Keywords bilateral CSDH - bilateral PCA infarction - postoperative cortical blindness
Introduction
Chronic subdural hematoma (CSDH) is a common condition requiring neurosurgical intervention
and most often results in a favorable outcome. It is usually seen after a trivial
head trauma leading to the rupture of the cortical bridging veins, but it can also
occur spontaneously in the presence of coagulopathy. Although unilateral CSDHs occur
more commonly, bilateral CSDHs are being increasingly diagnosed. The incidence of
bilateral CSDH has been reported as 16 to 20%.[1 ] Bilateral CSDHs usually manifest without any neurologic deficits, and have been
reported to be associated with rapid progression requiring early decompression. They
are also known to have higher recurrence rates. Blindness due to bilateral infarction
of the posterior cerebral artery (PCA) following bilateral chronic subdural evacuation
is an extremely rare entity. Only four cases have been reported so far, with this
case being the fifth one. The exact etiopathogenesis and mechanism of this rare complication
remain unknown. In all the previously reported cases, the patients suffered permanent
visual loss. The authors evaluate one such scenario in which evacuation of bilateral
chronic subdural hemorrhage was followed by bilateral PCA infarction and cortical
blindness.
Case Report
A 45-year-old man was admitted with complaint of holocranial headache for 2 months,
which progressively worsened and was not associated with vomiting or visual obscuration.
The patient had history of head trauma caused by fall from a two-wheeler 2 months
back. Clinical examination revealed no abnormalities. Computed tomography (CT) and
magnetic resonance imaging (MRI) scanning showed bilateral frontotemperoparietal chronic
SDH without parenchymal and vascular abnormality. There was no midline shift ([Fig. 1A ] to [D ]). Magnetic resonance angiography (MRA) and magnetic resonance venography (MRV) were
normal. Blood investigations were normal. There were no comorbid medical illness or
risk factors associated with coagulopathy. Bilateral frontal and parietal burr holes
and evacuation of CSDH was done. The procedure was uneventful.
The patient developed decreased vision in both the eyes in the immediate postoperative
period that proceeded on to complete blindness by the second postoperative day. On
clinical examination, there was no perception of light, the pupils were equal, and
reacting and fundus examination was normal. Except for cortical blindness, the patient
did not have any other neurologic deficit. Postoperative MRI revealed bilateral PCA
infarction. There was no midline shift and only a minimal residual subdural hemorrhage
([Fig. 1E ] to [K ]). Hematologic and rheumatologic assessment for coagulopathy was negative. Cardiac
assessment was normal. The lipid profile of the patient was within normal limits.
Transcranial ultrasound (USG) Doppler was done, which showed no abnormality in both
the intracranial and extracranial arteries. The blood flow and velocity in bilateral
PCAs were normal and symmetrical. A repeat MRI done after 2 weeks showed persistent
bilateral occipital lobe infarction. The patient was followed up for a period of 1 year
during which there was no recovery in the vision.
Fig. 1 Preoperative CT of brain (A, B ); preoperative MRI (C–E ); postoperative CT (F, G ); postoperative MRI (H ); postoperative MRI: DWI (I ); MRA (J ); MRV (K, L ). A–D showing bilateral frontotemporoparietal chronic SDH without midline shift. E–G showing postcraniotomy status with minimal residual chronic subdural without any
midline shift. H postoperative MRI DWI showing bilateral PCA territory infarction;
with normal MRA (I ) and MRV (J and K ).
Discussion
Cortical blindness is a rare neurologic condition characterized by loss of vision
in the presence of an intact anterior pathway. It is usually binocular with preserved
pupillary reflexes.[2 ] It occurs due to ischemia of the occipital cortex due to a local event such as embolism
or hemorrhage or, more commonly, due to global hypoperfusion. Aldrich et al have postulated
that the occipital cortex is very sensitive to systemic hypoxia because of its distant
location from the central cerebral circulation.[3 ] Cortical blindness has been associated with cerebral venous thrombosis, during pregnancy,
and PCA infarction. Rarer causes include occipital head trauma causing extradural
or subdural hemorrhage, carbon monoxide poisoning, and neoplasms. Common etiologic
factors for a PCA stroke include cardiogenic embolization, atheromatous disease of
the proximal vessels, dissection of the proximal vessel, and intrinsic PCA atheromatous
disease. Less common etiologies include migrainous cerebral infarction, hypercoagulable
disorders, illicit substance use, vasculitis, and fibromuscular dysplasia. Rare causes
include postsurgical especially cardiac surgery and following angiography—both cerebral
and coronary, wherein cortical blindness may occur due to disruption of the blood-brain
barrier following angiography, concurrent hypotension, embolism, and vasospasm.[3 ]
Cortical blindness occurring due to bilateral PCA infarction following bilateral chronic
subdural evacuation in the absence of any other associated risk factor is an extremely
rare presentation. Only four cases of blindness following surgical decompression of
CSDH have been reported and published in the literature so far. The exact pathophysiology
behind this rare complication remains to be understood.
