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A Case of Persistent Diplopia Postconcussion in a 34-Yr-Old Woman

Probert, Allan MD; Grafton, Lori MD

Author Information
American Journal of Physical Medicine & Rehabilitation: December 2021 - Volume 100 - Issue 12 - p e180-e182
doi: 10.1097/PHM.0000000000001772

CASE REPORT

History and Physical Examination

A 34-yr-old woman presented to our outpatient physiatry clinic for evaluation of persistent headaches 2 mos after a motor vehicle accident in which her stationary vehicle was rear ended at a stoplight. At the time of the accident, the patient did not lose consciousness and sought care at the emergency department immediately afterward. At that time, Glasgow Coma Scale score was 15, and computed tomography without contrast and magnetic resonance imaging of the brain and cervical spine revealed no acute abnormality. She was subsequently discharged with primary care follow-up. Her primary care provider recommended physical therapy and prescribed acetaminophen 650 mg twice daily for pain, which minimally improved symptoms until presentation at the physiatry clinic. Since the accident, she reported worsening intense, pressure-type frontotemporal headaches with radiation to the back of her head, neck, shoulders, and upper back bilaterally. The headaches were nonpositional, and she denied nausea, vomiting, or photophobia. She also reported intermittent double and blurred vision, tinnitus, as well as emotional instability, irritability, and a general feeling of overstimulation. Medical history was significant for C5-C6 disk bulge, obstructive sleep apnea, and endometriosis.

Physical examination revealed an obese female (body mass index = 36 kg/m2), who was intermittently tearful. Head and neck examination was remarkable for convergence insufficiency and nystagmus on rightward end gaze with extraocular movement testing, mildly decreased neck range of motion, and paraspinal cervical muscle tenderness at the level of C6-C7. Cranial nerves II-XII were otherwise normal. Mental status examination revealed that the patient was alert and fully oriented. Recall was 3/3 immediately and 2/3 at 5 mins; she was able to recall the third item with cueing. She was able to spell “world” forward and backward but had some difficulty with serial sevens. Sensory examination revealed decreased sensation to light touch over the fifth digits in both hands. Strength was graded 5/5 in bilateral upper and lower limbs. Reflexes were 2+ diffusely and symmetric. Romberg test was positive.

What is the differential diagnosis for this patient’s headache? Which visual changes are most concerning postconcussion?

Differential Diagnosis and Initial Management

The differential diagnosis of headache is broad and can be divided into primary or secondary causes (Table 1). Regarding primary headaches, the patient’s bilateral, band-like headache with cervical paraspinal muscle tenderness was not supportive of cluster-type or paroxysmal hemicrania headaches but was supportive of tension-type headache. In addition, given the lack of photophobia and aura as well as daily headache occurrence, migraines were also unlikely.1

TABLE 1 - Differential diagnosis of headache
Primary Headache Secondary Headache
Migraine headache
Tension headache
Trigeminal autonomic cephalalgia (cluster headache, paroxysmal hemicrania)
Hemorrhage (subarachnoid or intracerebral hemorrhage and epidural or subdural hematoma)
Stroke (ischemic or hemorrhagic)
Cerebral venous sinus thrombosis
Infection (meningitis, abscess)
Brain tumor
Giant cell arteritis
Idiopathic intracranial hypertension
Trigeminal neuralgia
Chiari I malformation
Posttraumatic headache (migraine, tension, or cervicogenic-type headaches)
Cerebrospinal fluid leak
Drug-related headache

In this stable, subacute-chronic headache, acute causes of secondary headache, such as hemorrhage, cerebral venous sinus thrombosis, meningitis, and stroke could be ruled out. Considering several causes of secondary chronic headaches, age of younger than 50 yrs, recent normal cerebellar tissue on magnetic resonance imaging, nontrigeminal nerve distribution headache, lack of orthostatic headache, and no previous medications could exclude giant cell arteritis, Chiari I malformation, trigeminal neuralgia, cerebrospinal fluid leak, and drug-induced headache, respectively.1

Although bilateral worsening headache associated with visual changes could be concerning for a mass-occupying lesion,1 another cause of secondary headache, this was felt to be unlikely given trauma acutely preceding headache and recent negative neuroimaging.

