later replaced after the danger of herniation has passed.
60. What is the most common cause of stenosis in the internal carotid artery just beyond the carotid bifurcation?
Atherosclerotic disease commonly leads to stenosis of the internal carotid artery just beyond the carotid bifurcation.

Thrombi formed on a stenotic internal carotid artery can embolize distally, giving rise to TIAs or infarcts of various carotid branches, esp the MCA, ACA, and ophthalmic artery.
61. Carotid stenosis symptoms
Carotid stenosis is associated with MCA territory symptoms such as contralateral face-arm or face-arm-leg weakness, contralateral sensory changes, contralateral visual field defects, aphasia, or neglect.

In addition, there may be ophthalmic artery symptoms such as ipsilateral monocular visual loss, and ACA territory symptoms such as contralateral leg weakness.
62. How can one assess the severity of a carotid stenosis?
Can be estimated noninvasively with Doppler ultrasound and MRA, although conventional angiography remains the gold standard.
63. Carotid endarterectomy
Treatment for symptomatic carotid stenosis. In this procedure the carotid artery is exposed surgically and temporarily clamped.

A longitudinal incision is made in the artery, and atheromatous material is shelled out from the internal carotid lumen, eliminating the stenosis.
64. Carotid occlusion
Sometimes an internal carotid artery can gradually or suddenly become 100% occluded, causing infarcts in the MCA, ACA, or ACA-MCA watershed territories.

Carotid occlusion may be completely asymptomatic if there is sufficient collateral flow via the anterior or posterior communicating arteries.
65. Common location of carotid occlusions
The occlusion usually occurs just beyond the carotid bifurcation, and the vessel then becomes filled with thrombus up to the level of the ophthalmic artery, which is perfused by collateral flow.

Emboli may become dislodged from the top of the thrombus and cause TIAs or strokes.
66. Treatment for carotid occlusions
In contrast to carotid stenosis, endarterectomy is not usually performed in cases of 100% carotid occlusion b/c of the risk of dislodging more emboli, and b/c the procedure has no proven benefit.
67. Random cause for watershed infarction with carotid stenosis?
A sudden drop in systemic BP - leads to infarction in the ACA-MCA watershed territory.
68. Carotid dissection
Head or neck trauam, and sometimes even minor events can cause a small tear to form on the intimal surface of the carotid or vertebrate arteries.

This may allow blood to burrow into the vessel wall, producing a dissection. A flap then protrudes into the vessel lumen, under which thrombus forms that can embolize distally.
69. Symptoms of a carotid dissection
Patients with a carotid dissection may describe feeling or hearing a pop at the onset.

They may hear a turbulent sound with each heartbeat and have an ipsilateral Horner's syndrome and pain over the eye.
70. Vertebral dissection
In a vertebral dissection, there is often posterior neck and occipital pain.

Sometimes dissection, particularly of the vertebral artery, leads to formation of a pseudoaneurysm that may rarely rupture, causing subarachnoid hemorrhage.
71. Vertebral vs. carotid dissection infarct locations
TIAs or infarcts occur in the anterior circulation with carotid dissection.

They occur in the posterior circulation with vertebral dissection.
72. Treatment of dissections
Dissection is usually treated with IV heparin followed by oral Coumadin to prevent thromboembolic events.
73. Sagittal sinus thrombosis
Sagittal sinus thrombosis is often associated with one of the hypercoagulable states. It occurs with increased frequency in pregnant women and within the first few weeks post partum.

Obstruction of the venous drainage usually causes elevated ICP.

In addition, the increased venous pressure can decrease cerebral perfusion, leading to infarcts. Seizures are common. Patients often have headaches and papilledema, and they may have depressed level of consciousness.

Treatment is usually with anticoagulation therapy, although this is controversial when hemorrhage has occurred.
74. Where do the superficial veins of the brain drain?
The superficial veins drain mainly into the superior sagittal sinus and the cavernous sinus.
75. Where do the deep veins of the brain drain?
The deep veins of the brain drain into the great vein of Galen.

Ultimately, nearly all venous drainage for the brain reaches the internal jugular veins.
76. Cavernous sinus
The cavernous sinus is a plexus of veins located on either side of the sella turcica that surrounds portions of the internal carotid artery and CN III, IV, V, and VI.

The cavernous sinus drains via the superior petrosal sinus into the transverse sinus, and via the inferior petrosal sinus into the internal jugular vein.
77. The confluence of the sinuses (AKA torcular Herophili)
The confluence of sinuses occurs where the superior sagittal, straight, and occipital sinuses join together and are drained by the transverse sinuses.

The torcula is often shaped in such a manner that most blood from the superior sagittal sinus enters the right transverse sinus, while most blood from the straight sinus enters the left transverse sinus.
78. What are the five major cortical veins?
1. Inferior anastomotic vein of Labbe, which drains into the transverse sinus
2. Superior anastomotic vein of Trolard, which drains into the superior sagittal sinus
3. Superficial middle cerebral vein, which drains into the cavernous sinus
4. Anterior cerebral veins*
5. Deep middle cerebral veins*

*Drains into the basal veins of Rosenthal, which then join the internal cerebral veins to form the great vein of Galen
79. Left MCA superior division infarct
Left MCA superior division infarct

1. Right face and arm weakness of the upper motor neuron type
2. Nonfluent, or Broca's, aphasia
3. In some cases there may also be some right face and arm cortical type sensory loss.
80. Left MCA inferior division infarct
Left MCA inferior division infarct

1. Fluent, or Wernicke's aphasia
2. Right visual field deficit
3. There may also be some right face and arm cortical type sensory loss.
4. Motor findings are usually absent, and patients may initially seem confused or crazy, but otherwise intact, unless carefully examined.
5. Some mild right sided weakness may be present, especially at the onset of symptoms.
81. Left MCA deep territory infarct
Left MCA deep territory infarct

1. Right pure motor hemiparesis of the upper motor neuron type.
2. Larger infarcts may produce cortical deficits as well, i.e. aphasia.
82. Left MCA stem infarct
Left MCA stem infarct

