Double Vision

Real Cases, Real Thinking, Real Medicine

Amie and Ben discuss a case of  gentleman in his 60's who presents with double vision. 

Can Ben figure out what is going on? 

As you listen, ask yourself: can you figure out the diagnosis? What would you have done in the situation?

Links & Resources

• RCPE Education: rcpe.ac.uk/education

Connect With Us

• Email: amie@homeofmedicine.com
• YouTube: Home of Medicine Channel

Disclaimer: All patient stories discussed in Home of Medicine are informed by real patient interactions. However, all identifying details have been removed or appropriately modified to protect patient confidentiality. 

This podcast is intended for education and professional development and should not replace independent clinical judgement or specialist consultation.

Transcript

Host [Dr. Amie Burbridge]: Hello and welcome to the Home of Medicine Podcast, a podcast in association with the Royal College of Physicians Edinburgh. I'm Dr. Amie Burbridge.

Guest [Dr. Ben Lovell]: And I'm Dr. Ben Lovell.

Host [Dr. Amie Burbridge]: Ben, I have a case for you. Are you ready?

Guest [Dr. Ben Lovell]: Yes, I'm very excited.

Host [Dr. Amie Burbridge]: This was a gentleman I saw on a post-take ward round. He was in his 60s, and he presented with a one-week history of double vision.

Guest [Dr. Ben Lovell]: Oh, neurophobia kicking in! Okay. What are your thoughts when I say double vision?

Host [Dr. Amie Burbridge]: Well, what are my thoughts? My thoughts are that I am going to have to put my thinking cap on. This isn't going to be a quick turnaround like an acute exacerbation of COPD requiring nebulizers, steroids, and antibiotics.

When analyzing double vision, we have to isolate where the problem originates:

• Is the lesion located within the central nervous system?
• Is the pathology affecting the extraocular muscles themselves?
• Or is it a problem within the cranial nerves that supply those extraocular muscles, presenting as an ophthalmoplegia?

First, I need to be absolutely sure it is true diplopia. Patients might report "double vision" when they actually mean blurred vision, tunnel vision, or a distinct refractive issue, such as a corneal problem or a dislocated lens. I would try to work out if this truly represents an extraocular muscle paresis, and then localise the lesion from the central to the peripheral nervous system.

Host [Dr. Amie Burbridge]: That is brilliant. Honestly, that is probably not what I did initially because as soon as I heard "double vision," my anxiety started. I flipped into what we have talked about before: Type 1 versus Type 2 thinking (thinking fast and thinking slow).

Type 1 thinking relies on rapid pattern recognition. It occurs when we have seen a presentation many times before; it is on the tip of our tongue and readily accessible in our consciousness.

When it comes to neurology and double vision, I really struggle with instant recognition. I immediately shifted into Type 2 thinking, which is slow, methodical, and forces you to go back to basic principles to figure out exactly what is going on.

Sifting through History and Comorbidities

Host [Dr. Amie Burbridge]: To carry on with the history: he had a one-week history of double vision present in both eyes. He described it as objects appearing four to six inches apart. Crucially, the diplopia resolved upon covering either eye, confirming it was binocular.

He also reported a permanent, noticeable, low frontal headache across the anterior aspect of his head. It wasn't severe, and he wasn't overly worried about it, but it had been present for the same duration as the double vision. He wore corrective lenses, but the diplopia persisted both with and without his glasses.

He denied having a cough, cold, chest pain, jaw claudication, speech changes, or any transient visual loss. There was no nausea or scalp tenderness. However, he noted that his left eye had a slight eyelid droop (ptosis) for the last day or two. Does that change your trajectory?

Guest [Dr. Ben Lovell]: A droopy eyelid immediately makes me consider conditions like Horner syndrome, meaning I need to evaluate the pupillary responses and check for associated signs.

Diplopia paired with a headache introduces distinct differentials:

• Is this a primary pathology causing both the headache and the nerve deficit?
• Or is it a secondary headache brought on by significant eye strain?

We also have to consider complex neuro-vascular or inflammatory conditions, though some entities like ophthalmoplegic migraine remain highly contentious in modern neurology, often reclassified as recurrent painful ophthalmic neuropathy.

I am still trying to methodically track the causes of diplopia down from the brainstem—starting with ischemic strokes and demyelination—working down to the cranial nerve nuclei, the peripheral nerve courses, and finally the neuromuscular junctions.

Did this happen to him previously?

Host [Dr. Amie Burbridge]: No, never.

Guest [Dr. Ben Lovell]: Does he have a history of migraines?

Host [Dr. Amie Burbridge]: No.

