disease, it causes spasticity and muscular atrophy The course is progressive and is ultimately fatal Anterior horn cell disease affects the most proximal component of the lower motor neuron unit Because these diseases affect the motor neurons, sensory function is normal Reflexes are generally lost early in the course of the disease Ultimately, muscle atrophy and fasciculations develop Cranial nerve nuclei are often affected as well Poliomyelitis is the classic example of an anterior horn cell disease, but it has been largely eradicated by immunization In 2014, anterior horn cell disease emerged in association with enterovirus D68 A peculiar entity that mimics poliomyelitis is idiopathic postasthmatic amyotrophy, or Hopkins syndrome It presents as a sudden onset of weakness, generally to weeks after an acute asthma attack Like polio, prognosis is poor, with all patients left with some degree of permanent paralysis The three pediatric types of spinal muscular atrophy (SMA) comprise a group of autosomal recessive genetic disorders in which the anterior horn cells in the spinal cord and motor nuclei of the brainstem are progressively lost There is widespread muscle denervation and atrophy The weakness is usually symmetric, progressive, and proximal, and presents anytime from birth to adulthood Later in the disease course, tongue fasciculations and diminished DTRs may occur Importantly, intellect and cardiac, sensory, and sphincter functions are preserved Spinal muscular atrophy I (acute infantile SMA, or Werdnig–Hoffman disease) is the most severe form of SMA The weakness and severe generalized hypotonia begin before months of age These patients never develop the ability to sit alone Death often occurs by years of age, usually from overwhelming pneumonia Spinal muscular atrophy II (chronic infantile SMA) usually has its onset of weakness between and 18 months These patients can sit alone, but can never walk In this “intermediate” SMA, survival to adulthood is expected Spinal muscular atrophy III (mild juvenile SMA, or Kugelberg–Welander disease) usually presents with weakness after 18 months These patients can walk without support Neuropathies (primary disorders of the axon or its myelin sheath) usually present as progressive symmetric distal weakness Weakness and sensory loss may move in a glove and stocking distribution Tendon reflexes are usually lost early Dysesthesias (“pins and needles” or burning sensations) usually occur in acquired conditions Guillain–Barré syndrome (GBS) , or acute inflammatory demyelinating polyradiculopathy (AIDP) , is the classic acquired immunologic neuropathic