Subarachnoid Hemorrhage: Causes, Symptoms, and Acupuncture Treatment

Subarachnoid hemorrhage (SAH) is a clinical syndrome resulting from the rupture of intracranial blood vessels, with blood entering the subarachnoid space. The etiologies of SAH are numerous, with common causes including: ① SAH due to an abnormal vascular network at the base of the brain (moyamoya disease); ② Rupture of congenital intracranial aneurysms or venous malformations; ③ Arterial rupture caused by hypertension or cerebral atherosclerosis; ④ Necrosis and rupture of arterial walls due to infectious emboli or cerebral arteritis from encephalitis or meningitis—including purulent, viral, tuberculous, syphilitic, fungal, leptospiral, and Brucella types; ⑤ Other less common causes, such as bleeding from brain tumors (including gliomas, hemangioblastomas, meningiomas, choriocarcinomas, and brain metastases), often referred to as tumor apoplexy; additionally, hematologic disorders and complications of anticoagulant therapy may also induce SAH. Blood entering the subarachnoid space can cause the entire brain or parts of its surface to appear purplish-red, with more pronounced staining at the base of the brain, cisterns, and sulci. When hemorrhage is massive, a thin layer of blood clots often covers the surface and base of the brain, and the cerebrospinal fluid (CSF) becomes bloody, with blood cells deposited in the sulci and cisterns. Over time, the red blood cells in the CSF lyse and release hemosiderin, turning the brain surface a dark brown color. In cases of heavy bleeding, blood clots may engulf the blood vessels and nerves at the base of the skull; when clots obstruct the CSF circulation pathways, they can lead to hydrocephalus and cerebral herniation. The pathological changes in the brain parenchyma mainly consist of patchy ischemic changes in the cortex and extensive white matter edema. Intracranial aneurysms are often saccular or fusiform, ranging in size from a sorghum grain to a soybean, and most frequently occur on the circle of Willis at the base of the skull.