Combo of above with:
1. Right hemiplegia
2. Right hemianesthesia
3. Right homonymous hemianopia
4. Global aphasia
5. There is often a left gaze preference, especially at the onset, caused by damage to the left hemisphere cortical areas important for driving the eyes to the right.
83. Right MCA superior division infarct
Right MCA superior division infarct

1. Left face and arm weakness of the upper motor neuron type
2. Left hemineglect is present to a variable extent.
3. In some cases there may also be come left face and arm cortical type sensory loss
84. Right MCA inferior division infarct
Right MCA inferior division infarct

1. Profound left hemineglect
2. Left visual field and somatosensory deficits are often present, however, these may be difficult to test convincingly b/c of the neglect.
3. Motor neglect w/decreased voluntary or spontaneous initiation of movements on the left side can also occur. However, even patients with left motor neglect usually have normal strength on their left side, as evidenced by occasional spontaneous movements or purposeful withdrawal from pain.
4. Some mild right-sided weakness may be present.
5. There is often a right gaze preference, especially at onset.
85. Right MCA deep territory infarct
Right MCA deep territory infarct

1. Left pure motor hemiparesis of the upper motor neuron type.
2. Larger infarcts may produce "cortical" deficits as well, such as left hemineglect.
86. Right MCA stem infarct
Right MCA stem infarct

Combo of the above with:
1. Left hemiplegia
2. Left hemianesthesia
3. Left homonymous hemianopia
4. Profound left hemineglect
5. There is usually a right gaze preference, especially at the onset, caused by damage to right hemisphere cortical areas important for driving the eyes to the left.
87. Left ACA infarct
Left ACA infarct

1. Right leg weakness of the upper motor neuron type
2. Right leg cortical type sensory loss
3. Grasp reflex, frontal lobe behavioral abnormalities, and transcortical aphasia can also be seen.
4. Larger infarcts may cause right hemiplegia
88. Right ACA infarct
Right ACA infarct

1. Left leg weakness of the upper motor neuron type
2. Left leg cortical type sensory loss
3. Grasp reflex, frontal lobe behavioral abnormalities, and left hemineglect can also be seen.
4. Larger infarcts may cause left hemiplegia
89. Left PCA infarct
Left PCA infarct

1. Right homonymous hemianopia
2. Extension to the splenium of the corpus callosum can cause alexia without agraphia
3. Larger infarcts including the thalamus and internal capsule may cause aphasia, right hemisensory loss, and right hemiparesis
90. Right PCA infarct
Right PCA infarct

1. Left homonymous hemianopia
2. Larger infarcts including the thalamus and internal capsule may cause left hemisensory loss and left hemiparesis.
91. Pure motor hemiparesis or dysarthia hemiparesis
Pure motor hemiparesis or dysarthia hemiparesis

Clinical features:
Unilateral face, arm, and leg upper motor neuron type weakenss, with dysarthria.

Locations:
Posterior limb of internal capsule*, ventral pons*, conona radiata, cerebral peduncle

*Most common
92. Ataxic hemiparesis
Ataxic hemiparesis

Clinical features:
Same as pure motor hemiparesis, but with ataxia on same side as weakness

Location:
Same as pure motor hemiparesis
93. Pure sensory stroke (thalamic lacune)
Pure sensory stroke (thalamic lacune)

Clinical features:
Sensory loss to all primary modalities in the contralateral face and body

Location:
VPL nucleus of the thalamus
94. Sensorimotor stroke (thalamocapsular lacune)
Sensorimotor stroke (thalamocapsular lacune)

Clinical features:
Combination of thalamic lacune and pure motor hemiparesis

Locations:
Posterior limb of the internal capsule, and either thalamic VPL or thalamic somatosensory radiation
95. Basal ganglia lacune
Basal ganglia lacune

Clinical features:
Usually asymptomatic, but may cause hemiballismus (involuntary flinging motions of the extremities)

Locations:
Caudate, putamen, globus pallidus, or subthalamic nucleus
96. 1. Profound weakness of the left leg, with mild weakness of the left arm and face, mild dysarthria, left leg hyperreflexia, and Babinski's sign
2. Left grasp reflex and motor impersistence
3. Left arm "out of control"
4. Unawareness of left sided weakness and abrasions, decreased response to pinprick on the left, tactile extinction on the left.
Dx: Embolic stroke causing an infarct in the right medial frontal lobe including foot motor cortex and supplementary motor area would be caused by occlusion of the right anterior cerebral artery.

In sum, right ACA infarct
97. Right homonymous hemianopia and left retro-orbital headache
PCA infarct which caused a left primary visual cortex infarct
98. 1. Right handed weakness and speech difficult "mixing up words"
2. Dim blurry vision in the left eye
3. Right leg suddenly gave out
4. High-pitched bruit audible over the left carotid artery
Very tight stenosis of the left internal carotid artery.
99. Decreased movements of right face (sparing forehead), profound right arm weakness, and mild right leg weakness

Also has nonfluent (Broca's) aphasia
Left MCA superior division infarct causing infarcts in the left primary motor face and arm areas, Broca's area, and adjacent left frontal cortex.
100. 1. Fluent aphasia with impaired comprehension and repetition
2. Blink to threat present only on the left
3. Greater grimace in response to pinprick on the left side than the right
4. Slightly increased tone in the right arm, with right Babinski's sign
Left MCA inferior division infarct causing lesions int he left temporal and parietal lobes, including Wernicke's area, optic radiations and somatosensory cortex.
101. Dysarthria and right face, arm, and leg paralysis with a right Babinski's sign
This is pure motor hemiplegia.

Most likely resulted from an ischemic infarct of the internal capsule.