Posttraumatic headache (PTH) is a common occurrence post–mild traumatic brain injury (mTBI).2 Headache symptoms may be nonspecific in nature or present as migraine, tension, or cervicogenic-type headaches.2 Given that mTBI with resultant PTH may be associated with tinnitus, visual changes (including convergence insufficiency and diplopia), emotional lability, and neurocognitive deficits,1,3,4 all of which the patient had, the headache was felt likely to be primarily a tension-type PTH. In addition, cervical strain injuries commonly occur during rapid acceleration-deceleration and subsequent flexion-extension of the neck,1 as might occur in a rear-ending motor vehicle accident. As the patient reported cervical paraspinal muscle tenderness, myofascial strain likely contributed to a cervicogenic headache.

A myriad of visual disturbances after mTBI may be present including, but not limited to, accommodative dysfunction, photosensitivity, visual field deficits, convergence insufficiency, and version deficits. However, it is important to note that some examination findings, such as pupillary abnormalities, diplopia, progressive vision loss, and ptosis require diagnostic consideration beyond mTBI.4

For several months after injury, her headaches and cervical paraspinal muscle spasms were managed with baclofen, transcutaneous electrical nerve stimulation, and physical therapy, in which cervical muscle stretching provided some relief. A topiramate trial for tension headache prophylaxis did not provide significant relief and was quickly discontinued because of an adverse effect of fatigue. Her diplopia persisted, and the patient was referred to ophthalmology, with ophthalmic examination revealing papilledema.

In a patient with visual changes, papilledema, and headache refractory to medical therapy, what would be the next best step in diagnosis?

Diagnostic Results

In the setting of headache and papilledema, neuroimaging must be done to rule out other secondary causes of elevated intracranial pressure (ICP).1,5 The patient was referred to neurosurgery, and brain magnetic resonance venography was performed, showing stenosis of the bilateral transverse venous sinuses (Fig. 1). In addition, the patient underwent a fluoroscopic-guided low-volume lumbar puncture (LP), which revealed an elevated opening pressure of 34 cm H2O and closing pressure of 20 cm H2O, and the diagnosis of idiopathic intracranial hypertension (IIH) was made.

FIGURE 1
FIGURE 1:
Axial magnetic resonance venography image demonstrating stenosis of the bilateral transverse cerebral venous sinuses. A. Right-sided transverse venous sinus stenosis. B. Left-sided transverse venous sinus stenosis.

What are the next best steps in management of patients both with and without rapidly progressing visual loss in IIH?

Management and Outcome

The patient was subsequently started on acetazolamide 500 mg twice daily, titrated up to 1000 mg twice daily,5 which led to visual symptom but not headache improvement. Because of the low-volume LP not alleviating her headache, it was determined by neurosurgery that a ventriculoperitoneal shunt would likely not provide relief and also be relatively contraindicated because of endometriosis history, leading to a potential route of seeding to the brain. Three months after the initial LP, she underwent a high-volume LP of 40 mL, which provided some relief and revealed opening and closing pressures of 34 cm H2O and 20 cm H2O, respectively. She then underwent a six-vessel diagnostic cerebral angiogram, which revealed bilateral transverse sigmoid junction stenosis, right greater than left, with a right-sided transstenosis pressure gradient of 12 cm H2O. Right-sided cerebral venous sinus stenting was then completed with a poststent gradient of 1 cm H2O. Over the course of a year, ophthalmology felt that her papilledema had resolved and her vision was spared. Currently, she remains clinically well and follows up regularly.

DISCUSSION

From our review, two previous cases in the literature have described IIH diagnoses after mTBI.6,7 Given this rare association, the goal of this case is to highlight the importance of recognizing IIH as a potential cause of visual changes and treatment-refractory headaches in the setting of mTBI. As there may be significant symptomatic overlap between PTH and IIH,1,5 it is unclear whether head trauma directly precipitated the development of IIH or whether IIH developed concurrently in the setting of trauma in this case. Regardless, it is imperative to recognize the possibility of IIH in this setting to prevent the sequela of untreated IIH, permanent vision loss.5

As exemplified by this case, IIH is characterized by symptoms of increased ICP and most commonly occurs in obese adult women of childbearing age.5 In addition, associations have been made with obstructive sleep apnea, polycystic ovarian syndrome, and Addison disease.5,8 Several exogenous substances and medications may also precipitate IIH, including tetracyclines, vitamin A and retinoids, and growth hormone.5,8

