Neurology eConsult Request (Page 1 of 2) Current Status: Submitted

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Diagnosis:

74 yo man with history of left sided CVA in 1990, unclear distribution; recently with episodic headache intermittently located in bilateral occiput, bilateral temples; MRI 6/2017 shows no acute abnormalities; mildly elevated ESR, otherwise labs WNL.

Please recommend further evaluation steps of headache if necessary, would you consider temporal artery biopsy in this case? Thanks.

Clinical Question per Referring Provider: Please evaluate patient’s complaint of recent onset, intermittent episodes of brief duration cephalgia—bilateral occiput/crown/bi-temporal distribution—with associated mildly elevated ESR/normal CRP—and discuss the whether to proceed with temporal artery biopsy.

Relevant Co-morbid Concurrent Concerns: Prior Stroke 1990 with residual R lower facial droop; Chronic Kidney Disease III, RLS, Gout Arthritis

Diagnostic Work-Up to Date: MRI Brain (7/10/2017); ESR, CRP (6/14/2017)

Therapeutic Interventions to Date for Chief Complaint: N/A

Medications/Allergies: Acetaminophen, Allopurinol, Losartan, Metoprolol, Tamsulosin

Pertinent ROS Findings: No relevant contributory symptoms noted, such as: malaise/fatigue, jaw claudication, limb weakness in a proximal distribution, limb claudication, peripheral neuropathy, fever, amaurosis fugax, scintillating scotoma, vertigo, unilateral hearing loss. Patient does have lower extremity cramping—quadriceps and calves.

Pertinent Physical Exam Findings: BP 104/72, Temp 36.7; Normocephalic/atraumatic; no temporal artery tenderness to palpation, no trismus, no malocclusion; PERRL; no musculoskeletal abnormalities reported; CN II-XII grossly intact except for R CN VII lower branch to angle of mouth, full strength in limbs and sensation to light touch reported intact.

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DiagnosisCase Summary: 74 yo gentleman with recent onset of intermittent, brief episodes of cephalgia in a bilateral occipital, crown and bi-temporal distribution, recently mildly improved, but persistent. The patient has no other associated features consistent with a primary headache syndrome (e.g. photophobia, nausea/vomiting, vertigo; rhinorrhea, lacrimation); or features suggestive of Giant Cell Arteritis (e.g. jaw claudication, malaise/fatigue, proximal limb muscle weakness or pain, scintillating scotoma or amaurosis fugax). Recent laboratory studies reveal a mildly elevated ESR (25 mm/h; note that it was 43 mm/h 3 years ago), normal CRP. Recent MRI Brain was reported to show no acute abnormalities or contributory findings relative to the chief complaint— but shows atrophy with prominent ventricles, small vessel ischemic changes, and absent findings in the mastoid, calvarium, dura, and only mild sinus disease.

Giant Cell Arteritis is a vasculitis of medium and large vessels, seldom present before the age of 50, and headache is the most common symptom (experienced by 72% of patients at some time and the initial symptom 33% of the time—most often throbbing, with associated scalp tenderness and striking focal tenderness of the affected superficial temporal or less often occipital artery—note that 1/3 of patients with headache may have no objective signs of superficial temporal artery inflammation. Greater than half (58%) of patients experience Polymyalgia Rheumatica—with PMR as the presenting symptom in 25% of patients—with fatigue and malaise occurring in 56% of patients and jaw claudication in 40% of patients. Most ominous, amaurosis fugax with 10% of patients experiencing it, of these 35% bilaterally and 50% affected with subsequent partial or total blindness if untreated.

Physical signs associated with Giant Cell Arteritis relate to involvement of various arteries; superficial temporal artery inflammation reveals erythema, pain on palpation, arterial nodularity, reduced pulsations on the affected side—rarely ischemic necrosis of the scalp and tongue occur. Almost 1/3 of patients have large-artery bruits or diminished pulses— predominantly carotid, and upper limb arteries more affected than lower limb. Ocular findings are striking in amaurosis fugax, and restriction in eye movements and oculosympathetic paresis (Horner Syndrome) occasionally occurs with anterior ischemic optic neuropathy and optic nerve infarction.

ESR and CRP elevation are often associated with Giant Cell Arteritis, and CRP may be more sensitive in some patients.

The clinical onset of Giant Cell Arteritis may be acute, subacute or chronic, and the median duration of symptoms before diagnosis is 1 month; rare patients may have PMR for several years before diagnosis.

