Superior and Middle Cluneal Nerve Entrapment: A Cause of Low Back and Radicular Pain.

BACKGROUND: The superior and middle cluneal nerves are sources of low back, buttock, and leg pain. These nerves are cutaneous branches of the lateral branches of the dorsal rami of T11- S4. Pain arising from entrapment or dysfunction of one or more of these nerves is called "cluneal nerve syndrome." A clear understanding of the anatomy underlying cluneal nerve syndrome and its treatment has been hampered by the very small size of the cluneal nerves and their complex, varying anatomy. Because of differing methods and foci of investigation, the literature regarding cluneal nerves has been confusing and even contradictory. OBJECTIVES: This paper provides a thorough critical literature review of cluneal nerve anatomy and implications for therapy. STUDY DESIGN: A modified scoping review. METHODS: The bibliographic trail of English language papers on the anatomy and treatment of cluneal nerve syndrome was used to resolve the contradictions that have appeared in some of the anatomic descriptions and, where applicable, to examine their implications for therapy. RESULTS: Recent anatomic and surgical investigations confirm a wider than previously realized range of central nervous system origins of these peripheral nerves, explaining why cluneal nerve dysfunction can cause a wide array of symptoms, including low back, buttock, and/or leg pain or "pseudosciatica." CONCLUSIONS: Cluneal nerve syndrome is characterized by a triad of pain, tender points, and relief with local anesthetic injections. The pain is a deep, aching, poorly localized low back pain with variable involvement of the buttocks and/or legs. Tender points are localized at the iliac crest or caudal to the posterior superior iliac spine. Muscle weakness and dermatomal sensory changes are absent in cluneal nerve syndrome. If the pain returns after injections, neuroablation, nerve stimulation, or surgical release may be needed.

Nerve Entrapment Headaches at the Temple: Zygomaticotemporal and/or Auriculotemporal Nerve?

BACKGROUND: Temple headaches are common, yet the anatomic etiology of headaches in this region is often confusing. One possible cause of temple headaches is dysfunction of the auriculotemporal nerve (ATN), a branch of the third division of the trigeminal nerve. However, the site of pain is often anterior to the described path of the ATN, and corresponds more closely to a portion of the path of a small branch of the second division of the trigeminal nerve called the zygomaticotemporal nerve (ZTN). OBJECTIVES: We present the anatomic and clinical differences between these 2 nerves and describe treatment approaches. Diagnosis is made by physical examination of the temporal fossa and the temporomandibular joint, and injection of local anesthetic over the tenderest nerve. RESULTS: In general, treatments of headaches that generated from the peripheral nerve attempt to neutralize the pain origin using surgical or interventional pain techniques to reduce nerve irritation and subsequently deactivate stimulated migraine centers. CONCLUSIONS: Treatment of temporal nerve entrapment includes medications, nerve injections, dental appliances, cryoneuroablation, chemical neurolysis, neuromodulation, and surgical decompression. KEY WORDS: Headache, migraine, trigeminal nerve, Frey's syndrome, zygomaticotemporal nerve, auriculotemporal nerve, temple pain, jaw pain, ear pain, tooth pain.

Treatment of phantom limb pain by cryoneurolysis of the amputated nerve.

The pathophysiology of phantom limb pain (PLP) is multifactorial. It probably starts in the periphery and is amplified and modified in the central nervous system. A small group of patients with PLP were questioned as to the portion of the phantom limb affected by pain (e.g., "great toe," "thumb"). In the stump, the corresponding amputated nerve was located with a nerve stimulator. With correct placement and stimulation, the PLP could then be reproduced or exacerbated. A small dose of local anesthesia was then injected, resulting in the disappearance of the PLP. If a peripheral nerve injection gave temporary relief, our final treatment was cryoanalgesia at this location. Evaluation of 5 patients, followed for at least 2.5 years, yielded the following results: 3 patients had excellent results (100%, 95%, and 90% decrease in complaints, respectively), 1 patient had an acceptable result (40% decrease), and 1 patient had only a 20% decrease in pain. Although both central and peripheral components are likely involved in PLP, treatment of a peripheral pain locus with cryoanalgesia should be considered. We propose the identification of a peripheral etiology may help match patients to an appropriate therapy, and cryoanalgesia may result in long-term relief of PLP.

