A 44-year-old male was transferred to our hospital for metastatic workup of multiple “ring enhancing lesions,” which were visualized on an outside-hospital MRI. He was scheduled for biopsy the next day, and a new set of pre-operative images were obtained and reviewed.
Question 1: Consider the images through the ring enhancing lesion in the left frontal lobe, which could have many etiologies. Which of the following possibilities are unlikely (can be more than one)?
A 56-year-old woman who started fingolimod 3 months ago for treatment of relapsing-remitting multiple sclerosis presented with abnormal vision in the right eye for 2 days. She denied any eye pain or headache, and describes the abnormality as blurred or distorted vision when she tries to read her computer screen. It improves if she closes her right eye. She thinks her peripheral vision is intact, but notes that shapes look distorted in her right eye when she looks directly at them. Her past medical history is significant for type II diabetes mellitus, poorly compliant with diet and oral hypoglycemics. Exam shows pupils to be equal and reactive without afferent pupillary defect. Acuities are 20/50 OD and 20/20 OS, with normal visual fields but abnormal Amsler grid with the right eye. Fundoscopic shows bitemporal disc pallor. MRI of the brain with and without contrast is acquired and shows stable burden of T2 lesions consistent with MS, without any abnormal gadolinium enhancement. Optical coherence tomography (OCT) shows central foveal thickness of 312uM OD and 268uM OS with a peri-foveal cystoid morphology.
A 37-year-old woman develops lower extremity numbness, weakness, and urinary retention that worsens rapidly over 4 days. Two years prior, she had a 2-week episode of intractable hiccups and nausea; gastroenterological evaluation was unrevealing and the symptoms resolved spontaneously. Current neurological examination shows severe paraparesis, loss of proprioception and vibration sense in the feet, and a spinal sensory level at T4. Emergent spinal cord MRI reveals an intramedullary lesion that extends contiguously from C6 to T5 vertebral levels and is associated with cord swelling and enhancement after gadolinium administration. Brain MRI shows scattered nonspecific subcortical white matter lesions. She is treated with IV methylprednisolone and achieves nearly complete resolution of her myelitis symptoms over the next 6 days.
— Dean M. Wingerchuk, MD, MSc, FRCP(C)
This question is related to the CME activity – Review of Neuromyelitis Optica. Participate in the webcast for more information on this topic.
I invite you to attend our seventh annual Mellen Update in Multiple Sclerosis, held at the InterContinental Hotel & Bank of America Conference Center on Friday, June 28, 2014. Our focus will be where we stand with treatment.
The past 5 years have yielded an explosion of new medications for MS. Deciding what medicines to begin and how to monitor and safeguard these medicines can be challenging for the busy clinician. Our keynote speaker this year, Dr. Jeff Dunn from Stanford Medical School, will discuss whether MS is truly one disease or perhaps several. Other speakers will review data on therapeutics and disease management.
We will have speakers on a diverse range of topics focused on what’s new and what’s important in the field: Vitamin D, MS pathology, treatment targets, MRI measures and symptoms management. This year we will address disability assessment and counseling as well as new technologies in MS and some exciting research work going on at the Mellen Center. We will focus on how treating MS patients affects the professional, reflecting a growing awareness of the importance of ‘mental health’ for clinicians to avoid burnout and job satisfaction issues. Building a better experience for our MS patients and initiating and monitoring the new MS medicines from an allied health professional point of view will be discussed.
A 33-year-old woman presented with blurred vision in her right eye, and retro-orbital pain when looking to the right. Exam showed a deafferented right pupil and diminished visual acuity to 20/80 OD. Brain MRI showed 3 periventricular T2 hyperintense lesions, none of which enhanced with gadolinium. She was treated with intravenous methylprednisolone and vision improved to baseline within 3 weeks. Six months later, follow-up brain MRI showed a new gadolinium enhancing lesion in the right frontal lobe. Although she had no symptoms, she was started on interferon beta injections. She did well on interferon beta with only mild post-injection flu-like symptoms. At follow-up 6 months later she was asymptomatic, but brain MRI scan showed 2 new gadolinium enhancing lesions in the left hemispheric white matter.
Based on information in the previous post, the correct answer is: Multiple Sclerosis.
The following progress was seen. The patient’s gait improved over 2-3 weeks but remained ataxic with inability to perform tandem gait. Partial left 6th nerve palsy with episodes of sudden onset hypersomnolence lasting 2-4 hours, occurring in the middle of eating lunch or dinner. Venous PCO2 up to 60mmHg during these episodes. The patient experienced periods of disinhibition and paranoia and concerns regarding cognitive function: slowed processing, word finding difficulties, and problems with working memory.
Patient history: A 16-year-old female, born at term with normal development. She is fully immunised, previously well and active, no previous neurologic symptoms, and no recent travel. She is one of 6 childen, her mother is Jamaican, father from Ghana and she has a 19-year-old sister with autism. No FHx MS, demyelination, or autoimmune conditions. Presenting problem: On November 2008 she had a headache – bifrontal, intermittent. She has no associated nausea, vomiting or visual symptoms; somnolence and fatigue. She is sleeping 18 hours per day and falling asleep in class; secondary amenorrhoea. In December 2008 she experienced emotional lability and irritability. In January 2009 she was unable to attend school due to somnolence, increasing headache severity, photophobia, and has blurred vision, dizziness and left facial pain.
In February 2009, she experienced ataxia. She fell once at bowling alley, has feeling of generalised weakness, is vomiting, and presented to hospital ER. She has no antecedent infections or vaccinations; no fever; no seizures, diplopia, bladder/bowel dysfunction, back pain; no cognitive decline; and no rashes or arthralgias. Examination findings: She is alert, GCS 15. MSE 29/30 (-1 recall). Cranial nerves are normal fundi, no RAPD, no ophthalmoplegia, normal facial sensation, and no facial weakness. Her limbs have normal tone and strength, normal sensation, reflexes increased on left compared to right, and dysmetria L upper and lower limb. She is unable to walk on admission due to ataxia.
Alexander D. Rae-Grant, MD
Clinical Associate Professor of Medicine
Cleveland Clinic Lerner College of Medicine
Director of Resident and Student Education
Mellen Center for Multiple Sclerosis Treatment and Research
Jennifer Hartman, PA-C
Claire Hara-Cleaver, CNP