Rehabilitation Management of Upper Limb Segmental Zoster Paresis Following Coronavirus 2019 Vaccination: A Case Report

INTRODUCTION

Segmental zoster paresis (SZP) is a relatively rare complication of herpes zoster (HZ), occurring in approximately 0.5%–5% of cases, and is characterized by focal muscle weakness.¹⁾ SZP typically emerges in the dermatome corresponding to the rash, usually with a delay of 2–3 weeks.²⁾ Although some reports suggest that a combination of steroids and rehabilitation may be effective,³⁾ there are currently no established guidelines for the management of SZP. Furthermore, a review of the literature reveals no specific recommendations regarding an appropriate approach, intensity, or timing of rehabilitation.

Because of a low awareness of SZP, delayed diagnosis and treatment are of significant concern. Motor deficits may present as cranial neuropathy including Horner syndrome,⁴⁾ radiculopathy, or mononeuropathy, further complicating diagnosis. Here, we present a case of SZP that demonstrated significant recovery with rehabilitation despite a delayed diagnosis and initiation of treatment at 1 month after onset.

CASE

A 74-year-old man developed rashes and numbness in his right forearm 2 weeks after receiving his fourth coronavirus disease 2019 (COVID-19) vaccine (Moderna). He had a 5-year history of diabetes mellitus with an HbA1c (NGSP) of 7.0%, without signs of diabetic neuropathy. Over the following 2 weeks, he developed progressive weakness in his right hand and fingers. His primary physician suspected HZ-related neuropathy and initiated treatment with pregabalin and mecobalamin. Although the rashes gradually resolved, the paralysis lingered and swelling developed. By Day 18, his right side grip strength was 0 kg, and the following Medical Research Council scale scores (MRCSS) were recorded for his right hand: wrist flexion, 3; finger abduction, 3. Magnetic resonance imaging of the brain and cervical spine revealed no abnormalities. Blood tests were positive for varicella zoster virus antibodies (IgG>128 times, IgM>5.35 times), confirming HZ-related neuropathy. Oral valaciclovir (1000 mg/day, 7 days) was initiated on Day 25.

The patient visited our hospital on Day 35 for rehabilitation consultation. Muscle weakness was prominent in the distal muscles of the right upper extremity (MRCSS: elbow extension, 3; wrist flexion, 3; finger flexion, 1; finger extension, 1). Nerve conduction studies (NCS) revealed slightly slowed motor nerve conduction velocity (MCV) in the median and ulnar nerves. Compound motor action potential (CMAP) amplitudes were at the lower limit of normal in the median nerve but slightly decreased in the ulnar nerve. Sensory nerve conduction velocities (SCVs) were nearly symmetric bilaterally for both the median and ulnar nerves, and sensory nerve action potential (SNAP) amplitudes were within the normal range. F wave persistence was 1/16 in the median nerve and 0/16 in the ulnar nerve. Needle electromyography (EMG) revealed positive sharp waves and fibrillation potentials (PSWs/Fibs) in the abductor pollicis brevis, first interossei dorsalis (FDI), extensor indicis (EIP), and triceps brachii (Tri) muscles but not in the biceps brachii and deltoid muscles. Voluntary motor unit potentials were absent in the FDI and EIP. Interference patterns were reduced in Tri. Given the location of the rashes (ulnar side of the forearm, Fig. 1), findings were consistent with C7-8 radiculopathy, likely involving the dorsal root ganglion and ventral horn, leading to a diagnosis of SZP.

Fig. 1.

 Photograph of patient’s forearm. Arrows indicate rashes on the dorsoulnar forearm, hand dorsum, and fourth finger, predominantly corresponding to the C8 dermatome.

Heat and swelling suggested active inflammation, so oral prednisolone (30 mg/day for 5 days) was administered, followed by loxoprofen (180 mg/day). Because needle EMG indicated active denervation, rehabilitation emphasized finger stretches to prevent contractures, avoiding strength training at this stage.

On Day 54, the patient was admitted to a nearby hospital for cerebral infarction in the left putamen. He developed mild right hemiparesis but exhibited no higher brain dysfunction. Standard post-stroke inpatient rehabilitation was provided for an estimated 1–2 h/day, five times a week. After discharge, he returned to our hospital on Day 70. At this time, independent finger movements were partially possible, but full extension remained limited, reflecting a mixture of cerebral and peripheral paresis. Weekly occupational rehabilitation was initiated with a focus on fine motor skill training.

By Day 90, the patient could write simple characters with the affected hand. By Day 98, MRCSS reached 5 in all elbow and wrist functions, and 4 in finger flexion and finger extension. By Day 113, the patient was able to use chopsticks proficiently for all meals. At this time, we gradually increased high intensity muscle-strengthening exercises such as resistance training.

On Day 147, MRCSS reached 5 in all major joints, and grip strength improved to 12 kg. Follow-up NCS showed significant improvements in MCVs, CMAP amplitudes, and F-wave occurrence rate of the median nerve and ulnar nerves, nearing normal values. EMG showed resolution of PSWs/Fibs in the EIP and reductions in the FDI and Tri. Interference patterns also improved. By Day 224, grip strength reached 21 kg, and outpatient rehabilitation was concluded based on nearly normal electrodiagnostic findings (see Fig. 2 and Table 1). Written consent was obtained from the patient for publication of this case report.

Fig. 2.

 Summary of clinical appearance including symptoms, medication, rehabilitation and timing of electrophysiological studies. STEF, simple test for evaluating hand function; VACV, valaciclovir; PSL, prednisolone; LSH, loxoprofen sodium hydrate.

Table 1.  Summary of electrophysiological findings.