Guest [Dr. Ben Lovell]: Any prior focal neurological deficits, numbness, weakness, or transient paralysis?

Host [Dr. Amie Burbridge]: Nothing at all.

Guest [Dr. Ben Lovell]: Is he historically prone to headaches?

Host [Dr. Amie Burbridge]: Not really.

Guest [Dr. Ben Lovell]: Has he noticed any structural changes to his pupils?

Host [Dr. Amie Burbridge]: He mentioned that both of his pupils looked larger to him, but it was difficult for him to definitively judge.

Guest [Dr. Ben Lovell]: Any altered facial sensation or asymmetry?

Host [Dr. Amie Burbridge]: Nothing, apart from the left eyelid droop and a sensation that his left eye was tearing slightly more than normal. He noted the onset of the double vision was sudden and has remained static since. On the ward round, he had walked into the bay, was sitting comfortably in his chair in day clothes, and looked clinically well.

Guest [Dr. Ben Lovell]: Is the double vision worse towards the end of the day or when he is fatigued?

Host [Dr. Amie Burbridge]: No diurnal variation or fatigability. Why do you ask?

Guest [Dr. Ben Lovell]: I was screening for Myasthenia Gravis. Fatigable weakness and variable diplopia are classic hallmarks. What about a history of thyroid dysfunction?

Host [Dr. Amie Burbridge]: No history of thyroid eye disease and no history of recent trauma.

Guest [Dr. Ben Lovell]: Let's look at his past medical history and current prescriptions.

Host [Dr. Amie Burbridge]: He has a 45-year history of Type 1 diabetes, hypertension, and non-alcoholic fatty liver disease. He was also reviewed by an ophthalmologist a few years ago and noted to have cataracts and stable glaucoma.

His medications include:

• Insulin on a basal-bolus regimen
• A statin
• Bendroflumethiazide
• Ferrous sulfate
• Doxazosin
• Omeprazole
• Aspirin
• Lisinopril

Guest [Dr. Ben Lovell]: The long-standing diabetes is an immediate red flag. Diabetes is a notorious cause of microvascular complications, leading to mononeuritis multiplex via micro-infarctions of the vasa nervorum supplying the peripheral nerves.

I have frequently seen diabetes manifest as an isolated abducens nerve palsy. Was his diplopia more pronounced on horizontal gaze to either side, or was it uniform in all directions?

Host [Dr. Amie Burbridge]: To be honest, I didn't ask that specific question during my intake.

Guest [Dr. Ben Lovell]: If we can localize the maximal diplopia to a specific gaze direction, we can pinpoint the weak extraocular muscle and determine if this is a microvascular mononeuropathy secondary to diabetes. What about his social history?

Host [Dr. Amie Burbridge]: He does not drink, has never smoked, lives with his sister, and is a retired healthcare worker.

Objective Physical Examination Findings

Host [Dr. Amie Burbridge]: This is where my neurology panic peaked. I can execute the physical examination steps perfectly, but interpreting complex, conflicting signs on the spot is where I struggle.

His vital signs were stable:

• Heart rate: 94 bpm (regular)
• Blood pressure: 140/74 mmHg
• Temperature: 36°C
• Respiratory rate: 14 breaths/min
• Oxygen saturations: 96% on room air

He was alert, conversational, and oriented. On inspection, he had a subtle left-sided ptosis. His pupils appeared somewhat dilated bilaterally, but they were equal and briskly reactive to light. There was no relative afferent pupillary defect (RAPD). His peripheral neurological and systemic examinations were normal, except for chronic bilateral lower limb edema.

When evaluating his extraocular movements, I noted a mild weakness of the left orbicularis oculi. Sensation was intact across all trigeminal distributions, and he could raise his eyebrows symmetrically.

However, looking at his eye deviations:

• The right eye demonstrated a complete inability to abduct laterally.
• The left eye displayed a ptosis, and I noted an apparent abduction deficit on the left as well.

Guest [Dr. Ben Lovell]: So, he presented with a bilateral abduction deficit?

Host [Dr. Amie Burbridge]: Yes, he could not fully abduct either eye. There were no gross visual field defects, though I documented a suspected, subtle left inferior nasal quadrantopia—which, in hindsight, may have just been an over-analysis on my part because I was feeling so anxious about the case!

Formulating the Differential Diagnosis

Guest [Dr. Ben Lovell]: If it were simply an isolated right abducens nerve palsy, it would point toward a classic diabetic microvascular mononeuropathy. However, bilateral abducens nerve palsies combined with a left-hand ptosis complicate the picture. You do not typically see concurrent, symmetrical microvascular infarctions of the exact same cranial nerve bilaterally without an underlying systemic driver.

