Give me clinical cases with questions and answers on topic of anatomy NEUROANATOMY

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neuroanatomy spinal cord cross section tracts Brown-Sequard

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Wallenberg lateral medullary syndrome brainstem anatomy

**Imaging Modality:** Sagittal Magnetic Resonance Imaging (MRI), T2-weighted sequence.

This diagnostic image set consists of brain MRI scans, including an axial T2-weighted sequence and two coronal views, demonstrating a subacute ischemic lesion. The axial view reveals a localized area of hyperintensity (bright signal) within the brainstem, specifically located in the medulla oblongata on the left side, as indicated by the yellow arrow. In the coronal sections, the lesion is shown as an elongated, hyperintense region extending vertically along the longitudinal axis of the medulla, reaching from the pontomedullary junction toward the caudal portion near the cervical spinal cord. The high signal intensity relative to the surrounding brain parenchyma suggests vasogenic edema or subacute infarction. Clinically, this imaging pattern of a medullary infarct extending caudally is associated with Opalski syndrome, a variant of lateral medullary syndrome (Wallenberg syndrome) that involves corticospinal fibers, leading to ipsilateral hemiparesis. The images serve as an educational example of brainstem vascular anatomy and the radiological presentation of specialized stroke syndromes.

**Imaging Modality:** Magnetic Resonance Imaging (MRI), Diffusion-Weighted Imaging (DWI) sequence.

**Imaging Modality:** Magnetic Resonance Imaging (MRI), Sagittal T2-weighted sequence.

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cranial nerve anatomy brainstem nuclei diagram

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internal capsule anatomy corona radiata cerebral hemisphere

Diagnostic neuroimaging featuring four axial slices of a brain, likely based on computerized tomography (CT) or MRI templates, displaying a cumulative lesion mask from a stroke research study. The image demonstrates the spatial distribution of cerebral infarcts across a subject group. A color-coded heat map overlay indicates lesion frequency per voxel: the spectrum ranges from red (1 subject) to yellow (maximum of 11 subjects), with a concentration of lesions visible in the left hemisphere encompassing the frontal, parietal, and temporal regions, including the corona radiata and internal capsule. Superimposed on the anatomy is a green tract-based spatial statistics (TBSS) white matter skeleton, representing the average group white matter pathways. The figure illustrates the anatomical overlap of ischemic damage in relation to major motor recovery-related neural pathways. This visual is designed for medical researchers and clinicians studying post-stroke neuroanatomy and diffusion tensor imaging (DTI) characteristics.

I now have comprehensive, authoritative content from multiple neurology textbooks. Let me compile the full, detailed clinical cases answer.

Clinical Cases in Neuroanatomy - Questions & Answers

Below are 8 carefully crafted clinical cases covering key neuroanatomy topics, each with detailed anatomical reasoning sourced from authoritative neurology textbooks.

CASE 1 - The Crossed Syndrome

Clinical Scenario

A 62-year-old man with hypertension suddenly develops severe dizziness, nausea, and vomiting. On examination you find:

Ipsilateral (right) face: Loss of pain and temperature sensation; ptosis, miosis, and anhidrosis (Horner's syndrome); hoarseness; dysphagia; ataxia of the limb
Contralateral (left) body: Loss of pain and temperature sensation (arm and leg)
Motor: No limb paralysis
Nystagmus present (horizontal, towards the lesion side)

Questions

Q1. What syndrome is this, and which artery is most likely occluded? Q2. Explain the anatomy behind each finding. Q3. Why is there NO limb weakness despite a major brainstem infarct? Q4. What is the characteristic "crossed" pattern in this syndrome?

Answers

A1. Wallenberg's Lateral Medullary Syndrome - caused by occlusion of the posterior inferior cerebellar artery (PICA) or the vertebral artery (VA) proximal to PICA.

A2. Anatomy of each finding:

Finding	Structure Damaged	Location
Ipsilateral face - pain/temp loss	Spinal trigeminal nucleus & tract (CN V)	Lateral medulla
Contralateral body - pain/temp loss	Spinothalamic tract (already crossed in spinal cord)	Lateral medulla
Horner's syndrome (ptosis, miosis, anhidrosis)	Descending sympathetic pathway	Lateral tegmentum of medulla
Dysphagia, hoarseness	Nucleus ambiguus (CN IX, X)	Lateral medulla
Vertigo, nystagmus	Vestibular nuclei	Lateral medulla
Ipsilateral limb ataxia	Inferior cerebellar peduncle	Lateral medulla

A3. No limb weakness because the corticospinal (pyramidal) tract runs in the medial medulla (the pyramids), which is supplied by the anterior spinal artery - not the PICA. The lateral medullary infarct spares the pyramids entirely. This is the defining feature that separates it from medial medullary syndrome.

