Vision and Rehabilitation After Brain Trauma (Part 2)

Eric Singman, MD, PhD,
Vision and Rehabilitation After Brain Trauma: Part 2

This is part two of a three-part article

This is part two of a three-part article published to

The Efferent Visual Pathways and How Brain Injury Can Affect Them

The efferent visual pathways include both voluntary and involuntary (otherwise known as autonomic) functions affecting the muscles within and surrounding the eye. The iris, an internal muscle of the eye, is what we recognize as the colored part of the eye with a central opening called the pupil. The iris stands directly in front of the natural lens and by contracting or relaxing, it controls the size of the pupil and thereby the amount of light that enters the eye. Like the iris, the ciliary body is a ring-shaped muscle that is attached around the natural lens and controls the ability of the lens to focus. Both of these muscles are in turn controlled by nerves of the autonomic nervous system.

The autonomic nerves controlling the internal muscles of the eye are of two types, sympathetic and parasympathetic. The sympathetic nerves employ chemicals identical or similar to adrenalin, and take a circuitous path to get from the brain to the eye, going by way of the neck, down to the chest and back up the neck to the head. Along the way, the sympathetic pathway helps control breathing, heart rate, blood pressure, sweating and even two millimeters of eyelid opening. Damage to this pathway from blunt trauma or shrapnel causes many problems including what is known as the Horner’s syndrome. In this condition, the patient will present with a small pupil, a somewhat droopy eyelid and decreased sweating on the affected side of the face. In addition, the patient may often describe a sense of fatigue with distance vision because the affected eye’s lens may not adjust focus normally. 

The parasympathetic pathway starts in the brainstem, where the brain starts to narrow as it merges with the spinal cord. The parasympathetic nerves to the eye socket cause the pupil to become small and cause the lens to focus for near work. Head trauma can damage this pathway and a patient will have a large pupil and difficulty focusing for reading. This pathwayalso can be damaged by elevated pressure in the brain which is why patients who suffer head trauma and have large or unreactive pupils are treated as critical emergencies. Many patients suffering head injury often need reading glasses earlier than what might be expected because of the reduced ability to focus at near. These patients may also have more problems with glare. However, it has not been confirmed that these problems are a direct result of damage to the parasympathetic pathways in every patient.

Attached to the outside of each eye is a team of six muscles. These extra-ocular muscles allow the eyes to not only look in every direction but to rotate as well so that visual images remain upright-appearing even when the head tilts. The nerves serving these ocular muscles all originate in the brainstem. These nerves are quite delicate and even a mild concussion can damage them. When this occurs, the affected muscle cannot help the eye move as quickly or completely as it should and the result is double vision, or diplopia. Patients will report doubled images as being displaced horizontally, vertically or even diagonally. Although images can also be torsionally displaced, patients have a much harder time expressing this complaint in specific terms. For this reason, neuro-ophthalmologists, orthoptists and behavioral optometrists, all of whom are particularly trained to evaluate eye teaming disorders, play a key role in diagnosing and treating diplopia.

The extra-ocular muscles normally work in unison so that the two eyes fixate on the same target and smoothly pursue that target when necessary. They permit the eyes to move in the same direction such as when a patient tracks an object that is moving up, down, right or left. They also allow the eyes to move in opposite directions (i.e., to cross or uncross) during times when a patient is tracking objects that are approaching or departing. Head trauma routinely causes a reduction in the ability of the eyes to work as a team. Convergence insufficiency is a reduction in the ability of the brain to make the eyes cross for close vision and is one of the most common deficits following concussion. Deficiency of smooth pursuits is also common. In this case, the eyes have difficulty following a moving object such as a swinging pendulum; the patient reports dizziness or even nausea trying to complete this simple visual task.

Nystagmus is a repetitive movement of the eyeball during which the eye seems to drift off target and then quickly corrects to re-gaze at the target. This condition can occur after brain injury and causes considerable reduction of visual clarity as well as a sense of dizziness. Although all the centers of the brain controlling the maintenance of fixation are not well understood, nystagmus often suggests damage to the centers of the brain associated with balance and equilibrium, specifically the cerebellum located at the back of the brain, and the vestibular system inside the ears. Even relatively mild trauma to the skull can cause damage to the delicate bony walls of the vestibular system. Patients might not have any hearing loss but still have balance problems or nystagmus. Interestingly, nystagmus from damage to the wall of the vestibular system may not be constant but rather might be initiated by a repetitive sound such as a ringing telephoneor by increased air pressure in the chest such as during inflation of a balloon; this is called Tullio’s phenomenon.

As mentioned previously, glare frequently occurs after traumatic brain injury, and it is unclear why this occurs. In some patients, it may be secondary to elevations in intracranial pressure. In others, it seems to accompany pain to the eyes and forehead from injury to a nerve at the back of the skull, just above the neck, called the Greater Occipital Nerve. This nerve exits from the base of the skull and runs forward to the eye socket. The pain from this nerve can be felt along its entire course and even gentle pressure on the nerve root can bring exquisite pain. Patients with this type of headache are sometimes misdiagnosed as having migraine headaches or even as being insincere because clinicians focus their attention on the forehead and eye rather than considering the Greater Occipital Nerve as the cause of this referred pain. In addition, pain from irritation of this nerve can appear months or years after the original injury and clinicians might not correlate the patient’s complaint of pain with a head trauma they suffered years before.

Posted on BrainLine March 2, 2011

From Stars and Stripes, March 2010,


Having sought the expertise of highly qualified doctor's of ophthalmology and behavioral optometry for several years. I found my first indication of Greater Occipital nerve injury by a doctor of neurologic chiropractic about a month ago. I found Dr . Singman on this site and continue to search for a conclusion to my search and finding a treatment.

That is horrible.  Police should be trained to listen to law abiding citizens instead of falsely accusing them.  I also have vision impairment due to brain injury; I am unable to use my eyes for reading.  I get horrible gastritis onsets when my brain goes on overload.  I am suffering from cerebral hypoxia; which means, my brain is constricted from getting enough oxygen.  There is not much support for our type of injury out there .

I wish police would read this, I have been stop thrown in jail, my eyes dont dilated right, my balane is off,I goto jail taking all the tests, and find no drugs in me, all because of head injury 34 years ago

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