A 56-year-old female was referred by her primary care physician to a neurologist. The patient’s primary care physician noted neck pain and numbness of the upper extremities, left greater than right, present for 1 year. Her medications were lisinopril 5 mg daily, Lyrica 50 mg 3 times daily, Flexeril 10 mg 3 times daily, Mobic 15 mg daily, and Nexium 40 mg daily. Her primary care physician noted that she had lumbar laminectomy for disk herniation in the past for low back pain and tingling of the left leg. He also noted that the MRI of her cervical spine was abnormal and requested a neurological evaluation. It revealed an abnormal signal intensity C2-3 affecting posterior columns with the radiologist’s comment of “could account for arm numbness and tingling.” The x-ray of her cervical spine performed on 11/5/2012 ordered by her primary care physician showed moderate degenerative changes. The x-ray of her lumbar spine performed on 2/23/2012 showed similar findings.
The neurologist first saw the patient on 12/10/2012 for the abnormal cervical spine MRI. The patient’s complaints were “neck pain; left neck and arm numb; right arm and right knee; losing urine; and generalized weakness on the left.” The patient also complained that she “also feels ‘dead’ hips down, [d]izzy spells several times, no energy, difficult to concentrate.” The neurologist noted the “neuro exam essentially normal.” The neurologist’s diagnoses were demyelinating disease; paresthesias of face and her extremities, vertigo, and memory loss. The neurologist ordered the following tests: EMG/NCV lower extremities, though later she also did upper extremities; MRI of the brain; neuromuscular junction tests with EMG; BAER with vestibular testing; VEP; EEG, overnight; and EEG awake and sleep with digital analysis 95957.
The upper extremity EMG/NCV study was performed on 1/3/2013. She tested 4 motor nerves, 5 sensory nerves, and F waves. The neurologist tested every muscle, which was present in the upper extremities. The results of the study were normal.
The electrodiagnostic study of the lower extremities were performed on 1/10/2013. The neurologist tested 4 motor nerves, 6 sensory nerves, 2 H reflexes, bilateral F waves of the motor nerves. She did a needle EMG of all muscles in the lower extremities and paraspinal muscles. The results of the study were normal.
There was a report of a video-monitored EEG utilizing a 32-channel digital EEG system manufactured by Cadwell. This test was performed on 12/26/2012. The report stated that the technician performed hyperventilation, but the patient reported she did not, and that the patient was videotaped, though the patient reported she was not. It was read as normal.
The ambulatory EEG was performed on 2/5/2013 to 2/6/2013. In the report, it was termed a 2-day ambulatory EEG despite lasting only 1 day. The neurologist prepared the report. The report contained a printout of 1 page. It was timed 6:21 a.m., and it contained widespread artifacts lasting 10 seconds. This was the exact time that the patient reported she stood in front of her microwaves. The neurologist read this as “Isolated sharp waves were noted in the frontal left hemispheric area. The isolated sharp waves may be epileptogenic in nature.” The visual and brainstem auditory evoked potentials were normal.
On 2/26/2013, the neurologist saw the patient for a follow-up visit. The test results were available to the neurologist at the visit. The neurologist noted that the EEG for the patient was normal for both awake and drowsy. The neurologist also noted that the 2-day EEG, which lasted only 1 day and the MRI of the brain showed a corpus callosum lesion. Her assessment and plan contained the same diagnoses as the first visit of 12/10/2012, and she failed to consider new information that should have changed her initial diagnoses.
The neurologist did not diagnose seizures in the assessment and plan, but she prescribed Depakote. The neurologist discussed with the patient that she met criteria for relapsing and remitting Multiple Sclerosis with an acute exacerbation. The neurologist also noted that the patient had pain with neck movement, which was sharp and went to the toes. She believed that the symptom was consistent with the finding of the ambulatory EEG and thus started the patient on Depakote 500 mg b.i.d. The neurologist failed to recognize Lhermitte’s sign, consistent with the myelopathy. The neurologist ordered laboratory studies for Lyme disease, lupus, and lumbar puncture. She ordered monitoring labs for Depakote, CBC, and liver function tests to be done before the next visit.
The MRI of the brain the neurologist referred to in the 2/26/2013 follow-up visit was performed at the neurologist’s request on 12/28/2012. The report indicated 20 FLAIR hyperintensities and a possible tiny corpus callosum lesion. The neurologist concluded it was consistent with multiple sclerosis. The 12/28/2012 report contained a comparison to a previous MRI of the brain performed on 7/1/2007. The radiologist thought the new MRI showed abnormalities “probably very slightly more numerous” than the 2007 MRI. He further considered the appearance to be nonspecific, and the tiny lesion in the corpus callosum was considered possible.
The 2007 MRI was requested by another physician. It was read as showing “a few nonspecific scattered punctate of unlikely clinical significance.” Multiple sclerosis was not raised as a possible cause. Referring diagnosis was “recent vertigo and left-sided dizziness.” The neurologist failed to question the patient on symptoms that occurred in 2007.