A4. The "crossed" pattern: Facial sensation loss is ipsilateral (trigeminal nucleus is in the medulla, ipsilateral to the infarct), while body sensation loss is contralateral (the spinothalamic tract has already crossed in the spinal cord before reaching the medulla). This ipsilateral face + contralateral body pattern is the hallmark "crossed" brainstem syndrome.

Source: Localization in Clinical Neurology, 8e - "The lateral medullary lesion (Wallenberg syndrome)... combination of a Wallenberg syndrome plus a contralateral hemiplegia" and K.J. Lee's Essential Otolaryngology - "Also called syndrome of the posterior-inferior cerebellar artery thrombosis or lateral medullary syndrome"

MRI showing lateral medullary infarction - Wallenberg syndrome variant (Opalski syndrome with corticospinal involvement)

CASE 2 - The Knife Wound

Clinical Scenario

A 28-year-old man is brought to the ER after a stab wound to the right side of his back at the T10 level. Neurological examination shows:

Right lower limb: Complete loss of voluntary movement; loss of vibration and proprioception (position sense)
Left lower limb: Loss of pain and temperature sensation (beginning 2 segments below T10, i.e., around T12)
Both limbs: Preserved crude touch
Bladder and bowel function: intact (incomplete lesion)

Questions

Q1. What spinal cord syndrome does this represent? Q2. Draw the tracts affected and explain the laterality of findings. Q3. Why does pain/temperature loss begin 1-2 segments BELOW the lesion level on the contralateral side? Q4. What is the prognosis for this injury?

Answers

A1. Brown-Séquard Syndrome (right-sided spinal cord hemisection at T10).

A2. Tracts affected:

RIGHT SIDE (ipsilateral to lesion - T10 hemisection):
├── Lateral corticospinal tract → IPSILATERAL motor loss (UMN signs)
└── Posterior columns (fasciculus gracilis/cuneatus) → IPSILATERAL loss of
    vibration, proprioception, fine discriminative touch

LEFT SIDE (contralateral):
└── Lateral spinothalamic tract (already crossed) → CONTRALATERAL loss of
    pain and temperature

A3. The 1-2 segment offset for contralateral pain/temperature loss: When pain and temperature fibers enter the spinal cord, they ascend 1-2 segments ipsilaterally in Lissauer's tract (dorsolateral fasciculus) before crossing anteriorly through the anterior commissure to join the contralateral spinothalamic tract. Therefore, the spinothalamic tract at T10 contains fibers from T11-T12 and below - not from T10 itself. The contralateral sensory loss begins at T12, not T10. Additionally, there may be a narrow band of ipsilateral pain/temperature loss at the exact lesion level.

A4. Prognosis - Best of all incomplete spinal cord syndromes:

80-90% regain bowel and bladder function
75% regain ambulatory status
70% become independent in activities of daily living

Source: ROSEN's Emergency Medicine - "Brown-Séquard syndrome carries the best prognosis of any of the incomplete spinal cord syndromes. Fully 80% to 90% of patients regain bowel and bladder function, 75% regain ambulatory status"

CASE 3 - The Locked-In Patient

Clinical Scenario

A 55-year-old man collapses. He is brought to the ER appearing "awake" - his eyes are open and he can blink - but he cannot move any limb, cannot speak, and cannot move his face. Family reports he seems to understand everything said to him. CT angiography shows basilar artery thrombosis with infarction of the ventral pons.

Questions

Q1. What syndrome is this? How does it differ from coma? Q2. Which tracts are damaged and which are spared? Q3. Why can the patient blink and move eyes vertically but NOT horizontally? Q4. How do you communicate with a locked-in patient?

Answers

A1. Locked-In Syndrome. The patient is fully conscious and aware but has no motor output to limbs or face. In coma, the patient is unaware and unresponsive. In locked-in syndrome, cognition and sensation are completely preserved - the patient hears, feels, and understands everything, but is "imprisoned" inside a non-functional body.

