The normal range of intracranial pressure, as measured by lumbar puncture, should be between 7.84 and 11.8 kPa (80 to 120 mmH₂O). Generally, intracranial pressure often increases to varying degrees after traumatic brain injury, while cases of low intracranial pressure are relatively rare. Occasionally, some patients may experience elevated intracranial pressure in the early stages post-injury, followed by the development of intracranial hypotension, with an incidence rate of approximately 5%. The so-called intracranial hypotension syndrome refers to a comprehensive set of symptoms that arise when a patient's lateral decubitus lumbar puncture pressure falls below 7.84 kPa. Its clinical manifestations are similar to those of increased intracranial pressure, but due to the differing treatment approaches, careful differentiation is essential. The causes of intracranial hypotension may primarily stem from post-traumatic cerebrovascular spasms, which inhibit the choroid plexus's ability to secrete cerebrospinal fluid, or may be secondary to cerebrospinal fluid fistula disease, shock, severe dehydration, hyponatremia, hyperventilation, or the excessive drainage of cerebrospinal fluid during surgery or lumbar puncture. Post-lumbar puncture headaches are well-known, with two possible mechanisms: one being the reflex inhibition of the choroid plexus caused by the lumbar puncture itself or functional disturbances in the hypothalamic cerebrospinal fluid secretion center; the other being the reduction in cerebrospinal fluid volume. Franksson once pointed out that when intracranial pressure ranges from 100 to 200 mmH₂O, cerebrospinal fluid can fistula disease into the epidural space through the lumbar puncture needle hole at a rate of up to 240 ml per day. Under normal circumstances, the total volume of cerebrospinal fluid is 100–160 ml, with a secretion rate of about 0.3 ml/min, producing 400–500 ml daily. Therefore, even a single rapid drainage of 20 ml of cerebrospinal fluid in a healthy individual can induce headaches. Grant et al. (1991) suggested that headaches may result from compensatory stirred pulse dilation. Additionally, during trauma, the forceful impact of cerebrospinal fluid into the spinal canal may tear the lumbar nerve root sleeve, potentially causing cerebrospinal fluid to fistula disease into the epidural space, leading to low intracranial pressure (Bell, 1960).

Post-traumatic intracranial hypotension typically occurs 1–2 hours after head injury, sometimes 2–3 days later, with headache being the most prominent symptom. The pain is often localized in the forehead and occipital region and worsens with an elevated head position. In severe cases, it may spread throughout the entire head and radiate to the neck, back, shoulders, or even the lower limbs. The headache alleviates or disappears when lying flat or in a head-down position. Previously, this positional headache was thought to be related to brain sagging, but recent MRI studies have not confirmed this. Therefore, the cause of the headache may be associated with traction or compression of intracranial blood vessels, reduced intracranial volume leading to adaptive changes in meningeal tension, or compensatory regulation of intracranial volume causing vascular dilation due to the redistribution of blood and cerebrospinal fluid. Other symptoms include vertigo and vomiting, which often occur with changes in head position or after severe headaches. Patients may experience dizziness, blurred vision, nausea, vomiting, a weak and rapid pulse, low blood pressure, photophobia, fatigue, anorexia, dehydration, and neck stiffness. In severe cases, consciousness disturbances may occur, ranging from drowsiness to unconsciousness. A few patients may also exhibit autonomic symptoms, such as significant fluctuations in vital signs and paroxysmal flushing of the face and neck. In rare cases, due to the loss of cerebrospinal fluid buoyancy and cushioning, cranial nerves may be directly compressed or stretched, leading to unequal pupil size and/or abducens nerve palsy. These symptoms can easily be mistaken for increased intracranial pressure and should be approached with caution.

The diagnosis of post-traumatic intracranial hypotension syndrome primarily relies on clinical features and lumbar puncture pressure measurement. Clinically, when a patient exhibits severe symptoms such as dizziness, headache, lack of strength, and anorexia after head injury, which are inconsistent with the severity of brain injury—especially if there is a clear pattern of headache worsening upon elevating the head and improving upon lowering it—the possibility of intracranial hypotension should be considered. If lumbar puncture in the supine position reveals a pressure below 80mmH₂O, the diagnosis is confirmed. A pressure below 40mmH₂O indicates grade III intracranial hypotension, often accompanied by severe dehydration and electrolyte imbalances. Due to the significant reduction in intracranial pressure, the brain volume shrinks, and intracranial veins dilate and become stretched, leading to oozing or bleeding. Consequently, the cerebrospinal fluid often appears yellow or contains varying amounts of red blood cells, with slightly elevated protein levels. In some cases, patients may even develop subdural hematomas. For this reason, some authors have suggested avoiding lumbar puncture in patients with intracranial hypotension to prevent further loss of cerebrospinal fluid, recommending instead ventricular drilling to assess intracranial pressure, which is both accurate and safe. In fact, with the advanced development of neuroimaging today, if clinical features align and CT or MRI has ruled out other confounding conditions, a therapeutic trial can be used for confirmation. This may involve lying flat or in a head-down position, inhaling a mixture of 5% CO₂

bubble_chart Treatment Measures

The treatment of post-traumatic intracranial hypotension syndrome may vary slightly depending on the {|###|}disease cause{|###|}, but the basic principles remain the same. Common treatment methods include: lying flat and resting without a pillow, and if necessary, adopting a foot-elevated and head-lowered position; increasing fluid intake, with approximately 1000ml of normal saline and 2500–3000ml of 5% glucose solution administered orally or intravenously daily; inhaling oxygen containing 5% CO₂ for 5–10 minutes per hour to dilate cerebral blood vessels, reduce resistance, and promote cerebrospinal fluid secretion; intravenous injection of 10–15ml of distilled water per day, which can reflexively stimulate cerebrospinal fluid production, though hemolytic reactions must be monitored; if necessary, intravenous infusion of 500–1000ml of 0.5% hypotonic saline per day can also increase cerebrospinal fluid; alternating left and right cervical sympathetic ganglion blocks with 10ml of 0.5% novocaine once daily can dilate intracranial blood vessels; injecting 10–15ml of normal saline or filtered air into the cerebral ventricles or 15–20ml of normal saline or air into the subarachnoid space via lumbar puncture can directly fill the subarachnoid space and stimulate cerebrospinal fluid secretion, though this carries the risk of post-lumbar puncture fistula disease; other medications beneficial for improving intracranial hypotension, such as foxtail millet alkaloids, ephedrine, adrenaline, posterior pituitary hormones, coffee bean alkaloids, pilocarpine, neostigmine, dextroamphetamine sulfate, urotropine, and corticosteroids, may also be administered in appropriate doses to aid recovery. Additionally, for patients with secondary intracranial hypotension, timely intervention targeting the {|###|}disease cause{|###|} is necessary, such as surgical repair of cerebrospinal fluid fistulas. According to literature, Cushing once documented a rare case where a dura mater puncture site remained unhealed nine months after lumbar puncture, with headaches resolving only after the fissure was clipped.