While observing the mass, we noticed she had a tail

This 44-year-old female presents with right wrist pain. You are shown five images. A coronal proton density (image 1), a coronal proton density fat suppression (image 2), two sagittal proton density fat suppression (images 3 and 4), and an axial or short-axis proton density (image 5). A hyperintense mass around the ulna is obvious.

Q1 – With regard to the pink arrows in images 1 and 2, what do you think the significance is?

Q2 – What is your differential diagnosis for a septated cystic mass of the wrist?

Q3 – What are masses that are associated with a “tail sign”?

Q4 – What is the most common location for ganglion pseudocyst in the wrist? How about the second most common?

Coronal PD

Coronal STIR

Sagittal STIR

Sagittal STIR

Axial PD

 

A1 – The pink arrows (images 1 and 2; 6 and 7) demonstrate a tail extending back to the joint capsule and subsheath portion of the extensor carpi ulnaris.

A2 – (a) ganglion pseudocyst, (b) epidermoid, (c) myxoma, (d) capsular cyst, (e) pisotriquetral bursal cyst, or (f) capsulosynovial cyst associated with inflammatory arthritis (such as rheumatoid).

A3 – (a) ganglion with a tail to either the capsule or sheath of a tendon, (b) neural tumor with a tail to a nerve, (c) aneurysm or pseudoaneurysm with a tail to a vessel, or (d) capsular or synovial cyst with a tail to a joint.

A4 – The most common is along the dorsal scapholunate interval near the dorsal limb of the scapholunate ligament (SL) and the radial limb of the intercarpal ligament. Sometimes these project at the junction of the scaphoid and base of the capitate dorsally.

The second most common location is along the palmar aspect of the wrist near the volar SL ligament and capsule near the base of the radioscaphocapitate extrinsic or the base of the radial lunatotriquetral ligament extrinsic.

In other words, a ganglion in this location is extremely atypical. Its intimacy with the extensor carpi ulnaris is problematic as it relates to dynamic motion (i.e. can restrict).

The blue arrow on image 8 also corroborates the dorsal tail of a ganglion pseudocyst, and the yellow arrow on image 9 shows the septated mass, sagittally.

In image 10, the green arrow shows the mass’s close proximity to the extensor carpi ulnaris (image 10, purple arrow), displacing it medially.

Coronal PD

Coronal STIR

Sagittal STIR

Sagittal STIR

Axial PD

 

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A close look at a transspatial thoracic spine abscess

This 55-year-old male patient has history of quadriplegia due to transsection of the upper cervical spinal cord (image 1, orange arrow). Within the last six months, the patient noticed an absence of muscle spasms from the lower lumbar and lower extremities.

At the level of the T11-T12 intervertebral disc space, large loculated fluid collection / abscess obliterates the central spinal canal and portions of the T11 and T12 vertebral bodies as well as extends to the posterior elements and soft tissues. Images 2 and 3 (red arrows) show the extent of the abscess extending from the prevertebral soft tissues through the intervertebral disc space, through the spinal canal, and into the posterior elements.

Fluid collection partially surrounds the descending aorta with edematous changes including the bodies of T11 and T12, and extends approximately two-thirds of the way of the L1 vertebral body. Abscess extends approximately from the level of T10 to L1 measuring 7.25cm in craniocaudal dimension (image 2, yellow line) and 2.00cm in anteroposterior dimension (image 2, blue line). The fluid component measures 7.09cm in the trans-sagittal dimension (image 2, pink line). Given the upper cervical spinal cord transsection, findings are consistent with an abscess likely related to underlying Charcot disease.

Image 4 shows the extent of the abscess (green arrow) obliterating the spinal canal, vertebral body, and posterior elements.

Sagittal T2 FSE

Sagittal T2 FSE

Sagittal T1

Axial T2 FSE

 

Diagnosis:
Large transspatial thoracic spine abscess related to underlying Charcot disease from prior cervical spinal cord transsection.

 

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What can happen when you combine a 33-year-old shoulder with weight lifting?

This 33-year-old weight lifter presents with anterior shoulder pain and popping.

Q1 – Using images 1 through 4, what are the imaging findings?

Q2 – What intraarticular AC joint pathology is most likely?

T2 TSE Sagittal SPAIR

T2

T2

T2 TSE Sagittal SPAIR

 

A1 – The diagnosis is clavicular osteolysis. Osteolysis of the clavicle more commonly affects younger adult males (mid 30s). MRI imaging characteristics include bone marrow edema of the distal clavicle, cysts or erosions of the distal clavicle, and a subchondral line within the distal clavicle (images 5 and 6, arrows). Additional imaging findings include resorption of the distal clavicle as well as periarticular swelling. Etiologies include fracture, AC joint dislocation as well as microtrauma related to sporting activities and weight lifting; especially bench and military pressing. Treatment is conservative (avoidance of overload activity, stretching, and steroid injection in particular) with resection of the distal clavicle reserved for refractory cases.

