Homonymous hemianopia and vision loss progress after gunshot wound, decompressive craniectomy

Early intervention and rehabilitation are crucial for recovery from traumatic neurologic injury.

We report a 23-year-old woman with right homonymous hemianopia and incomplete left inferior quadrantanopia and paracentral scotoma secondary to head trauma from a gunshot wound. The patient underwent decompressive craniectomy to relieve intracranial pressure with preservation of the bone flap in the abdominal cavity. This case demonstrates the complexity of managing ocular manifestations and cerebral swelling following trauma.

Traumatic brain injury is a common cause of homonymous hemianopia and is the causative etiology in more than 10% of such visual field deficits. It is more common for patients with traumatic brain injury to have multiple visual field defects in addition to diffuse cerebral damage and neurological defects. Early intervention is important to provide the highest likelihood of spontaneous recovery. For patients with traumatic neurologic injury, decompressive craniectomy is a life-saving procedure that in some cases may also maximize success with rehabilitation. Our patient presented with worsening visual defects 3 months after her trauma, which demonstrates the complexity of treating traumatic brain injury from both a neurologic and ophthalmologic perspective.

Patient case presentation

A 23-year-old woman presented to an ophthalmic practice in Kansas City, Mo., with a chief complaint of sudden loss of vision and associated symptoms of speech impairment and dizziness.

Three months prior, the patient suffered a gunshot wound to the back of the head. Due to severe intracranial swelling, part of the patient’s skull cap was removed and temporarily surgically implanted into her abdomen to be restored several months later after the risk of herniation decreased.

The patient was told to expect visual field loss as a result of the incident. She reported peripheral loss in addition to loss of vision in the top half of her right visual field.

The patient’s ocular history was unremarkable, with no surgeries or prior trauma. She was not taking any eye medications at the time of presentation but was prescribed Vicodin (hydrocodone, Abbott Laboratories), Prozac (fluoxetine hydrochloride, Eli Lilly), Symbicort (budesonide/formoterol fumarate dihydrate, AstraZeneca) and Proair HFA (albuterol sulfate, Teva Respiratory). Medical history was significant for depression. Family history was unremarkable, and social history was negative for smoking, illicit drugs and alcohol. Review of systems was likewise unremarkable.

Visual field analysis of the patient’s left and right eyes on 1/11/11 revealing an incomplete quadrantanopia and a right homonymous hemianopia.
Visual field analysis of the patient’s left and right eyes on 1/11/11 revealing an incomplete quadrantanopia and a right homonymous hemianopia.
Images: Silverstein SM, Rice GD, Silverstein DW
Visual field analysis on 4/8/11 revealing worsening visual fields.
Visual field analysis on 4/8/11 revealing worsening visual fields.

Visual acuity without correction on initial examination measured 20/40 in the right eye and 20/40 in the left eye with a modest myopic astigmatic correction. IOP was normal, measuring 17 mm Hg bilaterally via Goldmann applanation tonometry at 2:43 p.m. Motility was full and normal, and all aspects of the anterior segment and dilated funduscopic examination were within normal limits. There was no afferent pupillary defect. Visual field testing demonstrated a right homonymous hemianopia with incomplete left inferior quadrantanopia and paracentral scotoma in both eyes.

Three months after the initial visit, the patient presented with worsening visual fields, papilledema of the optic nerves and headaches. Visual acuity without correction measured 20/60 in the right eye and 20/50 in the left eye. A shunt was recommended to relieve intracranial pressure.

Discussion

This case presents important aspects of the ocular manifestations and management of the long-term treatment for traumatic neuro-ophthalmic injury. The pattern of symptoms seen in this patient is consistent with a gunshot wound to the occipital lobe. Two-thirds of patients with traumatic neurologic injury show no improvement or worsening symptoms after 3 months. Despite decompressive craniectomy, our patient reported decreased field of vision and worsening neurologic symptoms over the subsequent months, suggesting diffuse injury.

Decompressive craniectomy is a relatively common procedure in patients with neurologic trauma. The purpose of this life-saving procedure is to prevent further neurologic damage due to swelling and to improve the chances of recovery. The benefits of the procedure must be weighed against the risks, because 60% of patients who undergo decompressive craniectomy develop complications. These complications range from transient defects to life-threatening hydrocephalus. The most common complication is the “syndrome of the trephined,” which is a spectrum of worsening neurologic and cognitive defects usually occurring weeks to months after the procedure.

The bone flap produced in the procedure can be preserved ex vivo or in a number of in vivo locations, such as a subgaleal pocket or abdominal flap. Preserving the bone flap in vivo is a cost-effective way to preserve the bone flap and keep it sterile until the risk of damage due to swelling has decreased and the flap can be re-implanted. In this case, the segment of skull was preserved in an abdominal flap, a method that has become less preferred to preservation in a subgaleal pocket.

