(1) Peripheral neuropathy is common in polyneuritis caused by various reasons, such as toxic, metabolic and hereditary polyneuritis. The main manifestations are symmetrical sensory, motor and nutritional disorders of distal limbs, decreased muscle tension, disappearance of tendon reflex and muscle tenderness. Its main feature of ataxia is ataxia of limbs. The lower limb is heavier than the upper limb, and the distal limb is heavier than the proximal limb, which is aggravated when the eyes are closed. This type has deep sensory disturbance, without argyle-Robertson pupil and sphincter disturbance. The above three points can be differentiated from posterior bundle type or spinal tuberculosis.
(2) Patients with posterior rhizopathy and polyradiculitis may have ataxia, accompanied by paresthesia, paresthesia, myalgia, decreased muscle tone, disappearance of tendon reflex and increase of cerebrospinal fluid protein. Typical sensory ataxia occurs after spinal tuberculosis damages the roots and bundles. And may have lightning-like pain, waist-girdling sensation, sphincter dysfunction,
(3) Sensory ataxia of posterior bundle injury can occur in people who have injured the posterior bundle of spinal cord for various reasons, such as subacute combined degeneration, posterior spinal tumor and hereditary spinal ataxia. It is characterized by sensory separation, that is, the sense of touch and warm pain is not damaged, while the sense of position, pressure and vibration is reduced or disappeared. Patients with subacute degeneration often have pyramidal tract damage, including myasthenia, hyperreflexia and positive pathological signs, as well as polyneuritis and pernicious anemia. Gastric juice analysis often leads to the reduction of free acid. Posterior spinal cord tumors often have nerve root pain first, and then gradually develop into sensory ataxia symptoms, often accompanied by superficial sensory disturbance of conduction tract and pyramidal tract sign, lumbar intervertebral canal obstruction symptoms, and increased cerebrospinal fluid protein.
(4) Sensory ataxia may occur in the posterior fasciculus or its nucleus, pons and medial colliculus of the midbrain. The ataxia of medulla oblongata lesions is on the same side, and the ataxia of pons and central lesions is on the opposite side. It is characterized by the symptoms of ipsilateral cranial nerve damage, which is often accompanied by cerebellar ataxia.
(5) Thalamic lesions The causes of thalamic ataxia can be blood vessels, tumors and trauma. In addition to sensory ataxia in the contralateral hemisphere, there are spontaneous pain and superficial sensory disturbance in the contralateral hemisphere, and ataxia in the upper limb is more serious than that in the lower limb. Because the ventral thalamic nucleus is related to cerebellum, thalamic lesions are accompanied by cerebellar symptoms. Thalamic lesions lead to deep sensory disturbance. You can see the movements of hands and feet, especially the hands, which is called thalamic restless hands. When you close your eyes, your hands can't keep a certain posture and your fingers move, which is caused by the position perception disorder of your hands (pseudo-peristalsis of your hands and feet).
Second, cerebellar ataxia
(1) Cerebellar vermis disease mainly causes balance disorder, manifested as trunk ataxia, unstable standing and walking, and almost or completely normal limb ataxia, which is called cerebellar vermis syndrome. Acute progressive cerebellar vermis lesions are common in tumors, especially in children, such as medulloblastoma, astrocytoma and ependymoma. Metastatic tumors are more common in adults, and their clinical manifestations are progressive intracranial hypertension and trunk ataxia. This is most obvious when the patient is standing and walking. Usually, the body can shake backwards and fall, especially when turning around, the gait instability is obvious, the upper limb ataxia is not obvious, and it is often accompanied by dizziness and decreased muscle tension. Chronic progressive cerebellar vermis disease, from childhood, has progressive cerebellar ataxia, which is characterized by ocular telangiectasia; Adults have progressive cerebellar degeneration, cancerous cerebellar atrophy and alcoholic cerebellar degeneration. The main clinical manifestations are trunk ataxia and speech disorder.