A concurrent ptosis and diplopia frequently signal an oculomotor nerve palsy. If a compressive lesion like a posterior communicating artery aneurysm were responsible, the patient would typically present as acutely unwell, meningitic, or photophobic due to an aneurysmal subarachnoid hemorrhage.

We must also remember that the abducens nerve has a long, vulnerable intracranial course. Raised intracranial pressure (ICP) can cause a false localizing sign, stretching both abducens nerves over the petrous ridge, regardless of where the primary mass or pressure origin sits.

Could a single lesion be compressing an oculomotor nerve while driving up intracranial pressure enough to cause bilateral abducens palsies? He urgently needed neuroimaging. Did he get a CT head?

Host [Dr. Amie Burbridge]: Yes, the unenhanced CT brain was completely normal.

Guest [Dr. Ben Lovell]: If I were reviewing this patient on a post-take ward round, my immediate strategy would involve admitting him for an urgent inpatient MRI brain alongside a formal neurology consultation.

As a consultant, I often teach registrars that while making a definitive diagnosis is satisfying, 90% of a ward round's value lies in nailing down a safe, detailed, and actionable management plan. In an era of strict hospital flow and bed management, deciding whether a patient can be safely evaluated via outpatient pathways versus an acute inpatient stay takes precedence.

Host [Dr. Amie Burbridge]: I had a similar thought process. I suspected a multi-focal microvascular process, like a mononeuritis multiplex affecting both the oculomotor and abducens nerves. I clinically ruled out Giant Cell Arteritis (GCA) because there was no jaw claudication or scalp tenderness, making a systemic vasculitis less probable.

Guest [Dr. Ben Lovell]: GCA is actually an excellent thought, because temporal arteritis can occasionally present with complex, ischemic ophthalmoplegia without the classic profound vision loss.

Host [Dr. Amie Burbridge]: Because of the bilateral signs, I wanted to rule out an aneurysm, so I arranged a CT angiogram (CTA) alongside the MRI of the brain and orbits.

The results were reassuring:

• The CT angiogram showed no evidence of an intracranial aneurysm.
• The MRI demonstrated moderate small vessel ischemic disease, but was otherwise entirely normal.

Specialist Evaluation and Cognitive Biases

Guest [Dr. Ben Lovell]: That is intriguing. What else can cause a complex, combined ophthalmoplegia? Wernicke's encephalopathy can present this way, but he has no significant alcohol history. Neuromuscular junction disorders were ruled out, and rare mitochondrial cytopathies or a Miller Fisher variant of Guillain-Barré syndrome seem unlikely without ascending paralysis or loss of reflexes.

Anatomically, the oculomotor nucleus sits in the midbrain, while the abducens nucleus resides in the pons. A single structural brainstem lesion like demyelination would have to span multiple levels, which our clear MRI disproves. Could there have been an error in interpreting the physical signs?

Host [Dr. Amie Burbridge]: That is exactly what happened. The neurology team reviewed him and stated definitively that the patient did not have a left-sided oculomotor nerve palsy.

They agreed there was an anomaly in his ocular motility, but concluded the left eye was structurally and neurologically normal. The primary deficit was an isolated right abducens nerve palsy.

To explain why the unaffected left eye appeared abnormal, I looked into Hering’s Law of Equal Innervation.

Hering’s Law of Equal Innervation states that the nervous system sends an identical amount of motor input to the synergistic muscle pairs of both eyes simultaneously to maintain conjugate gaze.

When a peripheral nerve injury—like a right abducens palsy—paralyzes an extraocular muscle, the brain attempts to overcome the deficit by sending increased motor signals to that weak muscle. By law, that exaggerated signal is also delivered to the healthy yoke muscle in the opposite eye. This over-innervation can cause the normal eye to move eccentrically, creating the clinical illusion of a bilateral gaze palsy or a contralateral deviation.

Guest [Dr. Ben Lovell]: I love eponymous medical principles, but I have never come across Hering's law before! That beautifully explains the clinical confusion.

Host [Dr. Amie Burbridge]: Ultimately, the consultant neurologist, the ophthalmologist, and the orthoptics team all evaluated him and formally concluded that he had a microvascular abducens nerve palsy, secondary to his long-standing diabetes and hypertension, superimposed on underlying small vessel disease.

Guest [Dr. Ben Lovell]: While it is a definitive conclusion, an isolated cranial nerve palsy attributed entirely to microvascular disease can sometimes feel like an incomplete diagnosis. However, it fits the clinical history perfectly.

