Here is your chance to be an anatomy king or queen for a day. We plan on dispersing these anatomic snippets of the brain in small groups so as not to overwhelm you, however, you will find complete descriptions at MRI Online.

You are shown one T1 sagittal image of a 71-year-old male. Focus on the inferior frontal gyrus anteriorly which makes the letter M. Do you see the letter M? It is made up of three components.

Q1 – Can you identify these inferior frontal sulcus structures labeled in pink, blue, and yellow?

Q2 – The staircase descending sulcus labeled with a multitude of orange arrows, behind the pars opercularis, is representative of what sulcus?

Q3 – The purple arrow highlights what sulcus?

Q4 – The unlabeled gyrus in front of the purple arrow represents what?

Q5 – The pars opercularis of the inferior frontal gyrus is known as Brodmann area ___?

Q6 – The pars triangularis of the inferior frontal gyrus surrounds the anterior horizontal limb of the lateral sulcus and is bounded caudally by the anterior ascending limb of the lateral sulcus, white arrow, represents Brodmann area ___?

Q7 – Brodmann areas 44 and 45 are named after what famous French physician?

Sagittal T1 FSE

A1 – The pink arrow highlights the pars orbitalis, blue indicates the pars triangularis, and yellow is the pars opercularis.

A2 – Precentral sulcus.

A3 – Central sulcus of Rolando.

A4 – Precentral gyrus, a critical contributor to motor function.

A5 – Brodmann area 44.

A6 – Brodmann area 45.

A7 – Pierre Paul Broca who lived from 1824 to 1880. This French physician, anatomist and anthropologist is best known for the area named after him, namely Broca’s area. He ascertained that patients suffering from aphasia contained abnormalities in the left frontal region in this locus. Broca’s area abnormalities produce expressive aphasia. Expressive aphasia is characterized by partial loss of the ability to produce language (spoken, manual, or written), although comprehension remains intact. Speech is difficult and full of effort. It usually includes important words of content but omits functional words that only have grammatical significance and not real word meaning such as prepositions. Another name given to this is “telegraphic speech”. The person’s intended message can be understood but is usually grammatically incorrect. In severe forms of expressive aphasia a person may only speak with single-word utterances.

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A 55-year-old man presents with headache, neck pain and dizziness. See if you can answer the questions below by looking at images 1 through 3 before looking at the duplicate images with arrows (images 4 through 6).

Q1 – What is the salient finding on the presented MRI study?

(a) Cortical atrophy
(b) Dural venous thrombosis
(c) Pachymeningeal thickening
(d) Subdural hematoma
(e) Demyelinating plaques

Q2 – What is the most likely diagnosis?

(a) Sarcoidosis
(b) Bacterial meningitis
(c) Pseudotumor cerebri
(d) Intracranial hypotension
(e) Metastasis

Sagittal T1

Sagittal T1

Axial T2

A1 – (c) Pachymeningeal thickening. The salient finding on precontrast images is bilateral and symmetrical subdural fluid collections and pachymeningeal thickening.

Cortical atrophy (a) is false since supporting findings of cerebral atrophy, such as sulcal enlargement and ex vacuo ventricular enlargement, are not present. Dural venous thrombosis (b) is false given that T1-weighted images demonstrate slightly increased signal in the sinuses, but flow void is confirmed on T2-weighted images. No dural thrombosis is evident. Subdural hematoma (d) is false because there is no evidence of signal alterations associated with blood products on T1- or T2-weighted images. Demyelinating plagues (e) is also false. There are scattered T2 and FLAIR hyperintensities in the white matter of bilateral frontal lobes. However, these lesions do not demonstrate typical septocallosal distribution of MS demyelinating plaques.

A2 – (d) Intracranial hypotension. Diffuse, smooth, supra and infratentorial enhancement of the thickened dura mater is a classical finding of intracranial hypotension. Often, veins compensatorily distend (image 4, green arrow). Such compensatory distention includes the dural venous sinus flow void (image 5, green arrow).

Sarcoidosis (a) and pseudotumor cerebri (c) are false. Sarcoidosis and other granulomatous diseases, including tuberculosis, Wegener granulomatous, and fungal disease, may produce dural masses and pachymeningeal enhancement, though granulomatous processes typically affect the basilar leptomeninges rather than hemispheric convexities. They are often “lumpy-bumpy”. Bacterial meningitis (b) is false given that it is associated with leptomeningeal enhancement, not isolated pachymeningeal enhancement. It may be thick and irregular. Patients are usually very sick. Metastasis (e) is also false. Metastases, particularly breast, prostate, melanoma and RCC, can present with pachymeningeal enhancement. However, in the absence of medical history, metastasis is unlikely. Furthermore meningeal carcinomatosis often involves the leptomeninges (pia arachnoid) and may be “lumpy-bumpy”.