Internal capsule infarcts are most commonly caused by occlusion of the lenticulostriate arteries, which take their origin from the proximal MCA and supply the deep MCA territories.
102. 1. Right face, arm, and leg paralysis, w/right hyperreflexia and Babinski's sign
2. No response to pain on the right side except for weak flexion of the right leg
3. Global aphasia
4. No blink to threat on the right
5. Left gaze preference
6. Decreased right corneal reflex
Left MCA stem infarct
103. 1. Left facial weakness sparing the forehead, left arm weakness, and hyperreflexia
2. Mild dysarthria
3. Occasional extinction on the left side to double simultaneous visual or tactile stimulation
Right MCA superior division infarct
104. 1. Anosognosia
2. Left visual neglect
3. Extinction on the left to double simultaneous tactile stimulation
4. Moving the hand to the right of the page
5. Decreased spontaneous movements on the left side
6. Right gaze preference
7. No blink to threat on the left
8. Decreased spontaneous movements on the left side, with mildly decreased left nasolabial fold, and slightly brisker reflexes on the left
TIA followed by ischemic infarct of the right temporoparietal lobe which is supplied by the right MCA inferior division.
105. 1. Anasognosia, hemiasomatognosia
2. Left face, arm, and leg plegia with left Babinski's sign
3. No blink to threat on the left
4. No voluntary gaze to the left past the midline
5. No response to pinprick on the left side
Right MCA stem infarct
106. 1. Weakness of the proximal left arm and leg, with left hyperreflexia and Babinski's sign
2. Unsteady gait, veering to the left
3. Decreased leftward fast phases of optokinetic nystagmus
4. Right carotid bruit
Acute infarct in the right ACA-MCA watershed territory
107. 1. Right frontal headache
2. Weakness of the left face and arm more than the left, with left Babinski's sign
3. Mildly decreased light touch, pinprick, temp, vibration and joint position sense on the left side, with decreased left stereognosis and graphesthesia
4. Left visual and tactile extinction
Hemorrhage in the parietal lobe extending to the face and arm regions of the precentral gyrus.
108. What is the principal visual pathways from the two retinas to the visual cortex?
The visual nerve signals leave the retinas thru the optic nerves. At the optic chiasm, the optic nerve fibers from the nasal halves of the retinas cross to the opposite sides, where they join the fibers from the opposite temporal retinals to form the optic tracts.

The fibers of each optic tract then synapse in the dorsal lateral geniculate nucleus of the thalamus, and from there, geniculocalcarine fibers pass by way of the optic radiation to the primary visual cortex in the calcarine fissure area of the medial occipital lobe.
109. What are 4 other older areas of the brain in which visual fibers also pass?
1. From the optic tracts to the suprachiasmatic nucleus of the hypothalamus (control circadian rhythm)
2. Into the pretectal nuclei in the midbrain, to elicit reflex movement of the eyes to focus on objects of important and to activate the pupillary light reflex
3. Into the superior colliculus, to control rapid directional movement of the two eyes
4. In the ventral lateral geniculate nucleus of the thalamus and surrounding basal regions of the brain, presumably to help control some of the body's behavioral functions
110. So what are the main differences between the old and new system for transmission of visual signals?
The older system travels to the midbrain and the base of forebrain and is used for visual detection of form via the superior colliculus.

The new system is for direct transmission of visual signals into the visual cortex and is responsible for perception of virtually all aspects of visual form, colors, and other conscious vision.
111. What are the functions of the dorsal lateral geniculate nucleus?
The optic nerve fibers of the new visual system terminate in the dorsal lateral geniculate nucleus, located at the dorsal end of the thalamus, and also called simply the lateral geniculate body.

It has two principal functions:

1. It relays visual infection from the optic tract to he visual cortex by way of the optic radiation. (Very accurate)
2. It "gates" the transmission of signals to the visual cortex-- that is, to control how much of the signal is allowed to pass to the cortex.
112. What are the different layers of the fibers in the optic tract?

What is the composition of the dorsal lateral geniculate nucleus?
Half the fibers in each optic tract after passing the optic chiasm are derived from one eye and half from the other eye. However, the signals from the two eyes are kept apart in the dorsal lateral geniculate nucleus.

This nucleus is composed of six layers. Layer 2, 3, and 5 receive signals form the lateral half of the ipsilateral retina, whereas layers 1, 4, and 6 receive signals from the medial half of the retina of the opposite eye.
113. The dorsal lateral geniculate nucleus receives fibers from what two major sources?
1. Corticofugal fibers returning in a backward direction from the primary visual cortex to the lateral geniculate nucleus
2. Reticular areas of the mesencephalon.

*Both of these are inhibitory, and when stimulated, can turn off transmission thru selected portions of the dorsal lateral geniculate nucleus.
114. In what two ways is the dorsal lateral geniculate nucleus divided?
1. Layers 1 and 2 are called "magnocellular" layers b/c they contain large neurons; they receive inputs from large type Y retinal ganglion cells. This provides rapid conduction of visual info to the cortex. However, this system is colorblind and transmits only black and white info. Also, its point-to-point transmission is poor.

2. Layers 3-6 are called "parvocellular" layers b/c they contain large numbers of small to medium sized neurons; they receive inputs from type X retinal ganglion cells that transmit color and convey accurate point-to-point spatial information, but at only a moderate velocity of conduction.
115. Where is the primary visual cortex located?
The primary visual cortex lies in the calcarine fissure area, extending forward form the occipital pole on the medial aspect of each occipital cortex. This area is the termination of direct visual signals from the eyes.
116. How are signals from the retinas represented in the visual cortex?
Signals from the macular area of the retina terminate near the occipital pole, whereas signals from the more peripheral retina terminate at or in concentric half circles anterior to the pole but still along the calcarine fissure on the medial occipital lobe.

The upper portion of the retina is represented superiorly and the lower portion inferiorly.

*The fovea has several 100x as much representation in the primary visual cortex as do the most peripheral portions of the cortex.
117. What are the secondary visual areas (aka visual association areas)
The secondary visual areas lie lateral, anterior, superior, and inferior to the primary visual cortex. Most of these areas also fold outward over the lateral surfaces of the occipital and parietal cortex.

Secondary signals are transmitted to these areas for analysis of visual meanings.
118. Where is Brodmann's area 18?
On all sides of the primary visual cortex is Brodmann's area 18, which is where virtually all signals form the primary visual cortex pass next.

