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SAEM Clinical Images Series: Pain, Paralysis, and Rash

The patient is an 81-year-old female with a history of asthma and hypertension who presents to the Emergency Department with right-sided abdominal swelling for five days. Five days ago, the right side of her abdomen appeared to protrude more than the left. This protrusion then increased over the next 2-3 days. The patient was diagnosed with shingles to the right lower abdomen earlier that month, but her rash has now nearly resolved. She continues to have “electric” pain in the region of the prior shingles infection. She denies any fevers, abdominal trauma, vomiting, or changes in bowel or bladder habits. She has never had anything like this before.

 

Vitals: All vital signs are normal.

Abdomen: See image provided. There is a firm unilateral distention of the right lower abdomen without shifting dullness or fluid wave. No palpable masses are present. There is moderate tenderness over the protruding region but no rebound or guarding. Bowel sounds are present.

Skin: See image provided. Moderate tenderness to palpation over region.

CBC and CMP are unremarkable.

CT scan of the abdomen and pelvis: No evidence of acute abnormality. Normal appendix. Moderate stool burden.

This patient has a Zoster pseudohernia.

Varicella-Zoster Virus (Shingles).

Zoster pseudohernia (ZP) occurs when the zoster infection infiltrates a posterior thoracic dermatome, affecting the spinal nerve roots responsible for the motor function of the abdominal wall. ZP typically presents with a rapidly progressive unilateral outpouching of the abdomen, giving a hernia-like appearance, but with intact abdominal wall musculature. In most cases, the classic Herpes Zoster rash precedes ZP, however in up to 10% of patients ZP may be the first presenting sign of zoster. Although uncommon, the symptoms are often distressing to patients, with many presenting to emergency departments or surgical offices for initial evaluation. The diagnosis is clinical and is based on a history of zoster infection or classic zoster symptoms and lack of findings suggesting alternate pathology. Abdominal CT or other imaging is recommended to exclude tumors, true hernias, free fluid, or other possible causes of abdominal distention. Electromyography (EMG) can be used to support diagnosis and will typically be abnormal due to the dysfunction of the abdominal wall musculature. Complete recovery occurs in 70-80% of patients within about 4-5 months.

Take-Home Points

  • Zoster Pseudohernia is a rare presentation of herpes zoster infection resulting in dysfunction of the abdominal wall musculature.

  •  There is no specific treatment with most cases fully resolving within several months to one year.

  • Chernev I, Dado D. Segmental zoster abdominal paresis (zoster pseudohernia): a review of the literature. PM R. 2013 Sep;5(9):786-90. doi: 10.1016/j.pmrj.2013.05.013. PMID: 24054853.
  • Yoo J, Koo T, Park E, Jo M, Kim MS, Jue MS. Abdominal pseudohernia caused by herpes zoster: 3 case reports and a review of the literature. JAAD Case Rep. 2019 Aug 5;5(8):729-732. doi: 10.1016/j.jdcr.2019.06.019. PMID: 31440570; PMCID: PMC6698640.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.



By |2026-01-25T20:35:10-08:00Jan 26, 2026|Infectious Disease, Neurology, SAEM Clinical Images|
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SAEM Clinical Images Series: I Cannot Control My Right Side

CT

The patient is a 47-year-old female whose past medical history includes ESRD on dialysis, type 1 diabetes, and hypertension, who presents to the Emergency Department for uncontrollable right-sided movements of her body. The patient states these symptoms have been present for several weeks and have progressively worsened over the past week. She reports difficulty with ambulation secondary to these involuntary movements of the right side of her body. She denies any missed dialysis sessions. She denies fever, headaches, sensory problems, or any other complaints at this time.

Vitals: BP 201/88 HR 92 R 18 T 97.5 O2sat 99% room air.

General: Awake and alert, no acute distress.

Cardiovascular: Regular rate and rhythm with no murmur. Right upper extremity fistula with good thrill and no signs of infection.

Neurologic: GCS 15, moving all four extremities well. Cranial nerves intact, but repetitive twitching of the right side of the face is seen on examination. There are repetitive jerking movements of her right upper and right lower extremity. Sensation intact and equal bilaterally.

CMP: 

Na 127
K 4.5
Cl 92
HCO3 25
BUN 24
Creat 5.5
Glucose 540

Hyperintensity along the left lentiform nucleus.

Hemichorea-Hemiballismus Syndrome.

