Where are the Primary Visual Cortex and Primary Auditory Cortex located, and what are their Brodmann area numbers?

The Primary Visual Cortex (Brodmann area 17, striate cortex) lies along the banks of the calcarine sulcus in the occipital lobe; the Primary Auditory Cortex (Brodmann areas 41 and 42) lies in the transverse temporal gyri of Heschl within the superior temporal lobe.

What neurological deficits result from a Middle Cerebral Artery (MCA) stem occlusion?

Contralateral paralysis and sensory loss of the face and upper extremity (greater than lower extremity), contralateral homonymous hemianopia, ipsilateral gaze preference, and EITHER aphasia (if dominant left hemisphere) OR hemispatial neglect (if non-dominant right hemisphere).

Which gyri and Brodmann areas correspond to Broca's area and Wernicke's area in the dominant (usually left) hemisphere?

Broca's area lies in the inferior frontal gyrus (pars opercularis and pars triangularis, Brodmann areas 44 and 45); Wernicke's area lies in the posterior superior temporal gyrus (Brodmann area 22).

What syndrome results from a stroke of the non-dominant (usually right) inferior parietal lobule?

Contralateral (left) hemispatial neglect (hemi-inattention to the left side of space and one's own body), often accompanied by anosognosia (lack of awareness of illness), dressing apraxia, and constructional apraxia.

What is Cerebral Venous Sinus Thrombosis (CVST), what risk factors predispose to it, and why does it cause hemorrhagic venous infarctions?

Thrombosis of the dural venous sinuses (most commonly the superior sagittal or transverse sinus) associated with hypercoagulable states, pregnancy/puerperium, oral contraceptives, or local infection; impaired CSF absorption and venous congestion raise intracranial pressure and cause bilateral parasagittal hemorrhagic venous infarcts that do not conform to arterial territories (first-line treatment is therapeutic anticoagulation with LMWH or unfractionated heparin EVEN when venous hemorrhage is present).

What are the classic clinical presentation and major delayed complications of a ruptured saccular aneurysm (Subarachnoid Hemorrhage)?

Sudden-onset 'thunderclap' headache ('worst headache of my life') with meningismus; major complications include rebleeding (first 24–48h), cerebral vasospasm causing delayed ischemic stroke (days 3–14, prevented with oral nimodipine), communicating/non-communicating hydrocephalus, and SIADH/cerebral salt wasting.

How do lesions of the Cerebellar Hemispheres versus the Cerebellar Vermis/Flocculonodular Lobe differ clinically, and are cerebellar deficits ipsilateral or contralateral?

Cerebellar deficits are IPSILATERAL to the lesion (due to double decussation of cerebellar and motor tracts); lateral hemisphere lesions cause limb ataxia, dysmetria, intention tremor, and dysdiadochokinesia, whereas midline vermis/flocculonodular lesions cause truncal/gait ataxia, titubation, and nystagmus.

What are the anatomical origin, clinical presentation, and classic CT scan appearance of an Epidural Hematoma versus a Subdural Hematoma?

Epidural Hematoma: rupture of the middle meningeal artery (pterion trauma), often with a 'lucid interval', appearing as a biconvex (lens-shaped) hyperdensity bounded by suture lines; Subdural Hematoma: tearing of bridging veins (elderly/alcoholics/shaken baby), appearing as a crescent-shaped hyperdensity that crosses suture lines.

What are the three most common sites of saccular (berry) aneurysms in the Circle of Willis, and what systemic conditions predispose to them?

1) Anterior Communicating Artery (ACom, most common overall; can compress the optic chiasm causing bitemporal hemianopia), 2) Posterior Communicating Artery (PCom; classically compresses the adjacent Oculomotor Nerve [CN III], causing ipsilateral mydriasis ['blown pupil'] and 'down-and-out' ptosis), and 3) Middle Cerebral Artery (MCA) bifurcation; associated with Autosomal Dominant Polycystic Kidney Disease (ADPKD), Ehlers-Danlos syndrome, Marfan syndrome, aortic coarctation, and smoking/hypertension.

Which thalamic nuclei serve as motor relays for the Basal Ganglia and Cerebellum, and where do they project?

The Ventral Anterior (VA) and Ventral Lateral (VL) thalamic nuclei receive inputs from the globus pallidus internus and deep cerebellar nuclei (dentate) and project to the primary motor and premotor cortices.