Nerve/muscle	Finding	Day 35	Day 147	Day 224
NCS a
Median	CMAP amplitude, mV	4.5	6.1	4.4
	CMAP distal latency, ms	4.4	4.6	4.6
	MCV, m/s	48.0	52.5	49.9
	SNAP amplitude, μV	5.7	7.1	9.4
	SCV, m/s	45.5	43.8	41.7
	F wave	1/16	16/16	13/16
Ulnar	CMAP amplitude, mV	2.3	5.4	5.3
	CMAP distal latency, ms	3.0	3.1	3.5
	MCV, m/s	48.3	49.0	50.0
	SNAP, μV	12.1	13.3	24.7
	SCV amplitude, m/s	47.9	48.3	45.5
	F wave	0/16	16/16	16/16
EMG b
EIP	P	3	0	0
	Fib	4	0	0
	Int	0	2	4
FDI	P	3	2	0
	Fib	4	2	1
	Int	0	2	3
Tri	P	2	0	0
	Fib	2	1	0
	Int	2–3	3	4

P, Positive sharp waves; Fib, fibrillation potentials; Int, interference patterns.

^a Amplitudes and distal latency were stimulated at the wrist; ^b Valuations in EMG: 0, none; 1, occasionally observed; 2, reproducibly observed but not frequent; 3, frequently observed; 4, observed throughout exam.

DISCUSSION

We report a case of SZP post-COVID-19 vaccination, with a delayed diagnosis that achieved substantial motor recovery through rehabilitation. HZ infection is associated with host immunocompromised states. Although studies differ on whether COVID-19 vaccination increases HZ risk, reports suggest an incidence of approximately 3.3 cases per person-year after vaccination.^5,6)

Motor paresis is a relatively uncommon complication in HZ patients, with a prevalence rate of 0.5%–5%, and may be underrecognized by physicians.¹⁾ The variability of motor symptoms may contribute to a delay in diagnosis/treatment initiation. If motor symptoms develop approximately 2 weeks after HZ onset in or close to the involved dermatomal region, SZP should be considered in the differential diagnosis, irrespective of the neurological features or pattern of motor impairment. Treatment strategies generally include a combination of antiviral drugs, corticosteroids, and rehabilitation.³⁾ According to a previous report, only about half of patients with HZ who demonstrate motor fiber involvement in NCS develop clinical motor weakness. Furthermore, no relationship was found between the extent of electrophysiological abnormalities, such as changes in CMAP amplitude or MCV, and the occurrence of symptoms.⁷⁾ This may be because electrophysiological examinations were only performed once in the study, with the timing based on the onset of skin symptoms and not motor symptoms. Therefore when evaluating the severity or recovery in a specific case, a single point examination might be insufficient. As performed in the present case, serial electrophysiological examinations might be of importance for managing of rehabilitation.

Despite severe motor paralysis and a delay of over 1 month in the initiation of rehabilitation, our patient achieved favorable outcomes, suggesting that meaningful recovery is possible even with delayed diagnosis. Early administration of corticosteroids has been reported to prevent axonal degeneration and improve outcomes in SZP.³⁾ However, late diagnosis often limits the use of corticosteroids. In the present case, forearm swelling suggested sub-acute inflammation; therefore, even delayed steroid administration may have exerted a protective effect. Oral corticosteroids may also have contributed to the reduction of edema and pain, thereby facilitating the progression of rehabilitation.

Historically, SZP has been considered a condition with a favorable prognosis. For instance, a survey-based report from 1972 indicated that 55% of SZP cases in the limbs achieve “functional” recovery.⁸⁾ A recent study that compiled published case reports has reported similar outcomes, with full recovery observed in 15 of 21 patients, whereas only 1 patient had a persistent deficit.⁹⁾ In contrast, a study involving a higher proportion of older patients with diabetes mellitus reported no recovery in five of eight cases,¹⁾ indicating that careful attention is required in older patients with diabetes, similar to that in the present case. With typical recovery taking 1–2 years,¹⁰⁾ long-term rehabilitation management is essential.

In the present case, active denervation precluded early muscle-strengthening exercises because of the risk of overuse syndrome.¹¹⁾ Therefore, initial rehabilitation focused on stretches to prevent contractures. Given the long recovery time and generally favorable functional outcome, this appears to be a reasonable initial approach.

Because the treatment for cerebral infarction, including inpatient rehabilitation, was conducted at another hospital, detailed information on the rehabilitation program was unavailable. However, it is likely that range-of-motion exercises and fine motor skill training were performed for post-stroke hemiparesis. Intensive inpatient rehabilitation might well have contributed to the recovery from SZP.

Post-stroke rehabilitation primarily emphasized fine motor skills, after which strength training was gradually introduced. Follow-up NCS on Day 147 showed increased SNAP amplitudes and no decrease in CMAP amplitudes. Needle EMG showed a significant decrease in active denervation. These findings indicate that our therapeutic approach at this stage did not exert any negative effects, encouraging further strength training exercises. Final NCS and EMG showed near-normal findings, correlating with clinical improvement. No recurrence of active denervation was noted.

The coexistence of SZP and left putamen infarction complicates the interpretation of symptom origin and recovery in this case. Nevertheless, this case illustrates that even with delayed interventions, significant recovery is possible in SZP. As implemented in the present case, a stepwise rehabilitation approach can be feasible for post-SZP rehabilitation of the upper extremity; our approach initially focused on the prevention of contractures, shifting to fine motor skill exercises once voluntary movement became possible, and a subsequent increase in muscle strengthening exercises while monitoring for signs of progressive neurological deterioration. This study also highlights how NCS and needle EMG can confirm clinical recovery through objective testing. We expect that this study will serve as a supportive guide to manage SZP rehabilitation.