Skip lesions are common in the vessel, and as such, biopsy is rarely pursued at this time, and the diagnosis is clinical.

Based on the entirety of the patient’s presentation, it is unlikely that the cause of his symptoms is occult Giant Cell Arteritis; if his features evolve as described above, empirical treatment with corticosteroid and clinical/laboratory monitoring should be considered.

The most likely cause of the patient’s symptoms is cervicogenic neuralgia/occipital neuralgia—paroxysmal jabbing pain in the Greater (C2), Lesser (C2-3), and/or Third (C3) occipital nerve distribution. The origin of the injury is typically at either the C2-3 zygohypophysial joint or bilateral spasm/compression of the C2/C3 nerve roots by the trapezii and/or semispinalis capitii muscles. The pain has a sudden onset, can be severe and stabbing in quality, shock-like and brief—starting at the nuchal region and immediately spreading towards the vertex. Paroxysms can start spontaneously or be provoked by specific maneuvers; on examination, pressure/palpation/percussion over the occipital nerve trunks may reveal tenderness and/or elicit a painful paroxysm. Often cervical range of motion is limited and local posterior neck muscle spasm is found.

Although a local occipital nerve anesthetic block may transiently relieve the painful crises, it is non-specific and does not indicate a specific etiology.

For completeness’s sake, I recommend:

1. MRI C-spine imaging to fully define the anatomic structures involved and r/o a potential serious etiology.

2. If cleared by radiology, evaluation and treatment via Physical Therapy.

3. If necessary, consider local occipital anesthetic block as needed by an experienced provider.

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Neurology eConsult Request (Page 1 of 2) Current Status: Submitted

Patient Information

Name: Gender: Date of Birth: Address: Email: Phone: Mobile Phone: Insurance No: Language Account No. (MRN): Birthplace:

Referred From: Referred To:

Site: Provider: Address: Phone/Fax:

Referral Information

eConsult ID: Diagnosis: Status: Procedure(s): Auth Number: Additional Notes:

Decision Date:

Appointment:

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Please refer to progress note for details.

Elderly man of 83 with dementia who is taken care of by his two sons. I cannot rule out diversion. Reported hx of seizures for which he has been on clonazepam for a number of years. Had been on 1 mg BID. A UDS in the hospital in June was negative for drug. I inherited this patient and repeated a UDS in November which was negative for clonazepam but was + for 7-amino clonazepam >200 ng/ml. This was obtained about 10 am so I expect that he should have been positive for the drug itself. I have already started a wean due to the dementia and possible contribution to memory issues. I can not find any records that support the seizures. He is also on low dose gabapentin.

Is it reasonable to wean him off the clonazepam. Should I increase his gaba since he is already on this to cover any potential seizures? Should I start him on something else instead? Considered EKG but didn't know the quality of study since he would be on the clonazepam.

I have reviewed the attached clinical information for your patient. Please see below for my recommendations.

Diagnosis: Seizure Disorder

Further testing and evaluation: EEG

Treatment plan: OK to wean off Clonazepam. I do not like to increase Gabapentin dose due to following reason. Please also wean off Gabapentin over the period of one week and start Keppra.

“Gabapentin is associated with dizziness and somnolence the elderly are at increased risk of accidental injury (fall). The elderly have an increased risk of somnolence, peripheral edema, and asthenia”

Excerpt from: The Epilepsy Prescriber's Guide to Antiepileptic Drugs: Second Edition; Philip N Patsalos & Blaise F. D. Bourgeois

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DiagnosisPlease start Keppra for seizures:

Week 1: Keppra 125 mg BID

Week 2: Keppra 250 mg BID

Week 3: Keppra 375 mg BID and continue this dose.

Continue Keppra 375 mg BID but in future in the case of breakthrough seizure please increase dose to 500 mg BID.

Seizure precautions: No climbing higher than 4 feet off the ground. Adult supervision with all swimming. No unsupervised tub baths. No driving for 6 months after the last seizure or event in which there is a loss of consciousness. Smoking, drugs and alcohol use are discouraged. Females of childbearing age should be on a folic acid supplement—Folic acid 4mg once daily. All children and elderly patient on seizure medications should take a multivitamin with calcium and vitamin D. Use a curling iron with an automatic shut off to prevent burns. Close supervision while cooking. Use of a microwave is encouraged.