Kaene reported the first case in 1980 when the author documented seven cases with
permanent visual loss following decompression for tentorial herniation. The causes
were unilateral subdural hematoma in three patients and bilateral CSDH, bilateral
subdural empyema, traumatic intracerebral hematoma, and postoperative infarction in
one patient each. The authors speculated is that descending transtentorial herniation
occurring during the decompression could have led to the kinking of the bilateral
posterior cerebral arteries and consequent occipital lobe polar ischemia and infarction.
Among these patients, three went on to develop optic atrophy that indicated that both
damage to the anterior visual pathway and posterior circulation compression had occurred.[4 ]
Russegger et al have reported the second case of a 51-year-old patient who developed
bilateral blindness following decompression of a traumatic CSDH. The patient had bilateral
optic atrophy, and the authors have postulated breakdown of the altered vasoregulation
of the optic nerve occurring at the time of intracranial pressure drop during the
decompression had caused the optic atrophy and consequent amaurosis.[5 ]
The third and fourth case reports by Kudo et al describe two patients developing occipital
infarction and blindness following bilateral chronic subdural evacuation. Both the
patients had a poor Glasgow coma scale (GCS) on admission, and their CTs revealed
ambient and interpeduncular cistern compression. The authors have attributed the severe
sequelae to occipital infarction caused by central transtentorial herniation.[6 ]
The patient in this case reported by the authors presented with GCS 15, and preoperative
imaging did not reveal any midline shift. Also, there were no associated comorbid
illness or risk factors for stroke. A sudden drop in intracranial pressure (ICP) during
the decompression could cause vascular jeopardization to the optic pathways bilaterally,
but the presence of normal anterior pathway and selective posterior pathway involvement
occurring with cortical blindness as in our case goes against this theory. The authors
postulate descending transtentorial herniation that occurred during the evacuation
of the hematoma as the reason for the bilateral occipital infarction caused by the
kinking of bilateral PCAs against the tentorial margin. Another possible explanation
is the preexisting hypoxic insult to the PCA due to the chronic compression by the
bilateral subdural hematoma could have aggravated the infarction following the decompression.
In our case, the authors believe that preexisting chronic ischemia has led to the
decrease in brain volume, thereby giving space for the collection of the chronic subdural
hemorrhage, and subsequent surgical evacuation has caused the worsening of the ischemia
resulting in PCA infarction.
In recent times, bilateral CSDH is being recognized as a distinct entity with altered
hemodynamics in the cerebral circulation. Although the pathophysiology behind bilateral
subdurals is not well known, it is postulated that trauma to the bridging veins leads
to the hematoma similar to that of a unilateral chronic subdural hemorrhage. Age more
than 75 years, use of antiplatelet and anticoagulation medication, hemodialysis, and
preexisting coagulopathy are known to be risk factors for the occurrence of bilateral
CSDHs.[1 ] The clinical presentation is usually vague and variable, and neurologic deficits
occur less commonly. Most patients with bilateral CSDH present with headache, nausea,
and vomiting, Bilateral CSDHs are more common in the old-aged men and do not have
any midline shift on CT.[7 ] Several studies have also shown bilateral CSDH as a risk factor for recurrence.
Kurokawa et al have found rapid deterioration occurring in patients with CSDHs and
advocate early and simultaneous decompression in these patients even if they show
no or minor clinical deficits. They attribute the rapid aggravation due to the impaired
autonomic buffering capacity of the raised ICP and coagulofibrinolytic abnormality
in the hematoma.[8 ]
Tanaka et al in their study have suggested that CSDH may induce neurologic dysfunction
primarily through mechanical distortion of the central brain regions and transneural
depression occurring in the distant regions[9 ] Okuyama et al measured cerebral blood flow (CBF) in 34 patients with bilateral CSDH
and found that in the patients with brain shift, the CBF reductions are noted in the
frontal, parietal, and occipital cortices in the thin hematoma side and in the putamen
in the thick hematoma side. Based on their results, the authors postulated the shifted
force of the CSDH is accompanied by a secondary CBF reduction in the deep cerebral
regions and is the major cause of neurologic dysfunction.[10 ]
Conclusion
CSDH is a frequently encountered problem in neurosurgical practice. As Gelabert-Gonzalez
et al have stated: CSDHs are perceived as “common lesions that are easily treated
with a minimum morbidity and mortality.” Bilateral CSDH, however, is a separate entity
with altered pathophysiology and deranged cerebrovascular autoregulatory mechanisms,
and it needs to be treated with greater diligence. Early and simultaneous decompression
is recommended for bilateral CSDH to prevent rapid deterioration and neurologic sequelae.
Blindness following the evacuation of bilateral CSDH is an extremely rare complication,
and yet again it reinforces the fact that bilateral chronic subdural hemorrhage should
not be dismissed as a benign disorder.