A2 – The most common intraarticular abnormality associated with osteolysis clavicle is labral pathology (approximately one-third). This patient has a posterior labral tear with a paralabral cyst (images 7 and 8, arrows). Less commonly, partial-thickness rotator cuff tears are also present. This is a sub-type of “peel-back” labral pathology seen in weightlifters.

Diagnosis: “Weightlifters Shoulder” with clavicular osteolysis and posterior labral “peel-back”.

T2 TSE Sagittal SPAIR

T2

T2

T2 TSE Sagittal SPAIR

 

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Watch out for other diagnoses that look similar in this pediatric brain case

This 10-year-old male has a history of encephalitis.

Q1 – The most likely diagnosis is:

(a) Herpes encephalitis
(b) Adrenoleukodystrophy
(c) Acute disseminated encephalomyelitis
(d) Acyl-CoA oxidase deficiency
(e) Metachromatic leukodystrophy

Axial T2 FLAIR

TSE

T1 SE

T1W

 

A1 – (b) Adrenoleukodystrophy

Adrenoleukodystrophy (ALD) is an X-linked disorder affecting young males due to the accumulation of very long chain fatty acids from a genetic deficiency in perioxisomal oxidation related to ALDP gene mutation. Carrier females can be symptomatic. MRI appearance includes relative sparing of subcortical U fibers, posterior distribution, central areas of scarring, and an active leading edge of demyelination. There are childhood, adolescent and adult forms as well as spinal (adrenomyeloneuropathy) manifestations and forms limited to Addison’s disease.

Herpes encephalitis is more temporal and hemorrhagic. It also has a more acute, rather than chronic, progressive presentation. Meningeal enhancement is common.

Acyl-CoA oxidase deficiency (pseudo ALD) can have a similar appearance, but is rare and seen in neonates. The disease is progressive unlike acute disseminated encephalomyelitis, which is monophasic.

Arylsulfatase A is decreased in metachromatic leukodystrophy (MLD). It does not have a parieto-occipito-callosal predilection on MRI.

Besides X-linked ALD (symmetric), not very many diseases affect the splenium of the corpus callosum, especially symmetrically. Some include:

  • Lymphoma (mass effect)
  • Glioblastoma (mass effect)
  • Posterior reversible encephalopathy syndrome (PRES)
  • Marchiafava-Bignami disease (alcohol-related non-masslike)
  • Multiple sclerosis (patchy)
  • Infective [e.g. Influenza (reversible), rotavirus, mumps, adnovirus, and E. coli]
  • Hyperosmolar hyperglycemia (reversible)
  • Legionnaires’ disease (reversible)
  • Glufosinate Ammonium Poisoning (non-masslike)
  • Krabbes disease (non-masslike, symmetric)
  • Dai-Diffuse axonal injury (trauma, hemorrhage, siderosis)
  • Infarct (usually hypoxic type)
  • Post-shunt decompression
  • Venous thrombosis (internal cerebral veins and straight sinus)
  • Others: AIDs dementia complex; antiepileptic drugs; mild encephalopathy with reversible splenial lesion (MERS); hemolytic uremic syndrome (HUS)

*For a proposed scoring method on adrenoleukodystrophy (ALD), see the referenced article by Daniel J. Loes.

 

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Reference:

1. Loes DJ, et. al., Adrenoleukodystrophy: A Scoring Method for Brain MR Observations, American Journal of Neuroradiology, (1994) 15:1761-1766.

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At a glance, how would you assess this ankle?

This 43-year-old female presents with ankle pain and paresthesia. Using images 1 through 5, what is your diagnosis?

Axial T1 TSE

Axial T2 TSE

Sagittal T1 TSE

Sagittal STIR TE

Sagittal T1 TSE

 

When looking at image 6, note four tendons in the medial flexor compartment. This is known as “the sign of too many tendons”. The arrows in image 6 point to a complex longitudinal split tear of the posterior tibialis. This is also visualized on image 7 (arrow). Abnormal longitudinal high grade partial split tear is shown on images 8 and 9 (arrows).

In the setting of tendinosis and split tears, it is useful to identify the proximal-distal length of the tear. In this case, retromalleolar, inframalleolar, and postmalleolar segments are swollen and abnormal as the posterior tibialis courses behind the medial malleolus into the arch of the foot and navicular attachments. Periarticular arthropathic spurring is identified within the midfoot, sagittally.

Additionally, note unrelated prominent medial process of the navicular, which has close approximation to the anterior calcaneal process outlined on image 10 (arrows). This resembles fibrous coalition; however, no osseous edema. No bony bridging is noted. The navicular is simply dysplastic.

Axial T1 TSE

Axial T2 TSE

Sagittal T1 TSE

Sagittal STIR TE

Sagittal T1 TSE

 

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Anatomy Queen or King for a day

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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ACL contusion patterns: The importance of medial sided contusions

This 52-year-old male presents with knee pain following an injury one week ago.