Seizure first aid:

1. Stay calm and keep patient in a safe place.

2. DO NOT restrain the patient.

3. DO NOT place anything in their mouth. A patient does not swallow their tongue during a seizure.

4. Turn the patient on his/her side to keep their airway open.

5. Place something soft, if possible, under the patient's head to protect their head

6. Loosen anything tight around their neck.

7. Time the seizure and let it run it's course.

8. Pay attention to what the seizure looks like to be able to tell healthcare providers.

9. If provider does not give you emergency medicine then call 911 at seizure onset.

10. After the seizure is over, allow the patient to rest. It is normal for them to be tired after a seizure. If patient received emergency medication they will also be tired from that too. If the patient is not back to normal after waking up or recovering from a seizure then please call 911.

11. Do not give the patient anything to eat or drink after a seizure until they are fully awake and able to swallow safely.

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Neurology eConsult Request (Page 1 of 2) Current Status: Submitted

Patient Information

Name: Gender: Date of Birth: Address: Email: Phone: Mobile Phone: Insurance No: Language Account No. (MRN): Birthplace:

Referred From: Referred To:

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eConsult ID: Diagnosis: Status: Procedure(s): Auth Number: Additional Notes:

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Appointment:

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Diagnosis:

eConsult for headaches (see HPI from office visit).

Reason for consultation: Recurrence of headache.

Clinical Summary:This is a 25-year-old woman who developed moderate to severe migraine headaches for 1 month complicated by nausea and vomiting. The frequency is 3-4 time per week. Duration 3-4 hours. She also reported daily headaches for which she was taking daily Excedrin. Her neurological examination demonstrated sensory deficit. The rest of her neurological examination was normal.

Diagnosis:Migraine headache.Medication overuse headache (MOH), also called analgesic rebound headache.

Recommendation: Stop using Excedrin.Use abortive medication for migraine such as sumatriptan (Imitrex): A single dose of 50 mg (taken with fluids). If a satisfactory response has not been obtained at 2 hours, a second dose may be administered. The medication should be taken at early onset of headache to guarantee maximum efficacy. If persistence of nausea and vomiting despite early use of Imitrex, oral or rectal anti-emetic drug could be used (Prochlorperazine). Imitrex intranasal or subcutaneous administration is another alternative.It seems from the note that the trend of the claimant headache changed in the last month. If this is the case, I strongly recommend head MRI with and without contrast to rule out brain organic lesion.

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DiagnosisReferences :

1. Buse DC, Serrano D, Reed ML, et al. Adding Additional Acute Medications to a Triptan Regimen for Migraine and Observed Changes in Headache-Related Disability: Results From the American Migraine Prevalence and Prevention (AMPP) Study. Headache 2015;55:825-839.

2. Chessman AW, Detar DT. Review: history and physical examination can accurately identify migraine and the need for neuroimaging in patients with headache. Evid Based Med 2007;12:25.

3. Chessman AW, Detar DT. Review: history and physical examination can accurately identify migraine and the need for neuroimaging in patients with headache. ACP J Club 2007;146:23.

4. D'Amico D. Antiepileptic drugs in the prophylaxis of migraine, chronic headache forms and cluster headache: a review of their efficacy and tolerability. Neurol Sci 2007;28 Suppl 2:S188-197.

5. Fischer M, Frank F, Wille G, Klien S, Lackner P, Broessner G. Triptans for Acute Migraine Headache: Current Experience With Triptan Use and Prescription Habits in a Tertiary Care Headache Outpatient Clinic: An Observational Study. Headache 2016;56:952-960.

6. Orr SL, Aube M, Becker WJ, et al. Canadian Headache Society systematic review and recommendations on the treatment of migraine pain in emergency settings. Cephalalgia 2015;35:271-284.

7. Pringsheim T, Davenport WJ, Dodick D. Acute treatment and prevention of menstrually related migraine headache: evidence-based review. Neurology 2008;70:1555-1563.

8. Schmidt P. (381) Evaluation of headache pain response and nausea relief relative to triptan use and placebo in migraine patients treated with diclofenac potassium for oral solution. J Pain 2016;17:S70.