There is a stripe of hyperintensity along the left lentiform nucleus seen on head CT, which is a finding consistent with hemichorea- hemiballismus syndrome. This syndrome is a rare presentation that can occur in the setting of acute hyperglycemia or uncontrolled diabetes. Patients with hemichorea-hemiballismus syndrome typically present with involuntary movements of upper and lower limbs, usually unilaterally, but in even more rare cases bilateral symptoms may occur. Neuroimaging may show hyperintense lesions along the contralateral striatum of the affected extremities. Proposed pathophysiology of this syndrome includes hyperviscosity secondary to hyperglycemia and disruption of the blood- brain barrier, decrease in GABA availability in the striatum, and hypersensitivity of the dopamine system receptors due to decreased estrogen concentration in postmenopausal women. Treatment includes management of hyperglycemia; neurological symptoms typically resolve with glycemic control.

Take-Home Points

  • Hemichorea-hemiballismus syndrome can occur in the setting of hyperglycemia and uncontrolled diabetes, and it typically presents with unilateral involuntary movements of the body.
  • Neurological symptoms resolve with management of hyperglycemia and improved glycemic control.

  • Dong M, E JY, Zhang L, Teng W, Tian L. Non-ketotic Hyperglycemia Chorea-Ballismus and Intracerebral Hemorrhage: A Case Report and Literature Review. Front Neurosci. 2021;15:690761. Published 2021 Jun 23. doi:10.3389/fnins.2021.690761
  • Salem A, Lahmar A. Hemichorea-Hemiballismus Syndrome in Acute Non-ketotic Hyperglycemia. Cureus. 2021;13(10):e19026. Published 2021 Oct 25. doi:10.7759/cureus.19026

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-12-16T22:35:25-08:00Dec 19, 2025|Emergency Medicine, Neurology, SAEM Clinical Images|
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SAEM Clinical Images Series: Ptosis? A Don’t Miss Diagnosis!

ptosis

A 50-year-old female with no past medical history presented to the emergency department for a headache. She developed progressive dull, left-sided head pain with sinus pressure one week prior, associated with sleep disturbance. In addition, she described two days of left eyelid drooping. She had no fever, chills, cough, difficulty breathing, neck pain, jaw claudication, vision changes, dizziness, numbness, or recent weight loss. She also denied any recent trauma to the head or neck.

 

Vitals: BP 119/59; PR 92; Temp 37°C; RR 16; SpO2 100% on RA

General: Well-appearing, no acute distress.

HEENT: EOMI, left eyelid ptosis with miosis of left pupil.

Cardiovascular: RRR, normal S1/S2, no murmur.

Neurologic: Alert and oriented x 3, normal strength and sensation bilateral upper and lower extremities, left ptosis and miosis, otherwise cranial nerves II-XII unremarkable.

WBC: 8.9

INR: 0.9

This patient presented with Horner Syndrome, a triad of ipsilateral anhidrosis, miosis, and ptosis, the latter two of which are evident in this clinical image. Horner Syndrome presents when a lesion or insult disturbs the three-order sympathetic pathway that innervates the head, neck, and ipsilateral eye. Physical examination findings may be variable and/or subtle in patients with carotid dissection. Interestingly, isolated Horner Syndrome is the only abnormal physical finding in up to 50% of patients with carotid dissection. Further, patients with carotid dissection may present with only a partial Horner’s, with anhidrosis limited to the ipsilateral eyebrow, which can be difficult to identify. Evaluation of a patient with a new Horner Syndrome in the emergency department should include CT brain, CXR, and, if there is concern for carotid artery dissection, CTA or MRA head/neck. Carotid artery dissection is a neurologic emergency with significant morbidity and mortality ranging between 25-46% if left untreated. Management requires emergent neurology consultation with activation of the stroke team, as the treatment may require systemic thrombolytics and/or mechanical thrombectomy. Patients who present outside the time-window for stroke care, or who demonstrate resolving symptoms should be treated with antiplatelet or anticoagulant therapy. Notably, for patients with intracranial dissection or dissection involving the aorta, the preferred treatment is antiplatelet therapy in conjunction with neurology consultation.

Horner syndrome has a broad differential diagnosis including stroke, neoplastic disease (brain, neck or lung), vascular injury, demyelinating disease, lymphoma, and iatrogenic injuries. This patient’s Horner syndrome was attributable to a carotid artery dissection (the most common vascular cause of Horner’s). Carotid dissection may occur after blunt trauma to the neck, but also as a result of seemingly innocuous movements of the neck. For example, evidence suggests that yoga, massage, and roller coaster rides each may increase risk for carotid dissection.

Take-Home Points

  • Horner syndrome is the triad of ipsilateral anhidrosis, miosis, and ptosis, although physical exam findings may be subtle.

  • The differential for Horner Syndrome includes several urgent and emergent underlying etiologies.

  • Carotid artery dissection is an important cause of Horner Syndrome to consider in the appropriate clinical context.

