Spinal cord atrophy (SCA) describes the loss of tissue mass and subsequent shrinkage in this structure. This reduction in size is not a primary disease but rather a measurable consequence of underlying damage to the axons, myelin, or nerve cells within the cord itself. As the cellular components that make up the cord deteriorate, the overall volume decreases, which can be visualized on medical imaging. This tissue loss directly disrupts the signaling pathways, leading to neurological deficits that manifest as the symptoms of SCA.
Recognizing the Signs of Spinal Cord Atrophy
The specific symptoms of spinal cord atrophy depend heavily on the location and extent of the tissue loss within the cord’s cross-section. Damage to the descending motor tracts, which carry signals from the brain, results in profound motor symptoms. Patients often experience muscle weakness (paresis) or complete paralysis, typically affecting the limbs below the level of atrophy. This weakness can present as spasticity, where muscles are stiff and reflexes are exaggerated, or flaccidity, characterized by low muscle tone and absent reflexes.
Fine motor skills become challenging, and gait disturbances are common, ranging from a clumsy, uncoordinated walk to the complete inability to walk. Atrophy that affects the cervical region, located in the neck, is particularly impactful because it can compromise function in all four limbs, a condition known as tetraplegia. Over time, the muscles that are no longer receiving adequate nerve signals will also begin to visibly shrink, a process called neurogenic muscle atrophy.
Sensory pathways, which transmit information like touch, pain, and temperature back to the brain, are also frequently damaged. This can cause altered or reduced sensation (hypoesthesia), leading to patches of numbness or tingling (paresthesia) on the skin. A loss of proprioception, the body’s internal sense of where the limbs are positioned in space, can further exacerbate issues with balance and coordination.
Autonomic functions, which govern involuntary body processes, are also regulated by the spinal cord and can be compromised by atrophy, especially in the thoracic region (T6 and above). Symptoms include neurogenic bladder and bowel dysfunction, leading to difficulties with control and emptying. Cardiovascular regulation can be affected, sometimes resulting in orthostatic hypotension, a sudden drop in blood pressure upon standing. Changes in sexual function and the body’s ability to regulate temperature are further examples of compromised autonomic control.
Conditions That Lead to Spinal Cord Atrophy
Spinal cord atrophy is a secondary process that occurs after the initial insult or progressive destruction of neural tissue caused by a primary condition. One major category includes neurodegenerative and demyelinating disorders, such as Multiple Sclerosis (MS). In MS, atrophy is thought to reflect widespread axonal degeneration and nerve cell loss, which occurs independent of the acute inflammatory lesions. The duration of the disease plays a significant role in the degree of cord shrinkage observed over time.
Traumatic injury is another prominent cause, with Spinal Cord Injury (SCI) leading to rapid and progressive atrophy both above and below the level of the initial trauma. The initial physical damage is followed by a secondary injury cascade that includes cell death and axonal retraction, reducing the overall cord volume. Chronic compression, such as that caused by severe degenerative spinal events or long-term instability, can also result in localized atrophy. In these cases, the persistent mechanical pressure restricts blood flow and physically deforms the cord, leading to tissue loss.
Genetic disorders like Spinal Muscular Atrophy (SMA) are defined by the degeneration of motor neurons located in the anterior horn of the spinal cord. This specific loss of nerve cell bodies and their outgoing axons results in a measurable, focal atrophy of the spinal cord tissue. Inflammatory conditions, including chronic myelitis or infections like HTLV-1 associated myelopathy, also cause tissue destruction and subsequent atrophy.
Confirming a Diagnosis
The diagnostic process begins with a detailed neurological examination to assess a patient’s reflexes, muscle strength, and sensory perception. This physical evaluation helps the physician map the neurological deficits and localize the probable segment of the spinal cord that is affected. Findings such as hyperreflexia, spasticity, or a distinct pattern of sensory loss guide the subsequent imaging studies. The examination provides functional evidence that correlates with the structural changes of atrophy.
Magnetic Resonance Imaging (MRI) is the gold standard for visualizing the spinal cord and confirming the presence of atrophy. On an MRI scan, atrophy is quantified by measuring the spinal cord cross-sectional area (SCCSA), most commonly at the C2-C3 vertebral level in the cervical spine. A reduced SCCSA compared to healthy controls is a direct indication of tissue loss. The MRI also helps in identifying the underlying cause by revealing lesions, tumors, or signs of chronic compression, which is necessary to plan effective management.
Ancillary electrodiagnostic tests, such as Electromyography (EMG) and Nerve Conduction Studies (NCS), are often used to assess the functional consequences of the atrophy. NCS measures the speed and strength of electrical signals traveling along the nerves, while EMG evaluates the electrical activity within the muscles. These tests help differentiate between nerve root damage, peripheral nerve disorders, and primary spinal cord issues by showing patterns consistent with motor neuron loss or denervation.