No abstract

This study suggests that the risk of developing posttraumatic chronic daily headache is greater for less severe head injury compared with moderate/severe head injury. The reason for this relation is unclear.

In this study, using headache frequency as the primary metric, for the entire group, amitriptyline was superior to placebo in migraine prophylaxis at 8 weeks but, because of a robust placebo response, not at subsequent time points. For the subgroup with CDH, amitriptyline was statistically significantly superior to placebo at 8 weeks and 16 weeks with a similar but nonsignificant trend at 12 and 20 weeks. Compared with placebo amitriptyline is effective in CDH. Amitriptyline was also significantly effective in IM compared intragroup to its own baseline; however, placebo was equally effective in the same analysis. The reason for the robust placebo response in the IM group is not clear, but has been occasionally reported.

Results suggest that head and neck injury (HANI) accounts for approximately 15% of chronic daily headache (CDH) cases in this non-clinical population. The relationship between HANI and CDH was not limited to injuries proximate to CDH onset. The lifetime risk of CDH increases with increasing number of HANI.

Spontaneous intracranial hypotension (SIH) is a syndrome that was largely unknown until the advent of MRI. The incidence of SIH is estimated at 5 per 100,000, which is half the incidence of subarachnoid hemorrhage. The major feature is a postural headache of acute or subacute onset. This headache is absent or minimal when the patient is lying down and rapidly worsens to great intensity when the patient sits or stands. Other features may include nausea, vomiting, vertigo, tinnitus, and marked exacerbation by Valsalva maneuver. SIH is due to a leak of cerebrospinal fluid from a tear in the dural membrane, which occurs most often at the exit zones where the cervical spinal roots leave the subarachnoid space. Other leak sites may be the vestibular system, the cribriform plate, or the pituitary fossa. If the leak continues, the brain loses buoyancy within the cranial space and sags toward the foramen magnum. This, in turn, may produce subdural hygroma or hematoma, brainstem compression, focal cranial nerve palsies, or cerebellar tonsillar herniation. The initial therapy is generally strict bed rest. If this fails, an epidural blood patch is usually successful in sealing the leak and restoring brain buoyancy. A significant minority of patients require a repeat epidural blood patch. If the blood patch fails, a surgical approach may be needed. Repair of the leak and restoration of brain buoyancy will stop the postural headache and, in most cases, will reverse the complications.