The International Association for the Study of Pain defines hyperesthesia as “increased sensitivity to stimulation, excluding the special senses,” which “may refer to various modes of cutaneous sensibility including touch and thermal sensation without pain, as well as to pain.” While hyperesthesia can be used to describe any increased sensitivity to a stimulus, it is commonly used to describe a painful sensation from a stimulus.
Hyperesthesia is a common symptom of neuropathic pain. Neuropathic pain is defined by the International Association for the Study of Pain as “pain caused by a lesion or disease of the somatosensory system.” The neuropathic pain phenotype contains a spectrum of symptoms that can be roughly categorized into positive and negative symptoms. Hyperesthesia is a positive symptom of neuropathic pain. Positive symptoms are categorized as stimulus-dependent pain, stimulus-independent pain, and paresthesias. Neuropathic pain affects about 7-8% of the general population.
In this article, hyperesthesia will be defined as an increased cutaneous sensitivity manifesting as stimulus-dependent neuropathic pain. The most common hyperesthesias are allodynia and hyperalgesia. Allodynia is a pain caused by a stimulus that usually does not elicit a painful response (i.e., pain on light touch). Hyperalgesia is an exaggerated pain response to a stimulus that usually causes pain (i.e., out of proportion pain from a pinprick). While most neuropathic pain symptoms are contained within the dermatomal distribution of the affected nerve, hyperesthesia has been known to extend beyond the affected nerve’s distribution. This can sometimes obscure the correct diagnosis and lead to the inappropriate diagnosis of a psychosomatic disorder.
A detailed history and a thorough physical examination should be sufficient to identify the underlying etiology. Routine laboratories should be ordered as part of the workup. Special laboratory, diagnostic, and imaging tests may have to be ordered to make a definitive diagnosis of the etiology. Treatable and reversible etiologies should be promptly treated. The mainstay of treatment is symptomatic relief via pharmacological, non-pharmacological, and interventional therapies. Symptoms are typically challenging to eliminate, and patients will most likely continue to experience persistent symptoms. A multidisciplinary team approach has been shown to provide the most effective and lasting results.
Neuropathic pain symptoms, including hyperesthesia, develop secondarily to a disease or a lesion of the nervous system that results in abnormal functioning of the somatosensory system. The etiology of hyperesthesia can be categorized anatomically or etiologically. Anatomically speaking, the source can be either central or peripheral.
Epidemiological studies of hyperesthesia are technically challenging to perform. Barriers to performing accurate epidemiological studies include the vast amount of conditions that can cause hyperesthesia and the subjective nature of hyperesthesia. Two epidemiological studies that focused on the prevalence of chronic pain with neuropathic pain features estimated that the prevalence of neuropathic pain among the general population to be 7% to 8%.
One study that used a questionnaire to assess sensory symptoms in patients with painful diabetic neuropathy (PDN) and postherpetic neuralgia (PHN) found that allodynia was present in about 50% of the PHN patients. That study contained 1600 patients with PDN, of which 18% reported pain to light touch, and 14% reported occasional pain with heat or cold. Another study performed quantitative sensory testing of 1236 patients with diagnosed neuropathic pain. The study used both mechanical and thermal stimuli. Their results showed that 20% of patients had brush-provoked allodynia. The study also found that mechanical hyperalgesias (pinprick 29% and blunt pressure 36%) occurred more often than thermal hyperalgesias (hot 24% and cold 19%).
The pathophysiology of neuropathic pain has been extensively studied, and several important mechanisms have been identified. Some of the identified mechanisms provide clear explanations for the development of hyperesthesias. The mechanisms that lead to the development of hyperesthesia are central sensitization of the somatosensory system, peripheral sensitization of the somatosensory system, and dysfunction of endogenous pain inhibition. It is believed that mechanical hyperesthesia(e.g., light pinprick and light manual pressure) and mechanical allodynia (i.e., stroking the skin with a brush) is due to the sensitization of the somatosensory system (i.e., peripheral sensitization and central sensitization) and dysfunction of endogenous pain inhibition. Cold hyperesthesias are believed to be due to either peripheral sensitization or central disinhibition. Heat hyperesthesias are believed to be due to peripheral sensitization of nerve fibers.
History: A thorough history should be performed, as this should be sufficient to make a diagnosis of hyperesthesia.
Physical exam: A complete neurological exam should be performed in addition to a general focused physical exam.
The first step should be to determine whether the etiology is peripheral or central. It is essential to accurately diagnose the cause of hyperesthesia to provide treatment of any treatable underlying cause.
Imaging: imaging is typically not needed to diagnose hyperesthesia, but it helps diagnose specific conditions.
Treatment of hyperesthesia and other neuropathic pain symptoms is challenging but is best achieved by using a multidisciplinary team approach that can focus on treating underlying causes, administer pharmacotherapy, apply interventional therapy, address functional impairments, and provide mental health services if needed. Realistic goals for hyperesthesia should be established early on. Any comorbidities such as mood disorders or sleep disturbances should be addressed promptly. Patients typically require close follow-up to monitor response to therapy and continued evaluation of the underlying cause.
For peripheral neuropathy, the most common treatable causes are diabetes mellitis, hypothyroidism, and nutritional deficiencies. Other causes of hyperesthesia, such as nerve root compression or peripheral nerve entrapment, may be initially treated conservatively with symptomatic pharmacotherapeutic support, physical therapy, lifestyle modifications, and minimally invasive procedures (i.e., epidural steroid injection or peripheral nerve injection). However, if there is worsening or stagnation of function, surgery may be required.
Pharmacological treatments can be used to treat both central and peripheral causes of hyperesthesia. Of the pharmacological options available, antidepressants and antiepileptic drugs are the most widely used. General guidelines for treatment are provided below; however, recommendations for the treatment of choice for specific etiologies are provided.
First-line drugs: These drugs have the most substantial evidence to support their treatment of neuropathic pain symptoms. This group contains two classes of antidepressants and one class of antiepileptic drugs.
Not all patients will respond to monotherapy; in fact, 45% of individuals with neuropathic pain are on two or more medications for their pain. If a patient fails first-line monotherapy, they can be used in combination (i.e., gabapentinoid + TCA or SNRI).
Some interventional treatments currently being practiced lack robust trials to be recommended by the guidelines. Some of the interventions that require continued research are radiofrequency denervation of the dorsal root ganglion, adhesiolysis for FBSS, TENS, spinal cord stimulation, and motor cortex stimulation.
It is difficult to completely eliminate hyperesthesias and other neuropathic pain symptoms. This should be explained to the patient early during the treatment course. Monotherapy should be initially started; however, 45% of the patients with neuropathic pain are on two or more medications for their pain.
Complications of hyperesthesia include increased morbidity if symptoms are not controlled. The patient may also experience increased morbidity from extensive interventional procedures. Also, if the patient is started on potent opioids for treatment, the patient may become addicted.
Consultations with the following may be required:
Here are important points to take note of:
Early identification of hyperesthesia and other neuropathic pain symptoms is essential to start the patient on a proper treatment plan. The education of the patient early on during the treatment is necessary to establish realistic pain goals. Always treat with a multidisciplinary team approach. While the general practitioner is almost always involved in the care of patients with hyperesthesia, it is essential to consult with an interprofessional team of specialists that include pain medicine specialists, sleep medicine professionals, physical therapy, and occupational therapy. A psychiatrist and psychologist evaluations are recommended as many patients suffer from mood disorders.
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