Muscle weakness stupidly confused? I will teach you!

Decades of clinical experience tells you that myasthenia refers to the inability of the muscles to produce normal strength, and the loss of muscle strength to varying degrees.

The patient is consciously fatigued, and it is difficult to complete the activities or actions of daily life or professional life.

Video: The pathogenesis of muscle weakness For clinicians, the diagnosis of muscle weakness is very difficult.
What is the difficulty? Four Difficulties in Diagnosis and Treatment 1.
The clinical manifestations are highly similar.
The main complaint of the patient is very similar to the clinical manifestations.
If you are not a neurologist, you will feel that they all look the same.

For example, can you find the difference between these patients? Or based on the main complaints of these patients, can you make a preliminary judgment on their location diagnosis and qualitative diagnosis? Figure 1: Stupid and unclear 2.
Positioning diagnosis depends on electrophysiological support to a certain extent.
Although clinical judgment is very important, it relies on electrophysiological support.
Electrophysiology is a highly technical auxiliary examination.
Excellent electrophysiologists must Has a very strong clinical background.

Therefore, in many hospitals, electrophysiological reports are inaccurate.
Under the guidance of biased electrophysiological reports, if clinicians do not have a strong ability to integrate knowledge, they may be induced to make a wrong diagnosis.

 3.
There are many kinds of diseases.
At least hundreds of neuromuscular diseases can cause clinical muscle weakness.

 4.
Limited treatment means Many causes of myasthenia are hereditary, and the treatment means are limited.
The cause of myasthenia in patients with symptoms of myasthenia is mainly concentrated in acquired myasthenia, such as immune-mediated, drug poisoning-related, endocrine Related etc.

Clinical diagnosis roadmap To understand the mentality of myasthenia diagnosis from a macro level, "I will be at the top of the mountain and see the mountains and small mountains", which means that we can see the whole picture when we stand at a very high place.

So, let us first take a look at what are the major categories of muscle weakness symptoms? First of all, myasthenia can be divided into pseudomyasthenia and true myasthenia: pseudomyasthenia is more common.
For example, many patients with anxiety and physical symptoms say that they have muscle weakness.
This is pseudomyasthenia; true myasthenia is also Divided into upper motor neuron muscle weakness and lower motor neuron muscle weakness.

Among them, upper motor neuron muscle weakness is highly discernible, such as spinal cord disease, cerebral hemisphere or brain stem disease, which has characteristic accompanying symptoms and signs, which are easier to identify.

 The most difficult to identify is lower motor neuron muscle weakness.
According to the anatomical location of the disease, it can be divided into five categories: forefoot cell disease, nerve root plexus disease, peripheral neuropathy, neuromuscular junction disease, and muscle disease.

These lesions have their own general clinical characteristics: the forefoot cell lesions have obvious muscle jumping, obvious muscle atrophy, and asymmetric onset and development; most of the nerve root plexus lesions are accompanied by sensory disturbances, and weakness and paresthesias are distributed in segments; Neuropathy generally coexists with motor and sensory disturbances, and the distribution is mainly symmetrical at the distal extremities; neuromuscular junction disease is characterized by fluctuating and easy fatigue; the distribution of muscle pathology is characterized by proximal muscle weakness and head-lifting muscle weakness.
obvious.

Figure 2: The general idea of ​​the clinical diagnosis of muscle weakness.
These classifications based on anatomical parts are divided into two categories from the etiology: acquired and hereditary.

It seems simple, but in fact, it contains many, many disease diagnosis subdivisions under the general category, but the rough classification is our preliminary method for learning the diagnosis idea, from the "coarse to the fine", from the "coarse" diagnosis system Transition to a "finer" diagnostic system, and then further deepen it to a single disease, so that we can get a complete picture of similar disease groups.

 At the time of diagnosis, you can implement "check-in seating", and the single disease type after classification is the "seat".

