- Many neurological disorders simultaneously or consecutively affect the brain and spinal cord, however most neurologist find their comfort zone in attending the diagnosis via the brain access.
- This concept resulted in lagging of spinal cord imaging researches compared to brain ones and consecutive underestimation of the opportunity of an important tool sometimes essential to reach a definite diagnosis.
Degenerative Marrow Changes (Signal intensity changes) adjacent to the endplates of degenerated discs are a common observation on MR images.
This is a teaching lecture given twice by Prof. Dr. Mohamed Mohi Eldin, professor of neurosurgery, in the weekly conference of kasr El Aini Neurosurgery Department, Cairo University, November 2010 and January 2013.
Degenerative Marrow Changes (Signal intensity changes) adjacent to the endplates of degenerated discs are a common observation on MR images.
This is a teaching lecture given twice by Prof. Dr. Mohamed Mohi Eldin, professor of neurosurgery, in the weekly conference of kasr El Aini Neurosurgery Department, Cairo University, November 2010 and January 2013.
The caroticocavernous fistula is a specific type of dural arteriovenousfistula characterized by abnormal arteriovenous shunting within the cavernous sinus.
A caroticocavernous fistula results in high-pressure arterial blood entering the low-pressure venous cavernous sinus.
This interferes with normal venous drainage patterns and compromises blood flow within the cavernous sinus and the orbit.
The caroticocavernous fistula is a specific type of dural arteriovenousfistula characterized by abnormal arteriovenous shunting within the cavernous sinus.
A caroticocavernous fistula results in high-pressure arterial blood entering the low-pressure venous cavernous sinus.
This interferes with normal venous drainage patterns and compromises blood flow within the cavernous sinus and the orbit.
Idiopathic intracranial hypertension, Looking for the black cat in the dark r...Wafik Bahnasy
IIH is a disorder characterized by elevation of the ICP
without evidences of CSF cytochemical alterations,
dilated ventricles or mass lesions
◘ The annual incidence of IIH is increasing in association
with higher obesity rates, whereas recent scientific
studies indicate a possible role for androgen sex
hormones and adipose tissue in the pathogenesis of
the disease
True vs. pseudo papilledema, Dr. Jekyll and Mr. HydeWafik Bahnasy
◘ The term “ has been restricted to the description of optic disc swelling secondary to increased ICP
◘ Papilledema is the hallmark sign of IIH with or without associated retinal hemorrhages, folds, cotton wool spots, and exudates
◘ Papilledema results in dysfunction of the swollen ON fibers followed by progressive loss of the retinal nerve fibers, and lastly optic atrophy
◘ The threat of vision loss is correlated with the severity of papilledema
White matter hyperintensities, the invisible invaderWafik Bahnasy
WMHs is the most frequent type of CSVDs and a common incidental finding in MRI films of up to 70% of MRI images in individuals > 60 years, and 90% in those > 70 years.
Meticulous assessment of asymptomatic WMHs subjects reveals the presence of subtler cognitive, gait, balance and psychiatric disturbances.
Controversies in Tremor disorder, Beyound the resting and kinetic oscillationsWafik Bahnasy
(1) Tremor type identification is not always an easy mission.
(2) Always revise your initial diagnosis.
(3) Be flexible and able to change your initial diagnosis on the basis of new findings, manner of disease progression and response to treatment
◘ Management of WWE is a dynamic process needs the consideration of multidirectional effects of sex hormones and seizure management.
◘ The epileptologist should have a holistic view and be aware of the challenges he is facing including the impacts of AEDs on fertility, teratogenic risk, libido and contraception as well as AEDs concentrations change during pregnancy, postpartum, and lactation.
Refractory Status epilepticus: A Time TravelWafik Bahnasy
Status Epilepticus is a condition resulting from failure of the mechanisms responsible for seizure termination or the initiation of mechanisms, which leads to abnormally prolonged seizures (time point, T1) that might have long-term consequences (time point T2), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures.
Neuromyelitis optica spectrum disorders (NMOSD) is an autoimmune disorder of young adults' results from astrocytic aquaporin–4 (AQP–4) channelopathy. The AQP–4 IgG antibodies may be present in the context of some paraneoplastic disorders which should be suspected when NMOSD occurs in elderly patients.
Hematoma expansion after spontaneous intracerebral hemorrhageWafik Bahnasy
The size of the hematoma grows due to rebleeding in the next few hours after the onset in up to 40% of cases which results in early neurological deterioration, poor functional outcome and increased mortality.
