Traumatic chiasmal syndrome: A meta-analysis.

PURPOSE: To report a case presenting with bitemporal hemianopia due to traumatic chiasmal syndrome after head injury, and to compare the findings with individual case reports published in the literature.
METHODS: A detailed search was made in PubMed, MedIND, Taylor and Francis online and Wiley online library databases for individual case reports of traumatic chiasmal syndrome. All the case reports were read in full and the findings summarized in a table, which included details of the case who presented with bitemporal hemianopia as an index case.
RESULTS: All published cases of traumatic chiasmal syndrome appear to share some common features, such as injury to the frontal bone and fracture of the anterior skull base. Bitemporal hemianopia and visual acuity have a variable presentation, and do not appear to correlate with severity of injury. Isolated bitemporal hemianopia is rare and clinical improvement may or may not occur. CONCLUSIONS AND IMPORTANCE: Traumatic chiasmal syndrome should be considered as a differential diagnosis in patients presenting with bitemporal hemianopia after head injury causing frontal and anterior skull base fracture.

Introduction

Bitemporal hemianopia is a hallmark of optic chiasmal injury, because of the peculiar arrangement of the fibres of the optic nerves; various lesions, including tumour, inflammation, demyelination, ischemia and infiltration, can affect the optic chiasma. Traumatic chiasmal syndrome, which occurs due to an injury at the level of crossing fibres in the optic chiasma following trauma to the head, is characterised by bitemporal hemianopia or scotomata. Traumatic chiasmal syndrome is a rare occurrence, since only severe impact will damage the anatomically-privileged chiasma, and it is difficult to survive such an impact. The first case of traumatic chiasmal syndrome was reported by Nieden in 1883; several cases have since been reported. The current brief report describes a patient who presented with traumatic chiasmal syndrome, and compares the findings observed with those of individual cases reported in the literature.

Material and methods

A patient presenting with traumatic chiasmal syndrome was investigated and a systematic literature search was performed in the PubMed, MedIND, Taylor and Francis online and Wiley online library databases using the search term: “traumatic chiasmal syndrome” and “chiasmal injury”. Only individual case reports of traumatic chiasmal syndrome were selected to be included in this report, and all the case reports were read in full. Case reports with no follow-up findings were excluded. A table was prepared to provide an overview and to compare the salient aspects of the published case reports with the case being presented in this report.

Results

A total of 9 case reports were selected; the salient findings in these 9 cases are summarized in Table 1, in addition to details of our case.

Table 1

Salient features of individual case reports of traumatic chiasmal syndrome published in the literature and of the case described in the current brief report.

Sr. no.	Case reported by	Age	Sex	Mode of injury	Visual acuity	Visual field defect	Other deficits	CT/X- ray Findings	MRI findings	Outcome
1	Index case of the current report	39	M	Motorcycle accident	RE 6/6, LE 6/12	Bitemporal hemianopia (Fig. 1)	Anosmia, CSF rhinorrhea	CT: Comminuted frontal and anterior skull base fractures, bilateral frontal lobe hemorrhagic contusions and multiple frontal aeroceles	Normal optic chiasma (Fig. 2)	Vision improved to 6/9 in LE, Visual fields improved in both eyes (Fig. 3)
2.	Dutta et al.2	25	M	Closed head injury	RE 6/12, LE 6/60	Bitemporal hemianopia	Intermittent CSF rhinorrhea	CT: Orbital roof and basi sphenoid fracture	Frontal gyrus rectus herniation in sphenoid sinus with chiasmal edema	Marginal visual improvement
3.	Hughes et al.3	45	M	Road accident	BE 6/9	Complete bitemporal hemianopia	Bilateral anosmia, complete facial paralysis on the right with loss of taste and mild left hemiparesis	X- ray: Fracture of frontal bone		No improvement
4.	Hughes et al.4	31	M	Head on motor crash	RE 6/18, LE 1/60	RE – upper temporal quadrant defectLE – upper nasal island of vision only	3rd nerve paresis	X- ray: Fissured fracturein the left frontal bone, traversing the left frontal sinus, also involving left anterior and middle fossa		Significant improvement
5.	Logan et al.5	33	M	Road accident	RE 6/9,LE Counting fingers	Bitemporal hemianopia	CSF rhinorrhea, bilateral anosmia,LE limitation of ocular movements except lateral movements	Multiple frontal fracture, anterior fossa fracture involving sphenoid and ethmoid air sinus		No improvement
6.	Mohindra et al.6	17	M	Accidental fall	RE 6/60, LE 6/9	Bitemporal hemianopia	None reported	CT: Speck of air at interpeduncular and chiasmatic cistern	Isolated contusion of optic chiasma	No improvement
7.	Resneck et al.7	50	M	Automobile accident	BE 6/6	Bitemporal hemianopia	Absence of olfactory functions	X- ray: Fracture of right superior orbitCT: Pneumocephalus and fracture of sella turcica		No improvement
8.	Tang et al.8	17	M	Motor cycle accident	BE 20/25	Bitemporal hemianopia	Diplopia with exophoria, diabetes insipidus, decreased thyroid stimulating hormone and testosterone levels	Multiple facial and skull fractures, including fracture of lesser wing of the sphenoid	Hemorrhagic contusion of the frontal lobes, mild swelling on the left side of the optic chiasm	No change
9.	Vora et al.9	26	M	Motor vehicle accident	RE 6/6, LE 6/36	Complete bitemporal hemianopia	CSF rhinorrhea	Midline frontal bone fracture, basi sphenoid fracture, intraparenchymal hematoma in left frontal region	Central chiasmal contusion with thinning of nasal fibres	Vision improved to 6/6 both eyes but no improvement in fields
10.	Yazici et al.10	20	M	Motor vehicle accident	BE 20/20	Bitemporal hemianopia	Exotropia with RE fixation.	Fracture frontal, ethmoid and maxillary, fracture in the sellar region of sphenoid bone, air in the orbit and cranium	Thinning, shape deformity in the optic chiasm	No change in visual fields

