BACKGROUND: Peripheral Facial Palsy (PFP) is a facial paralysis with various etiologies, including idiopathic causes (Bell\'s palsy), infections, trauma, and genetic factors. Traditional treatments involve antiviral medications, corticosteroids, and physiotherapy. However, new therapies, such as Low-Level Laser Therapy (LLLT), are emerging with promising results.
METHODS: This case series reports on two patients with PFP treated with LLLT combined with Vitamin B1, B6, and B12 supplementation. The first case involved a 52-year-old female with PFP due to a viral infection. The second case was a 33-year-old male who developed PFP following a traumatic brain injury. Both patients received LLLT sessions every two weeks, targeting 10 points along the facial nerve pathway from the facial notch across the face. The laser device used was the Theraphy EC (DMC, Sao Carlos, SP, Brazil), with each point receiving 4 Joules of energy applied perpendicular to the skin after cleaning the face with water and soap to remove lipids that could interfere. The administration of Vitamin B was done using NEUROBIONTA tablets (Vitamin B1 + Vitamin B6 + Vitamin B12; Procter & Gamble, Santiago, Chile) with one tablet taken daily for 30 days.
RESULTS: After six to seven sessions, both patients showed significant improvement in facial muscle function and overall facial symmetry. In the first case, improvements were noted in muscle tonicity and facial movements, with the patient reporting reduced facial disfigurement. In the second case, notable recovery in facial mobility and symmetry was observed, with the patient experiencing decreased paresthesia and restored muscle functionality.
CONCLUSIONS: These findings suggest that LLLT, combined with Vitamin B1, B6, and B12 supplementation, may effectively improve facial muscle function and symmetry in PFP patients. The non-invasive nature and ease of application make LLLT a viable option for PFP treatment. Further studies with larger sample sizes and standardized protocols are necessary to confirm these results and establish LLLT as a standard treatment for PFP.

Wernicke\'s encephalopathy (WE) is a dangerous and potentially fatal neurological condition associated with thiamin deficiency. The standard treatment for WE is intravenous (IV) thiamin, but limited research describes optimal dosing. We present a case of a 40-year-old male with severe alcohol use disorder (AUD) and chronic malnourishment who developed WE. Upon administration of 100 mg IV thiamin, symptoms of WE persisted, but when the dose was increased to 500 mg, altered mental status and ophthalmoplegia resolved rapidly. IV thiamin is a reliable and low-risk treatment for WE, even when administered at high doses. High-dose IV thiamin (i.e., >/100 mg) can treat neurological symptoms and cognitive dysfunction in WE and should be considered for first-line treatment. Further study of WE diagnostic and treatment guidelines is warranted to maximize recovery potential.

Unless otherwise demonstrated, seizures during pregnancy that happen after 20 weeks of gestation are typically caused by eclampsia. In our clinical case we report the diagnostic challenge of Wernicke\'s encephalopathy occurring at 34 weeks and mimicking an eclamptic attack. This is about a 30-year-old female patient who suffers from hyperemesis gravidarum during her pregnancy. she has no known history of epilepsy .The patient was brought to the emergency room by medical transport at 34 weeks of gestation due to a seizure at home. The initial diagnosis was eclampsia. Emergency high-level extraction under general anesthesia was decided for maternal rescue. However, after extubation, the patient\'s condition deteriorated, with the onset of a confusion syndrome characterized by agitation, temporal-spatial disorientation, attention and vigilance disorders, and challenging communication. Angio MRI was performed, revealing signs consistent with Wernicke\'s encephalitis.

Individuals with alcohol use disorder frequently suffer from vitamin D deficiency, in addition to deficiencies in vitamins B12, folic acid and B1. This is due to inadequate dietary intake and behavioural changes. Each of these deficiencies results in different clinical symptoms. Subacute spinal cord degeneration, together with radicular and sensorimotor peripheral neuropathy, arises from B12 vitamin and folic acid deficiencies. B1 vitamin deficiency leads to Wernicke\'s encephalopathy, which can include the classical triad of symptoms (i.e. cognitive changes, ataxia and ophthalmoplegia). Sarcopenia is a consequence of a long-term deficiency of vitamin D. This current case report describes a 43-year-old female patient with alcohol use disorder who complained of dizziness, postural disturbance and episodes of intermittent paraesthesia. She was subsequently shown to have concomitant Wernicke\'s encephalopathy and sarcopenia due to vitamin D deficiency. This case report presents the diagnostic process undertaken to exclude conditions related to ataxia and paraparesis other than vitamins D and B1 deficiencies. It also emphasizes the importance of concomitant replacement of the depleted vitamins because the vitamin deficiency may occur simultaneously, which causes the accompanying manifestations of several clinical syndromes.

Homogenates of brain tissue from the frontal cortex at autopsy in patients with amyotrophic lateral sclerosis (ALS) showed dramatically reduced levels of the enzyme thiamine pyrophosphatase (TPPase), the enzyme responsible for the conversion of thiamine pyrophosphate (TPP) to thiamine monophosphate (TMP). Additionally, free thiamine (vitamin B1) and TMP levels have been shown to be significantly reduced in the plasma and cerebral spinal fluid (CSF) of patients with ALS. These findings suggest that there is impaired thiamine metabolism in patients with ALS. Impaired thiamine metabolism decreases adenosine triphosphate (ATP) production and is a well-established cause of neurodegeneration. Decreased levels of TPPase, resulting in decreased levels of TMP in the cells of the frontal cortex, might account for the focal neurodegenerative changes observed in motor neurons in ALS. Benfotiamine, a safe, lipid-soluble, highly absorbable thiamine analogue, significantly raises free thiamine, TMP, and TPP levels in the blood. A case in which benfotiamine may have positively impacted the symptoms of a patient with ALS is presented. The use of benfotiamine in patients with ALS appears to be a promising therapeutic option. Considering the severity and the lack of satisfactory treatment options associated with this disease, more research on the effects of benfotiamine on the course of ALS is urgently needed.