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Neurology eConsult Request (Page 1 of 2) Current Status: Submitted

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Patient is requesting an MRI because she is concerned she has MS. The does report having seizures associated with her menstrual cycle. Records available for review are a normal EEG and CT. Patient reports migraine headaches, these also appear to be cyclical. Patient reports she has tried many medications for migraines and has taken antidepressants and hormonal birth control but she states she is "sensitive" and responds differently than others. I don't believe an MRI is warranted for this patient. I believe she has migraines but am unsure how to treat them if she is not willing to take medications. I have encouraged her to see a GYN to discuss non hormonal methods to reduce her menstrual cycles.

My question is: given patient's complaints, is an MRI reasonable to rule out MS, and are there any recommendations for control of migraines outside of the triptans and antihypertensives that may be effective? I recommended amitriptyline, patient did not want to start anything without knowing if she has MS.

Age: 41 years

Reason for Consultation: Uncontrolled migraine headache. Head MRI medical necessity.

Clinical Summary: 41-year-old woman who developed menstrual migraine and a report of seizure associated with her migraine. Normal EEG. She tried several medications including antidepressant without clear documentation of the effect of these medications.

Diagnosis: Menstrual Migraine headache.

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DiagnosisRecommendation:

Head MRI with and without contrast could be helpful to manage this patient. I agree with the provider that MRI is not indicated to rule out MS in this case. The patient has no neurological evidence suggestive for this diagnosis. However, she has intractable headache associated to possible seizure (Normal EEG cannot exclude seizure) not controlled by migraine/pain medication. An organic brain lesion should be excluded. In addition, performing MRI may increase the patient willingness to follow the provider recommendation and use headache medications.

Menstrual migraine. Initial treatment of menstrual migraine should be the same as for migraine occurring at other times: a rapid-onset triptan administered early in the mild pain. An alternative to triptans is NSAIDs. One randomized trial found that mefenamic acid (500 mg every eight hours as needed) was superior to placebo in treatment of acute menstrual migraine (.Al-Waili NS. Treatment of menstrual migraine with prostaglandin synthesis inhibitor mefenamic acid: double-blind study with placebo. Eur J Med Res 2000; 5:176) Initial: 500 mg beginning at the onset of bleeding and associated symptoms, followed by 500 mg every 8 hours; continue for 2 to 3 days.

Reference:

Al-Waili NS. Treatment of menstrual migraine with prostaglandin synthesis inhibitor mefenamic acid: double-blind study with placebo. Eur J Med Res 2000; 5:176

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52 yo male with dx of MS in 2015. Patient does not want to be sent to OHSU for further management although disease progressed. I have little experience in choosing therapies. I am unclear if this is RRMS or secondary.

How do I differentiate from RRMS and secondary? Does this patient look like someone who can be managed in primary care or should I encourage neurology referral?

As he did not tolerate Copaxone, what medication should be tried next? I believe he was covered under a different insurance at time of dx which may be why he did not qualify for teriflunomide; now on Medicare. Is Medicare likely to cover and I should reconsider this?

How often is an MRI needed? Any other testing needed at this time? Any other considerations?

52 yo gentleman with at least a 3 year history of neurological deficits/neural imaging correlates (both intracranial and cervical spine lesions noted on imaging report) consistent with demyelinating disease, diagnosed as Multiple Sclerosis; not currently on disease modifying treatment; has progressive clinical disease; not currently seeing a neurologist or MS specialist. Significant questions regarding the patient's state of disease and future management have been asked by his Primary Care provider.

Although general opinions regarding the role of neural imaging to track disease progression, the role of disease modifying therapies and the management of progressive neurological complications/disability can be offered relative to current guidelines, it is in the patient's best interests to be seen and managed face-to-face by an MS Specialist. The diagnostic/therapeutic care this patient requires cannot be adequately addressed via an eConsult, and the standard of care for a patient with MS is beyond the scope of Primary Care.

Fortunately, a number of providers who specialize in MS are available in the geographic region, including a leading academic center as well as highly regarded private practice neurologists, all of whom can coordinate follow-up care with the referring provider to lessen the frequent travel burden to the patient. That said, he needs to be scheduled as soon as possible to schedule neural imaging and begin a new immunologic therapeutic regimen monitored by an MS Specialist.

I appreciate that the patient may be resistant to such advice, is generally not addressing his significant health concerns (BP 190/90, has not picked-up prescription for anti-hypertensive), but I cannot offer the level of instruction or support to the patient or provider for a disorder this complicated and serious via eConsult.

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