Infrapatellar saphenous neuralgia - diagnosis and treatment.

Persistent anterior knee pain, especially after surgery, can be very frustrating for the patient and the clinician. Injury to the infrapatellar branch of the saphenous nerve (IPS) is not uncommon after knee surgeries and trauma, yet the diagnosis and treatment of IPS neuralgia is not usually taught in pain training programs. In this case report, we describe the anatomy of the saphenous nerve and specifically the infrapatellar saphenous nerve branch; we also discuss the types of surgical trauma, the clinical presentation, the diagnostic modalities, the diagnostic injection technique, and the treatment options. As early as 1945, surgeons were cautioned regarding the potential surgical trauma to the IPS. Although many authors dismissed the nerve damage as unavoidable, the IPS is now recognized as a potential cause of persistent anterior and anteriomedial knee pain. Even more concerning, damage to peripheral nerves such as the IPS has been identified as the cause and potential perpetuating factor for conditions such as complex regional pain syndromes (CRPS). Because the clinical presentation may be vague, it has often been misdiagnosed and underdiagnosed. There is a documented vasomotor instability, but, unfortunately, sympathetic blocks will not address the underlying pathology, and therefore patients often will not respond to this modality, although the correct diagnosis can lead to rapid and gratifying resolution of the pathology. An entity unknown to the clinician is never diagnosed, and so it is important to familiarize pain physicians with IPS neuropathy so that they may be able to offer assistance when this painful condition arises.

A comparison of three doses of a commercially prepared oral midazolam syrup in children.

UNLABELLED: Midazolam is widely used as a preanesthetic medication for children. Prior studies have used extemporaneous formulations to disguise the bitter taste of IV midazolam and to improve patient acceptance, but with unknown bioavailability. In this prospective, randomized, double-blinded study we examined the efficacy, safety, and taste acceptability of three doses (0.25, 0.5, and 1.0 mg/kg, up to a maximum of 20 mg) of commercially prepared Versed((R)) syrup (midazolam HCl) in children stratified by age (6 mo to <2 yr, 2 to <6 yr, and 6 to <16 yr). All children were ASA class I-III scheduled for elective surgery. Subjects were continuously observed and monitored with pulse oximetry. Ninety-five percent of patients accepted the syrup, and 97% demonstrated satisfactory sedation before induction. There was an apparent relationship between dose and onset of sedation and anxiolysis (P < 0.01). Eight-eight percent had satisfactory anxiety ratings at the time of attempted separation from parents, and 86% had satisfactory anxiety ratings at face mask application. The youngest age group recovered earlier than the two older age groups (P < 0.001). There was no relationship between midazolam dose and duration of postanesthesia care unit stay. Before induction, there were no episodes of desaturation, but there were two episodes of nausea and three episodes of emesis. At the time of induction, during anesthesia, and in the postanesthesia care unit, there were several adverse respiratory events. Oral midazolam syrup is effective for producing sedation and anxiolysis at a dose of 0.25 mg/kg, with minimal effects on respiration and oxygen saturation even when administered at doses as large as 1.0 mg/kg (maximum, 20 mg) as the sole sedating medication to healthy children in a supervised clinical setting. IMPLICATIONS: Commercially prepared oral midazolam syrup is effective in producing sedation and anxiolysis in doses as small as 0.25 mg/kg; there is a slightly faster onset with increasing the dose to 1.0 mg/kg. At all doses, 97% of patients demonstrated satisfactory sedation, whereas 86% demonstrated satisfactory anxiolysis when the face mask was applied.