1. Diagnostic Criteria

**Subarachnoid Hemorrhage** Subarachnoid hemorrhage (SAH) commonly occurs in patients aged 40–60 years. Onset is typically sudden, with some patients experiencing prodromal symptoms such as headache and cranial nerve palsy. Precipitating factors include sudden physical exertion or emotional stress. Early manifestations may include severe headache, nausea, vomiting, and transient loss of consciousness. Coma occurs in only about 20% of patients, and some may present with focal or generalized epileptic seizures. In elderly patients, the clinical presentation is often atypical: headache is less prominent, while psychiatric symptoms and consciousness disturbances are more common. Severe cases may rapidly progress to deep coma, accompanied by decerebrate rigidity and brain herniation, potentially leading to death in a short time. **Key Signs** 1. **Meningeal Irritation Signs**: Nuchal rigidity typically appears within 2–3 days. Caution is needed for potential tonsillar herniation through the foramen magnum, which may cause sudden respiratory distress. Lumbar puncture is contraindicated in such cases. 2. **Hemiparesis**: Rupture of a middle cerebral artery aneurysm, often located in the Sylvian fissure, may cause hemiparesis, aphasia, hemisensory loss, or focal seizures. Hemiparesis is usually mild. Early (within 1 week) hemiparesis or hemisensory deficits may result from cerebral edema or intraparenchymal hemorrhage; later-onset deficits are often due to cerebral vasospasm. 3. **Cranial Nerve Deficits**: Oculomotor nerve palsy, abducens nerve palsy, optic atrophy, hemianopia, facial palsy, hearing impairment, and vertigo may occur. 4. **Ocular Findings**: Unilateral or bilateral papilledema, venous congestion, intraocular hemorrhage (retinal hemorrhage, sometimes subhyaloid hemorrhage), and occasionally hemorrhage into the anterior chamber causing severe or permanent vision loss. 5. **Hypertension**: A minority of patients develop transient hypertension post-hemorrhage, typically resolving within days to 3 weeks. 6. **Respiratory Patterns**: Initial rapid, deep, irregular respirations may become slow and irregular as intracranial pressure rises. Acute pulmonary edema may occur if the anterior hypothalamic nucleus is damaged. 7. **Fever**: Body temperature may rise post-hemorrhage, usually not exceeding 39°C. 8. **ECG Changes**: Approximately 50% of patients show ECG abnormalities, including prolonged QT interval, increased P-wave and U-wave amplitude, ST-segment elevation (or depression in some), and T-wave inversion. 9. **Gastrointestinal Manifestations**: Some patients vomit coffee-ground-like material or have melena. **Laboratory and Imaging Findings** 1. **Peripheral Blood**: About 1/3 to 1/2 of patients have leukocytosis (typically 10.0–20.0 × 10⁹/L). Erythrocyte sedimentation rate (ESR) may be elevated; blood glucose may be increased in a minority. 2. **Urinalysis**: Some patients have transient glycosuria and proteinuria, which usually resolves within a few days. 3. **Cerebrospinal Fluid (CSF)**: The hallmark of SAH is blood in the CSF. With small amounts of blood, CSF appears turbid; with larger amounts, it appears pink or bright red. Fresh hemorrhage yields red CSF; old hemorrhage yields yellow (xanthochromic) CSF due to erythrocyte lysis, peaking after a few days and persisting for about 3 weeks before clearing. Microscopy reveals numerous erythrocytes, some crenated. Protein content is elevated; glucose may also be increased. After centrifugation, the supernatant is yellow. CSF pressure (normal ≤200 mmH₂O) is often elevated (200–300 mmH₂O); a small proportion have normal pressure, and low pressure should raise suspicion of a blood clot obstructing CSF circulation. 4. **Cerebral Angiography**: This is the most direct method to confirm intracranial aneurysms and arteriovenous malformations, and the most reliable to assess vasospasm after SAH. 5. **Electroencephalography (EEG)**: In the acute phase, diffuse slow waves are common. If the hemorrhage disrupts the cerebral cortex, focal slow waves may appear at the injury site. After the acute phase, the EEG gradually normalizes. Mild cases may show no significant abnormalities. 6. **Radionuclide Cerebral Angiography**: Intravenous injection of a non-diffusible radionuclide followed by serial gamma-camera imaging allows dynamic assessment of cerebral perfusion and washout. 7. **CT Scan**: CT often fails to visualize the ruptured aneurysm sac but can demonstrate subarachnoid hemorrhage, secondary intracerebral hematoma, intraventricular hemorrhage, hydrocephalus, cerebral edema, cerebral infarction, brain herniation, and secondary brainstem hemorrhage. 8. **Electrocardiography (ECG)**: Acute-phase ECG may mimic myocardial infarction, showing ischemic changes, atrioventricular block, or atrial fibrillation, but cardiac enzyme levels remain normal.