The most widely used diagnostic criteria are the modified Dandy criteria,5 in which each of the following must apply: (1) signs and symptoms of elevated ICP, (2) absence of localizing neurologic signs other than possible cranial nerve VI palsy, (3) elevated CSF opening pressure on LP of greater than 25 cm H2O and normal CSF composition, (4) neuroimaging that suggests no other etiology, and (5) no other explanation for elevated ICP. Magnetic resonance venography with contrast is the preferred imaging modality over standard magnetic resonance imaging because of higher sensitivity to detect cerebral venous thrombosis, which may acutely present similarly to IIH.1,5 Neuroimaging should be followed by a diagnostic LP revealing elevated opening pressure.1,5

Goals of treatment in IIH are to eliminate symptoms and to prevent permanent vision loss.5 Treatment may be medical or surgical with an additional focus on weight loss.5 Thought to reduce the rate of CSF production, first-line medical therapy consists of carbonic anhydrase inhibitors, such as acetazolamide.5 The antiseizure medication, topiramate, because of weak carbonic anhydrase inhibitor effect, has also been used.5 In this patient’s case, topiramate was initiated for tension-type headache before suspicion of IIH and may not have provided significant relief because of the weak carbonic anhydrase inhibitor effect in addition to early discontinuation due to adverse effects. Loop diuretics, such as furosemide, may be used as adjunctive therapy to reduce CSF pressure.5

If patients have rapidly advancing visual loss or symptoms refractory to medical management, surgical therapy is preferred in the form of optic nerve sheath fenestration to reduce pressure on the optic nerve, ventriculoperitoneal shunting to reduce ICP, or venous sinus stenting in the case of stenosis.9

Interestingly, as with this patient, up to 90% of patients with IIH have cerebral transverse venous sinus stenosis.9 Given multiple potential pathophysiological mechanisms of IIH, it is unknown currently whether venous sinus stenosis develops as a consequence of increased CSF production or whether venous sinus flow abnormalities lead to increased ICP by reducing CSF absorption. Acute cerebral vascular flow reductions as well as chronic changes in cerebral vasculature autoregulation, leading potentially to an overall increase or decrease in vascular flow, have been well documented in mTBI.10 However, given so few reported cases of IIH in the setting of mTBI, more studies are needed to elucidate any relationship between the two conditions.

CONCLUSIONS

This case highlights the importance of recognizing IIH as a potential cause of vision changes and treatment-refractory headaches in the setting of traumatic brain injury, particularly in patients with known risk factors.

This case report conforms to all American Journal of Physical Medicine & Rehabilitation Resident Fellow Section CARE guidelines and reports the required information accordingly (see Supplemental Checklist, Supplemental Digital Content 1, https://links.lww.com/PHM/B281).

REFERENCES

1. Headache Classification Committee of the International Headache Society (IHS): The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 2013;33:629–808
2. Lucas S, Hoffman JM, Bell KR, et al.: Characterization of headache after traumatic brain injury. Cephalalgia 2012;32:600–6
3. Singh T, Seidman MD: Chapter 11: hearing disorders associated with mild traumatic brain injury (mTBI), in: Neurosensory Disorders in Mild Traumatic Brain Injury. Cambridge, MA, Academic Press, 2019:149–63
4. Kapoor N, Ciuffreda KJ: Vision disturbances following traumatic brain injury. Curr Treat Options Neurol 2002;4:271–80
5. Thurtell MJ, Wall M: Idiopathic intracranial hypertension (pseudotumor cerebri): recognition, treatment, and ongoing management. Curr Treat Options Neurol 2013;15:1–12
6. Sabo T, Supnet C, Purkayastha S: Secondary intracranial hypertension (pseudotumor cerebri) presenting as post-traumatic headache in mild traumatic brain injury: a case series. Childs Nerv Syst 2018;34:681–90
7. Rahman MI, Raveendran S, Kaliaperumal C, et al.: Pseudotumor cerebri following traumatic brain injury in a 29-year-old man. J Nat Sci Biol Med 2012;3:105–7
8. McGeeny BE, Friedman DI: Pseudotumor cerebri pathophysiology. Headache 2014;53:445–58
9. Kanagalingam S, Subramanian PS: Cerebral venous sinus stenting for pseudotumor cerebri: a Review. Saudi J Ophthalmol 2015;29:3–8
10. Wang Y, Nelson LD, LaRoche AA, et al.: Cerebral blood flow in acute concussion: preliminary ASL findings from the NCAA-DoD CARE consortium. Brain Imaging Behav 2019;13:1375–85
Keywords:

Idiopathic Intracranial Hypertension; Concussion; Diplopia

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