Is cerebellar ataxia all hereditary?

Ataxia does not have to be genetic.

It can be caused by traumatic brain injury, intracranial hemorrhage, and more.

Genetic ataxia is usually symptomatic as a child.

More than 60 should not be hereditary. It will not be passed on to future generations.

Cerebellar ataxia is hereditary and more common than adulthood. The main manifestations are ataxia of the limbs, mostly heavier in the lower limbs, nystagmus and poetic speech. Clinically it can be divided into 3 types:

No family history, only cerebellar involvement, no intention tremor, possible coarse normal cerebral cortical ataxia. If there is significant intention tremor, nystagmus, and late onset of dysphagia, olive, pontine, and cerebellar ataxia may occur. Cerebellar dentate nucleus ataxia may be present if cerebellar ataxia is present, with significant intention tremor, and lower extremity ataxia is mild or with convulsive braching and myoclonus.

Hereditary cerebellar ataxia (neurology) is the most common of all reported ataxias. The pathogenesis is unknown, and the lesions mainly involve the cerebellum, but the spinal cord and cranial nerves can also be partially affected. The mode of inheritance is autosomal dominant, and there is no significant difference in incidence between men and women.

If you find signs of disease, you should go to the hospital for examination in time, and if you find the symptoms, you will be able to do it in time, so that the effect will be greatly improved, and the disease will not be delayed. There is a certain genetic predisposition to the disease, but it is not necessarily passed on to future generations. Patients should go to a public hospital on the right track to stop the examination and **, stop functional exercise appropriately, and do not smoke and drink.

Cerebellar atrophy usually affects walking. Patients with cerebellar atrophy generally have symptoms such as dizziness, dizziness, unsteady walking, uncoordinated limbs, slurred speech, and plosive sounds, and the patient can be diagnosed by cranial magnetic resonance examination. The cerebellum can regulate the posture and balance of the limbs and coordinate the voluntary movements of the cerebellum, so the main symptoms of cerebellar atrophy are uncoordinated limb function and abnormal posture.

Patients should pay attention to rest when they are flat, so as not to cause blood supply to the brain.

Spinocerebellar ataxia (SCA) is a group of neurological genetic disorders caused by genetic mutations leading to degeneration of the cerebellum, brainstem, and spinal cord. The main clinical manifestations are progressive motor coordination dysfunction and balance disorders. Most are autosomal dominant, but can also be autosomal recessive, X-linked, and mitochondrial inherited.

**Principle. At present, there is no specific method for this disease, and symptomatic treatment can alleviate symptoms. Modalities include medications, surgery, and exercise.

Drugs**. 1. The combined application of buspirone, amantadine and gabapentin can improve the symptoms of ataxia.

2. Levodopa or dopamine agonists can alleviate extrapyramidal symptoms such as rigidity.

3. Neurotrophic drugs such as ATP, coenzyme A, inosine and B vitamins can be tried.

Related medicines. Spirone, amantadine, gabapentin, levodopa, ATP, coenzyme A, inosine, B vitamins.

Surgery**. If the condition requires, optic thalamic dissection may be done.

Other**. Training, physical, and assisted walking may help patients improve their quality of life.

**Cycle. The first cycle of spinal cord and cerebellar ataxia is generally 1 to 3 years, but there may be individual differences due to factors such as the severity of the disease, the first plan, the timing of the file, and the individual's physique.

Cerebellar ataxia is inherited and runs in families, and as long as one person in the family suffers from the disease, there is a 50% chance that the child will inherit it.

In general, hereditary spinocerebellar ataxia is common in cerebellar ataxia, and sporadic cases are also common, and the number of inherited generations is different in different inheritance methods, mainly including the following forms:

1. Autosomal dominant inheritance: it is the most common inheritance mode, which is mainly manifested in the continuous generations of patients in the family, and there is a 50% genetic probability for the offspring of the patient with a clear diagnosis, that is, when one of the parents is sick, the children have a 50% chance of developing the disease. In general, the autosomal dominant spinocerebellar ataxia subtype is commonly found in some ethnic patients, also known as SCA3 or Machado-Joseph disease, which is about more than half of the autosomal dominant spinocerebellar ataxia alumina.

Other subtypes such as SCA1, SCA2, SCA3, and SCA6 are rare, while SCA8, SCA12, SCA17, and SCA35 are extremely rare.

2. Autosomal recessive inheritance: the main feature is that when one of the parents is sick and the other parent is normal, the child may carry the disease-causing gene, but will not develop the disease;

Hereditary ataxia is a group of genetic degenerative diseases characterized by chronic progressive cerebellar ataxia, which is characterized by ataxia manifestations, genetic history, and spinal cord, brainstem, and cerebellar damage. In addition to cerebellar and conduction fiber involvement, this group of diseases often involves the pyramidal tract, spinal cord, cranial nerve nucleus, pontine nucleus, spinal ganglia, basal nucleus, and autonomic nervous system. Ataxia gait is the first symptom to emerge and gradually increase in embarrassment, and the most cautious eventually leads to bedridden, overlapping clinical symptoms, and is very complex, and the same family can show a high degree of heterogeneity.

Common symptoms: Friedreich ataxia is the most common idiopathic degenerative disease. Chromosomal recessive ataxia is often early and has unique clinical features, such as childhood.

Progressive gait ataxia of the limbs with neurological signs and symptoms such as pyramidal extrapyramidal signs, dysphonia, deep paresthesias, and non-neurological symptoms such as scoliosis, pes cavus, and cardiac impairment.