How Multiple Sclerosis Affects Reflexes

Multiple sclerosis disrupts reflexes throughout the body, and the disruption usually goes in a direction that surprises people: most reflexes become overactive rather than sluggish. Because MS damages the insulating myelin sheath around nerve fibers in the brain and spinal cord, the signals that normally keep reflexes in check lose their way, and the reflexes themselves become exaggerated, poorly timed, or both. This pattern shows up not only in the classic knee-jerk test but in eye movements, pupil responses, blood-pressure regulation, bladder control, and balance reactions. The specifics vary depending on where in the nervous system the damage lands, and they change as the disease progresses.

Why MS Typically Makes Reflexes Overactive

Reflexes are built as loops. A sensor detects something (a tap on the tendon, a flash of light, a drop in blood pressure), sends a signal along a nerve, and a response fires back. The brain and spinal cord constantly fine-tune these loops, dialing them up or down depending on context. In MS, demyelination and inflammation interrupt the descending signals that normally restrain spinal-cord reflexes. When that braking system fails, the reflex arc fires too easily, too strongly, or both.

This is why MS is classified as an upper motor neuron disease. The motor neurons in your spinal cord and brainstem are intact, but the signals coming down from the brain to modulate them are degraded. The result is hyperreflexia, meaning reflexes that are brisker and more forceful than they should be, often accompanied by spasticity and muscle stiffness. Hyporeflexia, or reduced reflexes, is not a typical sign of MS; when reflexes are diminished in someone with MS, clinicians usually look for a second problem affecting the peripheral nerves or spinal roots.

Deep Tendon Reflexes and Spasticity

The most familiar reflex test in a neurologist’s office is the tendon tap. A small hammer strikes the patellar tendon below the kneecap, the quadriceps contracts, and the lower leg kicks forward. In people with MS-related spasticity, this response is amplified in measurable ways. A study comparing MS patients with healthy controls found that it took less tapping force to trigger the reflex, yet the reflex produced more torque. Despite significant quadriceps weakness, the reflex “gain” was markedly higher, the muscle contracted faster, and the reflex loop delay was shorter, all indicating that the motor neurons and peripheral receptors were in a state of hyperexcitability. In effect, a larger proportion of the muscle was being recruited reflexively, including fast-twitch fibers that would not normally participate.¹

This creates an odd paradox. The muscles themselves are often weak because voluntary signals from the brain struggle to get through the damaged myelin. But the spinal reflex pathway, freed from its normal regulation, overcompensates. The muscle can snap to attention when tapped or stretched, even though it cannot generate the same force on command. That mismatch between reflex strength and voluntary strength is one reason spasticity feels so frustrating: your leg may stiffen and resist bending when you try to walk, yet feel weak when you try to push off a step.

How Spinal Reflexes Go Wrong During Walking

The hyperactive tendon response you see on an exam table becomes a real problem in motion. During normal walking, the nervous system modulates spinal reflexes on a millisecond-by-millisecond basis, ramping them up during the stance phase when the leg bears weight and dialing them back during the swing phase when the leg needs to move freely. Research on the H-reflex, a laboratory version of the stretch reflex measured via electrical stimulation of the nerve, shows that this modulation is impaired in people with MS and spasticity. In healthy walkers, H-reflex size changes are driven by the muscle’s activity level plus additional neural factors. In MS patients with spasticity, the modulation tracks only with the muscle’s excitation level, meaning the extra layer of neural control is missing.²

The practical consequence is stiff, poorly coordinated walking. If your spinal cord cannot suppress reflexes at the right moments during a stride, your muscles co-contract when they should be relaxing, your gait becomes labored, and tripping risk goes up. This is a distinct problem from pure muscle weakness and helps explain why some people with MS report that their legs feel “locked” or “robot-like” during movement rather than simply tired.

