Symptom: Lhermitte's Sign

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Symptom: Lhermitte's Sign

Postby jimmylegs » Mon Nov 20, 2017 2:49 pm

"A symptom is any subjective evidence of disease, while a sign is any objective evidence of disease. Therefore, a symptom is a phenomenon that is experienced by the individual affected by the disease, while a sign is a phenomenon that can be detected by someone other than the individual affected by the disease."

i don't know if lhermitte's can be detected by someone other than the affected patient. so for now at least, it's going into the symptom bucket.

Lhermitte's Sign: The Current Status (2015)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445188/
Lhermitte's sign was described by Marie and Chatelin and named after Jean Lhermitte. This sign is mostly described as an electric shock like condition by some patients of multiple sclerosis. This sensation occurs when the neck is moved in a wrong way or rather flexed. It can also travel down to the spine, arms, and legs, and sometimes the trunk. Demyelination and hyperexcitability are the main pathophysiological reasons depicted for the Lhermitte's sign. Other causes for Lhermitte's sign include transverse myelitis, behçet's disease, trauma, etc. This article reviews the Lhermitte's sign, its history, and its etiopathophysiology. Very few studies are available on Lermitte's sign and more research need to be done on the same to ensure its sensitivity and specificity.

Reassessment of Lhermitte’s sign in multiple sclerosis (2015)
https://link.springer.com/article/10.10 ... 015-0466-4

The reliability and diagnostic value of Lhermitte’s sign in multiple sclerosis (MS) has not been fully established. The purpose of this study was to determine the clinical, neurophysiological and neuroradiological correlations of Lhermitte’s sign in a cohort of MS patients and reassess the relevance of this phenomenon in the clinical history of the disease. A prospective study of 694 patients with MS and 110 age-matched healthy adults was evaluated by a structured questionnaire that included basic demographic data, age of onset, clinical characteristics of the disease, and the inquiry of Lhermitte’s sign. Cranial and spinal magnetic resonance imagings (MRI) and median and tibial somatosensory evoked potentials (SSEP) were performed at the same time. One hundred and twelve (16 %) patients were reported to have Lhermitte’s sign; 582 (84 %) patients did not experience Lhermitte’s sign during their disease duration (P < 0.026). No correlation was found between Lhermitte’s sign and age, gender, EDSS, and disease duration; 88 % of patients with Lhermitte’s sign had a demyelinating lesion on the cervical MRI. In negative Lhermitte’s sign group, 64 % patients had a positive MRI. SSEP conductions were delayed in 92 % of patients with positive Lhermitte’s sign and in 70 % of patients with negative Lhermitte’s sign. Regarding the data, a significant correlation was found between MRI lesion and Lhermitte’s sign (P < 0.001), and between SSEP abnormality and Lhermitte’s sign as well (P < 0.001). This study underlines the relevance of this phenomenon with neuroradiological and neurophysiological abnormalities.
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
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Re: symptom: lhermitte's sign

Postby jimmylegs » Mon Nov 20, 2017 3:12 pm

this guy's my kind of dumb@$$. i hadn't really considered how much worse it could have been. sounds like i was *lucky* to have that fall 2 yrs after symptom onset, which put the issue squarely on the front burner at last. and yeah the government and student health insurance plans came in pretty handy as well.

A B-wildering Case of Paraplegia: Cobalamin Deficiency (2013)
http://www.amjmed.com/article/S0002-934 ... 3/abstract

PRESENTATION
An uninsured patient delayed adequate medical evaluation until he suffered permanent damage from an easily-treated condition. The 36-year-old Caucasian man presented with spastic paraplegia, decreased lower-extremity sensation, and sphincter incontinence. He explained that his illness started about 4 years earlier with back pain and lower-extremity paresthesia. His primary care physician recommended spine imaging, which was never performed due to lack of health insurance. Records from this past visit were unavailable.
Over the ensuing years, the patient experienced slowly progressive lower-extremity weakness, eventually requiring the use of a cane. About 3 months prior to presentation, he fell and injured his left knee, which led to decreased ambulation and the need for a walker. He had not hurt his back. During this entire period, he never sought medical
attention, as he believed he would not be able to afford it. About 3 days prior to presentation, he developed urinary and fecal incontinence and was no longer able to move his legs. This prompted him to get medical care for the first time in 4 years.
...
Given the combination of neurologic and hematologic abnormalities, the patient’s serum B12 level was checked and found to be markedly low at 45 pg/mL. His serum folate
concentration was normal. Methylmalonic acid and homocysteine levels were both significantly increased at 40.46 mmol/L (reference, 0-0.4 mmol/L) and 141.6 mmol/L (reference, < 10 mmol/L), respectively; such paired elevations signal B12 deficiency.
...
Historically, B12 deficiency used to progress until it produced devastating neurologic disease, including myelopathy, neuropathy, neuropsychiatric abnormalities, and optic nerve atrophy. The myelopathy caused by B12 deficiency is called subacute combined degeneration of the spinal cord and manifests with symmetric dysesthesia, abnormal proprioception, and rarely, spastic para- or tetraparesis.1 In the era of fortified foods, prevalence of subacute combined degeneration of the spinal cord has likely decreased, with paresis being very uncommon today.2
Evolution to full-blown paraplegia is even more unusual, as patients are typically diagnosed and treated before the deficits progress to that degree. Most B12 deficiency cases seen by modern-day physicians are diagnosed during an evaluation for hematologic abnormalities. Neurologic symptoms, if present, tend to consist of mild sensory or balance defects.3,4
Because of this, B12 deficiency could be easily overlooked as a potentially reversible cause of severe neurologic dysfunction.
...
A review of 57 patients with subacute combined degeneration of the spinal cord confirmed by MRI suggests that factors associated with complete neurologic recovery include shorter duration of illness, male gender, age younger than 50 years, presence of Lhermitte’s sign (neck flexion elicits an electrical sensation down the back and into the limbs), and absence of sensory level, spinal cord atrophy, anemia, Romberg sign, and Babinski sign
...
At a 3-month follow-up visit, the patient’s blood counts and red blood cell indices had normalized. He was still wheelchair-bound but was able to move his toes. Although he had regained fecal continence, he continued to have urinary retention that required self-catheterization of the bladder. Members of the Departments of Gastroenterology and Endocrinology continue to monitor and manage his gastric carcinoid.
...
Our patient’s lack of financial resources and health insurance prevented him from pursuing spine imaging or further medical care after his initial presentation 4 years prior to diagnosis. It is unclear if a complete blood count was obtained on that initial visit. If it had been abnormal, an opportunity for a much earlier diagnosis and perhaps a much
better neurologic outcome may have been missed.
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
User avatar
jimmylegs
Volunteer Moderator
 
Posts: 10780
Joined: Sat Mar 11, 2006 3:00 pm


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