Host [Dr. Amie Burbridge]: Following that consensus, another member of the medical team requested an extensive laboratory workup, including inflammatory markers (ESR, CRP), an autoimmune vasculitis screen, HIV, syphilis serology, antiphospholipid antibodies, and an ANCA screen.

Given that four specialist teams had already agreed on a diabetic microvascular etiology, I wondered if it was truly necessary to run all of these specialized, expensive screening tests?

Guest [Dr. Ben Lovell]: This is a classic dilemma. It reminds me of my time as a junior doctor in gastroenterology. Patients would present with clear alcohol-related liver disease, yet we would routinely run exhaustive screening panels for vanishingly rare conditions like Wilson's disease or alpha-1 antitrypsin deficiency.

The goal of this exhaustive testing is to avoid premature closure—the diagnostic bias where we grab the first plausible hypothesis that fits and stop looking for alternative answers.

We must always remember Hickam’s Dictum: "A patient can have as many diseases as they damn well please." A patient with poorly controlled diabetes can concurrently develop an independent, treatable systemic vasculitis. If we assume it is always a diabetic complication and miss a reversible inflammatory process, we fail the patient. Running the screens is often a matter of due diligence.

Navigating Heuristics in Modern Healthcare

Host [Dr. Amie Burbridge]: I completely agree that premature closure is a significant diagnostic bias, and I have been caught out by it earlier in my career. Because of a significant medical error I made a decade ago, I now find myself working much slower. I struggle to rely on quick clinical intuition because I feel compelled to run through a full, analytical, hypothetico-deductive reasoning process for every single patient out of fear of missing a rare alternative diagnosis.

Guest [Dr. Ben Lovell]: At least you possess that self-awareness. Many clinicians operate under a state of unconscious bias. However, we must defend the appropriate use of heuristics—the mental shortcuts we take to process complex information rapidly.

While human factors research often frames heuristics negatively as a source of diagnostic error, they are essential tools for senior decision-makers. On a heavy acute take with dozens of complex admissions, you cannot build a exhaustive, ground-up theoretical framework for every single patient. You have to utilize safe pattern recognition to make efficient decisions.

The key is keeping a small part of your mind open to the possibility that your initial pattern recognition might be wrong, allowing you to adapt if the patient's clinical course changes. The continuous cycle of re-review built into our acute medical units ensures that if a heuristic fails, a colleague is there to catch the discrepancy before it causes harm.

Host [Dr. Amie Burbridge]: That is an excellent point. Knowing when to rely on safe pattern recognition and when to step back, slow down, and analyze a complex presentation from square one is the hallmark of true clinical experience.

Thank you, Ben, as always for your insights. And a huge thank you to our listeners! We recently reached number five in the UK medical podcast charts, which is incredible. Please remember to rate, review, and subscribe, and send any feedback to amie@homeofmedicine.com.

Thank you to the Royal College of Physicians Edinburgh, and we will see you next time. Goodbye!

Host: Dr. Amie Burbridge (Acute Medicine Consultant / General Physician)

• Guest: Dr. Ben Lovell (Acute Medicine Consultant)

Extracted Clinical & Diagnostic Entities

Clinical Concepts & Pathologies

• Binocular Diplopia: Double vision resulting from a misalignment of the visual axes, resolving upon closing either eye.
• Ophthalmoplegia: Paralysis or paresis of one or more of the extraocular muscles responsible for controlling eye movements.
• Ptosis: Drooping of the upper eyelid, which can indicate oculomotor nerve dysfunction or sympathetic pathway disruption.
• Mononeuritis Multiplex: Symmetrical or asymmetrical damage to at least two separate nerve areas, frequently driven by microvascular ischemic processes like diabetes.
• Abducens Nerve Palsy (Sixth Cranial Nerve): A deficit resulting in the inability to abduct the eye laterally due to weakness of the lateral rectus muscle.
• Oculomotor Nerve Palsy (Third Cranial Nerve): A neurological deficit characterized by ptosis, a dilated pupil, and a "down and out" deviation of the affected eye.
• Horner Syndrome: A triad of miosis, ptosis, and anhidrosis caused by a disruption of the sympathetic nerve supply to the eye.
• Myasthenia Gravis: An autoimmune neuromuscular junction disorder characterized by fluctuating, fatigable skeletal muscle weakness, frequently affecting extraocular movements.
• Giant Cell Arteritis (Temporal Arteritis): An inflammatory vasculitis of large and medium-sized arteries that can present with headaches, jaw claudication, visual loss, and complex cranial neuropathies.
• Premature Closure: A cognitive diagnostic error where a clinician jumps to a conclusion and terminates the diagnostic process before evaluating all alternate options.
• Herring’s Law of Equal Innervation: A physiological law stating that an equal and simultaneous volume of nervous innovation is delivered to the synergistic muscle groups of both eyes.
• Hickam’s Dictum: The medical principle that a patient's symptoms can be the result of multiple concurrent diseases rather than a single unifying diagnosis.