The right homonymous hemianopia with incomplete left inferior quadrant-anopia and paracentral scotoma seen in this case is a common manifestation of occipital lobe trauma. These visual field defects worsened dramatically in our patient. The symptoms have severely affected the patient’s quality of life, have caused a deep depression and have prevented her from driving.

The long-term prognosis for homonymous hemianopia is guarded, with 60% of patients showing improvement within the first 2 weeks, decreasing to 20% showing improvement after 1 to 2 months. Our patient followed this timeline of worsening symptomatology despite early intervention. Early intervention and rehabilitation are the most important factors in recovery from neurologic and ophthalmologic symptoms after traumatic injury.

Conclusion

This case illustrates the devolving nature of neurologic injury and how the ophthalmologic symptoms in these patients can be progressive and negatively affect the patient’s quality of life. Early intervention and rehabilitation are crucial in cases of traumatic neurologic injury. Interventions such as decompressive craniectomy save many lives but have a high rate of complications, and it is important to weigh the benefit-to-risk ratio. Our patient’s worsening neurologic and ophthalmologic symptoms could be caused by an initial diffuse injury or may have resulted from the decompressive craniectomy. Early rehabilitation is especially important for the ophthalmologic manifestations because spontaneous recovery from a homonymous hemianopia is rare after 3 months.

References:

  • Bruce BB, Zhang X, Kedar S, Newman NJ, Biousse V. Traumatic homonymous hemianopia. J Neurol Neurosurg Psychiatry. 2006;77(8):986-988.
  • Krishnan P, Bhattacharyya AK, Sil K, De R. Bone flap preservation after decompressive craniectomy — experience with 55 cases. Neurol India. 2006;54(3):291-292.
  • Stephens FL, Mossop CM, Bell RS, et al. Cranioplasty complications following wartime decompressive craniectomy. Neurosurg Focus. 2010;28(5):E3.
  • Stiver SI. Complications of decompressive craniectomy for traumatic brain injury. Neurosurg Focus. 2009;26(6):E7.
  • Wick J, Wade J, Rohrer D, O’Neill O. Use of decompressive craniectomy after severe head trauma. AORN J. 1999;69(3):517-525, 527, 529.
  • Zhang X, Kedar S, Lynn MJ, Newman NJ, Biousse V. Natural history of homonymous hemianopia. Neurology. 2006;28;66(6):901-905.

  • Steven M. Silverstein, MD, FACS, can be reached at Silverstein Eye Centers, 4240 Blue Ridge Blvd., Suite 1000, Kansas City, MO 64133. 816-358-3600; email: ssilverstein@silversteineyecenters.com.
  • Disclosure: Dr. Silverstein has no relevant financial disclosures.

We report a 23-year-old woman with right homonymous hemianopia and incomplete left inferior quadrantanopia and paracentral scotoma secondary to head trauma from a gunshot wound. The patient underwent decompressive craniectomy to relieve intracranial pressure with preservation of the bone flap in the abdominal cavity. This case demonstrates the complexity of managing ocular manifestations and cerebral swelling following trauma.

Traumatic brain injury is a common cause of homonymous hemianopia and is the causative etiology in more than 10% of such visual field deficits. It is more common for patients with traumatic brain injury to have multiple visual field defects in addition to diffuse cerebral damage and neurological defects. Early intervention is important to provide the highest likelihood of spontaneous recovery. For patients with traumatic neurologic injury, decompressive craniectomy is a life-saving procedure that in some cases may also maximize success with rehabilitation. Our patient presented with worsening visual defects 3 months after her trauma, which demonstrates the complexity of treating traumatic brain injury from both a neurologic and ophthalmologic perspective.

Patient case presentation

A 23-year-old woman presented to an ophthalmic practice in Kansas City, Mo., with a chief complaint of sudden loss of vision and associated symptoms of speech impairment and dizziness.

Three months prior, the patient suffered a gunshot wound to the back of the head. Due to severe intracranial swelling, part of the patient’s skull cap was removed and temporarily surgically implanted into her abdomen to be restored several months later after the risk of herniation decreased.

The patient was told to expect visual field loss as a result of the incident. She reported peripheral loss in addition to loss of vision in the top half of her right visual field.

The patient’s ocular history was unremarkable, with no surgeries or prior trauma. She was not taking any eye medications at the time of presentation but was prescribed Vicodin (hydrocodone, Abbott Laboratories), Prozac (fluoxetine hydrochloride, Eli Lilly), Symbicort (budesonide/formoterol fumarate dihydrate, AstraZeneca) and Proair HFA (albuterol sulfate, Teva Respiratory). Medical history was significant for depression. Family history was unremarkable, and social history was negative for smoking, illicit drugs and alcohol. Review of systems was likewise unremarkable.

Visual field analysis of the patient’s left and right eyes on 1/11/11 revealing an incomplete quadrantanopia and a right homonymous hemianopia.
Visual field analysis of the patient’s left and right eyes on 1/11/11 revealing an incomplete quadrantanopia and a right homonymous hemianopia.
Images: Silverstein SM, Rice GD, Silverstein DW
Visual field analysis on 4/8/11 revealing worsening visual fields.
Visual field analysis on 4/8/11 revealing worsening visual fields.