A2. Tracts damaged vs. spared:

Damaged (Ventral Pons)	Spared (Tegmentum)
Bilateral corticospinal tracts	Somatosensory pathways
Bilateral corticobulbar tracts (face, jaw, tongue)	Brainstem arousal (reticular formation) - consciousness
Horizontal gaze pathways (PPRF/CN VI nucleus)	Vertical gaze control (rostral midbrain tectum)
CN VI, VII nuclei affected	CN III, IV nuclei spared

A3. Vertical eye movements are controlled by the rostral midbrain (superior colliculus, pretectal area, riMLF - rostral interstitial nucleus of MLF). Horizontal eye movements depend on the pontine paramedian reticular formation (PPRF) and CN VI nucleus in the pons. Since the basilar artery infarct destroys the ventral pons, horizontal gaze is lost. But the midbrain vertical gaze centers are typically spared, so the patient retains the ability to look up/down and to blink (orbicularis oculi via CN VII can be partially preserved via extra-pyramidal pathways, and eyelid elevation via CN III midbrain).

A4. Communication: Patients can communicate using vertical eye movements or blinking (yes = one blink, no = two blinks). Modern eye-tracking computer interfaces have been developed that allow locked-in patients to write and communicate using only eye movements.

Source: Neuroanatomy through Clinical Cases, 3rd Edition - "Locked-in syndrome often spares vertical eye movements and eye opening. Patients with this syndrome can thus communicate using eye movements."

CASE 4 - The Horner's Triad

Clinical Scenario

A 45-year-old woman presents with a drooping right eyelid, a constricted right pupil, and the right side of her face does not sweat. She also has right arm and hand pain (burning quality). Chest X-ray reveals a mass at the apex of the right lung. She is a heavy smoker.

Questions

Q1. Name the syndrome and the likely underlying diagnosis. Q2. Describe the three-neuron sympathetic pathway - where does each neuron travel? Q3. What is the anatomical basis for each component of the triad (ptosis, miosis, anhidrosis)? Q4. If MRI showed a lesion in the lateral medulla instead, how would the presentation differ?

Answers

A1. Horner's Syndrome - caused here by a Pancoast tumor (superior sulcus lung carcinoma at the lung apex) invading the cervical sympathetic chain. This is a 3rd-order (post-ganglionic) Horner's syndrome.

A2. The Three-Neuron Sympathetic Pathway:

1st ORDER NEURON (central):
   Hypothalamus → descends through lateral brainstem
   → lateral funiculus of spinal cord → synapses at C8-T2 (ciliospinal center of Budge)

2nd ORDER NEURON (pre-ganglionic):
   C8-T2 → exits ventral root → travels over lung apex
   → over subclavian artery → superior cervical ganglion (synapses here)
   [THIS IS WHERE PANCOAST TUMOR COMPRESSES]

3rd ORDER NEURON (post-ganglionic):
   Superior cervical ganglion → travels along internal carotid artery
   → enters orbit → superior tarsal muscle + iris dilator + sweat glands

A3. Anatomical basis of each sign:

Ptosis (drooping eyelid): The sympathetic system innervates the superior tarsal muscle (of Müller), which contributes to upper lid elevation (~2 mm). Loss → partial ptosis. (Full ptosis = CN III palsy; Horner's ptosis is partial/subtle)
Miosis (constricted pupil): Iris dilator muscle (dilator pupillae) is sympathetically innervated. Loss of innervation → the parasympathetic sphincter pupillae dominates unopposed → miosis. Pupil fails to dilate in darkness.
Anhidrosis (lack of sweating): Sweat glands of the face are sympathetically innervated. The 3rd-order fiber from the superior cervical ganglion travels with the external carotid artery to facial sweat glands. Anhidrosis is present if the lesion is at or proximal to the superior cervical ganglion.

A4. Lateral medullary lesion (Wallenberg's) would cause Horner's syndrome by damaging the 1st-order descending sympathetic pathway in the lateral tegmentum. The presentation would ALSO include the full Wallenberg picture: ipsilateral facial pain/temp loss, contralateral body pain/temp loss, vestibular symptoms, and CN IX/X palsy - rather than the isolated Horner's + arm pain from tumor invasion.

