The role of cerebral ptosis in assessing recovery and prognosis in traumatic brain injury: a case report

Introduction

Cerebral ptosis is a rare condition where the eyelid droops due to brain issues, rather than muscle or nerve damage. This form of ptosis is linked to dysfunctions in parts of the brain like the cerebral cortex, thalamus, or brainstem, which indirectly control eyelid movement (1). It results from disruptions in the brain’s control of eyelid movement (1,2). Causes include strokes, tumors, or brain injuries. Diagnosis typically requires neuroimaging to identify brain lesions, and treatment focuses on managing the underlying brain condition, rather than correcting the eyelid directly.

A multidisciplinary approach involving neurologists, ophthalmologists, and neurosurgeons is often necessary for the diagnosis, monitoring, and treatment of cerebral ptosis, as it can offer important clues to the location and progression of brain damage. This collaboration helps distinguish cerebral ptosis from peripheral causes (such as cranial nerve III palsy or myasthenia gravis) and ensures appropriate management based on the underlying neurological condition (1,2). We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-24-243/rc).

Case presentation

We present a case involving a 46-year-old man admitted to the Neurorehabilitation Unit following a severe traumatic brain injury (TBI) due to an accidental fall at home. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal. Two months earlier, the patient had sustained a head injury resulting in an acute epidural hematoma on the left side, leading to a coma characterized by bilateral mydriasis and decerebrate posturing. He underwent emergency surgery to evacuate the hematoma, followed by a tracheostomy. After surgery, he remained in a comatose state, and was transferred to our unit for rehabilitation. Upon admission, his condition included occasional right eye opening and signs of a left third cranial nerve deficit. His responses were minimal, characterized by limb flexion, and he was breathing on his own through a tracheostomy tube. Initial computed tomography (CT) scans showed a reduction in brain swelling and signs of ex vacuo dilation, indicating brain tissue loss. A magnetic resonance imaging (MRI) performed later revealed areas of gliosis and necrosis in the left temporal and occipito-parietal regions and the right cerebral peduncle (Figure 1), reflecting widespread bilateral brain damage. Functional evaluations showed that brainstem auditory responses were normal, but cortical sensory responses were significantly reduced on the left side, suggesting an imbalance between brainstem and higher cortical processing. During the early stages of speech therapy, the patient was unresponsive, with eyes closed, sporadic swallowing, and a primitive sucking reflex, indicating severe brain dysfunction. A detailed neuro-ophthalmologic exam was performed to assess extraocular muscle function and exclude myogenic causes. MRI findings specifically supported a neurogenic origin of the ptosis rather than a direct muscle impairment.

Figure 1 Gliosis and necrosis in the left temporal and occipito-parietal regions and the right cerebral peduncle.

Over the following month, however, we observed gradual improvement. Somatosensory evoked potentials (SEPs) showed an N20 latency of 21 ms, as illustrated in Figure 2. The N20 wave, which reflects cortical somatosensory processing, indicated preserved but delayed conduction along the somatosensory pathways. This finding supported the presence of residual cortical activity and was consistent with the patient’s emerging signs of awareness. Upon admission, the patient exhibited occasional, reflexive right eye opening without voluntary control. However, over the following month, he demonstrated increasingly consistent and purposeful control of his right eyelid, including the ability to initiate and sustain eye opening in response to external stimuli. This improvement coincided with the partial recovery of the blink reflex and right eye movement, suggesting enhanced neural control and an evolving transition from reflexive to intentional motor function. These changes supported the initial neurological recovery observed in the patient, aligning with his shift from a vegetative state to a minimally conscious state (MCS). He began responding to simple commands by blinking his eyelids (once for “yes” and twice for “no”) and started following videos on a smartphone with his gaze, signaling a partial return of awareness and a shift from a vegetative state to an MCS. As the patient’s condition evolved towards MCS, the transition from bilateral to unilateral ptosis appeared to reflect improving neural control and asymmetrical brain recovery. This shift in ptosis became a critical marker of his neurological status, indicating the brain’s ongoing attempts to reorganize and heal. Notably, the patient’s neurological improvement, including the regained control of his right eyelid and transition to an MCS, occurred in the absence of pharmacological intervention. This suggests that the observed recovery was primarily driven by spontaneous neural reorganization during intensive neurorehabilitation.

Figure 2 Somatosensory evoked potentials recorded for the median nerve in both arms, displaying latencies (N9, N11, N13, N20, P25) and central conduction times. The table and graphs show cortical and cervical responses, aiding in evaluating neural pathway integrity.

Discussion

As seen in this case, the transition from bilateral to unilateral ptosis coincided with broader neurological and functional improvements. Alongside this shift, the patient began responding to simple commands by blinking (once for “yes”, twice for “no”), demonstrating an emerging ability to communicate. Additionally, he regained partial control of his right eyelid, exhibited recovery of the blink reflex, and showed increased right eye movement, allowing limited visual interaction with his environment. These changes were accompanied by improvements in gaze fixation and tracking, as the patient started following videos on a smartphone with his eyes. The combined improvements suggest a gradual recovery, consistent with the transition from a vegetative state to an MCS. These findings seem to reinforce the role of cerebral ptosis as a dynamic neurological marker, reflecting ongoing neural reorganization. So, cerebral ptosis serves as a key clinical marker in assessing severe brain injuries, providing insights into both the extent of neurological damage and the potential for recovery (3). Observations in TBI patients have shown that a shift from bilateral to unilateral ptosis, as patients progress from a vegetative state to an MCS, suggests neural reorganization and partial restoration of motor and arousal pathways (4). This change can be seen as a positive sign, indicating the brain’s gradual, albeit uneven, reestablishment of motor control. This transition from bilateral to unilateral ptosis has not been extensively studied as a marker of neural recovery in TBI patients. However, related research on pupillary responses, oculomotor dysfunction, and eyelid abnormalities in neurological disorders suggests that changes in eyelid function can serve as indicators of neural reorganization and functional recovery. Previous studies have highlighted the role of visual fixation and eye movement patterns in predicting neurological improvement, reinforcing the idea that eyelid control could be part of a broader recovery trajectory. Recent literature suggests that monitoring patients in both established and innovative ways can reinforce early prediction of potential transitions from a vegetative state to a MCS, which is critical. (4).