Sleep abnormalities in Gullian Barre Syndrome PatientsWafik Bahnasy
GBS had long been defined as a neurological disorder with various sensori-motor manifestations with little attention to its psychiatric and sleep manifestations.
Physiological reduction of the gonadal sex hormones in old ages results in declined neurogenesis especially in the hippocampus with the resultant age dependent memory and executive functions regressions.
Physiological reduction of the gonadal sex hormones in old ages results in declined neurogenesis especially in the hippocampus with the resultant age dependent cognitive impairment and risk of AD
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...
Tips, Pearls and Pitfalls of Spinal Cord MRI
1.
2.
3. ◘ Since the introduction of MRI, a breakthrough had
happened in neurological diagnosis.
◘ Many neurological disorders simultaneously or
consecutively affect the brain and spinal cord,
however most neurologist find their comfort zone in
attending the diagnosis via the brain access.
◘ This concept resulted in lagging of spinal cord imaging
researches compared to brain ones and consecutive
underestimation of the opportunity of an important
tool sometimes essential to reach a definite diagnosis.
4. To break the ice upon getting the diagnosis through the spinal axis and
increase the utilization of this important investigation
5. (1) In sagittal section:
- The region of the lesion (cervical, dorsal, conus)
- The extent of the lesion (SSTM, LETM).
- Cord swelling at the lesion.
(2) In axial sections:
- The location of the lesion (central, lateral, dorsal).
- The width of the lesion.
- Location of the spinal cord within the canal.
(3) Gadolinium enhancement:
- Pattern of enhancement (patchy, ring, flame).
- Persistent enhancement (> 3-months).
- Associated meningeal or vertebral enhancement.
(4) The vertebrae:
- Associated spondylitis.
- Spinal cord compression (disc bulge, spondylosis).
8. ◘ MS spinal cord MRI criteria:
(1) Short segment (≤ 2 vertebral bodies).
(2) Eccentric (predominantly dorso-lateral).
(3) < 50% of the cross spinal cord section.
(4) Ring enhancement (32% of cases).
◘ Value of MRI in MS:
(1) Support the diagnosis (DIT, DIS).
(2) Detects subclinical activities.
(3) Predicts treatment response as well as
functional outcome.
9. ◘ LETM ≥ 3 contiguous vertebral bodies.
◘ In axial sections:
(1) > 50% of the spinal cord cross section.
(2) Central cord predominance with > 70% of the
lesion resides around the central canal in the
central grey matter.
◘ Gadolinium enhancement may be patchy or the
more characteristic elliptical lens shaped ring-
enhancement which distinguishes NMOSD
from other causes of LETM but not MS.
◘ Enhancement disappears in < 3-months or
shortly after steroid therapy.
10. ◘ Usually affects the conus and thoracolumbar
spinal segment.
◘ T2 hyperintense lesion in axial sections, highly
restricted to the grey matter (H sign).
◘ Bilateral anterior ON involvement.
◘ Younger age of onset and a more favorable
outcome than AQP–4 positive cases.
◘ Characterized by simultaneous or rapid
sequential ONs and TM.
11. ◘ TM Consortium Working Group diagnostic criteria:
- Acute bilateral symptoms and signs with a clear sensory level.
- Progression from onset to nadir in 4 h to 21 days.
- Evidence of inflammation demonstrated by CSF pleocytosis,
elevated IgG index or MRI gadolinium enhancing lesion(s).
- Exclusion of other intra- or extra-axial pathologies (diagnosis of
exclusion).
- T2 / FLAIR hyperintense edematous spinal cord lesion (1–2
vertebral bodies length, but rarely LETM).
- Typically involving > 50% of the cord in cross-section.
- Variable enhancement in 38% of cases (not ring enhancement)
which rapidly disappear after steroid therapy.
(a, b) LETM.
(c, d) short segment
myelitis.
12. ֎ Spinal cord involvement is reported in up to 83% of
cases of ADEM.
◘ MRI is important to confirm the diagnosis of ADEM
despite the picture is not totally specific.
֎ Spinal cord MRI may show confluent, intramedullary
lesion(s), swollen cord in acute phase and variable
contrast enhancement.
◘ Brain T2 / FLAIR MRI reveals multifocal, hyperintense
poorly margined, white matter lesions (> 1 – 2 cm),
with/without grey matter involvement (especially
putamen and thalamus) and no evidence of DIT.
13. - Preceding infection or vaccination (> 70% of cases).
