No high blood pressure, type 2 diabetes, hyperlipidemia... why repeat cerebral infarction?

*It is only for medical professionals to read and refer to.
Be sure to pay attention to the patient's main complaint
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Cerebral infarction is the most common cerebrovascular disease.
Most patients have risk factors such as hypertension, type 2 diabetes, hyperlipidemia, smoking, alcoholism, obesity, etc.
However, if the patient does not have the above common risk factors and recurrent cerebral infarction, How should we think about it? Without further ado, let’s take a look at the case patient.
A 61-year-old female was admitted to the hospital on July 11, 2017 due to “slurred speech and skewed speech for 8 hours”
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Previous cerebral infarction for 1 month, left limb weakness, now oral aspirin enteric-coated tablets (100mg qd), clopidogrel bisulfate tablets (75mg qd), atorvastatin calcium tablets (20mg qn) treatment; deny hypertension , Diabetes, hyperlipidemia and other medical history
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Denies the history of smoking and alcoholism
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Physical examination: T 36.
7℃, P 82 times/min, R 20 times/min, BP 135/70mmHg
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Clear mind, slurred articulation, equilateral pupils on both sides, sensitive to light reflection, shallow left nasolabial fold, left tongue extension, soft neck, normal muscle tension of limbs, muscle strength of left upper limb 3, left lower limb Muscle strength level 4, right limb muscle strength level 5, bilateral somatic sensation is normal, bilateral tendon reflexes are normal, bilateral Pap sign is negative, bilateral K-sign is negative
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The heart rhythm is uniform, no murmurs are heard in each valve area; breath sounds in both lungs are clear, no dry and wet rales are heard; the abdomen is flat and soft, with no tenderness or rebound pain
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Auxiliary examination (2017.
6.
8): Brain MRI+MRA showed: the right frontal parietal occipital lobe and basal ganglia mostly diverged in subacute infarction, leukoaraiosis, and brain atrophy; brain MRA: cerebral arteriosclerosis, left brain The arteries were not clearly shown, and the right middle cerebral artery scoliosis segment and bilateral anterior cerebral arteries were severely stented (see the figure below)
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 Complete related examinations after admission: urine, stool routine, fasting blood glucose, renal function, electrolytes, myocardial enzymes, blood lipids, glycosylated hemoglobin, coagulation function, and thyroid function are normal
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Blood routine: the number of red blood cells is 3.
4 × 1012/L, and hemoglobin is 104 g/L
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Liver function: total protein 61.
30 g/L, albumin 32.
50 g/L
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Ferritin 426.
30 ng/ml
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Heart color Doppler ultrasound showed: mild tricuspid regurgitation
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Carotid artery color Doppler ultrasound showed multiple plaque formation in bilateral carotid arteries, and plaque formation in the initial segment of the right subclavian artery
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Brain MRI+MRA (see figure below): Scattered multiple subacute infarctions in the head of the caudate nucleus of the right frontal, parietal, and temporal lobes; old luminal infarcts in the right basal ganglia; leukoaraiosis; cranial MRA: cerebral artery Sclerosis, the left middle cerebral artery is not obvious, and the bilateral anterior and right middle cerebral artery scoliosis segments are severely stenosis
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Preliminary diagnosis of TOAST classification of cerebral infarction: large atherosclerosis
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The problem caused by the case.
The patient has been given secondary antibody and statin for secondary prevention.
Why did the patient relapse with cerebral infarction after only one month? The patient has no risk factors such as hypertension, type 2 diabetes, hyperlipidemia, smoking, alcoholism, obesity, etc.
Why is the intracranial vascular disease so severe? Solving the problem In an occasional round of the ward, the patient complained of dry mouth, which could not be significantly relieved even if he drank more water.
Asking the medical history, the patient had dry mouth and dry eyes symptoms for 2 years, and the symptoms gradually worsened
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Because the patient has symptoms of dry mouth and eyes, it is necessary to determine whether there is Sjogren’s syndrome.
