Difficulty walking without seeing toes

Introduction Eye movement disorder is a characteristic manifestation of progressive supranuclear palsy, with both eyes staring upwards and downwards. Generally speaking, starting from the two eyes will follow the paralyzed paralysis, the main complaint is that you can't see the difficulty of walking on the toes, or you can't see the food on the table. It is difficult to eat. The progressive loss and the upper vision function become complete vertical gaze, and the eyeball is fixed in the middle. Bit. In patients with more than 2/3 of the advanced stage, there may be bilateral paralysis of the eyes, and 1/3 of the patients have internuclear ophthalmoplegia. In some patients, the converging of the two eyes is not possible, the pupils are reduced, and light reflection and convergent reflexes exist.

Cause

(1) Causes of the disease

The cause of PSP is unknown, and although there are few familial clues, there is a lack of genetic evidence. The disease has similar narcolgic encephalitis-like neurofibrillary tangles in the brainstem. Some people suspect that it is associated with lentivirus infection, but there are no etiological clues in terms of poisoning, encephalitis, ethnicity and geographical factors.

(two) pathogenesis

At PSP, the striatum reduced 18F-dopa uptake and decreased D2R density. Dopamine (DA) and high vanillic acid (HVA) levels are reduced; cholinergic neurons are also involved, and choline acetyltransferase activity is reduced. The frontal lobe, striatum, thalamus, cerebellum glucose metabolism or glucose utilization and oxygen metabolism were significantly reduced, with the most prominent frontal lobe. A few patients showed diffuse glucose metabolism, but the frontal lobe and striatum were more obvious. Different from normal or increased striatum metabolism in PD, it may contribute to the identification of both.

Pathological features: extensive brain atrophy can be seen by the naked eye, including globus pallidus, substantia nigra, etc., and the lateral ventricle and third ventricle are enlarged. Microscopically, the pathological changes of the substantia nigra, globus pallidus-striatum pathway, quadrilateral superior mound, and white matter around the aqueduct were observed. The dense NFT was characteristically distributed and the nerve fiber mesh was formed. The latter is a filamentous structure embedded in the nerve fiber network, which does not depend on NFT alone, suggesting that PSP is a diffuse disease originating from the cytoskeleton. In addition, Tau-positive astrocytes were also found in the basal ganglia and brainstem. Other non-specific pathological changes include loss of neurons and gliosis, and the brain and cerebellar cortex are not affected.

an examination

Related inspection

Eye and sacral area CT examination neurological examination neurological immunological examination

Cerebrospinal fluid examination revealed an increase in CSF protein content in approximately one-third of patients.

1. About 1/2 of patients have non-specific diffuse abnormalities in EEG.

2. Head CT examination showed brain atrophy, MRI examination showed atrophy of the midbrain, with posterior enlargement of the third ventricle and atrophy of the anterior temporal lobe; some patients on T2WI could show low signal of the nucleus.

Differential diagnosis

Clinically, PSP should be noted with PD, post-encephalitis or arteriosclerotic pseudo-Parkinson's syndrome, cortical basal ganglia degeneration (CBGD), multiple system atrophy (MSA), diffuse Lewy body disease (DLBD), Creutzfeldt -Jacob disease (CJD) and other identification.

Parkinson's disease (PD) is also called tremor paralysis. Typical symptoms are resting tremor, muscle stiffness, and bradykinesia. Clinically, it is divided into primary, atherosclerotic, senile, encephalitis sequelae, and chemical poisoning according to different causes. Their main symptoms are basically the same, which is called Parkinson's syndrome.

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