- Typically monophasic (> 90% of cases), but in few cases
may be multiphasic or recurrent.
- Multifocal, polyfocal initial presentation.
- More common in pediatric population (< 10 years).
- Encephalopathy with either altered consciousness or
behavioral change.
- Bilateral simultaneous optic neuritis (in NMOSD always
sequential).
- CSF pleocytosis without oligoclonal bands.
14. ◘ Causes LETM with possible associated vertebral pathological collapse.
◘ Contrasted films show linear dorsal subpial and central canal enhancements (Trident Sign).
◘ Enhancement > 3 months is in favor of sarcoidosis rather than NMOSD.
15. ◘ Myelitis is a rare neuropsychiatric manifestations of
SLE.
◘ SLE results in acute short segment TM (LETM is
exceptional).
◘ In axial sections, SLE myelitis causes hyperintense
lesion involving both the grey and white matter to
a variable degree and the cord is swollen over it.
SLE myelitis; LETM (left) and
short segment (right)
16.
17. ◘ VDDSC is an increasingly used term in past decade,
due to better diagnosis in MRI films and as it
constitutes a potentially treatable disease.
◘ The thoracic spine cord has normal anterior position
owing to the normal dorsal kyphosis.
◘ Spinal cord attachments are predominantly lateral,
when laxed, the cord get stretched against the
dome of the mid-dorsal spine with consecutive
anterior displacement.
18. Notice the eccentric cord and the dilated heterogenous retro-spinal subarachnoid
space
19. ◘ The paired denticulate ligaments are lateral
extensions of the pia between the nerve roots
which anchor the spinal cord to the dura mater
and provide stability during flexion/extension
of the vertebral column.
◘ The subarachnoid space has fibrous trabeculae
attaching the pia matter to the arachnoid
membranes.
◘ The pia also extend as the filum terminal to fix
the lower spinal cord border with the coccyx.
20. ◘ A midline bi-layered arachnoid membrane
dissecting the retro-spinal subarachnoid space.
◘ In the cervical region, the septum is interrupted
and is formed of irregular bands.
◘ In the dorsal region, it is well developed and forms
a true membrane till the conus which could be
identified as a retro-spinal filling defect in CT
myelogram.
◘ The septum may have irregular developmental or
post-traumatic perforations.
Perforations in the septum
posticum
21. ◘ Consists of fibrous connective tissue bands of variable size that anchor the ventral aspect
of the dural sac with the anterior longitudinal ligament of the spinal canal.
Septum Posticum
Hofmann’s ligaments
22. (1) Lax denticulate ligament.
(2) Septum posticum fenestration followed by
focal arachnoiditis and thickening.
(3) Congenital dural defects.
(4) Tear and/or anterior traction of the Hoffman
ligament due to trauma or inflammation.
(5) Turbulent CSF flow and shearing stress result
in dural inflammation and tear.
23. ◘ It is a mild form of VDDSC with preserved rim of subarachnoid space between the ventral
aspect of the cord and the dura.
Septum Posticum PouchArachnoid septation (web)
24. ◘ CT myelogram and MRI show VDDSC, flattening of the posterior margin in axial sections
and focal indentation of the cord in sagittal sections “scalpel sign”.
25. ◘ Presented by progressive myelopathy with MRI reveals no intervening CSF space between the
cord and the dura.
◘ Herniation is a severe form of VDDSC where the spinal cord bulges through a dural defect.
26. ◘ The spinal cord projects across a dural defect.
◘ An anterior C-shaped kink of the cord with an
irregular posterior margin on sagittal sections.
◘ On axial section, the herniated cord is visible as a
protrusion through the dural defect.
◘ The herniated cord may be thinned out and may
show signal changes due to cord atrophy.
◘ The presence of normal CSF pulsation artifacts and
free CSF flow in phase contrast pulse in MRI
differentiates it from an arachnoid cyst.
27. The spinal cord is wrapped by a sheet of Duragen at the site of dural defect
28. ◘ Spinal arachnoid cysts (SAC) result from CSF inflow
into a small diverticulum in-between the 2 layers
of the septum posticum (intradural SAS) or
through a small dural defect (extradural SAS).
◘ The most common location of SAS is the dorsal
retro-spinal subarachnoid space where the septum
posticum is well developed.
◘ The arachnoid diverticulum may be congenital or
may develop secondary to trauma, infection or
iatrogenic (lumbar puncture or postsurgical).
29. (1) Type I SAC which describes extradural
arachnoid cysts without nerve root
involvement (including sacral meningocele).
