It’s NERVEmber and Consultant & Neurosurgeon – Zeljko Kojadinovic, MD, PhD wants us to think about the specific nerve disease – Shingles and how it mimics heart disease.
A Heart Attack — or Something Completely Different?
Imagine someone waking up with severe pain on the left side of their chest. The pain feels deep, sharp, and frightening. Their first thought is a heart attack. At the emergency department, doctors investigate a possible cardiac emergency. The evaluation is reassuring, but the pain continues. Three days later, small blisters appear along the painful area, extending from the back toward the front of the chest. Suddenly, the explanation becomes clear.
The pain was caused by shingles — but the rash had not yet appeared.
This illustrative scenario reveals a diagnostic challenge: herpes zoster can produce substantial nerve pain several days before its characteristic skin eruption. But what happens when the rash never appears? Or when the nerve pain has nothing to do with a virus?
The real question is not simply whether the heart is healthy. It is what structure is actually generating the pain.
Shingles: Why It Can Mimic Heart Disease and Why Early Recognition Matters
After chickenpox, the varicella-zoster virus remains inactive for years, sometimes decades, in sensory nerves (more precisely, in their ganglia). Shingles (herpes zoster) develops when the virus becomes active again. The intercostal nerves are among the nerves most commonly affected by shingles. Because these nerves supply the chest wall, viral inflammation can produce burning, stabbing, or deep constricting pain in the same region where patients may perceive heart-related pain. The characteristic blistering skin rash may appear several days after the pain begins, although some patients develop the rash without preceding pain.
Recognizing shingles early matters. Antiviral treatment is most effective when started promptly, ideally within 72 hours of rash onset, although treatment after this period may still be appropriate in selected patients. Antivirals can shorten the acute illness and reduce its severity.
Vaccination also substantially reduces the risk of shingles and postherpetic neuralgia. In the United States, recombinant zoster vaccination is recommended for adults aged 50 and older and for certain immunocompromised adults aged 19 and older.
What if the Shingles Rash Never Appears?
Occasionally, varicella-zoster virus reactivation occurs without the typical skin eruption. This is called zoster sine herpete. A patient may develop unilateral thoracic pain, burning, or hypersensitivity without blisters to reveal the underlying process.
Intercostal nerve irritation, thoracic radiculopathy, and musculoskeletal disorders may produce similar symptoms. When viral reactivation is suspected without a rash, careful clinical assessment and appropriate virological evidence may be needed.
The absence of visible skin changes should neither automatically exclude shingles nor become an explanation for every unexplained chest pain. This distinction is particularly important in patients with a previous history of shingles. New or recurrent pain in the same area may be related to postherpetic neuralgia, another nerve disorder, or a completely unrelated disease — including a heart attack. A previous diagnosis of shingles must never become a reason to overlook a potentially serious cardiac or other internal-organ condition.
When Shingles Is Over but the Pain Remains
For many patients, shingles-related pain improves as the skin lesions heal. For others, neuropathic pain continues. This is postherpetic neuralgia, a potentially disabling complication of herpes zoster.
Patients describe burning, electric shocks, stabbing sensations, or severe sensitivity to touch. Even clothing brushing against the affected skin may become intolerable. Persistent pain may reflect nerve injury and changes in how the nervous system processes pain. However, persistent pain after shingles should not automatically be attributed solely to nerve damage (neuropathy) caused by the virus. Even when the initial viral inflammation has resolved, the affected nerve may continue to generate pain on its own, while also remaining sensitive to mechanical irritation from surrounding muscles, fascia, rib movements, or thoracic spinal structures, as well as to persistent local inflammation and muscle spasms. These factors can trigger or amplify pain in an already sensitized nerve, sometimes becoming important contributors to its persistence.
In other words, nerve damage may explain how the pain started, but it does not necessarily explain everything that keeps it going.
The Intercostal Nerve (Intercostal Neuralgia): An Overlooked Source of Chest Pain
Shingles demonstrates how irritation and inflammation of thoracic nerves can generate severe chest pain. But a virus is not required for that. There are 11 pairs of intercostal nerves (T1–T11), while the twelfth thoracic nerve runs below the last rib and is called the subcostal nerve. Their sensory territories extend from the upper chest to the abdominal wall. Intercostal nerves travel beneath the ribs, carrying sensory signals from the chest wall toward the spinal cord. When irritated or injured, an intercostal nerve can produce pain extending from the back around the rib cage toward the front of the chest. Potential causes include trauma, thoracic surgery, scarring, nerve entrapment, and mechanical irritation associated with rib movement. The source may also lie in a thoracic nerve root irritated by disc herniation, spondylotic changes, tumors or other processes in the spinal canal. Pain that occurs in this way is called intercostal neuralgia.
The level of the affected nerve can dramatically change what disease the pain seems to suggest. Irritation of upper or middle thoracic nerves may produce pain over the heart or breast, while involvement of lower intercostal nerves may cause pain in the upper abdomen, sometimes resembling gallbladder, liver, or gastrointestinal disease.
Just as nerve pain can be mistaken for heart disease, the same diagnostic confusion can occur with these other organs — leading to repeated investigations while the actual source of pain remains overlooked.
Five Clues That Chest Pain May Be Nerve-Related
Once urgent causes have been appropriately evaluated, several findings may direct attention toward the chest wall and thoracic nerves.
- The pain follows a recognizable path.
A band extending from the back around one side of the chest may suggest intercostal nerve or thoracic root involvement. - Movement changes the pain.
Rotation, bending, coughing, or deep breathing may reproduce symptoms involving mechanically sensitive structures. - Pressure reproduces the familiar pain.
A specific tender point near a rib, intercostal space, or thoracic spine may help localize the source. - Sensation is altered.