  • Hakimi R, Sivakumar S. Imaging of Carotid Dissection. Curr Pain Headache Rep. 2019 Jan 19;23(1):2. doi: 10.1007/s11916-019-0741-9. PMID: 30661121.

  • Keser Z, Chiang CC, Benson JC, Pezzini A, Lanzino G. Cervical Artery Dissections: Etiopathogenesis and Management. Vasc Health Risk Manag. 2022 Sep 2;18:685-700. doi: 10.2147/VHRM.S362844. PMID: 36082197; PMCID: PMC9447449.

  • Flaherty PM, Flynn JM. Horner syndrome due to carotid dissection. J Emerg Med. 2011 Jul;41(1):43-6. doi: 10.1016/j.jemermed.2008.01.017. Epub 2008 Sep 14. PMID: 18790590.

  • Maloney WF, Younge BR, Moyer NJ. Evaluation of the causes and accuracy of pharmacologic localization in Horner’s syndrome. Am J Ophthalmol. 1980 Sep;90(3):394-402. doi: 10.1016/s0002-9394(14)74924-4. PMID: 7425056.

  • Stein DM, Boswell S, Sliker CW, Lui FY, Scalea TM. Blunt cerebrovascular injuries: does treatment always matter? J Trauma. 2009 Jan;66(1):132-43; discussion 143-4. doi: 10.1097/ TA.0b013e318142d146. PMID: 19131816.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-04-03T09:22:20-07:00Apr 4, 2025|Neurology, SAEM Clinical Images|
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Greater Occipital Nerve Block in the Emergency Department

Chief complaints of non-traumatic headaches represent approximately 2% of emergency department (ED) visits in the United States [1]. Headaches are classified as primary (standalone condition) or secondary (a symptom of another medical condition), with primary headaches being the more common type [2].

In the ED, it is critical to rule out life-threatening causes of headaches such as subarachnoid hemorrhages, stroke, or meningitis. Headaches such as migraines, occipital neuralgia, cervicogenic headaches, and cluster headaches while more benign may still be debilitating for patients (Figure 1).

GON headache types

Figure 1. Headaches that may benefit from greater occipital nerve blockade [illustration by Dr. Felipe Ocampo]

Treatment of such headaches includes supportive care, medications, and procedures, including blockade of the greater occipital nerve (GON) [3, 4]. Peripheral nerve blocks such as GON blockade provide pain relief and its effects may outlast the duration of the local anesthetic. The GON block is an efficient, low-cost, and safe intervention for treatment of such headaches in the ED [5, 6]. In this article, we review the GON block, its relevant anatomy, indications, and procedural technique.

Identifying the Greater Occipital Nerve

Anatomy

Bilaterally, the GON originates from the second cervical spinal nerve (C2) and innervates the posterior scalp [7].

After arising from the C2 spinal nerve, the fibers of the GON ascend through the fascial plane between the obliquus capitis inferior and semispinalis capitis muscles. The fibers then pierce the semispinalis capitis and travel deep to the trapezius muscle until exiting the aponeurosis inferior to the superior nuchal line where it lies subcutaneously, medial to the occipital artery (Figure 2). The nerve measures approximately 2.5 to 3.5 mm in diameter [8].

Anatomy of greater occipital nerve for block

Figure 2: Anatomy around the greater occipital nerve (occipital aspect of the skull) [illustration by Dr. Felipe Ocampo]

GON Block: Necessary Equipment

The basic supplies one should collect for the GON block procedure:

  • Chlorhexidine gluconate or isopropyl alcohol applicator
  • 5 mL syringe
  • 18 gauge needle for drawing solution
  • 2 to 4 mL of either: 0.25 – 0.5% bupivacaine or 1 – 2% lidocaine
    • Consider a 1:1 mix in the same syringe for both short and longer lasting relief,
    • Example: 1.5 mL 1% lidocaine + 1.5 mL 0.25% bupivacaine
  • 1.5 inch 25- or 27-gauge needle for injecting solution

Note about inclusion of corticosteroids: The data is weak except in the case of cluster headaches where it is moderate [9].

equipment for greater occipital nerve block

Figure 3. Basic equipment necessary to perform a GON block [illustration by Dr. Felipe Ocampo]

GON Block: Procedural Technique

Procedural Technique #1: Palpation Approach

Traditionally, the GON block can be done by palpating the external occipital protuberance (OP) and the mastoid process (MP). Anesthetic is injected approximately one-third the distance from the OP to the MP (Figure 4) [6]. With this approach, the nerve is targeted more distally from its origin, where it is found more superficially at a median depth of 8 mm [10]. Here, the occipital artery can typically be palpated lateral to the location of the greater occipital nerve but anatomy can vary [11].