(2) Type II SAC which include extradural
arachnoid cysts with nerve root
involvement.
(3) Type III SAC incorporate intradural
arachnid cysts.
31. ◘ Uniform fluid intense lesion in all MRI sequences, loss of normal CSF pulsation artifacts
during phase contrast imaging (spinal block) and smooth symmetric anterior spinal cord
displacements.
32.
33.
34. ◘ Before the era of MRI, SCI was a diagnosis of doubt with a common misdiagnosis inside the
trap of ATM while definitive diagnosis was kept only postmortem.
Aortic Atheroma Causing Cord
Ischemia
35. ◘ SCI comprises < 1% of all strokes and 5–8% of acute myelopathies.
◘ The onset is often dramatic (< 1-hour) and spinal cord MRI (DWI/ADC) show restricted
diffusion.
36. 1. Acute non-traumatic myelopathy.
2. MRI hyperintense lesion in a defined vascular
territory or watershed area on T2-WI.
3. No alternative diagnoses or cord compression.
A. Definite SCI:
- Vascular abnormality demonstrated on spinal angiogram
explanatory of the clinical presentation.
B. Probable SCI:
- Spinal angiogram negative or not available.
- Positive DWI or known stroke risk factors or mechanism
explanatory of the clinical presentation (i.e., severe
hypotension, hypercoagulable state)
C. Possible SCI:
- Spinal angiogram negative or not available.
- No identifiable risk factor or mechanism.
37. (A) Dissection or atheroma of aortic, vertebral,
subclavian arteries are the commonest causes.
(B) Procedure Related; aortic surgery, vertebral
angiography, intra-aortic balloon counter-
pulsation or renal artery embolization.
(C) Embolic; cardioembolic or decompression
sickness (diving).
(D) Vasculitis.
(E) Systemic hypotension and cardiac arrest.
(F) Hypercoagulable state and cocaine
abuse.
(G) Spinal-dural AVF. Vertebral artery dissection
38. (1) Typical ASA syndrome is bilateral loss of motor
function and pain/temperature sensation, with relative
sparing of deep sensation below the level of the lesion.
(2) Man in Barrel Syndrome due to central cervical
cord hypoperfusion (WSI between the branches of the
ASA and PSA) with consecutive painful bilateral
brachial diplegia and relative sparing of lower limbs.
(3) Progressive distal amyotrophy with wasting and
fasciculation due to chronic AHCs ischemia. May be
misdiagnosed as ALS but usually asymmetrical.
39. ◘ MRI shows bilateral T2 ventral and paracentral spinal cord pencil like linear hyperintensities in
sagittal sections, owl or snake eyes appearance in axial ones, cord swelling, ill-defined patchy
enhancement and associated vertebral body infarction.
Owl or snake eyes
Contrast
enhancement
Diffusion restrictionVertebral infarction
40. (1) Posterior spinal artery occlusion
results in dorsal columns involvement.
(2) Segmental (radicular) arteries
infarctions cause complete cord syndrome
(simulating idiopathic transverse myelitis).
(3) Sulco-commissural arteries occlusion
result in hemi-cord syndrome.
41. ◘ Results in mid-thoracic spinal cord WSI due to hypo-perfusion at its anastomosis with the
ASA usually during repair of aortic aneurysm.
42. ◘ Venous infarction in a patient with epidural and paraspinal abscesses.
◘ Notice the leptomeningeal enhancement and the increased bone marrow intensities due to
associated vertebral bodies ischemia.
43. ◘ It is the most common spinal vascular malformation
with progressive or stepwise course.
◘ MRI shows serpentine dilated peri-medullary
venous plexus with puzzle shaped LETM due to
peri-AVF spinal cord ischemia.
◘ The spinal lesion is hyperintense in T2-WI with a
hypointense rim made of stagnant deoxygenated
hemoglobin in the dilated capillaries.
◘ Gadolinium enhancement persists > 3 months.
44. Dilated and tortuous
draining vein
Feeding artery from
right vertebral artery
T2-and contrasted T1 with spinal cord lesion and
serpentine, dilated peri-medullary venous plexus
45.
46. ◘ It is the most common cause of myelopathy
accounting for 23% of cases (usually cervical).
◘ MRI shows hyperintense heterogenous T2 lesions
with flat, transversely oriented pancakelike
enhancement (width>height) at the site of
maximal compression.