Diagnostic Tools & Laboratory Panels

• Computed Tomography (CT) Brain: Initial unenhanced imaging to exclude acute structural pathology or hemorrhage.
• Computed Tomography Angiography (CTA): Vascular imaging utilized to rule out intracranial aneurysms.
• Magnetic Resonance Imaging (MRI) Brain & Orbits: High-resolution soft-tissue imaging to assess for small vessel ischemic disease, brainstem demyelination, or orbital lesions.
• Erythrocyte Sedimentation Rate (ESR) & C-Reactive Protein (CNP): Non-specific inflammatory biomarkers used to screen for systemic vasculitis.
• ANCA Screen (Antineutrophil Cytoplasmic Antibodies): Specialized serology to evaluate for small-vessel vasculitides.
• Vasculitis / Autoimmune Screen: A collection of specialized autoantibody panels used to exclude underlying connective tissue and rheumatological diseases.

This episode focuses on a male patient in his 60s who presented with a acute, one-week history of binocular diplopia and a low-grade frontal headache. The clinical narrative explores the challenges of mapping cranial neuropathies while managing cognitive biases like premature closure. 

What are the primary clinical considerations when evaluating acute binocular diplopia?

Physicians must first distinguish true ocular motility limitations from refractive errors or blurred vision by verifying if the symptom resolves upon covering either eye. The diagnostic approach involves localising the deficit along the neuroanatomical axis, differentiating central intracranial pathology from cranial nerve mononeuropathies or neuromuscular junction disorders.

How does premature closure impact complex neurological diagnoses?

Premature closure is a cognitive bias where a clinician accepts an initial diagnostic hypothesis before exploring all alternatives or fully validating the data. In complex cases, this can lead to missed secondary pathologies, as clinicians often cease investigations once a singular, common condition fits the primary clinical picture.

What is Herring's law of equal innervation in ocular motility?

Herring's law of equal innervation states that during conjugate eye movements, an equal and simultaneous nervous impulse is sent to the synergistic muscle pairs of both eyes. In the context of a unilateral cranial nerve palsy, the brain may overcompensate by increasing innervation to the paretic muscle, which simultaneously overstimulates the corresponding muscle in the unaffected eye, potentially mimicking a bilateral deficit.

Introduction

In this episode of the Home of Medicine Podcast, Dr. Amie Burbridge and Dr. Ben Lovell dive deep into a challenging neurological presentation on the post-take ward round. Listeners will learn how to systematically approach a patient presenting with acute double vision, how to differentiate between multiple cranial nerve palsies, and how to execute an effective diagnostic plan. The discussion also provides a transparent look into the psychology of medicine, balancing Type 1 (fast, heuristic-led) and Type 2 (slow, analytical) thinking, while warning against the dangers of premature closure.

Chapter Markers & Timestamps

• 00:12 – Introduction & Case Presentation: Dr. Amie Burbridge introduces a patient in his 60s presenting with a one-week history of double vision.
• 00:45 – Neurophobia & Initial Localisation: Dr. Ben Lovell shares his initial framework for breaking down diplopia, ocular muscles, and nerve pathways.
• 01:46 – Cognitive Processing: Type 1 vs. Type 2 thinking patterns when managing acute neurological complaints.
• 02:51 – Symbology & Clinical Secrets: Analysis of the patient's low frontal headache, ptosis, and history of diabetes.
• 06:21 – Differential Diagnosis Expansion: Considering neuromuscular junction disorders, thyroid eye disease, and microvascular ischemia.
• 09:23 – Objective Clinical Examination: Breaking down the cranial nerve examination findings and pupillary responses.
• 13:04 – Interpreting Bilateral Signs: Deconstructing false localizing signs and the potential role of raised intracranial pressure.
• 15:18 – Ward Round Strategy: Why the management plan takes precedence over diagnostic certainty in acute care.
• 19:31 – The Specialist Verdict: The neurology team's interpretation, Herring's Law of Equal Innervation, and final case consensus.
• 23:52 – The Cost of Due Diligence: A debate on mononeuritis multiplex screens, vasculitis investigations, and defensive medicine.
• 28:04 – Heuristics & Clinical Shortcuts: How senior decision-makers safely deploy rules of thumb within the health system.
• 33:05 – Epilogue & Wrap-up: Overcoming past medical errors and reclaiming clinical confidence.