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*For medical professionals only
The neurological symptoms of rheumatism are also too mysterious!
Synopsis:
Elderly men whose main complaint is "numb limbs for more than half a year", go around in circles or because of rheumatism? Lu Zhemin (interpreting physician), a resident physician of Peking University Health Science Center, and Yang Yue, deputy chief physician (commenting physician) of Peking University People's Hospital, met such a patient with complex conditions
.
Follow in their footsteps and unravel the truth about numbness in your limbs!
Case introduction
.
Current medical history: The patient developed numbness in the limbs half a year ago, bilateral symmetry, and no obvious relationship with
body position and activity.
The numbness of the lower limbs gradually increased, spreading to about 10cm below the knees, and there was a feeling of stepping on cotton on the feet, accompanied by hyperalgesia
.
Before 1 month, he was diagnosed in the Department of Orthopedics, Peking University People's Hospital, and the MRI of the cervical spine showed cervical spondylosis, which was ineffective
after nutritional nerve therapy.
Presented in the hospital's neurology department, electromyography showed possible
damage to the biulnar nerve and the common left peroneal nerve.
Consider peripheral neuropathy
.
Continued nutritional neurotherapy is ineffective
.
He is now admitted to the rheumatology department
of the hospital for further treatment.
Anamnesis: gastroesophageal reflux for more than 20 years, hypertension for more than 10 years, blood pressure up to 145/90mmHg
.
The patient was diagnosed with cataracts in both eyes 1 year ago and underwent left eye surgery
in the ophthalmology department of the hospital.
Shingles
was diagnosed by 2 months.
History of
lumbar disc herniation.
Personal history: Nearly 40 years of tobacco and alcohol history, and has quit smoking and drinking for 6 years
.
Auxiliary examination:
the patient's blood, urine, stool routine, biochemistry, coagulation, tumor markers were not obvious abnormalities, erythrocyte sedimentation rate, C-reactive protein, tuberculosis, hepatitis B, hepatitis C, AIDS, syphilis and other related tests were negative;
Immunoglobulin: IgE 558 IU/ml;
Lymphocyte subsets: helper/induced T cells 51.
44%, CD4/CD8 2.
54, B# 22.
99%, NK#43/ul, NK% 3.
64%;
HLA-B27（+）；
Cytokines: IL-10 7.
6 pg/ml;
ECG illustration: sinus heart rate, limb leads, low voltage;
Bone density: severe osteoporosis;
Echocardiography: mild tricuspid regurgitation;
Sacroiliac joint CT: it indicates bilateral degenerative changes of the sacroiliac joint, MRI of the lumbar spine shows degenerative changes of the lumbar spine, and degeneration of the lumbar intervertebral disc is bulging;
MRI of the brain shows mild white matter degeneration
.
There are many doubts, and the cocoons are peeled back Complex medical history with many doubts
.
First of all, the diagnosis of cervical spondylosis and lumbar disc herniation can be confirmed, but is the numbness of the patient's limbs caused by problems with the lumbar and cervical spine?
In addition to numbness in the limbs, the patient has no obvious low back pain and shoulder and neck pain, and is not accompanied by limb weakness
.
In addition, there is no obvious correlation between the patient's symptoms and postural activities, and combined with the patient's diagnosis and treatment in the orthopedic department, numbness
of the limbs caused by the cervical or lumbar spine can basically be excluded.
So, for an elderly man with high blood pressure, could numbness in the limbs be caused by cerebrovascular lesions? However, apart from numbness in the limbs, the patient did not have significant limb weakness and mobility impairment, and brain MRI did not support this diagnosis
.
Upon further history, the physician learned that the patient's symptoms progressed gradually from distal to proximal and were bilaterally symmetrical
.
Does this seem a bit like the legendary Guillain-Barré syndrome? Yes, Dr.
Lu Zhemin also took this into account, but after repeated medical history, the patient did not have any prodrome symptoms before the onset of the disease, and the symptoms progressed very slowly, except for numbness in the limbs, there was no limb weakness and other manifestations, which did not meet the clinical manifestations
of Guillain-Barré syndrome.
It turned out to be you - Sjogren's syndrome seems to have only one possibility left - connective tissue disease
。
Finally, whether the patient will have connective tissue disease, Dr.
Lu Zhemin shared, "It is well known that connective tissue diseases such as systemic lupus erythematosus and Sjogren's syndrome can affect the nervous system, and some patients will have nervous system involvement as the first manifestation
.
"
Although this patient has neurological lesions, he does not have the common clinical manifestations of connective tissue disease (fever, joint swelling and pain, rash, ulcers), and all inflammatory indicators are also negative, so it is necessary to continue to improve autoantibodies and other related tests to further clarify
.
"
Sure enough, the patient's autoantibody results suggested that the patient's ANA anti-centromere 1:1000, histone antibody (+), anti-SSA antibody (++), anti-R0-52 antibody (++), anti-centromere antibody (+++).
Ophthalmologic consultation suggests dry eye.
