A whiplash injury refers to an injury that occurs in the bone or soft tissue when an impact is applied to the neck by an acceleration-deceleration mechanism¹. Whiplash injury can cause pain in the neck and shoulder and in severe cases, neurological symptoms, such as dysphagia, vertigo, memory loss, and visual impairment. These clinical symptoms are defined as whiplash-associated disorders (WAD)².

Previous studies reported that 2% to 29% of patients complained of swallow-related problems after a whi-plash injury³. Although dysphagia significantly impacts a patient’s quality of life, the consequences of dysp-hagia that occurs after a whiplash injury have been underestimated. In particular, there are few reports on the treatment and progression of delayed-onset dysphagia following whiplash injuries.

This article reports the clinical features, treatment, and progression of a patient who complained of delayed dysphagia after a whiplash injury.

A 37-year-old female patient visited our outpatient clinic in the department of rehabilitation medicine complaining of progressive dysphagia.

Approximately one year ago, she was diagnosed with a whiplash injury due to a car accident that occurred after a collision with an oncoming vehicle. Cervical spine magnetic resonance imaging (MRI) performed after the accident showed disc protrusions at C2-7 and T1-4 and bilateral neural foraminal stenosis at C5-6. She underwent outpatient treatment at an oriental medicine hospital for neck and bilateral arm pain and arm weakness, with a diagnosis of whiplash injury.

Two months post-injury, her neck and arm pain persisted and the muscle weakness in both arms was aggravated, with markedly increased right-sided muscle weakness, which prompted her to visit the Depart-ment of Neurosurgery of our outpatient clinic. A physical examination revealed Medical Research Council (MRC) grade of 4 in her right shoulder flexor, shoulder exte-nsor and elbow flexor; 3 in elbow extensor; and 5 in the other muscles of the right upper limb. All muscles of the left upper limb were graded 5 on the MRC scale. The deep tendon reflex was normoactive, and no pathological reflex was observed. She reported hypesthesia in the right upper limb area corres-ponding to the C6 and C7 dermatomes. MRI revealed no significant differences compared to the previous image.(Fig. 1) A nerve conduction study was normal, and electromyography revealed abnormal spontaneous activities in the right C7 paracervical and right pro-nate teres muscles corresponding to right cervical radi-culopathy, mainly at the C6-7 level.(Table 1, 2) She complained of neck and bilateral arm pain with weak-ness, but there was no dysphagia. She was managed with conservative treatment, including analgesics. Since then, no additional traumatic events have occurred.

Table 1 . Nerve conduction study..

	Stimulation	Latency (ms)*	Amplitude	CV (m/s)
Sensory nerve
Rt. median (digit III)	Wrist	3.65	49.5	49.8
Rt. ulnar (digit V)	Wrist	3.13	42.4	58.4
Lt. median (digit III)	Wrist	3.23	60.7	56.0
Lt. ulnar (digit V)		3.18	40.3	57.2
Motor nerve
Rt. median (APB)	Wrist	3.39	13.1
	Elbow	7.19	12.7	56.5
Rt. ulnar (ADM)	Wrist	2.50	10.1
	Below elbow	4.90	10.1	66.8
	Above elbow	6.51	10.1	68.1
Lt. median (APB)	Wrist	3.07	15.4
	Elbow	6.41	12.9	63.0
Lt. ulnar (ADM)	Wrist	2.66	14.6
	Below elbow	5.00	14.0	68.3
	Above elbow	6.51	13.9	72.8

Amplitudes are measured in microvolt (μV, sensory) and millivolt (mV, motor)..

CV: conduction velocity, Rt.: right, Lt.: left, APB: abductor pollicis brevis, ADM: abductor digiti minimi..

*Sensory nerve: peak latency, motor nerve: onset latency..

Table 2 . Needle electromyography..

Muscle	IA	Fib	PSW	MUAP	Recruitment pattern
Rt. abductor pollicis brevis	NL	None	None	Large, polyphasic	Full
Rt. abductor digiti minimi	NL	None	None	NL	Full
Rt. flexor carpi radialis	NL	None	None	NL	Full
Rt. pronator teres	NL	2+	None	NL	Full
Rt. biceps	NL	None	None	NL	Full
Rt. deltoid	NL	None	None	NL	Full
Rt. supraspinatus	NL	None	None	NL	Full
Rt. infraspinatus	NL	None	None	NL	Full
Rt. C5 CPS	NL	None	NA	NA	NA
Rt. C6 CPS	NL	None	NA	NA	NA
Rt. C7 CPS	NL	2+	NA	NA	NA
Rt. C8 CPS	NL	None	NA	NA	NA
Rt. T1 CPS	NL	None	NA	NA	NA
Lt. C5 CPS	NL	None	NA	NA	NA
Lt. C6 CPS	NL	None	NA	NA	NA
Lt. C7 CPS	NL	None	NA	NA	NA
Lt. C8 CPS	NL	None	NA	NA	NA
Lt. T1 CPS	NL	None	NA	NA	NA

IA: insertional activity, Fib: fibrillation, PSW: positive sharp wave, MUAP: motor unit action potential, NL: normal, NA: not available, CPS: cervical paraspinalis..