surface anatomy injection site for greater occipital nerve block

Figure 4: Injection site for the greater occipital nerve block along the occipital surface of the scalp [illustration by Dr. Felipe Ocampo]

  1. Position patients with their head flexed forward with either technique:
    • Sitting on the edge of the bed with their palms (or a procedure stand with a pillow) supporting their face
    • Prone with a pillow under the chest
  2. Find landmarks by palpating the external OP and MP
  3. Your target will be approximately one-third the distance from the OP to MP
  4. Ensure there is no palpable pulse at your target
  5. After sterilizing the area, insert the needle approaching from an inferior angle.
    • If you hit periosteum/skull, withdraw the needle slightly
    • Aspirate to ensure that you are not in the occipital artery or another vessel
    • Inject the anesthetic solution (typically 1-3 mL per side)
    • Consider slightly withdrawing and advancing while injecting to bathe multiple planes in anesthetic
  6. Assess for numbness along the posterior scalp (within 5 minutes for lidocaine and 10-15 minutes for bupivacaine)

Note: A modified version of this technique is to ask patients to pinpoint the area where pain is maximal or originates and if in general distribution of the GON between the OP and MP, this can be targeted assuming no palpable pulse and/or blood on withdrawal of syringe.

Procedural Technique #2: Ultrasound-Guided Approach

For the ultrasound-guided approach, the GON is typically targeted more proximally from its origin, at the level of the C2 vertebra. Here, the GON lies within the fascia above the obliquus capitis inferior (OCI) at a median depth of 1.8 cm [10].

  1. Positioning: same as landmark approach above.
  2. Prep the skin and transducer before insertion of the needle.
  3. Apply a generous amount of ultrasound gel to the lower posterior scalp
  4. A high-frequency linear probe is used with the indicator pointing towards the scanner’s left in the axial view starting at the midline external occipital protuberance (OP). With this view, one can see the semispinalis capitis (SSC) on either side. Note that this view may not be attainable in a patient with longer hair.
  5. Then, the probe can be translated downwards until the bifid C2 spinous process is visualized – here the trapezius, SSC, and obliquus capitis inferior (OCI) are seen on either side.
  6. By rotating the probe obliquely and slightly laterally towards the ear of the affected side, one can visualize the GON lying in the fascia above the OCI. Once this view is achieved, lateral to medial in-plane technique can be used to position the needle (25-27 gauge needle) adjacent to the GON, injecting 1-3 mL of solution to achieve spread around the nerve.
    • Pro Tip: The GON is often not visualized on ultrasound, but as long as your other landmarks are clear (between the OCI and SSC), injecting the solution into the plane is sufficient as long as you visualize your needle tip and confirm you are not intravascular.
  7. As with the palpation method, assess for numbness along the posterior scalp after 5-15 minutes, depending on anesthetic used.

ultrasound GON block

Figure 5: Illustrated sonographic views around the greater occipital nerve (yellow); SSC – semispinalis capitis, OP – occipital protuberance, TM – trapezius muscle, OCI – obliquus capitis inferior, C2 – C2 vertebra [illustration by Dr. Felipe Ocampo]

Greater occipital nerve block GON ultrasound anatomy

Figure 6: Sonographic anatomy of the greater occipital nerve (GON); TM- trapezius muscle, SSC – semispinalis capitis, OCI – obliquus capitis inferior, C2 – C2 vertebra [image from Dr. Felipe Ocampo]

GON Block: Comparing Techniques

Choosing a GON block technique may be up to clinician and/or patient preference or equipment availability.

Studies comparing the 2 approaches seem to favor ultrasound-guided GON blockade at the proximal (C2) site due to:

  • Improved analgesia [10]
  • A theoretical lower risk of damaging the occipital artery because (a) it is further from the GON in the proximal ultrasound-guided approach and (b) the ability to visualize structures [11]
  • Easier skin disinfection as injection site tends to be below the hairline [10, 11]
  • Anatomical variants in GON location making the landmark-based/palpation approach less accurate [14]

GON Block: Contraindications and Adverse Effects

Absolute Contraindications

  • Patient refusal
  • Anesthetic allergy
  • Open skull defect
  • Infection at procedural site

Relative Contraindications

  • Coagulopathy
  • Arnold-Chiari Malformations
  • Inability to lie still

Adverse Effects

  • Hematoma
  • Local infection
  • Lesion to nerve
  • Allergy to local anesthetics
  • Local anesthetic systemic toxicity (LAST)
  • Intradural infiltration
  • Vasovagal syncope
  • Alopecia around injection site

Common Indications for GON Block

1. Occipital Neuralgia

Occipital Neuralgia (ON) is a painful condition characterized by paroxysmal, lancinating, stabbing headaches along the posterior scalp that can last seconds to minutes [2]. The etiology of ON is thought to be due to irritation or compression of the occipital nerves, most commonly the GON. Symptoms are usually unilateral but can be bilateral in a third of cases [15, 16].