In addition, the patient's bilateral salivary gland uptake and secretion of tracers showed serious impairment of salivary gland function, lip gland biopsy showed partial acinar atrophy with interstitial fibrosis, and a large number of lymphaplasmocytes infiltrated in the lobule, including 3-4 lymphocytes and >50 lymphocytes in the foci
.
At this point, the diagnosis of Sjogren's syndrome can be basically clear
.
So are the patient's neurological symptoms caused by Sjogren's syndrome? Immune-related tests of cerebrospinal fluid in patients showed ANA anti-centrocentrotype 1:1000, anti-SSA antibody (++), and neuroimmunologic tests also suggested this diagnosis
.
Finally, the doctor still considered the patient to be involved in the nervous system caused by primary Sjogren's syndrome (pSS), and gave the patient methylprednisolone 60mg*5d, and the c-egg 20g*5d; Cyclophosphamide 400 mg once every two weeks for 4 months
.
It was then extended to 1 time per month for 4 months
.
Then the hormone dose is regularly reduced, cyclophosphamide is changed to 2 tablets / day, orally
.
Finally, the patient's condition was stable and numbness was relieved
.
Neurological manifestations of pSS should be alerted to pSS as a chronic autoimmune disease.
Characterized by autoantibody secretion and exocrine monocyte infiltration, resulting in dryness of the mouth and eyes, and can also affect organs and nerve tissue
outside the gland.
It is reported that an average of 20% of patients with pSS can have neurological damage
.
pSS combined with neurological lesions can be anatomically classified into central nervous system (CNS) lesions, peripheral nervous system (PNS) lesions, and autonomic nervous system lesions
.
Compared with CNS, PNS is the most common site of involvement, particularly sensory polyneuropathy
.
Dr.
Lu Zhemin shared that at present, the pathogenesis of pSS mainly includes three aspects [1]:
1.
The mechanism of sensory neuron neuropathy and trigeminal neuropathy is T cellsInfiltrated dorsal root gangliitis
.
2.
The mechanism of multiple mononeuropathy is vasculitis of nerve-nourishing vessels and secondary changes
in neuroischemic infarction.
3.
CNS: Monocyte infiltration or anti-Ro/SSA antibodies induce CNS angiopathy is a possible mechanism
.
Summary:
1.
Neurological lesions caused by pSS are common and heterogeneous
.
2.
For neurological lesions that are difficult to explain with common causes, the possibility
of pSS should be considered.
3.
There may be poor treatment effect and poor prognosis, requiring multidisciplinary joint diagnosis and treatment
.
Deputy Chief Physician Yang Yue commented:
Although the clinical symptoms of patients are not typical, doctors still focus on the investigation of autoimmune diseases through this layer-by-layer, peeling and cocooning differential analysis, obtain certain clues through the positive of the patient's autoantibodies, further improve the ophthalmic salivary gland function and other examinations, get more evidence, and finally diagnose Sjogren's syndrome
through lip gland biopsy.
On the one hand, for patients with the involvement of the peripheral nervous system and the central nervous system, we should remember to distinguish
autoimmune diseases including Sjogren's syndrome, systemic lupus erythematosus, and systemic vasculitis.
On the other hand, for rheumatologists and immunologists, it is necessary to understand that Sjogren's syndrome, as a chronic autoimmune disease with weakened salivary and lacrimal glands, can have clinical manifestations of both exocrine gland involvement and the involvement
of many organs and systems outside the gland.
In clinical work, we should be particularly vigilant about the occurrence
of neuropathy.
Interpreting physicians
Dr.
Lu Zhemin (Interpreting Physician)
- Graduated from Peking University Health Science Center with a master's degree
Commenting physician
Yang Yue Deputy Chief Physician
- Deputy Chief Physician, Department of Rheumatology and Immunology, Peking University People's Hospital, Postdoctoral Fellow at Harvard Medical School and Massachusetts General Hospital
- International Research Fellow, American College of Rheumatology
- Participated in the drafting of the Asia Pacific Society of Rheumatology (APLAR) rheumatoid arthritis treatment guidelines, the compilation of "Kelly Rheumatology" and "Harrison Rheumatology", and the compilation of "Clinical Rheumatology Handbook" and other works
- He has served as the executive deputy editor of APLAR official newspaper, a contracted translation expert for the Chinese edition of Uptodate, published more than 30 academic papers in Chinese and English, and presided over the National Natural Science Foundation of China and the New Teacher Fund for Doctoral Programs of the Ministry of Education
Evaluation of the biostimulatory effects and the level of neocollagenesis of dermal fillers:a review[J].
Int J Dermatol,2022,61(10):1284-1288.
DOI:10.
1111/ijd.
16229.
This article is compiled from the "Medical Doctor Station" online video course, included in the "Rheumatology Clinical Classic Case Collection", for the full version of the course content, please log in to the Doctor Station APP to watch
.
Webusers who have downloaded the "Medical Doctor Station" can directly scan the QR code below to view the course
Source of this articleMedical Rheumatology and Immunology Channel Author Fan Zhihua Review of this articleChen Xinpeng Deputy Chief Physician Responsible EditorOrange
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