Ptosis often reveals specific brain dysfunctions that may not be immediately apparent through standard exams. A classic example is ptosis in Weber’s syndrome, which results from a midbrain stroke affecting the cranial nerve III and the cerebral peduncle. Recognizing cerebral ptosis as a sign of brain involvement helps identify areas of injury, informing treatment decisions. Additionally, cerebral ptosis may indicate complications such as increased intracranial pressure (ICP) or brainstem compression, factors that significantly influence prognosis and management approaches. Differentiating cerebral ptosis from other forms of ptosis requires a meticulous clinical approach, utilizing patient history, targeted neuroimaging, and functional testing to exclude peripheral causes (1-4).

In patients with TBI, eye ptosis can act as a significant prognostic indicator. While studies directly linking ptosis to prognosis are limited, previous research has demonstrated that alterations in pupillary responses and ocular motor functions are correlated with neurological outcomes in TBI patients. In particular, pupillary light reflex abnormalities have been associated with brainstem oxygenation and perfusion, suggesting that changes in pupil reactivity can serve as indicators of neurological dysfunction and have prognostic value. Additionally, the Neurological Pupil Index (NPi), an objective measure of pupillary reactivity assessed through automated pupillometry, has been linked to poorer outcomes in neurocritical care patients when values fall below 3. Ocular signs observed in patients with abnormal posturing, such as decerebrate or decorticate postures, further reflect the severity of neurological impairment and are associated with worse prognosis. Although ptosis has not been extensively studied as an independent prognostic marker, the relationship between ocular motor function and neurological outcomes suggests that changes in eyelid position may potentially reflect processes of neurological recovery or deterioration (5). Research underscores the importance of eye movement and fixation in assessing recovery trajectories in TBI patients (5). The presence of visual fixation within 24 hours of intensive care unit (ICU) admission has shown a correlation with improved functional outcomes, even outperforming traditional measures like the Glasgow Coma Scale (GCS) (6). Abnormalities in the pupillary light reflex, measured through quantitative pupillometry, are also linked to neurological decline, with a specificity of 91.67% for predicting deterioration. Such changes in pupil reactivity can signal neurologic decline, often preceding the onset of increased ICP (7). Although optic nerve sheath diameter (ONSD) measurements via CT scans have been associated with TBI severity, they do not consistently correlate with GCS scores, suggesting that while informative, ONSD alone may not directly predict outcomes related to eye function (8,9).

While eye ptosis can indicate severe underlying conditions, its predictive value varies based on the specific TBI context and accompanying neurological assessments. Following a TBI, eye ptosis can signal underlying brain injuries, especially when involving the brainstem, cranial nerves or extraocular muscles (i.e., edema) (10). However, its predictive accuracy for outcomes depends on the type of TBI and related neurological evaluations. Studies have demonstrated the critical role of neuroimaging, particularly MRI, in assessing brain injury severity in TBI patients. MRI can reveal underlying lesions, ischemia, or brainstem injuries contributing to ptosis and other neurological symptoms (11). Contrast enhancement of the oculomotor nerve on MRI may be observed in cases of ischemic isolated ptosis (12), and neurogenic ptosis can improve with treatment of the underlying cause (13). In pediatric TBI cases, MRI measures, including contusion volume and brainstem injury, have shown significant predictive value for long-term outcomes, particularly when combined with clinical assessments such as pupil reactivity and GCS scores (14,15). This multi-modal approach enhances the accuracy of outcome predictions beyond what clinical metrics alone can provide.

This case underscores the importance of recognizing cerebral ptosis as a dynamic marker of brain recovery in TBI patients. The progression from bilateral to unilateral ptosis mirrors the brain’s ongoing reorganization and highlights the adaptive nature of neural recovery. By closely monitoring these changes, clinicians can gain deeper insights into a patient’s recovery journey, helping to guide rehabilitation and set appropriate expectations for outcomes. Cerebral ptosis, particularly when it evolves from bilateral to unilateral, reflects the complex interplay of brain healing and the critical role of a multidisciplinary approach in optimizing care for patients with disorders of consciousness. Monitoring post-comatose patients is a core activity, and neurological registration (systematic tracking of neurological signs) must always be considered in conjunction with clinical signs. In our patient, the shift from bilateral to unilateral ptosis, combined with MRI findings and SEPs, suggested a sudden qualitative and quantitative improvement in neurorehabilitation. This monitoring provided, for example, the rationale for intensifying the treatment approach by incorporating more specific robotic interventions, such as adding the ArmeoSpring to the Erigo device after a few days, to further support motor recovery.

Conclusions

This case highlights the role of cerebral ptosis as a potential dynamic marker of neurological recovery in TBI patients. The progression from bilateral to unilateral ptosis paralleled broader functional improvements, suggesting neural reorganization. Monitoring these changes provided critical insights that guided rehabilitation strategies. Recognizing cerebral ptosis as part of a broader recovery trajectory may help clinicians optimize neurorehabilitation approaches and improve patient outcomes.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-24-243/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-24-243/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-24-243/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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