Postural Reflexes and Balance

When you stumble or the floor moves unexpectedly, your body fires automatic postural responses, quick muscle contractions in the legs and trunk to keep you upright. These are not the same as tendon-tap reflexes; they involve longer loops that route sensory information up through the spinal cord before triggering a corrective response. In MS, the sensory leg of this loop is slowed by demyelination. One study found that people with MS had postural response latencies averaging about 160 milliseconds compared with roughly 100 milliseconds in healthy controls, a delay of more than 50 percent. Those delays correlated strongly with slowed somatosensory conduction in the spinal cord, not with cerebellar damage.³

What’s interesting is how the body tries to compensate. Participants with MS produced postural responses that were normal or even larger than normal in amplitude. Their nervous systems seemed to recognize that the signal was arriving late and cranked up the volume to make up for lost time. This compensatory strategy works up to a point, but it has limits. A response that fires 60 milliseconds late is 60 milliseconds late regardless of how strong it is. That gap is where falls happen, and falls are one of the most common and feared complications of MS.

The Blink Reflex and Hidden Brainstem Damage

When the skin near your eye is tapped or an electrical stimulus hits the nerve above your eyebrow, you blink. This reflex travels through the brainstem, and its speed can reveal demyelination in pathways that an MRI might not flag clearly. Several studies have found prolonged blink reflex latencies in MS patients compared with healthy controls, even in people whose brainstems appear clinically unaffected.⁴ In one study, about 40 percent of patients who had no brainstem-related symptoms whatsoever still showed abnormal blink reflex results, suggesting subclinical damage that had not yet produced noticeable problems.⁵

Abnormalities in the blink reflex tend to be more pronounced in patients with longer disease duration and greater disability, and they are especially common when MRI shows brainstem lesions.⁶ This makes the blink reflex a useful, low-tech add-on to the diagnostic workup: it is cheap, quick, and can pick up damage that imaging misses. It also helps clinicians track disease progression without needing a new MRI every time.

Pupillary Reflexes and Optic Neuritis

Your pupils constrict when light hits the retina, a reflex that depends on intact optic nerves and brainstem pathways. Since optic neuritis, inflammation of the optic nerve, is one of the most common early symptoms of MS, it makes sense that the pupillary light reflex would be affected. Research using dynamic pupillometry shows that MS patients who have experienced optic neuritis have a reduced amplitude of pupil contraction and a longer delay before the pupil starts to constrict, compared with both healthy controls and MS patients without a history of optic neuritis.⁷

In clinical practice, this often shows up as a relative afferent pupillary defect, where swinging a light from one eye to the other causes the affected pupil to paradoxically dilate instead of constricting. That test has been part of the standard neurological exam for decades. Earlier work on pupillary light reflex latency in people with definite MS found abnormal direct responses in roughly a quarter to a third of patients, and the defect correlated with visual evoked potential abnormalities in the same eye.⁸ Even after optic neuritis resolves and vision improves subjectively, pupillary responses can remain sluggish, hinting at persistent axonal damage in the optic pathway.

The Vestibulo-Ocular Reflex and Dizziness

The vestibulo-ocular reflex keeps your vision stable when your head moves. If you shake your head while reading, your eyes counter-rotate to keep the text in focus. This reflex runs through the brainstem and cerebellum, regions commonly affected by MS. In a study of childhood-onset MS patients, one in five had abnormal vestibulo-ocular reflex gains, and the group as a whole showed significantly lower gains in multiple semicircular canal planes compared with healthy peers. Those with dizziness had even lower gains than those without.⁹

Impaired vestibular reflexes help explain the dizziness and oscillopsia (a sense that the visual world is bouncing) that many MS patients experience. These symptoms can be especially disorienting in environments with lots of visual motion, like busy streets or grocery store aisles. Work on pediatric MS also found that nearly half of young patients showed abnormalities in vestibular evoked responses, and the degree of impairment tracked with the volume of brainstem and cerebellar lesions on MRI.¹⁰ The fact that these deficits appear even in children and adolescents with MS underscores how early vestibular pathways can be involved.