Source: Bradley and Daroff's Neurology in Clinical Practice - "The classic Horner syndrome triad of sympathetic dysfunction consists of ipsilateral ptosis, miosis, and facial anhidrosis. The lesion may be anywhere along the three-neuron sympathetic pathway"

CASE 5 - "I Can't Move My Right Side But I'm Awake"

Clinical Scenario

A 70-year-old hypertensive man wakes up with sudden inability to move his right arm and leg. His face also droops on the right. Speech is dysarthric (slurred). There is no sensory loss. Brain MRI (DWI) shows a small lacunar infarct in the posterior limb of the left internal capsule.

Questions

Q1. What type of stroke syndrome is this? Where is the lesion? Q2. What specific structure/artery is typically involved in internal capsule lacunes? Q3. Why is the weakness "proportionate" (face = arm = leg equally affected)? Q4. How is an internal capsule lesion clinically different from a cortical (motor strip) lesion at the same level?

Answers

A1. Pure Motor Hemiplegia - a classic lacunar infarct syndrome. The lesion is in the posterior limb of the left internal capsule, producing contralateral (right) face, arm, and leg weakness.

A2. Vascular supply: The internal capsule posterior limb is supplied by the lenticulostriate arteries, which are small perforating branches of the middle cerebral artery (MCA). These are end-arteries with no collateral circulation, predisposing them to lacunar infarction in the setting of hypertensive small vessel disease.

A3. Proportionate weakness (face = arm = leg): In the internal capsule, the corticobulbar (for face) and corticospinal fibers (for arm and leg) are tightly bundled together in the genu and posterior limb, respectively, in a very compact space. A small lesion can simultaneously knock out all of these fibers together, producing equal weakness of face, arm, and leg. Contrast this with cortical lesions:

Motor cortex lesion → disproportionate weakness (arm > leg if frontal MCA territory, or leg > arm if parasagittal/ACA territory), often with cortical sensory signs and seizures
Capsular lesion → proportionate hemiplegia, no cortical signs (no aphasia, no seizure, no hemineglect)

A4. Cortical vs. Capsular lesion differences:

Feature	Cortical Motor Lesion	Internal Capsule Lesion
Weakness pattern	Disproportionate	Proportionate
Sensory loss	Common	Absent (pure motor)
Aphasia/neglect	Yes (if dominant/non-dominant)	Absent
Visual field defect	Possible	Absent
Seizures	More common	Less common
Size of lesion	Larger territory	Small lacune

Source: Localization in Clinical Neurology, 8e - "With internal capsular lesions, the hemiplegia is often proportionate..." and Adams and Victor's Principles of Neurology - "in the cerebral white matter (corona radiata) and internal capsule, the corticospinal fibers are intermingled"

CASE 6 - "I Can't Feel Anything Below My Waist"

Clinical Scenario

A 35-year-old man with a history of multiple sclerosis presents with sudden onset weakness in both legs and inability to feel pain, temperature, or light touch below the umbilicus (T10 dermatome). He also cannot tell if his bladder is full, and has urinary retention. MRI shows a demyelinating plaque at T8 in the anterior and lateral cord.

Questions

Q1. What cord syndrome does this represent, and what is the mechanism? Q2. Which specific tracts are damaged? What tracts are preserved? Q3. Explain the concept of a "sensory level" and how to determine it clinically. Q4. What would you find on examination: UMN or LMN signs? Why?

Answers

A1. Anterior Cord Syndrome (or near-complete transverse myelopathy in this MS case). The anterior and lateral cord damage destroys the corticospinal tracts and spinothalamic tracts while initially sparing the posterior columns.

A2. Tracts damaged vs. spared:

Tract	Location	Function	Status
Lateral corticospinal tract	Lateral funiculus	Voluntary motor	DAMAGED → bilateral weakness
Lateral spinothalamic tract	Anterolateral funiculus	Pain, temperature	DAMAGED → bilateral loss
Anterior spinothalamic tract	Anterior funiculus	Crude touch	DAMAGED
Posterior columns	Posterior funiculus	Vibration, proprioception	SPARED
Dorsal root fibers	Posterior horn	Segmental sensation	SPARED

A3. Sensory level: A "sensory level" is the dermatome below which sensation is abnormal. Clinically, you test pain (pinprick) and temperature from caudal to cranial up the trunk. The point at which sensation suddenly becomes normal is 1-2 levels ABOVE the actual cord lesion (due to the ascending tract offset). The level detected at T10 (umbilicus) suggests a cord lesion at approximately T8-T9 - matching the MRI finding.

