Symptoms depend on the type of<unk>  inherited. The main feature of the disease is progressive<unk> ity in the lower limbs due to pyramidal tract dysfunction. This also results in brisk reflexes, extensor plantar reflexes, muscle weakness, and variable bladder disturbances. Furthermore, among the core symptoms of<unk>  are also included abnormal gait and difficulty in walking, decreased vibratory sense at the ankles, and paresthesia. Individuals with<unk>  can experience extreme fatigue associated with central nervous system and neuromuscular disorders, which can be disabling. Initial symptoms are typically difficulty with balance, stubbing the toe or stumbling. Symptoms of<unk>  may begin at any age, from infancy to older than 60 years. If symptoms begin during the teenage years or later, then<unk>  gait disturbance usually progresses over many years. Canes, walkers, and wheelchairs may eventually be required, although some people never require assistance devices. Disability has been described as progressing more rapidly in adult onset forms. More specifically, patients with the autosomal dominant pure form of<unk>  reveal normal facial and extraocular movement. Although jaw jerk may be brisk in older subjects, there is no speech disturbance or difficulty of swallowing. Upper extremity muscle tone and strength are normal. In the lower extremities, muscle tone is increased at the hamstrings, quadriceps and ankles. Weakness is most notable at the iliopsoas, tibialis anterior, and to a lesser extent, hamstring muscles. In the complex form of the disorder, additional symptoms are present. These include: peripheral neuropathy, amyotrophy, ataxia, intellectual disability, ichthyosis, epilepsy, optic neuropathy, dementia, deafness, or problems with speech, swallowing or breathing. Anita Harding classified the<unk>  in a pure and complicated form. Pure<unk>  presents with<unk> ity in the lower limbs, associated with neurogenic bladder disturbance as well as lack of vibration sensitivity (pallhypesthesia). On the other hand,<unk>  is classified as complex when lower limb<unk> ity is combined with any additional neurological symptom. This classification is subjective and patients with complex<unk> s are sometimes diagnosed as having cerebellar ataxia with<unk> ity, intellectual disability (with<unk> ity), or leukodystrophy. Some of the genes listed below have been described in other diseases than<unk>  before. Therefore, some key genes overlap with other disease groups. Age of onset In the past,<unk>  has been classified as early onset beginning in early childhood or later onset in adulthood. The age of onsets has two points of maximum at age 2 and around age 40. New findings propose that an earlier onset leads to a longer disease duration without loss of ambulation or the need for the use of a wheelchair. This was also described earlier, that later onset forms evolve more rapidly.
Hereditary spastic paraplegia
Spinal muscular atrophy
Madras motor neuron disease
Tropical ataxic neuropathy
Spinal and bulbar muscular atrophy
Autosomal recessive cerebellar ataxia type 1
Distal hereditary motor neuronopathies
Congenital distal spinal muscular atrophy