1. Lesion Localization in Neuroradiology: Classic Neurologic Exam and Neuroimaging Correlates
eEdE-07
John A. Coburn, MD
Samuel I. Frost, DO
Tabassum A. Kennedy, MD
John-Paul J. Yu, MD, PhD
Department of Radiology
University of Wisconsin School of Medicine and Public Health

2. Disclosures None of the authors have any financial disclosures.
All diagrams used in this exhibit were created by the authors.

3. Objectives
Many pathologic processes affect the central nervous system in characteristic anatomic locations, producing predictable neurologic examination findings.
An understanding of common neurologic presentations can help the neuroradiologist target their search pattern and hone in on pathology that may otherwise go undetected.
In this exhibit, we highlight key neuroanatomic landmarks in a case-based format using lesions characteristically affecting these locations and their corresponding classic clinical presentation. A discussion regarding the functional anatomy of the neuroanatomic landmark of interest follows each case.

4. Case Contents Anatomy Review Gelastic Seizure
Upper Extremity Sensory Deficit
Palatal Myoclonus
Click on each box to view each case
Upper Extremity
Motor Deficit
Confusion, Ataxia & Vision Change
Fluent Aphasia
Double Vision &
Facial Weakness
Expressive Aphasia
Dysarthria & Gait Disturbance
Focal Visual Deficit
Vertigo & Crossed Hemisensory Deficits
Click on the icon to bring you back to this home page

5. Key Neuroanatomy: Lateral Convexity
Parietal Lobe
Frontal Lobe
Occipital Lobe
Temporal Lobe

6. Key Neuroanatomy: Lateral Convexity
Central sulcus
Precentral sulcus
Postcentral sulcus
Parieto-occipital
fissure
Precentral gyrus
Postcentral gyrus
Superior frontal gyrus
Sup. parietal lobule
Middle frontal gyrus
SMG
Inferior parietal lobule AG
Inferior frontal gyrus
AAR
POP PT
Superior frontal sulcus
Superior temporal gyrus
AHR
POR
Middle temporal gyrus
Inferior frontal sulcus
Inferior temporal gyrus
Lateral sulcus
Intraparietal
sulcus
Superior Temp. sulcus
Middle Temp sulcus
SMG Supramarginal gyrus; AG Angular gyrus; POR Pars orbitalis; PT Pars triangularis; POP Pars opercularis
AHR Anterior horizontal ramus of the lateral sulcus; AAR Anterior ascending ramus of the lateral sulcus

7. Key Neuroanatomy: Axial Vertex
Superior frontal sulcus
Inferior frontal sulcus
Inferior frontal gyrus
Middle frontal gyrus
Superior frontal gyrus
Precentral sulcus
Central sulcus
Precentral gyrus
Postcentral sulcus
Postcentral gyrus
Supramarginal gyrus
Lateral sulcus
Superior parietal lobule
Superior Temp sulcus
Angular gyrus
Intraparietal sulcus
Occipital gyri

8. Key Neuroanatomy: Midline Sagittal
Central sulcus
Ascending ramus of the cingulate sulcus
Parieto-occipital sulcus
Paracentral
lobule
Superior frontal gyrus
Cingulate sulcus
Precuneus
Cingulate gyrus
Corpus
callosum
Cuneus
Fornix
Parolfactory
area
Uncus
Lingual gyrus
Calcarine fissure
Hippocampal gyrus
Interthalamic adhesion
Fusiform gyrus
Inf. temporal gyrus
Collateral sulcus
Inferior temporal sulcus

9. 78 F with headache and focal left upper extremity sensory deficits
T1+C
FLAIR
HPI: 78 yo woman presents with gradual onset of headaches and extremity sensory changes that appear to be localized to her left upper extremity

10. 78 F with headache and focal left upper extremity sensory deficits
T1+C
FLAIR
Central sulcus
Post central gyrus
Axial T1, post contrast axial T1 and FLAIR images at the level of frontoparietal vertex demonstrate a focal enhancing mass along the right post central gyrus with associated vasogenic edema (blue arrow). The mass was dural based, resected and consistent with a meningioma.

