## 1 Introduction  
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the progressive degeneration of both upper and lower motor neurons [1, 2]. Currently, ALS is considered a multisystemic disease [3] that primarily affects motor neurons and has great genetic, clinical, and neuropathological heterogeneity [4]. The age group most at risk for developing this disease is 45 to 75 years old. Its most common form is sporadic (90% of cases), in which its pathogenesis is related to complex interactions between genetic and environmental factors. The remainder of the cases (10%) are of the familial type, where there is the presence of an autosomal dominant inheritance pattern proven by the occurrence of a family history of the disease [4]. The etiology of ALS is not yet fully understood, but it is known that there are interactions between genetic and environmental factors, in addition to aging-related dysfunctions [4]. The pathophysiology of ALS is marked by neuronal dysfunction with eventual cell death (neuronal apoptosis). Hypotheses guiding its pathophysiology include glutamate toxicity, oxidative stress, neuroinflammation, protein aggregation (e.g. TDP-43 protein),defects in RNA processing, mitochondrial dysfunction, axonal transport dysfunction, toxin exposure, and viral infections [5; 6]. In ALS, the first observation of symptoms usually occurs between the ages of 51 and 66 [7]. As the disease affects motor neurons, the most characteristic symptoms are muscle atrophy and weakness. The affected muscles are skeletal and those involved in breathing, speaking, and swallowing. In this way, a range of signs and symptoms can be observed, such as dysarthria, dysphonia, dysphagia, atrophy, and muscle weakness [4; 5]. Other signs and symptoms include drooling, fasciculations, hyperreflexia, sensory impairment, cramps, and emotional liability. Around 50% of patients will present other non-motor symptoms, related to cognitive and behavioral changes. One example is frontotemporal dementia in 10-15% of cases, clinically characterized by behavioral changes, impairment of executive functions, and/or language impairment [4]. The diagnosis of ALS is based on clinical history and physical examination, which shows signs of progressive dysfunction of the upper and lower motor neurons. It is usually supported by electrophysiological and neuroimaging studies, as well as laboratory tests, especially in cases of familial ALS. Exclusionary diagnoses should be considered [8]. The El Escorial criteria were developed to standardize ALS diagnosis for clinical research [9]. Early diagnosis can contribute to better clinical management of the disease. However, incorrect diagnoses early in the disease can delay the diagnosis of ALS. Studies show that the delay in diagnosing ALS can range from 9 to 24 months [7]. Currently, some guidelines address the treatment of ALS [5; 10; 11] and all recommendations support a multidisciplinary approach. Regarding drug treatment, although several clinical trials are underway, there are two drugs approved by the Food and Drug Administration (FDA): Riluzole and Edaravone. Riluzole acts as a glutamate antagonist and reduces its excitotoxicity, increasing survival by only about 3 to 6 months [12]. On the other hand, Edaravone acts to reduce oxidative stress and has been shown to improve the functional status and increase the survival of patients with ALS [13]. As a limitation, the treatment of the disease is focused on managing the symptoms that occur throughout the disease. Authors demonstrate that multidisciplinary care in ALS is capable of significantly increasing survival [14]. The prognosis for patients with ALS is unfavorable, but survival time after diagnosis varies greatly. The factors that lead to shorter survival of patients with ALS are bulbar onset, delay in diagnosis, rapid functional decline, pronounced loss of weight or body mass index (BMI), advanced age at the onset of symptoms, presence of frontotemporal dementia, and low forced vital capacity.