I have done a lot of inspections, but the cause of the headache is still unknown. How can the experts find out?

*Read only for medical professionals Headaches, Headaches, Annoying Headaches.
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How to Peel the Mists and See the Truth! In the face of headache patients, it is often annoying that all examinations are perfect, but the cause cannot be found! At this time, if the conventional medication doesn't work anymore, it will be a feeling of "not being called every day, but not working".
The patient has a headache, and the doctor also has a headache
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This article will introduce how a master of the gods can solve the headache puzzle through 4 questions, please scroll down! The patient, male, 51 years old, was admitted to the hospital on June 10, 2021
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One week before admission, the patient had a headache, which was obvious on the top of the head, felt a tight hoop on the top of the head, obvious pain, occasional feeling of stuffiness in the left ear, nausea and vomiting in severe cases, and the vomit was stomach contents.
Head trauma, denied chills and fever, and denied chest tightness and shortness of breath
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Then he came to the outpatient clinic, and the head CT showed no abnormality.
The blood routine showed high-sensitivity C-reactive protein: 6.
6mg/L, white blood cell count: 15.
70*109/L, neutrophils 81.
2%, and headache after treatment with mannitol.
Slight relief, surgical consideration of urinary tract infection, anti-infection with Laoxan cephalosporin
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▌ Past history of type 2 diabetes mellitus, taking sitagliptin to control blood sugar
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Had fungal cystitis for 1 year, taking fluconazole capsules 0.
4qd + flucytosine 1g qid
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He has a history of lumbar spondylosis, lumbar spondylolisthesis, and sometimes numbness of the left lower extremity
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Syphilis history of more than 10 years, regular treatment
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▌ Laser intracavitary lithotripsy for bilateral ureteral calculi was performed multiple times in the surgical history
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In March 2021, ureteral anastomosis will be performed in another hospital
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▌ Personal history of smoking for 30 years, 6 cigarettes per day
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▌ Plain CT scan of head: Figure 1: No obvious abnormality was found on CT head CT: No obvious abnormality was found
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▌ Physical examination after admission: T: 36.
5℃, R: 18 times/min, BP: 130/80mmHg, P: 70 times/min
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Physical examination: clear mind, clear articulation, slightly strong neck, equal size and round pupils, normal movement of both eyes, symmetrical bilateral nasolabial folds, no skewed corners of the mouth, centrally protruding tongue, normal muscle tension in the limbs, bilateral acupuncture Symmetrical spines, symmetrical tendon reflexes, right Babinski (+)
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The nose is steady on both sides
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Q: Is this patient a primary headache? Secondary headaches? Secondary headaches may indicate a more serious disease behind them.
Therefore, we must first rule out the possibility of secondary headaches.
The following figure lists the common red warning situations of secondary headaches
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Figure 2: Common Red Alert Situations for Secondary Headaches In this patient, a 51-year-old with a sudden onset of new-onset headaches, was highly considered secondary
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QWhat are the secondary causes of acute headache? How is this patient considered? Intracranial hemorrhage (spider blood, parenchymal hemorrhage) Intracranial vein thrombosis Reversible cerebral vasoconstriction syndrome Carotid or vertebral artery dissection Acute post-traumatic headache Hydrocephalus meningitis Drug-induced headache Intracranial tumor or above is a common cause of secondary causes of acute headache.
According to the patient's medical history, physical signs, head CT, cerebral hemorrhage, post-traumatic headache, angle-closure glaucoma, hydrocephalus, intracranial tumor, drug-induced headache Headaches are not currently supported, and those marked in bold need to be considered
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Auxiliary examination after admission: slide up and down to view the full content Imaging examination: Figure 3: No obvious abnormality of carotid artery + vertebral artery CTA: no obvious abnormality of bilateral common carotid artery, internal carotid artery and vertebral artery CTA
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Cerebrovascular CTA: CTA of intracranial blood vessels showed no obvious abnormality
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Figure 4: Abnormal signal of left superior temporal gyrus head MRI scan: abnormal signal of left superior temporal gyrus, inflammation? Enhanced + spectral imaging is recommended
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Figure 5: Abnormal signal in the left temporal lobe, no obvious enhancement.
Brain MRI enhancement: Abnormal signal in the left temporal lobe, no obvious enhancement
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Q: Consider the positioning and qualitative diagnosis of the patient in this case? Positioning diagnosis Figure 6: Positioning diagnosis and qualitative diagnosis Figure 7: Qualitative diagnosis and disease evolution On the 6th day of admission, the patient had a sudden headache, slurred speech, drooling at the right corner of the mouth, and no physical activity
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The symptoms were relieved in about 10 minutes .

Physical examination at the time of seizure: clear consciousness, clear articulation, incomplete motor aphasia, bilateral nasolabial fold symmetry, middle tongue extension, V-grade muscle strength of both upper extremities, V-grade of bilateral lower extremity muscle strength, decreased acupuncture sensation in left lower extremity , normal muscle tone of the limbs, right Babinski (+)
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Review lumbar puncture: cerebrospinal fluid pressure: 310mmH2O↑
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Cerebrospinal fluid routine: white blood cells 2 × 106/L
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Cerebrospinal fluid biochemical indicators: protein 1008.
4mg/L↑, sugar 4.
0mmol/L (synchronized blood sugar 5.
82mmol/L), chloride 124.
6mg/DL
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Cerebrospinal fluid bacterial culture (-), fungal culture (-), Cryptococcus not found
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Autoimmune brain-associated antibody (-)
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Skull MRV: Figure 8: The venous plexus is disordered, and the venous sinus is unclear.