Autonomic Reflexes and Blood Pressure Control

Not all reflexes involve skeletal muscle. Your cardiovascular system relies on the baroreflex, a feedback loop that detects changes in blood pressure and adjusts heart rate and blood vessel tone within seconds. When you stand up from a chair, baroreceptors in the carotid arteries sense the drop in pressure and trigger vasoconstriction and a slight uptick in heart rate to keep blood flowing to your brain. In MS, this reflex can be blunted. One study found that baroreflex sensitivity in MS patients was roughly half that of healthy controls, meaning the system responded less vigorously to pressure changes.¹¹

A separate investigation using neck pressure to stimulate carotid baroreceptors directly showed that people with MS had a blunted blood pressure response to a simulated drop in blood pressure. The problem was not in the heart’s output but in the blood vessels’ ability to constrict, suggesting the autonomic nerve fibers controlling vascular tone are specifically vulnerable.¹² The practical upshot is lightheadedness on standing, exercise intolerance, and sometimes fainting, symptoms that patients and even clinicians may not immediately attribute to MS.

Bladder Reflexes

Bladder function depends on a coordinated set of reflexes that tell the detrusor muscle when to contract and the sphincter when to relax. Spinal cord lesions in MS commonly disrupt these signals, producing neurogenic detrusor overactivity: the bladder contracts reflexively when it should be quietly filling. This leads to urgency, frequency, and incontinence, symptoms that affect a majority of people with MS at some point. A meta-analysis of rehabilitation approaches found moderate evidence that peripheral tibial nerve stimulation and pelvic floor muscle training can help manage this overactivity, offering non-drug options alongside the anticholinergic medications often prescribed.¹³

Managing Overactive Reflexes

Because hyperactive reflexes and spasticity are among the most functionally limiting features of MS, a significant amount of research has gone into taming them. The two most commonly prescribed oral medications are baclofen and tizanidine, both of which reduce the excitability of spinal motor circuits but through different mechanisms. A head-to-head trial found no significant difference in overall antispastic efficacy between the two, but baclofen was more likely to cause muscle weakness severe enough to impair walking and standing. Tizanidine, in some patients with moderate to marked leg weakness combined with high spasticity, appeared to improve mobility, a trade-off that mattered more to daily function than any lab measure of stiffness.¹⁴

For patients whose spasticity is severe and does not respond adequately to pills, intrathecal baclofen delivered by an implanted pump can be remarkably effective. One study used the stretch reflex itself as a dosing guide: as the baclofen dose was increased, the amplitude of the soleus stretch reflex fell in a tightly correlated fashion. At therapeutic doses, the stretch reflex amplitude dropped to about a tenth of untreated values, confirming that the drug was reaching its target in the spinal cord.¹⁵

Non-drug approaches also show promise. A systematic review of 32 randomized trials found moderate-to-low-certainty evidence that physical activity programs and transcranial magnetic stimulation, used alone or in combination with other treatments, can reduce spasticity in MS.¹⁶ Neuromuscular electrical stimulation is another approach under investigation. Early evidence suggests it can acutely reduce spinal excitability (as measured by the H-reflex) in MS patients with spasticity, offering a potential way to “reset” overactive circuits during rehabilitation sessions.¹⁷

What Reflex Testing Tells Clinicians About Disease Progression

Beyond the direct impact on daily life, reflex testing gives clinicians a window into how MS is progressing. The corticospinal tract, the main highway carrying motor commands from the brain to the spinal cord, can be assessed using transcranial magnetic stimulation. One study found that longer motor evoked potential latencies (the time it takes a magnetic pulse over the scalp to produce a muscle twitch in the hand) correlated with higher disability scores, while measures of cortical facilitation inversely correlated with the degree of structural damage in the tract’s white matter.¹⁸ In plainer terms, the worse the nerve fiber damage looked on advanced imaging, the less the brain could amplify its own signals, and the more disabled the patient was.

Blink reflex testing, pupillary response measurement, and vestibular function tests all serve similar double duty. They can reveal subclinical damage before symptoms appear, and tracking changes over time helps clinicians decide whether a disease-modifying therapy is holding the disease in check or whether a switch is needed. The fact that roughly 40 percent of MS patients without brainstem symptoms still show abnormal blink reflexes or abnormal sympathetic skin responses illustrates how much subclinical activity can be detected through simple electrophysiology. For patients, this means that a reflex test result can carry information about their disease that an MRI scan might miss, and that seemingly minor changes on an exam can signal real biological change in the nervous system.