Q1 – What is the most likely mechanism of injury in this individual with an ACL tear?

Q2 – What are the potential internal derangements associated with this knee contusion pattern?

Coronal PD Fat Sat

Sagittal PD Fat Sat

Sagittal PD Fat Sat

Sagittal PD Fat Sat

Sagittal PD Fat Sat

Axial T2

 

A1 – Image 7 demonstrates an acute ACL tear (blue arrow). In addition, osseous contusions are identified in the posterior aspect of the lateral compartment in both the lateral femoral condyle (red arrow) and lateral tibial plateau (yellow arrow). Image 8 (arrow) also demonstrates an osseous contusion in the anterior medial tibial plateau (anterior medial tibial rim sign). Radiologists are most familiar with pivot-shift contusions in the lateral compartment. However, medial compartment osseous contusions also occur, and are associated with higher-energy injuries. The most commonly reported mechanism with an anterior medial tibial rim sign is axial loading. Axial loading occurred in this 52-year-old male following a fall from a ladder. An anterior medial rim sign is identified in approximately 30% of individuals with acute ACL tears.

A2 – The rim sign is associated with a significant increased risk of contusions and fractures as well as posterolateral corner injuries and tears of the posterior horn lateral meniscus. Image 9 (arrow) indicates a torn popliteofibular ligament. Images 10 and 11 (arrows) indicate a complex tear of the posterior horn / root attachment of the lateral meniscus. Image 12 (arrows) demonstrates an impaction fracture of the posterolateral tibial plateau. The proposed etiology for the anterior medial rim sign is a contusion between the inferior pole of the patella and anterior medial rim. Patellar edema is less common than the edema in the anterior medial tibia, likely related to the relative hardness of the sesamoid bone relative to the tibia. The identification of edema in both the patella and anterior medial rim is uncommon, occurring in approximately 4% of all acute ACL tears.

Coronal PD Fat Sat

Sagittal PD Fat Sat

Sagittal PD Fat Sat

Sagittal PD Fat Sat

Sagittal PD Fat Sat

Axial T2

 

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Don’t miss the salient finding in this brain case

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).

 

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Be kind to your AC joint. It can only take so much.

Many of us have experienced pain in the shoulder. It is often attributed to some deep-seated joint abnormality, and we wonder if it is the dreaded rotator cuff tear. However, one of the most common causes of shoulder pain is premature degeneration from overuse of the acromioclavicular (AC) joint, the so-called “joint on top”. If there is pain on top, with grinding or crunching, odds are it is the AC joint that is causing the problem.

Believe it or not, almost no one over age 20 has a normal AC joint. It seems that this joint was not meant to sustain the amount of activity that we humans undertake throughout our lives. In particular, the advent of backpacks, as well as modern sport, has put undue stress on this structure.

Since almost everyone over age 20 has an abnormal AC joint, this post will attempt to address (1) when this joint is the cause of the symptoms, (2) when it needs to be addressed, (3) what exacerbates disease in this joint, and (4) what imaging findings cinch the diagnosis.

You are shown three coronal images of the left shoulder of a 39-year-old male. He presents with pain, limited range of motion, and arm weakness.

Q1 – What symptoms should point you in the direction of the AC joint as the cause of discomfort?

Q2 – What activities in young athletes particularly aggravate this problem?

Q3 – In image 2, see if you can locate the swelling in the joint, edema of bone, and erosions. Since everyone has some of these, how can an imager know that this joint is actually the cause of the patient’s symptoms?

Coronal T1W TSE

Coronal T2W SPAIR

Coronal T2W TSE

 

A1 – Pain on “top”; motion specific pain with the arms over the head; crunching or grinding noises that you can feel and sometimes hear.

A2 – Weightlifting (especially heavier weights), and performing the activities of bench pressing or military pressing. Most young men do this in the gym. A tip-off that this activity is occurring is the size of the shoulder muscles, especially the supraspinatus, trapezius and pectoralis major.

A3 – Check out image 5 for identification of some swelling (pink arrow), erosions and/or edema of bone (blue arrow), and further erosions (yellow arrow). Now look at image 6, the standard T2 sequence. In patients that have symptomatic acromioclavicular joint disease, there are often tip-offs on the less sensitive water weighted sequence:

(a) The swelling or high signal in the joint persists on the T2 weighted image as a sign of active disease (image 6, orange arrow).

(b) In younger patients there is often no other evidence of any other pathology or an alternative explanation.

(c) Finally, the patient’s muscularity suggests that weightlifting activity is occurring and exacerbating this condition, and corroborating your diagnosis.

Coronal T1W TSE

Coronal T2W SPAIR

Coronal T2W TSE

 

Check out MRI Online for more case review.

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Do you know why this patient has resting tremor and diplopia?

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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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.

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