OBJECTIVE: To investigate the platelet-rich plasma (PRP) effectiveness in patients with a long-lasting postviral olfactory dysfunction (LPOD).
METHODS: Forty-three consecutive patients with a long-lasting postviral OD were prospectively recruited. The injection of 1 mL of PRP was carried out in both olfactory clefts. The pre- to 6-month post-PRP injection change in olfaction was assessed with the olfactory disorder questionnaire (ODQ) and the threshold, discrimination, and identification (TDI) tests.
RESULTS: Forty-three patients received bilateral PRP injections (24 females). The mean age of patients was 58.9 ± 16.8 years. The mean duration of LPOD was 8.7 years. The pre to 6-month post-injection mean TDI significantly improved from 10.3 ± 10.2 to 20.12 ± 12.07 (p = 0.001). The mean ODQ significantly decreased from 29.8 ± 13.0 to 23.4 ± 11.3 (p = 0.013). The average change of the TDI and the ODQ were 9.8 and 6.4, respectively. Age was inversely associated with the 6-month threshold score.
CONCLUSIONS: PRP appears to be a promising therapeutic strategy for long-lasting postviral OD. Our findings support the conduction of controlled randomized trial in this population of patients.

UNASSIGNED: Although some patients with postviral olfactory dysfunction (PVOD) recover spontaneously, many others are left with the degree of smell loss and there are no established drugs for the treatment of patients with PVOD. Valproic acid (VPA) has been widely used for the treatment of epilepsy. Its potential neuroregenerative effects have been shown via animal studies. This is the first study to treat PVOD patients with VPA. This open-label, single-arm, phase II study was conducted to investigate the effects of VPA in patients with PVOD.
UNASSIGNED: The patients received oral tablets of VPA 200 mg twice a day for 24 weeks. In total, 11 patients with PVOD were recruited. Oder scores of recognition and detection threshold (measured with a T&T olfactometer), and visual analog scale were examined during the treatment.
UNASSIGNED: All odor scores significantly improved over time. Although the mean duration of olfactory dysfunction in this study was 11.5 months, both odor recognition threshold and odor detection threshold scores significantly improved 4 weeks after treatment initiation compared to the pre-treatment threshold scores. The olfactory recovery rates in patients treated with VPA were clearly better than those we previously reported in PVOD patients who received Toki-shakuyaku-san, the traditional treatment in Japan. The olfactory recovery rates of patients with PVOD at 12 weeks and 24 weeks of VPA treatment were both 77.8%, and the olfactory cure rates at 12 weeks and 24 weeks of VPA treatment were 33.3% and 44.4%, respectively. No serious adverse events were observed.
UNASSIGNED: VPA seems to be a safe treatment option in patients with PVOD. The effects of VPA treatment for PVOD patients should be studied with a controlled study design in the future.

OBJECTIVE: The aim of the study was to investigate whether olfactory fluctuations (OF) are pronounced in patients with sinonasal olfactory dysfunction (OD).
METHODS: The retrospective investigation included patients aged 18 years or older, who consulted a tertiary referral center for olfactory loss. Patients with normal smell function were excluded. Patients answered a structured questionnaire about their olfactory symptoms, with specific questions related to the presence of OF and its average frequency, amplitude, duration, time since most recent OF, and associated symptoms of self-reported OF. Patients also underwent clinical evaluation including a structured medical history and physical examination including nasal endoscopy. In addition, we assessed orthonasal olfactory function using Sniffin\' Sticks, and gustatory function using \"taste sprays\".
RESULTS: Participants included 131 men and 205 women (n = 336), aged 18 to 86 years (mean 50, SD 16). Patient-reported fluctuations occurred most frequently in sinonasal (38%), idiopathic (29%), and postviral (29%) OD. Amplitude of OF was highest in postviral OD (p = 0.009). Average frequency, duration, and the time since the most recent fluctuation were not significantly different between groups (all p\'s > 0.42). Odor discrimination (p = 0.002) and identification (p = 0.017) scores were higher among those individuals with OF.
CONCLUSIONS: Amplitude of OF may help distinguish postviral from other causes of OD, especially in patients presenting with equivocal symptoms of sinonasal disease.