We have improved the relevant examinations: three items of rheumatism: C-reactive protein 97.
50 mg/L; erythrocyte sedimentation rate 82mm/h; ENA polypeptide: strong anti-SSA antibody positive (+++), strong anti-Ro-52 antibody positive (+++); anti-nuclear antibody screening: anti-nuclear antibody (nuclear granule type) positive (+) 1:100, anti-double-stranded DNA negative (-); Labial gland biopsy: (lower lip) meets Sjogren’s syndrome (see picture below)
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Replace the TOAST classification for diagnosis of cerebral infarction: other types with clear causes; primary Sjogren's syndrome (pSS)
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 The treated patients were treated with aspirin enteric-coated tablets, atorvastatin calcium tablets, methylprednisolone tablets, and cyclophosphamide.
They were followed up for 2 years without recurring cerebral infarction
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 pSS is a chronic inflammatory autoimmune disease that mainly involves the exocrine glands.
It has many insidious symptoms.
The typical symptoms are dry mouth and dry eyes.
Symptoms outside the glands are related to the involved organs and can involve the skin, skeletal muscle, and kidneys.
, Lungs, digestive system, blood system and nervous system
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The incidence of central nervous system involvement in pSS is 0%-68%, which requires the attention of neurologists
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Its pathogenesis is mainly vasculitis, which mostly involves small blood vessels.
The most common are the subcortical white matter and blood vessels around the ventricles, and it can also involve large and medium blood vessels in the skull
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The clinical manifestations of central nervous system involvement in pSS are diverse, and the lesions can involve the brain and spinal cord
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Brain lesions can be divided into diffuse and focal lesions.
Diffuse lesions are mainly manifested as subacute or acute encephalopathy, aseptic meningoencephalitis, psychological and cognitive disorders, etc.
; focal lesions are common in cerebral infarction type , Mainly in the subcortical and periventricular white matter, manifested as local sensory and motor abnormalities, seizures and vision loss
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pSS with central nervous system damage common cranial MRI manifestations are multiple small lesions (<1cm) in subcortical and periventricular white matter, cerebellum, corpus callosum, and basal ganglia may also be involved, T1 low signal, T2 high signal, FLAIR high signal, enhanced Scanning is generally not significantly enhanced
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Need to pay attention to the identification of multiple sclerosis
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The current treatment of pSS is mainly to relieve symptoms, prevent the development of the disease and prolong survival.
There is no cure.
Those with systemic damage should be treated according to the damaged organ and its severity
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For patients with important organ involvement, glucocorticoid therapy should be used; for those with rapid disease progression, immunosuppressive agents such as cyclophosphamide and azathioprine can be used in combination
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If there is a central nervous system disease caused by pSS, high-dose glucocorticoid intravenous pulse therapy should be used together with cyclophosphamide
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As for cerebral infarction caused by pSS, there are case reports of combined use of antiplatelet aggregation and statins, but there are also cases of not combined use
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 References: 1.
Song Pu, Zhang Qingshan, Sun Huiqin.
Two cases of Sjogren’s syndrome with acute cerebral infarction[J].
Chinese Journal of Neurology, 2016, 49(10):796-797.
2.
Yang Dan, Qiao Lin, Zhao Lidan .
Primary Sjogren’s Syndrome with Cerebral Infarction A Case Report with Literature Review[J].
Journal of Peking University (Medicine Edition), 2016(6).
3.
Ma Jing, Tang Ling, Wang Xiufeng, et al.
Primary Dryness Syndrome complicated by cerebral infarction 1 case report and related literature review[J].
Stroke and Neurological Diseases, 2015(2).
4.
Chinese Medical Association Rheumatology Branch.
Guidelines for the diagnosis and treatment of Sjogren’s syndrome[J].
Chinese Rheumatism Academic Journal, 2010, 14(11):766-768.