What is the final consideration for this patient? Figure 9: The final diagnosis was: Intracranial Venous Sinus Thrombosis (CVST)
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Let us systematically review CVST, this imitative liar▌ Definition CVST refers to a special type of cerebrovascular disease characterized by obstruction of cerebral venous return, often accompanied by impaired absorption of cerebrospinal fluid, resulting in intracranial hypertension caused by various etiologies, It accounts for about 0.
5%-1% of cerebrovascular disease
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Figure 10: Schematic diagram of intracranial venous sinus Notes: green: superior sagittal sinus; light blue: inferior sagittal sinus; dark purple: straight sinus; orange: sinus confluence; dark blue: transverse sinus; yellow: sigmoid sinus; lilac: Jugular vein and bulb ▌ 8 common etiologies and risk factors About 15% of CVST cases have no known etiology.
Common etiologies and risk factors are as follows: 1.
Congenital factors: including thrombin deficiency, protein S and protein C deficiency, Leiden factor V mutation, thromboxane gene mutations
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2.
Infectious factors: otitis media, mastoiditis, sinusitis, meningitis, brain abscess and systemic infection
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3.
autoimmune diseases: systemic lupus erythematosus, Wegener's granulomatosis, sarcoidosis and Behcet's disease, ulcerative colitis and Crohn's disease and the like
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4.
Acquired thrombogenic state: including nephrotic syndrome, antiphospholipid antibody syndrome, hyperhomocysteinemia, pregnancy and puerperium
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5.
blood disorders: polycythemia, leukemia, anemia, paroxysmal nocturnal hemoglobinuria, and congenital or acquired coagulation disorders and the like
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6.
Drug: oral contraceptives, asparaginase, postmenopausal hormone replacement therapy, and steroid therapy
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7.
trauma and mechanical operations: head trauma, neck trauma involving the jugular vein, nerve surgery, lumbar puncture, jugular catheter operation or the like
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8.
Others: dural arteriovenous malformation, cerebral arteriovenous malformation, severe dehydration, wasting disease (cachexia, advanced cancer), heart failure, shock, ketoacidosis, high fever, intracranial tumor and other malignant tumors, etc.
Can cause or promote CVST
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▌ The clinical manifestations of the three common clinical manifestations of CVST are very different and have no specificity
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1.
Intracranial hypertension headache is the most common (90%) and the earliest manifestation is severe and diffuse, mostly progressive, bilateral, with vomiting
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There are also optic disc edema, progressive loss of vision and so on
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2.
Brain parenchymal damage manifests as epileptic seizures (40%), focal neurological deficits, and disturbance of consciousness
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3.
Venous obstruction manifestations Figure 11: Venous obstruction sites and corresponding manifestations ▌ Imaging manifestations Brain CT is the preferred method for neurological emergency
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Although about 25-30% of CVSTs have normal CT findings, they can be used to rule out other lesions
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Figure 12: Common imaging findings of CVST MRV is the most commonly used imaging method for diagnosing CVST
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Corresponding signs of venous sinus occlusion, poor venous imaging, dilated collateral veins, barrier veins, and scalp veins can be found
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However, the ability of MRV to display pure cortical veins is weak, and it cannot judge the direction of venous blood flow
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In the past, DSA was considered to be the main method for diagnosing CVST, but due to the continuous improvement and wide application of CT and MRI and its vascular imaging technology, invasive DSA is now less relied on to diagnose CVST.
This examination is possible when performing endovascular interventional therapy
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▌ 4 types of commonly used treatment methods 1.
Treatment of the cause of infection: control the infection, treat the primary tumor, and use sensitive antibiotics in a sufficient amount and course of treatment in a timely manner
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Non-infectious: treat primary disease, increase blood volume, reduce blood viscosity
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2.
Special treatment anticoagulation, thrombolysis, endovascular intervention
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3.
Symptomatic treatment of high intracranial pressure: dehydration to lower intracranial pressure
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Hyperthermia: Physical cooling
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Seizures: Antiepileptic
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4.
CVST patients without anticoagulation contraindications should receive anticoagulation therapy as soon as possible.
In the acute phase, low molecular weight heparin should be used at a dose of 90-100 IU/kg body weight, subcutaneously injected twice a day; or unfractionated heparin should be used.
The partial thromboplastin time was prolonged by 1.
5 to 2.
5 times
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The course of treatment lasts 1 to 4 weeks
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The safety and efficacy of low molecular weight heparin is slightly better than that of unfractionated heparin
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The small amount of intracranial hemorrhage and increased intracranial pressure associated with CVST are not absolute contraindications to anticoagulation
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After the acute phase, oral anticoagulants should be continued, warfarin is often used, and the target PT-INR value should be kept between 2 and 3
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For CVST with rapidly controllable risk factors, such as pregnancy, oral hormonal contraceptives, anticoagulation therapy can be given within 3 months; for CVST with unknown risk factors or mild hereditary thrombophilia, oral anticoagulation therapy should be continued 6 to 12 months; for CVST with more than 2 episodes or severe hereditary thrombophilia, long-term anticoagulation may be considered
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There is currently no evidence to support imaging-proven recanalization of occluded veins (sinus) as a basis for discontinuing oral anticoagulation
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The new oral anticoagulant dabigatran is similar in efficacy and safety to warfarin, but more convenient to use than warfarin
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Key points 1.
The identification of headaches is a headache, but there must be traces to follow
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2.
Patients with unexplained headache, papilledema, increased intracranial pressure, focal brain damage, epileptic seizures, varying degrees of disturbance of consciousness, cognitive or mental disorders, or patients with dural arteriovenous fistula, should be considered CVST possible, parallel correlation checks
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3.
For CVST, anticoagulation should usually be started as early as possible to improve prognosis
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