What Is the Striatum?

Striatum: One of the basal ganglia of the striatum. The striatum includes caudate and bean-shaped nuclei. These two nuclei are not completely separated and are connected on the ventral side of the front end. The lenticular nucleus is further divided into putamen and pale globules. Caudate nucleus and putamen are relatively new structures of striatum in phylogeny, collectively referred to as new striatum; pale globus is the oldest part of striatum, called old striatum. The striatum is a component of the extrapyramidal system that receives fibers from the cerebral cortex (mainly the frontal lobe) and thalamus. Most of the fibers emitted by the striatum originate from the pale globules, and these fibers enter the base of the thalamus. The main function of the striatum is to regulate muscle tension and coordinate various sophisticated movements. If the striatum is damaged, its function is impaired.

Striatum: One of the basal ganglia of the striatum. The striatum includes caudate and bean-shaped nuclei. These two nuclei are not completely separated and are connected on the ventral side of the front end. The lenticular nucleus is further divided into putamen and pale globules. Caudate nucleus and putamen are relatively new structures of striatum in phylogeny, collectively referred to as new striatum; pale globus is the oldest part of striatum, called old striatum. The striatum is a component of the extrapyramidal system that receives fibers from the cerebral cortex (mainly the frontal lobe) and thalamus. Most of the fibers emitted by the striatum originate from the pale globules, and these fibers enter the base of the thalamus. The main function of the striatum is to regulate muscle tension and coordinate various sophisticated movements. If the striatum is damaged, its function is impaired.

Chinese name

Striatum

Foreign name

Striatum

Definition

The main components of the basal ganglia

Include content

Lenticular nucleus and caudate nucleus

Classification

It can be divided into old and new striatum according to the occurrence of morning and evening

Neostriatum

Related to maintaining a fixed posture of the body

Old striatum

An important outgoing intermediate station in the extrapyramidal system

Features

Stability of voluntary movement, maintenance of muscle tone, etc.

Striatum overview

Striatum nigra degeneration: Striatum nigra degeneration. Can cause pigment loss, causing muscle rigidity, reduced movement, and slow action tremor. Elderly patients may have ataxia or orthostatic hypotension. Onset after middle age. The course of disease is 2-8 years. Head magnetic resonance showed striatum atrophy, substantia nigra degeneration, and later cerebellum and brain stem atrophy. No effective treatment.

Striatum striatum morphological structure and function

The striatum is one of the main neural structures of the extrapyramidal motor system. Including bean-shaped nucleus and caudate nucleus. The latter is divided into shells and pale balls. In terms of occurrence and fiber connection, the caudate nucleus and shell belong to the neostriatum, and the pale globus belongs to the old striatum. The head of the bean-shaped nucleus and the caudate nucleus are connected. There are nerve fibers at the junction and inside the bean-shaped nucleus to form gray and white stripes. This form is very clear on the horizontal section of the middle hemisphere. The caudate and bean-shaped nuclei are called striatum. The striatum is generally regarded as an important relay nucleus of the descending conduction beam of the cerebral cortex. The striatum functions are: maintaining normal muscle tension; maintaining coordination and relative stability of muscle groups during muscle movement. Clinically, the symptoms and signs of striatum can be classified into two types. A type of muscular dysfunction disorder, mostly manifested as increased muscle tension caused by slowness of movement, too little facial expression (mask face). Another type of dyskinesia often involves involuntary movements, such as tremors, hand and foot movements, and chorea. Such movements tend to increase when emotionally agitated, and disappear when sleeping peacefully.

Striatum and striatum related diseases

1. Parkinson's disease: Idiopathic Parkinson's disease is a non-hereditary progressive neurological disorder of the extrapyramidal system. In neuropathology, the obvious changes are the reduction of pigmented neurons and the appearance of eosinophilic inclusions in the substantia nigra. Its etiology is still unclear, although there is some evidence that it is related to environmental factors (such as the use of pethidine analogs containing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine [MPTP] Drug addicts may show Parkinson's syndrome). Extrapyramidal symptoms are mainly caused by dopamine deficiency in the striatum (ie, tail and putamen) caused by degeneration of the dopaminergic substantia nigra pathway. In addition to typical motor abnormalities (rest tremor, lead-like rigidity, bradykinesia, disappearance of normal posture reflexes, and abnormal gait), cognitive, perceptual, and memory impairments, or even total dementia, can occur in about one-third of patients. Depression is seen in about half of the patients. Many patients can also experience speech disorders, salivation, difficulty swallowing, and seborrheic dermatitis.