Wernicke\'s encephalopathy (WE) is a condition caused by a deficiency of vitamin B1. While there have been many reported cases of WE in the literature, there are few reports on the early stages of the disorder. In this report, we present a case of WE with urinary incontinence as the main clinical manifestation. A 62-year-old female patient was admitted to the hospital due to intestinal obstruction and did not receive vitamin B1 supplements for 10 days. Three days after her operation, she developed urinary incontinence. She also had mild mental symptoms, such as a little indifference. After consultation with a urologist and neurologist, the patient was immediately given intramuscular vitamin B1 at a dosage of 200 mg/day. After 3 days of supplementing with vitamin B1, her urinary incontinence and mental symptoms improved and were completely resolved after 7 days of treatment. Surgeons should be aware that when long-term fasting patients have urinary incontinence, it may be a symptom of WE, and they should be supplied with vitamin B1 in a timely manner without extensive examination.

A 42-year-old female was admitted with upper abdominal pain. Imaging studies and laboratory tests were performed to consider acute lipogenic pancreatitis. After symptomatic treatment, her abdominal pain was significantly relieved. However, the patient was accompanied by upper gastrointestinal obstruction, which was gradually relieved after long-term fasting, gastrointestinal decompression, and fluid rehydration. The patient developed dizziness and ataxia, which worsened. Cranial magnetic resonance imaging (MRI) indicated patchy abnormal signal shadows in the bilateral thalami and dorsal brainstem and suggested metabolic encephalopathy. Wernicke\'s encephalopathy (WE) was the initial diagnosis of suspicion, adequate vitamin B1 was immediately replenished until the complete resolution of symptoms, and the patient made a rapid and dramatic recovery.

BACKGROUND: Gayet-Wernicke\'s encephalopathy (GWE) is a neurological pathology caused by a Thiamine deficiency. While it is most often related to chronic alcoholism, GWE can occur in any situation that results in thiamine deficiency. It is a fairly common pathology that is frequently underdiagnosed and therefore under-treated, and is associated with a high mortality and morbidity rate. In the absence of pathognomonic signs, the diagnosis of GWE relies on a range of clinical, biological and radiological assessments. GWE is considered a medical emergency. We present a case of Gayet-Wernicke\'s Encephalopathy resulting from complete parenteral nutrition in an undernourished North African male operated for a left colon tumor. Through this report, our aim was to put the light on this often underknown disease and to remind the interest of thinking about this pathology in patients at risk of undernourishment especially in oncology.
METHODS: A 66-year-old North African male with no personal or family history was operated for a sigmoid colon tumor. He was put on exclusive parenteral nutrition on day thirteen post-operatively and presented with a GWE on day sixteen post-operatively. The patient was treated with intravenous vitamin B1 on day eighteen post-operatively and deceased on day twenty-four post-operatively.
CONCLUSIONS: Although most often associated with chronic alcoholism, GWE occurs in any situation where there is an increased energy demand or decreased nutritional intake especially in oncology. GWE is common but under-diagnosed and remains lethal if not treated urgently, hence the importance of prophylactic treatment.

Wernicke\'s encephalopathy (WE) is a rare, life-threatening neurological disease due to thiamine deficiency. It is most commonly associated with chronic alcoholism but is also associated with disorders of malabsorption and malnutrition. We present a case of a young female with idiopathic gastroparesis who developed Wernicke\'s encephalopathy due to poor oral intake and malnutrition as a result of gastroparesis. This case exemplifies that Wernicke\'s encephalopathy should be on the differential in patients who present with encephalopathy with a history of gastroparesis.

Thiamine deficiency (TD) in non-alcoholic hospitalized patients causes a variety of non-specific symptoms. Studies suggest it is not rare in acutely and chronically ill individuals in high income countries and is underdiagnosed. Our aim is to demonstrate data which help define the risk factors and constellation of symptoms of TD in this population. We describe 36 cases of TD in hospitalized non-alcoholic veterans over 5 years. Clinical and laboratory data were extracted by chart review +/- 4 weeks of plasma thiamine level 7 nmol/L or less. Ninety-seven percent had two or more chronic inflammatory conditions (CICs) and 83% had one or more acute inflammatory conditions (AICs). Of possible etiologies of TD 97% had two or more of: insufficient intake, inflammatory stress, or increased losses. Seventy-five percent experienced 5% or more weight loss. Ninety-two percent had symptoms with the most common being weakness or falling (75%) followed by neuropsychiatric manifestations (72%), gastrointestinal dysfunction (53%), and ataxia (42%). We conclude that TD is underdiagnosed in this population with consequent morbidity and mortality. TD likely develops because of inflammatory stress from CIC\'s compounded by AIC\'s combined with decreased energy intake or increased nutrient losses.