Which penetrating arteries are affected in Lacunar Strokes, what is the primary underlying pathology, and what are the four classic lacunar syndromes?

Lenticulostriate (MCA), thalamoperforating (PCA), and paramedian pontine (basilar) arteries damaged by chronic hypertension-induced lipohyalinosis and microatheromas; classic syndromes: 1) Pure motor hemiparesis (posterior limb of internal capsule), 2) Pure sensory stroke (VPL/VPM thalamus), 3) Ataxic hemiparesis, and 4) Dysarthria-clumsy hand.

In the Basal Ganglia, which specific structure is degenerated in Parkinson's disease, Huntington's disease, and Hemiballismus?

Parkinson's disease: loss of dopaminergic neurons in the Substantia Nigra pars compacta; Huntington's disease: atrophy of GABAergic medium spiny neurons in the Caudate and Putamen (striatum); Hemiballismus: lacunar stroke of the contralateral Subthalamic Nucleus.

How do the Direct and Indirect Pathways of the Basal Ganglia modulate thalamic excitation of the motor cortex?

The Direct pathway (excited by nigrostriatal D1 receptors) inhibits the GPi/SNr, thereby DISINHIBITING the thalamus to promote movement; the Indirect pathway (inhibited by nigrostriatal D2 receptors) excites the GPi/SNr via the subthalamic nucleus, thereby INHIBITING the thalamus to suppress unwanted movement.

What neurological deficits result from a Posterior Cerebral Artery (PCA) cortical stroke?

Contralateral homonymous hemianopia with macular sparing (due to dual collateral supply to the occipital pole from the MCA); if the dominant left PCA and splenium of the corpus callosum are infarcted, it also causes alexia without agraphia (inability to read despite intact writing).

How do strokes of the Superior Division versus the Inferior Division of the left Middle Cerebral Artery (MCA) differ clinically?

A left MCA Superior Division stroke affects the frontal lobe (precentral gyrus and Broca's area), causing contralateral face/arm weakness and Broca's aphasia; an Inferior Division stroke affects the temporal/parietal lobes, causing Wernicke's aphasia and visual field loss WITHOUT significant motor weakness.

What is Conduction Aphasia, which white matter tract is damaged, and what are its language characteristics?

Damage to the arcuate fasciculus (superior longitudinal fasciculus) and posterior perisylvian temporoparietal junction (supramarginal gyrus / area Spt) connecting Wernicke's and Broca's areas; speech is fluent and auditory comprehension is intact, but repetition is disproportionately and severely impaired with frequent phonemic paraphasias and self-correction attempts.

What causes Cortical Watershed (Borderzone) Infarcts, and how does an ACA-MCA watershed stroke present clinically?

Severe systemic hypotension, cardiac arrest, or bilateral carotid stenosis causing ischemia at the distal boundaries between major cerebral arteries; an ACA-MCA watershed stroke affects the proximal limb motor/sensory strip, producing 'man-in-a-barrel' syndrome (bilateral proximal shoulder and hip weakness with spared hands and feet).

What neurological deficits result from an Anterior Cerebral Artery (ACA) occlusion?

Contralateral motor paralysis and sensory loss predominantly affecting the lower extremity (leg and foot), urinary incontinence (damage to the paracentral micturition center), and abulia/personality changes or grasp reflex (medial prefrontal cortex).

What is Klüver-Bucy Syndrome, which brain structure is bilaterally damaged, and with what viral encephalitis is it associated?

Bilateral destruction of the amygdala (anterior temporal lobes), often secondary to HSV-1 encephalitis; characterized by hyperorality, hypersexuality, hypermetamorphosis (compulsive exploration of visual stimuli), emotional placidity/loss of fear, and visual agnosia.

What are the major arterial branches that form the Circle of Willis at the base of the brain?

The Anterior Communicating Artery (ACom), paired Anterior Cerebral Arteries (ACA), paired Internal Carotid Arteries (ICA), paired Posterior Communicating Arteries (PCom), and paired Posterior Cerebral Arteries (PCA) arising from the Basilar artery.

Where do Meyer's Loop and Baum's Loop travel, and what visual field defects result from lesions in each pathway?