On exam, there may be dysesthesia (abnormal perceptions of touch) or allodynia (pain to typically non-painful stimuli) of the posterior scalp. There may also be a positive Tinel’s sign along the course of the GON.

A GON block can be both diagnostic and therapeutic by providing immediate relief and can provide up to 2 months of symptom relief [12].

2. Migraine

A migraine is a complex disorder that can be divided into two major subtypes: without aura (75%) and with aura. The etiology of migraines is unclear but some theories describe involvement of the peripheral and central nervous system, the former of which may involve sensory input from nerves including the GON [17].

Migraine characteristics:

  • Migraine without aura involves recurrent episodes of headache lasting 4-72 hours with at least two of the following characteristics: unilateral, pulsatile, moderate to severe in intensity, aggravated by or causing avoidance of physical activity. A migraine headache occurs with at least one of the following symptoms: nausea and/or vomiting, photophobia, phonophobia.
  • Migraine with aura is characterized by transient neurological symptoms that precede or accompany the headache described above. Auras involve at least one unilateral disturbance of: visual, sensory, speech and language, motor, brainstem.
  • A diagnosis is made with at least 5 attacks meeting the above criteria.
  • Chronic migraines are diagnosed when episodes occur 15 or more days per month for 3 months or longer [2].

GON blockade may be helpful for the immediate treatment of migraine episodes or as an alternative treatment in refractory episodes [12]. It has been shown to be as effective as a regimen of intravenous NSAIDs and metoclopramide in patients with acute migraine headaches in the ED [18]. In a case series of patients in the ED with migraine headaches, there were improved symptoms on 2-week call backs of patients who had received a GON block [19]. For chronic migraines, GON block may be as effective as current prophylactic treatments [12].

3. Cervicogenic Headache

Cervicogenic headaches are thought to be due to referred pain from disorders or lesions of the cervical spine or soft tissues of the neck. These headaches tend to be unilateral, moderate to severe in intensity, and may localize to the occipital, frontotemporal, and periorbital regions [2, 20]. Etiology is thought to be due to nociceptive signals from injury of structures in the neck innervated by C1-3 converging into the trigeminal cervical complex [12]. There may be clinical or imaging evidence of cervical lesions.

On exam, there may be decreased cervical range of motion and worsening of the headache with provoking maneuvers.

GON blockade may support diagnosis of cervicogenic headaches by rapidly relieving symptoms and may provide prolonged remission of headaches [12]. One study showed reduced analgesic medication consumption for months in patients with refractory cervicogenic headaches who had received GON blockade [21].

4. Cluster Headache

Cluster headaches are excruciating unilateral headaches that typically localize to the orbit with attacks lasting 15 minutes to 3 hours in duration [2]. This condition is rare, affecting approximately 0.1% of the population, most commonly males in their thirties. The etiology of cluster headaches is unclear but theories describe an association with the trigeminovascular system, parasympathetic nerve fibers, and the hypothalamus [22].

Cluster headache characteristics:

  • Severe, unilateral, orbital or supraorbital and/or temporal in location
  • Attacks occur with at least one ipsilateral autonomic symptom of:
    • Conjunctival injection or lacrimation
    • Nasal congestion or rhinorrhea
    • Eyelid edema or forehead or facial sweating
    • Miosis or ptosis
    • Unilateral photophobia or phonophobia
  • May involve agitation or restlessness
  • Occur with a frequency of once every other day to 8 times per day

GON blocks have been shown to be effective in both the acute and prophylactic treatment of cluster headaches [13, 23, 24]. The data for using corticosteroids in GON blocks is strongest for cluster headaches [12].

Conclusions

In the emergency department, it is critical to evaluate for life-threatening headaches. However, when indicated for patients presenting with specific headaches, the GON block may be an effective and efficient tool in providing analgesia.

