DISCUSSION
Contrary to a frequent presentation of unilateral BG bleed, finding a bilateral basal ganglia bleed is out of the ordinary. The aetiopathogenesis in the circumstance of simultaneous bilateral basal ganglia hemorrhage remains unsettled. A handful of hypothesis has been postulated by different authors with reference to aforementioned context. The most common plausible pathogenesis is the concurrent rupture of bilateral micro aneurysms on lenticulostriate arteries by chance [7]. Other mechanism predicate that the initial hemorrhage results in specific hemodynamic ambience, such as reflex increase in blood pressure, evoking rupture of a second micro aneurysm on the contralateral side in a brief time span, which seems more credible[7] . Nonetheless, traumatic basal ganglia bleeding is uncommon, and bilateral basal ganglia hemorrhage after trauma is extremely rare. Concerning the trauma, two hypotheses has been put forward namely spontaneous or traumatic hemorrhage [8]. Spontaneous hemorrhage occurs when the blood pressure haul up impulsively due to emotional or physical strain and ruptures the lenticulostriate artery forming a hematoma. The genesis to this predicament being congenital vascular malformation, long term hypertension and diabetes mellitus [9]. Traumatic hemorrhage hypothesis surmise shearing force that cause the tear in the palladium branch of the anterior choroid artery. When a hefty coercion is imposed to the vertex, forehead, or occipital area directed towards the tentorium, there would be a reposition of the brain parenchyma through the tentorial notch with shredding and ripping of vessels by shearing forces, resulting in hemorrhages in the basal ganglia region. A few authority labels this as intermediary contusions [10]. The basal ganglia and thalami are profoundly metabolic brain domains, making them susceptible to hypoxic-ischemic injury, toxic poisoning (carbon monoxide, methanol, cyanide), metabolic anomalies (liver disease, Leigh disease, Wilson disease, hypoglycemia, and osmotic myelinolysis), and neuro degeneration [11]. The bilateral basal ganglia or thalami can also be targeted by focal flavi virus infection, toxoplasmosis, and primary CNS lymphoma [11,12]. Lately, with the emergence of global pandemic, the sinner being the SARS-CoV-2, it has been presumed that the ailment can be neurotropic via the trans cribriform or the hematogenous route [13]. The doubt as to why COVID 19 would predispose to bilateral ganglia hemorrhage remains open and undecided. Even so, the virion has been reported to predispose to a vulnerable hypercoagulable state, increasing the likelihood of cerebrovascular accident and ischemic stroke [14]. It is theorized that the aetiopathology of COVID 19 whether by direct invasion or via systemic inflammatory responses, may contribute to bilateral basal ganglia hemorrhage and to ensuing neurological deficits [15].
As outrageous it is to involve the bilateral basal ganglia, an impoverished outcome is always anticipated. Hereupon, debate come to light whether or not to intervene the patient surgically. On account of destruction of crossing and non-crossing fibers, bilateral diaschisis phenomenon, severely disrupted and altered level of consciousness, quadriparesis and pseudo bulbar palsy, compromised aftermath is contemplated [16]. While some professionals prefer an upfront evacuation of hematoma depending upon the volume, the others favor to lie in wait to undertake surgery immediately when there are signs of surge in intracranial pressure.
As luck would have it, our patient achieved an admissible recovery. We found it compelling that the patient could circumvent surgical intervention in the face of voluminous hematoma with bilateral involvement. Into the bargain, his neurological function also rectified making him a self-sufficient being.