Abbreviations:RE = right eye; LE = left eye; BE = both eyes; M = male; CT = computed tomography; MRI = magnetic resonance imaging; CSF = cerebrospinal fluid.

An analysis of the clinical details revealed that eight out of 10 cases had injury due to road accident while riding a motor vehicle, while one had closed head injury when the bus he was travelling in was targeted by a bomb and one had an accidental fall. The visual acuity after trauma ranged from normal to counting fingers. The extent of field defect, bitemporal hemianopia, was uncertain, being either complete or incomplete, with or without macular splitting. An analysis of the radiological reports revealed that all the cases had fracture of the frontal bone, along with the involvement of the anterior base of the skull. Magnetic resonance imaging (MRI) details were provided in five case reports, which showed some abnormality in the chiasma; the MRI report of the case being presented here did not reveal any chiasmal damage. Out of 10 cases, six did not show any improvement in the visual manifestations. Only one case presented with isolated bitemporal hemianopia, while the other cases had other accompanying manifestations, such as cerebrospinal fluid rhinorrhea, anosmia, 3rd nerve palsy and extraocular muscle injury.

Automated 30–2 analysis of both eyes at the first visit revealed temporal field defects, complete in the left eye and incomplete in the right eye.

Magnetic resonance imaging (left – sagittal section; right – coronary section) of the head three months after surgery. Areas of gliosis in the frontal region are seen, while the sella turcica, pituitary and optic chiasma appear normal (red circle). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Automated 30–2 fields on review, showing slight improvement in both eyes.

In our case, it is not clear why visual loss was gradually progressive. In previously reported cases, it appears that the onset of the visual loss was shortly after the trauma, and there was no progression several months thereafter, unlike the observation in our case.

Discussion

The optic chiasma is a structure located along the visual pathway at the point where the optic nerves of the right eye and left eye join each other. The nasal fibres of the retina decussate at the optic chiasma. It is the arrangement of the fibres at the chiasma that accounts for the typical visual field defects seen when a lesion occurs at the site. The most common field defect observed in patients with optic chiasmal injury is bitemporal hemianopia, although the field loss can be of varying degrees, as seen in this report. Traumatic chiasmal syndrome is a rare entity; in fact, the patient being described is the first such case documented among patients with trauma to the head who have been examined and treated at our institution.

In a study by Mejico et al., the most frequent cause of bitemporal hemianopia was found to be pituitary adenoma. A bitemporal field defect due to optic chiasmal damage after head injury occurs in 0.3% of cases. The field defect that develops after traumatic chiasmal syndrome is variable, and can manifest as either complete monocular blindness or incomplete subtle scotomas which may or may not involve the macula, suggesting that there is no specific pattern of field defects, as seen in this report. Traumatic chiasmal syndrome is usually seen following a fracture of the frontal bone along with multiple cranial fractures., Similar observations were made in the case being presented in the current report.

Two main types of head injury have been described, namely, contact injury and acceleration/deceleration injury. A contact injury is produced by direct impact, while acceleration/deceleration injury occurs following violent motion of the head, which results in subdural haemorrhage and diffuse axonal injury. Following trauma, the axons either undergo primary axotomy, which implies complete transection of the nerve due to mechanical shearing, or secondary axotomy, which implies slow degeneration of the nervous tissue.