References

  1. Goldstein JN, Camargo CA Jr, Pelletier AJ, Edlow JA. Headache in United States emergency departments: demographics, work-up and frequency of pathological diagnoses. Cephalalgia. 2006;26(6):684-690. doi:10.1111/j.1468-2982.2006.01093.x PMID 16686907
  2. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808. doi:10.1177/0333102413485658. PMID 23771276
  3. Austin M, Hinson MR. Occipital Nerve Block. [Updated 2023 Apr 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  4. Afridi SK, Shields KG, Bhola R, Goadsby PJ. Greater occipital nerve injection in primary headache syndromes–prolonged effects from a single injection. Pain. 2006;122(1-2):126-129. doi:10.1016/j.pain.2006.01.016. PMID 16527404
  5. Guner D, Bilgin S. Efficacy of Adding a Distal Level Block to a C2 Level Greater Occipital Nerve Block under Ultrasound Guidance in Chronic Migraine. Ann Indian Acad Neurol. 2023;26(4):513-519. doi:10.4103/aian.aian_169_23. PMID 37970254
  6. Levin M. Nerve blocks in the treatment of headache. Neurotherapeutics. 2010;7(2):197-203. doi:10.1016/j.nurt.2010.03.001. PMID 20430319
  7. Yu M, Wang SM. Anatomy, Head and Neck, Occipital Nerves. [Updated 2022 Oct 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  8. Güvençer M, Akyer P, Sayhan S, Tetik S. The importance of the greater occipital nerve in the occipital and the suboccipital region for nerve blockade and surgical approaches–an anatomic study on cadavers. Clin Neurol Neurosurg. 2011;113(4):289-294. doi:10.1016/j.clineuro.2010.11.021. PMID 21208741
  9. Benzon HT, Elmofty D, Shankar H, et al. Use of corticosteroids for adult chronic pain interventions: sympathetic and peripheral nerve blocks, trigger point injections – guidelines from the American Society of Regional Anesthesia and Pain Medicine, the American Academy of Pain Medicine, the American Society of Interventional Pain Physicians, the International Pain and Spine Intervention Society, and the North American Spine Society. Reg Anesth Pain Med. Published online August 7, 2024. doi:10.1136/rapm-2024-105593. PMID 39019502
  10. Greher M, Moriggl B, Curatolo M, Kirchmair L, Eichenberger U. Sonographic visualization and ultrasound-guided blockade of the greater occipital nerve: a comparison of two selective techniques confirmed by anatomical dissection. Br J Anaesth. 2010;104(5):637-642. doi:10.1093/bja/aeq052. PMID 20299347
  11. Gürsoy G, Tuna HA. Comparison of two methods of greater occipital nerve block in patients with chronic migraine: ultrasound-guided and landmark-based techniques. BMC Neurol. 2024;24(1):311. Published 2024 Sep 4. doi:10.1186/s12883-024-03816-8. PMID 39232647
  12. Santos Lasaosa S, Cuadrado Pérez ML, Guerrero Peral AL, et al. Consensus recommendations for anaesthetic peripheral nerve block. Guía consenso sobre técnicas de infiltración anestésica de nervios pericraneales. Neurologia. 2017;32(5):316-330. doi:10.1016/j.nrl.2016.04.017. PMID 27342391
  13. Blumenfeld A, Ashkenazi A, Napchan U, et al. Expert consensus recommendations for the performance of peripheral nerve blocks for headaches–a narrative review. Headache. 2013;53(3):437-446. doi:10.1111/head.12053. PMID 23406160
  14. Shim JH, Ko SY, Bang MR, et al. Ultrasound-guided greater occipital nerve block for patients with occipital headache and short term follow up. Korean J Anesthesiol. 2011;61(1):50-54. doi:10.4097/kjae.2011.61.1.50. PMID 21860751
  15. Djavaherian DM, Guthmiller KB. Occipital Neuralgia. [Updated 2023 Mar 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  16. Choi I, Jeon SR. Neuralgias of the Head: Occipital Neuralgia. J Korean Med Sci. 2016 Apr;31(4):479-488. https://doi.org/10.3346/jkms.2016.31.4.479. PMID 27051229
  17. Pescador Ruschel MA, De Jesus O. Migraine Headache. [Updated 2024 Jul 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  18. Korucu O, Dagar S, Çorbacioglu ŞK, Emektar E, Cevik Y. The effectiveness of greater occipital nerve blockade in treating acute migraine-related headaches in emergency departments. Acta Neurol Scand. 2018;138(3):212-218. doi:10.1111/ane.12952. PMID 29744871
  19. Yanuck J, Shah S, Jen M, Dayal R. Occipital Nerve Blocks in the Emergency Department for Initial Medication-Refractory Acute Occipital Migraines. Clin Pract Cases Emerg Med. 2019;3(1):6-10. Published 2019 Jan 22. doi:10.5811/cpcem.2019.1.39910. PMID 30775654
  20. Al Khalili Y, Ly N, Murphy PB. Cervicogenic Headache. [Updated 2022 Oct 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  21. Gabrhelík T, Michálek P, Adamus M. Pulsed radiofrequency therapy versus greater occipital nerve block in the management of refractory cervicogenic headache – a pilot study. Prague Med Rep. 2011;112(4):279-287. PMID 22142523
  22. Kandel SA, Mandiga P. Cluster Headache. [Updated 2023 Jul 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  23. Gönen M, Balgetir F, Aytaç E, Taşcı İ, Demir CF, Müngen B. Suboccipital steroid injection alone as a preventive treatment for cluster headache. J Clin Neurosci. 2019;68:140-145. doi:10.1016/j.jocn.2019.07.009. PMID 31326284
  24. Gordon A, Roe T, Villar-Martínez MD, Moreno-Ajona D, Goadsby PJ, Hoffmann J. Effectiveness and safety profile of greater occipital nerve blockade in cluster headache: a systematic review. J Neurol Neurosurg Psychiatry. 2023;95(1):73-85. Published 2023 Dec 14. doi:10.1136/jnnp-2023-331066. PMID 36948579
By |2025-03-26T14:01:20-07:00Mar 28, 2025|Expert Peer Reviewed (Clinical), Neurology|
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SAEM Clinical Images Series: When it is Not Just a Knot

