Homonymous hemianopia with corresponding ganglion cell layer loss and oculomotor nerve palsy in acute subdural hemorrhage

Homonymous hemianopia following acute SDH is rare, typically caused by posterior cerebral artery compression or optic tract injury from temporoparietal contusions.[1,2] We report a unique case of homonymous hemianopia with pupil-involving third nerve palsy after SDH, accompanied by ganglion cell complex (GCC) thinning on optical coherence tomography (OCT) despite no occipital lobe lesion. Case History A 53-year-old man sustained a head injury in a road traffic accident, with transient loss of consciousness. CT scan revealed a thin hyperdense rim along the falx and right tentorial leaflet, consistent with acute SDH hygroma [Fig. 1a]; no occipital infarct was seen. A left orbital floor fracture was also present. Initial ophthalmic examination showed a normal right eye; the left eye had periorbital edema, conjunctival congestion, a sluggish 4 mm pupil without relative afferent pupillary defect, and no enophthalmos. He was managed conservatively, stabilizing by day four. Follow-up revealed a left pupil-involving partial third nerve palsy, though fundus examination remained normal [Fig. 2]. Repeat CT on day five showed bilateral subdural hygromas [Fig. 1b].Figure 1: Computed tomography (CT) brain in sagittal view (a) showing a thin rim of blood along the falx ceberi, (b) resolving on 5th dayFigure 2: Fundus of (a) right eye and (b) left eyeAt one month, the third nerve palsy had nearly resolved. However, perimetry demonstrated left congruous homonymous hemianopia without macular sparing [Fig. 3]. OCT revealed GCC thinning in the left sectors of both eyes, corresponding to the visual field defect [Fig. 4]. Magnetic resonance imaging (MRI) was recommended but declined by the patient.Figure 3: (a) and (b) Showing decreased retinal sensitivity in the nasal half of the right eye and the temporal half of the left eye, respectivelyFigure 4: OCT image showing thinning of ganglion cell layers over the nasal half of the right eye and the temporal half of the left eye, respectively. OCT = Optical coherence tomographyDiscussion Visual field deficits following SDH are most often attributed to injury involving the occipital cortex or optic radiations.[1–3] In the present case, however, conventional imaging revealed no evidence of such involvement. The absence of macular sparing argued against primary occipital damage, while OCT demonstrated GCC thinning, consistent with retrograde degeneration likely originating from an optic tract injury.[4,5] CT, though readily available and the standard first-line modality in trauma, often fails to detect subtle contusions or evolving ischemic changes [Fig. 5]. Such lesions may only become evident radiologically after 8–12 weeks, when they appear as chronic infarcts. MRI remains the most sensitive modality for detecting parenchymal or pathway lesions that underlie visual field deficits.[3–5] Unfortunately, in this case, MRI could not be pursued due to financial constraints, limiting definitive anatomical correlation.Figure 5: Computed tomography (CT) brain in axial view – showing no evidence of occipital infarction noted on day one and day fifth of the accident, respectivelyDespite these imaging limitations, the persistent field defect, together with OCT evidence of inner retinal thinning, strongly supports an underlying traumatic visual pathway injury. This case highlights the complementary role of structural and functional testing—namely, OCT and automated perimetry—in traumatic brain injury. These assessments can reveal clinically relevant visual dysfunction even when neuroimaging appears unremarkable. Accordingly, clinicians should consider perimetry and OCT as part of the evaluation of patients presenting with cranial nerve palsy or visual complaints after head trauma.[4,5] Early identification of field defects may improve patient counseling, prognostication, and long-term rehabilitation planning. Conclusion Perimetry and OCT are valuable tools for detecting post-traumatic visual pathway injury when standard imaging appears normal. Their use should be considered in patients with cranial nerve palsy or visual complaints after head trauma to aid early diagnosis and management. Authors’ contributions 1. Dr Nishkarsh Bansal – concept, design, definition of intellectual content, literature search, data acquisition, and manuscript preparation. 2. Dr Swathi M – interpretation of imaging and investigations, manuscript editing, manuscript review, and overall supervision. 3. Dr Sudha Menon – patient management, data acquisition, manuscript editing, and manuscript review. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship: Nil. Conflicts of interest: There are no conflicts of interest.