Meyer's loop carries inferior retinal fibers (superior visual field) through the temporal lobe -> lesion causes contralateral superior quadrantanopia ('pie in the sky'); Baum's loop carries superior retinal fibers (inferior visual field) through the parietal lobe -> lesion causes contralateral inferior quadrantanopia ('pie on the floor').

How do you clinically distinguish Broca's (expressive) aphasia from Wernicke's (receptive) aphasia?

In Broca's aphasia, speech is non-fluent, telegraphic, and effortful with intact comprehension and high patient frustration; in Wernicke's aphasia, speech is fluent ('word salad' with paraphasias) with severely impaired auditory comprehension and lack of insight.

Which gyri and Brodmann areas correspond to the Primary Motor Cortex and the Primary Somatosensory Cortex?

The Primary Motor Cortex lies in the precentral gyrus of the frontal lobe (Brodmann area 4); the Primary Somatosensory Cortex lies in the postcentral gyrus of the parietal lobe (Brodmann areas 3, 1, and 2).

What is Dejerine-Roussy (Thalamic Pain) Syndrome?

A lacunar stroke of the posterolateral thalamus (VPL/VPM nuclei) that initially causes contralateral complete hemisensory loss, followed weeks to months later by severe, burning contralateral neuropathic pain and allodynia.

What passes through the Anterior Limb, Genu, and Posterior Limb of the Internal Capsule?

Anterior limb: frontopontine and thalamocortical (anterior thalamic radiation) fibers; Genu: corticobulbar tract (motor to cranial nerve nuclei); Posterior limb: corticospinal tract (motor to body) and somatosensory radiations from VPL/VPM.

Which brain structures are damaged in Wernicke-Korsakoff Syndrome due to Thiamine (Vitamin B1) deficiency, and what is the clinical triad?

Hemorrhagic necrosis of the mammillary bodies, dorsomedial thalamic nuclei, and periaqueductal gray matter; acute Wernicke encephalopathy presents with confusion, ophthalmoplegia/nystagmus, and gait ataxia, which can progress to irreversible Korsakoff psychosis (anterograde/retrograde amnesia and confabulation).

How is the cortical homunculus somatotopically organized from medial to lateral along the precentral and postcentral gyri?

The genitalia, foot, and lower extremity are represented medially in the interhemispheric fissure (paracentral lobule, supplied by the ACA), while the trunk, hand, face, and tongue are represented along the lateral convexity (supplied by the MCA).

Which specific thalamic nuclei relay Somatosensory (body vs face), Visual, and Auditory information, and to which cortical areas do they project?

VPL (body somatosensory via spinothalamic/medial lemniscus) and VPM (face somatosensory via trigeminothalamic + taste) project to primary somatosensory cortex; LGN (visual) projects to calcarine cortex; MGN (auditory) projects to Heschl's gyri.

What is Anton Syndrome, and what cortical lesion produces it?

Cortical blindness caused by bilateral Posterior Cerebral Artery (PCA) occlusion of the occipital lobes, characterized by complete visual loss combined with confabulation and anosognosia (the patient denies being blind).

What four neurological deficits constitute Gerstmann Syndrome, and where is the causal lesion located?

Agraphia (without alexia), acalculia, finger agnosia, and left-right disorientation; caused by a lesion of the dominant (usually left) angular gyrus (Brodmann area 39) in the inferior parietal lobule.

How do Transcortical Motor Aphasia and Transcortical Sensory Aphasia differ from Broca's and Wernicke's aphasias?

Transcortical aphasias (often caused by watershed infarcts around perisylvian language zones) mirror the fluency and comprehension deficits of Broca's or Wernicke's aphasia, RESPECTIVELY, but REPETITION remains completely intact.

What is Prosopagnosia, and which cortical region is damaged?

The inability to recognize familiar faces (including one's own face in a mirror) despite intact visual acuity, caused by a lesion of the fusiform gyrus (occipitotemporal gyrus, often bilateral or right-sided PCA territory).

Neurology: Cerebral Cortex Brodmann Areas, Circle of Willis, Stroke Syndromes & Aphasias

Clinical neurology and neuroanatomy of cerebral cortex Brodmann areas, cortical homunculus, Broca/Wernicke/conduction/transcortical aphasias, Circle of Willis berry aneurysms, ACA/MCA/PCA/lacunar/watershed stroke syndromes, thalamic nuclei, internal capsule, basal ganglia, and cerebellum.