As a note, transient pachymeningeal enhancement can also be seen after cranial surgery and uncomplicated lumbar puncture.

Sagittal T1

Sagittal T1

Axial T2

Q3 (BONUS) – Which is not a supporting image finding of spontaneous intracranial hypotension in this case?

(a) Decreased dimension of the suprasellar cistern
(b) Empty sella
(c) Venous distension
(d) Effacement of the basal cisterns
(e) Tonsillar ectopia

A3 (BONUS) – (b) Empty sella. Supporting imaging features of spontaneous intracranial hypotension (SIH) include all but empty sella. Empty sella could be seen with idiopathic intracranial hypertension (IIH), previously known as pseudotumor cerebri. In spontaneous intracranial hypotension, venous engorgement at the dura mater across the sella turcica could produce reactive hyperemia and increase in size of the pituitary gland. Other supporting findings of SIH include small slit-like ventricles (image 6, green arrows) bowing of optic chiasm, flattening of the pons against the clivus, dural thickening and intense enhancement with extrathecal cerebrospinal fluid collection. Retroclival venous engorgement (image 4, green arrow) is a useful sign on sagittal T1 MRI supporting spontaneous intracranial hypertension.

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References:

1. Saindane Am. Recent Advances in Brain and Spine Imaging. Radiol Clin N Am. Feb 2015.
2. Smirniotopoulos JG, Murphy FM, Rushing EJ, Rees JH, Schroeder JW. Patterns of contrast enhancement in the brain and meninges. Radiographics. 2007 Mar-Apr;27(2):525-51.
3. Park ES, Kim E. Spontaneous intracranial hypotension: clinical presentation, imaging features and treatment. J Korean Neurosurg Soc. 2009 Jan; 45(1):1-4.
4. Medina JH, Abrams K, Falcone S, Bhatia RG. Spinal imaging findings in spontaneous intracranial hypotension. AJR Am J Roentgenol. 2010 Aug;195(2).

Imaging signs on MR can be a helpful tipoff toward the correct diagnosis. Take a look at this textbook example in today’s neurological imaging case.

This 71-year-old male presents with resting tremor and diplopia. Is the most likely diagnosis Parkinson’s disease, Lewy body dementia, Progressive supranuclear palsy, Alzheimer’s disease, or Frontobasal degeneration? Have a look at images 1 and 2, and see if you can generate a diagnosis.

Clue: Do you have a hummingbird feeder in your yard?

FLAIR Axial IR

T1 Sagittal

Image 2 supplement – “Hummingbird Sign”

This patient was diagnosed with progressive supranuclear palsy (PSP), also known as Steele-Richardson-Olszewski syndrome or Richardson’s syndrome. The condition is associated with supranuclear ophthalmoplegia, pseudobulbar palsy, nuchal dystonia, dementia, gradual progressive monophasic disease onset at age 40 or older, and prominent posterior instability in the first year of the disease.

PSP is a tauopathy like frontotempolobar dementia (formerly known as Pick’s disease). Tau is a microtubule-associated protein which, in the normal human brain, is distributed by axons. Neurofibrillary tangles and tau protein filaments are found in cases of Alzheimer’s disease.

Sometimes, PSP has early brainstem involvement with a frontal predominance. It is typical for there to be more posterior fossa and brainstem involvement than in classic Parkinson’s disease. Midbrain atrophy, divergence of the red nuclei, dilatation of the third ventricle, atrophy of the superior cerebellar peduncle, and frontocortical atrophy are common. The hummingbird sign is used to describe mid-sagittal imaging appearance of PSP, at the midbrain level (image 2, yellow arrows).

In addition to the midbrain atrophy in PSP, the dentate nucleus (not shown) is markedly involved. This leads to its main efferent pathway, the brachium conjunctivum or superior cerebellar peduncle being affected and atrophic.  Its fibers pass into the brainstem and decussate at the inferior colliculi before synapsing at the red nucleus and ventrolateral nucleus of thalamus.

Q1 – What diseases found in the brain are linked to tau proteins?

(a) Pick’s disease
(b) Alzheimer’s
(c) Progressive supranuclear palsy (PSP)
(d) Wilson’s disease
(e) a, b, and c

Q2 – The “hummingbird sign” is typical of:

(a) Parkinson’s disease
(b) Progressive supranuclear palsy (PSP)
(c) Wilson’s disease
(d) Hurler’s disease
(e) None of the above

Q3 – The “big panda sign” is typical of:

(a) Parkinson’s disease
(b) Progressive supranuclear palsy (PSP)
(c) Wilson’s disease
(d) Hurler’s disease
(e) NF-2

Q4 – The “swallow tail sign” is typical of:

(a) Parkinson’s disease
(b) Progressive supranuclear palsy (PSP)
(c) Wilson’s disease
(d) Multisystem atrophy
(e) None of the above