A4. UMN signs: Below the level of the lesion, UMN features are expected:

Hypertonia (spasticity)
Hyperreflexia (exaggerated DTRs)
Positive Babinski's sign (extensor plantar response)
No muscle atrophy (lower motor neurons intact)
Clonus may be present

The LMN features (flaccidity, atrophy, fasciculations) would only appear at the exact level of the lesion (where anterior horn cells may be destroyed), not below.

CASE 7 - The Diplopia and Facial Weakness

Clinical Scenario

A 58-year-old diabetic man wakes up with double vision and right facial weakness. On examination: complete inability to abduct the right eye; the right eye is deviated medially at rest; all other eye movements are preserved. Right lower motor neuron facial palsy (forehead spared on left but affected on right - i.e., complete right facial palsy). No limb weakness. MRI shows a small infarct in the right pons.

Questions

Q1. Why are CN VI and CN VII both affected by a single pontine lesion? Q2. What is Millard-Gubler syndrome? What additional finding would suggest this? Q3. Explain the anatomy: why does a CN VI nucleus lesion cause a conjugate gaze palsy rather than just an isolated abduction deficit? Q4. Distinguish peripheral CN VII palsy (Bell's palsy type) from central CN VII palsy on examination.

Answers

A1. CN VI and CN VII nuclei are both located in the dorsal pons tegmentum. The CN VII (facial nerve) fascicles loop around the CN VI nucleus in the dorsal pons - forming the facial colliculus visible as a bulge on the floor of the 4th ventricle. Therefore, a single pontine lesion can simultaneously damage both CN VI and CN VII at their root-exit zones or nuclei.

A2. Millard-Gubler Syndrome: An infarct of the ventral pons affecting:

CN VI fascicles → ipsilateral lateral rectus palsy (medial deviation/esotropia)
CN VII fascicles → ipsilateral LMN facial palsy
Corticospinal tract → contralateral hemiplegia (crossed hemiplegia)

If the corticospinal tract is spared (as in this case), the syndrome is incomplete. The complete Millard-Gubler would have right CN VI + right CN VII palsies PLUS left body hemiplegia.

A3. CN VI nucleus lesion → Conjugate gaze palsy (not just abduction deficit): The CN VI nucleus contains two types of neurons:

Motor neurons → axons form CN VI nerve → innervate ipsilateral lateral rectus
Internuclear neurons → axons cross and ascend in the contralateral MLF (medial longitudinal fasciculus) → reach the contralateral CN III nucleus → drive medial rectus for conjugate gaze

A nucleus lesion destroys BOTH populations. Result: the eyes cannot move toward the lesion side at all (conjugate gaze palsy), not just limited abduction. Compare: a lesion of only the CN VI nerve fascicle would produce isolated abduction failure with preserved adduction of the contralateral eye.

A4. Central vs. Peripheral CN VII palsy:

Feature	Central (UMN) palsy	Peripheral (LMN) palsy - Bell's type
Forehead sparing	YES - forehead spared (bilateral cortical input to upper face)	NO - forehead involved (complete ipsilateral palsy)
Tear secretion	Normal	Reduced (if proximal lesion)
Taste	Normal	Impaired (if proximal to chorda tympani)
Hyperacusis	Absent	Present (if proximal to nerve to stapedius)
Site of lesion	Above facial nucleus (cortex/corona radiata/internal capsule)	Facial nucleus or peripheral nerve
Cause	Stroke, tumor	Idiopathic, VZV, Lyme disease

In this case, the complete right CN VII palsy including forehead confirms a LMN (nuclear/fascicular) lesion in the pons - not a central lesion.

Source: Bradley and Daroff's Neurology in Clinical Practice - "A peripheral seventh cranial nerve palsy usually accompanies a lesion of the sixth cranial nerve nucleus."

CASE 8 - The Vision Field Defect

Clinical Scenario

A 68-year-old man with atrial fibrillation presents after a transient ischemic attack. Neurological exam reveals he cannot see objects in his left visual field in both eyes (left homonymous hemianopia). He cannot read any written text despite having normal acuity (he can see faces, objects, colors). He can still write. MRI shows an infarct in the left occipital lobe and left splenium of the corpus callosum.

