Hyperreflexia describes an involuntary, exaggerated muscle contraction in response to a stimulus, such as a tap on a tendon. This means the body’s deep tendon reflexes are overactive. While a brisk reflex might be a normal variation, when it is pronounced or occurs alongside other symptoms, it indicates an underlying health issue. Understanding the cause helps determine whether the finding is a temporary physiological change or a sign of a chronic condition affecting the nervous system.
The Mechanism Behind Overactive Reflexes
The body’s reflexes are controlled by a simple circuit called the reflex arc, which involves sensory nerves, the spinal cord, and motor nerves leading to the muscle. This arc operates automatically without needing input from the brain. A separate set of nerve pathways, known as the Upper Motor Neurons (UMNs), descend from the brain and brainstem to the spinal cord.
These UMN pathways normally exert a continuous, dampening influence on the spinal reflex arc, regulating its sensitivity. When a lesion or injury damages the UMNs, this descending inhibitory control is lost entirely. The loss of inhibition leaves the reflex arc unchecked, leading to the disinhibition of the Lower Motor Neurons (LMNs) in the spinal cord.
With the LMNs hyper-excitable, even a mild stimulus can trigger an exaggerated muscle contraction, resulting in hyperreflexia. Damage to the central nervous system, which houses the UMNs, is the most frequent cause of chronic hyperreflexia. The severity of the hyperreflexia often correlates with the extent of the damage to these regulatory pathways.
Chronic Conditions Affecting the Central Nervous System
Hyperreflexia is a sign of damage to the UMN pathways and can indicate several chronic neurological disorders. A stroke causes immediate injury to UMNs, often leading to hyperreflexia on the side of the body opposite the brain lesion. This exaggerated response may develop weeks or months after the initial event, once the temporary period of spinal shock resolves.
Spinal cord injuries result in hyperreflexia below the level of the damage. The UMN pathways are severed, isolating the spinal cord segments below the injury from the regulatory control of the brain. The deep tendon reflexes in the limbs below the injury become hyperactive, sometimes accompanied by spasticity and clonus (a rhythmic, involuntary muscle contraction).
Multiple Sclerosis (MS) results from the autoimmune destruction of the myelin sheath surrounding nerve fibers in the central nervous system. The demyelination creates scattered lesions that disrupt the flow of inhibitory signals along the UMN tracts. The location and size of these lesions determine which reflexes are affected.
In Amyotrophic Lateral Sclerosis (ALS), hyperreflexia is a sign of UMN involvement. It often occurs simultaneously with signs of LMN damage, such as muscle weakness and fasciculations (muscle twitching). This unique combination of UMN and LMN signs is highly characteristic of ALS.
Metabolic and Temporary Triggers
Not all causes of hyperreflexia involve chronic, structural damage to the UMN pathways; some result from systemic issues that temporarily increase nerve excitability. Hyperthyroidism, where the thyroid gland produces excessive hormones, speeds up the body’s metabolism. This heightened state of cellular excitement can lead to brisk reflexes that resolve once the underlying thyroid condition is treated.
Severe imbalances in electrolytes can also trigger hyperreflexia. Low levels of calcium (hypocalcemia) or magnesium (hypomagnesemia) increase the excitability of nerve and muscle cells. Correcting these mineral deficiencies through targeted treatment typically normalizes the reflex response.
Acute toxic states or withdrawal syndromes can also present with exaggerated reflexes. For example, Tetanus releases a toxin that blocks inhibitory neurotransmitters, leading to painful muscle spasms and systemic hyperreflexia. Withdrawal from depressant substances like alcohol or benzodiazepines can cause a temporary state of nervous system over-activity. These systemic causes are distinct from UMN lesions because they do not involve permanent nerve damage and can often be reversed.
How Doctors Evaluate Reflexes and Next Steps
A doctor evaluates reflexes during a physical examination using a reflex hammer to quickly tap various tendons, such as the knee or elbow. The response is graded on a standardized scale, typically ranging from 0 to 4+. A grade of 2+ is considered a normal, average response. Responses graded 3+ (brisk) or 4+ (hyperactive with clonus) indicate hyperreflexia.
A doctor pays close attention to the symmetry of the response, as a difference between the right and left sides is often more meaningful than overall briskness. The presence of clonus is a specific indicator of a neurological problem. The doctor also looks for other signs of UMN damage, such as muscle weakness and spasticity, to place the hyperreflexia in a broader clinical context.
If hyperreflexia is found, the next steps involve a comprehensive neurological workup to determine the root cause. This may include brain or spinal cord imaging, such as an MRI, and laboratory tests to check for metabolic or infectious causes.