It is important to recognize that idiopathic Parkinson's disease is only one of Parkinson's syndromes. Another large group of diseases called "atypical Parkinson's syndrome" can have neurological signs that are difficult to distinguish from Parkinson's disease. Drugs (i.e. antipsychotics, metoclopramide, reserpine), toxins (e.g. MPTP, manganese, carbon tetrachloride, carbon disulfide), metabolic diseases (e.g. Wilson disease), encephalitis (e.g. Parkinson's syndrome after encephalitis) ), And various neurodegenerative ("Parkinson's syndrome") lesions (such as progressive supranuclear palsy, substantia nigra degeneration, Shy-Drager multiple system atrophy), etc. can cause Parkinson's syndrome.

The goal of Parkinson's disease therapy is to effectively reduce functional impairment with the lowest dose of anti-Parkinson's disease drugs. The patient's ability to perform daily activities such as labor, walking, getting up or standing up, dressing, and eating should be a determinant of dose adjustment. The impairment of these functional abilities is generally manifested by bradykinesia and dysregulation. Other signs of Parkinson's disease, such as tremor and rigidity, are usually of little use in determining whether treatment is adequate. Treatment is symptomatic rather than curative, and generally tends to supplement striatum dopamine, stimulate striatum dopamine receptors, and block central cholinergic receptors, the latter being less useful than the first two.

Although drug therapy is the main method for treating Parkinson's disease, non-drug therapy is also important. Exercise, speech therapy, physical therapy, and psychotherapy are all beneficial. In terms of optimal treatment, support and involvement of relatives is essential.

2. Striate internal capsular infarction: anterior choroidal artery blood supply area infarction: anterior choroidal artery (AChA) infarction was first reported by some scholars in 1925. AChA originated from the internal carotid artery approximately 3 mm distal to the posterior communication artery. On the posterior side, a few start from the middle cerebral artery or posterior communicating artery, and the proximal end sends out branches to supply below the optic cross, optic tract, gray nodules, and papillary bodies; and then sends out important striated internal saccular arteries to the internal sac. The hind two thirds, the medial part of the pale bulb, the audiovisual radiation, and the tail of the caudate nucleus. After entering the inferior corner of the lateral ventricle via the choroid, the hair branches to the hippocampus, hook, amygdala, hippocampus and anterior dentate gyrus. It ends in the choroid plexus of the lateral ventricle. AChA varies a lot, but the branches to the optic tract, brain feet, inner capsule hind limbs, and choroid plexus are relatively fixed. AChA is characterized by a long stroke, a thin lumen, a wide range of blood supply, and the lack of collateral circulation. Once occluded, especially the striatum, the cystic artery will cause typical "trilateral" symptoms (isotropic blindness on the opposite side of the lesion). , Contralateral hemiplegia and anaesthesia), at this time, it can be considered that the infarction of AChA area is narrow striatum internal sac infarction, and the brain CT manifests as a low-density foci of the entire internal sac hindlimb, which are mostly stick-shaped and less flaky. A craniocerebral MRI showed a strip-shaped lesion in the hindlimb of the inner capsule, showing a low T1 signal and a high T2 signal. In general, the striated endocystic infarction also includes infarcts in the blood supply area of the striatum. The lesions are mostly in the front of the stigma nucleus, the forelimbs of the internal capsule, and the knee. They are characteristic "ton" shaped lesions. It is academically easy to distinguish from AChA infarction. Due to the wide range of AChA blood supply, in addition to the symptoms of "triangularity", sometimes there are visual symptoms such as flowering, whitening, and blurred vision in the eyes; vertical and lateral paralysis of the eyeballs, and mild to moderate lesions in the main hemisphere. Speech impairment, non-dominant hemisphere lesions may appear lateral neglect; bilateral AChA infarcts may have varying degrees of consciousness impairment, cognitive decline and pseudobulbar paralysis.