11. Sensorimotor Cortex
The central sulcus is an important sulcus which divides the primary cortex (precentral gyrus) within the frontal lobe from the primary sensory cortex (post central gyrus) within the parietal lobe.
Identifying the central sulcus:
The sagittally oriented superior frontal sulcus (which divides the superior frontal gyrus from the middle frontal gyrus) terminates within the precentral sulcus. The sulcus immediately posterior to the precentral sulcus is typically the central sulcus.
The central sulcus is the main sulcus that extends to the midline.
The pars marginalis or “pars bracket sign” is a paired short sulcus immediately posterior to the central sulcus.
Identify the “hand knob”. U shaped segment of the precentral gyrus corresponding to upper extremity motor function
Superior frontal sulcus
Precentral sulcus
Central sulcus
Postcentral sulcus
Pars Marginalis
Precentral gyrus
Postcentral gyrus

12. 56 M with right upper extremity weaknessCT
DWI
ADC
FLAIR
HPI: 56 yo male who presents with the acute onset of right upper extremity weakness which began 4 hours prior to presentation. A stroke was suspected and a stroke code was activated.

13. 56 M with right upper extremity weaknessCT
DWI
ADC
FLAIR
Hand Knob
Axial CT at the level of the vertex demonstrates no hemorrhage or evidence for cytotoxic edema. An MR was subsequently performed which demonstrates a small focus of diffusion restriction consistent with infarction (red arrow) within the left precentral gyrus co-localizing to the “hand knob” on the homunuclus (blue arrow).

14. 55 M with fluent aphasia
DWI
FLAIR
HPI: A 55 year old male presents with acute onset speech difficulty. The evaluating neurologist states the patient’s speech deficits are consistent with a fluent aphasia.

15. 55 M with fluent aphasia
DWI
FLAIR
Axial diffusion-weighted and sagittal T2-FLAIR images demonstrate areas of restricted diffusion with associated T2-FLAIR hyperintense signal involving the left posterior superior temporal (STG) and supramarginal gyri (SMG), consistent with early subacute infarct.

16. Wernicke’s Aphasia
Lesions involving Wernicke’s area lead to speech errors known as phonemic paraphasic errors, in which the phonemes (consonant or vowel sounds distinguishing one word from a different but similar word) are chosen incorrectly. These errors are cardinal features of Wernicke’s aphasia, a type of fluent aphasia.
Wernicke’s area was classically thought to be involved in speech comprehension, although modern evidence indicates a role in speech production, including phonologic retrieval, as well as the monitoring, feedback and correction of self-produced speech.
Middle temporal gyrus
Superior temporal gyrus
SMG AG
Wernicke’s area (outlined in green) refers to the dominant (left) hemispheric posterior perisylvian region, including the posterior superior temporal gyrus and supramarginal gyrus (SMG). The angular gyrus (AG) is located posterior to the SMG.

17. 26 M with expressive aphasia
T1+C
FLAIR
HPI: A 26 year old male presents with gradual onset speech difficulty. The evaluating neurologist states the patient’s speech deficits are consistent with an expressive aphasia.

18. 26 M with expressive aphasia
T1+C
FLAIR PT
Insula
POP
POP PT
Insula
Axial T2, sagittal T1 post contrast and coronal FLAIR MR images of the brain demonstrate an expansile T2/FLAIR hyperintense non enhancing mass involving the left pars triangularis (PT) and pars opercularis (POP) of the left inferior frontal gyrus as well as the insula. The mass was resected and pathology was consistent with an oligodendroglioma.

19. Broca’s aphasia IFS AAR AHR PCS POP POR PT PT POP Broca’s area POP PT
Inferior frontal gyrus PT
POP
POR
POP PT
POR
Broca’s area refers to the pars triangularis (PT) and pars opercularis (POP) of the dominant (typically left) inferior frontal gyrus. The pars orbitalis (POR), PT and POP comprise the inferior frontal gyrus. The POR is separated from the PT by the anterior horizontal ramus (AHR) of the lateral sulcus. The anterior ascending ramus (AAR) of the lateral sulcus separates PT from POP. [IFS = inferior frontal sulcus; PCS = inferior extent of the precentral sulcus]
Broca’s area is involved in the motor component of speech production. Broca’s aphasia is an expressive aphasia characterized by non-fluent, scarce production of speech, with poor articulation in the form of short sentences with only a few words. PT
POP

20. 69 M with visual field deficit and confusion
FLAIR
DWI
TOF
HPI: A 69 yo male presents with acute onset of visual disturbance and confusion.

