A woman in her 50’s with a past medical history of meningitis approximately 10 years ago and concussion 5 years before then went for chiropractic manipulation of her cervical spine. Two weeks later she developed neck and head pain. She returned to the chiropractor for further manipulation that consisted mostly of deep cervical tissue massage. It did not relieve her headache. Her headaches progress, becoming bilateral and intractable bilateral. Any attempt at a bowel movement would increase the pressure in her head as did sitting upright. When she lay down, her headaches did slightly improve. There was no diplopia, focal motor weakness, or sensory loss. Two months earlier she recalls striking her head when reaching for a kitchen utensil.
CT scan on admission showed bilateral subacute subdural hematomas with a left to right midline shift. (Fig. 1A). CTA showed no arterial or venous abnormalities. (Fig. 1B).
Figure 1. A) Initial non-contrast CT with bilateral mixed subdural collections and no improvement following 4 days of medical management (B).
The differential diagnoses included post-traumatic subdural hematomas secondary to incidental trauma and CSF leak leading to spontaneous intracranial hypotension (SIH). Despite bedrest and medical management the positional headaches worsened and the subdural collections enlarged. (Fig. 1B). MRI imaging of the entire spine and CT Myelography failed to identify a site of leakage. Inferior displacement and crowding of the cerebellar tonsils and midbrain became evident. Bilateral burr hole evacuation of the subdural collections ensued. Thin membranes were present, consistent with the chronicity of the subdurals. (Fig. 2A and B). Mild improvement in the mass effect and midline shift were noted, but positional headaches persisted.
Figure 2. A) NCT post bilateral burr hole decompression with slight improvement; B) Persistent collections and bilateral dural enhancement with downward displacement of tonsils on coronal MRI; C) Normal Tonsillar Position Reference
Now that the mass effect of the subdural collections had been dealt with, we proceeded with the presumed diagnosis of intracranial hypotension and its treatment. Under fluoroscopic control, an LP was done at L4-5. The opening pressure was less than 5 cm of water. Twenty-five mL of autologous blood was injected as an epidural blood patch was then done at this level (Fig. 3A).
Figure 3. A) Epidural Blood Patch contrast performed at L4-5; B) 2-month FU NCT confirms near-complete resolution of bilateral subdural collections.
Within six hours of the blood patch, the patient was able to walk without headache. Within 36 hours, she was discharged. Follow up CTs and clinical evaluations over the next 3 months showed progressive resolution of her subdural collections and near-complete clinical recovery (Fig. 3B).
Spontaneous intracranial hypotension (SIH) is characterized by postural headache and low opening pressure at lumbar puncture (<6 cm H20) without obvious causes such as trauma or iatrogenesis. Cranial magnetic resonance and CT imaging often reveal small subdural collections with minimal mass effect, occasional dural enhancement, venous sinus dilatation, or downward displacement of the brain (“Brain Sag”). “Spontaneous” can often overlook incidental trauma, such as minor falls, chiropractic manipulation, or recent iatrogenesis (i.e. epidural anesthesia or recent surgery) and should be elicited in a careful historical inquiry. The condition is thought to be benign in most patients, however, some patients may experience progressive and intractable symptoms. In addition, episodic cranial neuropathies may often be present and confusing on initial evaluation, including nonreactive, dilated pupils (3rd), paresis of vertical gaze (4th), or 9th-12th Lower Cranial Neuropathy deficits which may result in disturbed speech, swallowing, coughing, deglutition, sensory functions, taste, or autonomic functions, neuralgic pain, dysphagia, head, pharyngeal, or neck pain, cardiac or gastrointestinal compromise, or weakness of the trapezius, sternocleidomastoid, or the tongue muscles.
On occasion, tearing of bridging veins may produce subdural hematomas (SDHs) and mass effect, which in some patients may lead to rapid deterioration, even coma, and require emergent surgical decompression or interventions. The diagnosis of spontaneous intracranial hypotension should be considered in patients presenting with subdural hematoma in the absence of trauma and with normal clotting. Imaging of the site of CSF leak is often inconclusive, as the small volume of total CSF (90-150 cc), the physiologic kinetics, small rate/volume of leakage, and resorption limits visualization of the leak anatomically. Lumbar puncture should be performed under fluoroscopic guidance to confirm positioning, as the low pressure associated with this condition may result in a “dry tap”, which also necessitates the use of a digital manometer to measure the opening pressure rather than the traditional gravity based manometer. Subdural hematomas secondary to intracranial hypotension may recur following surgical drainage if treatment of the underlying cause of CSF leak is not done. Epidural blood patches (blind or targeted) are felt to be the best primary treatment strategy even without identifying the site of leakage, and have been shown to be successful in the majority of patients, and can be repeated for patients who do not respond to initial treatment or experience recurrence of symptoms. (References 1-5)
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