Therefore, Brodmann's area 18 is called visual area II.
119. How is the visual cortex organized structurally?
The visual cortex is organized structurally into several million vertical columns of neuronal cells, each column having a diameter of 30-59 um. The same vertical columnar organization is found throughout the cerebral cortex. Each column represents a functional unit.
120. Distance of transmission and layers
The signals that pass outward to layers 1, 2, and 3 eventually transmit signals for short distances laterally in the cortex.

Conversely, the signals that pass inward to layers 5 and 6 excite neurons that transmit signals much greater distances.
121. What are color blobs in the visual cortex?
Interspersed among the primary visual columns as well as among the columns of some of the secondary visual areas are special column-like areas called color blobs.

They receive lateral signals from adjacent visual columns and are activated specifically by color signals. Therefore, it is presumed that these blobs are the primary areas for deciphering color.
122. How do the visual signals interact from the two separate eyes?

1/2
The visual signals from two separate eyes are relayed thru separate neuronal layers in the lateral geniculate nucleus. These signals still remain separated from each other when they arrive in layer 4 of the primary visual cortex. In fact, layer 4 is interlaced w/stripes of neuronal columns; the signals from one eye enter the columns of every other stripe, alternating w/signals from the second eye.
123. How do the visual signals interact from the two separate eyes?

2/2
This cortical area deciphers whether the respective areas of the two visual images from the two seaparate eyes are in register with one aother. In turn, the deciphered information is used to adjust the directional gaze of the separate eyes so that they will fuse w/each other.

*Allows for a person to distinguish the distance of objects via steropsis.
124. What are the 2 major pathways for analysis of visual information?
1. The fast position and motion pathway
2. The accurate color pathway
125. What is the fast position and motion pathway?
This pathway is used to analysis the 3D position, gross form, and motion of objects.

In other words, this pathway tells where every object is during each instant and whether it is moving.

After leaving the primary visual cortex, the signals flow into the posterior midtemporal area and upward into the broad occipitoparietal cortex, where it analyzes the 3D aspects of somatosensory signals.
126. What types of signals are transmitted in the fast position and motion pathway?
The signals transmitted in this fast position and motion pathway are mainly from the large Y optic nerve fibers of the retinal Y ganglion cells, transmitting rapid signals but depicting only black and white with no color.
127. What is the accurate color pathway?
The color info passes from the primary visual cortex into secondary visual areas of the inferior, ventral, and medial regions of the occipital and temporal cortex.

This pathway is concerned with such visual feats as recognizing letters, reading, determining the texture of surfaces, determining detailed colors of objects, and deciphering from all this info that the object is and what it means.
128. What does the primary visual cortex detect?
The areas of maximum excitation occur along the sharp borders of the visual pattern. Thus, the visual signal in the primary visual cortex is concerned with mainly the contrasts in the visual scene rather than with noncontrasting areas.
129. What controls the intensity of stimulation in most neurons?
The intensity of stimulation of most neurons is proportional to the gradient of contrast, that is, the greater the intensity difference between light and dark areas, the greater the degree of stimulation.
130. What else does the primary visual cortex detect?

What are simple cells?
It not only detects the existence of lines and borders in the retinal image but it also detects the direction of orientation of each line or border; whether it is vertical or horizontal.

This is believed to result from linear organizations of mutually inhibiting cells that excite second-order neurons when inhibition occurs all along a line of cells where there is a contrast edge.

Thus for each such orientation of a line, specific neuronal cells are stimulation; these are called "simple cells". They are found mainly in layer 4.
131. What are complex cells?
As the visual signal progresses farther away from layer 4, some neurons respond to lines that are oriented int eh same direction but are not position specific.

That is, even if a line is displaced moderate distances laterally or vertically in the field, the same few neurons will still be stimulated if the line has the same direction. These cells are complex cells.
132. What happens as one goes farther into the analytical pathway of the visual cortex?
More characteristics of each visual scene are deciphered, such as lines of specific lengths, angles, or other shapes.
133. What is the mechanism of color contrast analysis?
The mechanism of color contrast analysis depends on the fact that contrasting color, called "opponent colors," excite specific neuronal cells.

It is presumed that the initial details of color contrast are detected by simple cells, whereas more complex contrasts are detected by complex and hypercomplex cells.
134. What is the effect of removing the primary visual cortex?
Causes loss of conscious vision - blindness. However, blind people can still, at times, react to changes in light intensity, to movement, or rarely even to some gross patterns of vision.

This vision is believed to be observed by neuronal pathways that pass from the optic tracts mainly into the superior colliculi and other portions of the older visual system.
135. What is perimetry?
To Dx blindness in specific portions of the retina, one charts the field of vision for each eye by a process called perimetry.

In all perimetry charts, a blind spot caused by alack of rods and cones in the retina over the optic disc is found about 15 degrees lateral to the central point of vision.
136. What is scotomata?
Occasionally, blind spots are found in portions of the field of vision other than the optic disc area.

Such blind spots are called scotomata; they freq are caused by damage to the optic nerve resulting from glaucoma (too much fluid pressure in the eyeball), from allergic reactions in the retina, or from toxic conditions such as lead poisoning or excessive use of tobacco.
137. What is retinitis pigmentosa?
In this disease, portions of the retina degenerate, and excessive melanin pigment deposits int eh degenerated areas.

Retinitis pigmentosa usually causes blindness in the peripheral filed of vision first and then gradually encroaches on the central areas.
138. Destruction of the optic chiasm causes...?
It prevents the crossing of impulses from the nasal half of each retina to the opposite optic tract.

Therefore, the nasal half of each retina is blinded, which means that the person is blind in the temporal field of vision for each eye b/c the image of the field of vision is inverted on the retina by the optical system of the eye.