Visual acuity without correction on initial examination measured 20/40 in the right eye and 20/40 in the left eye with a modest myopic astigmatic correction. IOP was normal, measuring 17 mm Hg bilaterally via Goldmann applanation tonometry at 2:43 p.m. Motility was full and normal, and all aspects of the anterior segment and dilated funduscopic examination were within normal limits. There was no afferent pupillary defect. Visual field testing demonstrated a right homonymous hemianopia with incomplete left inferior quadrantanopia and paracentral scotoma in both eyes.

Three months after the initial visit, the patient presented with worsening visual fields, papilledema of the optic nerves and headaches. Visual acuity without correction measured 20/60 in the right eye and 20/50 in the left eye. A shunt was recommended to relieve intracranial pressure.

Discussion

This case presents important aspects of the ocular manifestations and management of the long-term treatment for traumatic neuro-ophthalmic injury. The pattern of symptoms seen in this patient is consistent with a gunshot wound to the occipital lobe. Two-thirds of patients with traumatic neurologic injury show no improvement or worsening symptoms after 3 months. Despite decompressive craniectomy, our patient reported decreased field of vision and worsening neurologic symptoms over the subsequent months, suggesting diffuse injury.

Decompressive craniectomy is a relatively common procedure in patients with neurologic trauma. The purpose of this life-saving procedure is to prevent further neurologic damage due to swelling and to improve the chances of recovery. The benefits of the procedure must be weighed against the risks, because 60% of patients who undergo decompressive craniectomy develop complications. These complications range from transient defects to life-threatening hydrocephalus. The most common complication is the “syndrome of the trephined,” which is a spectrum of worsening neurologic and cognitive defects usually occurring weeks to months after the procedure.

The bone flap produced in the procedure can be preserved ex vivo or in a number of in vivo locations, such as a subgaleal pocket or abdominal flap. Preserving the bone flap in vivo is a cost-effective way to preserve the bone flap and keep it sterile until the risk of damage due to swelling has decreased and the flap can be re-implanted. In this case, the segment of skull was preserved in an abdominal flap, a method that has become less preferred to preservation in a subgaleal pocket.

The right homonymous hemianopia with incomplete left inferior quadrant-anopia and paracentral scotoma seen in this case is a common manifestation of occipital lobe trauma. These visual field defects worsened dramatically in our patient. The symptoms have severely affected the patient’s quality of life, have caused a deep depression and have prevented her from driving.

The long-term prognosis for homonymous hemianopia is guarded, with 60% of patients showing improvement within the first 2 weeks, decreasing to 20% showing improvement after 1 to 2 months. Our patient followed this timeline of worsening symptomatology despite early intervention. Early intervention and rehabilitation are the most important factors in recovery from neurologic and ophthalmologic symptoms after traumatic injury.

Conclusion

This case illustrates the devolving nature of neurologic injury and how the ophthalmologic symptoms in these patients can be progressive and negatively affect the patient’s quality of life. Early intervention and rehabilitation are crucial in cases of traumatic neurologic injury. Interventions such as decompressive craniectomy save many lives but have a high rate of complications, and it is important to weigh the benefit-to-risk ratio. Our patient’s worsening neurologic and ophthalmologic symptoms could be caused by an initial diffuse injury or may have resulted from the decompressive craniectomy. Early rehabilitation is especially important for the ophthalmologic manifestations because spontaneous recovery from a homonymous hemianopia is rare after 3 months.

References:

  • Bruce BB, Zhang X, Kedar S, Newman NJ, Biousse V. Traumatic homonymous hemianopia. J Neurol Neurosurg Psychiatry. 2006;77(8):986-988.
  • Krishnan P, Bhattacharyya AK, Sil K, De R. Bone flap preservation after decompressive craniectomy — experience with 55 cases. Neurol India. 2006;54(3):291-292.
  • Stephens FL, Mossop CM, Bell RS, et al. Cranioplasty complications following wartime decompressive craniectomy. Neurosurg Focus. 2010;28(5):E3.
  • Stiver SI. Complications of decompressive craniectomy for traumatic brain injury. Neurosurg Focus. 2009;26(6):E7.
  • Wick J, Wade J, Rohrer D, O’Neill O. Use of decompressive craniectomy after severe head trauma. AORN J. 1999;69(3):517-525, 527, 529.
  • Zhang X, Kedar S, Lynn MJ, Newman NJ, Biousse V. Natural history of homonymous hemianopia. Neurology. 2006;28;66(6):901-905.

  • Steven M. Silverstein, MD, FACS, can be reached at Silverstein Eye Centers, 4240 Blue Ridge Blvd., Suite 1000, Kansas City, MO 64133. 816-358-3600; email: ssilverstein@silversteineyecenters.com.
  • Disclosure: Dr. Silverstein has no relevant financial disclosures.