II. Treatment

(1) Acupoints

1. **Motor Area (Healthy Side):** Corresponds to the projection of the precentral gyrus (primary motor cortex) onto the scalp. The upper point is located 0.5 cm posterior to the midpoint of the anterior-posterior midline (the line connecting the glabella to the most prominent point of the external occipital protuberance). The lower point is at the intersection of the eyebrow-occipital line and the anterior margin of the temporal hairline. The line connecting these two points is the motor area. The upper 1/5 of the motor area treats contralateral lower limb paralysis; the middle 2/5 treats contralateral upper limb paralysis; the lower 2/5 treats contralateral central facial palsy, motor aphasia, drooling, and speech disorders. 2. **Sensory Area (Healthy Side):** Corresponds to the projection of the postcentral gyrus (primary sensory cortex) onto the scalp. It lies 1.5 cm posterior and parallel to the motor area. The upper 1/5 treats contralateral lumbosacral pain, numbness, paresthesia, as well as pain in the posterior head and neck, and tinnitus; the middle 2/5 treats contralateral upper limb pain, numbness, and paresthesia; the lower 2/5 treats contralateral facial numbness, hemicrania, trigeminal neuralgia, toothache, and temporomandibular arthritis. 3. **Vasomotor Area (Healthy Side):** Located on a line 3 cm anterior and parallel to the motor area. The upper 1/2 treats contralateral lower limb edema; the lower 1/2 treats contralateral upper limb edema, and can also treat primary hypertension. 4. **Foot Motor-Sensory Area (Healthy Side):** Located 1 cm posterior to the upper point of the sensory area, 1 cm lateral to the anterior-posterior midline, and extending 3 cm anteriorly as a parallel line. It treats lower limb paralysis, contralateral lumbosacral pain and numbness, cortical nocturnal enuresis, cortical dysuria, cortical urinary incontinence, uterine prolapse, and rectal prolapse. 5. **Speech Area 2 (Healthy Side):** Draw a line parallel to the anterior-posterior midline from the parietal eminence. From a point 2 cm posterior to the parietal eminence along this line, extend a vertical line 3 cm downward. This area treats anomic aphasia. 6. **Speech Area 3 (Healthy Side):** Located 1.5 cm above the ear apex, on a horizontal line extending 4 cm posterior from the midpoint of the Vertigo-Auditory Area. It treats sensory aphasia.

(2) Methods

For subarachnoid hemorrhage, clinical acupoint selection follows the same principles as for other cerebrovascular diseases, primarily based on presenting symptoms. For example, when hemiplegia, hemianopsia, hemisensory disturbance, motor aphasia, drooling, or tongue paralysis occur, needle the motor area and the upper, middle, and lower points of the sensory area. If sensory aphasia or nominal aphasia is present without motor aphasia, the lower 2/5 of the motor area and sensory area may be omitted, and Speech Area 2 or Speech Area 3 should be added instead. Most patients do not develop edema of the upper or lower extremities after onset; if edema does occur, the vasomotor area may be added. After selecting the required needling areas, position the patient in a sitting or lateral lying position. Use a 30-gauge, 1.5-cun filiform needle. Perform routine local disinfection, then apply relay needling (jie li ci) and horizontal needling (ping ci) to puncture all selected areas. Retain the needles for 1 hour, with manipulation every 20 minutes (twisting frequency: 200 times per minute). Remove the needles after 1 hour. Treatment is given once daily, with 10 sessions constituting one course; rest for 5 days before the next course.

III. Commentary

Subarachnoid hemorrhage generally has a favorable prognosis, especially in middle-aged patients with good physical condition, relatively minor bleeding, and first-time onset. After surviving the critical period, such patients rarely develop sequelae. If sequelae do occur, the aforementioned treatment can help promote rapid recovery. For patients with larger bleeds, poorer physical condition, or advanced age, sequelae often remain after the critical period; however, appropriate application of the same treatment can still yield quite good results. Early intervention in this disease can facilitate the early restoration of brain cells. Most patients treated with the aforementioned method rarely experience lasting sequelae.

Etiology and Subarachnoid Hemorrhage Causes

Subarachnoid hemorrhage (SAH) arises from the extravasation of blood into the subarachnoid space, a compartment between the arachnoid mater and pia mater. The most prevalent subarachnoid hemorrhage causes include the rupture of saccular aneurysms, which account for approximately 85% of spontaneous cases. Other etiologies encompass arteriovenous malformations, dural arteriovenous fistulas, and rarer conditions such as moyamoya disease, characterized by an abnormal vascular network at the base of the brain. Additionally, subarachnoid hemorrhage risk factors such as hypertension, cigarette smoking, excessive alcohol consumption, and a family history of aneurysms significantly predispose individuals to vascular rupture. Non-aneurysmal causes, including cerebral vasculitis, arterial dissection, and coagulopathies, also contribute to the clinical spectrum. Understanding these diverse causative mechanisms is crucial for targeted prevention and acute intervention.