This is called bitemporal hemianopsia. Such lesions freq result from tumors of the pituitary gland pressing upward from the sella turcica on the bottom of the optic chiasm.
139. What causes homonymous hemianopsia?
Interruption of the optic tract denervates the corresponding half of each retina on the same side as the lesion; as a results, neither eye can see objects to the opposite side of the head.
140. What are the three pairs of muscles that control the eye movements?
1. Medial and lateral recti
2. Superior and inferior recti
3. Superior and inferior obliques

The medial and lateral recti contract to move the eyes side to side. The superior and inferior recti contract to move the eyes upward or downward. The oblique muscles function mainly to rotate the eyeballs to keep the visual fields in the upright position.
141. Besides CN 3, 4, and 6, what else controls the eye movements?
The interconnections among the brain stem nuclei by way of the nerve tract called the medial longitudinal fasciculus (MLF) also controls the eye movements.

Each of the three sets of muscles to each eye is reciprocally innervated so that one muscle of the pair relaxes while the other contracts.
142. What is perhaps the most important movement of the eyes?
Fixation movemetns, to fix on a discrete portion of the field of vision. Fixation movements are controlled by two neuronal mechanisms.:
1. Voluntary fixation movements
2. Involuntary fixation movements
143. What controls the voluntary fixation movements?
A cortical field located bilaterally in the premotor cortical regions of the frontal lobes.

Bilateral dysfunction or destruction of these areas makes it difficult or almost impossible to unlock the eyes from one point of fixation and move them to another point. It is usually necessary to blink the eyes or put a hand over the eyes for a short time, which then allows the eyes to be moved.
144. What causes the fixation mechanism in the eyes to lock on the object of attention (involuntary fixation movements)?
The fixation mechanism that causes the eyes to lock on the object once it is found is controlled by the secondary visual areas in the occipital cortex, located mainly in the anterior to primary visual cortex.

When this area is destroyed bilaterally in an animal, the animal has difficulty keeping its eyes directed toward a given fixation point or may become totally unable to do so.
145. What type of mechanism is involuntary locking fixation?

What are three types of continuous movements in the eyes?
It results from negative feedback mechanisms that prevent the object of attention from leaving the foveal portion fo the retina.

There are three types of continuous movements in the eyes:
1. Continuous tremor at 30-80 Hz caused by successive contractions of the motor units in the ocular muscles
2. A slow drift of the eyeballs in one direction or another
3. Sudden flicking movements that are controlled by the involuntary fixation mechanism
146. What are saccades?
The jumps in the eye fixations are called saccades, and the movements are called opticokinetic movements.

Also, the brain suppresses the visual image during saccades, so that the person is not conscious of the movements from point to point.
147. What is pursuit movement?
They eyes can also remain fixed on a moving object, which is called pursuit movement. A highly developed cortical mechanism automatically detects the course of movement of an object and then rapidly develops a similar course of movement for the eyes.
148. What part of the brain is mainly responsible for turning the eyes and head toward a visual disturbance?
The superior colliculi. To help in this directional movement of the eyes, the superior colliculi also have topological maps of somatic sensations from the body and acoustic signals from the ears.
149. What nerve fibers are responsible for these rapid turning movements?
The optic nerve fibers from the eyes to the colliculi that are responsible for these rapid turning movements are branches from the rapidly conducting Y fibers, with one branch going to the visual cortex and the other going to the superior colliculi.

In addition to causing the eyes to turn toward a visual disturbance, signals are relayed from the superior colliculi thru the MLF to other levels of the brain stem to cause turning of the whole head and body.
150. What fuses the visual images from the two eyes?
The visual cortex plays an important role in fusion. Interactions occur between cortical neurons in the lateral geniculate nucleus and cause interference excitation in specific neurons when the two visual images are not "in register" that is, they are not fused.

This excitation presumably provides the signal that is transmitted to the occulomotor apparatus to cause convergence or divergence or rotation of the eyes so that fusion can be re-established. Once the corresponding points of the two retinas are in register, excitation of the specific "interference" neurons in the visual cortex disappears.
151. What is the neural mechanism of stereopsis for judging distances of visual objects?
Even when the two eyes are fused with each other, it is still impossible for all corresponding points in the two visual images to be exactly in register at the same time. Furthermore, the nearer the object is to the eyes, the less the degree of register.

This degree of nonregister provides the neural mechanism for stereopsis, an important mechanism for judging the distances of visual objects up to about 200 feet.
152. What is the basis for the neuronal cellular mechanism for steropsis?
Some of the fiber pathways from the retinas to the visual cortex stray 1 to 2 degrees on each side of the central pathway. Therefore, some optic pathways from the two eyes are exactly in register for objects 2 meters away; still another set of pathways is in register for objects 25 meters away.

Thus, the distance is determined by which set or sets of pathways are excited by nonregister or register.
153. What is strabismus?
AKA squint or cross-eye, means lack of fusion of the eyes in one or more of the visual coordinates.

There are three tyeps:
1. Horizontal
2. Torsional
3. Vertical

Combinations of two or even all three of the different types of strabismus often occur.
154. What causes strabismus?
It is often caused by abnormal "set" of the fusion mechanism of the visual system. That is, in a young child's early efforts to fixate the two eyes on the same object, one of the eyes fixates satisfactorily while the other fails to do so, or they both fixate satisfactorily but never simultaneously.

Soon the patterns of conjugate movements of the eyes become abnormally "set" in the neuronal control pathways so that the eyes never fuse.
155. What causes suppression of the visual image from a repressed eye?
In a few pts w/strabismus, the eyes alternate in fixing on the object of attention. In other pts, one eye alone is used all the time, and the other eye becomes repressed and is never used for precise vision.

The visual acuity of the repressed eye develops only slightly, sometimes remain 20/400 or less. If the dominant eye then becomes blinded, vision in the repressed eye can develop only to a slight extent in adults but far more in younger children.
156. Where do the parasympathetic pre- and postganglionic fibers arise in the eye?

What do these nerves do?
The parasympathetic preganglionic fibers arise in the Ediner-Westphal nucleus and then pass in CN III to the ciliary ganglion, which lies immediately behind the ey.

There, the preganglionic fibers synapse w/postganglionic parasympathetic neurons, which in turn send fibers thru ciliary nerves into the eyeball.

