Keywords
vertex - epidural hematoma - trauma - quadriparesis
Introduction
Vertex epidural hematomas (VEHs) are rare and account for 1 to 8% of all epidural
hematomas (EDHs).[1] The location of a vertex EDH causes an unusual clinical-radiologic presentation
and can be a diagnostic challenge. The clinical picture of VEH is variable, and the
patient may present with headache, vomiting, and other features of raised intracranial
pressure (ICP) such as abducent nerve palsy.[2] Many authors have reported upper motor neuron signs and motor weakness.[1]
[3] Consequently, diagnosis can be delayed with fatal consequences; the mortality rate
is therefore high and reported to range between 18 and 50%.[4] However, timely surgery can gratify results. VEHs should therefore be considered
as a possibility in patients with traumatic brain injury (TBI) with quadriparesis,
especially when the spine is normal.
We report a case of VEH presenting with quadriparesis that is infrequently reported
in literature.
Discussion
EDHs at the vertex are very rare. This is probably due to dense dural adhesions of
superior sagittal sinus to the overlying bone particularly at the sagittal suture.
The bleeding source could be the veins, venous sinuses, the fracture itself, or diffuse
dural bleeding caused by dural stripping.[3]
[5] As many as 92 to 100% of the cases were associated with a fracture at the level
of the vertex, but exact incidence of source of bleeding in these could not be evidenced.[4]
[5]
[6]
[7] EDHs of venous origin are usually small and progress gradually presenting with features
of raised ICP without lateralizing signs. Source of bleeding in our case appeared
to be multiple tiny points along the sagittal sinus. Many authors reported headache,
vomiting, and raised ICP as major clinical symptoms.[6] Paraplegia and motor weakness are also important manifestations.[6]
[7]
[8]
[9] In the series of 14 patients, published by Borzone and coworkers, all 14 patients
had hemiplegia and 5 had headache too.[1] Safavi-Abbasi and coworkers had published a case report of vertex EDH with monoplegia.[10] Kiboi and Muriithi reported a case of bilateral upper limb decerebrate posture.[11] Our patient appears to have extensive direct bilateral compression of motor strip
by the hematoma with associated edema around contusions as a cause of quadriparesis.
Many authors have noted the problems associated with the diagnosis of VEHs by conventional
axial CT. The difficulty arises because of the location of the clot at the apex of
the brain. At this location, the near isodensity of the hematoma and bone and volume
averaging effects of routine CT scanning with relatively thick slices (10 mm) make
the diagnosis more difficult.
Most other authors emphasize coronal MRI and CT as the most important diagnostic tools.
We believe that coronal CT scanning or coronal reconstructions are preferable and
sufficient in all clinically suspected cases of VEHs. With coronal views, the real
size of the clot can be estimated and prompt surgical intervention without a time-consuming
diagnostic delay can follow. Rapid diagnosis and surgical intervention are crucial
to limit complications and death from the progressive event.
Surgical strategy proposed by many authors suggest bicoronal skin flap with separate
bilateral fronto parietal craniotomy leaving bone along superior sagittal sinus.[8]
[12]
[13] Also, multiple hitch stitches all around the craniotomy site, including along the
sagittal sinus, would control bleeding effectively.[8] Other techniques that are described include free duraplasty, direct stitching, clipping
of the sinus, and the pedunculated duraplasty.[14]
Some authors believe that extradural hematomas do not always require surgical evacuation,
depending on the patient's level of consciousness and the size of the hematoma. However,
this position is controversial and the exception rather than the rule for large hematoma.[15]
[16]
[17] Conservative management of VEHs has also been discussed,[17] and should be chosen with great caution.
Conclusion
VEHs should be considered as a possibility in patients of TBI with quadriparesis,
especially when the spine is normal. Patients with signs of raised ICP or paralysis
should undergo CT scanning with thin cuts and coronal reconstructions to verify the
location and size of the clot. Rapid surgical intervention, especially in patients
with progressive symptoms, can limit morbidity and mortality. The lesson learnt from
the case is that regardless of poor GCS and late presentation, surgical decompression
of VEHs may result in excellent recovery from the resultant quadriparesis.