The patient’s clinical symptoms, signs, and other examination results are the “tickets”.
If the patient enters the venue with 4 rows and 3 seats, then you need to have this “seat” within your cognition so that the number can be matched.
, The diagnosis will naturally be straightened out. It can be concluded that our diagnostic ability depends on our cognitive boundaries.
As much as we can recognize, we have as many "seats".
After the patient comes, we can give the corresponding "seats".

 Speaking of the underlying thinking, we must implement it.
In the diagnosis of neurological diseases, localized diagnosis and qualitative diagnosis are particularly important.
Next, let's take a look at how to localize and diagnose muscle weakness.

Location diagnosis 1.
Medical history prompts location The medical history plays an important role in the initial location diagnosis.

Assuming that a patient’s limbs are weak, the diagnosis process shown in the following figure can be drawn: through purposeful design of questions one by one, the general diagnosis direction is obtained; then physical examination and electrophysiological examination are gradually verified, and the final result is correct.
Diagnosis and timely treatment.

Figure 3: Medical history prompts positioning 2.
Physical examination prompts positioning Through physical examination, we can find many physical signs, and different physical signs suggest lesions in different locations.

 For example, in patients with anterior horn cell disease, symptoms of atrophy are more severe than symptoms of weakness.

The patient has visually detectable fasciculation, obvious dysarthria, insignificant abnormal sensation, flail arm/flail leg, split/anti-split hand muscle atrophy.

Among them, split hands are more common in motor neuron disease, and anti-split hands are more common in Hirayama disease.

Figure 4: Physical examination prompts are located in the physical examination, and constantly discovering details can help us consolidate the basis for diagnosis and make a correct diagnosis.

Examples of some signs: Figure 5: Examples of some signs of neuromuscular diseases Figure 8).

Figure 7: Electromyography is the cornerstone of the diagnosis of muscle weakness.
Figure 8: Magnetic resonance is sometimes useful.
In the left A, the brachial plexus is obviously thickened.
In the figure B, the left lumbar plexus is obviously thickened.
In the figure C, the lumbar plexus and spinal plexus are visible.
Obviously atrophy, Figure D shows partial strengthening of the lumbar plexus.

The different MRI sequences on the right of the figure indicate different pathological and physiological conditions.

Qualitative diagnosis Remember the Midnights principle.
For the diagnosis of muscle weakness, whether it is peripheral nerve or muscle disease, there is actually a phenomenon-the coexistence of multiple diagnoses.

 What is "multiple diagnosis coexistence"? In more fashionable terms, it is a "mix and match".

That is, for a patient, our diagnosis is based on multiple dimensions.

l Clinical diagnosis (peroneal syndrome, congenital myopathy, etc.
) l Laboratory diagnosis (GQ1b antibody syndrome, etc.
) l Pathological diagnosis (rod myopathy, cytoplasmic myopathy, etc.
) l Molecular diagnosis, for example, one The patient has symptoms consistent with congenital myopathy.

But after muscle biopsy, rod-shaped myopathy was found at the pathological level, then the diagnosis transitioned to pathological diagnosis, which turned out to be rod-shaped myopathy.

However, after gene second-generation sequencing, a heterozygous mutation in the NEB gene was discovered, and the patient's diagnosis became rod-shaped disease type 2.
In this process, our diagnosis gradually deepened from appearance to substance.

Figure 9: Summary of examples of multi-diagnosis coexistence Diagnosis ideas: start with any clue→preliminary induction and check the seat→establish the diagnosis hypothesis→deduct the necessary clues according to the hypothetical diagnosis→correspond to the performance of the real patient, and perform multiple induction→verify the diagnosis Figure 10: Diagnosis flow chart.
In summary, to improve diagnostic capabilities, we must expand our knowledge boundaries and understand the connections between clues in different dimensions and the underlying pathology and physiology.

 In the course of Professor Zhao Chongbo, there are more detailed explanations of the classification of disease types and more details on positioning and qualitative diagnosis, as well as practical operations on 9 cases.
The space is limited, so I will not write more here.
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