Burning, numbness, tingling, hypersensitivity, or pain from light touch may indicate neuropathic involvement. - Cardiac investigations are reassuring, but the chest wall and thoracic nerves have not been examined systematically.
These findings are useful clinical clues, not independent methods of ruling out heart disease.
Limitations of Tests for Chest Pain
Patients often assume that normal investigations mean no physical explanation exists. But every diagnostic test has limitations. An ECG evaluates cardiac electrical activity. Echocardiography examines cardiac structure and function. Neither identifies whether an intercostal nerve becomes irritated during trunk rotation. Even MRI may not reveal every painful process. However, reassuring routine cardiac tests do not exclude every cardiac disorder. Coronary microvascular dysfunction and coronary vasospasm may require additional evaluation when clinically suspected.
For diagnosing intercostal neuralgia, a careful clinical examination remains essential, sometimes supplemented by targeted diagnostic nerve blocks.
Finding the Real Pain Generator: Three Essential Questions
An injured intercostal nerve, a compressed thoracic nerve root, and a painful rib joint or costochondral junction (often diagnosed as costochondritis) may produce remarkably similar symptoms — but they do not necessarily require the same treatment.
Throughout my clinical practice and international telehealth consultations, I have encountered many patients whose persistent pain had been attributed to diseases of internal organs, even though repeated investigations failed to adequately explain their symptoms. Despite differences in healthcare systems, the same diagnostic problem appears worldwide: the organ where pain is felt receives extensive attention, while the nerves and surrounding structures that may actually generate the pain remain overlooked. In many of these patients, a focused neurological and musculoskeletal assessment helped identify the previously unrecognized source of pain.
My diagnostic approach to thoracic pain is based on answering three essential questions:
First: Which anatomical structure is actually generating the pain, if organ disease is excluded?
Is it an intercostal nerve, a thoracic nerve root, a rib joint, or surrounding tissue? Targeted examination, sensory mapping, selected movements, imaging review, and occasionally diagnostic nerve blocks may help clarify the source.
Second: What pathological process is affecting that structure?
Is there nerve injury, compression, inflammation, mechanical irritation, or persistent sensitization?
Third: What is keeping the pain active?
Persistent pain may be maintained by multiple interacting factors. These include mechanical overload, repetitive strain, muscle and fascial dysfunction, ongoing inflammation, metabolic disturbances such as insulin resistance, excess body weight, nutritional deficiencies, hormonal disorders, and impaired tissue recovery. Peripheral and central sensitization, autonomic dysfunction, poor sleep, physical deconditioning, psychological stress, medication effects, and other medical conditions may further contribute to pain persistence. Identifying these factors requires a systematic diagnostic algorithm to assess and, where appropriate, confirm or exclude each potentially relevant contributor, so that important factors are not overlooked. The original pathological process may explain how the pain began, but successful treatment also requires identifying and addressing the contributing factors that continue to maintain or aggravate it.
The objective is to move from a symptom label (such as thoracic pain) or a general diagnosis (such as intercostal neuralgia) to an anatomically and patho-physiologically meaningful diagnosis. When we identify the structure generating the pain, the pathological process affecting it, and the contributing factors that trigger, aggravate, or maintain that process, we can develop a targeted and potentially more effective treatment strategy.
Treatment Must Address the Pain Generator, the Pathological Process, and Contributing Factors
Effective treatment requires more than selecting medication for a particular type of pain. It must address the anatomical source, the pathological process affecting it, and the factors that contribute to its development or persistence.
For neuropathic pain, medications such as gabapentin, pregabalin, or certain antidepressants may be appropriate. Topical treatments can also help patients with localized postherpetic neuralgia.
When mechanical irritation, muscle dysfunction, or other musculoskeletal contributors are identified, targeted rehabilitation, movement modification, and appropriate local treatments may be beneficial. Selected patients may also benefit from diagnostic or therapeutic nerve blocks and other interventions.
Metabolic disturbances, nutritional deficiencies, chronic inflammation, sleep disorders, and other relevant contributing factors should also be assessed and addressed when present.
The goal is not simply to reduce pain temporarily, but to treat its underlying cause and the factors that continue to aggravate or maintain it.
Never Ignore a Possible Heart Emergency
New, severe, or worsening chest pain requires prompt medical evaluation, particularly when accompanied by breathlessness, sweating, fainting, or other concerning symptoms. A single normal ECG cannot reliably exclude acute coronary syndrome. Depending on clinical risk, assessment may require cardiac biomarkers, repeated ECGs, or additional investigations.
Shingles, intercostal neuralgia, and heart disease are not mutually exclusive.
First exclude what may be life-threatening. Then investigate what may have been overlooked.
Conclusion
When cardiac investigations do not explain persistent chest pain, the diagnostic process should not simply end.
Once serious cardiac conditions have been appropriately excluded, other possible sources of chest pain should be investigated, including shingles, intercostal nerve irritation, and disorders of the chest wall or thoracic spine. These conditions can produce pain that closely resembles heart disease but cannot be identified by routine cardiac tests.
Successfully treating thoracic pain requires identifying the anatomical structure generating the pain, the pathological process affecting it, and the contributing factors that trigger, aggravate, or maintain that process. Only then can treatment be appropriately targeted at the underlying causes rather than the symptoms alone.
About the Author: Zeljko Kojadinovic, MD, PhD, is a consultant neurosurgeon with more than 30 years of clinical experience, including over 15 years of international hospital practice. His clinical work focuses on the diagnosis and treatment of complex neuropathic and chronic pain conditions, with particular emphasis on identifying the underlying pain generator and providing individualized treatment recommendations.
Alongside his hospital practice, he also provides international telehealth consultations and specialist second opinions for patients with complex and persistent pain conditions.