Figure 1. Cervical spine magnetic resonance imaging (MRI) taken after the accident. (A) Sagittal image, (B) Axial image at the C5-6 level, (C) Axial image at the C6-7 level.

A year after the accident, the patient visited the Department of Rehabilitation Medicine in our outpa-tient clinic because of worsening neck pain and dysp-hagia symptoms. She reported that her neck pain had progressed to include a tightness sensation. As this symptom intensified, she started experiencing odyno-phagia, and intermittent aspiration symptoms while drinking. The patient’s upper limb pain and weakness persisted without any notable worsening over time. A physical examination revealed no significant changes in the MRC scale of both upper limbs and any other neurological signs compared to the previous exami-nation. In an additional evaluation related to dysphagia, reduced tongue strength was observed, with difficulty in chewing due to weakened mastication, and early fatigue symptoms appeared when consuming appro-ximately a quarter of the previous intake. For this reason, the patient’s diet was supplemented with additional enteral nutrients by oral intake. Stiffness of the sternocleidomastoid and anterior scalene muscle and movement restriction in the rotation and flexion of the neck were observed. Decreased hyolaryngeal elevation and pharyngeal strength, and low voice volume were noted. Compensatory behaviors, such as neck extension during swallowing, were accompanied by repeated swallowing.

A videofluoroscopic swallowing study (VFSS) was performed to assess swallowing function. VFSS revealed decreased laryngeal elevation and impaired upper esophageal sphincter opening in the pharyngeal phase. Furthermore, the Penetration-Aspiration Scale (PAS) score was 3 for pureed food and 7 for liquid food.(Fig. 2A) Brain computed tomography showed no abnormal findings. Laryngeal needle electromyography showed abnormal spontaneous activities, such as fibrillation potential and positive sharp waves, with normal duration and amplitude of motor unit action potential in both cricothyroid muscles, and normal findings in both thyroarytenoid muscles. A follow-up nerve con-duction study and needle electromyography in the upper extremities did not reveal any definite changes.

Figure 2. VFSS showed decreased residue in the pyriformis sinus and the vallecular fossa. (A) Before rehabilitation therapy, (B) Three months after therapy.

The patient received treatment for dysphagia to strengthen the suprahyoid muscle, increase the opening of the cricopharyngeal sphincter, and improve phar-yngeal contraction and laryngeal elevation. Furthermore, the patient underwent neck muscle massage and stre-tching to alleviate muscle tension in the neck. Three months after treatment, the patient showed impro-vement in neck pain and odynophagia. However, intermittent aspiration symptoms still accompanied liquid intake. Follow-up VFSS revealed decreased residue in the pyriformis sinus and vallecular fossa. It also showed improvements in PAS scores from 3 to 1 for pureed food and 7 to 3 for liquid food.(Fig. 2B)

Thereafter, the patient continued rehabilitation and complained of pain exacerbation when performing exercises involving excessive neck flexion. Accordingly, chin tuck against resistance and Shaker exercises were discontinued. Treatment primarily consisted of neck stretching and pharyngeal muscle strengthening exe-rcises, such as the Mendelsohn maneuver, Masako maneuver, and supraglottic swallowing.

In the swallowing function evaluation, which was re-evaluated after two months, the Swallowing Ability and Function Evaluation test score improved from 63 to 69 and from moderate to mild. An increase in food intake was also observed. After five months, although right arm pain and weakness persisted, the patient did not complain of discomfort when consuming any type of food and recovered to the extent that she did not complain of symptoms related to swallowing.

The complex symptoms and signs that occur after the acute phase of whiplash injury are called WAD, and dysphagia is one of them. According to previous studies, 7% to 34% of patients reported experiencing problems related to swallowing after whiplash injury. However, there are few studies on the mechanisms of delayed dysphagia and the course of treatment.

This patient initially complained of symptoms rela-ted to radiculopathy with persistent neck pain acco-mpanied by radiating pain to the arm. However, the pattern of neck pain later changed to neck pain that seemed to be tightening. As this symptom gradually worsened, it was accompanied by dysphagia, odyno-phagia and intermittent aspiration when drinking water. According to a longitudinal analysis, self-reported dysphagia after whiplash injury showed a higher inci-dence in the later stage (<3-12 months) than in the early stage (<1-2 weeks), and the symptoms also showed a worsening pattern⁴. Similarly, our patient did not complain of dysphagia symptoms in the early stages; these, symptoms appeared later.

However, whether delayed-onset dysphagia is due to other causes should be confirmed. In this case, where the patient presented with arm pain and weak-ness followed by swallowing difficulty, atypical neuro-pathies such as neuralgic amyotrophy, which rarely affect cranial nerves, may also be considered. However, neuralgic amyotrophy is characterized by intense pain that usually lasts for a few hours to three weeks, followed by a dull ache and muscle weakness that can persist for several months⁵. However, in this case, given the characteristics and course of pain and the findings of electromyography and imaging tests, the results more strongly support cervical radiculopathy over other disorders.