OBJECTIVE: Postinfectious olfactory dysfunction (PIOD) is the most common etiology of olfactory dysfunction, and olfactory training (OT) is an accepted treatment modality for PIOD. Some studies have investigated OT in Korean patients, but they involved odorants unfamiliar to Koreans or had no control group. The aim of this study was to verify the efficacy of OT in PIOD patients, using odorants familiar to Koreans and including a control group.
METHODS: We enrolled a total of 104 Korean patients with PIOD over the 3-year study period. All participants were assessed using endoscopy and an olfactory function test at the baseline assessment and 3 months after OT. The olfactory function test was performed using the Korean version of Sniffin\' stick (KVSS) II. Nasal and psychological function was evaluated using a visual analog scale and the Mini-Mental State Examination. OT was performed over a period of 3 months, using five odorants (rose, lemon, cinnamon, orange, and peach).
RESULTS: OT improved olfactory function in approximately 40% of subjects over a period of 12 weeks compared to non-OT subjects. A comparison of changes between the initial and follow-up assessments demonstrated that the OT group had significantly better olfactory results for the total KVSS II, threshold, and identification scores than the non-OT group. The degree of olfactory improvement after OT was affected by the initial score.
CONCLUSIONS: The effects of OT in patients with PIOD were demonstrated in this study. A meaningful contribution of this study is that Korean patients were tested using odors familiar to them in comparison with a control group.

BACKGROUND: Olfactory dysfunction is a prevalent problem with a significant impact on quality of life and increased mortality. Limited effective therapies exist. Platelet-rich plasma (PRP) is an autologous biologic product with anti-inflammatory and neuroprotective effects. This novel pilot study evaluated the role of PRP on olfactory neuroregeneration in patients with hyposmia.
METHODS: Seven patients who had olfactory loss greater than 6 months in duration, no evidence of sinonasal inflammatory disease, and no improvement with olfactory training and budesonide topical rinses were enrolled in this preliminary study. Patients received a single intranasal injection of PRP into the mucosa of the olfactory cleft. The Sniffin\' Sticks olfactory test consisting of threshold, discrimination, and identification measurements (TDI) was administered at the beginning of the study and at 1 and 3 months.
RESULTS: All patients reported a subjective improvement of their smell shortly after injection but then stabilized. At 3-month post-treatment, two patients with functional anosmia (TDI < 16) did not improve significantly. Five patients with hyposmia (TDI > 16 but <30) showed an improvement with 60% achieving normosmia (TDI > 30) at 3-month follow-up. On average, patients with baseline TDI > 16 improved by 5.85 points with the most significant improvement in the threshold subcomponent. There were no adverse outcomes from intranasal PRP injections.
CONCLUSIONS: PRP appears safe for use in the treatment of olfactory loss, and preliminary data suggest possible efficacy, especially for those with moderate yet persistent loss. Further studies will help determine optimal frequency and duration of use.
UNASSIGNED:

Early reports have suggested that smell loss may be an early symptom associated with the pandemic known as coronavirus disease 2019 (COVID-19). The possibility that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) might cause olfactory dysfunction is certainly plausible. Patients presenting to specialized smell clinics are commonly diagnosed with upper respiratory infection (URI)-associated olfactory loss and most are presumed to be viral related. In acute phases of infection, it is common to experience some smell loss as a result of nasal inflammation, mucosal edema, and obstruction of airflow into the olfactory cleft. In most cases, these episodes of smell loss are self-limiting and coincide with resolution of URI symptoms. However, in some cases the smell loss persists for months to years and this is presumed to occur through a more direct olfactory insult by the virus. It remains too early to know whether infection with SARS-CoV-2 causes persistent olfactory dysfunction. However, given the scale of this pandemic, if SARS-CoV-2 does cause chronic olfactory loss in even a small portion of those infected, then the overall population prevalence could be quite large. This review provides a brief, practical overview of viral-associated olfactory loss, realizing that evidence related to COVID-19 will likely not be clear for some time. Our goal is to highlight the existence and importance of this condition and provide information geared for both providers and patients. Practical suggestions regarding evaluation and treatment will be provided, realizing that there may be constraints on medical resources and the nature of this pandemic remains dynamic.