For more advanced nuanced thoughts (“putaminal slit sign” and “the smudging sign”), read on. Differential subtle features of similar diseases:

• PSP can be differentiated from multisystem atrophy-P (Parkinson type) using a midbrain diameter of less than 14mm on the sagittal scan in the AP dimension.
• Multisystem atrophy cerebellar-type (MSA-C) may be differentiated from PSP and idiopathic Parkinson’s disease by the “hot-cross bun sign” or “pontine cross sign” seen in MSA-C.
• Putaminal low signal intensity helps differentiate MSA from idiopathic Parkinson’s disease.
• The “putaminal slit sign” differentiates a parkinsonian-type or MSA-P type from progressive supranuclear palsy and standard idiopathic Parkinson’s disease.
• Zona compacta atrophy results in confluence or “the smudging sign” between the substantia nigra and red nucleus hypointensity in classic Parkinson’s disease.
• Corticobasal degeneration is characterized by global atrophy or asymmetric atrophy which helps differentiate it from the other entities.
• Classic Parkinson’s or idiopathic Parkinson’s disease should be suspected when there is resting tremor, rigidity, hypokinesia, but not upward gaze palsy as in PSP.
• Some later stage Parkinson’s patients may have visual hallucinations, but this is more typical of Lewy body dementia.

A1 – (e) a, b, and c

A2 – (b) Progressive supranuclear palsy (PSP)

A3 – (c) Wilson’s disease

A4 – (a) Parkinson’s disease

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For more case review, check out MRI Online.

References: 

1. Kornenko, Aronin.  Neuroradiology

2. Cossotini M et al. MRI of the Substantia Nigra. Radiology 2014.  Jun;271(3): 831-838.

3. Quattrone A et al. MR Imaging Differentiation of PSP from Parkinson’s. Radiology 2008; 246: 214-221.

This 57-year-old female presents with hippocampal atrophy, sudden cognitive decline, and visual disturbances.

Q1 – Using images 1 and 2, what is the most likely diagnosis?

(a) Thrombosed aneurysm
(b) Pituitary apoplexy
(c) Craniopharyngioma
(d) Choristoma

Coronal T2 FSE

Coronal T1 SE

A1 – (b) Pituitary apoplexy

Q2 – Which statement is false about pituitary apoplexy?

(a) Often requires urgent surgical decompression
(b) Often requires steroid therapy
(c) Occurs with microadenoma
(d) May be present with ophthalmoplegia
(e) May be associated with subarachnoid hemorrhage

Q3 – Which statement is false about prolactin-secreting adenomas?

(a) May be invasive with skull base destruction
(b) May be diagnosed with greater than 95 percent accuracy by prolactin greater than 200 ng/ml
(c) Mild elevations of prolactin (<100 ng/ml) can be related to medications, hypothyroidsm, or “stalk effect”
(d) Microadenomas may demonstrate the “hook effect” on laboratory studies

Pituitary apoplexy may often present as ophthalmoplegia, visual loss, and confusion in a patient with known pituitary macroadenoma.

Pituitary apoplexy is a surgical emergency requiring acute decompression. Steroid administration is required for endocrine support as the patient may exhibit acute pituitary insufficiency. Sometimes, intravenous T3 is also required.

Pituitary apoplexy may be associated with subarachnoid hemorrhage as well as vasospasm.

Prolactinomas are known to be invasive and, when large, can produce skull base erosion.

Prolactin is the only pituitary hormone which is regulated by an inhibitory mechanism. Large nonsecreting lesions which compress the pituitary stalk can result in elevations of the prolactin described as “stalk effect.” Elevations on this basis are relatively small as are those secondary to medications or hypothyroidism. A rule of thumb in elevating prolactin elevations is that the percentage of chance of a lesion being a secreting prolactinoma is about half of the level, so a prolactin of greater than 200 has an essentially 100 percent chance of being a prolactinoma.

Falsely low prolactin in the face or a large or invasive prolactinoma may represent the “hook effect” where the binding sites of the RIA antibody become saturated and the antibody curve is no longer proportional to the amount of prolactin. This is resolved by performing serial dilutions. This effect never occurs in microadenomas, but rather in macroadenomas.

A2 – (c) Occurs with microadenoma

A3 – (d) Microadenomas may demonstrate the “hook effect” on laboratory studies

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What is causing sudden right-side blindness in this 10-year-old girl?
What are the best MRI next steps for this stroke patient?
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For more case review, check out MRI Online.

References:

1. Diagnostic Imaging Brain Osborn et. al. Amirsys.

2. Greenberg MS Handbook of Neurosurgery. Thieme.

3. Liu JK, Couldwell WT Contemporary management of prolactinomas. Neurosurg. Focus 2004: 16 (4)