Previous studies have suggested muscle tension dysphagia⁶, superior laryngeal nerve⁷ and hypoglossal nerve⁸ damage due to traction injury, and articular dysfunction⁹ as mechanisms for dysphagia after whiplash. Since the dysphagia symptoms occurred one year after the in-jury in our case, the possibility of damage to the superior laryngeal and hypoglossal nerves due to traction injury was low. However, articular dysfun-ction or muscle tension dysphagia may be considered. According to a qualitative study, an increase in mu-scle tone and stiffness occurs after whiplash injury, similar to the clinical features of muscle tension dysphagia¹⁰. Muscle tension dysphagia most commonly presents swallowing symptoms such as difficulty in swallowing, odynophagia, choking, sensation of food sticking in the throat, and coughing¹¹. In addition, it is not uncommon for voice change to accompany muscle tension dysphonia. Given the similarity of our patient’s complaints to these symptoms, it is plausible to consider increased muscle tension as the underlying mechanism of dysphagia. In our case, the abnormal spontaneous activities in both cricothyroid muscles revealed in the laryngeal needle electromyography study also support the possibility of this effect. In a prospective study, where patients with muscle tension dysphagia were treated to release laryngeal muscle tension, all patients showed improvement in dysphagia symptoms¹¹. We similarly performed treatment to reduce the increased muscle tension through stretching exe-rcises, and our patient’s symptoms improved.

Chewing problems and tongue pain have been reported as swallowing-related outcomes after a whip-lash injury³. These issues often manifest as reduced or painful jaw movement, which is more prevalent among patients with WADs¹². Additionally, patients with reduced or painful jaw movement exhibited re-duced tongue strength and decreased endurance during chewing¹³. Furthermore, it has been reported that a few patients develop late onset impairments in jaw movement following an acute whiplash injury¹⁴.

One study was conducted on the effect of neck- specific exercise in patients with WAD, and showed a greater effect on pain reduction than in patients who performed general exercise¹⁵. The treatments conducted in this study consisted mainly of isometric extension, flexion, and rotation. However, in our patient, neck pain and dysphagia were exacerbated when bending exercises were performed during treat-ment. Therefore, therapy consisted mainly of neck extension exercises and pharyngeal muscle streng-thening exercises, and the patient’s symptoms improved after this therapy. This suggests that a therapeutic approach differentiated from patients who only com-plained of simple neck pain is needed for patients with dysphagia. This also indicates the importance of determining the presence or absence of symptoms related to early dysphagia in patients with WAD. Fur-thermore, treatment involving an indirect osteopathic approach and myofascial release that specifically targets the tongue is known to be effective for abnormal tongue mobility in a patient with WAD¹⁶. Nevertheless, further research is necessary as there is currently no established treatment for dysphagia after whiplash injury. In addition, as the delayed dysphagia that occurred after whiplash injury improved after several months of swallowing treatment, we realized the impo-rtance of treatment for dysphagia in these patients.

A limitation of this case report is that a compre-hensive nerve conduction study and needle electro-myography including additional upper limb and tongue muscles were not performed to differentiate other neurological disorders, owing to improved dysphagia symptom. In the future, it would be beneficial and instructive to proceed with a comprehensive nerve conduction study and needle electromyography.

This report describes a case of delayed dysphagia after a whiplash injury following a traffic accident and the effect of five months of rehabilitation treatment for dysphagia. We found that treatment aimed at releasing muscle tension can be beneficial in dysp-hagia after a whiplash injury compared to conventional dysphagia therapy. Because it also presents different symptoms including decreased tongue strength and dysfunction of jaw movement, a differentiated treatment approach is needed for the management of dysphagia after a whiplash injury. However, further research is needed to establish the exact mechanisms of its deve-lopment and treatment.

We obtained informed consent from the patient for this study, and IRB approval was obtained.

The authors declare that they have no conflict of interest.

Jungyun Kim (ORCID ID: 0000-0003-3439-9075): Conceptualization, Data curation, Formal analysis, Inve-stigation, Resources, Writing – original draft, Writing – review & editing, Yung Jin Lee (ORCID ID: 0000- 0003-4479-9136): Conceptualization, Investigation, Project administration, Resources, Supervision, Writing – review & editing, Mi Jin Hong (ORCID ID: 0000- 0002-4170-0762): Conceptualization, Formal analysis, Investigation, Writing – review & editing, Dong-Jin Chae (ORCID ID: 0000-0003-4258-5572): Conceptua-lization, Formal analysis, Investigation, Writing – review & editing, Jong Bum Park (ORCID ID: 0000-0002-0087- 845X): Conceptualization, Formal analysis, Investigation, Writing – review & editing.