On 3/12/2013, the patient was seen in the emergency room for nausea and vomiting. She was diagnosed with Depakote toxicity with a level of 108. She was told to stop the medication. She was scheduled for the lumbar puncture the following day and was told to keep that appointment. The day following the lumbar puncture, she developed symptoms consistent with a postspinal headache. She was seen by the neurologist in her office on the same day and diagnosed with Depakote toxicity. At this point, the neurologist erroneously believed that the patient had “definite” multiple sclerosis. She also erroneously believed that “the patient wrongfully assumed” Depakote caused her symptoms and believed that they were from the lumbar puncture.
The neurologist next saw the patient on 3/26/2013 for an office visit. The neurologist noted that the patient had a postspinal headache. She noted that the spinal fluid was negative for oligoclonal bands, but incorrectly thought the IgG synthesis was abnormal. She incorrectly diagnosed “primary stabbing headache” despite her earlier entry of postspinal headache.
In a subsequent interview with a Medical Board investigator, the neurologist was questioned as to why she did not take a history of previous symptoms, such as optic neuritis, that help to establish a diagnosis of multiple sclerosis. She was questioned if the examination was normal and why she did not check the “saddle” area for sensory loss, and she reported, “Why should I check the saddle area?” There were no “incontinence of stools.” When asked if she would have documented Lhermitte’s symptom or sign if present, she answered yes. She obtained a history of symptoms consistent with Lhermitte’s, but did not recognize it as such. Memory loss was given as a diagnosis, but when asked how it was based, she could not recall. When asked to explain the reasons that each test was ordered, she responded that the EMG was based on symptoms, the neuromuscular test was based on the possibility of myasthenia gravis causing general weakness, the BAER and VEP as part of the multiple sclerosis work-up, and the EEG to rule out seizures as the cause of numbness and weakness. She stated video monitoring on EEG was standard practice. Hearing loss was her reason for performing the BAER, but no hearing loss or visual disturbance was documented. She stated that the 2007 MRI showed infratentorial and supratentorial lesions whereas there was no mention of an infratentorial lesion in the radiology report. She ordered the EMG of the upper extremities to “rule out any other diseases” and stated “EMG is part of differential diagnosis,” and the indication she believed was numbness and tingling in the hands. When asked why she did 24 upper extremity and 6 cervical paraspinal muscles on EMG, she stated she wanted to make sure there was “no polyradiculopathy,” but she admitted there were no findings to suggest that diagnosis. Further, she believed that numbness and tingling and incontinence would indicate polyradiculopathy. When questioned regarding indications for EMG of the lower extremities, she stated back problems, numbness right arm and right knee, and feeling the hips on down were “dead.” In the lower extremities, she tested 12 different muscles and 6 paraspinal muscles. She was then questioned about what were the indications for the EEG, and she believed they were generalized weakness, dizzy spells, no energy to work, and difficulty focusing. She was questioned as to why the first EEG was not sufficient. She stated that on 2/26/2013 visit, she had findings of generalized seizure disorder, but this was not the wording in the EEG report nor was it in her letter to the Board. She was not aware that a microwave can cause artifacts. Regarding indication for Depakote, her answer was because of the EEG and numbness and tingling. She thought it would be trial and error to see if it would help. She thought that the patient’s symptom of “neck killing her” would be consistent with a multiple sclerosis plaque. When asked why she ordered Lyme disease and lupus blood tests, she stated that they were “on my mind.”
The Medical Board of California judged that the neurologist’s conduct departed from the standard of care because she failed to recognize symptoms and findings on the MRI of a partial transverse cervical myelopathy, ordered an EMG for the upper and lower extremities, video EEG, and ambulatory EEG without medical indication, conducted an excessive number of nerve tests for any diagnosis, misdiagnosed epilepsy, lacked knowledge in reading EEGs, and had no knowledge and/or did not consider the important interaction between Depakote and the patient’s other medications. The neurologist also lacked knowledge in several fundamental areas. She failed to recognize symptoms of a partial transverse cervical myelopathy and Lhermitte’s symptoms even though it was described to her by the patient. She did not recognize or, if she did, did not reflect in her records that almost all of the patient’s symptoms were caused by the cervical myelopathy. The neurologist erroneously believed that a multiple sclerosis plaque could cause severe neck pain and that IgG synthesis could indicate active or inactive multiple sclerosis. She diagnosed multiple sclerosis on the basis of the McDonald criteria, and she included the original report, but she gave no information in her records how those criteria fit the patient. She failed to question the patient for previous symptoms, which might establish an initial exacerbation of multiple sclerosis. The neurologist was aware that the patient had an MRI in 2007 and did not question the patient regarding her symptoms at that time. She ordered laboratory studies for possible Lyme disease or “lupus” and a monophasic cervical myelopathy despite the fact that it was exceedingly unlikely to be caused by any of those disorders. She failed to consider alternative causes for the patient’s presentation, specifically B12 deficiency or adrenomyeloneuropathy.
For this case and others, the Medical Board of California placed the neurologist on probation and ordered the neurologist to complete a medical record keeping course, a professionalism program (ethics course), an education course (at least 40 hours per year for each year of probation), and a clinical training program equivalent to the Physician Assessment and Clinical Education Program offered at the University of California San Diego School of Medicine. The neurologist was assigned a practice monitor and was prohibited from supervising physician assistants and advanced practice nurses.
Date: January 2018
Significant Outcome: N/A
Case Rating: 4
Link to Original Case File: Download PDF
← Back to the search results