21. 69 M with visual field deficit and confusion
FLAIR
DWI
TOF
Sagittal FLAIR, axial diffusion and time of flight MRA of the posterior circulation demonstrate cytotoxic edema within the lingual gyrus of the left occipital lobe and medial left temporal lobe (blue arrows) consistent with an infarction within the posterior cerebral artery (PCA) distribution related to occlusion of the left P1 segment (red arrow).

22. Visual Field Deficits R L
Parieto-occipital sulcus
Cuneus
Calcarine fissure
Lingual gyrus
Lingual gyrus
The occipital lobe, the primary visual cortex, is separated from the parietal lobe by the parieto-occipital sulcus. The calcarine fissure divides the occipital lobe into 2 primary lobes, the cuneus and the lingual gyrus.
Opto-retinal mapping is maintained along the visual pathway. The right and left occipital lobes receive temporal and nasal input from each eye. The input below the equator is mapped to the cuneus and above the equator is mapped to the lingual gyrus. R L
The visual field deficit in this patient with an infarct involving the left lingual gyrus corresponds to a right superior quadrantanopia.

23. 30 M with gelastic seizures
T1 +C
FLAIR
HPI: A 30 year old male is been treated for chronic, medically refractory epilepsy. One of his seizure types consists of a rising epigastric sensation, followed by the development of giggling or staring.

24. 30 M with gelastic seizures
T1 +C
FLAIR
Sagittal precontrast T1, coronal post contrast and coronal FLAIR images demonstrate a well circumscribed T1 isointense, T2/FLAIR mildly hyperintense, nonenhancing lobular mass arising from the left inferior aspect of the tuber cinereum (blue arrow).

25. Tuber Cinereum of Hypothalamus
Tuber cinereum hamartoma – Gelastic seizures
Normal Comparison
Mamillary Body
Hamartoma
Optic Chiasm
Tuber Cinereum of Hypothalamus
The tuber cinereum is an eminence of gray matter on the lower aspect of the hypothalamus, bordered anteriorly by the optic chiasm and posteriorly by the mammillary bodies. It forms part of the floor of the third ventricle, and its lower surface is the root of the pituitary infundibulum.
Tuber cinereum hamartomas are congenital tumors composed of neurons organized in poorly demarcated clusters that serve as a direct epileptogenic focus. The hypothalamus plays an important role in the mediation of emotional responses, although the specific reason that tuber cinereum hamartomas are associated with gelastic (laughing) seizures is incompletely understood.

26. 33 M with palatal myoclonus
FLAIR
T2 *
T2 *
Case courtesy of Dr. Kelli Dawson, University of Wisconsin Hospitals and Clinics
HPI: A 33 year old male presents for follow up MR imaging after suffering traumatic brain injuries 12 months prior. His previously documented injuries include grade III diffuse axonal injury. The patient demonstrates persistent symptoms of palatal myoclonus.

27. 33 M with palatal myoclonus
FLAIR
T2 *
T2 *
Case courtesy of Dr. Kelli Dawson, University of Wisconsin Hospitals and Clinics
Axial T2 and sagittal T2-FLAIR images of the brainstem demonstrate hyperintensity and enlargement of the right inferior olivary nucleus, consistent with hypertrophic olivary degeneration (HOD) (blue arrows). Two adjacent slices from axial T2* GRE sequence demonstrate focal hemosiderin deposition consistent with prior diffuse axonal injury affecting the dorsal brainstem in the right central tegmental tract (orange arrows), resulting in the HOD seen in the FLAIR sequences