Postviral gastroparesis can result from a variety of viral infections and may cause severe, persistent gastrointestinal symptoms. We report the case of an 85-year-old man with one year of persistent nausea, epigastric pain, early satiety, and 25-pound weight loss after an episode of viral gastroenteritis contracted on a cruise ship. The patient reported that he had tested positive for norovirus shortly after the onset of symptoms. Esophagogastroduodenoscopy revealed no abnormalities, and his symptoms persisted despite treatment for a positive serum H. pylori IgG antibody. Lab workup, including hemoglobin A1c, was otherwise normal, and computed tomography (CT) angiography was unremarkable. A gastric emptying study performed one year after the onset of illness revealed moderate gastroparesis. While most cases of postviral gastroparesis resolve within a year or less, there are a few reports of gastroparetic symptoms lasting two to three years or longer. The pathophysiology might involve a slowly reversible injury to gut neuromodulator cells. Antiviral treatment has not been shown to be effective; symptomatic treatment with antiemetic and prokinetic drugs may be helpful in some cases.

Lassa fever is a zoonotic disease endemic in some West African countries. It is exported to countries in America, Asia, and Europe. Antivirals against Lassa fever are important to provide a cure in patients with the disease and provide protection against it. In addition, due to the potential utilization of Lassa virus as a bioterrorism agent, vaccines against the disease can be utilized as a counterterrorism measure. Developing antiviral compounds and vaccines against the disease requires understanding of the pathogenesis of Lassa fever and its disease course, including the signs, symptoms, complications, and sequelae. An important sequela of Lassa fever is ataxia. A few cases of postviral ataxia following Lassa fever have been described in the literature. This review focuses on highlighting these cases, the gaps in scientific knowledge where further research is needed, and possible ways of diagnosing postviral ataxia after Lassa fever in resource-limited settings.

The authors report a case of fatal acute encephalopathy following influenza infection, with slightly atypical pathological and imaging findings. A healthy 8-year-old boy with probable recent influenza A/B infection admitted for refractory seizures was placed on phenobarbital coma and later developed hemodynamic instability. Magnetic resonance imaging revealed bilateral cerebral and cerebellar white matter lesions and microhemorrhages. Following his demise, the autopsy revealed a large area of necrosis in the right centrum semiovale with similar lesions in the temporal and cerebellar regions. Microscopically, there was extensive coagulative necrosis, compatible with necrotizing white matter encephalopathy, and neuronal loss suggesting superimposed hypoxic-ischemia. The acute progressive neurologic deterioration was partly reminiscent on acute necrotizing encephalopathy, a condition recently associated with influenza A. In acute necrotizing encephalopathy, typical brain findings are characterized by bilateral thalamic necrosis/petechiae with variable white matter edema. The somewhat atypical findings in our case can relate to superadded cardiovascular collapse and hypoxic-ischemic effects.

OBJECTIVE: The aim of this study was to evaluate the effects of olfactory training (OT) on olfactory function in patients with persistent postinfectious olfactory dysfunction (PIOD).
METHODS: Randomized, single-blind, controlled, multicenter crossover study.
METHODS: Twelve tertiary university medical centers participated. Investigations were performed at three visits (baseline, after 18 weeks, and after 36 weeks), including only subjects with PIOD of <24-months duration. At each visit, participants received detailed assessment of olfactory function. Seventy subjects trained with high concentrations of four odors for 18 weeks; the other half (n = 74) trained with low concentrations of odors. For the following 18 weeks this regimen was switched.
RESULTS: After 18 weeks, olfactory function improved in the high-training group in 18 of 70 participants (26%), whereas only 11/74 improved in the low-training group (15%). In subjects with a duration of olfactory dysfunction of <12 months, olfactory function improved in 15/24 participants (63%) of the high-training group and in 6/31 participants (19%) of the low-training group (P = .03).
CONCLUSIONS: OT improves PIOD, and the use of odors at higher concentrations is beneficial to improvement. OT is a safe procedure and appears to be particularly useful in patients who start OT within 12 months after the onset of the disorder. OT is the first successful therapy regime in patients with PIOD.
METHODS: 1b.