Level: intermediate
Languages: en → en
Cards: 32
Markdown: Neurology: Cerebral Cortex Brodmann Areas, Circle of Willis, Stroke Syndromes & Aphasias (.md)

Flashcards (32)

#	Front (Term / Question)	Back (Definition / Answer)
1	Where are the Primary Visual Cortex and Primary Auditory Cortex located, and what are their Brodmann area numbers?	The Primary Visual Cortex (Brodmann area 17, striate cortex) lies along the banks of the calcarine sulcus in the occipital lobe; the Primary Auditory Cortex (Brodmann areas 41 and 42) lies in the transverse temporal gyri of Heschl within the superior temporal lobe.
2	What neurological deficits result from a Middle Cerebral Artery (MCA) stem occlusion?	Contralateral paralysis and sensory loss of the face and upper extremity (greater than lower extremity), contralateral homonymous hemianopia, ipsilateral gaze preference, and EITHER aphasia (if dominant left hemisphere) OR hemispatial neglect (if non-dominant right hemisphere).
3	Which gyri and Brodmann areas correspond to Broca's area and Wernicke's area in the dominant (usually left) hemisphere?	Broca's area lies in the inferior frontal gyrus (pars opercularis and pars triangularis, Brodmann areas 44 and 45); Wernicke's area lies in the posterior superior temporal gyrus (Brodmann area 22).
4	What syndrome results from a stroke of the non-dominant (usually right) inferior parietal lobule?	Contralateral (left) hemispatial neglect (hemi-inattention to the left side of space and one's own body), often accompanied by anosognosia (lack of awareness of illness), dressing apraxia, and constructional apraxia.
5	What is Cerebral Venous Sinus Thrombosis (CVST), what risk factors predispose to it, and why does it cause hemorrhagic venous infarctions?	Thrombosis of the dural venous sinuses (most commonly the superior sagittal or transverse sinus) associated with hypercoagulable states, pregnancy/puerperium, oral contraceptives, or local infection; impaired CSF absorption and venous congestion raise intracranial pressure and cause bilateral parasagittal hemorrhagic venous infarcts that do not conform to arterial territories (first-line treatment is therapeutic anticoagulation with LMWH or unfractionated heparin EVEN when venous hemorrhage is present).
6	What are the classic clinical presentation and major delayed complications of a ruptured saccular aneurysm (Subarachnoid Hemorrhage)?	Sudden-onset 'thunderclap' headache ('worst headache of my life') with meningismus; major complications include rebleeding (first 24–48h), cerebral vasospasm causing delayed ischemic stroke (days 3–14, prevented with oral nimodipine), communicating/non-communicating hydrocephalus, and SIADH/cerebral salt wasting.
7	How do lesions of the Cerebellar Hemispheres versus the Cerebellar Vermis/Flocculonodular Lobe differ clinically, and are cerebellar deficits ipsilateral or contralateral?	Cerebellar deficits are IPSILATERAL to the lesion (due to double decussation of cerebellar and motor tracts); lateral hemisphere lesions cause limb ataxia, dysmetria, intention tremor, and dysdiadochokinesia, whereas midline vermis/flocculonodular lesions cause truncal/gait ataxia, titubation, and nystagmus.
8	What are the anatomical origin, clinical presentation, and classic CT scan appearance of an Epidural Hematoma versus a Subdural Hematoma?	Epidural Hematoma: rupture of the middle meningeal artery (pterion trauma), often with a 'lucid interval', appearing as a biconvex (lens-shaped) hyperdensity bounded by suture lines; Subdural Hematoma: tearing of bridging veins (elderly/alcoholics/shaken baby), appearing as a crescent-shaped hyperdensity that crosses suture lines.
9	What are the three most common sites of saccular (berry) aneurysms in the Circle of Willis, and what systemic conditions predispose to them?	1) Anterior Communicating Artery (ACom, most common overall; can compress the optic chiasm causing bitemporal hemianopia), 2) Posterior Communicating Artery (PCom; classically compresses the adjacent Oculomotor Nerve [CN III], causing ipsilateral mydriasis ['blown pupil'] and 'down-and-out' ptosis), and 3) Middle Cerebral Artery (MCA) bifurcation; associated with Autosomal Dominant Polycystic Kidney Disease (ADPKD), Ehlers-Danlos syndrome, Marfan syndrome, aortic coarctation, and smoking/hypertension.
