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.