 Hello everyone, myself Nadeem Ahmed, a third year PG resident, Department of Radio Diagnosis, Jawaharlal Nehru Medical College, AMU-Ligard, going to present a case on amortrophic lateral sclerosis. A 30-year female presented in opiative with history of progressive weakness of bilateral upper and lower limb for one year. Few months later, the patient developed generalized fasciculations, dysarthria and dysphasia. On examination, generalized fasciculations were observed with no muscular trophy. Tendon reflexes were increased, sensation and coordination were normal. The patient's informed concern for description of the case was given. Motor nerve conduction study was performed in the right ulnar and perinodial nerves. The parameters of sensory nerve conduction in the ulnar and sural nerves were normal. Parameters of motor unit action potentials such as amplitude, duration and size index were found to be significantly increased in each of the examined muscles, suggesting neurogenic abnormalities such as chronic denervation. According to the revised L-ascorial criteria, clinically definite ALS was diagnosed and MRI brain and spine was advised. This axial T2 cut section of MRI brain shows hyperintensity along the course of corticospinal tract. This axial flare scan shows hyperintensity along the course of corticospinal tract. This is SWI imaging showing blooming in both pre-central gui-ri also known as motor band sign. So, immunotrophic lateral sclerosis is also known as motor neuron disease or low-garrick disease. Ideology, upper motor neuron is in the primary motor cortex and sent exons inferiorly along the corticospinal tract to pass through the brainstem, decuss it at the cervical medullary junction and travel into the spinal cord. ALS is characterized by progressive degeneration of motor neuron in the both brain and spinal cord. Pathology, evidence of widespread muscle atrophy affecting limb and intercostal muscles and the diaphragm is typical at autopsy. The major historical pathological change in ALS is loss of motor cortex, brain stem and anterior haunts of the spinal cord. Epidemiology, ALS has an incidence of 1 to 2 per 1 lakh and is the most common motor neuron disease. ALS is mostly sporadic, 10 to 15 percent cases are familial. The average age of one-sided in familial ALS is 10 years earlier than in sporadic ALS. Presentation, signs of both UMN and element disease are generally required for the clinical diagnosis. Evidence of UMN degeneration includes hypertonicity, hyperreflexia and pathologic reflexes. Element disease results in muscle fasciculations, atrophy and weakness. Disease onset is typically ensued as at least 30 percent of anterior haunts are lost before weakness becomes clinically apparent. Natural history, although median survival from diagnosis to death is between three and four years, 10 percent of patients survive beyond 10 years. Death is generally from respiratory failure due to diaphragm weakness. On imaging, T2 flare hyperintensity is unusual but can occur anywhere from the subcortical white matter through the posterior limb of internal capsule, cerebral peduncle, pons to medullary pyramids and spinal cord. Changes are usually most prominent in the posterior limb of internal capsule and several peduncles. T2 weighted SWI image may demonstrate hyperintensity in the precentral cortex, also known as motor band sign as seen. Differential diagnosis, the major differential diagnosis of ALS is the normal hyperintensity of compact, fully myelinated white matter tracts. Another diagnostic consideration is primary lateral sclerosis. PLS is a juvenile autosomal resistive motor neuron disease that affects only motor neuron. Valerian degeneration can cause T2 flare hyperintensity along the corticospinal tract but is unilateral. Other disorders that may demonstrate T2 hyperintensity along the corticospinal tract including demyelinating and inflammatory disease, metabolic disorders such as acute hypoglycemic coma and infiltrating neoplasm. Discussion, fasciculations were present in our characteristic clinical finding in ALS. Fasciculations, however, are a non-specific finding related to neuropathic dysfunction. Fasciculation are not considered of clinical significance for ALS without associated evidence of neurogenic changes on needle EMG in the motor units reported as fasciculation. Such motor unit abnormalities were not seen. Electrodiagnostic studies in patients with possible ALS are critical for not only adding in the diagnosis but also helpful helping to provide information that could be consistent with a different potentially treatable diagnosis. And conclusion, a metrophy lateral sclerosis should be considered in patients with a rapidly progressive unexplained neuropathic process. This should be true even if there are atypical clinical and electrodiagnostic findings. Absence of response to therapy and development of upper modern neuroscience should reinforce the possibility that ALS may be present. Since ALS is a fatal illness, however, the possibility of this disease in patients with ALS clinical should not diminish the need for a thorough diagnostic evaluation and treatment trials. Thank you.