knot

A 12-year-old male with a history of hydrocephalus status post ventriculoperitoneal (VP) shunt placement presented with an abdominal “knot.” The patient’s mother noticed the knot two days ago, on the right anterolateral thorax, which has steadily been increasing in size. The patient had no known trauma to the area or had been bitten or stung by any insect. He has otherwise been complaining of a headache, generalized, without positional changes, improved with home acetaminophen, ice pack, and rest. There were otherwise no associated vision changes, nausea, vomiting, mental status changes, or fever.

Vitals: T-36.2°C; HR 74 bpm; BP 144/75 mm Hg; RR 20; O2 Sat 96% RA

General: Well-appearing teenager in NAD.

HEENT: NC/AT. PERRL approximately 2-3 mm bilaterally. EOMI.

Neck: Supple, no meningismus.

Chest Wall: Induration to the right anterolateral thorax 5 cm x 4 cm without erythema, fluctuance, or drainage, non-tender to palpation.

Neurological: Alert. No focal neurological deficit observed.

Normal

The cause of the knot is subcutaneous cerebrospinal fluid from a shunt malfunction. The ultrasound images show characteristic “cobblestoning,” indicating fluid in the subcutaneous tissue, around a linear hyperechoic object, the catheter of the VP shunt. On the plain film imaging, a disconnect was found between the thoracic and abdominal portions of the VP shunt. Up to 80% of patients with VP shunts will have experienced a shunt malfunction after 12 years, according to one study, with fractured tubing causing shunt failure in around 15% of all cases (1).

Nausea, vomiting, headache, irritability, or decreased mental status are common but nonspecific findings in shunt malfunction. Pediatric patients may present with other signs such as bulging fontanelles, increasing head circumference, or feeding and behavioral changes. An increase in the interval ventricular size can be seen in neuroimaging but can be absent in as many as 20% of patients (2). If there is a high degree of clinical suspicion for shunt malfunction, normal or unchanged neuroimaging should not preclude neurosurgical consultation.

Take-Home Points

  • In the United States, mechanical causes of VP shunt malfunction are the most common presentation, such as catheter obstruction, fracture along the clavicle or ribs, degradation of tubing, and migration of the distal catheter due to changes in height or weight.
  • Rarely, patients can develop an accumulation of CSF at the distal catheter of the VP shunt due to migration into the abdominal wall forming an abdominal pseudocyst.
  • In patients with VP shunts, abdominal complications should be considered as a sign of shunt malfunction.
  • Consider pertinent physical exam findings and POCUS to confirm the diagnosis of shunt malfunction at the distal catheter.

  • Sainte-Rose C, Piatt JH, Renier D, Pierre-Kahn A, Hirsch JF, Hoffman HJ, Humphreys RP, Hendrick EB. Mechanical complications in shunts. Pediatr Neurosurg. 1991-1992;17(1):2-9. doi: 10.1159/000120557. PMID: 1811706.

  • Reynolds RA, Ahluwalia R, Krishnan V, Kelly KA, Lee J, Waldrop RP, Guidry B, Hengartner AC, McCroskey J, Arynchyna A, Staulcup S, Chen H, Hankinson TC, Rocque BG, Shannon CN, Naftel R. Risk factors for unchanged ventricles during pediatric shunt malfunction. J Neurosurg Pediatr. 2021 Sep 24;28(6):703-709. doi: 10.3171/2021.6.PEDS2125. PMID: 34560626.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-02-19T12:57:12-08:00Feb 21, 2025|Neurology, Pediatrics, SAEM Clinical Images, Ultrasound|
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Trick of the Trade: Cut IV extension tubing for 2-person ultrasound guided nerve block

illustration nerve block ultrasound guided needle

Ultrasound-guided procedures are difficult enough just identifying the anatomy. Performing a nerve block with the ultrasound in one hand and the needle in the other hand adds extra challenges. The simplest 1-person approach involves attaching a syringe with local anesthetic directly to the end of the procedural needle. A 2-person approach involves attach the syringe to a custom tubing-needle setup such as below. However, this custom setup may not be readily available.