◘ Axial sections show circumferential sparing grey
matter
◘ Persistent lesional enhancement > 3-months and up
to 2-years after successful surgery.
50. The cross sectional distribution of lesion is of ultimate diagnostic importance
51. (1) NMOSD.
(2) Confluent ADEM lesion
(3) Anterior spinal artery occlusion.
(4) Spinal venous infarction
(5) Neuro-sarcoidosis.
(6) Paraneoplastic myelopathy.
(7) Primary CNS lymphoma.
(8) Exceptional causes of LETM:
- MS especially in pediatric
population.
- Idiopathic ATM.
- Vasulitic myelopathy.
Paraneoplastic LETM
Tract specific enhancement
52. (1) Spondylotic myelopathy.
(2) Spinal-dural AVF.
(3) Intramedullary metastasis
(4) Paraneoplastic myelopathy.
(5) Primary CNS lymphoma.
◘ Pattern and persistence of gadolinium
enhancement are important red flags to
revise your diagnosis.
53. ◘ Results from cervical spinal cord ventral
displacement during neck flexion with consecutive
chronic ASA ischemia.
◘ Characterized by progressive asymmetrical distal
amyotrophy of C7, C8 and T1 innervated muscles
with pyramidal tract and sensory sparing.
◘ T2 / MRI shows mid-cervical cord hyperintensities
with anterior displacement of the cord on flexion
and widening of the posterior epidural space.
54. ◘ The spinal cord remains one of the areas in
which ultra-high fields strength MRI have
great impacts:
(1) The small spinal cord diameter needs high spatial
resolution for lesion localization and grey/white
matter differentiation.
(2) Faster examination time.
(3) Better post-processing of structured films.
(4) Lower necessity for contrast enhancement.
55. [1] Salama et al. J Neuroimmunol. 2018; doi: 10.1016/j.jneuroim.2018.08.014
[2] Baghbanian et al. Journal of the Neurological Sciences. 2018; doi: 10.1016/j.jns.2018.02.028
[3] Bruscolini et al. Autoimmun Rev. 2018; doi: 10.1016/j.autrev.2018.01.001
[4] Xu et al. Mult Scler Relat Disord. 2019; doi: 10.1016/j.msard.2018.09.040
[5] Zalewski et al. JAMA Neurol. 2019; doi: 10.1001/jamaneurol.2018.2734
[6] Kramer. Continuum (MINNEAP MINN). 2018; doi: 10.1212/CON.0000000000000595
[7] Flanagan et al. ANN NEUROL 2014; doi: 10.1002/ana.24184
[8] Conway et al. Mult Scler. 2017; doi: 10.1177/1352458516650512
[9] Eroglu et al. World Neurosurgery. 2019; doi: 10.1016/j.wneu.2018.11.005
[10] Sadek and Sepahia. Clinical Neurology and Neurosurgery. 2019; doi: 10.1016/j.clineuro.2019.03.014
[11] Chellathurai et al. Asian Spine J. 2018; doi: 10.4184/asj.2018.12.2.224
[12] Bhattacharyya. The American Journal of Medicine. 2018; doi: 10.1016/j.amjmed.2018.03.009
[13] Cohen-Adad. NeuroImage. 2017; doi: 10.1016/j.neuroimage.2018.04.009
[14] Barry et al. Neuroimage. 2018; doi:10.1016/j.neuroimage.2017.07.003
[15] Prados et al. Scientific Reports. 2016; doi: 10.1038/srep36151
[16] Jeng et al. Korean J Radiol 2015; doi: 10.3348/kjr.2015.16.5.1119
[17] Barreras, et al. Neurology. 2018; doi: 10.1212/WNL.0000000000004765
[18] Zalewski et al. Neurology. 2018; doi: 10.1212/WNL.0000000000004796
[19] Koelman and Mateen. J Neurol. 2015; doi: 10.1007/s00415-015-7694-7
[20] Zalewski et al. J Neurol Neurosurg Psychiatry. 2017; doi:10.1136/jnnp-2016-314738
[21] Soni et al. Neuroradiol J. 2019; doi: 10.1177/1971400918806634
[22] Flanagan. World Congress of Neurology, 2017.
[23] French et al. Journal of Clinical Neuroscience. 2017; doi: 10.1016/j.jocn.2017.02.051
[24] Ghali et al. Journal of Clinical Neuroscience. 2018; doi: 10.1016/j.jocn.2017.10.090
[25] Lee et al. World Neurosurgery. 2018; doi: 10.1016/j.wneu.2018.05.199