Muscle relaxers slow down nerve signaling in your brain, producing sedation, drowsiness, and reduced muscle tension. They do this by amplifying the activity of your brain’s main “calm down” chemical, a neurotransmitter called GABA. That mechanism is what makes them effective for muscle spasms, but it’s also what causes brain fog, dizziness, and other cognitive side effects. If you’re wondering about chemical hair relaxers instead, those affect the brain through a different route, and this article covers both.
How Muscle Relaxers Change Brain Signaling
Most prescription muscle relaxers work inside the brain and spinal cord rather than directly on your muscles. They target GABA, the primary inhibitory neurotransmitter in the central nervous system. GABA’s job is to quiet nerve activity. Muscle relaxers boost that quieting effect, which is why tight or spasming muscles loosen up, but it’s also why your thinking, coordination, and reaction time take a hit at the same time.
GABA-producing neurons are spread across areas of the brain involved in movement, memory, hormone regulation, and sleep, including the hippocampus, thalamus, basal ganglia, hypothalamus, and brainstem. When a muscle relaxer amplifies GABA across all of these regions simultaneously, the effects aren’t limited to your sore back. Your entire central nervous system dials down a notch.
Short-Term Effects on Thinking and Coordination
The most immediate brain-related effects of muscle relaxers are the ones you can feel within an hour of taking a dose. Common ones include drowsiness, blurred vision, dizziness, and clumsiness or unsteadiness. Some people describe a general “fuzziness,” where they can’t think as quickly or clearly as usual. Getting up too fast from a chair or bed can cause lightheadedness or faintness, because the drug is also affecting blood pressure regulation in the brainstem.
These effects are strongest in the first few days of use and tend to soften somewhat as your body adjusts. But they don’t disappear entirely as long as you’re taking the medication, which is why muscle relaxers carry warnings about driving and operating machinery.
What Happens to Your Sleep
Muscle relaxers often make people sleepy, so it seems logical that they’d improve sleep quality. The reality is more nuanced. In a study of fibromyalgia patients, cyclobenzaprine (one of the most commonly prescribed muscle relaxers) increased total sleep time and reduced evening fatigue. However, it did not fix the abnormal brain wave patterns seen during non-REM sleep in those patients, and it didn’t improve pain scores or mood.
In other words, muscle relaxers can help you stay asleep longer, but the sleep you get may not be as restorative as it appears. Spending more hours in bed doesn’t automatically mean your brain is cycling through the deep and REM sleep stages it needs for memory consolidation and tissue repair.
The Anticholinergic Problem
Several muscle relaxers also interfere with another neurotransmitter called acetylcholine, which plays a central role in memory, attention, and learning. This “anticholinergic” activity is an unintended side effect of the drug’s chemical structure, not something it was designed to do. The result can be dry mouth, constipation, and urinary retention on the body side, and confusion, poor concentration, and memory lapses on the brain side.
Not all muscle relaxers carry the same anticholinergic load. Orphenadrine, for example, has significant anticholinergic effects, while tizanidine works through a different mechanism and carries less of this burden. The problem is that anticholinergic effects stack. If you’re also taking an antihistamine, an antidepressant, or a bladder medication, the combined impact on acetylcholine in your brain can be substantial.
Long-Term Use and Cognitive Decline
One of the more concerning findings involves the connection between prolonged muscle relaxer use and Alzheimer’s disease risk. A nationwide case-control study found that people who used muscle relaxers for more than a year had a 12% higher risk of developing Alzheimer’s compared to non-users. Shorter use (under a year) carried a smaller but still statistically significant 4% increase in risk.
The association was not uniform across all muscle relaxers. Orphenadrine, with its strong anticholinergic properties, showed a 19% increased risk at higher cumulative doses. Tizanidine, which works differently, showed no association with Alzheimer’s at all. This pattern suggests that the acetylcholine-blocking mechanism, rather than muscle relaxation itself, may be driving the cognitive risk.
The American Geriatrics Society’s 2023 Beers Criteria, a widely used guideline for medication safety in older adults, recommends avoiding most skeletal muscle relaxers for musculoskeletal complaints in people over 65. Baclofen and tizanidine are the two exceptions excluded from that warning. For older adults especially, the brain-related risks of these medications often outweigh their benefits for routine aches and spasms.
Dependence and Withdrawal
Your brain adapts to any substance that repeatedly alters its chemistry, and muscle relaxers are no exception. With regular use over weeks or months, your nervous system recalibrates around the drug’s presence. Neurons become less sensitive to GABA on their own, meaning they need the medication to maintain the same level of calm signaling. This is neuroadaptation, and it’s the biological basis of physical dependence.
When you stop abruptly, the brain finds itself in an overstimulated state. Withdrawal symptoms can include anxiety, insomnia, irritability, increased muscle tension, and in some cases, seizures (particularly with drugs closely related to benzodiazepines). Research into prolonged withdrawal from GABA-enhancing drugs has found that some people experience lingering neurological symptoms, both physical and psychological, well beyond the acute withdrawal window. The mechanisms behind these extended effects are not fully understood, but they appear to differ from the rebound that happens in the first few days after stopping.
Tapering slowly under medical guidance, rather than stopping cold, gives the brain time to readjust its own GABA production and sensitivity.
Chemical Hair Relaxers and the Brain
If you searched this topic thinking about hair straightening products rather than medications, the answer is different but still worth knowing. Chemical hair relaxers contain compounds that can act as endocrine disruptors, meaning they interfere with your body’s hormone signaling. These chemicals enter the body through the scalp, particularly when the skin is burned or irritated during application, which creates direct entry points for absorption.
Endocrine disruptors can affect the brain in several ways. They alter thyroid function, and thyroid hormones are essential for the creation and migration of new brain cells, the specialization of neurons, and the formation of myelin (the insulating coating that helps nerve signals travel quickly). Any disruption to thyroid signaling, particularly during fetal development, childhood, or adolescence, can affect how the brain develops and functions.
These chemicals can also mimic or block sex hormones like estrogen, testosterone, and progesterone. Progesterone in particular helps shape brain structure and influences neurotransmitter systems involved in mood and cognition, including the same GABA, dopamine, and glutamate pathways affected by muscle relaxers. Chemicals with estrogenic or anti-androgenic activity can activate or suppress hormonal pathways that guide brain development and reproductive function.
The brain effects of hair relaxer chemicals are subtler and slower than popping a muscle relaxer pill. They accumulate over years of repeated exposure rather than producing immediate drowsiness. The concern is less about how you feel after one salon visit and more about the cumulative hormonal disruption from regular use over a lifetime, especially for people who started using relaxers in childhood.