28. Hypertrophic olivary degeneration
FLAIR
FLAIR
FLAIR T2 RN RN DN
ION
ION DN
ION
Sequential coronal T2-FLAIR images from anterior to posterior (first 3 images from left to right) demonstrate the dentato-rubro-olivary pathway (i.e. Guillain-Mollaret triangle), comprised of the inferior olivary nucleus (ION), the ipsilateral red nucleus (RN), and the contralateral dentate nucleus (DN), which in this case demonstrates abnormal signal due to gliosis from prior tumor resection, resulting in HOD. Final image (far screen right) demonstrates classic findings of high T2 signal and hypertrophy of the inferior olivary nuclei seen in bilateral HOD.
The efferent fibers travel from the dentate nucleus to the contralateral red nucleus via the superior cerebellar peduncle. The tract decends from the red nucleus to the ipsilateral inferior olivary nucleus via the central tegmental tract. The afferent pathway originates from the inferior olivary nucleus to the contralateral cerebellum. Disruption of the dentato-rubro-olivary pathway affects the reflex arc that controls fine voluntary movements, and classically presents with palatal myoclonus.

29. 41 F with confusion, ataxia, and vision changes
FLAIR
FLAIR
HPI: A 41 year old female with history of gastric bypass who “drinks too much” (per her husband), presents with subacute onset global confusion, marked bilateral lower extremity weakness, ataxia, evidence of peripheral neuropathy, and recent onset blurred vision.

30. 41 F with confusion, ataxia, and vision changes
FLAIR
FLAIR
Axial T2-FLAIR images demonstrate hyperintense signal involving the periaquedectal grey matter (blue arrow, banks of the third ventricle (orange arrows) and mammillary bodies (white arrows).

31. Wernicke’s Encephalopathy
Thiamine is a water soluble vitamin and important cofactor for key enzymes in the Krebs and pentose-phosphate cycles. Rapid depletion can occur in those with poor nutrition, particularly those with chronic alcoholism. Wernicke’s encephalopathy (WE) classically presents with the triad of altered consciousness, ocular movement dysfunction and ataxia. Other signs of nutritional deficiency, such as polyneuropathy, can also occur.
MR findings of T2 signal abnormality (with diffusion restriction in the acute phase) involving the periaqueductal grey matter, walls of the third ventricle, mammillary bodies, with variable involvement of the medial thalami, caudate nuclei and frontal and parietal cortex is typical. Abnormal post-contrast enhancement involving the mammillary bodies, periaqueductal grey matter and medial thalami is another feature. MB
PAG
Thiamine deficiency leads to impaired cerebral energy metabolism, focal lactic acidosis, and disruption of cellular osmotic gradients, among other abnormalities, which have a tendency to effect the periventricular and periaqueductal regions, where thiamine-related glucose and oxidative metabolism is abundant.

32. 32 F with double vision and facial weakness
FLAIR T2 T1
HPI: A 32 year old female with history of multiple sclerosis presents with new double vision and left facial weakness. On physical examination, the patient has a left horizontal gaze palsy and dense left sided facial weakness (including loss of forehead wrinkling and left facial droop) consistent with lower motor neuron deficits referable to left cranial nerves VI and VII.

33. 32 F with double vision and facial weakness
FLAIR T2 T1
Sagittal T2-FLAIR, axial T2 and T1 weighted images at the level of the pons demonstrate a lesion that is T2/FLAIR hyperintense (white arrow) and T1 hypointense (orange arrow) involving the left facial colliculus, consistent with a demyelinating lesion in this patient with known multiple sclerosis.

34. Facial colliculus syndromeVI VI
VII
VII
Pons
The facial colliculi are paired small elevations (blue arrows) protruding from the dorsal pons into the fourth ventricle. They are formed by motor fibers from the facial nerve nucleus curving backward and laterally around the posterior aspect of the abducens nucleus prior to joining parasympathetic and special sensory fibers of the facial nerve and assuming an anterolateral course in the caudal pons.
A lesion affecting the facial colliculus will cause deficits of the abducens nerve and motor fibers of the facial nerve, leading to ipsilateral CN VI and VII palsies, manifesting as ipsilateral horizontal gaze palsy and lower motor neuron pattern facial weakness. This presentation has been termed the “facial colliculus syndrome”.