Questions

Q1. Trace the visual pathway from retina to cortex and explain the hemianopia. Q2. What is alexia without agraphia, and what is the anatomy of this "disconnection syndrome"? Q3. If the infarct were more anteriorly placed (in the temporal lobe), what visual field defect would result and why? Q4. What is "macular sparing" and when does it occur?

Answers

A1. Visual pathway and homonymous hemianopia:

VISUAL PATHWAY (left visual field → right cortex):
Left visual field → falls on NASAL retina of right eye + TEMPORAL retina of left eye
Both → Nasal fibers CROSS at optic chiasm; temporal fibers stay ipsilateral
→ Right optic tract (carries all fibers from left visual field)
→ Right lateral geniculate nucleus (LGN) of thalamus
→ Right optic radiations:
   - Inferior fibers → loop into temporal lobe (Meyer's loop)
   - Superior fibers → through parietal lobe
→ Right primary visual cortex (striate cortex, calcarine fissure, V1)

Left occipital infarct destroys the left visual cortex → left homonymous hemianopia (left visual field lost in BOTH eyes). The deficit is "congruent" (identical in both eyes) when the lesion is at or posterior to the LGN.

A2. Alexia without Agraphia (Pure Alexia) - the "Disconnection Syndrome": This is one of the most elegant neuroanatomy concepts. The mechanism:

Left occipital infarct → left visual cortex destroyed → the patient's left hemisphere cannot receive any visual input (both eyes now only project right visual field information to the right cortex)
The splenium (posterior corpus callosum) infarct → severs the connection between the right visual cortex and the left angular gyrus (the language/reading center)
Result: Visual information reaches the intact right visual cortex, but CANNOT cross to the left angular gyrus for reading
Writing is preserved because the left hemisphere motor system and language areas are intact - the patient can write from internal language representations
Reading requires visual input to reach the angular gyrus - this pathway is severed

Analogy: "The patient can write a letter but cannot read what they just wrote."

A3. Temporal lobe optic radiation lesion - "pie in the sky" defect: Meyer's loop carries the inferior optic radiation fibers (from the inferior retina → representing the superior visual field) and sweeps anteriorly into the temporal lobe before looping back. A temporal lobe lesion causes:

Contralateral superior homonymous quadrantanopia ("pie in the sky")
Superior visual field of both eyes is lost
A parietal lobe lesion would cause the opposite: inferior homonymous quadrantanopia ("pie on the floor")

A4. Macular (central) sparing:

The macula (central 5° of vision, area of highest acuity) is represented at the occipital pole, which has dual blood supply from both the PCA and MCA
In PCA territory infarction, the occipital pole may be spared by MCA collaterals
This produces homonymous hemianopia with preservation of central vision = macular sparing
Clinical importance: Patients with macular sparing often retain usable vision and can still read (unlike complete hemianopia)

Source: Localization in Clinical Neurology, 8e - "An intriguing 'disconnection syndrome' in a literate person occurs if there is damage to the left visual cortex and splenium of the corpus callosum... resulting in alexia without agraphia or pure alexia, occasionally associated with right-sided achromatopsia"

Quick Summary Table - Lesion Localization

Case	Lesion Site	Key Syndrome	Hallmark Finding
1	Lateral medulla	Wallenberg's	Crossed facial/body sensory loss + Horner's, NO weakness
2	Unilateral spinal cord T10	Brown-Séquard	Ipsilateral motor/proprioception loss + Contralateral pain/temp loss
3	Ventral pons (bilateral)	Locked-in	Quadriplegia + intact consciousness + preserved vertical gaze
4	Cervical sympathetic (Pancoast)	Horner's syndrome	Ptosis + miosis + anhidrosis (ipsilateral)
5	Posterior limb internal capsule	Pure motor hemiplegia	Proportionate face/arm/leg weakness, no sensory loss
6	Anterior/lateral cord	Anterior cord syndrome	Motor loss + pain/temp loss; vibration/proprioception spared
7	Dorsal/ventral pons	Millard-Gubler (partial)	CN VI + CN VII palsy + crossed hemiplegia if corticospinal involved
8	Left occipital + splenium	PCA territory infarct	Homonymous hemianopia + alexia without agraphia

Sources: Localization in Clinical Neurology 8e; Neuroanatomy through Clinical Cases 3rd Edition; Adams and Victor's Principles of Neurology 12th Edition; Bradley and Daroff's Neurology in Clinical Practice; ROSEN's Emergency Medicine; K.J. Lee's Essential Otolaryngology

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