These nerves excite (1) the ciliary muscle that controls focusing of the eye lens and (2) the sphincter of the iris that constricts the pupil.
157. Where do the sympathetic pre- and postganglionic fibers arise in the eye?

What do these nerves do?
The sympathetic innervation of the eye originates in the intermediolateral horn cells of T1. From there, sympathetic fibers enter the sympathetic chain and pass upward to the superior cervical ganglion, where they synapse w/postganglionic neurons.

Postganglionic sympathetic fibers then spread along the surfaces of the carotid artery and successively smaller arteries until they reach the eye.

There, the sympathetic fibers innervate the radial fibers of the iris (which open the pupil) as well as several EOM of the eye.
158. Accommodation results from?
Contraction or relaxation of the eye ciliary muscle. Contraction causes increased refractive power of the lens, and relaxation causes decreased power.
159. What regulates accommodation?
Accommodation of the lens is regulated by a negative feedback mechanism that automatically adjusts the refractive power of the lens to achieve the highest degree of visual acuity.
160. What are the 4 different types of clues that help to change the lens strength in the proper direction?
1. Chromatic aberration appears to be important. That is, red light rays focus lightly posteriorly to blue light rays b/c the lens bends blue rays more than red rays. This clue relays info to the accommodation mechanism whether to make the lens stronger or weaker
2. When the eyes fixate on a near object, the eyes must converge. The neural mechanisms for convergence cause a simultaneous signal to strength the lens of the eye
3. B/c the fovea lies in a hollowed-out depression that is slightly deeper than the remainder of the retina, the clarity of focus in the depth of the fovea is different from the clarity of focus on the edges. This could give clues about which way the strength of the lens needs to be changed
4. In has been found that the degree of accommodation of the lens oscillates lightly all the time at a freq of up to 2 Hz. The visual image becomes clearer when the oscillation of the lens strength is changing in the appropriate direction and becomes poorer when the strength is changing in the wrong direction
161. What areas of the brain control accommodation?
The brain cortical areas that control accommodation closely parallel those that control fixation movements of the eyes, with analysis of the visual signals in Brodmann's cortical areas 18 and 19, and transmission of motor signals to the ciliary muscle thru the pretectal area in the brain stem, then thru the Edinger-Westphal nucleus, and finally by way of the parasympathetic nerve fibers to the eyes.
162. What is miosis and mydriasis?
Stimulation of the parasympathetic nerves also excites the pupillary sphincter muscle, thereby decreasing the pupillary aperture; this is called miosis.

Conversely, stimulation of the sympathetic nerves excites the radial fibers of the iris and causes pupillary dilation, called mydriasis.
163. What can damage the pupillary reflexes?
A few CNS diseases damage transmission of visual signals from the retinas to the Edinger-Westphal nucleus, thus sometimes blocking the pupillary reflexes. Such blocks freq occur as a result of CNS syphlis, alcoholism, encephalitis, and so forth.

The block usually occurs in the pretectal region of the brainstem, although it can result from destruction of some small fibers in the optic nerves.
164. What happens when the final nerve fibers in the pathway thru the pretectal area to the Edinger-Wesphal nucleus are damaged?
These nerve fibers are mostly of the inhibitory type. When their inhibitory effect is lost, the nucleus becomes chronically active, causing the pupils to remain mostly constricted, in addition to their failure to respond to light.

*However, the pupils can constrict a little more if the Edinger-Westphal nucleus is stimulated thru some other pathway.
165. What is the pupillary reaction to accommodation?

What is an Argyll Robertson pupil
When the eyes fixate on a near object, the signals that cause accommodation of the lens and those that cause convergence of the two eyes cause a mild degree of pupillary constriction at the same time.

This is called the pupillary reaction to accommodation.

*A pupil that fails to respond to light but does respond to accommodation and is also very small (an Argyll Robertson pupil) is an important diagnostic sign of CNS disease - often syphilis.
166. What is Horner's syndrome?

What causes it?
1. Miosis
2. Anhydrosis
3. Ptosis
4. Flushing

It is caused by interruption of the sympathetic nerves to the eye. Interruption freq occurs in the cervical sympathetic chain.
167. As light enters the eye and passes thru the lens, where is the info projected?
As light enters the eye and passes thru the lens, it forms and image on the retina that is inverted and reversed.

Info from the upper visual space is projected on to the lower retina, and the lower visual space projects to the upper retina.

Similarly, the right part of the visual pace projects to the left hemiretina of each eye, and vice versa.
168. What is the fovea?
The central fixation point for each eye is the fovea and it is the region of the retina w/the highest visual acuity. The fovea corresponds to the central 1-2 degrees of visual space. Although it is small, info from the fovea is represented by about half of the fibers in the optic nerve and half of the cells in the primary visual cortex.
169. What is the macula?
The macula is an oval region approx 3x5 mm that surrounds the fovea and also has relatively high visual acuity. It occupies the central 5 degrees of visual space.
170. What is the optic disc and nerve?
About 15 degrees medial to the fovea is the optic disc, which is the region where the axons leaving the retina gather to form the optic nerve.

There are no photoreceptors over the optic disc. This creates a small blind spot about 15 degrees lateral and slightly inferior to the central fixation point for each eye.
171. Where does the optic nerve exit the orbit?
The retinal ganglion cells send their axons into the optic nerve, which exits thru the orbital apex via the optic canal of the sphenoid bone to enter the cranial cavity.
172. What is the optic chiasm?
There is a partial crossing of fibers in the optic chiasm. Thus, fibers from the left hemiretinas of both eyes end up in the left optic tract, while fibers from the right hemiretinas end up in the right optic tract.

In order to accomplish this, the nasal (medial) retinal fibers for each eye, which are responsible for the temporal (lateral) hemifields, cross over in the optic chiasm.
173. Lesions of the optic chiasm often produce...?
Lesions of the optic chiasm therefore often produce bitemporal (bilateral lateral) visual field defects.
174. Lesions of the eye, retina, or optic nerves produce...?
Monocular visual field defects
175. What cause homonymous visual field defects?
B/c of the crossover in the optic chiasm, lesions proximal to the chiasm (optic tracts, lateral geniculate, optic radiations, or visual cortex) generally produce homonymous visual field defects, meaning that the defect occurs in the same portion of the visual field for each eye.
176. Where does the optic chiasm lie in the brain?