IV and extension tubing attached to needle

Trick of Trade: Cut Standard IV Extension Tubing

Required equipment:

  • Ultrasound linear probe
  • 10 cc syringe
  • IV tubing
  • Procedural needle
  • Shears

IV extension injection port

Almost all standard IV extension tubing that connects IV fluid bags to a peripheral IV have an injection port near the downstream end.

  1. Clamp the IV tubing just upstream from the injection port and cut off all the unused upstream IV tubing.
  2. Attach a 10 cc syringe with local anesthetic to the injection port.
  3. Attach the other end of this IV tubing (Luer lock attachment) to the procedural needle.
  4. Prime the IV line with the anesthetic.
  5. Perform the nerve block with one person advancing the needle under ultrasound guidance, while the other person aspirates and injects the anesthetic when needed.

Video: 2-person ultrasound-guided nerve block with cut IV tubing

Bonus Tip: This approach is applicable to many procedures requiring aspiration or instillation of anesthetic, such as peritonsillar abscess aspiration.

Read more from the Tricks of the Trade series.

By |2024-10-23T07:23:46-07:00Oct 23, 2024|Neurology, Tricks of the Trade, Ultrasound|
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SAEM Clinical Images Series: Doubly Double Vision

palsy

A 52-year-old female with a past medical history of hypertension and prediabetes presented to the emergency department with double vision that started one day prior to arrival. She stated that her double vision improved when she closed one eye. She denied trauma, headache, neck pain, dizziness, dysphagia, numbness, tingling, weakness, or gait instability.

 

Vitals: BP 181/119; HR 76; RR 18; T 98.4°F; O2 saturation 96% on room air

General: No acute distress, well-appearing

Neurologic: AOx3; Following commands. Speech without dysarthria. PERRLA. EOM: incomplete abduction of the L and R eye. No facial asymmetry. Tongue protrudes midline. No pronator drift. 5/5 strength in all extremities. Sensation is intact throughout. Finger to nose is normal. Gait is narrow and steady.

None

Cranial nerve 6 (CN VI), also known as the abducens nerve, is responsible for ipsilateral eye movement. CN VI palsy presents clinically with the inability to abduct the eye resulting in horizontal diplopia. Patients often present complaining of double vision that is worse with lateral gaze. Other symptoms on presentation may include headache, nausea, vomiting, hearing loss, and recent viral symptoms. CN VI is typically diagnosed clinically by an inability to abduct the eye. It is the most common oculomotor palsy in adults and can be caused by damage anywhere along the course of the abducens nerve. Etiologies in adults include ischemia, trauma, neoplasm, demyelinating lesions, increased intracranial pressure, and infection. Risk factors include microvascular disease such as hypertension and inflammatory conditions. Bilateral CN VI nerve palsy without associated intracranial abnormalities is rare. Importantly, abducens nerve palsy is the second most common oculomotor palsy in children and a frequent presenting sign of an intracranial tumor. Children with CN VI palsy should be evaluated for ataxia and other gait disturbances which may indicate a brainstem glioma.

Depending on the presenting symptoms and medical history, the workup should include an MRI/MRA brain to evaluate for microvascular ischemia and cerebrovascular accident. Treatment of CN VI palsy should be targeted at the underlying cause. In cases of CN VI palsy due to microvascular ischemia, symptoms often self-resolve. In children, treatment includes alternating patching of the eyes, but this has not been shown to be effective in adults.

Take-Home Points

  • CN VI palsy is the most common oculomotor palsy in adults and presents with an inability to abduct the eye.
  • Treatment of CN VI palsy should target the underlying pathology which may include infection, trauma, neoplasm, or increased intracranial pressure.
  • CN VI palsy in children may indicate an intracranial tumor and workup should include a full neurologic examination and intracranial imaging when appropriate.

  • Graham C, Gurnani B, Mohseni M. Abducens Nerve Palsy. 2023 Aug 24. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 29489275.

    Merino P, Gómez de Liaño P, Villalobo JM, Franco G, Gómez de Liaño R. Etiology and treatment of pediatric sixth nerve palsy. J AAPOS. 2010 Dec;14(6):502-5. doi: 10.1016/j.jaapos.2010.09.009. PMID: 21168073.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2024-09-28T21:34:14-07:00Oct 7, 2024|Neurology, SAEM Clinical Images|
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