10	Which thalamic nuclei serve as motor relays for the Basal Ganglia and Cerebellum, and where do they project?	The Ventral Anterior (VA) and Ventral Lateral (VL) thalamic nuclei receive inputs from the globus pallidus internus and deep cerebellar nuclei (dentate) and project to the primary motor and premotor cortices.
11	Which penetrating arteries are affected in Lacunar Strokes, what is the primary underlying pathology, and what are the four classic lacunar syndromes?	Lenticulostriate (MCA), thalamoperforating (PCA), and paramedian pontine (basilar) arteries damaged by chronic hypertension-induced lipohyalinosis and microatheromas; classic syndromes: 1) Pure motor hemiparesis (posterior limb of internal capsule), 2) Pure sensory stroke (VPL/VPM thalamus), 3) Ataxic hemiparesis, and 4) Dysarthria-clumsy hand.
12	In the Basal Ganglia, which specific structure is degenerated in Parkinson's disease, Huntington's disease, and Hemiballismus?	Parkinson's disease: loss of dopaminergic neurons in the Substantia Nigra pars compacta; Huntington's disease: atrophy of GABAergic medium spiny neurons in the Caudate and Putamen (striatum); Hemiballismus: lacunar stroke of the contralateral Subthalamic Nucleus.
13	How do the Direct and Indirect Pathways of the Basal Ganglia modulate thalamic excitation of the motor cortex?	The Direct pathway (excited by nigrostriatal D1 receptors) inhibits the GPi/SNr, thereby DISINHIBITING the thalamus to promote movement; the Indirect pathway (inhibited by nigrostriatal D2 receptors) excites the GPi/SNr via the subthalamic nucleus, thereby INHIBITING the thalamus to suppress unwanted movement.
14	What neurological deficits result from a Posterior Cerebral Artery (PCA) cortical stroke?	Contralateral homonymous hemianopia with macular sparing (due to dual collateral supply to the occipital pole from the MCA); if the dominant left PCA and splenium of the corpus callosum are infarcted, it also causes alexia without agraphia (inability to read despite intact writing).
15	How do strokes of the Superior Division versus the Inferior Division of the left Middle Cerebral Artery (MCA) differ clinically?	A left MCA Superior Division stroke affects the frontal lobe (precentral gyrus and Broca's area), causing contralateral face/arm weakness and Broca's aphasia; an Inferior Division stroke affects the temporal/parietal lobes, causing Wernicke's aphasia and visual field loss WITHOUT significant motor weakness.
16	What is Conduction Aphasia, which white matter tract is damaged, and what are its language characteristics?	Damage to the arcuate fasciculus (superior longitudinal fasciculus) and posterior perisylvian temporoparietal junction (supramarginal gyrus / area Spt) connecting Wernicke's and Broca's areas; speech is fluent and auditory comprehension is intact, but repetition is disproportionately and severely impaired with frequent phonemic paraphasias and self-correction attempts.
17	What causes Cortical Watershed (Borderzone) Infarcts, and how does an ACA-MCA watershed stroke present clinically?	Severe systemic hypotension, cardiac arrest, or bilateral carotid stenosis causing ischemia at the distal boundaries between major cerebral arteries; an ACA-MCA watershed stroke affects the proximal limb motor/sensory strip, producing 'man-in-a-barrel' syndrome (bilateral proximal shoulder and hip weakness with spared hands and feet).
18	What neurological deficits result from an Anterior Cerebral Artery (ACA) occlusion?	Contralateral motor paralysis and sensory loss predominantly affecting the lower extremity (leg and foot), urinary incontinence (damage to the paracentral micturition center), and abulia/personality changes or grasp reflex (medial prefrontal cortex).
19	What is Klüver-Bucy Syndrome, which brain structure is bilaterally damaged, and with what viral encephalitis is it associated?	Bilateral destruction of the amygdala (anterior temporal lobes), often secondary to HSV-1 encephalitis; characterized by hyperorality, hypersexuality, hypermetamorphosis (compulsive exploration of visual stimuli), emotional placidity/loss of fear, and visual agnosia.
20	What are the major arterial branches that form the Circle of Willis at the base of the brain?	The Anterior Communicating Artery (ACom), paired Anterior Cerebral Arteries (ACA), paired Internal Carotid Arteries (ICA), paired Posterior Communicating Arteries (PCom), and paired Posterior Cerebral Arteries (PCA) arising from the Basilar artery.