35. 66 F with dysarthria and gait disturbance
HPI: A 66 year old female being treated for pseudomembranous colitis developed new onset dysarthria and ataxia. Her medication list included metronidazole for treatment of her infection.

36. 66 F with dysarthria and gait disturbance
An axial T2-weighted image at the level of the brainstem and cerebellum demonstrates symmetric hyperintense signal in the dentate nuclei of the cerebellar hemispheres bilaterally (arrows).

37. 66 F with dysarthria and gait disturbance
The abnormal signal on T2-weighted images resolved after removal of the offending medication.

38. Dentate nucleus– Metronidazole neurotoxicity
The paired dentate nuclei of the cerebellum appear to have anatomically separate, functionally distinct motor and non-motor domains. The dorsal dentate projects to cortical areas involved in coordination and control of motor activity, the ventral dentate projects to premotor and posterior parietal areas thought to be involved in higher cognitive and visuospatial functions.
Metronidazole neurotoxicity-induced encephalopathy is a rare complication of metronidazole use. The clinical presentation of reported cases shows commonalities such as dysarthria and gait disturbance, with other variable features such as extremity weakness.
MR findings include T2-FLAIR hyperintense signal almost always involving the dentate nuclei, with other commonly affected areas including the midbrain (tectum, red nucleus, and tegmentum around periaqueductal gray matter), dorsal pons (the vestibular nucleus, superior olivary nucleus, and the abducens nucleus), dorsal medulla, and corpus callosum (splenium). These lesions are always bilateral and symmetric.
Medulla
Dentate
Midbrain
Splenium
Normal axial FLAIR images at the level of the medulla, dentate nuclei, midbrain and splenium demonstrating common areas of involvement in metronidazole toxicity, including the dorsal medulla (white arrowheads), dentate nuclei, red nuclei, periaqueductal gray, and splenium.

39. 41 M with vertigo and crossed hemisensory deficits
DWI
HPI: A 41 year old male presents with nausea and vomiting, vertigo, right face tingling, and clumsiness of the right hand. Physical examination demonstrates right arm dysmetria, and right face and left body hemisensory changes.

40. 41 M with vertigo and crossed hemisensory deficits
DWI
Axial pre-contrast T1-weighted and DWI images demonstrate a focus of restricted diffusion in the right dorsolateral medulla (red arrow), consistent with acute infarct. There is crescentic, intrinsically T1 hyperintense signal in the right vertebral artery (blue arrow), consistent with intramural hematoma related to a vascular dissection.

41. Lateral medullary (Wallenberg) syndrome
Wallenberg syndrome is caused by an infarct of the lateral medulla due to compromise of the posterior inferior cerebellar artery (PICA). In younger patient’s this is commonly caused by vertebral artery dissection with secondary compromise of PICA. In older patient’s this can be caused by thromboembolic disease.
Classically, patient’s with Wallenberg syndrome present with a Horner syndrome (ipsilateral ptosis, miosis and anhydrosis), ipsilateral ataxia, and ipsilateral face and contralateral body sensory changes (so-called “crossed hemisensory deficits”), but they may present with varying combinations of deficits referable to the lateral medulla.
The clinical presentation is due to involvement of a combination of nuclei and tracts in the dorsolateral medulla. Involvement of descending sympathetic tracts leads to Horner’s syndrome. Involvement of the inferior cerebellar peduncle and spinal trigeminal nucleus/tracts leads to ipsilateral cerebellar signs and facial sensation deficits, respectively. Contralateral hemibody pain/sensory deficits are due to involvement of the spinal lemniscus (ie spinothalamic) tracts, which decussate at the level of the spinal cord prior to ascending into the medulla. Variable involvement of the vestibular nuclei and nucleus ambiguus may lead to symptoms of vertigo and dysarthria/dysphagia, etc.
Vertebral artery
PICA
Commonly affected: Spinal lemniscus, spinal trigeminal nucleus, tract of spinal trigeminal nucleus, inferior cerebellar peduncle
Occasionally affected: Dorsal vagal nucleus, nucleus solitarius, vestibular nuclei, nucleus ambiguus