It was previously believed that the principal mechanism involved in chiasmal injury following trauma to the head involved tearing of the crossing fibres due to mechanical stretching of the chiasma. However, Traquair et al. suggested that the pial vessel, which supplies the chiasma, undergoes tearing due to stretching, resulting in the functional impairment of the optic chiasma. Hughes et al., who were unable to detect any anatomical disruption of the chiasma itself, opined that the damage was probably due to compromised blood supply to the central area of the chiasma, thus substantiating the theory suggested by Traquair et al. However, the chiasma is known to be richly supplied by anastomoses between branches of the anterior communicating artery with the chiasmal artery, anterior cerebral artery, internal carotid artery, posterior communicating artery, anterior choroidal artery, middle cerebral artery and prechiasmal arcade; hence, the vascular theory for chiasmal damage may not completely explain why the lesion occurs. Hassan et al., in their case report, opined that the mechanism of the injury to the optic chiasma following trauma to the head may vary from individual to individual, being due to one or more of the following: i) mechanical stretch or mechanical tear; ii) contusion haemorrhage; iii) contusion necrosis; and iv) compression necrosis., The most likely pathologic mechanism for traumatic optic chiasmal injury is contusion necrosis or avulsion. In contusion necrosis, there is disruption of axonal transport, followed by breakdown of the axonal cell membrane after several hours. The reason for the involvement of only the decussating fibres, and sparing of the other fibres, remains unclear.

Very rarely, isolated (without accompanying manifestations) bitemporal hemianopia is seen in patients with traumatic chiasmal syndrome, as seen in only one previous case report. Other possible manifestations of traumatic chiasmal syndrome, some of which have been described in the case reports analyzed here, include first cranial nerve palsy, third cranial nerve palsy, fourth cranial nerve palsy, fifth cranial nerve palsy, sixth cranial nerve palsy, seventh cranial nerve palsy, eight cranial nerve palsy, cerebrospinal fluid rhinorrhea, carotid cavernous fistula, carotid aneurysm, panhypopituitarism, diabetes insipidus, meningitis, intrasellar hematoma and pneumatocele.

Savino et al., in their study on 11 patients with traumatic chiasmal syndrome, opined that the severity of visual field defect does not necessarily correlate with the severity of the head injury or associated neurological deficits. The loss of visual field seldom improves; it either remains stationary or may worsen. Out of 10 cases listed in Table 1, six cases did not show any improvement in the visual fields. However, some cases might show improvement in the visual acuity and visual field, as seen in three of the case reports,, and in the index case. Also, Anderson et al. reported a case which showed improvement in the visual field. The exact cause for this improvement cannot be ascertained; however, if the mechanism of injury had been due to vascular compromise, then re-establishment over time of vascular channels or development of new anastomoses between the arteries supplying the chiasma might have improved the functionality of the optic chiasma.

The investigation of choice for traumatic chiasmal syndrome is magnetic resonance imaging. However, as seen in the case being presented in the current report, the MRI may not show any anatomical abnormality of the chiasma that could explain the bitemporal field defect. Hence, it is not always necessary to perform MRI unless there are other neurological deficits. Ostri et al., in their case report, concluded that measurement of the retinal nerve fibre layer thickness by optical coherence tomography can be an effective, non-invasive tool in diagnosing an optic chiasmal lesion. Due to the paucity of cases being reported, management guidelines for traumatic chiasmal syndrome are yet to be established. The mecobalamin capsules which were prescribed to the index case in this report may not have contributed to the improvement of the visual acuity and visual fields, as its role in human subjects is inconclusive. Patients should be followed up regularly to check for any new neurological signs or symptoms other than involvement of the optic pathway.

To summarize, traumatic chiasmal syndrome should be suspected in a patient with bitemporal hemianopia occurring after trauma to the frontal bone associated with anterior skull base fracture, with or without other accompanying manifestations.

Conclusion

Although traumatic chiasmal syndrome is rare, it is important to identify this entity when it does occur; it should be considered as a differential diagnosis in a patient with bitemporal field loss after head trauma. Thus, unnecessary neurological diagnostic and investigative procedures can be avoided in such patients.

Patient consent

Consent to publish the case report was not obtained, because this case report does not contain any personal information that could lead to the identification of the patient.

Acknowledgments and disclosures

Funding

No funding or grant support.

Conflicts of interest

The following authors have no financial disclosures: VML, PAT, AAH.

Authorship

All authors attest that they meet the current ICMJE criteria for Authorship.