21	Where do Meyer's Loop and Baum's Loop travel, and what visual field defects result from lesions in each pathway?	Meyer's loop carries inferior retinal fibers (superior visual field) through the temporal lobe -> lesion causes contralateral superior quadrantanopia ('pie in the sky'); Baum's loop carries superior retinal fibers (inferior visual field) through the parietal lobe -> lesion causes contralateral inferior quadrantanopia ('pie on the floor').
22	How do you clinically distinguish Broca's (expressive) aphasia from Wernicke's (receptive) aphasia?	In Broca's aphasia, speech is non-fluent, telegraphic, and effortful with intact comprehension and high patient frustration; in Wernicke's aphasia, speech is fluent ('word salad' with paraphasias) with severely impaired auditory comprehension and lack of insight.
23	Which gyri and Brodmann areas correspond to the Primary Motor Cortex and the Primary Somatosensory Cortex?	The Primary Motor Cortex lies in the precentral gyrus of the frontal lobe (Brodmann area 4); the Primary Somatosensory Cortex lies in the postcentral gyrus of the parietal lobe (Brodmann areas 3, 1, and 2).
24	What is Dejerine-Roussy (Thalamic Pain) Syndrome?	A lacunar stroke of the posterolateral thalamus (VPL/VPM nuclei) that initially causes contralateral complete hemisensory loss, followed weeks to months later by severe, burning contralateral neuropathic pain and allodynia.
25	What passes through the Anterior Limb, Genu, and Posterior Limb of the Internal Capsule?	Anterior limb: frontopontine and thalamocortical (anterior thalamic radiation) fibers; Genu: corticobulbar tract (motor to cranial nerve nuclei); Posterior limb: corticospinal tract (motor to body) and somatosensory radiations from VPL/VPM.
26	Which brain structures are damaged in Wernicke-Korsakoff Syndrome due to Thiamine (Vitamin B1) deficiency, and what is the clinical triad?	Hemorrhagic necrosis of the mammillary bodies, dorsomedial thalamic nuclei, and periaqueductal gray matter; acute Wernicke encephalopathy presents with confusion, ophthalmoplegia/nystagmus, and gait ataxia, which can progress to irreversible Korsakoff psychosis (anterograde/retrograde amnesia and confabulation).
27	How is the cortical homunculus somatotopically organized from medial to lateral along the precentral and postcentral gyri?	The genitalia, foot, and lower extremity are represented medially in the interhemispheric fissure (paracentral lobule, supplied by the ACA), while the trunk, hand, face, and tongue are represented along the lateral convexity (supplied by the MCA).
28	Which specific thalamic nuclei relay Somatosensory (body vs face), Visual, and Auditory information, and to which cortical areas do they project?	VPL (body somatosensory via spinothalamic/medial lemniscus) and VPM (face somatosensory via trigeminothalamic + taste) project to primary somatosensory cortex; LGN (visual) projects to calcarine cortex; MGN (auditory) projects to Heschl's gyri.
29	What is Anton Syndrome, and what cortical lesion produces it?	Cortical blindness caused by bilateral Posterior Cerebral Artery (PCA) occlusion of the occipital lobes, characterized by complete visual loss combined with confabulation and anosognosia (the patient denies being blind).
30	What four neurological deficits constitute Gerstmann Syndrome, and where is the causal lesion located?	Agraphia (without alexia), acalculia, finger agnosia, and left-right disorientation; caused by a lesion of the dominant (usually left) angular gyrus (Brodmann area 39) in the inferior parietal lobule.
31	How do Transcortical Motor Aphasia and Transcortical Sensory Aphasia differ from Broca's and Wernicke's aphasias?	Transcortical aphasias (often caused by watershed infarcts around perisylvian language zones) mirror the fluency and comprehension deficits of Broca's or Wernicke's aphasia, RESPECTIVELY, but REPETITION remains completely intact.
32	What is Prosopagnosia, and which cortical region is damaged?	The inability to recognize familiar faces (including one's own face in a mirror) despite intact visual acuity, caused by a lesion of the fusiform gyrus (occipitotemporal gyrus, often bilateral or right-sided PCA territory).