Department of Neurosurgery, National Neurosciences Centre, Peerless Hospital Complex,
Kolkata, West Bengal, India.
   

A 6-year-old boy presented in an unconscious state with history of holocranial headache and vomiting of two days duration. There was no history of seizures or fever. He was afebrile but tachypneic, was localizing with both upper limbs, with no eye opening or verbal response (Glasgow Coma Scale of E1M5V1). Pupils were equal in size and reacting to light. Both plantars had withdrawal response. There was a history of fall, 3 weeks ago, following which he lost consciousness for 20 minutes and was then apparently normal except for complaints of occipital pain and was treated conservatively. Computed tomography (CT) scan revealed a left-sided hypodense extra-axial mass in the posterior fossa compressing the left cerebellar hemisphere and brain stem effacing the perimesencephalic cistern with 4th ventricular shift (Fig 1). His hematological parameters were normal. He underwent left cerebellar burr hole and evacuation of the hematoma under general anesthesia. Intraoperatively, altered liquid blood under pressure was drained and underlying dura was normal. A diagnosis of chronic extradural hematoma (EDH) was made. He regained consciousness the following day and was neurologically normal at follow-up, two months later.

(a)	(b)
Fig. 1 Axial CT scan images (a,b) showing a hypodense biconvex extra-axial collection in the posterior fossa on the left side with 4th ventricular shift, cisternal effacement and rounding of the third ventricle.

One of the well-described classical presentations of patients with acute extra dural hematoma is a history of transient loss of consciousness following injury with subsequent recovery for a variable period before lapsing back into unconsciousness. This period of transient neurological recovery is called the lucid interval and occurs in 14-21% of patients with extra dural hematoma [1]. While there is no consensus on how long this period may span, it has been described by Ganz as lasting from a few hours to a few days [2]. The length of the lucid interval will be longer if the accumulation of blood is slow, as in venous origin of bleed or if there is significant shunting of blood outwards through the epidural veins [2].

Given the absence of fresh bleeding (in imaging) in this case the probable pathophysiology is expansion of the initial EDH by fluid, flowing in down an osmotic gradient, like in a chronic subdural hematoma leading to brain stem compression and 4th ventricular shift.

Posterior fossa constitute around 4-13% of all extradural hematomas [3], and sudden worsening after an initial hypo-symptomatic period has been reported [4]. This worsening has been reported only in the acute stage, though 11% of all extradural hematoma become chronic over time [1]. To predict patients likely to require surgery, Bozbuga, et al., [5] noted that acute posterior fossa EDHs having perimesencephalic cisternal effacement and 4th ventricular shift were more likely to require intervention. This patient too demonstrated both these features on imaging, though the hematoma had become chronic.