Where do the optic tracts go from here?
The optic chiasm lies on the ventral surface of the brain, beneath the frontal lobes, and just in front of the pituitary gland.

It is therefore susceptible to compression by pituitary tumors and other lesions in this vicinity.

The optic tracts wrap around the midbrain laterally to reach the lateral geniculate nucleus of the thalamus.
177. What happens when the axons of the retinal ganglion cells in the optic tracts enter the lateral geniculate nucleus (LGN) of the thalamus?
The axons form synapses on neurons in the LGN of the thalamus, which in turn project to the primary visual cortex.
178. What is the extrageniculate visual pathway?
A minority of fibers in the optic tract bypass the LGN to enter the brachium of the superior colliculus.

These retinal fibers form the extrageniculate visual pathways, which project mainly to the pretectal area and superior colliculus.
179. REVIEW: What is the importance of the pretectal area?
The pretectal area is important in the pupillary light reflex and projects to the parasympathetic nuclei controlling the pupils.
180. REVIEW: What is the importance of the superior colliculus?
The superior colliculus and pretectal area are important in directing visual attention and eye movements toward visual stimuli. The superior colliculus and pretectal area therefore project to numerous brainstem areas involved in these functions, as well as to association cortex (lateral parietal cortex and frontal eye fields of the prefrontal cortex) via relays in the pulvinar and lateral posterior nucleus of the thalamus.
181. So what is the difference between the retino-tecto-pulvinar-extrastriate cortex pathway & the retino-geniculo-striate pathway?
The retino-tecto-pulvinar-extrastriate cortex pathway functions in visual attention and orientation.

The retino-geniculo-striate pathway functions in visual discrimination and perception.
182. What are the six layers of the LGN?
Numbered from 1-6 from ventral to dorsal.

The first 2 magnocellular layers relay information from M cells of the retina (gross stimulus features or movements), while layers 3 thru 6, the parvocellular layers, relay information from P cells (sensitive to fine visual detail any colors).

*The info from each eye remains segregated even after passing thru the LGN. The segregation is preserved b/c axons from the ipsilateral and contralateral retinas synapse onto different layers of the LGN.
183. The axons leaving the LGN go where?
The axons leaving the LGN enter the white matter to sweep over and lateral to the atrium and temporal horn of the lateral ventricle (thru the C shape of the lateral ventricle) and then back toward the primary visual cortex in the occipital lobe.
184. What are the optic radiations?
As the axons go to the primary visual cortex in the occipital lobe, these axons fan out over a wide area, forming the optic radiations.

Axons from the contralateral and ipsilateral retinal layers of the LGN are intermingled in the optic radiations, so lesions of the optic radiations usually cause homonymous defects affecting the contralateral visual field.
185. The fibers of the lower optic radiations go where?

What is Meyer's loop?
The fibers of the inferior optic radiations arc forward into the temporal lobe, forming Meyer's loop. They then project to the lower bank of the calcarine fissure.

The lower optic radiations carry information from the inferior retina or the superior visual field.
186. The fibers of the superior optic radiations go where?
The upper optic radiations pass under the parietal lobe and project to the superior bank of the calcarine fissure.

The upper optic radiations carry information from the superior retina or the inferior visual field.
187. Temporal lobe lesions or lesions to the lower bank can cause what defect...?
Contralateral homonymous superior quadrantanopia ("pie in the sky").
188. Parietal lobe lesions or lesions to the upper bank can cause what defect...?
Contralateral homonymous inferior quadrantanopia ("pie in the floor")
189. How is the primary visual cortex organized?
The primary visual cortex is retinotopically organized.

The region of the fovea is represented near the occipital pole, while more peripheral regions of the ipsilateral retinas and contralateral visual fields are represented more anteriorly along the calcarine fissure.
190. What are the portions of the medial occipital lobe above and below the calcarine fissure called?
Above is the cuneus (wedge)

Below is the lingula (little tongue)
191. Most input to the primary visual cortex arrives at which cortical layer?
Cortical layer 4. B/c of its functional importance in this region of the brain, layer 4 is relatively thick and is subdivided into sublaminae.

Layer 4B contains numerous myelinated axon collaterals resulting in the pale-appearing stria of Gennari, which is visible in sections of the gray matter even with the naked eye.
192. Where is motion analyzed?
The magnocellular layers of the LGN project mainly to layer 4Cα, conveying info about movement and gross spatial features.
193. Where is form analyzed?
The parvocellular layers of the LGN, carrying fine spatial information, terminate mainly in layer 4Cβ.
194. Where is color analyzed?
Information about color is also relayed by the parvocellular layers, as well as by the interlaminar zones, to specialized regions of cortical layers 2 and 3 called blobs b/c of their appearance on staining w/the histochemical marker cytochrome oxidase.
195. From the primary visual cortex (area 17), where do the neurons project?
From the primary visual cortex (area 17), neurons project to extrastriate regions of visual association cortex, including areas 18, 19, and other regions of the parieto-occipital and occipitotemporal cortex.
196. What are the two main streams of higher order visual processing that originate from the primary and secondary visual cortex?
1. Dorsal pathways
-project to the parieto-occipital association cortex
-answers the question "Where?" by analyzing motion and spatial relationships btwn objects and btwn the body and visual stimuli.

2. Ventral pathways
-projects to the occipitotemporal association cortex
-answers the question "What?" by analyzing form, with specific regions identifying colors, faces, letters, and other visual stimuli.
197. How can one differentiate occipital migraines from occipital seizures?
Migraines typically have fortification scotoma (zigzagging lines).