Clinical Presentation and Subarachnoid Hemorrhage Symptoms

The hallmark of SAH is the sudden onset of a severe, thunderclap headache, often described by patients as the worst headache of their life. Accompanying subarachnoid hemorrhage symptoms may include nausea, vomiting, photophobia, meningismus (neck stiffness), and transient or persistent loss of consciousness. Focal neurological deficits, such as cranial nerve palsies (commonly the oculomotor nerve), hemiparesis, or aphasia, can arise from direct mass effect or secondary vasospasm. Seizures occur in a subset of patients at ictus. The clinical severity is often graded using the Hunt and Hess or World Federation of Neurological Surgeons scales, which help predict outcomes. Prompt recognition of these symptoms is critical, as delayed diagnosis can lead to devastating neurological injury.

Diagnostic Imaging and Subarachnoid Hemorrhage CT Scan Findings

Non-contrast computed tomography (CT) of the head is the initial diagnostic modality of choice for suspected SAH. Classic subarachnoid hemorrhage CT scan findings include hyperdense material within the basal cisterns, Sylvian fissures, and cortical sulci, indicating acute blood. The distribution of blood can suggest the location of a ruptured aneurysm; for instance, blood localized to the interhemispheric fissure may point to an anterior communicating artery aneurysm. The sensitivity of CT is highest within the first 6 to 12 hours post-ictus, declining with time as blood is reabsorbed. CT angiography is often performed concurrently to identify the underlying vascular lesion. In cases where initial CT is negative but clinical suspicion remains high, lumbar puncture to detect xanthochromia is essential for confirmation.

Acute Care and Subarachnoid Hemorrhage Treatment Options

Initial management focuses on stabilizing vital signs, securing the airway, and preventing rebleeding. Definitive subarachnoid hemorrhage treatment options include surgical clipping or endovascular coiling of the ruptured aneurysm. The choice between these modalities depends on aneurysm morphology, location, and patient factors. Medical adjuncts involve administering nimodipine, a calcium channel blocker, to mitigate delayed cerebral ischemia, and maintaining euvolemia to prevent vasospasm. Aneurysmal subarachnoid hemorrhage management also requires close monitoring in a neurointensive care unit for complications such as rebleeding, cerebral vasospasm, hydrocephalus, and hyponatremia. External ventricular drainage may be necessary for acute hydrocephalus. Early intervention and multidisciplinary care are paramount to optimize outcomes.

Rehabilitation and Subarachnoid Hemorrhage Recovery Time

The trajectory of recovery post-SAH is highly variable and influenced by the initial severity of the bleed, patient age, and comorbidities. Subarachnoid hemorrhage recovery time can span weeks to months, with many survivors experiencing persistent cognitive deficits, including memory impairment, executive dysfunction, and fatigue. Physical rehabilitation, occupational therapy, and neuropsychological support are integral to the recovery process. While some patients achieve functional independence, others may require long-term care. The risk of long-term complications, such as epilepsy and chronic hydrocephalus necessitating shunt placement, underscores the need for sustained follow-up. Early and intensive rehabilitation can significantly improve quality of life and functional outcomes.

Preventive Strategies and Subarachnoid Hemorrhage Risk Factors

Modifying subarachnoid hemorrhage risk factors is a cornerstone of prevention. Hypertension control, smoking cessation, and moderation of alcohol intake are primary targets. Screening for unruptured intracranial aneurysms may be considered in high-risk populations, such as those with a family history of SAH or autosomal dominant polycystic kidney disease. For patients with identified unruptured aneurysms, prophylactic treatment (clipping or coiling) may be offered based on size, location, and growth characteristics. Public health initiatives emphasizing awareness of warning signs and risk reduction are essential to decrease the incidence of this devastating condition. Continued research into genetic predispositions and novel therapeutic targets holds promise for future preventive strategies.