42. Summary
Knowing the clinical history can aid in the detection of pathology on neuroimaging studies.
A firm understanding of neuroanatomy and important imaging landmarks can allow the radiologist to precisely localize and characterize pathology.
Sup. parietal lobule

43. References
1. Binder JR. The Wernicke area: Modern evidence and a reinterpretation. Neurology Dec 15;85(24): DeWitt I, Rauschecker JP. Wernicke's area revisited: parallel streams and word processing. Brain Lang Nov;127(2): Sinanović O, Mrkonjić Z, Zukić S, Vidović M, Imamović K. Post-stroke language disorders. Acta Clin Croat Mar;50(1): Kim J, Kwon Y, Yang Y, et al. Clinical experience of modified diffusion-weighted imaging protocol for lesion detection in transient global amnesia: an 8-year large-scale clinical study. J Neuroimaging Jul-Aug;24(4): Bartsch T, Deuschl G. Transient global amnesia: functional anatomy and clinical implications. Lancet Neurol Feb;9(2): Bartsch T, Döhring J, Rohr A, Jansen O, Deuschl G. CA1 neurons in the human hippocampus are critical for autobiographical memory, mental time travel, and autonoetic consciousness. Proc Natl Acad Sci U S A Oct 18;108(42): Huynh N, Stemmer-Rachamimov AO, Swearingen B, Cestari DM. Decreased vision and junctional scotoma from pituicytoma. Case Rep Ophthalmol May;3(2): Parvizi J, Le S, Foster BL, et al. Gelastic epilepsy and hypothalamic hamartomas: neuroanatomical analysis of brain lesions in 100 patients. Brain 2011: 134; 2960– Wu J, Gao M, Shen J-X, Qiu S, Kerrigan JF. Mechanisms of intrinsic epileptogenesis in human gelastic seizures with hypothalamic hamartoma. CNS neuroscience & therapeutics. 2015;21(2): Palacios E, Wasilewska E, Alvernia JE, Figueroa RE. Palatal myoclonus secondary to hypertrophic olivary degeneration. Ear Nose Throat J Jul;88(7): Elefante A, Puoti G, Senese R, et al. Non-alcoholic acute Wernicke's encephalopathy: role of MRI in non typical cases. Eur J Radiol Dec;81(12): Kirkpatrick C. Facial colliculus syndrome. University of Iowa Health care ophthalmology and visual sciences website. Accessed 4/12/ Kim E, Na DG, Kim EY, Kim JH, Son KR, Chang KH. MR imaging of metronidazole-induced encephalopathy: lesion distribution and diffusion-weighted imaging findings. AJNR Am J Neuroradiol Oct;28(9): Dum RP, Strick PL. An unfolded map of the cerebellar dentate nucleus and its projections to the cerebral cortex. J Neurophysiol Jan;89(1): Day GS, Swartz RH, Chenkin J, Shamji AI, Frost DW. Lateral medullary syndrome: a diagnostic approach illustrated through case presentation and literature review. CJEM Mar;16(2): Foroozan R. Chiasmal syndromes. Curr Opin Ophthalmol Dec;14(6): Lee AG, Siebert KJ, Sanan A. Radiologic-clinical correlation. Junctional visual field loss. AJNR Am J Neuroradiol Jun-Jul;18(6): Milea D, LeHoang P. An unusual junctional scotoma. Surv Ophthalmol Nov-Dec;47(6): Transient global amnesia. Mayo Clinic Diseases and Conditions website. July 18, Accessed April 23, Bartsch T, Deuschl G. Transient global amnesia: functional anatomy and clinical implications. Lancet Neurol Feb;9(2): Bartsch T, Döhring J, Rohr A, Jansen O, Deuschl G. CA1 neurons in the human hippocampus are critical for autobiographical memory, mental time travel, and autonoetic consciousness. Proc Natl Acad Sci U S A Oct 18;108(42): Enzinger C, Thimary F, Kapeller P, et al. Transient global amnesia: diffusion-weighted imaging lesions and cerebrovascular disease. Stroke Aug;39(8):