When pts instead experience pulsating colored lights or moving geometric shapes, occipital seizures should be suspected, although occipital seizures may also produce migrainelike visual phenomena at times.
198. What is a release phenomenon?
Patients w/visual deprivation in part or all of the visual fields caused by either ocular or CNS lesions may occasionally see objects, people, or animals in the regions of vision loss, especially during the early stages of the deficit.
199. What is Bonnet syndrome?
Visual hallucinations that occur in elderly pts as a result of impaired vision have been called Bonnet syndrome.
200. What causes monocular scotoma?
A lesion of the retina. Common causes include retinal infarcts, hemorrhage, degeneration, or infection.

If the lesion is severe enough, the entire retina may be involved, causing monocular visual loss.
201. Lesions of the optic nerve cause...?
Monocular visual loss or monocular scotomas, which may be partial or incomplete depending on the severity of the lesion.

Common causes include glaucoma, optic neuritis, elevated ICP, anterior ischemic optic neuropathy, optic glioma, schwannoma, meningioma, and trauma.
202. Damage to the optic chiasm typically causes...?
Bitemporal hemianopia.

Common lesions in this area include pituitary adenoma, meningioma, craniopharyngioma, and hypothalamic glioma.
203. What causes incongruous homonymous visual field defects?

What causes congruous homonymous visual field defects?
Anterior retrochiasmal lesions (optic tracts, LGN, optic radiations) cause incongruous homonymous visual field defects.

Posterior retrochiasmal (visual cortex) lesions cause more congruous homonymous visual field defects.
204. What causes contralateral homonymous hemianopia?
Lesions of the optic tracts are relatively uncommon, and usually cause a contralateral homonymous hemianopia. They are usually associated with lesions of the LGN,

Possible lesions include tumors, infarct, or demyelination.
205. What is a visual consequence of an MCA inferior division infarct?
Lesions involving the temporal lobe, such as MCA inferior division infarcts, can interrupt the lower optic radiations as they loop thru the temporal lobe.

This causes a contralateral superior quadrantanopia or pie in the sky visual defects.
206. What is a visual consequence of an MCA superior division infarct?
Lesions involving the parietal lobe, such as MCA superior division infarcts, can interrupt the upper portions of the optic radiations, as they pass thru the parietal lobe.

Therefore, parietal lesions cause a contralateral inferior quadrantanopia, or pie on the floor visual defects.
207. Lesions of the entire optic radiation cause....?
Lesions of the entire optic radiation or the entire primary visual cortex cause a contralateral homonymous hemianopia.
208. Lesions to the upper bank of the calcarine fissure cause...?

Lower bank lesions?
Lesions to the upper bank cause a contralateral inferior quadrantanopia, while lesions to the lower bank cause a contralateral superior quadrantanopia.
209. What is macular sparing?
Partial lesions of the visual pathways occasionally result in a phenomenon called macular sparing. This occurs b/c the fovea has a relatively large representation for its size, beginning in the optic nerve and continuing to the primary visual cortex.

Macular sparing can also occur in visual cortex b/c either the MCA or the PCA may provide collateral flow to the representation of the macula in the occipital pole.
210. What other lesions can also cause a relative sparing of central vision?
External compression of the optic nerve, as is seen in elevated ICP, may cause concentric visual loss (constricted visual field).
211.
221. What are the 3 main causes of impaired blood flow in the ophthalmic artery?
1. Emboli, often atheromatous material arising from ipsilateral internal carotid stenosis
2. Stenosis, usually associated w/diabetes, hypertension, or elevated ICP
3. Vasculitis, for example in temporal arteritis
222. What causes a monocular altitudinal scotoma?
Occlusion of the inferior branch of the right or left ophthalmic artery by an embolus.
223. What can cause a binocular altitudinal scotoma?
Binocular altitudinal scotoma can be caused by bilateral occlusion of the posterior cerebral artery (PCA) branches supplying the lingular gyri.
224. What is amaurosis fugax?
Transient occlusion of the retinal artery caused by emboli results in a transient ischemic attack of the retina called amaurosis fugax, w/browning out or loss of vision in one eye for about 10 minutes, sometimes described as being like a window shade moving down or up over the eye.

*It may be a warning sing for an impending retinal or cerebral infarct.
225. What is a common cause of amaurosis fugax?
A common cause of amaurosis fugax is ipsilateral internal carotid artery stenosis which causes artery-to-artery emboli.
226. What is the blood supply of the LGN?
THe LGN has a variable blood supply arising from several vessels, including the anterior choroidal artery (ACA), thalamogeniculate artery, and posterior choiroidal artery (PCA).

Infarcts of the LGN typically produce a contralateral homonymous hemianopia. In addition, there may be an associated contralateral hemiparesis or hemisensory loss due to involvement of the nearby posterior limb of the internal capsule and thalamic somatosensory radiations.
227. What about basilar artery disease?
Sometimes disease of the basilar artery, which supplies both PCAs can cause bilateral PCA ischemia or infarcts.

A bilateral altitudinal scotoma is strongly suggestive of vertobrobasilar insufficiency causing bilateral infarcts or TIAs.
228. Dark purplish brown spot in the upper part of vision on right side that disappeared when covered the right eye. +Soft right carotid bruit and scotoma in the upper nasal quadrant of the right eye.
Embolus arising from the right internal carotid artery resulting in a branch retinal artery occlusion in the right eye.
229. Monocular visual loss in the left eye, improving to a monocular central scotoma; left afferent pupillary defect; left optic disc pallor
Left optic nerve; optic neuritis of the left eye.
230. Bitemporal hemianopia and long-standing menstrual irregularity and infertility
Meningioma (could've been a pituitary adenoma but pathology said not).
231. Left homonymous hemianopia
Tumor in the right temporal lobe
232. Throbbing bilateral or right occipital pain, fortification scotoma and left inferior quadrantanopia in a 57 y/o male
Given his age, a brain tumor such as glioblastoma or brain metastasis should be considered first as the cause of his migraine-like headaches and visual field cut.

Of not, arteriovenous malformations (AVMs) can cause migraine headaches that recur in the same location; they can also cause hemorrhage, ischemia or infarcts, resulting in focal deficits.

Dx: a large AVM involving the superior portions of the right occipital lobe located predominantly above the calcarine fissure.